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Clinical Cases in Anesthesia
Clinical Cases in Anesthesia
Allan P. Reed, MD
Professor
Department of Anesthesiology
Icahn School of Medicine at Mount Sinai
New York, New York
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Clinical cases in anesthesia / [edited by] Allan P. Reed, Francine S. Yudkowitz. -- Fourth edition.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4557-0412-5 (hardcover : alk. paper)
I. Reed, Allan P., editor of compilation. II. Yudkowitz, Francine S., editor of compilation.
[DNLM: 1. Anesthesia--Case Reports. 2. Anesthesiology--Case Reports. WO 200]
RD82.3
617.9'6--dc23
2013035684
vii
viii Contributors
Why a fourth edition? Clinical Cases in Anesthesia, fourth edition, differs from
Previous editions of Clinical Cases in Anesthesia stand conventional anesthesia textbooks. It is not intended to
out as some of the most widely available anesthesia texts replace journals or tomes. Instead, this book offers select
worldwide. The first edition was initially conceived as topics that are most likely to present in the course of cur-
a study guide for the oral board examination. Dating rent practice. Many cases are repeated from previous edi-
back to 1989, its succinct descriptions of relevant basic tions, and many are new. Although some classic questions
sciences and clinical applications of those sciences in anesthesia care remain the same over decades, ap-
garnered praise among board candidates. As its reputa- proaches change based on emerging information. The
tion grew, the book was used by residents, fellows, and new version updates these areas invoking information
practicing anesthesiologists throughout the United contained in the American Society of Anesthesiologists
States. Clinical Cases in Anesthesia soon became popular guidelines and practice parameters. The entire section on
in other English-speaking countries and nations where Intensive Care Medicine is offered in response to readers’
medical education was conducted in English. This suc- requests. Some cases have been eliminated for lack of
cess was expanded by translation into Russian. Editions relevance to modern anesthetic encounters. Use of central
2 and 3 were created as updates. They were equally well venous catheters and pulmonary artery catheters has been
received, culminating in a Chinese translation of the de-emphasized to comport with current trends.
third edition. English, Russian, and Chinese versions of While expanding the text, we have attempted to main-
Clinical Cases in Anesthesia reach anesthesia practitioners tain its relevance to oral examination board review and
on most of the planet. contemporary anesthesia practice. The practice of anesthe-
Recently, readers have asked for an updated and sia is complex and relies on in-depth knowledge across
expanded version of the book they have relied on for so multiple medical specialties. It is our hope that this new
many years. Clinical Cases in Anesthesia, fourth edition, edition will further fulfill the goals of the original book, as
answers that request. New medical sciences, techniques, well as convey the importance of basic anatomy, physiol-
and concepts require a fresh look at modern anesthesia ogy, and pharmacology to safe and quality patient care.
practice. Our goal is to enhance understanding of basic The editors are grateful to our authors, who are dedi-
and clinical sciences with brief, focused, and clear expla- cated practitioners and teachers. Without their contribu-
nations. Tables and boxes do more than just summarize tions, this book would not be possible.
important information. They allow for quick, easy refer-
ences that can be reviewed and provide crucial facts for Allan P. Reed, MD
immediate patient care. Francine S. Yudkowitz, MD, FAAP
xiii
S EC TION 1
CARDIOVASCULAR
SYSTEM
1
CASE 1
QUESTIONS
1. What are the determinants of myocardial oxygen 4. Describe the considerations for performing
supply? surgery on patients with drug-eluting coronary
2. Explain the determinants of myocardial oxygen stents.
consumption (demand). 5. Is perioperative !-adrenergic blockade indicated
3. What are the pharmacologic alternatives for this patient?
for treating myocardial ischemia in this 6. How should this patient be monitored
patient? intraoperatively?
A 65-year-old man with hypertension, familial hypercho- diastolic interval. The left coronary artery is perfused dur-
lesterolemia, type 2 diabetes mellitus, and angina pectoris ing diastole. The right coronary artery is perfused during
presented for resection of a sigmoid colon tumor. Stress both diastole and systole. It is important to prevent short-
imaging demonstrated an anteroseptal region of ischemia. ening of the diastolic interval by preventing increases in
Coronary angiography showed a critical lesion of the left heart rate. Coronary perfusion pressure is maintained by
anterior descending coronary artery and a 50% stenosis of ensuring normal to high diastolic arterial pressure and nor-
the proximal circumflex coronary artery. Percutaneous mal to low left ventricular end-diastolic pressure (LVEDP).
transluminal coronary angioplasty with drug-eluting stent
(DES) implantation was performed successfully on the 2. Explain the determinants of myocardial oxygen
left anterior descending lesion 6 weeks before surgery. consumption (demand).
The patient was maintained on metoprolol, aspirin, and
clopidogrel therapy. Clopidogrel was discontinued 7 days Heart rate, myocardial contractility, and myocardial wall
before surgery. tension are the three major determinants of myocardial
General anesthesia was induced with etomidate, mid- oxygen consumption. Heart rate is probably the most im-
azolam, and fentanyl. Maintenance anesthesia consisted portant parameter regulating myocardial oxygen supply-
of oxygen, sevoflurane, and fentanyl. Muscle relaxation demand balance. Decreasing heart rate increases oxygen
was provided with vecuronium. During tumor mobiliza- supply by prolonging diastole (allowing for more subendo-
tion, the heart rate increased from 70 to 120 beats per cardial perfusion) and decreases oxygen demand. The as-
minute. Blood pressure remained stable at 130/70 mm sociation between tachycardia and myocardial ichemia is
Hg. On the V5 electrocardiogram (ECG) lead, 2 mm of well documented. Severe bradycardia should be avoided
horizontal ST-segment depression was noted, but no because it causes decreased diastolic arterial pressure and
abnormality was seen in lead II. An additional dose of increased LVEDP. !-Adrenergic blocking drugs are com-
fentanyl was associated with slowing of the heart rate to monly used to maintain mild bradycardia in patients
95 beats per minute but no change in the ST-segment with CAD.
depression in V5. Myocardial contractility refers to the ability of the heart
to generate force at a given preload. Myocardial contractil-
1. What are the determinants of myocardial oxygen ity is very difficult to measure and is poorly described by
cardiac output or even left ventricular ejection fraction.
supply?
Determination of loading conditions and measurement of
A major concern in the anesthetic management of patients velocity, force, and extent of muscle shortening facilitate
with coronary artery disease (CAD) is maintaining a favor- description of myocardial contractility. Decreased myo-
able balance between myocardial oxygen supply and de- cardial contractility is associated with decreased myocar-
mand (Figure 1-1). Myocardial oxygen supply is tenuous in dial oxygen demand, and decreasing myocardial contrac-
patients with CAD because blockages in coronary arteries tility may be beneficial in patients with CAD. Specifically,
by atherosclerotic plaques, thrombi, and emboli disrupt the agents that depress myocardial contractility but are not
flow of oxygen-rich blood to heart muscle distal to the potent vasodilators may be beneficial as long as coronary
obstruction. Coronary perfusion is preserved by maintain- perfusion pressure is maintained. Examples of such agents
ing both coronary perfusion pressure and length of the include midazolam and etomidate.
2
1 Coronary Artery Disease 3
Calcium-channel entry blockers are a less common The 2009 ACC/AHA focused update on perioperative
component of medical therapy for patients with CAD. ! blockade recommends the following:
Their role as intraoperative agents for the management • In patients undergoing surgery, !-adrenergic block-
of myocardial ischemia is less clear. There is some evi- ers should be continued for patients already receiv-
dence that preoperative calcium-channel entry blocker ing them.
therapy may increase the incidence of intraoperative • In patients who have CAD, have evidence of cardiac
myocardial ischemia. However, these agents may be car- ischemia, or are at high cardiac risk, !-adrenergic
dioprotective against reperfusion injury and significantly blockers should probably be initiated preoperatively
improve diastolic dysfunction. Short-acting calcium- and considered intraoperatively to titrate heart rate
channel blockers such as nicardipine may be useful in and blood pressure during vascular or intermediate-
controlling hypertension and reducing afterload during risk surgery.
myocardial ischemia. • !-Adrenergic blockers should not be given to patients
Phenylephrine, a “pure” "-adrenergic agonist, is the undergoing surgery who have an absolute contraindi-
agent of choice for treatment of hypotension in myocar- cation to receiving them.
dial ischemia because it increases diastolic pressure with • In patients undergoing noncardiac surgery, it is not
no change (or a slight decrease) in heart rate. Drugs advisable to give high doses of ! blockers to patients
with !-adrenergic effects, such as ephedrine, dobuta- not currently taking them.
mine, and dopamine, increase the heart rate, increase Continuation of preoperative !-adrenergic block-
myocardial contractility, and may have minimal to re- ade during the 48-hour perioperative period is a
ductive effects on diastolic arterial pressure. All of these current Surgical Care Improvement Program quality
!-adrenergic actions are undesirable during myocardial measure.
ischemia.
6. How should this patient be monitored
4. Describe the considerations for performing intraoperatively?
surgery on patients with drug-eluting coronary
The most important modality for monitoring this patient
stents.
intraoperatively is a multiple-lead ECG system. Of the
Current American College of Cardiology/American ECG changes of myocardial ischemia that are present
Heart Association (ACC/AHA) guidelines recommend on a standard 12-lead ECG, 89% can be detected by a
delaying elective surgery for 12 months after implanta- V5 precordial ECG lead alone. Since the late 1970s, the
tion of a DES. In patients who cannot wait that long recommendation has been to follow limb lead II and
for their surgery, such as patients undergoing cancer precordial lead V5 simultaneously for detection of intra-
operations, careful assessment of the risks and benefits operative myocardial ischemia. This combination reflects
of withdrawing thienopyridine therapy must be under- the distribution of both the right and the left coronary
taken. A cardiologist should be consulted to assess the arteries and should enable #90% of ischemic episodes to
degree of myocardium at risk, and the possibility of be detected.
continuing antiplatelet therapy through the periopera- Current operating room ECG systems are usually
tive period should be considered. Many surgeons agree capable of continuous ST-segment monitoring. Gener-
to operate with continued aspirin therapy, but few ally, this monitoring determines the relationship of the
agree to continue thienopyridine. Additionally, there is ST segment 60–80 msec after the J-point (junction
no current evidence that “bridging therapy” with low- between the QRS complex and the ST segment) to the
molecular-weight heparin or short-acting antiplatelet baseline (during the PQ interval). Ischemia may be
therapy is beneficial. Increased vigilance for acute peri- defined as #0.1 mV of horizontal or downsloping ST-
operative myocardial infarction is required for all pa- segment depression or #0.2 mV of ST-segment eleva-
tients undergoing surgery within the first 12 months tion. These systems are rendered less effective by left
(and possibly longer) after DES placement. ventricular hypertrophy and frequent electrocautery
and are not useful in left bundle-branch block or ven-
5. Is perioperative !-adrenergic blockade indicated tricular pacing.
Transesophageal echocardiography (TEE), if avail-
for this patient?
able, is an extremely sensitive method of detecting
!-Adrenergic blockers are part of routine care for pa- myocardial ischemia. TEE is performed by continu-
tients with unstable angina and recent myocardial infarc- ously imaging the transgastric short-axis view of the
tion. !-Adrenergic blocker therapy should be initiated left ventricle. The images represent distributions of the
within the first 24 hours for ST-segment elevation myo- three major coronary vessels. The attention of busy
cardial infarction in patients who do not have signs of practitioners is frequently diverted from continuous
heart failure, evidence of low cardiac output, increased TEE observation by other important tasks. Changes in
risk for cardiogenic shock, or other relative contraindica- regional wall motion are not specific for myocardial
tions (i.e., P–R interval #0.24 seconds, second-degree ischemia, even if they are highly sensitive. Additionally,
or third-degree heart block, asthma, or reactive airway equipment cost and need for specialized training limit
disease). the use of TEE.
1 Coronary Artery Disease 5
QUESTIONS
1. How do you evaluate cardiac risk in a patient 5. Which intraoperative monitors would you use?
scheduled for noncardiac surgery? 6. What additional drugs would you have prepared?
2. How is cardiac status evaluated before elective 7. What anesthetic technique would you use?
noncardiac surgery? 8. How would you manage this patient postoperatively?
3. What is the cardiac risk in this patient, and what
additional investigations should be performed?
4. What are the implications for anesthetic manage-
ment when coronary revascularization is performed
before noncardiac surgery?
A 68-year-old woman with multiple cardiac risk factors information about the balance of myocardial oxygen con-
experienced sudden onset of crushing substernal chest sumption and delivery. Additionally, the presence of left-
pain. Despite aggressive thrombolytic therapy, the patient sided or right-sided failure (jugular venous distention,
had electrocardiogram (ECG) evidence of a transmural peripheral edema, pulmonary edema, or S3) and the pre-
anterolateral myocardial infarction (MI). She developed sence of murmurs should be assessed.
acute cholecystitis 3 weeks later and was scheduled for Routine laboratory tests, electrolytes, blood urea nitro-
cholecystectomy. gen, creatinine, and complete blood counts may have
some predictive value of cardiac risk. These tests may re-
veal the presence of anemia, hypokalemia from diuretic
1. How do you evaluate cardiac risk in a patient therapy, and increasing creatinine levels heralding renal
scheduled for noncardiac surgery? insufficiency. Also, specific cardiac drug levels such as di-
goxin should be considered. Point-of-care testing for the
Initial Approach
efficacy of medications such as clopidogrel and aspirin
Preoperative cardiac evaluation and assessment include may be useful as well. Chest radiograph aids in assessing
a review of the history, physical examination, and labora- heart size and shape. An ECG should be obtained; how-
tory results. Knowledge of the planned surgical proce- ever, a normal ECG may be present in 50% of patients
dure is also important. The history should assess the with CAD. The most common ECG findings in patients
following: with CAD are ST-T wave abnormalities (65%–90%),
• Severity and reversibility of coronary artery disease LV hypertrophy (10%–20%), and pathologic Q waves
(CAD) (e.g., risk factors, anginal patterns, history of MI) (0.5%–8%). ECGs are indicated for patients with at least
• Left ventricular (LV) and right ventricular function one clinical risk factor who are undergoing vascular surgi-
(e.g., exercise capacity, pulmonary edema, pulmo- cal procedures or for patients with known congestive
nary hypertension) heart failure (CHF), peripheral arterial disease, or cere-
• Presence of symptomatic arrhythmias (e.g., palpita- brovascular disease who are undergoing intermediate-risk
tions, syncopal or presyncopal episodes) surgical procedures. ECGs are not indicated for asymp-
• Coexisting valvular disease tomatic patients undergoing low-risk surgical procedures.
• Presence of a pacemaker or implantable cardio- Further evaluation depends on the results of the afore-
verter defibrillator mentioned preliminary investigations and the planned
Comorbidities that commonly occur in patients with surgical procedure.
CAD include peripheral vascular disease, cerebrovascular
disease, diabetes mellitus, renal insufficiency, and chronic Assigning Clinical Risk
pulmonary disease. A calculation of the patient’s meta-
bolic equivalents (METs) of tasks helps to determine The standard of care, as of this writing, is defined by the
cardiac risk (Figure 2-1). American College of Cardiology/American Heart Asso-
On physical examination, particular attention should ciation (ACC/AHA) 2007 Guidelines for Perioperative
be paid to the vital signs, specifically heart rate, blood Cardiovascular Evaluation and Care for Noncardiac
pressure, and pulse pressure. These parameters provide Surgery. The general paradigm is that patients are
6
2 Recent Myocardial Infarction 7
kph indicates kilometers per hour; MET, metabolic equivalent; and mph, miles per hour.
FIGURE 2-1 ■ Metabolic equivalent of tasks (METs). Modified from Fleisher LA, et al. ACC/AHA 2007 guidelines on perioperative cardiovascu-
lar evaluation and care for noncardiac surgery: A report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. J Am Coll of Cardiol 50: e159-e242, 2007. Based on Hlatky MA, et al. A brief self-administered questionnaire to determine
functional capacity (the Duke Activity Status Index). Am J Cardiol 64: 651–4, 1989; and Fletcher GF, et al. Exercise standards: statement for
healthcare professionals from the American Heart Association. Circulation 86: 340–4, 1992.
risk-stratified based on clinical risk factors (Box 2-1), TABLE 2-1 Risk Stratification for Surgical
surgical procedures (Table 2-1), and noninvasive testing. Procedures
In elective procedures, this algorithmic approach should
be used by internists, surgeons, and anesthesiologists as a Cardiac Risk Stratification Procedure Example
cardiovascular evaluation strategy.
In the past, numerous classification systems (e.g., High Aortic and other major
vascular surgery
Goldman, Detsky, and Eagle) were designed to predict the Peripheral vascular surgery
risk of cardiac morbidity. These classification systems did
not include patients with high-risk conditions that are Intermediate Intraperitoneal and
intrathoracic surgery
considered to be major predictors of perioperative cardiac Carotid endarterectomy
Head and neck surgery
Orthopedic surgery
Prostate surgery
BOX 2-1 Clinical Risk Factors Low Endoscopic procedures
Superficial procedures
MAJOR CLINICAL RISK FACTORS Cataract surgery
Breast surgery
• Unstable coronary syndromes Ambulatory surgery
• Unstable or severe angina
• Recent myocardial infarction
• Decompensated heart failure
• Significant arrhythmias
• Severe valvular disease
events (PCE). The ACC/AHA 2007 Guidelines reflect
INTERMEDIATE CLINICAL RISK FACTORS Lee’s Revised Cardiac Risk Index, which is the most com-
• History of ischemic heart disease monly used system today. Another commonly employed
• History of compensated or prior heart failure system is the National Surgical Quality Improvement
• History of cerebrovascular disease Program risk model. Both of these models assess patients
• Renal insufficiency with high-risk characteristics and are more applicable
today.
MINOR CLINICAL RISK FACTORS
Unstable angina is a major clinical predictor of PCE
• Advanced age (!70 years old) in the ACC/AHA Guidelines, whereas chronic stable
• Abnormal eletrocardiogram angina is an intermediate clinical predictor of PCE.
• Left ventricular hypertrophy
Fleisher and Barash (1992) suggested that patients should
• Left bundle-branch block
• ST-T abnormalities be classified in a more functional way. They contended
• Rhythm other than sinus rhythm that not all patients with stable angina have the same
• Uncontrolled systemic hypertension disease process (i.e., coronary anatomy, frequency of
ischemia, and LV function). The number of ischemic
8 SECTION 1 Cardiovascular System
episodes is especially difficult to quantitate without some arrhythmias with uncontrolled ventricular rate. Minor
sort of continuous monitoring (i.e., ambulatory ECG). predictors include abnormal ECG (i.e., LV hypertrophy,
This information is probably important because !75% left bundle-branch block, and ST-T wave abnormalities).
of ischemic episodes are silent, and !50% of patients Rhythm other than sinus (e.g., atrial fibrillation) is also a
with CAD (not just diabetics) have silent ischemia. It minor clinical predictor.
is unclear what the role of silent ischemia is in myocardial Patients with valvular heart disease are difficult to
injury, although it seems to portend a worse prognosis evaluate because the lesions cause changes that are inde-
if present in patients with unstable angina or patients pendently associated with increased risk (i.e., CHF,
after MI. rhythm changes). However, severe valvular disease is
The relationship between history of MI and PCE var- considered a major clinical predictor. If aortic stenosis is
ies significantly based on the age of the infarction. Recent symptomatic, the surgery generally should be postponed
infarctions are defined by cardiologists as infarctions or canceled for possible aortic valve replacement or other
within the last 7–30 days and are acknowledged as a ma- intervention before elective surgery. Patients with severe
jor clinical predictor of PCE. Prior MI by history or aortic stenosis undergoing noncardiac surgery have a
pathologic Q waves on ECG is an intermediate clinical mortality rate of approximately 10%.
predictor. Interpretation of history of MI and PCE is
complicated in anesthesia practice because anesthesiolo- Assigning Surgical Risk
gists traditionally refer to recent infarctions as occurring
within the preceding 6 weeks to 6 months. Classic “rein- In addition to patient characteristics, risk is determined
farction” studies from data collected 20–40 years ago by the surgical procedure (see Table 2-1). Higher risk
found that patients with an infarct within 3 months had surgeries include procedures with greater potential for
a 5.7%–30% incidence of reinfarction. Between 3 and hemodynamic cardiac stress. Such stressors could be
6 months, the risks range from 2.3%–15%, and an infarct alterations in heart rate, blood pressure, intravascular
!6 months before surgery is associated with a 1.9%–6% volume, clotting, oxygenation, neurohumoral activation,
incidence. The mortality rate of repeat MI was about blood loss, and pain.
50%, and this figure varies very little among the various It is generally agreed that patients with a “combined”
studies. The lower numbers in each group are from the risk of PCE (i.e., based on patient and surgical factors)
study of Rao et al. (1983), in which aggressive hemody- of !10% warrant further evaluation. Noncardiac surgi-
namic monitoring was used and patients recovered in the cal procedures associated with the highest PCE rate are
intensive care unit postoperatively. The problem with mostly vascular surgical procedures. Peripheral vascular
applying these data to modern care is that they precede and aortic surgeries have high PCE rates, whereas
the widespread use of " blockers, coronary interventions, carotid artery surgery has PCE rates of about 5%.
and enzyme-based diagnosis of infarctions. Nevertheless, Although the data are still emerging, it appears that
there is no doubt that more recent MIs represent a sig- endovascular repairs have low associated risk. The high
nificant risk factor for PCE. The severity of the infarc- PCE rate of vascular surgical procedures is usually
tion must also be considered. attributed to the high incidence of CAD in patients
Medical literature distinguishes mortality rates in undergoing vascular surgery (estimated to be 90%) and
Q wave versus non–Q wave MIs, infarctions involving to the stress imposed on the myocardium by hemody-
the right versus the left coronary artery distribution, un- namic changes.
complicated versus complicated infarctions (i.e., recurrent The metabolic changes induced by surgery, such as
pain, CHF, or arrhythmias), and negative versus positive increased levels of stress hormones and increases in plate-
post-MI exercise stress test results. It seems reasonable let adhesiveness, are also implicated as factors that in-
to assume that mortality rates from all recent MIs should crease PCE. Nonvascular surgical procedures associated
not be classified together based solely on the time since with higher morbidity and mortality include intratho-
the infarction. racic and intraabdominal surgeries. Presumably, the in-
CHF in the general population has a poor prognosis. creased risk is because of the greater hemodynamic
The 5-year survival rate is approximately 50%, although changes associated with large fluid shifts, compression of
this may be improving with modern afterload-reduction the great veins, and aberrations in cardiopulmonary
and antiarrhythmic therapies. The 1-year mortality rate is function during thoracic surgery. Emergency surgery is
approximately 30% in patients with LV ejection fractions also associated with increased risk. Procedures associated
#30%. The ACC/AHA guidelines include uncompen- with a lower risk of PCE include extremity surgery,
sated CHF as a major clinical predictor and compensated transurethral prostate resections, and cataract surgery.
or prior CHF as an intermediate clinical predictor. The risk of surgery must always be included in the esti-
Arrhythmias are a common problem, especially in mation of patient risk, and this is constantly changing
elderly patients. Arrhythmias are usually benign except in owing to the emergence of less invasive techniques that
patients with underlying heart disease, in whom they serve cause less physiologic disturbance.
as markers for increased morbidity and mortality. Many The assignment of “cardiac risk” to a particular patient
patients with LV dysfunction and arrhythmias die as a re- for a particular surgical procedure is difficult, but there
sult of LV failure and not an arrhythmia. Acknowledged are guidelines and an algorithm that should be followed
major clinical predictors include high-degree atrioven- (Figure 2-2). The need for further evaluation depends on
tricular block, symptomatic ventricular arrhythmias in the whether the information gained would change the planned
presence of underlying heart disease, and supraventricular surgical or anesthetic management. These changes in
2 Recent Myocardial Infarction 9
Perioperative surveillance
Need for emergency and postoperative risk
Step 1 Yes Operating room
noncardiac surgery? stratification and risk factor
management
No
No
Proceed with
Step 3 Low risk surgery Yes
planned surgery
No
Step 5 No or unknown
Intermediate Intermediate
Vascular surgery Vascular surgery
risk surgery risk surgery
Consider testing if it will Proceed with planned surgery with HR control Proceed with
change management or consider noninvasive testing planned surgery
if it will change management
FIGURE 2-2 ■ Algorithm for managing a patient with cardiac disease undergoing noncardiac surgery. ACC/AHA, American College of
Cardiology/American Heart Association; HR, heart rate; METs, metabolic equivalents. Modified from Fleisher LA, et al. ACC/AHA 2007
guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: A Report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines. J Am Coll of Cardiology 50: e159-e242, 2007.
* Refer to Box 2-2
† Refer to Figure 2-1
‡ Noninvasive testing may be considered before surgery in specific patients with risk factors if it will change management.
management might include altering the surgical proce- BOX 2-2 Active Cardiac Conditions
dure to one associated with lower risk, medical or surgical Requiring Noninvasive Testing
treatment of CAD, perioperative anticoagulation, or per-
haps more aggressive intraoperative and postoperative • Unstable coronary syndromes
monitoring. Although many of these strategies sound • Unstable angina
logical, there is relatively weak evidence of outcome • Recent myocardial infarction
improvements with interventions. • Decompensated heart failure
• Significant arrhythmias
• High-grade atrioventricular block
2. How is cardiac status evaluated before elective • Mobitz II atrioventricular block
noncardiac surgery? • Third-degree atrioventricular block
• Symptomatic ventricular arrhythmias
Based on the evaluation described in Question 1, further • Supraventricular arrhythmias (including atrial fibrilla-
investigation of the patient’s cardiac status before elective tion) with uncontrolled ventricular rate (heart rate !100
noncardiac surgery may be warranted. Indications for beats per minute at rest)
preoperative ECGs are discussed in Question 1. Patients • Symptomatic bradycardia
with active cardiac conditions (Box 2-2) should undergo • Newly recognized ventricular tachycardia
noninvasive stress testing, which includes exercise stress • Severe valvular disease
testing, dobutamine stress echocardiogram, and intrave- • Severe aortic stenosis
nous dipyridamole/adenosine myocardial perfusion • Mean pressure gradient !40 mm Hg
• Aortic valve area #1.0 cm2
imaging with both thallium 201 and technetium 99m. • Symptomatic
Myocardial revascularization by percutaneous coronary • Symptomatic mitral stenosis
angioplasty and stent placement or coronary artery bypass • Progressive dyspnea on exertion
grafting (CABG) before elective noncardiac surgery for • Exertional presyncope
PCE risk reduction is not recommended in patients with • Heart failure
stable CAD. However, coronary revascularization before
10 SECTION 1 Cardiovascular System
noncardiac surgery is useful in patients with the following assume the patient has significant CAD. If time permits,
conditions: transesophageal echocardiography (TEE), specifically as-
• Stable angina with left main coronary artery sessing wall motion, LV ejection fraction, and mitral
stenosis valve function, provides useful information.
• Stable angina with three-vessel disease See Question 2 for indications for myocardial revascu-
• Stable angina with two-vessel disease and significant larization prior to elective noncardiac surgery for PCE
proximal left anterior descending artery stenosis and risk reduction.
either ejection fraction #50% or ischemia on non-
invasive testing 4. What are the implications for anesthetic
• High-risk unstable angina or non–ST-segment ele- management when coronary revascularization
vation MI is performed before noncardiac surgery?
• Acute ST-segment elevation MI
Elective noncardiac surgery is not recommended Increasingly, patients who have received a percutane-
within 4–6 weeks of placement of a bare metal coronary ous coronary artery intervention (PCI) are scheduled
stent (BMS) or within 12 months of placement of a drug- for elective noncardiac surgery. The type of intervention—
eluting coronary stent (DES) in patients in whom discon- balloon angioplasty, BMS, or DES—determines how
tinuing thienopyridine or aspirin/thienopyridine therapy long the patient must remain on antiplatelet therapy
is required. Elective noncardiac surgery is also not rec- and when elective surgery should be performed. The
ommended within 4 weeks of coronary artery balloon 2007 ACC/AHA guidelines do not specify a timing
angioplasty. recommendation for noncardiac surgery after CABG,
but they present data in which patients received vascu-
3. What is the cardiac risk in this patient, and what lar surgery a median of 29 days (Dutch Echocardio-
graphic Cardiac Risk Evaluation Applying Stress Echo-
additional investigations should be performed?
V [DECREASE-V] study) and 48 days (Coronary
This patient is an elderly woman with known CAD and a Artery Revascularization Prophylaxis [CARP] study)
recent MI who is undergoing emergency surgery. Several after CABG. The 2004 and 2011 Guidelines for Coro-
important factors require consideration. The first of nary Artery Bypass Graft Surgery do not recommend a
these is the patient’s course after MI. If she has recurrent specific time to wait after CABG. It seems reasonable
pain, CHF, or late ventricular arrhythmias (!48 hours to wait 4–6 weeks after CABG before performing non-
after MI) she has a 15%–30% risk of death or reinfarc- cardiac surgery, if possible; the decision to proceed
tion in the first year after MI even without surgery. should be directed by the same algorithm presented in
Another issue is whether there was evidence of reper- the 2007 ACC/AHA guidelines.
fusion after thrombolytic therapy. Evidence of reperfu- The 2007 ACC/AHA guidelines regarding type of
sion includes pain relief, reperfusion arrhythmias, large stent placement, antiplatelet therapy, and timing of
increases in creatine phosphokinase enzyme levels, and elective surgery are summarized in Table 2-2. Briefly,
an improvement in the ECG without evidence of MI. dual antiplatelet therapy is recommended for 1 month
Anticoagulant therapy is important. Heparin therapy for patients with a BMS and for 1 year for patients
used for patients with recurrent chest pain would need with a DES. Thereafter, aspirin should be continued
to be stopped before surgery. More recent studies suggest indefinitely. Prolongation of dual antiplatelet therapy in
that the timing may be very important. Patients in patients with a DES should be considered in the follow-
whom heparin was stopped for !9.5 hours were more ing circumstances:
likely to develop recurrent ischemia requiring urgent • Previous stent thrombosis
intervention. • Left main stent placement
Most patients who have received thrombolytic therapy • Multivessel stent placement
have significant residual stenosis in vessels that have been • Stent placed in the only remaining coronary artery
reperfused, and they often undergo early cardiac cathe- or graft
terization, especially if they had a complicated infarction. Elective surgery should be postponed until after dual
Some centers treat patients who are doing well the same antiplatelet therapy is no longer warranted (i.e., 1 month
as any patient with a recent uncomplicated MI—a modi- for patients with BMS, 1 year for patients with DES).
fied symptom-limited stress test is performed before Aspirin should be continued into the perioperative pe-
discharge (on post-MI days 5–7), and a symptom-limited riod, unless the benefit of decreasing surgical bleeding
stress test is performed 6 weeks later. outweighs the risk of stent thrombosis.
The presence of sepsis is an important consideration. In the case of emergent or urgent surgery, dual anti-
Hemodynamic changes associated with sepsis may in- platelet therapy should be continued into the periopera-
crease demands on the myocardium, including increased tive period if possible. If continuing dual antiplatelet
cardiac output because of endotoxin-induced vasodila- therapy is impossible, aspirin should be continued, and
tion and myocardial depression from myocardial depres- the thienopyridine should be restarted as soon as possible
sant factor. Also, hypotension from septic shock may to avoid a PCE.
decrease coronary artery perfusion pressure leading to A difficult situation arises when patients require PCI
myocardial ischemia. before urgent surgery. The type of PCI is determined by
If the patient must have an urgent surgical procedure when the surgery needs to be performed (i.e., 2 weeks vs.
and no additional cardiac studies have been performed 1 month) and whether antiplatelet therapy can continue
(e.g., stress test or coronary angiogram), one should into the perioperative period. If dual antiplatelet therapy
2 Recent Myocardial Infarction 11
BMS, Bare metal stent; DES, drug-eluting stent; OR, operating room.
*Aspirin should be continued throughout the perioperative period. If stopping aspirin is considered,
the risk of stent thrombosis should be weighed against the risk of surgical bleeding.
†
If patient is still on thienopyridine, it should be continued as soon as possible after surgery.
is contraindicated for the planned surgical procedure and compared with the “gold standard” (myocardial lactate
it must be performed within the next month, balloon extraction). ST-segment depressions and T-wave mor-
angioplasty would be indicated. If the surgery can be phology changes are most commonly seen. However, in
delayed for 1 month, a BMS can be placed. In this situa- some patients, the ECG is not an effective intraoperative
tion, a DES would not be indicated, especially if dual monitor of myocardial ischemia, including patients with
antiplatelet therapy needs to be discontinued. Each situ- LV hypertrophy, conduction abnormalities, and ventricu-
ation involves weighing the risk of bleeding during sur- lar pacemaker dependence. Computerized ST-segment
gery and urgency of the surgery versus the possibility of continuous analysis can be useful to monitor patients
a catastrophic cardiac event. with known CAD or patients undergoing vascular sur-
gery to detect myocardial ischemia.
The use of PACs may be reasonable in patients at risk
5. Which intraoperative monitors would you use?
for major hemodynamic disturbances that are easily
A general goal is to maintain intraoperative hemodynam- detected with PACs. Routine use is not recommended
ics within 20% of preoperative values. In addition to the and can cause harm. Although PACs may be useful in
standard intraoperative monitors, other monitors that selected groups of patients, there are no recent conclu-
should be considered include invasive continuous intraar- sive data showing benefit over risk. Potential complica-
terial catheters, pulmonary artery catheters (PACs), and tions include vessel or cardiac perforation, arrhythmia,
TEEs. An intraarterial catheter allows for beat-to-beat pulmonary embolism, and incorrect management based
blood pressure monitoring. Although 40% of intraopera- on data misinterpretation. The development of V waves
tive ischemic episodes are not related to aberrations in on the pulmonary artery wedge pressure waveform may
hemodynamics, some studies demonstrate that inadequate be an indication of myocardial ischemia, but it is neither
management of hemodynamic abnormalities may increase sensitive nor specific enough to be regarded as a reliable
risk. Hypotension (blood pressure #30% baseline for monitor for this purpose (Figure 2-3). However, the
!10 minutes) was shown to be a strong predictor of PCE usefulness of the PAC extends beyond its questionable
in one study. There are no studies showing conclusively ability to detect ischemia. The PAC provides informa-
that hypertension is associated with adverse outcome. tion about the patient’s intravascular volume status;
An intraarterial catheter also offers the ability to per- provides a quantitative estimate of myocardial compli-
form laboratory testing throughout the intraoperative ance; and allows for calculation of cardiac output and
period; this would facilitate optimizing metabolic and other hemodynamic measurements, such as systemic
respiratory derangements. Glucose management is im- vascular resistance and stroke volume.
portant because hyperglycemia is an independent predic- TEE is the most sensitive detector of intraoperative
tor of cardiovascular risk and is directly related to mortal- ischemia by demonstrating regional wall motion abnor-
ity during MI. Finally, point-of-care testing is necessary malities and is capable of detecting ischemia earlier than
for rapid determination of anticoagulation levels and any other modality. Use of TEE requires specialized skills
adequate reversal. and training as defined by the American Society of Echo-
Tachycardia has not been definitively shown to be asso- cardiography. Although its usefulness in detecting is-
ciated with PCE, although studies suggest a relationship. chemia is well established, it is unclear what TEE changes
Also, hypothermia may increase myocardial oxygen de- are predictive of PCE. Several older studies did not find
mand and has been shown to be an independent predictor LV wall motion abnormalities were predictive of cardiac
of morbid cardiac events. Temperature should be moni- morbidity. Also, regional wall motion abnormalities
tored, and normothermia should be maintained. during ischemia sometimes do not resolve when ischemia
An effective tool for monitoring myocardial ischemia has dissipated. Finally, TEE provides additional physio-
in anesthetized patients is a multiple-lead ECG. Moni- logic information, such as estimates of LV ejection frac-
toring precordial chest leads V4 and V5 detects !90% of tion and intravascular volume status, which may help with
ischemic events that would be seen on a 12-lead ECG, intraoperative management in patients with ventricular
although it has been reported to have only 9% sensitivity dysfunction.
12 SECTION 1 Cardiovascular System
SUGGESTED READINGS
Cohen MM, Duncan PG, Tate RB: Does anesthesia contribute to op-
erative mortality? JAMA 260:2859, 1988.
FIGURE 2-3 ■ Relationship between the ECG, pulmonary artery Fleisher LA, Barash PG: Preoperative cardiac evaluation for noncardiac
(PA) waveform, and pulmonary capillary wedge pressure surgery: a functional approach. Anesth Analg 74:586, 1992.
(PCWP) waveform is illustrated in normal circumstances and in Fleisher LA, Beckman JA, Brown KA, et al.; American College of Cardi-
the presence of V waves. There is widening of the PA waveform ology; American Heart Association Task Force on Practice Guidelines
and loss of the dicrotic notch in the presence of V waves. The (Writing Committee to Revise the 2002 Guidelines on Perioperative
peak of the V wave occurs about the same time as the T wave Cardiovascular Evaluation for Noncardiac Surgery); American Society
on the ECG. of Echocardiography; American Society of Nuclear Cardiology; Heart
Rhythm Society; Society of Cardiovascular Anesthesiologists; Society
for Cardiovascular Angiography and Interventions; Society for Vascu-
lar Medicine and Biology; Society for Vascular Surgery: ACC/AHA
2007 guidelines on perioperative cardiovascular evaluation and care
for noncardiac surgery: a report of the American College of Cardiol-
ogy/American Heart Association Task Force on Practice Guidelines
6. What additional drugs would you have prepared? (Writing Committee to Revise the 2002 Guidelines on Perioperative
Intravenous nitroglycerin, esmolol, and vasopressors should Cardiovascular Evaluation for Noncardiac Surgery) developed in col-
laboration with the American Society of Echocardiography, American
be immediately available to treat ischemia and hemody- Society of Nuclear Cardiology, Heart Rhythm Society, Society of
namic aberrations. Phenylephrine is particularly useful in Cardiovascular Anesthesiologists, Society for Cardiovascular Angiog-
restoring myocardial blood flow in hypotensive patients raphy and Interventions, Society for Vascular Medicine and Biology,
without causing major increases in myocardial oxygen and Society for Vascular Surgery. J Am Coll Cardiol 50:e159, 2007.
Fletcher GF, Balady G, Froelicher VF, et al.: Exercise standards: a
consumption owing to tachycardia. " Adrenergic blockers statement for healthcare professionals from the American Heart
should be managed as per the 2009 ACC/AHA guidelines Association. Circulation 91:580, 1995.
on perioperative " adrenergic blocker management (see Goldman L, Caldera DL, Nussbaum SR, et al.: Multifactorial index of
Chapter 1 for further elaboration). cardiac risk in noncardiac surgical procedures. N Engl J Med
297:845, 1978.
Hillis LD, Smith PK, Anderson JL, et al.: 2011 ACCF/AHA Guideline
7. What anesthetic technique would you use? for Coronary Artery Bypass Graft Surgery: executive summary: a
report of the American College of Cardiology Foundation/American
Anesthetic technique has not been shown to be a predic- Heart Association Task Force on Practice Guidelines. Circulation
tor of PCE. There are several trials involving different 124:2610, 2011
Hlatky MA, Boineau RE, Higginbotham MB, et al.: A brief self-
subsets of patients, including patients who underwent administered questionnaire to determine functional capacity
vascular or abdominal surgery that showed no difference (the Duke Activity Status Index). Am J Cardiol 64:651, 1989.
in outcome between patients who received epidural ver- Lee TH, Marcantonio RE, Mangione CM, et al.: Derivation and pro-
sus general anesthesia. A trial by Cohen et al. in 1988 spective validation of a simple index for prediction of cardiac risk of
showed a possible increase in 30-day mortality in patients major noncardiac surgery. Circulation 100:1043, 1999.
Mangano DT: Perioperative cardiac morbidity. Anesthesiology 72:153,
who received monitored anesthesia care; however, this 1990.
may have been the result of selection bias. The anesthetic Mangano DT, Goldman L: Preoperative assessment of patients with
technique used should be based on patient assessment, known or suspected coronary disease. N Engl J Med 333:1750, 1995.
maintenance of stable intraoperative hemodynamics, and Park KW, Lee J, Breen P, et al.: The risk of perioperative cardiac com-
plications is high in major vascular surgery performed within a month
adequate postoperative analgesia. Tachycardia should be of coronary artery bypass graft surgery. Anesth Analg 94:S63, 2002.
avoided in patients with CAD. Agents such as ketamine Rao TL, Jacobs KH, El-Etr AA: Reinfarction following anesthesia in
and pancuronium are probably best avoided. patients with myocardial infarction. Anesthesiology 59: 499, 1983.
CASE 3
QUESTIONS
1. Name possible etiologies for dilated 3. Which monitors would you use for this patient in
cardiomyopathy. the perioperative period?
2. Explain the pathophysiology of dilated 4. How would you anesthetize this patient?
cardiomyopathy.
A 55-year-old man with dilated cardiomyopathy (DCM) pulsus alternans (i.e., regular alternation of pressure
presented for open reduction and internal fixation of a pulse amplitude with a regular rhythm), and pulmonary
tibial fracture. He had been in a motor vehicle accident. edema. Complete recovery from infectious myocarditis
Past medical history included alcohol abuse, orthopnea, is usually the case, but there are exceptions, such as myo-
dyspnea on exertion, and several episodes of pulmonary carditis associated with diphtheria or Chagas disease.
edema. The patient’s medications included digoxin, furose- Diphtheria can produce either right or left bundle-branch
mide, and captopril. Physical examination revealed bibasi- block. The combination of diphtheria and bundle-branch
lar rales and S3 gallop. A gated blood pool scan showed a block has a mortality rate of approximately 50%. If com-
left ventricular ejection fraction of 15%. Cardiac catheter- plete heart block ensues, the mortality rate is 80%–100%.
ization indicated a left ventricular end-diastolic pressure Chagas disease can lead to right bundle-branch block
of 25 mm Hg, a cardiac index of 1.8 L/min/m2, 2! mitral and other arrhythmias in 80% of patients. Viral infec-
regurgitation, and no coronary artery disease. tions, mycotic infections, and helminthic myocardial
involvement have varying clinical profiles that include
1. Name possible etiologies for dilated arrhythmias, CHF, pericarditis, or valvular or vessel
obstruction. The noninflammatory variety of DCM also
cardiomyopathy.
manifests with the clinical picture of myocardial failure
DCM can be genetically derived or acquired and can but in this case secondary to toxic, degenerative, or infil-
exist in both inflammatory and noninflammatory forms. trative processes in the myocardium. In some cases, the
The genetic form comprises 20%–35% of DCM and exact etiology is unknown (idiopathic DCM).
is usually inherited in an autosomal dominant pattern, Alcoholic cardiomyopathy is a typical hypokinetic,
although there are also X-linked recessive and mitochon- noninflammatory cardiomyopathy associated with
drial patterns of inheritance. DCM is a common cause of tachycardia and premature ventricular contractions that
heart failure with a prevalence of 36 per 100,000 people. progresses to left ventricular failure with incompetent
DCM is characterized by ventricular chamber enlarge- mitral and tricuspid valves. This cardiomyopathy is
ment and systolic dysfunction with normal left ventricular probably due to direct toxic effects of ethanol or its
wall thickness. metabolite, acetaldehyde, which releases and depletes
The inflammatory variety, or myocarditis, is usually cardiac norepinephrine. In chronic alcoholics, acute
the result of infection or parasitic infestation. Myocardi- ingestion of ethanol produces decreases in contractility,
tis manifests with a clinical picture of fatigue, dyspnea, elevations in ventricular end-diastolic pressure, and
and palpitations that usually occur in the first weeks increases in systemic vascular resistance. Alcoholic car-
of infection. Palpitations progress to overt congestive diomyopathy is classified into three hemodynamic
heart failure (CHF) with cardiac dilation, tachycardia, stages (Table 3-1).
13
14 SECTION 1 Cardiovascular System
3. Which monitors would you use for this patient 4. How would you anesthetize this patient?
in the perioperative period?
Avoidance of myocardial depression is the goal of
Electrocardiogram (ECG) monitoring is essential in the anesthetic management (Table 3-2) for patients with
management of patients with DCM, particularly pa- DCM. All the potent volatile anesthetic agents are
tients with myocarditis. Ventricular arrhythmias are myocardial depressants. For this reason, these agents,
common, and the development of complete heart block especially in high concentrations, are probably best
requires rapid diagnosis and pacing. The ECG is also avoided in patients with DCM. An opioid and sedative-
useful for monitoring ischemic changes when CAD is hypnotic anesthetic can be employed instead. Etomi-
associated with cardiomyopathy, as in amyloidosis. Inva- date and ketamine are acceptable anesthetic induction
sive continuous intraarterial blood pressure monitoring agents, whereas thiopental and propofol are relatively
during surgery provides continuous blood pressure in- contraindicated.
formation and a convenient route for obtaining arterial For a patient with a severely compromised myocardium,
blood gases. the synthetic piperidine opioids (e.g., fentanyl, sufentanil,
Aortic Stenosis
Amanda J. Rhee, MD • Alexander J. C. Mittnacht, MD • David L. Reich, MD
QUESTIONS
1. Describe the symptoms of and long-term prognosis 6. How is hypotension best treated in a patient with
for aortic stenosis. aortic stenosis?
2. Identify the etiology of aortic stenosis. 7. How would you anesthetize this patient for cardiac
3. What is the significance of aortic valve area and or noncardiac surgery?
how is it calculated? 8. What are anesthetic considerations for transcatheter
4. Why is it important to maintain sinus rhythm? aortic valve implantation?
5. What is the treatment for supraventricular
tachyarrhythmias or bradyarrhythmias?
A 65-year-old woman presented for aortic valve replace- radius (R), and wall thickness (h) is described by the law
ment. She had a history of congestive heart failure of Laplace: T ! (P " R)/2h.
(CHF). Cardiac catheterization showed a peak systolic Tension generation in myocytes is the most inefficient
gradient of 90 mm Hg between the left ventricle and the way of performing cardiac work because it requires large
aorta. During anesthetic induction with fentanyl and ve- amounts of oxygen. In patients with left ventricular hyper-
curonium, the patient developed a junctional rhythm and trophy, oxygen delivery is decreased because left ventricu-
severe hypotension. lar end-diastolic pressure (LVEDP) is increased. Increased
LVEDP decreases coronary perfusion pressure (CPP).
1. Describe the symptoms of and long-term prognosis CPP is defined as diastolic aortic pressure minus LVEDP.
As the severity of AS increases, a decrease in diastolic
for aortic stenosis.
aortic pressure compromises CPP even more. The hy-
The classic symptoms in patients with severe aortic ste- pertrophied myocardium also results in decreased left
nosis (AS) are angina, syncope, and CHF. Life expectancy ventricular compliance and higher left ventricular filling
in untreated cases is approximately 5 years after develop- pressures, which leads to diastolic dysfunction and im-
ing angina, 3 years after developing syncope, and 2 years paired cardiac filling. Neovascularization of the pressure-
after developing CHF. Angina is present in approxi- overloaded heart is inadequate for the degree of hyper-
mately 66% of patients with critical AS, but only about trophy. Finally, the isovolumic phase of relaxation is
50% have clinically significant coronary artery disease inappropriately long, shortening the filling period of
(CAD). Patients without CAD develop angina because of diastole, which diminishes the time for coronary perfu-
inadequate oxygen delivery to hypertrophied myocar- sion. For all these reasons, patients with AS are prone to
dium. There is also evidence that patients with moderate developing myocardial ischemia during anesthesia.
to critical AS (i.e., aortic valve area 0.7-1.5 cm2) are at Syncope is the initial symptom of AS in 15%–30% of
increased risk for morbidity, which worsens with the on- patients. It is usually exertional and is caused by exercise-
set of symptoms. Some clinicians recommend that aortic induced vasodilation in the face of a fixed cardiac output.
valve replacement should be performed promptly in CHF portends the worst long-term prognosis. CHF occurs
symptomatic patients. However, percutaneous interven- when the heart has exceeded its capacity to compensate for
tions, such as balloon valvuloplasty and percutaneous pressure work with myocardial hypertrophy. The heart
transcatheter aortic valve implantation (TAVI), may be progressively dilates, and symptoms of left ventricular fail-
indicated depending on the clinical situation. ure appear.
Concentric left ventricular hypertrophy occurs in AS,
as defined by increasing left ventricular wall thickness in 2. Identify the etiology of aortic stenosis.
a symmetric fashion without ventricular dilation. The
advantage of a hypertrophied myocardium is the greater AS may be congenital or acquired. In adults, a congeni-
intraventricular pressure generated with a smaller in- tally bicuspid valve may become calcified and stenotic.
crease in wall tension. The relationship between wall Senile calcification of a trileaflet aortic valve is common
tension (T), intracavitary pressure (P), left ventricular in patients #70 years old. Rheumatic AS is almost always
17
18 SECTION 1 Cardiovascular System
associated with rheumatic mitral valve disease. This eti- prolonged isovolumic relaxation phase and decreased early
ology is becoming less common in developed countries ventricular filling, which leads to increased dependence on
because of the widespread use of antibiotic therapy. the atrial kick. The onset of nonsinus rhythm is often as-
sociated with marked hypotension because stroke volume
3. What is the significance of aortic valve area and is decreased from loss of the atrial kick. It is difficult for
patients with AS to compensate for the loss of sinus
how is it calculated?
rhythm because marked increases in left atrial pressure
The normal aortic valve area is 2.5-3.5 cm2. According would be required to maintain an adequate stroke volume.
to the American College of Cardiology/American Heart
Association (ACC/AHA) guidelines, valve area $1.0 cm2, 5. What is the treatment for supraventricular
peak transvalvular velocity #4.0 m/sec, and mean transval-
tachyarrhythmias or bradyarrhythmias?
vular gradient #40 mm Hg are considered to be parame-
ters of hemodynamically severe AS (Table 4-1). Treatment of arrhythmias in patients with AS must be
In cardiac catheterization laboratories, aortic valve accomplished rapidly to prevent hemodynamic decom-
areas are calculated using the modified Gorlin equation, pensation. Cardioversion should be considered as the
which in its simplified form states that the valve area is first-line therapy in unstable patients with supraventricu-
proportional to the flow across the valve divided by the lar tachyarrhythmias. In stable patients, a therapeutic
square root of the mean pressure gradient. A variation of diagnostic maneuver (e.g., vagal stimulation, adenosine)
this formula is the Hakki equation: Valve area ! cardiac should be attempted.
output/√peak pressure gradient. When the exact underlying rhythm is identified, treat-
Using echocardiography, the aortic valve area can be ment usually consists of %-adrenergic blockers (e.g., esmo-
calculated using the continuity equation, which is based lol), amiodarone, or cardioversion, depending on the rhythm.
on the principle that the stroke volume is equal in the left Amiodarone is the preferred drug in patients with impaired
ventricular outflow tract (LVOT) and the aortic valve: cardiac function (ejection fraction $40%, CHF) or when
ventricular tachycardia cannot be ruled out. Volume loading
Velocity-time-integral(LVOT) " area(LVOT) ! may be beneficial to treat rhythms without an atrial kick,
velocity-time-integral(aortic valve) " area(aortic valve) such as atrial fibrillation and junctional tachycardia.
Transvalvular peak-to-peak gradients are calculated Bradyarrhythmias should be treated with anticholiner-
using the modified Bernoulli equation: gics, combined &-adrenergic and %-adrenergic agonists, or
atrioventricular sequential pacing. The ideal heart rate
Transvalvular gradient ! 4 " (maximum velocity)2 is probably 70–80 beats per minute. This rate allows for
Transvalvular gradients underestimate the degree of adequate diastolic filling, while providing sufficient cardiac
AS in low cardiac output states because of diminished output in a heart with a relatively fixed stroke volume.
flow across the valve. Despite flow dependence, a mean
pressure gradient #40 mm Hg or a peak pressure gradi- 6. How is hypotension best treated in a patient with
ent #80 mm Hg implies severe AS. In the near future,
aortic stenosis?
new techniques that employ postprocessing of three-
dimensional echocardiographic data may result in im- Patients with severe AS do not tolerate hypotension.
proved accuracy compared with current two-dimensional Even brief episodes of hypotension may lead to hemody-
imaging and Doppler interrogation. namic decompensation. Based on optimization of pre-
load, afterload, heart rate, and contractility (Table 4-2),
the priorities of treatment to restore cardiac output
4. Why is it important to maintain sinus rhythm?
should include the following:
Atrial systole normally contributes approximately 15%– • Preservation of blood pressure using vasoconstrictors
20% of the total stroke volume; in AS, this increases to to increase afterload
40%–50%. The atrial “kick” is crucial in preserving left • Restoration of sinus rhythm
ventricular filling (and stroke volume) in AS because pas- • Intravenous fluids to maintain preload
sive filling is decreased owing to the noncompliant left • Maintenance of heart rate in the normal range
ventricle. This diastolic dysfunction is characterized by a • Maintenance of myocardial contractility
If the etiology of hypotension is not immediately obvi-
ous, empiric treatment with an &-adrenergic receptor ago-
nist (e.g., phenylephrine) should be attempted to preserve
TABLE 4-1 Aortic Valve Area CPP and avoid the vicious cycle of irreversible ischemia.
Category Valve Area (cm2)
Generally, pure &-adrenergic receptor agonists are the
preferred vasoconstrictor agents because they do not cause
Normal 2.5–3.5 tachycardia, which preserves diastolic filling time.
Mild stenosis 1.5–2.5
Moderate stenosis 1.0–1.5 7. How would you anesthetize this patient for
Severe stenosis 0.7–1.0
cardiac or noncardiac surgery?
Critical stenosis $0.7 Premedication in patients with AS should be adminis-
tered carefully. Oversedation may lead to hypotension
4 Aortic Stenosis 19
and decreased CPP, whereas undersedation may result in Anesthesia can be maintained with many different
anxiety, tachycardia, and myocardial ischemia. Patients techniques as long as preload, afterload, heart rate, and
with AS are critically sensitive to preload; adequate intra- contractility are controlled to avoid adverse hemody-
vascular volume status has to be ensured before anes- namic responses. Opioids, benzodiazepines, potent vol-
thesia induction. Systemic vascular resistance must be atile anesthetics, and nitrous oxide all should be titrated,
maintained at all times. Sympatholysis associated with paying careful attention to maintaining perfusion pres-
neuraxial anesthesia often requires use of vasoconstrictive sure. Tachycardia, bradycardia, and loss of sinus rhythm
medications and invasive monitoring. Neuraxial tech- all are problematic. Stroke volume across the stenotic
niques may be relatively contraindicated in patients with aortic valve is relatively fixed and is lower than normal;
severe AS. Arrhythmias are poorly tolerated, so mainte- an &-agonist, such as phenylephrine, is the agent of
nance of a sinus rhythm is imperative. A defibrillator choice for treating hypotension.
should be readily available, or defibrillator pads may be
placed preemptively, especially in reoperative cardiac 8. What are anesthetic considerations for
surgery and minimally invasive aortic valve replacement
transcatheter aortic valve implantation?
where internal paddles may not be as effective or may be
impossible to use. TAVI is a method by which a bovine bioprosthetic aortic
Perioperative monitoring should be guided by the valve is inserted through a catheter superimposing the
recommendations of the American Society of Anesthesi- existing aortic valve and replacing its function. It is most
ologists (ASA). Patients with AS are at increased risk for commonly used in patients with severe AS. The first
ischemia and arrhythmias, and electrocardiogram (ECG) valve approved for TAVI by the U.S. Food and Drug
monitoring should include leads II and V5. Intraarterial Administration (FDA) is the Sapien valve (Edwards Life-
monitoring should be used to monitor blood pressure sciences Corporation, Irvine, CA), which was approved
precisely for rapid recognition and treatment of hemo- in November 2011. The CoreValve (Medtronic Inc.,
dynamic derangements, especially in situations where Minneapolis, MN) is used in the United States at the
rapid fluid shifts or hemodynamic alterations are ex- present time for investigational purposes only. These two
pected. Pulmonary artery catheters are no longer rou- valves have similarities and individual limitations, but the
tinely used solely to estimate left-sided filling pressures overall procedure is similar.
because of absence of evidence to support the value of Depending on the patient’s comorbidities and proce-
this information. If a pulmonary artery catheter is inserted, dural approach, either general anesthesia or monitored
placement must be performed with extreme caution be- anesthesia care (deep sedation) can be performed. There
cause arrhythmias and (rarely) heart block may occur. are a few reports of neuraxial techniques, but they are not
However, pulmonary artery catheters may be advanta- widely accepted. Monitoring should include standard ASA
geous for monitoring mixed venous oxygen saturations, monitors, continuous intraarterial pressure monitoring
cardiac outputs, and transvenous pacing capability. before induction of anesthesia, and a large-bore central
The main goals for inducing anesthesia in patients with venous catheter through which pressures can be measured.
AS are to avoid major alterations in preload, afterload, Transesophageal echocardiography (TEE) is used to eval-
heart rate, and contractility (see Table 4-2). Etomidate, uate the patient’s baseline disease, aid in determining suit-
opioids, and midazolam are reasonably good choices but ability of valve placement, monitor the heart and valve
should be titrated to effect. Vecuronium and cisatracurium during the procedure, and evaluate successful placement
are neuromuscular blockers with favorable hemodynamic after valve deployment. Pulmonary artery catheters, cere-
profiles. Ketamine and pancuronium may increase heart bral oximetry, and anesthetic depth monitors should be
rate and should be avoided. Thiopental may cause de- considered. The need for rapid blood transfusion must
creased preload and myocardial contractility and probably also be anticipated and prepared for.
should be avoided or titrated to effect at reduced dosages. The CoreValve is a self-expanding device that contin-
The dosage and rate of administration of propofol should ues to expand over 48 hours; the risk of new conduction
also be reduced to avoid hypotension. abnormalities continues until expansion is complete.
20 SECTION 1 Cardiovascular System
Placement of a transvenous pacing wire is strongly rec- • Valve malfunction with inadequate opening of all
ommended during this time period. The Sapien valve is leaflets
not self-expanding, so the need for a transvenous pacing • Aortic regurgitation
wire is evident immediately after deployment of the valve. During the procedure, wires and catheters in the heart
The most common approach is retrograde by trans- may cause ventricular arrhythmia. Manipulation of the
catheter insertion through the femoral or axillary artery, aorta, other arteries, or the heart can lead to vessel injury,
which may be established percutaneously or via a surgical perforation, or dissection with the potential for massive
cutdown. TAVI can also be performed by direct access bleeding.
through the aorta after thoracotomy or sternotomy. Less
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Cook DJ, Housmans PR, Rehfeldt KH: Valvular heart disease—
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made, the right ventricle is paced at a rapid rate to de- (eds): Kaplan’s Cardiac Anesthesia—The Echo Era, 6th edition.
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Guidelines (Writing Committee to Revise the 2002 Guidelines on
decreased forward flow. Blood pressure may need to be Perioperative Cardiovascular Evaluation for Noncardiac Surgery);
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norepinephrine, or vasopressin. After obtaining an an- Cardiology; Heart Rhythm Society; Society of Cardiovascular Anes-
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tricular pacing is begun again to decrease cardiac output Surgery: ACC/AHA 2007 Guidelines on perioperative cardiovascular
as the valve is rapidly deployed. There is a brief period evaluation and care for noncardiac surgery: a report of the American
during which valve expansion creates a significant ob- College of Cardiology/American Heart Association Task Force on
struction of flow through the aorta. After the valve is Practice Guidelines (Writing Committee to Revise the 2002 Guide-
deployed, pacing is stopped, and the blood pressure may lines on Perioperative Cardiovascular Evaluation for Noncardiac
Surgery) developed in collaboration with the American Society of
need to be supported again with vasopressors. Successful Echocardiography, American Society of Nuclear Cardiology, Heart
valve placement should reestablish forward flow. After Rhythm Society, Society of Cardiovascular Anesthesiologists, Society
the procedure, the patient should recover in an intensive for Cardiovascular Angiography and Interventions, Society for Vascu-
care setting. lar Medicine and Biology, and Society for Vascular Surgery. J Am Coll
Cardiol 50:e159, 2007.
Possible deployment complications include the fol- Furukawa A, Abe Y, Tanaka C, et al.: Comparison of two-dimensional
lowing: and real-time three-dimensional transesophageal echocardiography
• Arrhythmia (e.g., complete heart block) in the assessment of aortic valve area. J Cardiol 59:337, 2012.
• Obstruction of the coronary arteries with native Kertai MD, Bountioukos M, Boersma E, et al.: Aortic stenosis: an un-
aortic valve leaflets that are pressed against the inner derestimated risk factor for perioperative complications in patients
undergoing noncardiac surgery. Am J Med 116:8, 2004.
aortic wall Leon MB, Smith CR, Mack M, et al.: Transcatheter aortic-valve
• Global ischemia from periods of low output during implantation for aortic stenosis in patients who cannot undergo
pacing surgery. N Engl J Med 363:1598, 2010.
CASE 5
Mitral Stenosis
Amanda J. Rhee, MD • Alexander J. C. Mittnacht, MD • David L. Reich, MD
QUESTIONS
1. What are the etiology and pathophysiology of mi- 5. How would you anesthetize this patient?
tral stenosis? 6. Describe the treatment for hypotension in patients
2. How are preload, afterload, heart rate, and with mitral stenosis.
contractility managed in patients with mitral 7. What therapies are recommended for perioperative
stenosis? right ventricular failure?
3. Explain methods for optimizing the patient’s 8. Describe specific considerations for mitral valve
condition preoperatively. repair, replacement, or percutaneous techniques.
4. What intraoperative monitoring would be
appropriate?
A 77-year-old woman with severe mitral stenosis was (i.e., New York Heart Association [NYHA] classifica-
scheduled for mitral valve repair or replacement and tricus- tion). The 10-year survival rate for patients with symp-
pid valve annuloplasty. On admission to the hospital, she toms of dyspnea on exertion is approximately 80%
had severe pulmonary edema and atrial fibrillation, with a without surgery. The 10-year survival rate for patients
rapid ventricular response. She weighed 55 kg. Cardiac with disabling NYHA class III (dyspnea with minimal
catheterization revealed mitral stenosis, pulmonary hyper- activity) and class IV (dyspnea at rest) symptoms is
tension, and tricuspid regurgitation. approximately 15% without surgery.
It previously had been thought that the left ventricle is
1. What are the etiology and pathophysiology “protected” from pressure or volume overload. Although
some degree of left ventricular “protection” may be present
of mitral stenosis?
for most cases of mild mitral stenosis, as the disease pro-
Mitral stenosis is frequently rheumatic in origin. In many gresses, it is likely to cause varying degrees of left ventricu-
patients, there is a latency period of 30–40 years between lar failure. Additionally, left ventricular contractility may be
the episode of rheumatic fever and the onset of clinical
symptoms. Dyspnea is the most common symptom. The
initial presentation is often due to an episode of atrial fibril-
lation resulting from atrial dilation or an exacerbation of
symptoms from an unrelated condition, such as pregnancy,
thyrotoxicosis, anemia, fever, or sepsis. Other common
symptoms include fatigue, palpitations, chest pain, throm-
boembolic events, and hemoptysis (from pulmonary vascu-
lar congestion).
The normal adult mitral valve orifice is 4–6 cm2. As
the orifice narrows to !2 cm2, the pressure gradient
between the left atrium and left ventricle increases to
maintain adequate flow and filling of the left ventricle.
The high left atrial pressure causes pulmonary venous
congestion, which eventually leads to pulmonary edema,
particularly in the presence of tachycardia (Figure 5-1).
Tachycardia shortens diastole and diminishes the time
available for flow across the mitral valve; this impairs
left atrial emptying and left ventricular filling. Cardiac
output decreases, pulmonary congestion increases, and
decompensation ensues. A mitral valve area !1 cm2 is
considered critical. However, the decision to perform
valve surgery is usually based on the severity of symptoms FIGURE 5-1 ■ Pathophysiology of mitral stenosis.
21
22 SECTION 1 Cardiovascular System
impaired by rheumatic involvement of papillary muscles treatment for the fixed obstruction resulting from mitral
and mitral anulus. Left ventricular posterobasal regional stenosis. However, medical optimization is mainly geared
wall motion abnormalities may result. However, it is pos- toward heart rate control to promote ventricular filling
sible that left ventricular function might also be impaired and reduce pulmonary vascular congestion. Medical ther-
by a leftward shift of the interventricular septum owing to apy includes "-adrenergic blockers or calcium-channel
right ventricular pressure overload. Pulmonary hyperten- blockers or both for heart rate regulation or cardiac gly-
sion and right ventricular failure are often observed in cosides if there is left or right ventricular dysfunction.
mitral stenosis. If there is bronchial reactivity, glucocorticoids may be
helpful. Pulmonary vascular congestion is treated with
2. How are preload, afterload, heart rate, diuretics and salt restriction. Diuretic-induced hypokale-
and contractility managed in patients mia is corrected to prevent digitalis toxicity and arrhyth-
mias. These medications are continued until the time of
with mitral stenosis?
surgery.
The goals for preload, afterload, heart rate, and contrac- Treatment of acute-onset rapid atrial fibrillation in-
tility are the major guiding principles of intraoperative cludes anticoagulation and rate control with digoxin,
management for patients with mitral stenosis. High left calcium-channel blockers, and "-adrenergic blockers.
atrial pressures are required to maintain filling of the left Hemodynamic instability requires immediate electrical
ventricle (preload) through the stenotic mitral valve. Hy- cardioversion and pharmacologic cardioversion in select
povolemia and venodilating drugs should be avoided. patients.
Afterload (systemic vascular resistance) should be kept Patients with mitral stenosis are unusually hemody-
high to maintain perfusion pressure in the face of a rela- namically sensitive to opioids and central nervous system
tively low and fixed cardiac output. Heart rate should depressants; however, adequate preanesthetic medication
be kept slow to maximize diastolic filling of the left is important for preventing anxiety-induced tachycardia.
ventricle. Contractility should be maintained to preserve Monitoring should be provided when administering
stroke volume. The hemodynamic goals in mitral steno- these medications to avoid or treat decreases in systemic
sis are summarized in Table 5-1. vascular resistance or preload.
Right ventricular failure is common in mitral stenosis.
Parameters should be optimized for the right ventricle 4. What intraoperative monitoring would be
and the left ventricle. For example, optimization of left appropriate?
ventricular preload is important while also guarding
against exacerbation of pulmonary congestion. Also, In addition to the American Society of Anesthesiolo-
tachycardia can be detrimental in mitral stenosis; how- gists (ASA) standard monitoring requirements, inser-
ever, a normal to mildly elevated heart rate is beneficial tion of an intraarterial catheter before induction is rec-
in right ventricular failure, where the cardiac output of ommended to follow blood pressure carefully during
the right ventricle becomes more heart rate–dependent. induction. Tachycardia during intubation or hypoten-
These seemingly contradictory management goals must sion related to induction agents should be recognized
be balanced based on each patient’s dynamic physiologic and treated rapidly to prevent catastrophic outcomes.
status and needs. Pulmonary artery catheters may be useful in these pa-
tients, but placement of a pulmonary artery catheter is
3. Explain methods for optimizing the patient’s not without risks. The risks include arrhythmias, heart
block, and pulmonary artery perforation. Benefits of
condition preoperatively.
pulmonary artery catheters include data on left atrial
In patients with mitral stenosis, it is essential to opti- filling pressure, pulmonary artery pressure, cardiac out-
mize hemodynamics preoperatively. There is no medical put, mixed venous oxygen saturation, and pulmonary
and systemic vascular resistance. In the presence of in pulmonary hypertension because it does not cause pul-
right ventricular dysfunction, knowledge of pulmonary monary vasoconstriction. Vasoconstriction is necessary
artery pressures is particularly important because suc- during hypotension because it is essential to preserve vital
cessful therapy includes decreasing right ventricular organ perfusion in the face of fixed low cardiac output.
afterload. "-Adrenergic agonists cause tachycardia and vasodilation,
Transesophageal echocardiography (TEE) provides in- which are undesirable effects in patients with mitral ste-
formation about biventricular function, left atrial dimen- nosis. Ephedrine, dopamine, dobutamine, and epineph-
sions, and valvular function. TEE allows for visualization rine are relatively contraindicated before valvular repair.
of left and right ventricular filling and function. Mitral
valve area can be calculated using pressure half-time mea- 7. What therapies are recommended for
surements or the continuity equation using Doppler inter- perioperative right ventricular failure?
rogation techniques. TEE permits evaluation of valvular
pathology and guidance for surgical decision making re- After mitral valve replacement, weaning from cardiopul-
garding repair versus replacement as well as evaluation of monary bypass is sometimes complicated by pulmonary
the valve or prosthesis after cardiopulmonary bypass. hypertension and right ventricular failure. Monitoring
left atrial pressure may be helpful in the most difficult
cases because a gradient is often present between the
5. How would you anesthetize this patient?
pulmonary capillary wedge and left atrial pressures. Fac-
Opioids (e.g., fentanyl, sufentanil, remifentanil), benzodi- tors that predispose to pulmonary vasoconstriction (e.g.,
azepines, and etomidate all are reasonable choices for anes- hypoxia, hypercarbia, acidosis, light anesthesia, and hy-
thetic induction in patients with mitral stenosis (Table 5-2). pothermia) should be corrected.
Opioids also have the advantage of increasing vagal tone The main goals in the anesthetic management of right
and slowing heart rate, usually without associated hypo- ventricular failure are to reduce right ventricular after-
tension. Short-acting barbiturates, such as thiopental, pro- load, optimize right ventricular preload, maintain right
duce undesirable venodilation and myocardial depression. ventricular coronary perfusion, and support right ven-
Ketamine is relatively contraindicated on the basis of its tricular contractility. In the presence of preexisting pul-
tachycardic effects. Volatile agents produce both myocar- monary hypertension and increased pulmonary vascular
dial depression and vasodilation and should be used cau- resistance, right ventricular failure responds favorably to
tiously in low concentrations. Propofol should be used with pulmonary vasodilation. Drugs with pulmonary vasodi-
caution. Theoretically, the most suitable neuromuscular lating activity that are used after termination of cardio-
blocking agents for mitral stenosis are succinylcholine, pulmonary bypass include nitroprusside, nitroglycerin,
vecuronium, rocuronium, and cisatracurium. Large boluses prostaglandin E1 (or other prostanoid therapies, such as
of pancuronium are relatively contraindicated because they prostacyclin or iloprost), or an endothelin antagonist.
produce tachycardia. However, none of these medications is selective for the
pulmonary circulation, and their use may be limited by
6. Describe the treatment for hypotension in patients systemic effects. Milrinone, a phosphodiesterase III in-
hibitor, increases right ventricular contractility and has
with mitral stenosis
pulmonary vasodilating properties. This pharmacologic
Hypotension is best treated with an #-adrenergic agonist, profile makes phosphodiesterase III inhibitors appealing
such as phenylephrine, which increases arterial blood pres- in the treatment of right ventricular failure. Inhaled aero-
sure and decreases heart rate via baroreceptor-mediated solized milrinone is an emerging therapy that may be
reflexes. Vasopressin can also be used and may be preferable used for selective pulmonary vasodilation.
Hypertrophic Obstructive
Cardiomyopathy
Amanda J. Rhee, MD • Alexander J. C. Mittnacht, MD • David L. Reich, MD
QUESTIONS
1. Describe the anatomic abnormalities in hypertrophic 4. What monitoring is required in patients with
obstructive cardiomyopathy. hypertrophic obstructive cardiomyopathy?
2. What changes in preload, afterload, heart rate, 5. What are the considerations for anesthetic man-
and contractility optimize hemodynamic perfor- agement of patients with hypertrophic obstructive
mance for patients with hypertrophic obstructive cardiomyopathy?
cardiomyopathy? 6. What are special considerations for anesthetic
3. What are the treatment options for hypertrophic management of labor and delivery in patients with
obstructive cardiomyopathy? hypertrophic obstructive cardiomyopathy?
A 28-year-old woman with hypertrophic obstructive identified in autopsy specimens, especially in areas of myo-
cardiomyopathy (HOCM) presented for labor and deliv- cardial fibrosis. This coronary artery disease may play some
ery. She was initially managed by the obstetrician with role in the etiology of myocardial ischemia in these patients.
intravenous butorphanol but became progressively more Obstruction to left ventricular outflow is caused by hy-
uncomfortable. The anesthesiologist was consulted for pertrophic muscle at the interventricular septum and systolic
further management. anterior motion (SAM) of the anterior leaflet of the mitral
valve. SAM is associated with mitral regurgitation and a
1. Describe the anatomic abnormalities in posteriorly directed jet. SAM previously was thought to
be caused by a Venturi effect of the rapidly flowing blood
hypertrophic obstructive cardiomyopathy.
in the LVOT. A more recent theory suggests that changes in
HOCM is the most common genetic cardiovascular the position of the leaflet coaptation zone relative to the
disease, with a prevalence of approximately 1 in 500 interventricular septum and changes in blood flow caused by
young people in the United States. It is an autosomal blood hitting the bulging septum may physically push the
dominant genetic disorder and is an important cause of anterior mitral valve leaflet into the LVOT during systole. In
heart failure at any age. HOCM is usually defined by other words, the hypertrophied ventricular septum causes
a hypertrophied, nondilated left ventricle that occurs in the mitral valve to be positioned more anteriorly in the
the absence of other causative diseases for hypertrophy, left ventricular cavity, bringing the leaflet coaptation point
such as chronic hypertension and aortic stenosis. It oc- closer to the interventricular septum than normal. Excessive
curs in either obstructive or nonobstructive forms. The anterior mitral valve tissue in combination with the more
obstructive forms feature a dynamic pressure gradient anterior position of the mitral valve causes the anterior
across the left ventricular outflow tract (LVOT). Other mitral valve leaflet to protrude into the LVOT. Additionally,
conditions can produce the picture of obstructive car- the hypertrophied ventricular septum changes blood flow in
diomyopathy secondary to significant infiltration of the the LVOT, redirecting it behind and lateral to the enlarged
ventricular wall, as in Pompe disease, in which a massive anterior mitral valve leaflet and pushing it into the septum.
accumulation of cardiac glycogen in the ventricular wall Consequently, a dynamic subaortic pressure gradient is
produces ventricular outflow obstruction. present. The outflow tract obstruction, by causing in-
HOCM, hypertrophic cardiomyopathy, asymmetric creased pressure in the ventricular chamber, can result in
septal hypertrophy, and idiopathic hypertrophic subaortic hypertrophy of the remainder of the ventricular muscle.
stenosis all are terms applied to the same disease process. As the ventricle hypertrophies, ventricular compliance
The main anatomic feature of HOCM is a hypertrophied decreases, and passive filling of the ventricle during dias-
ventricular muscle at the septum base in the LVOT. The tole is limited. The ventricle increasingly depends on atrial
histologic appearance is a disorganized mass of hypertro- systole (atrial kick) to maintain ventricular end-diastolic
phied myocardial cells extending from the left ventricular volume and, ultimately, cardiac output. Occasionally,
septal wall; the mass may involve the papillary muscles. HOCM is associated with right ventricular outflow tract
Intramural (small vessel) coronary artery disease has been obstruction as well.
25
26 SECTION 1 Cardiovascular System
2. What changes in preload, afterload, heart rate, !-adrenergic blockers, verapamil is administered, which
and contractility optimize hemodynamic also depresses systolic function and improves diastolic
performance for patients with hypertrophic function. Patients whose symptoms are refractory to this
obstructive cardiomyopathy? combination may be treated with disopyramide, a type
IA antiarrhythmic medication that decreases systolic
Determinants of the severity of the ventricular obstruction function and causes some peripheral vasoconstriction.
in HOCM are the following: Amiodarone is commonly administered for the control
• Systolic volume of the ventricle of supraventricular and ventricular dysrhythmias.
• Force of ventricular contraction Nonmedical treatment options are surgical myotomy or
• Transmural pressure distending the outflow tract myectomy, percutaneous transluminal septal myocardial
Large systolic volumes in the ventricle distend the out- ablation, alcohol septal ablation, septal coil embolization,
flow tract and reduce the obstruction. Paradoxically, when mitral valve replacement or valvuloplasty, or a combination
ventricular contractility is increased, the outflow tract is of these. Potential complications of surgical correction of
narrowed, which increases the obstruction and decreases the LVOT obstruction include complete heart block and
cardiac output. When aortic pressure (afterload) is elevated, immediate or late formation of a ventricular septal defect
there is an increased transmural pressure distending the secondary to septal infarction. Dual chamber pacing and
LVOT during systole, and this reduces the degree of implantable cardioverter-defibrillator devices are helpful to
obstruction. Conversely, during periods of systemic maintain sinus rhythm and treat arrhythmias that might
vasodilation, the outflow tract is narrowed. This results otherwise lead to sudden cardiac death. The reported annual
in a marked decrease in cardiac output and mitral regur- mortality rate is 1% to 3%, with deaths mostly resulting
gitation, as the mitral valve becomes the relief point for from ventricular arrhythmias, sudden cardiac death, progres-
ventricular pressure (Table 6-1). sive heart failure, and atrial fibrillation with embolic stroke.
3. What are the treatment options for hypertrophic 4. What monitoring is required in patients with
obstructive cardiomyopathy? hypertrophic obstructive cardiomyopathy?
Medical therapy of HOCM is based on the administra- Patients with HOCM may be extremely sensitive to slight
tion of !-adrenergic blockers (Table 6-1). The specific changes in ventricular volume, blood pressure, heart
regimen is tailored to an individual patient’s pathologic rate, and rhythm resulting in hemodynamic catastrophe.
profile. The beneficial effects of !-adrenergic blockers Monitoring should allow for continuous assessment of
are likely due to depressed systolic function, improved these parameters, particularly in patients with severe ob-
diastolic filling, and better relaxation. However, it is still struction. In patients with HOCM presenting for septal
unclear whether life expectancy is prolonged by this myectomy, an electrocardiogram (ECG), intraarterial
treatment. In patients whose symptoms are refractory to catheter, and central venous catheter are necessary.
A pulmonary artery catheter may be considered. Two- may exacerbate LVOT obstruction. An effort should be
dimensional transesophageal echocardiography (TEE) made to blunt this response (e.g., deepening the anes-
provides useful data on ventricular performance, the thesia) before stimulation. Inotropes, !-adrenergic ago-
dynamic mechanism of LVOT obstruction, and accom- nists, and calcium are relatively contraindicated for the
panying mitral regurgitation. After septal myectomy, same reason. Transmural distending pressure can be
TEE provides invaluable information about residual decreased by hypotension secondary to anesthetic drugs,
obstruction and mitral regurgitation. TEE can also be hypovolemia, or positive pressure ventilation. Tachy-
useful for detecting surgical complications, such as cardia is poorly tolerated in patients with HOCM be-
ventricular septal perforation. cause it decreases systolic ventricular volume, narrow-
In patients with HOCM scheduled for noncardiac ing the outflow tract. Atrial contraction is extremely
procedures, monitoring should provide some indication important to filling of the hypertrophied ventricle.
of ventricular volume, force of ventricular contraction, Nodal rhythms should be aggressively treated, using
and transmural pressure distending the outflow tract. atrial pacing if necessary.
Central venous pressure could be an indicator of ven- Anesthesia can be induced intravenously or by inha-
tricular volume in procedures that do not result in major lation of a potent anesthetic agent. Ketamine and pan-
volume shifts or alterations in ventricular function. An curonium are best avoided because of their sympatho-
intraarterial catheter is almost always indicated for beat- mimetic effects. Historically, halothane was the most
to-beat blood pressure monitoring during major regional efficacious potent volatile agent because it decreases
or general anesthesia in patients with symptomatic heart rate and myocardial contractility, has the least
HOCM. Intraoperative TEE is the most accurate moni- effect on systemic vascular resistance (SVR), and tends
tor of ventricular loading conditions and performance in to minimize the severity of LVOT obstruction when
HOCM. volume replacement is adequate. Isoflurane and desflu-
rane cause pronounced peripheral vasodilation and are
5. What are the considerations for anesthetic less desirable. Sevoflurane decreases SVR to a lesser
management of patients with hypertrophic extent and may be the preferred inhaled volatile anes-
thetic at the present time. Agents that release hista-
obstructive cardiomyopathy?
mine, such as morphine, are not recommended because
Anesthetic management of patients with HOCM re- of the venodilation and hypovolemia that they produce.
volves around optimization of intravascular volume, High-dose opioid anesthesia causes minimal cardiovas-
ventricular contractility, and transmural distending cular side effects along with bradycardia and may be a
pressure of the outflow tract (see Table 6-1). Blood loss, useful anesthetic technique in these patients. Preopera-
sympathectomy secondary to spinal or epidural anes- tive !-adrenergic blocker or calcium channel blocker
thesia, nitroglycerin, or postural changes can decrease therapy should be continued. Intravenous propranolol,
preload. Sympathetic stimulation caused by tracheal metoprolol, esmolol, or verapamil can be administered
intubation or surgical manipulation results in an in- intraoperatively to improve hemodynamic performance
crease in contractility and tachycardia, both of which (Table 6-2).
6. What are special considerations for anesthetic HOCM is a challenging situation, and emergency delivery
management of labor and delivery in patients with services should be available. Elective cesarean delivery
hypertrophic obstructive cardiomyopathy? should be considered if symptoms of HOCM are severe.
Cardiac Pacemakers
and Defibrillators
Marc E. Stone, MD • Himani Bhatt, MD
QUESTIONS
1. What are the different types of pacemakers? 12. How do you determine if a patient is pacemaker
2. How does a pacemaker work? dependent, and how should this be managed in the
3. What do the pacemaker codes represent? perioperative period?
4. Explain physiologic pacing. 13. Should a magnet be used?
5. What is mode switching? 14. Does an implantable cardioverter-defibrillator have
to be deactivated in the perioperative period?
6. Describe rate-adaptive pacing.
15. What should be done if a patient with a deactivated
7. What is cardiac resynchronization therapy? implantable cardioverter-defibrillator experiences
8. What is an implantable cardioverter-defibrillator? fibrillation?
9. How is a patient with a cardiac implantable electronic 16. How can one know if a cardiac implantable
device managed in the perioperative period? electronic device requires interrogation before
10. How is the type of device present determined? discharging the patient from an intensive care
11. What is electromagnetic interference, and how setting?
does it affect cardiac implantable electronic
devices?
A 59-year-old man with diverticulitis and dilated cardio- BOX 7-1 Indications for Implantation
myopathy presented for a hemicolectomy. Concurrent of Cardiac Pacemakers
medical issues include coronary artery disease, coronary
artery bypass graft, congestive heart failure, hypertension, • Sinus node dysfunction (symptomatic bradycardia)
mild renal insufficiency, and hiatal hernia. A pacemaker • AV conduction block
and implantable cardioverter-defibrillator (ICD) are pre- • Postablation of AV node or junction
sent. Medications include aspirin, warfarin, enalapril, • Third-degree AV block after myocardial infarction
• Significant carotid sinus hypersensitivity
fluoxetine, metoprolol, lansoprazole, and zolpidem. He • Congenital complete heart block
has no known drug allergies. • Long QT syndrome
• Refractory heart failure (cardiac resynchronization therapy)
1. What are the different types of pacemakers?
AV, Atrioventricular.
In modern practice, cardiac pacing can be provided in
numerous ways and by a range of devices, including
transcutaneous pacing pads; temporary external pacing pulse generator functions as anode) is that the distance
devices connected to transvenous or epicardial wires; between the anode and cathode is much smaller, and this
and highly sophisticated, multifunctional, programmable, confers a reduced susceptibility to electromagnetic inter-
permanently implanted pulse generators with permanent ference (EMI). Typically, pacemaker leads are placed in
intracardiac or epicardial leads. Indications for cardiac pac- the right atrial appendage, in the right ventricle, or in
ing are generally guided by two main factors: symptomatic both in a dual-chamber device (Figure 7-1).
arrhythmias and conduction abnormalities (Box 7-1).
Pacing impulses can be delivered to a single chamber 2. How does a pacemaker work?
(atrium or ventricle), dual chambers (atrium and ventri-
cle), or multiple chambers (e.g., biventricular pacing for In an asynchronous mode of programming, pacing im-
cardiac resynchronization therapy [CRT]). Bipolar leads pulses are delivered to the chamber where a lead resides
(cathode and anode present on the lead itself) have pre- at a set rate regardless of spontaneous electrical activity. In
dominantly been used since the late 1990s. The advantage a sensing mode, electrical activity can be detected in the
of bipolar leads (compared with unipolar leads where the chamber where a lead resides, and depending on device
29
30 SECTION 1 Cardiovascular System
Adapted from Bernstein AD, Daubert JC, Fletcher RD, et al.: The revised NASPE/BPEG generic code for antibradycardia, adaptive-rate and
multisite pacing. Pacing Clin Electrophysiol 25:260, 2002.
7 Cardiac Pacemakers and Defibrillators 31
inhibition or triggering of pacing of both the atrium increased minute ventilation are also available, and a
and the ventricle. DDD mode is a very versatile and blended sensor detecting both accelerations and changes
physiologic mode that is commonly programmed in thoracic impedance are used in certain devices. Preop-
for various clinical scenarios. eratively, it may be beneficial to disable the rate-adaptive
Asynchronous modes (e.g., AOO, VOO, DOO) are pacing function for some patients to avoid unnecessarily
most often used for emergency situations (e.g., acute rapid rates of pacing that may be diagnostically confusing
high-degree AV conduction block, asystole) or in an in the perioperative period.
environment (e.g., operating room) where EMI (e.g.,
electrocautery) can cause inhibition of pacing based on 7. What is cardiac resynchronization therapy?
sensed intrinsic electrical activity, especially in patients
who are pacemaker dependent. A risk of an asynchro- The fifth position in the NASPE/BPEG code provides
nous mode of pacing is competition with a spontaneous information about the presence or absence of multisite
underlying rhythm and the potential to deliver a pacing pacing, which implies either there is more than one lead
impulse at a vulnerable portion of the cardiac cycle, in a single cardiac chamber or there is biventricular pac-
leading to an arrhythmia (e.g., ventricular fibrillation ing. The former refers to attempts to suppress atrial
from an “R on T” phenomenon). fibrillation with more than one lead in the atrium, but
this is not currently clinically relevant. The latter refers
to biventricular pacing as CRT, which is beneficial in
4. Explain physiologic pacing.
restoring synchrony in some patients with heart failure
AV synchrony optimizes ventricular filling and, ulti- and left ventricular dysfunction.
mately, cardiac output. Dual-chamber pacing modes can Advanced cardiac failure is often accompanied by
sense and trigger or inhibit pacing in one or both cham- sinus or AV node dysfunction and intraventricular con-
bers. Such a mode of pacing (i.e., AAI, DDD) is “physio- duction defects that delay the onset and completeness of
logic” because it ensures that the atrial rate is the same as right or left ventricular systole in at least one third of
the ventricular rate and that an atrial systole immediately patients with heart failure. This delay causes dyssyn-
precedes every ventricular systole. This pacing can be chrony between and within left and right ventricular
especially important in patients with ischemic cardiomy- contractions, further impairing cardiac output, and
opathy or diastolic dysfunction, where an atrial kick and has been shown to increase the risk of death in these
AV synchrony improve cardiac output. In addition to patients.
improved hemodynamics, physiologic pacing modes min- CRT entails AV sequential biventricular pacing to
imize AV valvular insufficiency that occurs with isolated optimize the timing and completeness of the right and left
ventricular pacing and retrograde atrial depolarization. ventricular contractions, “resynchronizing” and optimiz-
These modes may reduce the incidence of atrial tachyar- ing cardiac function. CRT has been shown to improve
rhythmias, reducing potential thromboembolic events cardiac output, hemodynamics, heart failure symptoms,
from stasis in a noncontracting atrium. and quality of life in patients with heart failure. CRT is
currently indicated for reduction of symptoms in patients
with moderate to severe heart failure (New York Heart
5. What is mode switching?
Association [NYHA] class III or IV) who remain symp-
Mode switching refers to an automatic reprogramming of tomatic despite stable, optimal medical therapy and who
a pacemaker to prevent tracking of a sudden rapid atrial have a left ventricular ejection fraction (LVEF) of #35%
rate to the ventricle. Once sinus rhythm has been restored, and QRS duration $130 msec.
the pacemaker should revert quickly to the original pro-
gramming. Mode switching refers to an automatic, tempo-
8. What is an implantable cardioverter-defibrillator?
rary reprogramming of the device to prevent symptoms
resulting from a rapidly paced ventricular rate. An ICD is a device capable of detecting a malignant
ventricular arrhythmia and delivering therapy (e.g.,
shock) to terminate the arrhythmia. Sensing of electrical
6. Describe rate-adaptive pacing
activity from the right ventricular lead enables the ICD
The ability to increase the heart rate when needed is cru- to detect and classify the apparent heart rate as ventricu-
cial to optimal systemic perfusion. Rate modulation (also lar fibrillation (VF) or ventricular tachycardia (VT)
called rate adaptation) is a functionality incorporated into based on predetermined and programmed heart rate
most modern pacemakers that allows the device to “zones” and to provide an appropriate treatment. All
increase the paced heart rate automatically when needed modern ICDs also have pacemaker capabilities in case
to meet metabolic demands. The fourth letter of the defibrillation results in bradycardia or asystole (“post
NASPE/BPEG code designates the presence or absence shock therapy”—often VVI mode at 55–60 beats per
of rate modulation. This functionality is accomplished minute) and programming that allows for antitachycar-
according to a computerized algorithm in proportion to dia pacing that can potentially terminate VT.
the change in certain monitored physiologic variables. The main indication for implantation of an ICD is the
The most common sensor currently employed is a piezo- prevention of death caused by a lethal arrhythmia (e.g.,
electric accelerometer to sense vibrations and accelera- VF or VT). Modern ICDs can terminate VF in $98%
tions secondary to bodily motion. Sensors detecting a of episodes, and prevention of sudden death secondary
change in thoracic impedance ostensibly secondary to to arrhythmia has been shown to increase survival in
32 SECTION 1 Cardiovascular System
where significant EMI is anticipated intraoperatively. Magnet application to an ICD would not create an
Reprogramming of a pacemaker to an asynchronous asynchronous mode of pacing from the associated pace-
mode is recommended at the present time only for maker programming. Any desired reprogramming of the
pacemaker-dependent patients. This reprogramming pacemaker in a patient with an ICD would require a man-
can potentially be accomplished with a manufacturer- ufacturer-specific programming device to effect alterations
specific programmer or by magnet application (discussed to the programming (as explained subsequently).
later). Patients who are not pacemaker dependent should
not be reprogrammed to an asynchronous mode because 13. Should a magnet be used?
of the risk of competition of paced beats with a sponta-
neous rhythm and the potential “R on T” phenomenon It has become common practice to use a magnet to alter
that may produce ventricular fibrillation. However, it is the behavior of a CIED perioperatively because it is often
recommended that rate modulation should be suspended more convenient and may be safer for the patient than
(if feasible) for patients who do not require reprogramming formal reprogramming. However, the programmed mag-
(rate modulation is not a consideration in asynchronous net response of a device should ideally be ascertained in
modes of pacing). advance if magnet application is to be considered a ratio-
nal plan to prevent (or rescue from) inhibition of pacing
12. How do you determine if a patient is pacemaker or prevention of a defibrillatory shock owing to EMI.
dependent, and how should this be managed in Application of a magnet to a modern pacemaker usu-
ally produces an asynchronous mode of pacing. The con-
the perioperative period?
figuration and the programming of the device determine
It is critical to know if patients are dependent on their the specific mode of asynchronous pacing one obtains
pacemakers before going to the operating room. This (e.g., AOO, VOO, DOO), and the remaining battery life
information may be available in chart notes or may be determines the rate. There may also be default settings
ascertainable from the patient, the family, the manufac- that vary by manufacturer. Assuming an appropriate mag-
turer of the device, or the pacemaker clinic where the net response is programmed, once the magnet is applied
patient receives care. A history that the device was im- over the pulse generator, asynchronous pacing persists for
planted for symptomatic bradycardia or syncope or after a as long as the magnet remains in place. Removal of the
successful AV nodal ablation suggests pacemaker depen- magnet results in reversion to baseline settings. This
dence. If such information is unavailable, one should response is always seen with a Medtronic pacemaker
examine or obtain an electrocardiogram (ECG). Pace- (Minneapolis, Minnesota), (and would likely be seen with
maker dependence should be assumed if every P-wave or pacemakers from other manufacturers), but the magnet
QRS complex on the ECG is preceded by a pacemaker response is programmable in devices from Boston Scientific
spike. If an Industry Employed Allied Healthcare Pro- (Natick, Massachusetts), St. Jude (St. Paul, Minnesota),
fessional or other consultant interrogates the device, he and Biotronik (Berlin, Germany), and the response may
or she would be able to recognize pacemaker depen- vary (e.g., there may be none, or the device may first cap-
dency (there would be no spontaneous ventricular activ- ture a snapshot of recent events or conduct a battery test).
ity when the pacemaker is programmed to VVI mode at The more recent introduction of magnetic resonance
a low rate). Provocative maneuvers to elicit bradycardia imaging–compatible devices with programmable magnet
(e.g., prolonged Valsalva maneuver; administration of a responses brings a new set of considerations, emphasizing
small dose of esmolol, adenosine, or edrophonium) are the need to know what is present and how it is pro-
not recommended. grammed before proceeding into the operating room and
The recognition (or assumption) of pacemaker depen- simply assuming that a magnet application would produce
dence should prompt a plan to protect the CIED from an asynchronous mode of pacing when needed.
effects of EMI intraoperatively. Current recommenda- Application of a magnet to an ICD should disable
tions state that pacemaker-dependent patients should detection of arrhythmias and would protect against
have their devices reprogrammed to an asynchronous an inappropriately delivered defibrillatory shock as a
mode to protect from EMI intraoperatively, when the result of exposure to EMI; however, the magnet re-
site of surgery or EMI is close (e.g., #15 cm) to the sponse is potentially programmable in devices from
location of the device and leads. This reprogramming Boston Scientific, St. Jude, and Biotronik, and one
can be accomplished with a manufacturer-specific pro- needs to ensure that magnet response is enabled in a
gramming device or, potentially, with a magnet (assum- given patient’s device. Assuming the magnet response
ing no ICD is present, magnet response is enabled, and to be enabled, a critical concept to understand is that
the device is accessible during the procedure). If the site the nominal magnet response across the industry is to
of surgery or EMI is remote (e.g., $15 cm) from the deactivate an ICD. In other words, if a patient has an
location of the device and leads, magnet response is ICD that is also providing pacing, magnet application
known, and the device would be accessible during the would deactivate only the ICD, and one would not
surgical procedure, one may decline reprogramming obtain an asynchronous mode of pacing from the
the device in advance, reserving magnet application to device. If one desires asynchronous pacing in a patient
create an asynchronous mode of pacing as a rescue with an ICD, the device must be programmed with
maneuver, if needed. a manufacturer-specific programmer. This situation
7 Cardiac Pacemakers and Defibrillators 35
BOX 7-4 Recommended Indications for Interrogation of Cardiac Implantable Electronic Devices
(CIEDs) before Patient Discharge or Transfer from a Monitored Environment*
• Hemodynamically challenging surgeries, such as cardiac • Emergent surgery where the site of EMI exposure was
surgery or significant vascular surgery (e.g., abdominal above the umbilicus
aortic aneurysm repair) • Cardiothoracic surgery
• Significant intraoperative events, including cardiac • Procedures that emit EMI with a greater probability of
arrest requiring temporary pacing or cardiopulmonary affecting device function
resuscitation and events that required external electrical • Logistic limitations that would prevent reliable device
cardioversion evaluation within 1 month from their procedure
*Patients with CIEDs reprogrammed before the procedure that left the device nonfunctional, such as disabling tachycardia detection in an ICD.
EMI, electromagnetic interference.
From Crossley GH, Poole JE, Rozner MA, et al.: The Heart Rhythm Society/American Society of Anaesthesiologists expert consensus statement
on the perioperative management of patients with implantable defibrillators, pacemakers and arrhythmia monitors. Facilities and patient
management: executive summary. Heart Rhythm 8:e1, 2011.
Cardiac Tamponade
Cesar Rodriguez-Diaz, MD
QUESTIONS
A 54-year-old man with atrial fibrillation underwent because it is more compliant than the left ventricle and
percutaneous pulmonary vein isolation under general has a lower filling pressure. At this phase, stroke vol-
anesthesia earlier in the day. In the recovery room, he ume is diminished, but cardiac output may be main-
became tachycardic, hypotensive, and short of breath tained by a higher heart rate. Last, as further fluid
and complained of chest tightness. Electrocardiogram accumulates, intrapericardial pressure equalizes with
(ECG) revealed low QRS complexes and electrical alter- left ventricular filling pressure, and cardiac output be-
nans. Cardiac tamponade is suspected. comes severely compromised.
4. How is cardiac tamponade diagnosed? basis for pulsus paradoxus. Because cardiac tamponade
tends to affect right ventricular filling more than left
Diagnosis of cardiac tamponade requires a high index of ventricular filling, it is beneficial to maintain spontane-
suspicion. Transthoracic echocardiography has proved to ous inspiration.
be the imaging modality of choice because of its portabil-
ity and availability. It allows visualization of pericardial 6. What variants of cardiac tamponade have been
fluid and its effect on cardiac filling. Expected echocar-
described?
diographic findings of cardiac tamponade are summa-
rized in Box 8-2. Chest x-ray might be useful for large Usually in cardiac tamponade, CVP and PACWP range
pericardial effusions as previously discussed. from 15–30 mm Hg. Low-pressure cardiac tamponade
has been described in hypovolemic patients with a CVP
5. How does spontaneous respiration affect of 6–12 mm Hg. A fluid challenge might unmask classic
ventricular filling in cardiac tamponade? tamponade signs. Hypertensive cardiac tamponade has
been described when hypertensive patients develop tam-
Spontaneous inspiration in healthy subjects promotes ponade physiology but maintain an elevated blood pres-
right ventricular filling secondary to increased intratho- sure, presumably from increased sympathetic activity.
racic venous flow caused by negative intrathoracic pres- Regional tamponade occurs when a loculated effusion
sure. In contrast, during inspiration, left ventricular obstructs filling of a single chamber.
filling is decreased because of expansion of the pulmo-
nary vascular bed. In tamponade physiology, this phe-
7. How is cardiac tamponade treated?
nomenon is exaggerated. During inspiration, the right
ventricle fills, causing the ventricular septum to bulge The goal of management of cardiac tamponade ultimately
into the left ventricle and result in a markedly reduced is to relieve intrapericardial pressure by pericardiocentesis.
left ventricular stroke volume; this is the physiologic Medical management of cardiac tamponade aims at main-
taining cardiac output and perfusion pressure while the
pericardial effusion can be drained. Aggressive fluid hydra-
BOX 8-1 Cardiac Tamponade Findings tion to maintain increased CVP to overcome intrapericar-
dial pressure is the initial step in management. Tachycardia
NONSPECIFIC SYMPTOMS should be maintained and promoted to maximize cardiac
• Shortness of breath output in the setting of low stroke volume. Systemic vas-
• Chest tightness cular resistance should be optimized to maintain coronary
• Dizziness perfusion pressure in the setting of low cardiac output.
• Distended neck veins Contractility should be maintained or increased to opti-
• Shock mize cardiac output. #-Receptor and $-receptor agonist
CLASSIC FINDINGS infusions, such as epinephrine, dobutamine, dopamine,
and norepinephrine, should be instituted if needed.
• Pulsus paradoxus
• Beck triad (dilated neck veins, muffled heart tones, Pericardiocentesis can be performed bedside under
hypotension) echocardiographic guidance, in the catheterization labo-
• ECG ratory under fluoroscopic guidance, or in the operating
• Low voltage in all leads room under direct surgical vision. Possible complications
• Electrical alternans of pericardiocentesis include arrhythmias, coronary artery
• Pulmonary artery catheter injury, hemothorax, pneumothorax, and hepatic injury.
• CVP " PADP " PACWP In rare cases, transient biventricular dysfunction accom-
• Absent y descent on right atrial and wedge pressures panied by pulmonary edema has been described; the
• Enlarged cardiac silhouette on chest x-ray mechanism for this is unclear. Sudden increases in ven-
CVP, central venous pressure; ECG, electrocardiogram; PACWP,
tricular filling, neurohormonal etiology, or reduced coro-
pulmonary artery capillary wedge pressure; PADP, pulmoanry artery nary artery flow during cardiac tamponade have been
diastolic pressure. implicated in the mechanism.
8 Cardiac Tamponade 39
8. How would you anesthetize a patient with cardiac activity, provides analgesia, and produces hypnosis. Local
tamponade? anesthesia should still be used to minimize the amount of
ketamine required. After the procedure, the patient
The primary anesthetic goal is to maintain cardiac output should be monitored closely, preferentially in an inten-
with: sive care unit, to watch for complications or effusion
• Spontaneous respiration reaccumulation.
• Tachycardia
• Maintained vascular tone
• Aggressive hydration
• Promoting contractility SUGGESTED READINGS
Standard ASA monitors are applied. An intraarterial D’Cruz I, Rehman AU, Hancock HI: Quantitative echocardiographic
catheter is placed for beat-to-beat monitoring of hemody- assessment in pericardial disease. Echocardiography 14:207, 1997.
Domino KB, Bowdle TA, Posner KL, et al.: Injuries and liability related
namic status; however, the procedure should not be de- to central vascular catheters: a closed claims analysis. Anesthesiology
layed because of difficulty obtaining access. Preferentially, 100:1411, 2004.
pericardiocentesis should be performed in an awake pa- Maisch B, Seferovic PM, Ristic AD, et al.; Task Force on the Diagnosis
tient with local anesthesia to avoid potentially deleterious and Management of Pericardial Diseases of the European Society of
Cardiology: Guidelines on the diagnosis and management of pericar-
hemodynamic effects of anesthetic drugs. Vasodilation, dial diseases: executive summary: the Task Force on the Diagnosis
myocardial depression, or positive pressure ventilation and Management of Pericardial Diseases of the European Society of
could lead to cardiovascular collapse. However, awake Cardiology. Eur Heart J 25:587, 2004.
pericardiocentesis is not always possible in an uncoopera- Reddy PS, Curtiss EI, Uretsky BF: Spectrum of hemodynamic changes
tive patient, especially a child. in cardiac tamponade. Am J Cardiol 66:1487, 1990.
Reydel B, Spodick DH: Frequency and significance of chamber
If general anesthesia is necessary, intravenous ket- collapses during cardiac tamponade. Am Heart J 119:1160, 1990.
amine is the drug of choice because it usually maintains Spodick DH: Current concepts: acute cardiac tamponade. N Engl
spontaneous respiration, has indirect sympathomimetic J Med 349:684, 2003.
CASE 9
QUESTIONS
1. What is a ventricular assist device? 8. Which monitoring devices are necessary for
2. What are important preanesthetic considerations anesthetic management of a patient with a left
for patients with a left ventricular assist device? ventricular assist device?
3. What anesthetic agents and techniques are 9. When are central venous catheters or pulmonary
appropriate for a patient with a left ventricular artery catheters helpful in patients with a left
assist device? ventricular assist device?
4. What are the goals for fluid management in a 10. What are the parameters on the HeartMate II left
patient with a left ventricular assist device? ventricular assist device console?
5. Should anticoagulation be reversed for the surgical 11. How long do HeartMate II device batteries last?
procedure? 12. What alarms might I hear annunciated, and of
6. What antibiotic coverage is necessary for a patient what alert conditions do I need to be aware?
with a left ventricular assist device? 13. What are important postoperative considerations
7. How should implantable cardioverter-defibrillators in a patient with a left ventricular assist device?
and pacemakers be managed perioperatively in a
patient with a left ventricular assist device?
A 60-year-old man with end-stage heart failure presented for intermediate-term or long-term use as a “bridge-
for colonoscopy. He had a left ventricular assist device to-transplantation.” In patients who are not eligible for
(LVAD) as a bridge-to-transplantation. He last took war- transplantation, some devices have been approved as “desti-
farin 5 days ago. nation therapy” as a final, permanent management strategy
A 55-year-old man with an LVAD and stage IV for end-stage heart failure. In many instances, a period of
sacral decubitus ulcer presented for débridement and VAD support can improve multiorgan failure and improve
myocutaneous flap closure. The surgeon requested a patient’s status to become eligible for transplantation; in
the prone position. The patient was receiving a con- such instances, VADs are used as a “bridge-to-improved-
tinuous heparin infusion with a partial thromboplastin candidacy.” Devices also are available that can provide cir-
time of 70 seconds. culatory support as a “bridge-to-immediate-survival” (e.g.,
A 64-year-old man with intraabdominal hemorrhage from acute cardiogenic shock) and as a “bridge-to-next-
presented for exploratory laparoscopy and possible lapa- decision” (e.g., in a patient with uncertain neurologic or
rotomy 2 days after appendectomy. He had an LVAD as multiorgan status after a cardiac arrest).
destination therapy. His international normalized ratio VADs function by collecting blood from the failing
(INR) was 2.0 and his hematocrit was 23% after receiv- ventricle and pumping it downstream into the systemic
ing 2 units of packed red blood cells. circulation. An LVAD provides support for the left ven-
tricle by draining blood most commonly from the apex of
the left ventricle and returning it by pump to the ascend-
1. What is a ventricular assist device?
ing aorta. A right ventricular (RV) assist device provides
Ventricular assist devices (VADs) are pumps implanted to support for the right ventricle by draining blood from the
assist the failing ventricle and maintain systemic perfusion. right atrium and returning it by pump to the main pul-
Various VADs are approved for use in the United States, monary artery. Some VADs are implanted within the
and an even larger variety are used worldwide. Some VADs body, and some remain paracorporeal during support,
are intended for short-term use after an acute cardiac event connected to long cannulas implanted in the heart and
as a “bridge-to-recovery,” and some devices are intended great vessels.
40
9 Patient with a Left Ventricular Assist Device Presenting for Noncardiac Surgery 41
First-generation LVADs (approved in the mid-1990s) only the ease of implantation but also the relative percentage
were pulsatile devices that were intended to capture the of patients who can receive one. Further miniaturized de-
entire potential output of the failed ventricle and eject a vices are available for pediatric patients. Several advantages
physiologic stroke volume. Their output was pulsatile, have been demonstrated for continuous flow compared with
although the “pulse” rarely coincided with the underly- pulsatile flow, including potentially less hemolysis, lower in-
ing cardiac rhythm because the devices were generally cidence of thromboembolic complications, reduced stroke
set to eject only when they were full. Outputs were gen- rate, silent operation, and decreased incidence of RV failure
erally about 5 to 8 L per minute as long as intravascular during LVAD support. Continuous flow devices do not seek
volume status and RV function were adequate. Filling to decompress the left ventricle completely (which alters the
relied on gravity drainage augmented by residual ven- geometry of the right ventricle in an unfavorable way) but
tricular contractions. Ejection was accomplished by instead provide true left ventricular “assistance.”
either pneumatic or electrically controlled mechanical As of this writing, in the United States, it is most likely
compression of the blood chamber within the device. that a patient with an LVAD presenting for a noncardiac
First-generation pulsatile VADs have essentially been surgery has a HeartMate II LVAD (Thoratec Corporation,
supplanted worldwide by the second generation of VADs Pleasanton, CA) (Figure 9-1). The HeartMate II is a min-
and are now rarely used. iaturized axial flow pump with an internal volume of
Second-generation VADs (currently being implanted) 63 mL and a potential maximum output of 10 L per minute
provide nonpulsatile circulatory support with miniaturized against a mean arterial pressure (MAP) of 100 mm Hg.
impellers. The design of the impeller varies but can essen- The U.S. Food and Drug Administration approved the
tially be “axial” (similar to an Archimedean screw) or cen- HeartMate II as a bridge-to-transplantation in 2008 and
trifugal. Although some devices use bearings and impellers for destination therapy in 2010.
with fixed attachment, the impellers can also be magnetically More widespread acceptance of VADs has occurred as a
levitated, and some are hydrodynamically suspended by the result of a demonstrated decreased incidence of complica-
patient’s flowing blood (so-called third-generation devices). tions associated with the HeartMate II compared with
The next generation devices generally are much smaller previous LVADs, new understandings of risk factors that
than the first-generation devices, which has increased not may result in complications, increased patient management
Heart
Percutaneous
Power Power
lead exiting
lead lead
body
HeartMate II
LVAD or “heart
pump”
HeartMate II LVAS
System Controller
FIGURE 9-1 ■ Schematic of implanted HeartMate II. (Reprinted with the permission of Thoratec Corporation, Pleasanton, CA.)
42 SECTION 1 Cardiovascular System
experience over the years, significant improvement in mul- prolonged intubation predisposes to pulmonary infections
tiorgan function in patients with VADs, and very favorable and requires prolonged sedation. There is no reason for
published data from clinical trials of new continuous flow patients to remain intubated just because they have a VAD.
devices. The increasing use of VADs and enhanced survival
of patients with VADs mean that more and more patients 4. What are the goals for fluid management in a
with devices are presenting for elective noncardiac proce- patient with a left ventricular assist device?
dures. Anesthesiologists should become familiar with VADs
and related physiology. Intravascular volume status is a critical determinant of
LVAD output. Regardless of the type of device present
2. What are important preanesthetic considerations (pulsatile or continuous), intravascular volume must be
optimally maintained. Adequate “preload” was especially
for patients with a left ventricular assist device?
important with first-generation pulsatile devices that de-
The preoperative clinical status of a patient with an LVAD pended on a full blood chamber to trigger ejection, but it
is the result of multiple factors, including end-organ dam- is also very important for the current generation of non-
age sustained during low cardiac output states before VAD pulsatile LVADs. Hypovolemia resulted in hypotension
implantation, complications following implantation, cur- with pulsatile devices because the rate of LVAD filling
rent surgical problems, and preexisting comorbidities. Some slowed, which led to a slower rate of LVAD ejection and a
patients with an LVAD are ambulatory and appear to be decrease in overall output because the stroke volume was
uncompromised. Others have varying degrees of renal, he- fixed. With nonpulsatile devices, hypovolemia results in an
patic, pulmonary, or central nervous system insufficiency. underfilled arterial tree and possibly left ventricular “suck-
A thorough preoperative evaluation of all major organ sys- down” owing to the continuous nature of the LVAD
tems is essential even for minor procedures. Another con- pumping action (“suckdown” is the industry word used to
sideration is that further deterioration in the perioperative refer to the physical sucking empty of the LV). The goal
period may preclude full recovery or disqualify a patient for perioperative fluid management is to maintain a eu-
from later heart transplantation. Preoperative discussions volemic, if not slightly hypervolemic, state (assuming the
with knowledgeable colleagues, the surgeon, and the physi- right ventricle is able to handle the volume load).
cian managing the VAD are strongly encouraged. Issues to Decreased RV function is another important reason for
be considered include the following: inadequate “preload” to an LVAD, and all attempts must
• Perioperative fluid management be made to prevent abrupt increases in pulmonary vascular
• Perioperative anticoagulation resistance that may impair the ability of the right ventricle
• Perioperative antibiotic prophylaxis to get blood to the left ventricle (e.g., as a result of hyper-
• Perioperative management of pacemakers and implant- carbia, hypoxia, hypothermia, acidosis, pain, administered
able cardioverter-defibrillators (ICDs) !-agonist vasoconstrictors). The effect of surgical posi-
• Appropriate location for postoperative recovery (i.e., tioning and retractors also must be considered in regard to
postanesthesia care unit [PACU] vs. intensive care “preload,” and high intrathoracic pressures (e.g., from ex-
unit [ICU]) cessively large tidal volumes) should be avoided because
• Postoperative pain management venous return to the heart is impeded.
3. What anesthetic agents and techniques are 5. Should anticoagulation be reversed for the
appropriate for a patient with a left ventricular surgical procedure?
assist device?
There is a significant risk of thromboembolic events as-
No specific anesthetic agents are contraindicated in the sociated with extracorporeal circulation, and this requires
presence of a VAD. The selection of anesthetic agents and anticoagulation during VAD support. For example, the
the dosages used should be appropriate for the procedure HeartMate II currently requires an INR in the vicinity of
and should take into account the potentially dysfunctional twice the normal value, but ongoing experience is defin-
unsupported right ventricle in a patient with an LVAD as ing the optimal level of maintenance anticoagulation fur-
well as any other existing comorbidities as in any other pa- ther. The anesthesiologist, the surgeon, and the physician
tient. Most patients with a VAD receive a general anesthetic managing the VAD should discuss this important issue in
because of the requisite anticoagulation associated with advance to determine a safe anticoagulation regimen for
extracorporeal support through the VAD. However, in the perioperative period that balances the concern for
select cases, superficial regional blocks placed with ultra- surgical bleeding with the risk of thrombus formation and
sound guidance or a regional intravenous technique (e.g., a thromboembolism. In elective situations, requisite warfa-
Bier block) may be appropriate. Major conduction anesthet- rin therapy is sometimes discontinued preoperatively
ics (e.g., spinals, epidurals) are generally contraindicated. and converted to carefully monitored heparin infusions.
Intubation and extubation criteria are the same as for any Unless it has been discussed and agreed to beforehand,
patient. First-generation VADs were large and were im- heparin infusions should not be routinely and automati-
planted in a preperitoneal pocket, requiring “full stomach” cally discontinued “on call to the operating room” by
precautions (e.g., consideration of rapid sequence induction, the anesthesia staff. Although the surgeon usually desires
etc). The current generation of VADs has been miniatur- discontinuation of anticoagulation perioperatively, full
ized, and patients are no longer necessarily relegated reversal should not occur without agreement of the physi-
to “full stomach” status. Whenever possible, early (if not cian managing the VAD because this may result in a
immediately postoperative) extubation is desirable because thromboembolic event. If anticoagulation is to be fully
9 Patient with a Left Ventricular Assist Device Presenting for Noncardiac Surgery 43
reversed, the perioperative plan must be clearly eluci- associated with altered device behavior should be as-
dated, understood, and followed by all parties involved in sumed to be due to unrecognized EMI. All settings
the care of the patient. Most surgical procedures (except should be returned to baseline after the procedure.
possibly neurosurgical, ophthalmologic, and spine cases) A full discourse on the perioperative management of
can proceed in the presence of mild or even moderate an- pacemakers and ICDs is beyond the scope of this chapter
ticoagulation; however, scrupulous attention to hemostasis (see Chapter 7), but a comprehensive up-to-date review on
is required intraoperatively. Fresh frozen plasma or cryo- the subject was published more recently (see Suggested
precipitate or both may be infused to decrease the level of Readings). All anesthesia practitioners should become fa-
anticoagulation toward the lower limit of manufacturer’s miliar with the recommendations in the current American
recommendations. Frequent measurements of hemostatic Society of Anesthesiologists (ASA) practice advisory regard-
potential (e.g., partial thromboplastin time, thromboelas- ing perioperative management of patients with pacemakers
tography, INR) are important to balance the dual poten- and ICDs and in the 2011 expert consensus statement on
tial complications of hemorrhage and thromboembolism. this subject from the Heart Rhythm Society.
Antiplatelet medications should be discussed in advance.
8. Which monitoring devices are necessary for
6. What antibiotic coverage is necessary for a anesthetic management of a patient with a left
patient with a left ventricular assist device? ventricular assist device?
The perioperative antibiotic regimen should be appro- Standard ASA monitors (cardiac rhythm, blood pressure,
priate for the planned procedure but needs to be dis- oxygenation, ventilation, and temperature) are routine
cussed among the surgeon, the anesthesiologist, and the for every patient undergoing anesthetic procedures.
physician managing the VAD. Preoperative antibiotic First-generation LVADs essentially captured the entire
coverage for most procedures includes broad-spectrum output of the failed side of the heart and, when full,
antibiotics for gram-positive and gram-negative bacteria, ejected their physiologic “stroke volume” in a pulsatile
taking local flora into account. Antibiotics for anaerobes fashion into the arterial circulation immediately down-
are prudent for intraabdominal procedures. Antifungals stream from the failing ventricle. Standard perioperative
should be considered in patients who may be at higher monitoring was reliable; however, this is not the case
risk; this may include patients with recent treatment with with newer generation LVADs. Newer continuous flow
an antibiotic course or multiple indwelling catheters. In- devices provide nonpulsatile flow, although some pulsa-
fection of an LVAD itself is a catastrophic but rare compli- tility is often manifest during support. The two standard
cation. The most common site of infection involving ASA monitors that are potentially most affected by a
LVADs is in the tract of the percutaneous driveline that nonpulsatile circulation are noninvasive blood pressure
generally exits the body on the right side of the abdomen, and pulse oximetry measurements.
often between the upper and lower quadrants. Drivelines Noninvasive blood pressure measurements work in a
should be excluded from the sterile field by sterile drapes. patient with a continuous flow LVAD as long as there is suf-
ficient pulsatility. Although the MAP may be normal, the
7. How should implantable cardioverter-defibrillators pulse pressure often is small. Completely normal readings
and pacemakers be managed perioperatively in a (e.g., 120/80 mm Hg, MAP 93 mm Hg) may be present in
partially recovered, well-compensated euvolemic patients;
patient with a left ventricular assist device?
however, readings such as 86/65 mm Hg (MAP 72 mm Hg)
Perioperative management of pacemakers and ICDs are are commonly encountered and do not necessarily indicate
the same in patients with LVADs as in other patients. To a problem. After induction, a brief period of relative hypo-
devise a rational plan for perioperative management, one volemia from associated vasodilation results in lost pulsatil-
needs to ascertain what is present, how it is programmed, ity unless preload is adequately replenished. Pulsatility is
and that it is functioning as intended. One needs to un- routinely lost if a patient with a VAD becomes significantly
derstand the level of dependency on any pacemaker pres- hypovolemic from blood loss or major fluid shift. An inva-
ent and the expected response to magnet application. sive arterial monitoring catheter is often needed for cases
Generally, for any procedure in which electromagnetic with anticipated major fluid shifts. Because it can be difficult
interference (EMI) may be encountered (e.g., from surgi- to place arterial catheters in patients without a pulse, ultra-
cal electrocautery), ICDs should be deactivated (either sound guidance is necessary. Alternatively, it is possible to
with a magnet or with a programmer) after placement of decrease pump speed transiently to allow for increased pul-
external defibrillator pads, and patients with pacemakers sation in patients who can tolerate it. An arterial line is also
should have their device reprogrammed to an asynchro- helpful for assessment of oxygenation because pulse oxim-
nous mode (by programmer if an ICD is also present or etry does not work without a pulse. Cerebral oximetry is a
possibly by a magnet if no ICD is present). A magnet very helpful monitor of oxygenation in situations where
would not affect the behavior of a pacemaker if an ICD pulsatility is lost or there is minimal pulsatility at baseline.
is present. More recent recommendations suggest that a
site of EMI distant from the device (e.g., subumbilical 9. When are central venous catheters or pulmonary
site of surgery) poses little risk of interference with device artery catheters helpful in patients with a left
behavior. Vigilance must be maintained intraoperatively ventricular assist device?
for appropriate device function, cautery dispersal pads
should be appropriately placed to divert current away Trending of central venous pressure (CVP) measure-
from the device, and sudden hemodynamic changes ments can be helpful to understand the RV volume status,
44 SECTION 1 Cardiovascular System
and central vascular access is often used when large fluid an anesthetic if volume status and RV function are kept
shifts are anticipated. Optimal LVAD function depends on optimized.
adequate intravascular volume. Although the incidence may There are four parameters on the display: pump
be less with second-generation devices being implanted at flow, pump speed, pump power, and pulsatility index
the present time, LVADs do increase the risk of RV failure. (Figure 9-2).
Decompression of the left ventricle by an LVAD causes a Pump flow (L per minute) is an estimate of device out-
leftward shift of the interventricular septum, resulting in put derived from the speed of impeller rotation and power
altered RV geometry, increased RV compliance, and de- consumption. Flows encountered clinically usually range
creased RV contractility. Also, high output from an LVAD from 4 to 6 L per minute, but the device is capable of
increases RV preload. Sometimes this increased RV preload flowing 10 L per minute against an MAP of 100 mm Hg.
alone is enough to exacerbate RV dysfunction in patients Pump speed (rpm) is the number of revolutions
with moderate-to-severe RV dysfunction. Although an op- per minute at which the impeller is rotating. In most
timally functioning LVAD reduces RV afterload and often situations, this is a set and fixed value. Speeds encoun-
improves RV function in patients with normal pulmonary tered clinically usually range from 9000 to 9600 rpm.
vascular resistance (PVR), patients with fixed elevated PVR Increases in speed facilitate ventricular unloading by in-
may experience increased RV afterload owing to increased creasing flow through the pump. If the amount of flow
right-sided and pulmonary artery flows. Finally, moderate- exceeds the available volume in the ventricle, a “suck-
to-severe tricuspid regurgitation occasionally results from down” occurs. Decreasing the speed increases the vol-
dilation of the tricuspid anullus during LVAD support. ume in the left ventricle.
In addition to monitoring CVP to detect developing Pump power (watts) is the power required to spin the
RV failure and to guide fluid management, central ve- impeller at the set speed and is partially determined by flow.
nous access is useful for drug infusions and the potential Increases in speed or flow require increased power. Power is
introduction of transvenous pacing wires. Additionally, generally 5 to 7 W. A gradual increase in power over time
one can calculate systemic vascular resistance (SVR) by suggests developing thrombus in the pump. A sudden
substituting the VAD output for the cardiac output in the increase in power requirement may suggest significantly
hemodynamic formula. The calculation is as follows: increased afterload, thrombus, or other obstruction to rotor
rotation. One should always investigate abrupt increases in
SVR " power not explainable by an increase in pump speed.
[(MAP # CVP)/LVAD output] $ 80 dynes/sec/cm5 Pulsatility index is a unitless measure of the flow pulse
Central catheters are a potential source of sepsis (the difference between maximum flow and minimum
and should be avoided when not absolutely necessary. flow) through the device averaged over 15-second intervals.
Pulmonary artery catheters are a “double edged sword.” Pulsatility index is affected by myocardial contractility and
Although they allow for sampling of mixed venous preload and directly reflects the amount of assistance pro-
oxygen saturation and monitoring of pulmonary artery vided by the device. The relationship between pulsatility
pressures, they provide little other useful information in index and the amount of assistance is an inverse one (e.g.,
patients with an LVAD, because the LVAD console offers a higher pulsatility index indicates less assistance being
a continuous display of the “cardiac” output. Pulmonary provided, and a lower pulsatility index indicates more
artery catheters increase the risk of pulmonary artery assistance). Unless the ventricle is completely akinetic (or
rupture in patients with pulmonary hypertension. Pul- perhaps fibrillating), there is always some contractility,
monary artery catheters can be helpful in the pharmaco- which creates pulses of flow through the device, and this is
logic management of pulmonary hypertension. If the what is being measured. Optimization of preload improves
patient has a CVP catheter, SVR can be calculated with- the contractility of any ventricle through the Starling
out a pulmonary artery catheter as outlined previously.
Although it is not quantitative, one can sometimes infer
that the SVR has abruptly increased a patient with an
LVAD when the residual volume in the pump abruptly
increases (first-generation LVADs only) or if the power
readout (described subsequently) abruptly increases
(second-generation LVADs only). Transesophageal echo-
cardiography is the intraoperative monitor of choice if
one is concerned about failure of an unassisted ventricle,
if one needs to confirm volume status, or if one suspects
a device-related problem.
mechanism. In a euvolemic patient, pulsatility index is patient. The patient is always transported to the procedural
usually in the range of 4 to 6. Pulsatility index decreases suite or operating room on battery power, and unless there
with hypovolemia and increases with myocardial recovery. is a very good reason not to, as with all other life-support and
A low (or decreasing) pulsatility index likely indicates the lifesaving equipment in the operating room, it is prudent to
need to increase preload or possibly to increase contractil- ensure a connection to main A/C power during the intraop-
ity. RV dysfunction can lead to a decreased filling of the left erative period and in the recovery location (e.g., PACU).
ventricle.
12. What alarms might I hear annunciated, and of
11. How long do HeartMate II device batteries last? what alert conditions do I need to be aware?
According to the manufacturer, a pair of wearable, recharge- Various alerts may be annunciated from the controller or
able HeartMate II batteries powers the HeartMate II LVAD displayed on the clinical screen, but a thorough discussion
for approximately 3 to 5 hours, depending on the charge of all possible conditions is beyond the scope of this chap-
status of the batteries and the hemodynamic condition of the ter. Figure 9-3 shows alarm conditions, potential causes,
Yellow Controller Cell SC CELL MODULE LOW The battery module that
1 Beep Every (on System Monitor) powers the System
Replace the System Controller Battery Module.
4 Seconds DRIVER CELL LOW Controller audible alarm
(on Display Module) is depleted.
Rapidly Flashing Green
Power Symbol
1. Reconnect or tighten disconnected/loose power lead.
2. If alarm continues, check System Controller power lead and PBU power lead
One of the power leads
and 4 Green Battery 1 Beep Every POWER CABLE for damage.
is damaged or
Fuel Gauge Lights Second DISCONNECTED 3. If System Controller power lead or PBU power lead is damaged, replace the
disconnected.
Controller and/or replace thr PBU cable.
4. Obtain a new backup System Controller for this patient, if necessary.
Flashing Once Per
Second
NONE on PBU
w/System Monitor
NONE: No WARNING: Low Speed Pump is operating below Connect System Controller to System Monitor (audio alarm will stop) and
1 Beep Every 4
Warning Light Operation low speed limit. increase fixed speed setting or reduce low speed limit.
Seconds when on
Batteries or PBU
w/Display Module
FIGURE 9-3 ■ Summary of HeartMate II alarm conditions and manufacturer-suggested actions. (Reprinted with the permission of
Thoratec Corporation, Pleasanton, CA.)
46 SECTION 1 Cardiovascular System
QUESTIONS
1. Explain the physiology of transplanted hearts. 6. Which intraoperative monitors are recommended
2. Is reinnervation of the transplanted heart a for patients with a heart transplant?
concern? 7. Which emergency drugs are likely to be effective
3. Which immunosuppressive medications are in a patient with a heart transplant?
typically used after heart transplantation? 8. When antagonizing neuromuscular blockade in a
4. What are the preanesthetic concerns for patients patient with a heart transplant, do anticholinergics
with a heart transplant? also need to be given?
5. What anesthetic techniques are applicable to
patients with a heart transplant?
A 57-year-old man with hypertension, elevated serum a transplanted heart. One should not expect an
cholesterol, and mild renal insufficiency presented for increased heart rate from drugs with vagolytic
laparoscopic cholecystectomy. His past medical history actions (e.g., atropine, pancuronium, meperidine),
was significant for heart transplantation at age 55 for and similarly one should not expect a decreased
idiopathic dilated cardiomyopathy. His medications in- heart rate from drugs with vagotonic actions
cluded nifedipine, tacrolimus, azathioprine, prednisone, (e.g., acetylcholinesterase inhibitors, opioids). Drugs
atorvastatin, and omeprazole. that have both direct and indirect actions maintain
their direct effects on the denervated heart. Digoxin
maintains its positive inotropic effects on the graft
1. Explain the physiology of transplanted hearts.
but does not slow the heart rate through its para-
The donor heart is denervated during harvesting, and sympathetic mediated effects on the atrioventricular
once it is transplanted into the recipient, there is neither (AV) node.
direct efferent nor afferent neural innervation of the • Because of lack of direct sympathetic innervation
graft through autonomic or somatic pathways. Although of the heart, there are delayed and decreased sym-
denervation results in inability of the transplanted heart pathetic responses to laryngoscopy, intubation,
to respond to extrinsic neural signals, intrinsic myocar- painful stimuli, and light anesthesia. However, if a
dial mechanisms and reflexes remain intact. Although the stimulus is prolonged, increasing levels of circulat-
transplanted heart functions in isolation from the ner- ing catecholamines eventually result in an appro-
vous system, it retains the ability to respond to humoral priate tachycardia or perhaps an exaggerated one
factors circulating in the blood (e.g., catecholamines) through direct stimulation of myocardial adrener-
directly through myocardial receptors. The overall result gic receptors.
is a predictable physiology. Despite denervation, intrinsic myocardial mechanisms
The results of cardiac denervation are as follows: remain intact in the transplanted heart, as follows:
• Lack of tonic vagal input to the transplanted heart • The denervated myocardium responds normally to
results in relative tachycardia, usually around 90 to circulating or administered catecholamines (e.g., epi-
100 beats per minute. nephrine, norepinephrine) and direct-acting sympa-
• All autonomic reflexes that would normally alter thomimetic agents (e.g., isoproterenol, dobutamine)
the heart rate are gone. One should expect no through direct stimulation of myocardial adrenergic
change in heart rate with carotid massage, from receptors. In this regard, one should be aware that
acute hypertension or hypotension, or from a denervation appears to induce a downregulation of
Valsalva maneuver. !1 receptors, so most !-adrenergic receptors on the
• Drugs that alter the heart rate indirectly (i.e., via denervated myocardium tend to be of the !2 subtype.
the autonomic nervous system), either by intent or • The Frank-Starling mechanism (i.e., increased pre-
by side effect, do not have their usual effects on load results in increased stroke volume) remains
47
48 SECTION 1 Cardiovascular System
intact and is the primary mechanism for increased human graft, and there is no evidence at the present time
cardiac output in response to exercise or stress. For that reinnervation of transplanted human hearts is a
this reason, it is important to maintain adequate pre- clinically important phenomenon in the first few years
load in a patient after heart transplantation. Because after transplantation.
they already have an elevated heart rate, the only
way patients after heart transplantation can initially 3. Which immunosuppressive medications are
increase cardiac output in response to increased meta- typically used after heart transplantation?
bolic demand is through increased stroke volume.
Any further increases in heart rate and cardiac output A typical immunosuppressive maintenance regimen
with prolonged exercise or stress are the results of might consist of a selective T-cell inhibitor such as
increased levels of circulating catecholamines and are tacrolimus, a nonspecific purine antimetabolite such
slightly delayed in onset (and resolution). as mycophenolate mofetil, and a corticosteroid such
• Metabolic autoregulation of coronary blood flow in as prednisone. Characteristics of these medications are
response to changes in acid-base status (pH) and summarized in Table 10-1. Tacrolimus has replaced
carbon dioxide tension remains intact. cyclosporine because of a more favorable side-effect
• There is normal electrical impulse formation and profile. Mycophenolate is preferred over azathioprine
conductivity in the transplanted heart along the because of decreased mortality and rejection. When
usual pathways from the donor sinoatrial (SA) nephrotoxicity or malignancy is present, antiprolifera-
node, but first-degree AV block is a common find- tive agents such as sirolimus and everolimus may be
ing. Previous techniques for heart transplantation employed. In the immediate postoperative period, car-
involved leaving behind cuffs of native right and diac transplant recipients may be given interleukin-2
left atrial tissue to facilitate the anastomoses. As a receptor antagonists such as basiliximab or polyclonal
result, two P waves were seen on the electrocar- antithymocyte antibodies (Thymoglobulin), but these
diogram (ECG), one from the native heart and are unlikely to be encountered when patients present
the other from the donor heart (Figure 10-1). for noncardiac surgery.
The electrical discharge from the native SA node Although immunosuppressive agents are key to sur-
was unable to cross the suture line and did not vival after cardiac transplantation, they also have some
result in depolarization of the donor heart. Cur- very detrimental side effects. Cyclosporine and tacroli-
rent surgical technique involves bicaval anasto- mus tend to cause renal insufficiency, hepatotoxicity,
moses, so there is no native SA node left behind, hypertension, neurotoxicity, and potentially seizures by
and subsequently only a single P wave is expected lowering the seizure threshold. Azathioprine primarily
to be seen on the ECG. The cuff of left atrial tis- causes hematologic toxicity, resulting in thrombocytope-
sue contains the entry site for the four pulmonary nia and anemia, but also causes hepatotoxicity. Steroids
veins. can cause hypertension, diabetes, adrenal insufficiency,
pancreatitis, and psychiatric disturbances.
2. Is reinnervation of the transplanted heart Side effects such as those listed in Table 10-1 may
require medical management. However, other side
a concern?
effects of these medications often necessitate surgical
Whether or not significant reinnervation occurs in trans- management, and these side effects constitute some of
planted human hearts remains to be determined. There the most frequent indications for noncardiac surgery in
is laboratory evidence of varying levels of functional rein- patients after transplantation. For example, steroids
nervation in nonhuman experimental models of cardiac not only impair white blood cell function but also pre-
transplantation, and there are some reports in the litera- dispose to peptic ulceration, aseptic bone necrosis, and
ture supporting varying degrees of apparent sympathetic cataracts. Patients taking long-term high-dose steroids
reinnervation late in the posttransplantation period may present for drainage of abscesses; orthopedic pro-
("5 years postoperatively) in human patients. However, cedures on the hip, knee, elbow, or shoulder; explor-
reinnervation appears to be incomplete at best in the atory laparotomy; bowel resection for perforated viscus
FIGURE 10-1 ■ ECG strip of lead II from a patient with a cardiac transplant in sinus rhythm. Although the graft SA node is depolarizing
the transplanted heart at approximately 80 beats per minute, there is another, smaller P wave marching through this strip at an inde-
pendent rate, reflecting depolarization of the retained native SA node. The arrows indicate several native P waves; however, others
may be present, buried within the complexes, giving the appearance of an irregular rate of native SA node discharge.
10 Noncardiac Surgery after Heart Transplantation 49
and diverticulitis; and ophthalmologic procedures re- information, further information regarding prior episodes
lated to cataracts and retinal detachments. of rejection (if any) and ventricular function can usually
Cyclosporine, tacrolimus, and azathioprine tend to be obtained from the patient’s cardiologist. This infor-
cause biliary stasis, and patients taking these agents often mation from the cardiologist is especially important in
present for cholecystectomy. Nonspecific gastrointestinal patients whose transplantation was performed a few years
toxicities of these agents can also cause severe symptoms ago because a patient after cardiac transplantation is
(e.g., nausea, vomiting, diarrhea, anorexia, abdominal subject to accelerated atherosclerotic coronary artery
pain) mimicking an intraabdominal process that occa- disease (possibly the result of a vasculitis from low-level,
sionally prompts exploratory laparotomy. Sirolimus may subclinical rejection). The likelihood of significant coro-
cause oral ulcerations and poor wound healing along nary artery occlusion increases directly with time from
with severe lower extremity edema. transplantation, with a reported 10% to 20% incidence
Immunosuppression in general predisposes patients at 1 year, 25% to 45% incidence at 3 years, and 50%
to certain types of malignancies. Immunosuppressed incidence at 5 years.
patients sometimes present for diagnostic procedures Although some benign arrhythmias are common after
such as lymphoma staging, node sampling, and resection transplantation (e.g., incomplete right bundle-branch
of gynecologic or skin malignancies. block, premature atrial contractions, occasional prema-
ture ventricular contractions, and first-degree AV block),
4. What are the preanesthetic concerns for patients more ominous rhythms in the perioperative period might
be a sign of acute rejection. Given the propensity toward
with a heart transplant?
accelerated atherosclerotic disease, one should always
The primary concern preoperatively is the function of consider that new perioperative arrhythmias accompa-
the transplanted heart. Unless there is rejection, a patient nied by hypotension might be a sign of ischemia.
with a heart transplant does not usually perceive any During the preoperative evaluation, special attention
functional limitations and is classified as New York Heart should be paid to renal and hepatic function because im-
Association class I or II status. Because of a lack of affer- pairment of these organs is a major side effect of immu-
ent innervation, patients do not experience angina in nosuppressive therapy. When impairment is present, one
response to myocardial ischemia. However, just as in must carefully evaluate for acid-base and electrolyte de-
any other patient, one needs to assess the adequacy rangements. A complete blood count should be reviewed
of ventricular function. If the preanesthetic history and for anemia and thrombocytopenia because hematologic
physical examination do not provide adequate assessment toxicity is a major side effect of azathioprine.
50 SECTION 1 Cardiovascular System
Infection is a major source of morbidity and mortal- in systemic vascular resistance. An epidural technique
ity for immunosuppressed patients after transplanta- with a gradual increase of anesthetic level results in better
tion. Aseptic technique is mandatory for all invasive hemodynamic stability.
procedures, including intravenous line placement. Pro-
phylactic antibiotics are routinely employed where 6. Which intraoperative monitors are recommended
appropriate. for patients with a heart transplant?
Many immunosuppressive regimens include fairly high
doses of corticosteroids at some point. Unless the patient Monitoring requirements are the same for patients with
has recently been tapered off steroids, the issue of a a heart transplant undergoing a noncardiac procedure
preoperative “stress dose” should be discussed with the as for other patients. In the absence of rejection, graft
primary physician. function is usually fairly good, and a noninvasive blood
Finally, given the dependence of the graft on the pressure cuff and standard American Society of Anesthe-
Frank-Starling mechanism (discussed previously), one siologists monitors usually suffice. Invasive monitoring
must ensure an adequate intravascular volume status of arterial and central venous pressures is generally
before anesthetic induction. employed only if there is hemodynamic instability or if
indicated by the planned procedure. Required endomyo-
5. What anesthetic techniques are applicable to cardial biopsies to monitor rejection are preferentially
performed via the right internal jugular vein, and one
patients with a heart transplant?
should use the left internal jugular or subclavian veins
General, spinal, and epidural anesthesia; regional block- for central access if possible. When available, transesoph-
ade (e.g., axillary block, wrist block, ankle block, Bier ageal echocardiography may be preferable to invasive
block); and local anesthetic infiltration all have been used monitoring.
successfully in patients with a heart transplant, and the
requirements are similar to other patient populations. In 7. Which emergency drugs are likely to be effective
terms of general anesthesia, the choice of agent is not in a patient with a heart transplant?
so crucial as how the agent is employed. Generally, the
overwhelming experience is that induction agents, ben- Only direct-acting inotropic and chronotropic agents
zodiazepines, opioids, and inhaled potent volatile agents are immediately effective. Epinephrine is usually the
are usually well tolerated. All the usual caveats apply in direct-acting inotropic agent of choice. Direct-acting
the presence of renal or hepatic dysfunction. Just as in chronotropic agents include epinephrine, isoprotere-
any other patient, one must titrate to effect. Whenever nol, and dobutamine. Pacing (via external pacing pads
possible, one should plan a technique that allows early or a transvenous pacing wire) is also an option to
(if not immediate) postoperative extubation because increase heart rate. For reasons previously discussed,
prolonged intubation may increase the chances of pul- atropine is not likely to increase heart rate in the
monary infection. denervated graft. Vasoconstrictors (including phenyl-
The plasma levels of various anesthetic agents that ephrine, norepinephrine, and vasopressin) act on the
depend on P-450 metabolism may be increased or de- vasculature directly and are not affected by the dener-
creased by immunosuppressive agents and anticonvul- vated status of donor organs. For most situations, small
sants and can themselves alter immunosuppressant bolus doses of epinephrine and phenylephrine are
blood levels. This situation can be potentially danger- effective, and these are used as first-line agents when
ous if increased blood levels of immunosuppressant necessary.
agents result in undesirable side effects (e.g., nephro- Ephedrine is a noncatecholamine sympathomimetic
toxicity of cyclosporine and tacrolimus). For example, agent with direct and indirect actions on $-adrenergic
agents that compete for P-450 metabolism (e.g., furose- and !-adrenergic receptors. The indirect actions of
mide) can decrease cyclosporine elimination resulting ephedrine come from enhanced release of norepineph-
in increased blood levels. Conversely, agents that in- rine. Although ephedrine can be used advantageously in
crease cyclosporine metabolism (e.g., barbiturates) can a patient with a heart transplant, it is not usually consid-
reduce blood levels. ered a first-line emergency drug because at least part of
It is believed that neuromuscular blockade is aug- its desired action must await the subsequent release of
mented by cyclosporine and can be antagonized by norepinephrine.
anticonvulsants often given to patients taking azathio- Dopamine has both direct and indirect effects. It is
prine, but this should not pose a problem if neuromus- the immediate precursor of and causes the release of nor-
cular blockade is closely monitored. The dose for muscle epinephrine. In a patient after cardiac transplantation,
relaxants is not altered. dopamine would initially be expected to exert only its
Regardless of technique, volume depletion and acute direct dopaminergic effects (e.g., coronary and splanch-
vasodilation (e.g., as may occur with spinal anesthesia) are nic arterial vasodilation) through dopaminergic recep-
poorly tolerated because the transplanted heart initially tors. The vasoconstrictive $-adrenergic effects and the
depends on the Frank-Starling mechanism to maintain desired !-adrenergic effects on heart rate and contractil-
cardiac output. Sudden vasodilation is not compensated ity come only from subsequently released norepineph-
by reflex tachycardia. One can perform a spinal anesthetic rine. Taking into account all of these effects, dopamine
in a patient with a heart transplant, but one must be pre- may not be the optimal first-line choice when inotropy or
pared to augment preload and prevent sudden decreases chronotropy is urgently needed.
10 Noncardiac Surgery after Heart Transplantation 51
QUESTIONS
1. What are the major determinants of myocardial 5. What intraoperative monitoring techniques can be
oxygen supply and demand? used to detect myocardial ischemia?
2. How is coronary artery disease treated, and which 6. What are the advantages and disadvantages of
medications should be continued perioperatively? on-pump versus off-pump coronary artery bypass
3. What are the preanesthetic concerns in a patient grafting?
with coronary artery disease? 7. What are unique anesthetic considerations related
4. What anesthetic technique is used for coronary to off-pump coronary artery bypass grafting?
artery bypass grafting?
A 72-year-old man with a history of smoking, hyperten- artery supplies the lateral wall and in left dominant
sion, diabetes mellitus type 2, and mild chronic renal in- circulation (15% of people) gives rise to the poste-
sufficiency presented for off-pump coronary artery bypass rior descending artery.
grafting (OPCAB). Preoperative cardiac catheterization • Coronary perfusion pressure (CPP). CPP is deter-
revealed three-vessel coronary artery disease (CAD) with mined by the difference between aortic pressure
65% stenosis of the left main coronary artery, 95% steno- and ventricular pressure. During systolic contrac-
sis of the mid-left anterior descending artery, 75% stenosis tion, the pressure in the left ventricle approaches
of the circumflex artery, and 80% stenosis of the right aortic pressure, so no coronary perfusion occurs
coronary artery. Transthoracic echocardiography showed during this time. The left ventricle is almost
normal left ventricular function without significant valvu- entirely perfused during diastole, whereas the
lar abnormalities. His medications were metoprolol, lisin- right ventricle is perfused during both systole
opril, aspirin, metformin, and sublingual nitroglycerin. and diastole. CPP for the left ventricle is the
difference between the aortic diastolic pressure
1. What are the major determinants of myocardial (ADP) and the left ventricular end-diastolic pres-
sure (LVEDP):
oxygen supply and demand?
The myocardium normally extracts 65% of the oxygen in CPP ! ADP " LVEDP
arterial blood compared with extraction of 25% by other • Heart rate. Because nearly all perfusion of the left
tissues. An increase in myocardial demand for oxygen can ventricle occurs during diastole, the duration of
be met only by an increase in coronary blood flow, not by diastole is also a significant determinant of coro-
increased oxygen extraction. nary perfusion. Increases in heart rate result in a
The major determinants of myocardial oxygen supply disproportionately greater decrease in diastolic
include the following: time resulting in decreased coronary perfusion.
• Coronary anatomy. Myocardial blood supply derives • Arterial oxygen content. Hemoglobin concentration
from the left and right coronary arteries. The right and oxygen saturation need to be optimized to
coronary artery normally supplies the right atrium maintain adequate supply. The optimal hemoglo-
and most of the right ventricle and in right domi- bin concentration and transfusion trigger remain a
nant circulation (85% of people) gives rise to the matter of debate.
posterior descending artery, which supplies part The major determinants of myocardial oxygen demand
of the interventricular septum and the inferior wall include the following:
of the left ventricle. It also usually supplies the sino- • Basal oxygen requirements. Basal requirements account
atrial node (60% of patients) and the atrioventricu- for about 20% of the oxygen requirements.
lar node (85% of patients). The left coronary artery • Left ventricular wall tension (T). T is directly propor-
bifurcates into the left anterior descending artery tional to the intraventricular pressure (P) and ventricu-
and the circumflex arteries. The left anterior de- lar radius (r) and inversely proportional to ventricular
scending artery supplies the septum of the left ven- wall thickness (h): T ! Pr/2h. Increases in either pre-
tricle and the anterior wall, whereas the circumflex load (increased radius) or afterload (increased pressure)
52
11 Coronary Artery Bypass Grafting 53
increase T and oxygen demand. The increase in previous coronary artery stent procedure, necessitating
oxygen demand secondary to an increase in afterload treatment with aspirin and clopidogrel to prevent early
is usually compensated by an increase in CPP and stent thrombosis. Antiplatelet therapy is also used after
oxygen supply. CABG to reduce postoperative ischemic complications.
• Heart rate. Increases in heart rate increase oxygen Aspirin has strong efficacy in the prevention of early
demand, while decreasing oxygen supply, increasing graft thrombosis after CABG. However, controversy ex-
the potential for myocardial ischemia. ists in regard to preoperative antiplatelet therapy. The
• Contractility. Decreased myocardial contractility risk of hemorrhagic complications needs to be weighed
is associated with smaller oxygen requirements. against the potential antiischemic benefits of antiplatelet
However, if CPP is decreased, the oxygen supply therapy.
is decreased. The premature discontinuation of antiplatelet therapy in
patients with coronary artery stents presenting for noncar-
2. How is coronary artery disease treated, and which diac surgery increases the risk of stent thrombosis, myocar-
dial infarction, and death. It is ideal to delay elective noncar-
medications should be continued perioperatively?
diac surgery for 4 to 6 weeks after bare metal stent
To avoid ischemia, a balance between myocardial oxygen implantation and at least 12 months after drug-eluting stent
supply and demand must be maintained. The medications implantation. If surgery cannot be postponed, a discussion
used to treat CAD attempt to maintain this balance by with the surgeon and the patient’s cardiologist is necessary
either reducing the demand for or increasing the supply to determine the risk versus benefit of temporarily stopping
of myocardial oxygen. antiplatelet therapy compared with the risk of bleeding
complications. If it is determined that clopidogrel therapy
needs to be interrupted, owing to the risk of bleeding com-
!-Adrenergic Blockers
plications, aspirin therapy should be continued if possible,
By antagonizing the effects at # receptors, these agents and clopidogrel should be restarted as soon as possible.
reduce heart rate (increasing diastolic time) and contrac-
tility. Myocardial oxygen consumption is decreased, and 3-Hydroxy-3-methylglutaryl-coenzyme
coronary perfusion is improved. # Blockers are beneficial
A Reductase Inhibitors (Statins)
for most patients with CAD, particularly if their heart
rates are increased. When acutely administered in ade- 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG CoA)
quate dosage, # blockers have been shown to significantly reductase inhibitors have a variety of important effects in-
reduce myocardial oxygen demand and the incidence of dependent of their primary purpose as lipid-lowering
atrial and ventricular arrhythmias. The current American agents. They appear to possess potent antiinflammatory
College of Cardiology/American Heart Association and antithrombotic effects. Statins have also been shown to
(ACC/AHA) guidelines on perioperative cardiovascular decrease myocardial reperfusion injury after cardiac sur-
evaluation and care for noncardiac surgery recommend gery. The current ACC/AHA guidelines on perioperative
that # blockers should be continued in patients who have cardiovascular evaluation and care for noncardiac surgery
been taking them before surgery and should be started in recommend continuing statins in patients currently taking
patients who are at high risk for cardiovascular disease, as them and considering starting statins in patients with at
defined by the presence of more than one clinical risk least one clinical risk factor (see Box 11-1) undergoing
factor (Box 11-1), and who are undergoing high-risk or intermediate-risk surgery. Postoperative withdrawal of
intermediate-risk surgery. statin treatment is independently associated with increased
in-hospital mortality after CABG.
Antiplatelet Agents
Intraaortic Balloon Pump
Many patients present for coronary artery bypass grafting
(CABG) while being treated with platelet inhibitors. An intraaortic balloon pump is a mechanical device that
Aspirin is a well-recognized component of primary and increases myocardial oxygen perfusion while increasing
secondary prevention strategies for all patients with CAD. cardiac output and myocardial oxygen delivery. It ac-
The combination of aspirin and clopidogrel has been tively deflates in systole, increasing forward blood flow
shown to improve outcome after acute coronary syn- by reducing afterload. It actively inflates in diastole,
drome. Many patients presenting for CABG underwent a increasing blood flow to the coronary arteries. These
actions combine to decrease myocardial oxygen de-
mand and increase myocardial oxygen supply. The
preoperative use of intraaortic balloon pumps in high-
BOX 11-1 Clinical Risk Factors (Revised risk patients undergoing CABG has shown promising
Cardiac Risk Index) results in improving outcomes.
• History of ischemic heart disease
• History of congestive heart failure 3. What are the preanesthetic concerns in a patient
• History of cerebrovascular disease with coronary artery disease?
• Diabetes mellitus
• Renal insufficiency The anesthesiologist needs to be aware of any comor-
bidities the patient has and plan accordingly. Patients
54 SECTION 1 Cardiovascular System
with CAD often have a history of hypertension, diabetes, 5. What intraoperative monitoring techniques can be
cerebrovascular disease, and chronic renal disease. Many
used to detect myocardial ischemia?
also have a history of smoking.
Patients with hypertension have intravascular hypo- Intraoperative detection of ischemia depends on the rec-
volemia and may become hypotensive after induction ognition of ischemic changes by ECG, hemodynamic
of anesthesia. Patients with severe diabetes mellitus manifestations, and new-onset regional wall motion ab-
are at risk for autonomic and peripheral neuropathy normalities (RWMAs) seen on transesophageal echocar-
that can lead to silent myocardial ischemia and delayed diography (TEE).
gastric emptying. Appropriate prophylaxis for a “full • ECG. The simultaneous monitoring of leads V5 (ante-
stomach” should be considered. If a patient has signifi- rior wall) and II (inferior wall) allows for the detection of
cant cerebrovascular disease, a higher blood pressure 90% of ischemic episodes. In addition, this monitoring
is required to maintain cerebral perfusion pressure. allows for detection of atrial and ventricular dysrhyth-
Chronic renal disease may affect the elimination of mias, another possible manifestation of ischemia. Early
certain medications. ischemic changes usually involve T-wave inversions
Premedication in the preoperative period may be very followed by ST segment depression.
important in a patient presenting for CABG. Premedica- • TEE. The earliest sign of myocardial ischemia is
tion with benzodiazepines and opioids reduces apprehen- systolic RWMAs, which occur within seconds of
sion and provides analgesia for potentially painful events reduced coronary perfusion. TEE is more sensitive
before induction (e.g., vascular cannulation). This pre- than ECG at detecting myocardial ischemia. The
medication may help prevent preoperative anginal epi- routine use of TEE is now recommended for all
sodes elicited by tachycardia secondary to anxiety or patients undergoing CABG or OPCAB surgery.
painful stimuli. After premedication, all patients should The transgastric short-axis midpapillary muscle
receive supplemental oxygen and monitoring with pulse view of the left ventricle is commonly used because
oximetry, electrocardiogram (ECG), and noninvasive it visualizes myocardium supplied by all three major
blood pressure. coronary arteries. New RWMAs detected intraop-
eratively are not specific for myocardial ischemia
4. What anesthetic technique is used for coronary because they may frequently occur secondary to
artery bypass grafting? nonischemic causes, such as changes in loading con-
ditions, alteration in cardiac electrical conduction,
A balanced general anesthetic is the most commonly post-CPB pacing, or poor myocardial preservation.
performed anesthetic technique, but it needs to be tai-
lored to the individual patient. Most hypnotics, opioids, 6. What are the advantages and disadvantages of
and volatile agents have been used in different combina- on-pump versus off-pump coronary artery bypass
tions for the induction and maintenance of anesthesia
grafting?
with good results. The main considerations in choosing
an induction technique for patients undergoing CABG For many years, CABG was primarily performed with
are left ventricular function and coronary pathology. Ad- the use of CPB, which allowed for a bloodless and
ditionally, limiting the amount of opioids or the use of immobile surgical field. Conventional CPB and aortic
short-acting drugs is encouraged in patients eligible for cross-clamping risks generalized systemic inflammatory
fast-tracking and early extubation. responses that cause hemodynamic instability and affects
Interest in thoracic epidural anesthesia for cardiac sur- all organs, especially the heart, lungs, and kidneys. Cere-
gery, whether as the primary anesthetic technique or as a bral dysfunction likely results from emboli that dislodge
supplement to general anesthesia, has steadily increased. from the aorta during cross-clamping, cannulation, and
Thoracic sympathectomy appears to have favorable proximal vein graft anastomosis. The introduction of
effects on the heart and coronary circulation. Heightened OPCAB into practice was an attempt to decrease the
concerns about the risk of devastating neurologic injury adverse clinical consequences of conventional CPB and
secondary to the profound anticoagulation needed for aortic cross-clamping.
cardiopulmonary bypass (CPB) have limited its routine The introduction of mechanical stabilizer devices that
use in the United States. minimized motion around the anastomosis site (indepen-
Steadily increasing evidence from laboratory and clin- dent of heart rate) allowed for performing CABG with-
ical studies suggests that inhalation anesthetic agents out the use of CPB (i.e., “off-pump”). The ability to ex-
have favorable properties in patients undergoing CABG. pose the posterior surface of the heart to access the
There has been a major resurgence in their popularity as posterior descending and circumflex arteries was vital for
the primary anesthetic in patients undergoing cardiac the multivessel application of this technique. This ability
surgery owing to the current routine use of fast-track depends on placing suction devices on the apex of the
anesthesia techniques. Inhalation anesthetics are thought heart without producing major hemodynamic compro-
to protect the myocardium against ischemia by their abil- mise. About 30% of CABG procedures are likely per-
ity to elicit the same protective cellular responses that are formed off-pump.
seen with ischemic preconditioning. The latter has been Numerous studies analyzing whether OPCAB reduces
shown to reduce myocardial infarction size after periods morbidity and mortality compared with conventional
of ischemia. CABG have reported conflicting results. The final word
11 Coronary Artery Bypass Grafting 55
regarding difference in outcome and which patients may multiple comorbidities may be scheduled for OPCAB to
benefit from an OPCAB technique is still years away. avoid CPB and aortic cross-clamping.
Anticoagulation in patients undergoing OPCAB is
7. What are unique anesthetic considerations an area of controversy. Some surgeons prefer low-dose
related to off-pump coronary artery bypass heparinization (e.g., 100 to 200 units/kg heparin) with a
target activated clotting time (ACT) of 250 to 300 seconds,
grafting?
whereas others choose full heparinization (e.g., 300 units/kg)
The continuous, intensive involvement of the anesthesi- with a target ACT of greater than 480 seconds during the
ologist is perhaps more crucial during OPCAB than procedure. ACT is measured every 30 minutes, and heparin
during on-pump CABG. Relative to on-pump CABG, is administered to maintain the target ACT.
OPCAB extends the range of surgeon-induced hemody-
namic changes the anesthesiologist encounters. Surgical
manipulations can cause various cardiac anatomic distor- SUGGESTED READINGS
tions including compression of the right ventricle and Despotis GJ, Joist JH: Anticoagulation and anticoagulation reversal
distortion of the mitral valve anulus. Anesthesiologists with cardiac surgery involving cardiopulmonary bypass: an update.
must be able to anticipate and communicate with J Cardiothorac Vasc Anesth 13(4 Suppl 1):18, 1999.
surgeons to minimize the adverse impact of these changes Fuster V, Moreno PR, Fayad ZA, et al.: Atherothrombosis and high-risk
plaque: part I: evolving concepts. J Am Coll Cardiol 46:937, 2005.
on the heart and other vital organs. With a skilled sur- Lombard FW, Mathew JP: Neurocognitive dysfunction following
geon, the changes are usually modest or easily treated by cardiac surgery. Semin Cardiothorac Vasc Anesth 14:102, 2010.
the Trendelenburg position, judicious volume expansion, POISE Study Group, Devereaux PJ, Yang H, Yusuf S, et al.: Effects
and use of vasoconstrictors or inotropes. However, severe of extended-release metoprolol succinate in patients undergoing
changes secondary to acute ischemia, unrecognized right non-cardiac surgery (POISE trial): a randomised controlled trial.
Lancet 371:1839, 2008.
ventricular compression, or severe mitral regurgitation Raphael J: Physiology and pharmacology of myocardial preconditioning.
may occur, necessitating emergent conversion to CPB. Semin Cardiothorac Vasc Anesth 14:54, 2010.
The anesthesia technique in patients undergoing OP- Schwann NM, Hillel Z, Hoeft A, et al.: Lack of effectiveness of the
CAB does not differ much from the anesthesia technique pulmonary artery catheter in cardiac surgery. Anesth Analg
113:994, 2011.
for on-pump CABG. It can depend on the indication for Shroyer AL, Grover FL, Hattler B, et al.: Veterans Affairs Randomized
OPCAB. Patients with advanced age, significant ascend- On/Off Bypass (ROOBY) Study Group: On-pump versus off-pump
ing aortic disease, poor left ventricular function, and coronary-artery bypass surgery. N Engl J Med 361:1827, 2009.
S ECTI O N 2
RESPIRATORY SYSTEM
56
CASE 12
One-Lung Ventilation
Steven M. Neustein, MD • James B. Eisenkraft, MD
QUESTIONS
1. Describe the anesthetic evaluation before lung 8. What clinical problems are associated with
resection. placement and use of double-lumen endobronchial
2. How are ventilation and oxygenation monitored tubes?
noninvasively during surgery, and how do these 9. What complications are related to placing the
monitors work? patient in the lateral decubitus position?
3. What are the indications for one-lung ventilation? 10. How are pulmonary perfusion and ventilation
4. Describe the use of single-lumen endotracheal altered during one-lung ventilation?
tubes and bronchial blockers for one-lung 11. How is hypoxemia that occurs during one-lung
ventilation. ventilation treated?
5. If a double-lumen tube is to be used, which would 12. Describe the role of a thoracostomy tube after
be preferable, a left-side or right-side tube? pulmonary resection.
6. Describe the proper technique for placing a 13. Describe a commonly used pleural drainage
double-lumen endobronchial tube. system.
7. How is correct positioning of the double-lumen 14. What are the potential complications after
endobronchial tube assessed? thoracotomy?
A 70-year-old man presents for resection of a left up- and atelectasis and to guide bronchodilator therapy.
per lobe tumor. He has a long history of cigarette Spirometry is a noninvasive test that provides data on
smoking. lung volumes and gas flow rates. Flows are tested before
and after bronchodilator therapy, such as albuterol
1. Describe the anesthetic evaluation before lung by inhaler, to determine reversible obstructive airway
disease. Improved flows after bronchodilator therapy
resection. indicate preoperative adjustments in the bronchodilator
Preoperative evaluation begins with the same basic regimen.
information required before all anesthetics. Next, it is Pulmonary function tests that may correlate with out-
determined whether the patient is in optimal condition come include forced expiratory volume in 1 second
for the planned procedure or whether further preopera- (FEV1), forced vital capacity (FVC), maximum voluntary
tive evaluation or preparation is indicated. Finally, ventilation, and ratio of residual volume to total lung
an assessment is made to predict lung function after capacity (RV/TLC). Based on how much lung tissue is to
resection. Specific pulmonary evaluation includes be resected, predicted postoperative (PPO) function can
history of cough, sputum production, chest pain (pos- be calculated. A PPO FEV1 !40% has been associated
sibly pleuritic), dyspnea, wheezing, arm pain (resulting with improved outcome. FVC "50% of predicted or
from a Pancoast tumor invading the brachial plexus), RV/TLC !50% of predicted may indicate higher risk.
weakness (resulting from myasthenic syndrome), other Spirometry reflects respiratory mechanics, whereas
endocrine syndromes (caused by tumors secreting gas exchange is assessed by measuring the diffusing
hormones), and weight loss (hypoproteinemia). Physical capacity for carbon monoxide (DLCO). A PPO DLCO
examination includes auscultation for wheezing, rales, "40% indicates reduced lung parenchymal function and
and rhonchi. Wheezing may require treatment with is a predictor of increased risk.
bronchodilators, and infected sputum is treated with Cardiopulmonary reserve can be evaluated by measuring
antibiotics. Chest radiograph, tomography, computed the maximal oxygen consumption (V̇O2max). A V̇O2max
tomography, and magnetic resonance imaging provide "10 mL/kg/min indicates very high risk, and a V̇O2max
further information about the tumor site, structures !20 mL/kg/min indicates reduced risk. Other tests of car-
involved, and possible airway compromise. diopulmonary reserve include exercise oximetry, in which a
Lung function tests are indicated to predict the risk of decrease in oxygen saturation by pulse oximetry (SpO2) of
respiratory failure, right heart failure (cor pulmonale), 4% during exercise may indicate increased risk. A simple
57
58 SECTION 2 Respiratory System
test is stair climbing; inability to climb more than one flight of arterial blood (CaO2) is given by the following
of stairs is associated with increased risk, and ability to climb equation:
three or more flights of stairs reflects decreased risk.
If lung function results are poor, split lung function CaO2 $ [(Hb % 1.34 % SaO2) & (PaO2 % 0.003)]
testing (ventilation/perfusion radiospirometric studies)
can be done to allow calculation of PPO lung function. Normal arterial oxygen content can be calculated by
Ultimately, the operative decision to perform pneumo- substituting variables as shown, assuming that the patient
nectomy versus lobectomy versus wedge resection is a is breathing room air, the SpO2 is 97%, and the PaO2 is
clinical one in which the patient’s overall condition is 97 mm Hg:
considered.
CaO2 $ [(15 % 1.34 % 0.97) & (97 % 0.003)]
2. How are ventilation and oxygenation monitored $ 19.5 & 0.29
noninvasively during surgery, and how do these $ approximately 20 mL oxygen/100 mL blood
monitors work?
However, this calculation requires invasion of an ar-
The purpose of ventilation is to remove carbon dioxide tery for blood sampling.
(CO2) from the lungs. The average 70-kg man produces Noninvasive monitoring of oxygenation is most com-
approximately 220 mL per minute of CO2 and normally monly achieved using pulse oximetry, which is a standard
maintains an arterial carbon dioxide tension (PaCO2) of of care. Pulse oximetry uses a combination of two tech-
40 mm Hg. If removal of CO2 is impaired or if production nologies: (1) spectrophotometry of oxygenated and deoxy-
increases and ventilation does not increase, PaCO2 in- genated Hb and (2) optical plethysmography. The latter
creases. Arterial blood gas analysis provides the ultimate detects pulsatile components of changes in light transmit-
monitor of ventilation: PaCO2. In the lungs, CO2 diffuses ted through tissue. Each pulse oximeter probe has two
into alveoli, and in areas where ventilation and perfusion light-emitting diodes that emit light at 660 nm and 940 nm
are well matched, alveolar CO2 tension (PACO2) approxi- as well as one photodetector. The ratio of the pulse-added
mates PaCO2. PACO2 may be sampled as end-tidal carbon absorbances at 660 nm to that at 940 nm is related through
dioxide (PETCO2) and analyzed by various technologies to an empirically derived algorithm, to a saturation estimate
provide a noninvasive estimation of PaCO2. Overall, that is designated SpO2. Pulse oximeter readings have
PETCO2 is normally 4–6 mm Hg less than PaCO2. In- a standard deviation of approximately &2% in the satura-
creases in physiologic dead space or a decrease in alveolar tion range of 70%–100%. The accuracy decreases at lower
ventilation results in increased PaCO2. SpO2 levels. Nevertheless, pulse oximeters are valuable
Capnography is the science of measuring and displaying as monitors of saturation trends. Pulse oximeters are inac-
CO2 as a concentration plotted against time (capnogram). curate or may fail in the presence of poor perfusion (e.g.,
The CO2 concentration in gas mixtures may be measured vasoconstriction from low cardiac output or cold extremi-
using many technologies, the most common of which is ties), venous pulsations, severe peripheral vascular disease,
infrared light spectroscopy. Although mass spectrometry, intravascular dyes, dyshemoglobins, certain nail polishes,
infrared (IR) acoustic spectroscopy, and Raman scattering and certain pigmentations. If doubt exists regarding the
have been used in the past, the monitors that used these validity of pulse oximeter readings, an arterial blood gas
technologies are no longer in production. IR light spec- sample should be drawn for blood gas tension analysis and
troscopy is based on 4.3 #m (4300 nm) wavelength IR ra- saturation analysis in a laboratory cooximeter.
diation absorbance by intermolecular bonds in the CO2
molecule. The greater the number of CO2 molecules pres- 3. What are the indications for one-lung ventilation?
ent, the greater the absorbance of radiation. Gas is drawn
through a sample cell (cuvette), and IR light of 4.3 #m is One-lung ventilation is indicated for isolation and protec-
passed through the cell. Transmission of light through the tion of one lung from contamination by the other lung or
gas sample to a photodetector is inversely proportional to for selective ventilation of one lung only. Indications for
the tension of CO2 in the gas sample. Such systems are in separating the lungs include prevention of blood or pus
widespread use, and sampling may be of the sidestream or spillage and bronchopulmonary lavage. Situations in which
mainstream (in the airway) design. hemorrhage or infectious material might affect the contra-
By continuously following the tension of CO2 lateral lung include bronchiectasis, lung abscess, and hemo-
against time, the highest value is designated end-tidal ptysis. The ability to control the distribution of ventilation
and defines exhalation, and the lowest value is desig- between lungs improves exposure for thoracic surgery.
nated inspiratory and defines inspiration. Continuous Positive pressure ventilation through a single-lumen tube
capnography is considered the standard of care because risks losing large amounts of tidal volume through a bron-
it provides a continuous monitor of ventilation and, chopleural fistula or pneumothorax in the case of a giant
with certain limitations, can provide a noninvasive unilateral lung cyst. Surgical exposure is improved during
estimate of PaCO2. pneumonectomy, descending thoracoabdominal aortic
Oxygenation is monitored best by sampling arterial aneurysm repair, and resection of midesophageal and upper
blood and analyzing it for tension (PaO2), hemoglobin esophageal lesions. One-lung ventilation is needed for
(Hb) saturation with oxygen (fractional saturation, video-assisted thoracoscopy because the surgeon cannot
i.e., O2Hb/total Hb), and total Hb. The oxygen content operate endoscopically on an inflated lung.
12 One-Lung Ventilation 59
4. Describe the use of single-lumen endotracheal side of thoracotomy. Placement of a left-side DLT is
tubes and bronchial blockers for one-lung frequently prudent. In an adult, the left main stem
ventilation. bronchus is 5–6 cm in length, and the right main stem
bronchus is 1.5 cm in length. The right upper lobe
Bronchial blockers can be placed through single-lumen bronchus is more likely to be accidentally occluded by
tracheal tubes. This practice eliminates the need for the endobronchial tube than the left upper lobe bron-
changing a single-lumen tube to a double-lumen tube chus. Resection of the left lung necessitates continuous
(DLT) at the beginning of a case in which single-lumen ventilation of the right lung. Obstruction of the right
tubes had been placed for an initial bronchoscopy. It also upper lobe bronchus is likely to lead to hypoxemia during
eliminates the need for replacing DLTs with single- one-lung ventilation. For this reason, some anesthesiolo-
lumen tubes at the conclusion of surgery. That might be gists routinely place a left-side DLT regardless of the side
required if bronchoscopy is performed or preferred if of surgery, unless it is specifically contraindicated because
the patient’s airway is to be kept intubated. When using of the presence of a diseased left main stem bronchus or
bronchial blockers, single-lumen tubes of sufficient di- if the bronchus is likely to become part of the surgical
ameter are employed to accommodate both the blocker field, such as in a sleeve resection. If a left-side DLT is
and a fiberscope, which is needed for correct placement. placed too distally, it may lead to hypoxemia if the left
Endotracheal tubes cannot be too close to the carina, upper lobe is not adequately ventilated.
especially in the case of left-sided thoracic surgery, Some anesthesiologists routinely place the endobron-
because there will not be enough space to manipulate chial tube on the side ipsilateral to the pulmonary resec-
a blocker into the left main stem bronchus. It may be tion. With this arrangement, obstruction of the upper
necessary to rotate the endotracheal tube such that the lobe bronchus by the endobronchial tube is not as likely
concave side is on the left or to turn the patient’s head to to cause hypoxemia because this is the lung that is
the right for the bronchial blocker to enter the left main deflated during one-lung ventilation, and oxygenation
stem bronchus. continues via the tracheal lumen. Also, before chest clo-
The most commonly used bronchial blockers are the sure, reinflation of the remaining lung ipsilateral to the
Uniblocker (Fuji Systems, Tokyo, Japan), Cohen blocker tube can be verified by direct inspection. If the upper
(Cook, Bloomington, IN), and Arndt blocker (Cook). lobe fails to reinflate, the bronchial cuff is deflated so that
The first commercially available blocker was the Univent the upper lobe can be ventilated from the tracheal lumen.
tube (Fuji Systems). The Univent tube is a combined Alternatively, the DLT can be withdrawn until the distal
single-lumen endotracheal tube and an integral bronchial end of the endobronchial tube is proximal to the upper
blocker. The single-lumen tube is equipped with a nar- lobe bronchial orifice, or the side opening in the DLT
row internal lumen through which a balloon-tipped can be realigned with the right upper lobe orifice. In the
bronchial blocker is advanced into the right or left main case of a pneumonectomy, an ipsilaterally placed tube
stem bronchus. With the bronchial blocker retracted and must be withdrawn to a position where the distal end of
deflated, the tube is positioned by standard techniques the tube is in the trachea before division of the main stem
into the trachea. The tube is turned 90 degrees toward bronchus. Withdrawal may also become necessary if the
the side to be blocked, and the blocker is advanced under intubated bronchus is involved in the surgery.
flexible fiberoptic bronchoscopic guidance into the A different approach used by a smaller percentage of
appropriate bronchus. The balloon is inflated, and lung anesthesiologists is to place the DLT routinely into the
separation is confirmed by auscultation of breath sounds. nonoperative side. This strategy prevents damage from
More rapid collapse of the lung follows deflation of the placing the tube into a diseased bronchus. However,
blocker balloon and disconnection from the anesthesia placement of a right-side DLT for a left thoracotomy may
breathing circuit. After successful lung collapse, reinfla- lead to hypoxemia during one-lung ventilation, as dis-
tion of the blocker’s balloon and connection to the anes- cussed earlier. This approach may be the most prudent
thesia breathing circuit allow for ventilation of one lung course in the case of pneumonectomy, or sleeve resection,
and collapse of the other. The blocker of the Univent because surgery would not be affected by the presence of
tube is now available as an independent blocker, the Uni- a tube.
blocker, which is bent near the tip. Because the lumen of
a bronchial blocker is small, deflation of the blocked lung
6. Describe the proper technique for placing
is slower than when a DLT with larger lumens is used.
When placed, a blocker tends to dislocate more than a a double-lumen endobronchial tube.
DLT, especially when placed on the right side because The largest size DLT that can easily pass the glottis may
of its location near the carina. There is more space in be preferred. The advantages of placing a larger size tube
the left main stem bronchus to seat the balloon of the are as follows:
bronchial blocker. • Less air is required to inflate the endobronchial tube
cuff.
5. If a double-lumen tube is to be used, which would • A large lumen facilitates suctioning.
• Malposition of the tube distally in the bronchus is
be preferable, a left-side or right-side tube? less likely.
There is no one correct answer to this question. Differ- Clear polyvinyl chloride disposable Robertshaw-type
ent approaches to the choice of DLTs depend on the DLTs are available in sizes 41F, 39F, 37F, 35F, and 28F
60 SECTION 2 Respiratory System
intended for intubation, and slide the tube distally using the
fiberscope as a guide until resistance is met. If the trachea
was easy to intubate, instead of remanipulating the tube
within the patient, the tube can be removed from the
patient entirely, and the procedure can be repeated.
A right-side tube almost always goes to the correct
(right) side, but a left-side tube sometimes passes to the
wrong side. A left-side tube should not be allowed to
remain in the contralateral side because there is no open-
ing for the right upper lobe bronchus on a left-side tube.
Rotating the patient’s head to the right, as is performed
for left endobronchial rigid bronchoscopy, may facilitate
passage of the tube to the left side.
Ventilation of the lung while the endobronchial lumen
is clamped should provide breath sounds and chest move-
ment only on the side opposite the bronchus intended for
intubation, provided that the tube has been placed in the
appropriate bronchus (Figure 12-4). Inability to ventilate FIGURE 12-6 ■ Left endobronchial tube is placed too shallow in
the trachea (endobronchial cuff is inflated).
FIGURE 12-5 ■ Left endobronchial tube is placed too deeply into FIGURE 12-7 ■ Left endobronchial tube is placed too deep in the
the bronchus (both cuffs are inflated). left bronchus (only the tracheal cuff is inflated).
62 SECTION 2 Respiratory System
lung compliance and ventilation. Rolls beneath the hips nondependent lung from atelectasis stimulates the
and lower axilla lift the chest wall off the table and hypoxic pulmonary vasoconstriction (HPV) response,
improve dependent lung ventilation. which leads to further diversion of blood to the depen-
Maintaining the lateral decubitus position for a long dent (ventilated) lung. HPV is a local mechanism that
time leads to transudation of fluid in the dependent lung, constricts pulmonary vessels and diverts blood flow
causing interstitial pulmonary edema, known as “down- to the better oxygenated (ventilated) portions of
lung syndrome.” Administration of large amounts of the lung. Continued blood flow to the hypoxic lung
intravenous fluid increases left atrial pressure and leads constitutes true shunt. The stimulus for HPV appears
to further transudation of fluid. to be related to mixed venous blood (PV O2 ) and PAO2.
Peripheral nerve injuries from pressure or stretching Active HPV can decrease blood flow to hypoxic lung
may also occur. Padding the lower extremities and by approximately 50%, decreasing shunt and improv-
placing a low axillary roll help prevent injury to the ing PaO2.
peroneal nerve and brachial plexus. The dependent eye In numerous in vitro and in vivo animal studies, HPV
should remain clear of head supports, and the depen- has been shown to be inhibited by potent inhaled anesthet-
dent ear pinna should not fold over itself. An arterial ics and vasodilators. Intravenous agents such as ketamine,
catheter placed in the dependent arm allows for con- opioids, and benzodiazepines do not appear to inhibit
stant monitoring of excessive pressure on the dependent HPV. The effects of anesthetics on HPV are difficult to
axillary artery. demonstrate clinically because of the many confounding
variables present in patients undergoing surgery. If hypox-
10. How are pulmonary perfusion and ventilation emia occurs secondary to shunting, adding remifentanil
may allow less volatile agent to be used, decreasing the
altered during one-lung ventilation?
impact on HPV (Box 12-3).
During two-lung ventilation in the lateral decubitus
position, ventilation is preferentially diverted to the 11. How is hypoxemia that occurs during one-lung
nondependent lung, and perfusion is primarily directed ventilation treated?
to the dependent lung. When the nondependent lung is
collapsed, ventilation to that side is eliminated, but some In the past, ventilation of the dependent lung with large
perfusion persists. Blood passing through the deflated tidal volumes (10–12 mL/kg) was recommended during
lung does not exchange gas with alveoli and is called one-lung ventilation to prevent atelectasis. Increased
shunted blood. This unoxygenated venous (shunted) airway pressures also reduce transudation of fluid from
blood mixes with oxygenated blood from the dependent pulmonary capillaries. However, too much of an increase
lung in the pulmonary vein and left atrium, resulting in airway pressure may increase dependent lung pulmo-
in a significant overall decrease in oxygen tension. Ex- nary vascular resistance (PVR) and divert blood flow to
change of CO2 is not affected by one-lung ventilation to the nondependent lung. Large tidal volumes create a risk
the same extent as is oxygenation because CO2 diffuses for volutrauma and barotrauma from the associated
readily across alveolar-capillary membranes in the de- higher airway pressures leading to acute lung injury.
pendent (ventilated) lung. At the present time, most thoracic anesthesiologists
Additionally, hypercarbia is better tolerated than ventilate the lung with tidal volumes of 5–8 mL/kg of
hypoxia. There is a reduction in pulmonary blood flow ideal body weight. These smaller tidal volumes should be
to the nondependent lung during one-lung ventilation, accompanied by positive end expiratory pressure (PEEP)
which tends to decrease the shunt fraction (Box 12-2). to prevent atelectasis in the ventilated lung.
Gravity, surgical compression, and ligation of nonde- Ventilatory rate is adjusted to maintain PaCO2 near
pendent pulmonary vessels all decrease blood flow 40 mm Hg; this is usually achieved with a rate similar
to the nondependent lung. Alveolar hypoxia in the to that employed during two-lung ventilation. During
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Curr Opin Anaesthesiol 23:7, 2010. Neustein SM, Kahn P, Krellenstein DJ, et al.: Incidence of arrhythmias
Fujiwara M, Abe K, Mashimo T: The effect of positive end-expiratory after thoracic surgery: thoracotomy versus video-assisted thoracoscopy.
pressure and continuous positive airway pressure on the oxygenation J Cardiothorac Vasc Anesth 12:659, 1998.
and shunt fraction during one-lung ventilation with propofol anesthesia. Nurozler F, Argenziano M, Ginsburg ME: Nitric oxide usage after
J Clin Anesth 13:473, 2001. posttraumatic pneumonectomy. Ann Thorac Surg 71:364, 2001.
Giordano CR, Gravenstein N: Capnography. p. 245. In Ehrenwerth J, Slinger PD, Johnston M: Preoperative assessment for pulmonary
Eisenkraft JB, Berry JM (eds.): Anesthesia Equipment: Principles and resection. J Cardiothorac Vasc Anesth 14:202, 2000.
Applications, 2nd edition. Mosby, Philadelphia, 2013.
CASE 13
Thoracoscopy
Steven M. Neustein, MD • James B. Eisenkraft, MD
QUESTIONS
1. What procedures are performed under video- 4. How can hypoxemia from shunting during one-
assisted thoracoscopy? lung ventilation be treated?
2. What are the advantages of video-assisted 5. What complications can occur with video-assisted
thoracoscopy over traditional thoracotomy? thoracoscopy?
3. What anesthetic techniques can be used for
video-assisted thoracoscopy?
A 60-year-old man with a long history of cigarette spread to allow intrathoracic access, and sometimes rib
smoking presents for video-assisted thoracoscopy (VAT) resection is required. There is a high incidence of tachyar-
and wedge resection of a mass in the upper lobe of the rhythmias after thoracotomy, which may be related to
right lung. postoperative pain. Epidural analgesia and intercostal
nerve blocks are very effective for postoperative pain
1. What procedures are performed under video- management and may lead to a lower incidence of ar-
assisted thoracoscopy? rhythmias. VAT is followed by less pain and respiratory
impairment than open thoracotomy, allowing for earlier
Minimally invasive thoracic surgery can be performed discharge to home.
with VAT. Typically, three to five small incisions (portals)
are created to allow entry of instruments into the tho- 3. What anesthetic techniques can be used for
racic cavity. A camera is connected to a monitor on which
video-assisted thoracoscopy?
the visual field is displayed.
VAT can be used for biopsy of intrathoracic structures, VAT is usually performed under general anesthesia. It is
such as lung, pleura, and mediastinal masses. If the biopsy essential to provide excellent lung deflation and maintain
is positive for cancer, open thoracotomy for a more exten- oxygenation using one-lung ventilation (OLV). With a
sive resection, such as lobectomy or pneumonectomy, thoracotomy incision, surgeons can manually retract the
may be the next step. Other lung surgical procedures that lung if necessary, providing greater access and exposure.
can be performed with VAT include resection of bullae, Under VAT, however, inadequate lung deflation hampers
treatment of pneumothorax or empyema, and diagnosis exposure and surgical access. Less than full lung collapse
and treatment of thoracic trauma. may necessitate thoracotomy, which is associated with
Esophageal surgery can be performed with VAT, in- greater morbidity and mortality.
cluding esophagomyotomy for achalasia, which can also OLV can be achieved with a double-lumen tube
be performed via the abdomen with laparoscopy and (DLT), which allows for lung deflation by egress of gas
thoracoscopy. Traditionally, the Ivor Lewis esophagec- through the tracheal tube lumen. As soon as the patient
tomy was performed through the use of laparotomy and is turned to the lateral decubitus position, and the posi-
right thoracotomy incisions. tion of the tube is rechecked, the lung to be operated on
Pericardial surgery can be performed with VAT, in- is deflated, and OLV is instituted.
cluding pericardiectomy as treatment for pericardial An alternative to a DLT is a bronchial blocker. The
effusion. Excision of a pericardial cyst and “takedown” of most commonly used blockers are the Arndt (Cook,
the internal mammary artery for coronary artery bypass Bloomington, IN), Cohen (Cook), and Uniblocker (Fuji
grafting can also be performed with VAT. Systems, Tokyo, Japan). The first bronchial blocker avail-
able commercially was the Univent tube. This is a single-
2. What are the advantages of video-assisted lumen silicone tube that has a small separate lumen along
thoracoscopy over traditional thoracotomy? the anterior concave wall. The separate lumen contains a
small hollow bronchial blocker that can be advanced 10 cm
VAT requires only small incisions compared with a much beyond the tip of the Univent tube. Once the blocker
larger thoracotomy incision. Surgery via thoracotomy has been advanced into the bronchus to be blocked, a
requires cutting across chest wall muscles. Ribs are usually brief apneic period allows for partial lung collapse before
67
68 SECTION 2 Respiratory System
69
CASE 14
QUESTIONS
A 63-year-old woman with a brain tumor presents to maintain normal CBF. At the upper level of auto-
for bifrontal craniotomy in the supine position. She is regulation, cerebral blood vessels are maximally
neurologically intact but recently experienced head- constricted (i.e., resistance to flow is high), and CBF
aches, nausea, and blurred vision. Magnetic resonance increases linearly with increasing CPP. Integrity of the
imaging (MRI) revealed a large meningioma near the blood-brain barrier (BBB) is lost at these high pressures,
sagittal sinus. After induction of anesthesia and the and transudation of fluid occurs resulting in cerebral
start of surgery, the surgeon begins drilling a burr hole edema. Autoregulatory compensation generally occurs
in the skull. End-tidal carbon dioxide (ETCO2) starts over 1–3 minutes.
to decrease within 5 minutes, and the patient becomes The second parameter affecting CBF is arterial car-
hypotensive. bon dioxide tension (PaCO2). Increasing levels of PaCO2
produce elevated levels of extracellular hydrogen ions,
which induce cerebral vessel smooth muscle relaxation
1. What is cerebral autoregulation?
and vasodilation. Consequently, cerebral vascular resis-
Cerebral autoregulation is the control process by which tance decreases, increasing CBF by twofold. This effect
cerebral blood flow (CBF) is maintained constant plateaus at a PaCO2 of approximately 80 mm Hg. Con-
over a wide range of cerebral perfusion pressure (CPP) versely, decreasing PaCO2 increases cerebral vasocon-
(Figure 14-1). CPP represents the difference between striction, and CBF decreases. At a PaCO2 of 20 mm Hg,
mean arterial pressure (MAP) and intracranial pressure cerebral vasoconstriction is maximal, and CBF decreases
(ICP). Autoregulation adjusts cerebral vessel caliber by 50%. Further decreases in PaCO2 have no greater
as CPP changes. Normal CBF is 45–65 mL/100 g of vacoconstricting influence. These physiologic changes
brain tissue per minute. It is coupled to alterations remain in effect for several hours, after which cerebro-
in cerebral metabolic rate, which is linked to oxygen spinal fluid (CSF) bicarbonate levels decrease to com-
consumption (CMRO2). CBF parallels the changes in pensate for induced CSF alkalosis. When CSF pH
CMRO2. Several parameters affect CBF (Box 14-1). returns toward normal, respiratory alkalosis no longer
Autoregulation maintains CBF at a CPP of approxi- provokes cerebral vasoconstriction. The PaCO2
mately 50–150 mm Hg. At CPP !50 mm Hg, cerebral response at the limits of autoregulation can be blunted.
blood vessels achieve maximal dilation (i.e., resistance If CPP is low and cerebral vessels are maximally dilated,
to flow is low), and CBF decreases in direct proportion lowering PaCO2 would have little beneficial effect on
to CPP. Chronically hypertensive patients undergo an cerebrovascular resistance.
upward shift of autoregulation to higher perfusion pres- The third parameter affecting CBF is arterial oxygen
sures. Consequently, these patients require higher CPP tension (PaO2). At a PaO2 !50 mm Hg, CBF increases
70
14 Intracranial Mass, Intracranial Pressure, Venous Air Embolism, and Autoregulation 71
TABLE 14-1 Central Nervous System Effects of Anesthetic Agents and Adjuvants
Agent Effect Agent Effect
Potent inhalation Lowers CMRO2 Curare Decreases MAP
agents Increases cerebral blood flow by Cerebral vasodilator
vasodilation; this effect is prevented
by prior hyperventilation
Desflurane Similar to isoflurane, rapid uptake Pancuronium Increases heart rate
Increases MAP
Enflurane Increases CSF production Vecuronium* No significant effects
Decreases CSF reabsorption
Halothane Decreases CSF production Atracurium Large bolus doses may release
Decreases CSF reabsorption histamine, predisposing to
decreased MAP and cerebral
vasodilation
Isoflurane* No effect on CSF production Alfentanil Decreases MAP
Increases CSF reabsorption Decreases CPP
May protect from ischemia
Sevoflurane Autoregulation maintained at 1.5 MAC Fentanyl* With normal or low PaCO2
plus N2O, decreases CMRO2,
decreases CBF
With increased PaCO2, cerebral
vasodilator
Nitrous oxide No change in CMRO2, CSF production, or Remifentanil Decrease in MAP
CSF reabsorption No change in ICP
Cerebral vasodilating effects inhibited by Very short-acting
hyperventilation Increases CSF reabsorption
Expands intradural air
Expands venous air emboli
Barbiturates* Decreases CMRO2 Sufentanil Decreases CVR
Decreases CBF Increases CBF
Cerebral vasoconstrictor
Decreases CSF production
Increases CSF reabsorption
Ketamine Increases ICP Lidocaine Low dose: Decreases CBF,
Increases CBF and decreases CMRO2
Increases MAP High dose: Increases CBF,
No change in CMRO2 and increases CMRO2
No change in CSF production
Decreases CSF reabsorption
Etomidate* Similar to barbiturates Sodium No effect on CBF despite cerebral
Myoclonus indistinguishable from seizures nitroprusside vasodilatation
Decreases MAP
Increases CBV
Benzodiazepines* Decreases CBF Nitroglycerin Increases CBF
Decreases CMRO2 Increases CBV
Decreases MAP
Propofol Decreases MAP Hydralazine Increases CBF
Increases CBV
Decreases MAP
Onset 10–20 minutes
Succinylcholine Increases CMRO2 Labetalol* Decreases MAP
Increases CBF No effect on CBV
Increases muscle spindle activity;
diminished by pretreatment with
nondepolarizing neuromuscular blocker
CBF, Cerebral blood flow; CBV, cerebral blood volume; CMRO2, cerebral metabolic rate of oxygen consumption; CPP, cerebral perfusion
pressure; CSF, cerebrospinal fluid; CVR, cerebrovascular resistance; ICP, intracranial pressure; MAC, minimum alveolar concentration;
MAP, mean arterial pressure.
*Recommended for patients with increased ICP.
14 Intracranial Mass, Intracranial Pressure, Venous Air Embolism, and Autoregulation 73
and CBF. Barbiturates, notably thiopental, reduce that the duration of action of nondepolarizing muscle
CMRO2 primarily and CBF secondarily. Thiopental acts relaxants is reduced by various anticonvulsant medications.
as a cerebral vasoconstrictor. CO2 reactivity is main- However, the mechanism is unclear. Most patients
tained but is quantitatively reduced compared with the requiring craniotomy are treated with anticonvulsants,
awake state. Cerebral autoregulation is also maintained and the nondepolarizing muscle relaxant dosing regi-
intact. Thiopental is an excellent drug to reduce ICP men requires alteration. Atracurium and cisatracurium
acutely; however, amounts sufficient to induce an isoelec- seem to be largely resistant to these effects, most
tric electroencephalogram can produce significant hemo- likely because metabolism is achieved by Hoffman
dynamic side effects. elimination.
Ketamine can cause a significant increase in CBF Opioids are known to produce respiratory depression,
without an important effect on metabolic rate. It is not which results in an increase in PaCO2. Consequently,
considered a wise choice in most neurosurgical settings. opioids are administered sparingly in a spontaneously
However, small to moderate doses in a background of breathing patient with cerebral disease. Opioids at low
volatile anesthetic or intravenous infusion have not doses produce very little effect on CBF, provided that
been shown to be significantly harmful. Trauma pa- PaCO2 is not allowed to increase. During controlled
tients with hypovolemia and concurrent injuries may be ventilation with normocapnia or hypocapnia, opioids
suitable candidates for ketamine because blood pressure provide significant advantages. Independently, fentanyl
and CPP may be more easily maintained. Etomidate seems to have little effect on CBF or CMRO2, but
behaves similarly to thiopental and is an appropriate when combined with N2O, it decreases CMRO2 and
induction agent for patients who cannot tolerate the CBF, which is due to the hemodynamic changes caused
hemodynamic effects seen with thiopental. Myoclonus, by this combination of anesthetic agents. It increases
which occurs after etomidate administration, may be the rate of CSF reabsorption without affecting its rate
difficult to differentiate from seizure activity. Benzodi- of production. There has been controversy about how
azepines offer beneficial effects on elevated ICP by and whether opioids, such as sufentanil and alfentanil,
reducing CBF and CMRO2, without meaningful effects increase ICP. With cerebral autoregulation intact, a
on CSF dynamics. decrease in blood pressure results in compensatory
Propofol, a short-acting intravenous agent used for vasodilation to maintain CBF. This vasodilation in-
induction and maintenance of anesthesia, appears to creases cerebral blood volume and ICP. Interest in
maintain the relationship between CBF and CMRO2. remifentanil for neurosurgery has increased because of
Propofol does not cause cerebral vasodilation and does its rapid onset and offset and titratability to changing
not interfere with the normal response to PaCO2. It is stimuli. It is frequently used as a component of TIVA.
often used to supplement volatile agents during crani- However, the lack of residual analgesia requires a
otomies or as part of total intravenous anesthesia (TIVA) plan for postoperative pain relief and blood pressure
techniques. It is particularly useful for procedures in control.
which neurophysiologic monitoring is used, but it must Sodium nitroprusside is a direct-acting smooth mus-
be kept in mind that it produces dose-dependent de- cle relaxant that produces arteriolar and venous dila-
creases in blood pressure. Propofol has become the tion. It is sometimes used in neurosurgery for control of
mainstay for TIVA and has essentially replaced sodium arterial blood pressure. Although it acts as a cerebral
thiopental as an induction agent for most neurosurgical vasodilator and decreases MAP, it has little effect on
cases. CBF. However, cerebral blood volume is increased, and
Muscle relaxants have no direct intracerebral effects ICP may be elevated. If ICP is increased, use of sodium
because they do not cross the BBB. Nevertheless, they nitroprusside is best avoided. Thiopental, lidocaine, or
possess indirect effects because of their actions in the labetalol should be used instead. Nitroglycerin is pri-
periphery, which are sometimes significant. There is marily a venodilator and coronary vasodilator that acts
clear evidence from both experimental animals and by relaxing smooth muscle and works on the intracere-
humans that succinylcholine can increase ICP under bral venous capacitance vessels. Labetalol, a mixed #/$
conditions of intracranial hypertension. The magnitude blocker, decreases MAP by reducing systemic vascular
of the increase is typically small and transient. It has resistance and depressing cardiac output. It has no
been shown in humans that ICP changes caused by direct effect on cerebral blood vessels. Nicardipine, a
succinylcholine can be blocked by preadministration calcium channel blocker, is a newer option for blood
of a defasciculating dose of a nondepolarizing relaxant. pressure control in the perioperative period and has no
A probable mechanism is the massive fasciculation- deleterious effects on ICP or CBF.
induced afferent barrage from muscle spindles to the
brain that causes transient increases in metabolic rate
4. What are the signs and symptoms of increased
and coupled increases in CBF. The decision to use this
agent is determined by the need to secure the airway intracranial pressure?
rapidly. Pretreatment with a small dose of a nondepo- Gradual, chronic increases in ICP cause few signs and
larizing agent is helpful and recommended. symptoms. Symptoms of acute intracranial hyperten-
Nondepolarizing agents, such as vecuronium, sion are likely caused by decreased CPP resulting in
rocuronium, and cisatracurium, have no significant cerebral ischemia or mechanical forces on the brain-
hemodynamic or ICP effects. There is clear evidence stem, which thrust intracranial contents through
74 SECTION 3 Central Nervous System
the foramen magnum. These may include headache, the patient’s head promotes drainage of venous blood
nausea, vomiting, and mental status changes. Cushing from the brain and is effective at reducing brain bulk.
triad, consisting of Cheyne-Stokes respirations, in- Obstruction of venous outflow (e.g., by improperly
creased systolic blood pressure (with resultant increase placed tape around the neck, improper positioning of
in pulse pressure), and bradycardia, can be seen when the patient) is often an overlooked cause of increased
intracranial hypertension is associated with a mass brain volume. Acutely lowering ICP via hyperventila-
effect. Acute increases in ICP can cause loss of tion (PaCO2 reduction) is frequently employed for in-
consciousness, hypertension, bradycardia, absent brain- tubated patients. Hyperventilation is simple to perform
stem reflexes, cranial nerve dysfunction, decerebrate and results in rapid and dramatic decreases in ICP.
posturing, apnea, irregular respiration, fixed and Alteration of PaCO2 within the range of approximately
dilated pupils, and death as a result of impaired medul- 20–80 mm Hg causes parallel changes in CBF. CBF-
lary perfusion (Box 14-2). reducing and ICP-reducing effects of hyperventilation
are acute and most effective during the first 12–24 hours
of hyperventilation. A typical value to aim for is PaCO2
5. How is intracranial pressure monitored?
of 30–35 mm Hg because there is little benefit to be
Ventriculostomy is the most common method of mea- gained from lower PaCO2 values. The main complica-
suring ICP. A catheter is placed through a burr hole and tion of hyperventilation is reduction of CBF, which
into the anterior horn of a lateral ventricle. Obliteration gives rise to cerebral ischemia. Until more recently,
of the ventricle because of tumor or edema may create hyperventilation was implemented in all patients sus-
technical difficulties inserting the catheter. Subdural pected to have increased ICP, but neuronal ischemia
bolts also serve to measure ICP. These devices are caused by hyperventilation has now been demonstrated
placed via a twist drill hole in the calvaria and a small in humans.
hole in the dura. They are less invasive than ventricu- The two other intracranial compartments, CSF and
lostomy but provide only local pressure data instead of brain parenchyma, are also amenable to volume reduction.
global information. Subdural bolts can become infected CSF withdrawal can occur through a ventriculostomy, and
and lack the potential to withdraw CSF for lowering production of CSF can be reduced by acetazolamide, a
ICP. Proper positioning requires the bolt head to be carbonic anhydrase inhibitor. Brain edema may respond to
aligned in the same plane as underlying brain. Catheters osmotic or loop diuretics, such as mannitol or furosemide,
or electronic transducers placed in the epidural space respectively. The resulting diuresis reduces intravascular
can also be used for ICP monitoring. Lumbar subarach- volume and cerebral blood volume. The onset of action
noid catheters are used occasionally. The patient should of mannitol is approximately 30 minutes, and its effect
be placed in the horizontal position; otherwise, the is accelerated by furosemide. Use of osmotic agents re-
accuracy of these devices is impaired. Abrupt with- quires a globally intact BBB with only minimal areas of
drawal of CSF through lumbar subarachnoid catheters disruption.
risks brain herniation. Struggling or coughing against a tracheal tube should
be prevented, and this is best accomplished via adminis-
tration of sedative agents such as benzodiazepines, barbi-
6. How is increased intracranial pressure treated?
turates, propofol, opioids, and muscle relaxants. Systemic
Treatment of increased ICP may begin by changing the hypertension, tachycardia, and straining increase CMRO2
patient’s position. More recent studies have shown that and CBF (Box 14-3).
a change to the reverse Trendelenburg position in
anesthetized patients rapidly reduces ICP. Elevation of
7. How is venous air embolism detected and treated? BOX 14-5 Acute Treatment of Venous Air
Embolism
Venous air embolism (VAE) is a potentially life-threatening
event that must be detected and treated promptly. It Notify surgeons to identify open sinuses
is often associated with cases performed in the sitting Close sinuses surgically or flood field with saline and
position, but it can occur under certain physiologic cir- apply bone wax
cumstances. In neurosurgical procedures, air may enter Increase venous pressure in head
the venous system via noncollapsible venous channels, Lower head relative to heart
such as dural sinuses and diploic veins. When the head is Place table in Trendelenburg position
elevated above the heart, a pressure gradient can exist, Jugular vein compression
Positive end expiratory pressure*
which facilitates air entrainment. In the sitting position,
Discontinue N2O administration
the incidence of VAE is almost four times higher than the Support cardiovascular system
incidence in other positions (45% versus 12%). Air can Volume
also be entrained from pin sites during a stereotactic Inotropes
biopsy in the semisitting position. Vasopressors
Monitoring for VAE (Box 14-4) generally includes a
precordial Doppler, capnometer, pulse oximeter, and N2O, Nitrous oxide.
*Controversial.
esophageal stethoscope. When placed properly, precor-
dial Dopplers can detect 0.1 mL of air. Transesophageal
echocardiography is also sensitive for detecting and
recognizing intracardiac air but is not generally used in source of air entrainment, venous pressure in the head
this setting because of technical difficulty and cost. Air should be increased in an attempt to force blood
collects at the superior vena cava and the right atrium through the concealed opening; this is accomplished by
junction. lowering the head relative to the heart or occluding
Pulmonary artery catheters may provide valuable venous outflow from the head with jugular compres-
information because pulmonary artery pressures in- sion. If N2O is being used, administration should cease
crease during VAE. Pulmonary artery catheters and immediately. Rapid diffusion of N2O into air bubbles
central venous pressure catheters are inefficient means expands their volume, creating mechanical obstruction
of VAE aspiration. Continuous ETCO2 monitoring to flow, and hemodynamic compromise. Volume, ino-
demonstrates rapid decline as VAE ensues. Arterial tropes, and vasopressor administration contribute to
PaCO2 increases as ETCO2 decreases, increasing hemodynamic support, churning large air pockets
the gradient between these two measurements. The into smaller ones to be carried out to the pulmonary
difference increases as alveolar dead space increases. If peripheral blood vessels.
minute ventilation remains constant, the divergence The application of positive end expiratory pressure
between PaCO2 and ETCO2 may represent a useful (PEEP) in an attempt to increase central venous pres-
marker for the severity of VAE. Sensitive mass spec- sure and decrease the magnitude of VAE is controver-
trometry can show increases in expired nitrogen as the sial. High levels of PEEP greatly increase the risk of
VAE is eliminated through the lung. However, the hypotension in patients who are already intravascularly
sensitivity of current nitrogen monitoring technology depleted. Right atrial pressure may be increased in the
may be insufficient to detect subclinical VAE. Classically, face of lowered left atrial pressure, predisposing the
the “mill wheel” murmur heard through an esophageal patient to paradoxical air embolism through a patent
stethoscope is associated with intracardiac air. foramen ovale. Application of PEEP probably should be
When detected, VAE requires rapid treatment limited to situations in which all other attempts at pre-
(Box 14-5). The surgeon must be alerted immediately venting continuous VAE have failed.
when VAE is suspected so that open sinuses may be Even moderate amounts of VAE may result in de-
identified and flooded with saline or closed surgically creased PaO2. Initial treatment should be supportive with
to halt air entrainment. In the absence of an obvious enhanced inspired oxygen concentrations guided by
pulse oximetry and arterial blood gas determinations.
Postoperatively, patients may develop an interstitial pul-
monary process that usually resolves in 24–48 hours.
BOX 14-4 Monitors for Detection of Venous
Air Embolism 8. What are contraindications to the sitting position?
Precordial Doppler There are no absolute contraindications to the sitting
Transesophageal echocardiography position; however, each patient requires careful evalu-
Mass spectrometry (end-tidal nitrogen) ation to determine the feasibility of the sitting position
Capnography (ETCO2) and risks for complications. Specific contraindications
Pulse oximetry
Pulmonary artery pressure
involve the presence of a patent foramen ovale or sus-
Esophageal stethoscope pected intracardiac shunt. Other conditions that may
predispose to development of complications are hemo-
ETCO2, End-tidal carbon dioxide. dynamic instability or noted cerebral compromise
76 SECTION 3 Central Nervous System
when sitting upright preoperatively. Other concerns eloquent brain functions such as speech, motor, and
involve positioning of the neck, which may impair sensory to minimize neurologic resection. Craniotomy
spinal cord perfusion in the patient with severe cervi- in the awake state has been performed since ancient
cal arthritis. The sitting position is used infrequently times. Present-day indications include resection of a
today, to avoid its inherent problems. Many surgeons lesion in the eloquent or speech center of the brain.
now employ the lateral, prone, or supine position with Surgical procedures for the treatment of epilepsy,
the head turned. tumors, or arteriovenous malformation are sometimes
performed in an awake patient. With refinement of
neurophysiologic monitoring techniques, awake crani-
9. How would you induce and maintain anesthesia in
otomies are necessary in only a small percentage of
this patient? patients. However, surgery for movement disorders has
The preoperative assessment of this patient includes increased the use of this technique.
evaluation of mental status and determination of acute Intraoperative complications of awake craniotomy
increased ICP. Coexisting diseases optimally should be include restlessness and agitation. These complications
treated before arrival in the operating room. MRI reveals may occur when the patient is overly sedated yet experi-
a large mass that has slowly increased in size. This patient ences discomfort. More serious complications are
can be induced in the typical manner with caution to hypoventilation, nausea, and seizures. A change in the
avoid additional increases in ICP. Intravenous anesthetic level of sedation often resolves these problems. It is
induction is followed by moderate hyperventilation until important to maintain good rapport with the patient,
neuromuscular blockade is achieved. Thiopental and which should have been established preoperatively.
propofol are commonly used for induction with an opi- Positioning of the patient to avoid discomfort, allowing
oid, such as fentanyl, to blunt hemodynamic response to surgical access and avoidance of a claustrophobic atmo-
laryngoscopy and intubation. Moderate hyperventilation sphere, is essential and requires cooperation of the
is achieved to an ETCO2 of 28–30 mm Hg. A radial entire operating room staff. The evolution of anesthetic
artery catheter and additional intravenous lines may be techniques has progressed from fentanyl and droperidol
placed after endotracheal intubation. The potential to the current use of propofol infusion with alfentanil or
for blood loss may be considerable, and large-bore remifentanil. Intraoperative nausea is rare with the use
intravenous catheters are recommended. Mannitol is of propofol infusions. Dexmedetomidine (Precedex),
commonly administered at a dose of 0.5–1.0 g/kg. a selective #2-adrenergic agonist, is a newer agent used
Maintenance of anesthesia may proceed with low doses for continuous intravenous sedation. Dexmedetomidine
of volatile agent (i.e., !1 MAC) and continuous infusion has been shown to produce sedation and analgesia with-
or bolus doses of opioids and muscle relaxants. N2O may out respiratory depression. The onset is slower than
be administered at a concentration of 50%, if surgical propofol, and it must be administered by infusion; this
conditions do not indicate a “tight brain.” Intravenous may be beneficial for older patients, pediatric patients,
fluid administration generally requires isotonic crystalloid or potentially debilitated patients and has been used
solutions; colloids are also useful for maintenance of in- throughout intraoperative testing. Seizure control is
travascular volume. Extensive blood loss is replaced with sometimes necessary and can be managed effectively
packed red blood cells. Hypotonic solutions exacerbate with thiopental (1 mg/kg) or a benzodiazepine (midazolam).
cerebral edema and are generally contraindicated, and Terminating the seizure requires careful titration of
glucose-containing solutions are avoided unless truly sedatives to avoid apnea.
necessary to treat diagnosed hypoglycemia.
Neurosurgery is characterized by periods of intense
stimulation followed by minimal pain during brain re-
section. Hypertension may occur and is treated promptly SUGGESTED READINGS
to prevent bleeding and potential cerebral swelling. The Bendo AA, Luba K: Recent changes in the management of intracranial
use of $-adrenergic blockers in addition to adequate hypertension. Int Anesthesiol Clin 38:69, 2000.
anesthesia is recommended throughout. Blood pressure Joshi S, Ornstein E, Young WL: Cerebral and spinal cord blood flow.
p. 17. In Cottrell JE, Young WL (eds): Cottrell & Young’s Neuroan-
control is especially important on closure and emer- esthesia. Mosby, St Louis, 2010.
gence. Patients who have had an uneventful procedure Manninen PH, Balki M, Lukitto K, et al.: Patient satisfaction for awake
are expected to emerge promptly at the end of surgery craniotomy for tumor surgery: a comparison of remifentanil and
for neurologic evaluation. Extubation is managed care- fentanyl in conjunction with propofol. Anesth Analg 102:237, 2006.
Smith DS, Osborn IP: Posterior fossa: anesthetic considerations. p. 340.
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Intracranial Aneurysm
Arthur E. Schwartz, MD
QUESTIONS
1. How are patients graded after subarachnoid 4. Which monitors are indicated for patients
hemorrhage from a ruptured aneurysm? undergoing intracranial aneurysm clipping?
2. What are the most serious complications after 5. How is arterial blood pressure controlled?
subarachnoid hemorrhage from aneurysm 6. What is cerebral vasospasm, and how is it treated?
rupture? 7. How is aneurysm rupture during aneurysm
3. What are treatment options? clipping managed?
A 55-year-old woman was admitted with severe headache 3. What are treatment options?
and decreased consciousness. A subarachnoid hemor-
rhage (SAH) from a ruptured intracranial aneurysm was Treatment of intracranial aneurysm is by either craniot-
diagnosed. omy or endovascular therapy. After angiography, endo-
vascular treatment most often consists of packing the
1. How are patients graded after subarachnoid aneurysm with detachable coils. In many centers, endo-
vascular embolization is the preferred treatment. There
hemorrhage from a ruptured aneurysm?
may be a preference for craniotomy in younger patients.
The incidence of SAH is about 10–15 per 100,000 The most common complication of endovascular treat-
person-years. Angiography shows that 80%–85% of ment is ischemic injury. The second most common com-
cases of SAH are due to an intracranial aneurysm. plication is vascular perforation. Aneurysms without a
Cerebral aneurysms are most often found at bifurca- sufficiently narrow neck may require complex techniques
tions near the circle of Willis, and the risk of rupture is for endovascular embolization. Some cases require bal-
increased with increasing size. SAH almost always loon-assisted coiling. Sometimes a stent is initially placed
manifests with rapid onset of severe headache. The in the artery whose lumen feeds the aneurysm. Thereaf-
presence of other signs and symptoms is used for clini- ter, coils are introduced across the stent wall into the
cal grading of patients. The Hunt-Hess clinical grade aneurysm cavity.
classification is widely used (Table 15-1). The World Classic treatment consists of craniotomy and clipping
Federation of Neurologic Surgeons Grading System of the aneurysm. Most centers attempt early clipping
has also gained acceptance. after SAH to prevent rebleeding and permit safe induc-
tion of hypertension and hypervolemia as treatment of
2. What are the most serious complications after vasospasm.
subarachnoid hemorrhage from aneurysm
rupture? 4. Which monitors are indicated for patients
undergoing intracranial aneurysm clipping?
The most serious sequela of SAH is rebleeding. The
incidence of rebleeding after aneurysm rupture is ap- In addition to routine monitoring for general anesthesia,
proximately 15% in the first week and about 10% in patients with aneurysm should have intraarterial mea-
the second week. Morbidity and mortality after rebleed surement of blood pressure. The intraarterial catheter is
are great and have motivated the trend toward early best inserted before anesthetic induction because hyper-
intervention after aneurysm rupture. tension associated with laryngoscopy increases the risk
Cerebral vasospasm is also a major cause of morbidity of rupture. A urinary catheter is also indicated as in all
and mortality after SAH. Symptomatic brain ischemia craniotomies.
from vasospasm occurs in 15%–35% of patients. Angio- Many centers use electrophysiologic monitoring for
graphic evidence of vasospasm occurs in 70% of patients. aneurysm surgery when temporary arterial occlusion is
Vasospasm may lead to cerebral infarction. SAH often anticipated during surgical dissection of the aneurysm.
leads to hydrocephalus and may result in dangerously In these cases, arterial branches feeding the aneurysm
elevated intracranial pressure. may be temporarily occluded with surgical clips to
77
78 SECTION 3 Central Nervous System
Carotid Endarterectomy
Arthur E. Schwartz, MD
QUESTIONS
1. What are indications for carotid endarterectomy? 5. What interventions may reduce the risk of
2. What is the alternative to carotid endarterectomy? neurologic injury?
3. What are the most serious perioperative 6. Explain the risks of postoperative blood pressure
complications associated with carotid instability.
endarterectomy?
4. Intraoperatively, how is the patient’s neurologic
status monitored?
A 68-year-old man with a history of transient ischemic include cerebral infarction, transient ischemia, and cogni-
attacks presented for carotid endarterectomy (CEA). tive dysfunction. Cardiovascular complications include
cardiac ischemia, dysrhythmia, hypotension, hyperten-
sion, and myocardial infarction. Ischemic cerebral injury
1. What are indications for carotid endarterectomy?
may result from embolization of thrombus or air during
CEA reduces the risk of stroke in symptomatic patients with surgical manipulation. It may also result from decreased
significant carotid artery stenosis. Symptomatic patients cerebral perfusion during temporary carotid artery occlu-
with !70% luminal narrowing of the carotid artery had sion. Arterial stenosis or occlusion after CEA may also
improved outcome after surgery compared with patients produce an ischemic insult. Patients with atherosclerotic
receiving medical treatment alone. Symptoms include tran- disease of the carotid arteries often have similar pathology
sient ischemic attack, reversible ischemic neurologic deficit, of coronary vessels.
and nondisabling stroke. Asymptomatic patients with sig-
nificant luminal narrowing are considered for CEA if the 4. Intraoperatively, how is the patient’s neurologic
risk of perioperative morbidity and mortality is low.
status monitored?
The choice of techniques for assessing neurologic status
2. What is the alternative to carotid endarterectomy?
depends on whether regional or general anesthesia is
Carotid artery angioplasty with placement of an arterial used. With regional anesthesia, intermittent evaluation of
stent is a reasonable alternative treatment for carotid ar- motor strength, sensation, and language is performed.
tery stenosis. This technique involves placing an endovas- This evaluation should be timed to coincide with inter-
cular catheter, usually from the femoral artery, with fluo- ventions of relatively high risk. High-risk periods include
roscopic guidance, through the great arteries and heart to carotid artery manipulation, arterial occlusion, and reper-
the carotid artery. Balloon dilation of the stenosis is per- fusion. The choice and timing of sedation may markedly
formed. A filter or other device may be temporarily posi- interfere with proper evaluation. For example, adminis-
tioned distal to the lesion to limit embolization of material tration of a benzodiazepine may elicit reemergence of a
to the brain. After angioplasty, a stent is positioned at the focal deficit that was observed during an ischemic event
site to maintain arterial patency. The safety and efficacy of and subsequently resolved.
angioplasty with stent placement compare favorably with With general anesthesia, neurologic status is most of-
surgical treatment. It may be the only practical treatment ten assessed by electroencephalogram (EEG), somatosen-
for cases of high-grade carotid stenosis in which the lesion sory evoked potentials (SSEPs), motor evoked potential
is located distally and poorly accessible to surgery. (MEPs), or transcranial Doppler (TCD). EEG is the most
widely used and considered the “gold standard” for
3. What are the most serious perioperative monitoring neurologic function during general anesthe-
complications associated with carotid sia. It is the most sensitive method for detecting cerebral
ischemia in unconscious patients. Sensitivity depends on
endarterectomy?
the number of electrode channels monitored and the ex-
The most serious perioperative complications of carotid sur- perience of the person evaluating the EEG. EEG changes
gery are neurologic and cardiac. Neurologic complications indicative of ischemia are most likely to be observed from
80
16 Carotid Endarterectomy 81
electrodes positioned near the anatomic site of brain with increased by 10%–20% during temporary arterial occlu-
ischemia. Unilateral changes, especially changes observed sion. Intravenous phenylephrine is most often employed
in regions dependent on the operative artery, are more for this purpose. Surgical placement of a temporary vas-
likely to reflect ischemic insult. EEG changes most in- cular shunt during carotid artery occlusion also improves
dicative of ischemia are decreased amplitude (voltage), cerebral blood flow. However, this shunt may prolong
slowing (decreased frequency), or burst suppression. It is surgical time, obscure surgical exposure, and promote
useful to maintain a steady state of anesthetic agent dur- embolization.
ing monitoring to appreciate EEG changes that are not After reperfusion, ischemic and infarcted brain may
confounded by altered anesthetic dose. be at risk for reperfusion injury. Usually arterial blood
SSEPs depend on processing of signals from stimulation pressure is reduced to near normal before reperfusion.
of a peripheral nerve. Because the response is described by The choice of anesthetic agent for CEA is controversial.
latency and amplitude alone, analysis of SSEPs may require In a randomized study comparing potent inhalation anes-
less experience or training than EEGs. SSEPs are probably thetics, EEG evidence of ischemia occurred at higher cere-
less sensitive than EEGs for detecting ischemia. Ischemia is bral blood flows in patients anesthetized with halothane
indicated by an increase in latency or a decrease in ampli- compared with isoflurane; this may support the use of iso-
tude of the SSEP waveform. This change is of greatest flurane in these patients. There is no widely accepted pref-
concern when it is unilateral and on the operative side. erence for either a primarily opioid-based or inhalation
MEPs involve stimulation of the motor cortex by elec- anesthetic technique. In any case, rapid emergence from
tromagnetic signal. Motor response is measured in the general anesthesia, permitting timely assessment of neuro-
corresponding extremity. Muscle relaxants decrease or logic function, facilitates diagnosis of neurologic deficit
eliminate the response. Inhalation anesthetics also diminish resulting from cerebrovascular occlusion. Rapid emergence
the response. MEPs are very sensitive to cerebral ischemia. allows for more rapid intervention, such as therapeutic
TCD is used to measure middle cerebral artery blood surgical reexploration, cerebral thrombolysis, or angio-
flow velocity on the ipsilateral side. It does so by assess- plasty, if indicated.
ing the Doppler shift of sound waves reflected by moving Control of arterial carbon dioxide tension also is con-
red blood cells in the artery. It is also extremely sensitive troversial. Mild hypocapnia may reduce cerebral blood
for the detection of embolic material. Embolization is flow but may also preferentially shunt blood from normal
common during carotid surgery and depends on surgical brain to ischemic brain. Most practitioners maintain
technique and the presence of atherosclerotic plaque or arterial carbon dioxide tension near normal.
entrained air. Positioning of detector probes may be
quite cumbersome, and readings markedly depend on 6. Explain the risks of postoperative blood pressure
the probe direction (angle of insonation). Any movement
instability.
of the Doppler probe may result in diminished or lost
waveforms. CEA in proximity to the carotid sinus may result in arterial
Cerebral oximetry may be useful. Less common is blood pressure fluctuations postoperatively. Carotid artery
cerebral blood flow measurement by washout of intraar- angioplasty and stent placement may alter carotid wall
terial or intravenous xenon-133. mechanical properties, increasing baroreflex sensitivity.
Heightened baroreceptor responsiveness may lead to
5. What interventions may reduce the risk of impaired cardiovascular autonomic activity and may con-
tribute to postoperative morbidity and mortality. Increased
neurologic injury?
baroreceptor responsiveness results in an increased inci-
Ischemic neurologic insult from carotid artery surgery may dence of hypotension and bradycardia after CEA. These
result from arterial embolization during surgical manipula- conditions are most often successfully treated with intrave-
tion, decreased cerebral perfusion during temporary arte- nous phenylephrine and atropine. In contrast to conven-
rial occlusion, reperfusion injury, or unintentional arterial tional CEA, surgical techniques that include transection of
occlusion after surgery. Arterial embolization during surgery the carotid sinus nerve are likely to increase the incidence
is very common and often depends on surgical technique of postoperative hypertension. This hypertension is usu-
and the presence of atherosclerosis. Surgical placement ally treated with "-adrenergic blockers, calcium-channel
of a shunt may increase the incidence of embolization. blockers, or peripheral vasodilators. Hemodynamic dys-
In many centers, shunts are inserted only if indicated by function after carotid surgery is most often transient and
ischemic changes after carotid artery occlusion or other is best managed in an intensive care unit setting.
evidence of poor cerebral collateral circulation. Although
thiopental may improve outcome after focal ischemia, it is
SUGGESTED READINGS
not widely employed for maintenance of general anesthesia
because of dose-dependent delayed awakening and its he- Augoustides JG: Advances in the management of carotid artery disease:
focus on recent evidence and guidelines. J Cardiothorac Vasc Anesth
modynamic effects. Hypothermia also improves outcome 26:166, 2012.
after focal cerebral ischemia. However, it has not gained Blackshear JL, Cutlip DE, Roubin GS, et al.; CREST Investigators.
wide acceptance for carotid artery surgery. Hypothermia Myocardial infarction after carotid stenting and endarterectomy:
has numerous adverse myocardial effects. results from the carotid revascularization endarterectomy versus
stenting trial. Circulation 123:2571, 2011.
Decreased cerebral perfusion during temporary arte- Brott TG, Hobson RW 2nd, Howard G, et al.: Stenting versus endar-
rial occlusion is most often treated with deliberate hyper- terectomy for treatment of carotid-artery stenosis. N Engl J Med
tension. In many centers, systemic arterial pressure is 363:11, 2010.
CASE 17
Electroconvulsive Therapy
Ethan O. Bryson, MD • Charles H. Kellner, MD
QUESTIONS
An 88-year-old, 72-kg man with a history of treatment- number of treatments. In addition, the period of asystole
refractory major depressive disorder was referred for elec- during stimulus application is typically longer with unilat-
troconvulsive therapy (ECT). He received a successful eral electrode placement. For patients who are at increased
course of ECT during an episode of depression in 1968 and risk for a cardiovascular event during treatment, the risks
was in remission until about 2 years ago. He did not recall associated with an increased number of treatments needs to
any problems with either the treatment or the anesthesia. be evaluated if unilateral electrode placement is considered.
This episode was characterized by depressed mood, poor
sleep, thoughts to join his deceased parents, feelings of guilt 2. Do you have enough information to proceed with
about burdening his wife, and passive suicidal ideation. His
general anesthesia?
medical history was significant for hypertension, treated
with amlodipine and metoprolol. Additional medications The tasks of the anesthesiologist are to determine if the
included daily famotidine, finasteride, levothyroxine, patient is an acceptable anesthetic candidate for ECT, to
lorazepam, mirtazapine, quetiapine, rosuvastatin, docu- create a humane and safe anesthetic without suppressing
sate sodium (Colace), Senna, and tamsulosin. the therapeutic seizure, to mitigate or manage the physi-
ologic effects of the treatment, and to manage the tran-
sient effects of the anesthetics including management of
1. What is electroconvulsive therapy?
the airway. General anesthesia is required, and patients
ECT is the application of electrical stimuli to the brain receiving ECT should have the same quality of anesthetic
to induce a therapeutic seizure. ECT is an effective treat- evaluation as patients undergoing anesthesia for a surgical
ment for major depressive disorder, bipolar disorder, procedure. A thorough history should be taken.
catatonia, and schizophrenia. Most patients referred for A complete list of current medications should be ob-
ECT are seriously depressed, often suicidal or psychotic tained because some medications are known to interact
and unable to function because of their psychiatric with either the treatment or the anesthetic (Box 17-1).
illness. These patients have typically failed medical treat- Patients presenting for ECT are usually taking multiple
ment. ECT has been a safe and effective therapy for psychotropic medications. These medications may in-
refractory depression and other mental illnesses since its clude tricyclic antidepressants (TCAs), lithium carbon-
introduction. Most treatment-associated morbidity and ate, monoamine oxidase inhibitors (MAOIs), selective
mortality have been attributed to cardiovascular sequelae serotonin reuptake inhibitors (SSRIs), antipsychotics,
related to the physiologic response to treatment. benzodiazepines, and miscellaneous second-generation
ECT can be administered with either bilateral or unilat- antidepressants such as bupropion.
eral electrode placement. Bilateral electrode placement is TCAs block the reuptake of norepinephrine at the
associated with more rapid improvement but also portends postganglionic sympathetic nerve endings, resulting in
increased risk of short-term and long-term memory impair- increased baseline sympathetic tone. In these patients,
ment. Unilateral electrode placement is associated with less direct-acting sympathetic agents are preferred to indirect-
risk for memory-associated problems, but the clinical re- acting agents that increase the release of norepinephrine.
sponse may be slower and the patient may require a greater Several categories of drugs must be used cautiously with
82
17 Electroconvulsive Therapy 83
BOX 17-1 Anesthetic Implications of Selected psychiatric illnesses and may have no other treatment
Psychotropic Agents options. Consequently, the risk of death with no treat-
ment can be high enough to trump other concerns. Rela-
TCAs block reuptake of norepinephrine at postganglionic tive contraindications that may make anesthetic manage-
sympathetic nerve endings ment more complicated include the following:
• Drug levels of certain SSRIs (i.e., fluoxetine) may • Increased intracranial pressure (may be exacerbated
increase two to five times when used with TCAs during treatment)
MAOIs block the metabolism of catecholamines • Recent hemorrhagic stroke (!1 month) (increased
• Baseline sympathetic tone is increased risk for rebleed)
• Interaction with meperidine or indirect-acting sympa- • Retinal detachment (may be exacerbated during
thomimetic agents may lead to hypertensive crises,
seizures, and hyperpyrexia
treatment)
SSRIs block serotonin reuptake pump via the 5-hydroxy- A history of a recent myocardial infarction (!1 month)
tryptamine 1A receptor and unstable angina are not contraindications to ECT as
• Serotonin release is inhibited long as the patient is managed appropriately. Tachycardia
• 5-Hydroxytryptamine 1A receptors may be downregu- and hypertension occur frequently during ECT; either
lated one can predispose to repeat infarction. Cardiology con-
• There is little effect on norepinephrine reuptake sultation is important to assess risk and plan for appropri-
• An association with “serotonin syndrome” (restlessness, ate treatment. Severe coronary artery disease is a common
chills, ataxia, and insomnia), in combination with lith- life-threatening problem that can be exacerbated by ECT.
ium or carbamazepine, may be fatal The likelihood that further myocardial injury may occur as
Lithium carbonate prolongs neuromuscular blockade
Benzodiazepines may increase resistance to ECT by increasing
a result of treatment should be weighed against the risks of
the seizure threshold withholding ECT. It could be helpful to know the location
of lesions for which stent implantation is contraindicated,
the amount of myocardium at risk, and the results of
postinfarction stress tests because adverse hemodynamic
TCAs, antihypertensives, potent volatile agents, and conditions could occur during ECT. Patients should be
anticholinergics. given adequate " blockers and be normotensive before
MAOIs block the metabolism of catecholamines, in- treatment. Short-acting " blockers, such as esmolol, may
creasing baseline sympathetic tone as well. The interac- be administered during treatment along with nitroglycerin
tion between MAOIs and meperidine or indirect-acting or other short-acting agents to maintain blood pressure
sympathomimetic agents has been shown to lead to within the acceptable range. Clopidogrel and warfarin, if
hypertensive crises, seizures, and hyperpyrexia. indicated, may be continued.
Patients who have a history of pseudocholinesterase
deficiency or who are at risk for malignant hyperthermia 4. How are implanted cardioverter-defibrillators
present special problems. Both of these issues relate to and pacemakers managed for electroconvulsive
succinylcholine, a depolarizing muscle relaxant. Patients therapy?
with pseudocholinesterase deficiency are at risk for pro-
longed neuromuscular blockade if given succinylcholine, Artifacts produced by fasciculations from succinylcho-
so an alternative agent such as rocuronium should be line or interference from ECT might be misinterpreted
administered. Succinylcholine is contraindicated in pa- by a pacemaker or implantable cardioverter-defibrillator
tients with malignant hyperthermia because it is a known (ICD). Two approaches exist. One school of thought
trigger for the disease. suggests deactivating ICDs before ECT. The other
In the present case, none of the medications the pa- school of thought recommends allowing ICDs to func-
tient is taking appears to present a problem, but his blood tion normally. The rationale for deactivating ICDs
pressure is elevated. Because ECT is associated with before ECT is based on concern that artifacts gener-
acute but transient elevations in blood pressure, one ated during treatment could be interpreted as a treat-
needs to confirm that the patient has received his antihy- able rhythm by the internal device, resulting in dis-
pertensive medications according to schedule and that charge. Theoretically, such artifacts could result from
his blood pressure is within the expected range given his fasciculations in close proximity to sensing leads or from
history before proceeding. Additional antihypertensive electromagnetic interference produced by ECT devices.
medications may be administered immediately before the Unnecessary defibrillation from ICDs risks an electrical
procedure or on an “as-needed” basis to keep the systolic shock delivered during repolarization, R on T phenom-
pressure less than 200 mm Hg. The patient’s blood pres- enon, and real ventricular arrhythmias. Proponents of
sure should be measured frequently throughout the peri- allowing ICDs to function normally point out that even
operative period (every 1 to 2 minutes). an induced ventricular arrhythmia would be best treated
by the ICD. Because most treatment-associated mor-
3. Are there any relative or absolute bidity and mortality have been attributed to cardiovas-
cular sequelae of ECT, the benefit of allowing ICDs to
contraindications to electroconvulsive therapy?
remain active most likely outweighs the small risk of
ECT is generally a low-risk procedure, but many patients erroneous activation owing to artifact or interference.
who receive ECT fall into the “high-risk” category. Deactivation of ICDs is generally simple. A magnet
Some patients referred for ECT have life-threatening placed over most modern devices prevents defibrillation
84 SECTION 3 Central Nervous System
but allows the pacemaker function to continue. Reacti- the anesthetic and the neuromuscular blockade. In the
vation of most modern ICDs is achieved by removing United States, the drug of choice for induction of general
the magnet (Chapter 7). anesthesia is the ultra-short-acting barbiturate methohexi-
For a patient who has an implanted pacemaker, it is tal, although propofol and ketamine can also be used.
important to know why the device was placed. Although The advantage of using methohexital is rapid induction of
modern pacemakers are resistant to electromagnetic general anesthesia without adversely altering therapeutic
interference associated with ECT, there is a small risk of seizures. Additionally, methohexital is rapidly redistrib-
malfunction related to the treatment. Consequently, it is uted out of the brain so that the patient awakens soon after
prudent to have external pacing equipment available for the treatment has been performed. Propofol is not the
pacemaker-dependent patients. Theoretically, interfer- first-choice anesthetic for these procedures because it is
ence could either inhibit pacemaker output or reset the potently anticonvulsant and may raise seizure threshold or
device to a committed pacing mode (DOO or VOO). decrease seizure threshold. However, propofol has been
Applying a doughnut magnet to the pacemaker converts shown to be beneficial in patients with a history of pro-
it to a committed mode. Placing the doughnut magnet longed ECT-induced seizures and patients with a history
prevents inhibition of the device should interference of nausea and vomiting after ECT.
occur, and normal pacemaker function is restored on Succinylcholine is the drug of choice for neuromus-
magnet removal. Magnet application is not always re- cular blockade because of the short duration of these
quired. It is reasonable to have the magnet available for treatments. For patients in whom use of succinylcho-
application if inhibition of pacemaker output is noted line is contraindicated, rocuronium is an acceptable
coincident with treatment. Even if the device has been alternative.
placed into magnet mode, posttreatment interrogation is
not routinely required, but it should be performed by a 7. What concerns exist for the immediate postictal
trained individual when there is evidence of pacemaker period?
reset (i.e., asynchronous pacing). If there is any question,
a 12-lead electrocardiogram (ECG) should be obtained Return of spontaneous respiration generally occurs within
after the procedure (Chapter 7). 3 to 5 minutes after succinylcholine administration, which
is usually before emergence from general anesthesia. Ven-
5. What are the physiologic effects tilatory support via bag-valve-mask devices is indicated
until patients have adequate tidal volumes and are able to
of electroconvulsive therapy?
support their own airways without assistance. During this
The stimulus applied to the brain during ECT initially period, it is important to look for signs of light anesthesia
results in a profound parasympathetic surge. Asystole and residual paralysis, which may suggest prolonged suc-
during this period is common and may persist through- cinylcholine action requiring further ventilatory support
out the stimulus application. After stimulus termina- and either a reduction in succinylcholine dose on subse-
tion, the resulting seizure is accompanied by a pro- quent treatments or the use of a different neuromuscular
found sympathetic surge, commonly with associated blocking agent altogether. Hemodynamic instability is
tachycardia and hypertension. The elevation in blood common during this time, and patients who require tight
pressure is significant, and systolic blood pressure may blood pressure control should have their blood pressure
increase by 40% over baseline secondary to the increase checked frequently in the postictal period and receive
in sympathetic activity. If the patient does not have a medications as needed. Agitation after a seizure can result
seizure and asystole persists, treatment with atropine from hypoxia or hypercarbia as well as from the effects of
coupled with one or two rounds of chest compressions treatment. It is important to ensure appropriate oxygen-
may be necessary. In cases in which the risk of pro- ation and ventilation before administering posttreatment
longed asystole is high, pretreatment with an anticho- sedation.
linergic, such as glycopyrrolate, is often indicated.
One example is stimulus dose titration. Dose titration 8. Describe the events that lead to pulmonary edema
involves administration of increasing electrical stimuli after electroconvulsive therapy.
until a seizure is produced.
Elevated serum creatine phosphokinase has been re- Although very rare, pulmonary edema associated with
ported after ECT. Elevations of isoenzymes specific for ECT has been reported and may be due to numerous
myocardial infarction (CK-MB) are not observed with- causes, including negative pressure and neurogenic
out damage to the myocardium, even in patients with pulmonary edema. Negative pressure pulmonary edema
documented coronary artery disease and prior infarction. results when the patient attempts to inspire against a
closed glottis. Lax pharyngeal muscles are unable to lift
6. What is an appropriate anesthetic soft tissues out of the airway, allowing for upper airway
collapse and obstruction. Simultaneously, strong diaphragm
for electroconvulsive therapy?
and intercostal muscles generate substantial negative intra-
Anesthesia for ECT can directly influence the efficacy of thoracic pressures. Negative intrapleural pressures created
treatment. The goals are to induce general anesthesia in this way can overcome the Starling forces that keep
without increasing the seizure threshold, provide adequate plasma within capillaries. Fluid is drawn into alveoli,
muscle relaxation to prevent patient injury during motor resulting in pulmonary edema. Prevention is aimed at
seizures, and manage the patient until recovery from both restoring pharyngeal muscle tone, maintaining airway
17 Electroconvulsive Therapy 85
Spine Surgery
Stacie G. Deiner, MD
QUESTIONS
1. Does severe cervical stenosis necessitate awake 5. What are the concerns for prone positioning in
fiberoptic intubation? this patient?
2. How is chronic pain managed during major spine 6. Is there a safe range for mean arterial pressure
surgery? during spine surgery; what are the risks of induced
3. Explain the mechanism by which intraoperative hypotension?
neurophysiologic monitoring helps detect evolving 7. How would you use your knowledge of propofol
spinal injury; are there any contraindications to its pharmacology to ensure a rapid but safe
use? emergence?
4. How would you alter your anesthetic plan to
facilitate neurophysiologic monitoring?
A 73-year-old man with spinal cord compression pre- more movement of the cervical spine than a well-executed
sented for posterior cervical fusion (C3-6). For the past fiberoptic intubation. Some channel-type videolaryn-
year, he has experienced neck pain and increasing weak- goscopes (e.g., Airway Scope (AWS) S-100; [Pentax-AWS
ness and “tingling” in his right arm. His medications in- system]; AWS; Pentax, Tokyo, Japan, and AirTraq [ATQ;
cluded sustained-release oxycodone, 40 mg twice a day, Prodol Meditec, Vizcaya, Spain]) have been shown to
and oxycodone 5 mg/acetaminophen 650 mg, 2 tablets produce less cervical spine movement relative to direct
every 4 hours, although he did not take his medication the laryngoscopy. Glidescopes (Glidescope® videolaryngo-
morning of surgery. Radiology studies showed severe scope (Verathon, Bothell, WA) have been shown to cause
cervical spinal cord compression. The neurophysiologic less cervical spine movement at C2-5 but similar move-
monitoring team monitored somatosensory evoked po- ment to direct laryngoscopy at other levels, which means
tentials (SSEPs), motor evoked potentials (MEPs), and that Glidescopes are not a better choice for cases with
electromyography (EMG) beginning after induction to more rostral cervical instability. However, the Glidescope
obtain a baseline before positioning. does produce improved views, even with a cervical im-
mobilization collar in place. The advantage of these alter-
1. Does severe cervical stenosis necessitate awake native devices is their larger field of view, making them
fiberoptic intubation? better choices for an airway with a large amount of secre-
tions or blood or debris, such as in a trauma patient.
The decision to perform an awake fiberoptic intubation for
patients with cervical spine disease depends on the location
of the injury or disease, the risk of aspiration (full stomach), 2. How is chronic pain managed during major spine
the anticipated relative ease of mask ventilation, and the surgery?
patient’s ability to cooperate with airway anesthesia. Awake
Preoperative
fiberoptic intubation is the “gold standard” to minimize
neck movement caused by mask ventilation and direct la- Although transdermal systems (e.g., fentanyl patch)
ryngoscopy. Additionally, any patient who has risk factors should not be initiated, they should be continued if
for difficult mask ventilation (i.e., obesity, !55 years old, already in use. Patients should be instructed to take their
history of snoring, lack of teeth, the presence of a beard, oral medications, with the exception of nonsteroidal
Mallampati class III or IV, abnormal mandibular protrusion antiinflammatory drugs, which should be discussed with
test) should be considered for awake intubation. In an unco- the surgeon. For opioid-tolerant patients who refrain
operative patient, one must weigh the risk of induction from pain medication on the morning of surgery, the
versus movement from agitation or inadequate airway anes- daily opioid consumption can be calculated and con-
thesia. Induction before tracheal intubation is an option for verted to the equivalent intravenous morphine dosage.
patients who are not at increased risk for aspiration and for This calculation provides an approximation of the daily
whom mask ventilation is not predicted to be difficult. opioid intake, some of which should be administered
Videolaryngoscopes may be useful to secure the airway intravenously during surgery. Converting oral opioids
in patients with limited mobility, although they can cause to an intravenous dose is controversial; however, the
86
18 Spine Surgery 87
underlying principle is that surgical patients who are 3. Explain the mechanism by which intraoperative
opioid-tolerant require opioid dosing based on their neurophysiologic monitoring helps detect evolving
usual consumption. spinal injury; are there any contraindications to
Oral gabapentin can reduce morphine consumption
its use?
and pain scores in the first 12 hours after surgery. The
optimal preoperative dose to maximize pain control and Three major categories of neurophysiologic monitoring
minimize side effects ranges from 600 to 900 mg. The are routinely performed for spine surgery: SSEPs, MEPs,
most common side effects are nausea and vomiting, light- and EMG.
headedness, and ataxia. Because many patients with • SSEPs monitor the integrity of the dorsal columns
chronic pain have experience with gabapentin, it is pru- of the spinal cord. An electrical or magnetic impulse
dent to ascertain effective dosing for each individual is delivered to the periphery, producing electrical
patient. In some cases, side effects limit use of gabapen- potentials that propagate through the spinal cord to
tin. Based on this information, a decision can be made for the brain. The waveform that is generated can be
or against administering gabapentin preoperatively and measured at the level of the spinal cord proximal to
at what dose. the surgical field or at the brain (Figure 18-1).
• MEPs monitor the integrity of the anteriorly located
Intraoperative motor tracts of the spinal cord. An electrical or
magnetic impulse is delivered to the brain or spinal
Methadone can be an important part of the intraoperative cord proximal to the surgical site and measured as D
opioid regimen in opioid-tolerant patients undergoing and I waves with epidural electrodes on the surgical
major spine surgery. A single bolus dose of methadone field (less common) or as compound muscle action
(0.2 mg/kg) may reduce postoperative opioid use and potentials measured by pairs of needles over the
visual analog scale scores for 48 hours postoperatively. muscle corresponding to the monitored nerve (more
Ketamine can also be a useful adjunct during spine sur- common).
gery because it is profoundly analgesic and may improve • EMG is a measurement of electrical activity generated
the quality of intraoperative monitoring. Especially for by muscle contraction, monitored by two electrodes
opioid-dependent patients, the use of intraoperative in or near a muscle. Two major types of EMG are
ketamine (0.5 mg/kg on induction of anesthesia, with recorded during surgery:
continuous infusion at 10 "g/kg/min terminated at wound • Passive or free run—continual monitoring of a
closure) can reduce opioid requirements and pain scores muscle for spontaneous activity
up to 48 hours to 6 weeks later without an increase in side • Stimulated EMG—an electrical stimulus is applied
effects. The mechanism of action of ketamine includes near or to a nerve, and the response is recorded
N-methyl-d-aspartate receptor antagonism. over the muscle
FIGURE 18-1 ■ Signal loss in SSEP trace. Top arrow indicates normal; bottom arrow indicates loss.
88 SECTION 3 Central Nervous System
Neuromonitoring is sensitive for spinal cord injury patient positioning, the effects of muscle relaxants used
from any etiology. Surgical causes include ischemia from for intubation should have dissipated or been antago-
trauma, compression, or transection. In addition to surgi- nized. The intravenous anesthetic infusion should be
cal causes, there have been many reports of loss of signals immediately available to avoid having to readminister a
from malpositioning during surgery. A classic example bolus to restore adequate blood levels.
would be an impending brachial plexus injury. Loss of The components of an anesthetic for spine surgery
signal in an area where the surgeon is not working and not involving neurophysiologic monitoring include the
associated with a prior deficit should alert the anesthesi- following:
ologist to recheck the positioning of the affected limb. • For amnesia, propofol infusion is most commonly
A more global loss of signal could be associated with used, sometimes in combination with ketamine,
a change in the anesthetic depth (e.g., introduction of dexmedetomidine, or less than 0.5 minimum alveo-
potent inhalation agent, bolus of an intravenous agent, or lar concentration (MAC) of a potent inhalation
muscle relaxant) or a significant physiologic change such agent.
as hypotension or severe anemia. • For analgesia, an opioid infusion is used.
Although SSEPs and MEPs monitor the integrity of a The choice of which particular agent is administered
tract, they may be unable to detect injury of a single nerve depends on the patient’s underlying medical conditions
root. EMG allows the identification of a single nerve, and whether the patient is opioid-tolerant. Administra-
especially in cases where the anatomy is abnormal (e.g., tion of potent inhalation anesthetics depends on which
scar tissue, tumor). EMG is extremely sensitive and can neurophysiologic monitoring is used during the surgery.
detect activation of only 1% to 2% of a muscle’s fibers. Compared with SSEPs, MEPs are more sensitive to the
Commonly monitored nerves include the following: effects of inhalation agents. Studies suggest that a rela-
• Cervical nerve roots during spine surgery (C2-7) tively low-dose volatile agent (i.e., 0.25 to 0.5 MAC) is
• Lumbosacral (L2-S2) during spine surgery enough to suppress single pulse transcranial stimuli.
• Facial nerve during acoustic neuroma surgery or Although more aggressive stimulation patterns can pro-
parotid surgery duce compound muscle action potential responses in
• Recurrent laryngeal nerve during anterior cervical some patients, others are entirely unattainable. Patient
surgery factors that may contribute to volatile agent sensitivity
• Cranial nerves during brainstem surgery include myelopathy secondary to chronic spinal cord
Relative contraindications for evoked potential moni- compression and diabetic neuropathy.
toring include the following: Similarly, muscle relaxant infusion is controversial be-
• Implanted pacemaker cause the relationship between MEPs and train-of-four
• Functioning implantable cardioverter-defibrillator— responses is not linear. It is possible for a patient to have
in high-risk cases may need to disable antitachyar- one or two twitches with train-of-four monitoring but
rhythmia function absent MEPs.
• Implanted metal in the cranial vault (e.g., aneurysm Stimulation of the cervical motor tracts causes jaw
clips) contractions and may result in bite-related patient injury.
• Epilepsy These injuries range from lingual hematoma to mandib-
• Increased intracranial pressure ular fracture. Tracheal extubation may be precluded if
• Convexity defects of the skull hematoma formation is significant. Bite-blocks are rec-
In all cases, the risks of surgery without neurophysio- ommended during cervical tract motor stimulation.
logic monitoring must be weighed against the risk of However, it is still possible to sustain oral injuries even
arrhythmia, seizure, or thermal injury. with a bite-block in place. Compression of the rear por-
tion of the tongue (usually on the opposite side of the
4. How would you alter your anesthetic plan tracheal tube) can occur.
to facilitate neurophysiologic monitoring?
5. What are the concerns for prone positioning in
Both MEP and SSEP monitoring are affected to some this patient?
degree by all anesthetics. The goal is to create a constant
depth of anesthesia during acquisition of baseline signals Most spine surgeries are performed in the prone posi-
that would be maintained throughout surgery. This tion, which may improve ventilation in many cases.
approach avoids introducing an anesthetic or a physio- However, malpositioning may lead to significant morbid-
logic change that could be confused with surgical injury ity. In osteoporotic patients and patients with cervical
to the spinal cord. instability, particular attention should be given to posi-
Inhalation anesthetics cause a decrease in waveform tioning. Before induction, patients should be allowed to
amplitude and an increase in latency. Intravenous anes- position themselves for comfort in the supine position.
thetics with two exceptions, etomidate and ketamine, to After induction and tracheal intubation, it is important to
varying degrees cause a decrease in waveform amplitude log roll the patient safely with in-line stabilization of the
and an increase in latency. Etomidate and ketamine may neck. Whether a commercially available table and frame
increase waveform amplitude. Dexmedetomidine infusion or a regular operating table with bolsters and padding is
appears to have no deleterious effects on neuromonitoring. used, the overall goals are the same. The patient’s neck
During MEP monitoring, muscle relaxants should not should be maintained in neutral position with a foam
be administered. If MEP monitoring is instituted before headrest or cervical traction device. Horseshoe headrests
18 Spine Surgery 89
have fallen out of favor for prone positioning because of antifibrinolytics such as aminocaproic acid. Aminocaproic
an association with postoperative blindness when they acid has been shown to decrease intraoperative require-
impinge on the lateral canthus of the eye. Every effort ments for transfusion, although there is a small risk of
should be made to avoid positioning the patient with the thrombosis. Generally, a loading dose is followed by an
face turned to one side because this is associated with infusion continued throughout the case.
postoperative blindness and stroke.
Arm positioning may be challenging in patients who had 7. How would you use your knowledge of propofol
previous shoulder surgery or traumatic injury. Positioning pharmacology to ensure a rapid but safe
is often dictated by the need for intraoperative fluoroscopy emergence?
or x-ray. Most often, patients undergoing cervical spine
surgery have their arms secured at their sides. The surgeon Rapid awakening after long surgery using total intrave-
may tape the patient’s shoulders down to improve visualiza- nous anesthesia (TIVA) requires advanced planning
tion of the lower cervical and upper thoracic spine during because the time required for drug elimination is depen-
routine fluoroscopy or to help contour a wound for incision dent on the infusion duration. Context-sensitive half-life
and closure. Care must be taken to avoid overaggressive is the time required for the plasma concentration of a
traction on the shoulders and brachial plexus because this drug to decrease by 50% after cessation of an infusion
can lead to neurologic injuries. Occasionally, traction on designed to maintain a constant concentration. Based on
the shoulders may need to be released during surgery based pharmacologic studies, a 50% reduction in plasma drug
on neurophysiologic monitoring changes suggestive of concentration is necessary for recovery after a steady-state
undue stretch on the brachial plexus. infusion of most intravenous hypnotics (Figure 18-2).
Patients undergoing lumbar surgery have their arms Based on these findings, cessation of the intravenous
positioned at 90 degrees in all planes, supported by arm anesthetic after a prolonged procedure may be necessary
boards. Typically, the shoulder is abducted, with minimal 40 minutes before surgical finish. Commonly, during
shoulder flexion and 5 to 10 degrees of internal rotation. closure of the incision, neuromonitoring is discontinued,
Neuromonitoring can help assess neck and brachial and if necessary, a potent inhalation agent can be added.
plexus position throughout surgery. Processed electroencephalography (EEG) monitoring
Finally, lengthwise bolsters should be placed to support may give some insight into tapering anesthetic infusions
the patient from the tip of the shoulders to the iliac crests with respect to amnesia, although it is not helpful as an
allowing the abdomen to hang freely; this provides for index of immobility. Sevoflurane and propofol affect
venous return and diaphragmatic excursion during venti- movement to noxious stimuli differently at equivalent
lation. Legs should be bent at the knees. The hips may be levels of consciousness. At an equivalent depression of the
extended to create lordosis of the lumbar spine for fusion processed EEG, sevoflurane suppresses the blink reflex
or flexed for decompression procedures without fusion. more than propofol, indicating different pharmacody-
All pressure points and areas where peripheral nerves are namic properties of these anesthetics at the brainstem
subject to compression (e.g., ulnar nerve at the elbow, level. The differential level of immobility at similar levels
peroneal nerve at the fibular head) should be padded with of hypnosis can make titration of TIVA during spine
foam, and the wrist should be in a neutral position to surgery without the use of muscle relaxants complex.
protect the median nerve. Although an immediate postoperative neurologic exami-
nation is desirable, extubation of the trachea should not
6. Is there a safe range for mean arterial pressure be attempted unless accepted extubation criteria are met.
during spine surgery; what are the risks of Caution should be exercised if the patient is extremely
edematous or there is evidence of hemodynamic instability.
induced hypotension?
“Adequate” intraoperative blood pressure during spine
300
surgery is a complicated issue. Both the brain and the spinal
Context-sensitive half-time (minutes)
SUGGESTED READINGS Sloan TB, Heyer EJ: Anesthesia for intraoperative neurophysiologic
Jameson LC, Janik DJ, Sloan TB: Electrophysiologic monitoring in monitoring of the spinal cord. J Clin Neurophysiol 19:430, 2002.
neurosurgery. Anesthesiol Clin 25:605, 2007.
Lee LA, Roth S, Posner KL, et al.: The American Society of Anesthe-
siologists Postoperative Visual Loss Registry: analysis of 93 spine sur-
gery cases with postoperative visual loss. Anesthesiology 105:652, 2006.
CASE 19
Transsphenoidal Hypophysectomy
Irene P. Osborn, MD
QUESTIONS
A 44-year-old man with marked features of acromeg- and IGF-I levels are controlled via several interac-
aly presents for transsphenoidal hypophysectomy. The tions rather than stimulating growth directly. GH in-
patient reports increasing shoe size, glove size, and duces the release of IGF-I, which promotes DNA,
worsening sleep apnea. Magnetic resonance imaging RNA, and protein synthesis as well as cell and tissue
revealed a pituitary mass. Laboratory findings are growth.
within normal limits with the exception of serum glu-
cose, which is 170 mg/dL. The patient does not have 2. What symptoms are typical of acromegaly?
any allergies and does not take medications at home.
Past surgical history includes carpal tunnel release bi- The structural changes of acromegaly cause chronic pain
laterally. He denies other medical problems. and discomfort. These symptoms reduce quality of life
and life expectancy. Changes include skeletal overgrowth
deformities (particularly of the hands, feet, and face),
1. What is acromegaly?
cardiovascular disease (hypertension, enlarged heart),
Acromegaly was previously considered a rare disease. arthropathy, neuropathy, and respiratory obstruction
However, more recent European studies and improved (Boxes 19-1 and 19-2).
screening suggest that clinically significant pituitary
adenomas occur in 1 per 1064 people. Growth hor- 3. How is acromegaly treated?
mone (GH)–secreting tumors of the pituitary consti-
tute at least 10% of benign pituitary tumors. The pitu- Acromegaly is a severe, often chronic disease with in-
itary gland is anatomically and functionally separated creased mortality rates if it is not treated appropriately.
into the anterior pituitary (adenohypophysis) and pos- Treatment options include surgery, medical therapy, and
terior pituitary (neurohypophysis). In children, GH- radiation. Each modality has specific advantages and dis-
secreting tumors cause gigantism; acromegaly occurs advantages.
in adults whose epiphyses have fused. Acromegaly is Surgical therapy is the primary treatment for most
most common in patients 20–60 years old, with equal symptomatic adenomas. There are several surgical ap-
distribution between the genders. The diagnosis is gen- proaches to pituitary masses. Most pituitary masses can
erally made 10–15 years after the onset of pathologic be removed adequately via a transsphenoidal approach.
GH secretion. There is a twofold to fourfold increase This approach is associated with less morbidity (e.g.,
in mortality versus the general population. If un- hypopituitarism, diabetes insipidus) and mortality than
treated, 50% of patients with acromegaly die before transcranial resections and radiation. Larger lesions with
age 50 years. The most common cause of death is car- extensive growth outside the sella are best approached
diac and may be the result of hypertension, coronary through craniotomy.
artery disease, compensatory hypertrophy as a result of Oral medical therapy includes bromocriptine, a dopa-
generalized somatomegaly, or the direct effects of GH mine agonist, and levodopa, a dopamine precursor. These
on the heart. agents suppress hypothalamic-mediated GH levels and
Acromegaly results from excess secretion of GH decrease tumor size. In addition to somatostatin analogues,
and subsequent elevation of circulating and locally these agents may offer alternatives to surgery in debili-
produced insulin-like growth factor I (IGF-I). GH tated or elderly patients.
91
92 SECTION 3 Central Nervous System
BOX 19-1 Airway Changes in Acromegaly arrhythmias in the presence or absence of volatile agents.
Hypertension and bleeding during intrasellar exploration
ANATOMIC may be controlled effectively with appropriate anesthetic
Hypertrophy depth and intravenous administration of !-adrenergic
• Facial bones—large bulbous nose blockers or vasodilators. Practical considerations include
• Nasal turbinates difficulty in positioning of large extremities and place-
• Soft palate ment (if needed) of intraarterial catheters. Also, a throat
• Tonsils pack is inserted to prevent aspiration of blood from oro-
• Epiglottis pharyngeal pooling. The throat pack is removed at the
Glottic stenosis end of surgery, before extubation.
Impaired mobility of cricoarytenoid joints
Compression of recurrent laryngeal nerves
Limitation in head and neck mobility 5. Describe the airway management concerns
for patients with acromegaly.
PHYSIOLOGIC
Development or exacerbation of sleep apnea Airway assessment begins with careful history taking and
Hoarseness physical examination. Airway obstruction is one of sev-
Dyspnea eral mechanisms that are associated with difficult airway
management in these patients. Compared with patients
without acromegaly, this group of patients presents a
higher incidence of predicted and unpredicted difficult
intubations and problematic mask ventilation. A recent
BOX 19-2 Peripheral Effects of Excess
history of an uneventful intubation may be reassuring;
Growth Hormone
however, anatomic and physiologic changes over the
ANATOMIC course of 1–5 years may change that. Typical features,
such as large tongue, large epiglottis, distortion of the
Skeletal overgrowth
• Gigantism larynx, and soft tissue swelling, complicate visualization
• Enlarged hands and feet of the larynx in patients with acromegaly. Patients with-
• Distortion of facial features out hoarseness or dyspnea and with adequate mouth
• Prognathism opening may be cautiously approached in the routine
Soft tissue overgrowth manner. Only oral intubation or tracheostomy can be
• Enlarged lips, tongue, epiglottis, and vocal cords considered for transsphenoidal surgery because nasal in-
• Visceromegaly tubation would obstruct the surgical field. Patients are
Connective tissue overgrowth instructed preoperatively that mouth breathing will be
• Recurrent laryngeal nerve paralysis required in the postoperative period because of bilateral
Peripheral neuropathy
nasal packs.
• Carpal tunnel syndrome
The American Society of Anesthesiologists Difficult
PHYSIOLOGIC Airway Algorithm is a good framework to treat failed
Glucose intolerance intubation and difficult ventilation. Although it may
Hypertension be prudent to secure the airway with the patient awake,
Osteoarthritis fiberoptic-guided intubation is often challenging because
Osteoporosis of excessive soft tissue in the oropharynx. Minimizing
Skeletal muscle weakness mechanical trauma to the upper airway and vocal cords is
an important consideration because additional edema can
result in airway obstruction after tracheal extubation. An
awake and responsive patient is needed for safe removal
4. What are the anesthetic considerations of the tracheal tube.
for patients with acromegaly?
6. What structures lie within the transsphenoidal
The constellation of physical manifestations of acro-
megaly, especially heart and lung disease, combined with
surgical field?
upper airway involvement, presents particular concern The sella turcica, within the body of the sphenoid, pro-
to the anesthesiologist. Cardiac complications in patients vides bony protection for the pituitary gland. The dia-
with acromegaly have been described, and cardiomegaly phragma sella is a roof of dura pierced by the pituitary
can occur with or without coexisting hypertension. stalk with its arachnoid, which extends to the hypothala-
Many typical acromegalic features suggest difficult air- mus. The cavernous sinus surrounds the walls of the sella
way management in these patients (see Question 5). and contains the cavernous portion of the internal ca-
An anesthetic technique appropriate for most patients rotid artery and cranial nerves III, IV, and VI. The fifth
with acromegaly focuses on opioids, volatile agent, ni- cranial nerve, which provides facial and eye sensation, is
trous oxide, and muscle relaxants. Many surgeons use in the outside wall of the cavernous sinus. The optic
intranasal epinephrine-containing local anesthetics and nerves converge above the diaphragm to form the chiasm.
cocaine as part of their presurgical preparation. The use Arterial bleeding during transsphenoidal hypophysec-
of these solutions reduces bleeding but also may lead to tomy may be from the carotid artery or its branches, and
19 Transsphenoidal Hypophysectomy 93
NEUROMUSCULAR SYSTEM
94
CASE 20
Depolarizing Neuromuscular
Blockade
Michael T. Bialos, MD • James B. Eisenkraft, MD
QUESTIONS
1. What is the differential diagnosis for a healthy 5. Explain the potential side effects of
patient whose vital signs are stable but who is succinylcholine administration.
not “waking up” after general anesthesia? 6. What are the contraindications to succinylcholine
2. How is normal neuromuscular transmission administration?
accomplished? 7. What is the best and safest neuromuscular
3. Describe the mechanism of action of blocking drug for rapid-sequence induction?
succinylcholine. 8. Are there any drugs that could replace
4. How is the action of succinylcholine terminated? succinylcholine in the future?
An otherwise healthy, 16-year-old boy weighing 60 kg is administered shortly before the end of a procedure? The
scheduled for urgent appendectomy. Following preoxy- metabolism of each drug must be considered as well. Is
genation, rapid-sequence induction is carried out with there something interfering with the metabolism of one
propofol 130 mg, fentanyl 150 !g, and succinylcholine or more agents? Are small amounts of many agents work-
80 mg intravenously. Cricoid pressure is maintained ing additively to produce unconsciousness and apnea?
throughout induction. Direct laryngoscopy and tracheal Metabolic disturbances in a patient with normal vital
intubation are easily accomplished. Ventilation is con- signs can also produce prolonged unconsciousness and
trolled and anesthesia is maintained with 2% sevoflurane apnea. Hyponatremia, which can be produced by plasma
in 80% oxygen with air. During surgery, the patient dilution during transurethral prostate surgery, can lead
receives 500 mL of 0.9% saline and 1 g of cefazolin. Vital to severe mental status changes. Hypoglycemia, which
signs are stable throughout, and the procedure is com- may follow insulin administration in a fasting patient, can
pleted 35 minutes after induction of anesthesia. As the also produce unconsciousness. Hypocalcemia, which may
skin is being closed, sevoflurane is discontinued, and follow administration of multiple units of banked blood
100% oxygen is administered. At 20 minutes after the end products, can lead to such profound weakness as to pro-
of the procedure, the end-tidal concentration of sevoflu- duce apnea, especially in malnourished and frail patients.
rane is 0.0%, heart rate and blood pressure are increasing, Finally, prolonged hypotension and hypoperfusion can
end-tidal carbon dioxide (ETCO2) is 35 mm Hg, and result in global neurologic sequelae. Misuse and misinter-
there is no spontaneous respiration. pretation of blood pressure monitoring devices can lead
to this type of disaster. Documented cases exist of a
1. What is in the differential diagnosis for a healthy patient undergoing surgery and general anesthesia in the
patient whose vital signs are stable but who is not sitting position, with a noninvasive blood pressure cuff
“waking up” after general anesthesia? on the calf. The pressure gradient between the brain
and the lower extremities can be significant. Prolonged
Assuming stable and appropriate blood pressure, heart hypoperfusion of the brain has resulted in adverse out-
rate, arterial oxygen saturation, core temperature, and comes despite “normal” blood pressure readings that
ETCO2, the differential diagnosis can be divided into were measured in a dependent lower extremity.
three main categories: anesthetic drugs, metabolic distur-
bances, and neurologic problems. 2. How is normal neuromuscular transmission
It is important to consider every drug administered
during the perioperative course, including opioids, ben- accomplished?
zodiazepines, potent inhaled anesthetics, neuromuscular As the action potential of a motor neuron depolarizes
blocking agents, and other drugs such as ketamine and its terminal, an influx of calcium ions causes vesicles con-
dexmedetomidine. Did an opiate-naïve patient receive taining acetylcholine to fuse with the terminal mem-
enough fentanyl to produce apnea after a short proce- brane, releasing acetylcholine into the synaptic cleft.
dure? Was a long-acting neuromuscular blocking drug Acetylcholine molecules diffuse across the synaptic cleft
95
96 SECTION 4 Neuromuscular System
and bind to nicotinic cholinergic receptors on the motor For normal intubating doses of 0.6–2 mg/kg intrave-
end plate (Figure 20-1). The binding of acetylcholine nously, succinylcholine has a duration of action of roughly
to these receptors produces conformational changes in 5–10 minutes. Several abnormalities can prolong the
transmembrane ion channels that allow sodium and cal- duration of action of succinylcholine. Hypothermia can
cium ions to flow into the muscle cell, generating an end slow the action of pseudocholinesterase. Low plasma
plate potential. If enough receptors are bound by acetyl- pseudocholinesterase levels, as found in pregnancy, renal
choline, the motor end plate potential will be strong failure, and hepatic failure, can prolong the action of suc-
enough to depolarize the perijunctional membrane of the cinylcholine. However, because normal pseudocholines-
muscle fiber, and voltage-controlled sodium channels terase breaks down succinylcholine so efficiently, even
within this portion of the muscle membrane will open, low plasma levels of this enzyme usually do not prolong
producing the beginning of an action potential, which is the duration of action of succinylcholine to "30 minutes.
propagated along the muscle fiber. Some patients may have genetically determined abnor-
mal pseudocholinesterase that does not break down
succinylcholine. Approximately 1 in 50 patients has one
3. Describe the mechanism of action
normal and one abnormal gene (heterozygous) coding
of succinylcholine. for pseudocholinesterase, which results in a moderately
Succinylcholine is the only depolarizing neuromuscular prolonged drug action of 20–30 minutes. Approximately
blocking drug in clinical use. Its blocking properties 1 in 3000 patients are homozygous for the gene coding
are due to the chemical mimicry of acetylcholine. Succi- that produces atypical pseudocholinesterase. These
nylcholine acts as an agonist at the nicotinic cholinergic patients have virtually no working pseudocholinesterase
receptors at the motor end plate, producing a muscle enzyme and have very prolonged neuromuscular block
action potential and the muscle fasciculations associated after administration of a normal intubating dose of suc-
with succinylcholine administration. However, in con- cinylcholine, possibly up to 8 hours. In these cases, pa-
trast to acetylcholine, succinylcholine is not metabolized tients must remain sedated, intubated, and supported
by acetylcholinesterase, and the concentration of succi- with mechanical ventilation until the drug has been me-
nylcholine in the synaptic cleft remains relatively high tabolized by other pathways. There is presently no clini-
for a period of time. As long as succinylcholine remains cally approved reversal agent for succinylcholine-induced
in the synaptic cleft, it binds to nicotinic cholinergic re- neuromuscular blockade.
ceptors there. The result is continuous motor end plate
depolarization and neuromuscular blockade. 5. Explain the potential side effects
of succinylcholine administration.
4. How is the action of succinylcholine terminated?
Succinylcholine is the only depolarizing neuromuscular
In normal subjects, succinylcholine is very rapidly metabo- blocking agent available to practicing clinicians. The drug
lized by plasma pseudocholinesterase. The metabolism of has a host of potentially lethal side effects. With so many
succinylcholine by this enzyme is normally so efficient that nondepolarizing neuromuscular blocking agents available
only a fraction of the drug injected in a peripheral vein today, why is it still in such widespread clinical use? The
ever reaches the nicotinic cholinergic receptors in the answer is its rapid onset of action (30–45 seconds) and
synaptic cleft. As plasma succinylcholine levels decrease superior skeletal muscle relaxation. It is faster and more
with metabolism, succinylcholine molecules diffuse away efficacious than any other paralytic agent given in a rea-
from the neuromuscular junction, restoring normal neu- sonable, safe, and effective dose; this may be due to the
romuscular transmission. relative “overdose” that clinicians routinely administer
20 Depolarizing Neuromuscular Blockade 97
before laryngoscopy (1.5 mg/kg is four to five times the 60 minutes of discontinuing succinylcholine infusion
95% effective dose [ED95] of this drug). In normal me- in normal metabolizers. Neostigmine may speed the re-
tabolizers, the offset of succinylcholine, without pharma- covery from a phase II block, although the response to
cologic antagonism, is reliably faster than that of any other anticholinesterases is unpredictable.
neuromuscular blocking drug. Succinylcholine generally
produces optimum relaxation for laryngoscopy, which is 6. What are the contraindications to succinylcholine
extremely important for obtaining adequate laryngeal
views. Should intubation and mask ventilation prove to administration?
be difficult or impossible, succinylcholine’s short duration The contraindications to succinylcholine administration
of action offers the greatest likelihood that patients will are listed in Box 20-1.
recover spontaneous ventilation before hypoxemia ensues.
There is no other neuromuscular blocking agent currently 7. What is the best and safest neuromuscular
available that can provide this type of “fast on, fast off”
performance. blocking drug for rapid-sequence induction?
So why not use succinylcholine routinely? Many prac- Rapid-sequence induction and intubation is a technique
titioners still do, but it is imperative to understand the designed to facilitate expeditious tracheal intubation
potential pitfalls and side effects. and protect from aspiration of gastric contents. The
The greatest hazard in the use of succinylcholine is the objective is to minimize the time between loss of pro-
potential for sudden and severe hyperkalemia, possibly tective airway reflexes and tracheal intubation with a
leading to cardiac arrest. In normal patients, serum potas- cuffed tracheal tube. The concept of rapid-sequence
sium levels increase approximately 0.5 mEq/L after an induction and intubation has evolved slowly starting
intubating dose. Patients with spinal cord injuries, severe with the introduction of succinylcholine in the early
burns, crush injuries, intraabdominal sepsis, or prolonged 1950s and the description of cricoid pressure a decade
immobilization commonly have proliferation of extrajunc- after that. Much controversy surrounds the current un-
tional nicotinic cholinergic receptors. These receptors are derstanding of what constitutes the best set of drugs and
the result of upregulation after a relative loss of motor techniques to perform the safest rapid-sequence induc-
neuron function, and if they are stimulated by succinyl- tion and intubation.
choline, a sudden increase of potassium (several mEq/L) The FDA approves only two neuromuscular blocking
may result. A similar clinical scenario can result from the drugs for this purpose at the present time: succinylcholine
administration of succinylcholine to young male patients and rocuronium. The choice of drug depends on the par-
with undiagnosed myopathy. In the early 1970s, the ticular patient and the clinical scenario. Most practicing
United States Food and Drug Administration (FDA) is- clinicians agree that succinylcholine produces the most
sued a “black box” warning concerning the use of succinyl- profound relaxation of jaw muscles and laryngeal muscles
choline in young and adolescent boys because of the pos- in the shortest period of time, and it remains the best op-
sibility of hyperkalemic cardiac arrest in patients with tion in otherwise healthy patients. In addition, the relax-
undiagnosed myopathy. When the need to secure an air- ant effect of succinylcholine is almost always limited to
way as quickly as possible arises in a young male patient, 5–10 minutes in normal metabolizers, providing a good
the practitioner must use his or her best judgment when possibility for the early return of spontaneous ventilations
weighing the risks and benefits of the airway emergency should intubation or ventilation be more difficult than
against the rare, but potentially fatal, possibility of undiag- anticipated. This property of succinylcholine provides a
nosed myopathy and hyperkalemia. distinct safety advantage over long-acting nondepolariz-
Another remote but potentially deadly problem with ing neuromuscular blocking drugs in patients who are
succinylcholine is that it is a recognized malignant hyper-
thermia trigger. It must be avoided in any patient who
may be susceptible to malignant hyperthermia. Likewise,
in any facility where succinylcholine is being used, there
BOX 20-1 Contraindications to
must be adequate supplies of malignant hyperthermia
Succinylcholine Administration
rescue drugs, including dantrolene, and medical staff
trained to recognize and treat an episode of malignant Allergy to succinylcholine
hyperthermia. Known or suspected malignant hyperthermia
Other complications associated with the administration Pseudocholinesterase deficiency or abnormality
of succinylcholine include masseter muscle spasm, myal- Spinal cord transection
gias, increased intraocular and intracranial pressures, and Stroke "72 hours old
allergic reactions. Prolonged immobilization
Although not technically a side effect, prolonged ad- Crush injury
ministration of succinylcholine as an infusion, especially Intraabdominal sepsis
Burn injury "72 hours old
without neuromuscular monitoring, can lead to phase II
Muscular dystrophy
neuromuscular blockade. A phase II block is character- Multiple sclerosis
ized by fade on train-of-four stimulation, the pattern of Amyotrophic lateral sclerosis
response typical of nondepolarizing muscle relaxants. Rhabdomyolysis
Patients in phase II blockade must receive positive pres- Significant hyperkalemia
sure ventilation. A phase II block typically resolves within
98 SECTION 4 Neuromuscular System
super obese (and may be impossible to ventilate) or have similar to that of succinylcholine, and any new depolariz-
other airway abnormalities that could make laryngoscopy ing drug developed would almost certainly have the same
challenging. side-effect profile as succinylcholine owing to its action as
As described earlier, succinylcholine has many hidden a depolarizing agent.
dangers. A patient in need of rapid-sequence induction Sugammadex is a novel drug designed to encapsulate
and intubation often has sustained trauma, spinal cord rocuronium (and vecuronium) molecules, effectively termi-
injury, prolonged immobilization, or severe infection. In nating their bioavailability. Sugammadex may offer a major
such cases, the risk of extrajunctional cholinergic recep- breakthrough in the antagonism of nondepolarizing neuro-
tor proliferation is high. Using succinylcholine in these muscular blocking drugs. It is more efficacious than neo-
patients poses a risk of severe hyperkalemia. Succinylcho- stigmine in antagonizing profound rocuronium-induced
line must be avoided in patients with a known malignant and vecuronium-induced blockade. By itself, sugammadex
hyperthermia risk, allergy to the drug, or known myopa- does not affect neuromuscular function, and, in contrast
thy. In patients for whom succinylcholine is considered to neostigmine and other anticholinesterases, it does not
possibly harmful, clinicians must weigh the risks and ben- create cholinergic excess. Sugammadex would effectively
efits and consider inducing neuromuscular blockade with allow clinicians to use large overdoses of rocuronium to
rocuronium. produce profound relaxation rapidly for however brief
Although succinylcholine 1 mg/kg intravenously a time period desired, followed by complete antagonism
usually produces excellent intubating conditions within within 1–2 minutes. Use of sugammadex could end the
45–60 seconds, a “double dose” of rocuronium 1.2 mg/kg need for development of ultra-short-acting nondepolariz-
must be used to meet the FDA-approved standard for ers to replace succinylcholine. Although sugammadex is
rapid-sequence induction (note that 1.2 mg/kg is four approved and widely used in Europe, it has not yet gained
times the ED95 dose). Even then, good intubating condi- FDA approval for use in the United States. In rare cases, a
tions may not be achieved for 90 seconds in most patients. hypersensitivity reaction may occur shortly after adminis-
In terms of unanticipated reactions, rocuronium is a very tration of sugammadex.
safe drug. The only significant contraindication to its use
is known allergy to steroid-type neuromuscular blocking
drugs. So why not use rocuronium routinely for rapid- SUGGESTED READINGS
sequence induction and intubation? Antagonism of neu- Baumann A, Studnicska D, Gerard A, et al.: Refractory anaphylactic
romuscular blockade with rocuronium 1.2 mg/kg intrave- cardiac arrest after succinylcholine administration. Anesth Analg
nously cannot be accomplished for at least 30 to 60 109:137, 2009.
El-Orbany M, Connolly LA: Rapid sequence induction and intubation:
minutes. Should the patient be impossible to intubate and current controversy. Anesth Analg 110:1318, 2010.
impossible to ventilate, there is no chance for recovery of Godai K, Hasegawa Moriyama M, Kuniyoshi T, et al.: Three cases
spontaneous ventilation before hypoxemia develops. In of suspected sugammadex-induced hypersensitivity reactions. Br J
cases where the patient is at risk for aspiration of gastric Anaesth 109:216, 2012.
Lee C, Jahr JS, Candiotti KA, et al.: Reversal of profound neuromuscular
contents, and the use of succinylcholine is contraindi- block by sugammadex administered three minutes after rocuronium.
cated, clinicians must carefully evaluate the patient and Anesthesiology 110:1020, 2009.
consider the potential for impossible ventilation. Predic- Lee C, Katz RL: Clinical implications of new neuromuscular con-
tion of impossible supraglottic ventilation is an indication cepts and agents: so long, neostigmine, so long sux. J Crit Care 24:
for awake intubation or awake tracheostomy. 43, 2009.
Marsch SC, Steiner L, Bucher E, et al.: Succinylcholine versus ro-
curonium for rapid sequence intubation in intensive care: a prospective,
8. Are there any drugs that could replace randomized controlled trial. Crit Care 15:R199, 2011.
Martyn JAJ, Richtsfeld M: Succinylcholine-induced hyperkalemia in
succinylcholine in the future? acquired pathologic states. Anesthesiology 104:158, 2006.
Martyn JAJ, White DA, Gronert GA, et al.: Up- and down-regulation
Succinylcholine is an old drug that has been available to of skeletal muscle acetylcholine receptors, effects on neuromuscular
clinicians for 6 decades. Given all of the potential side blockers. Anesthesiology 76:822, 1992.
effects of this drug, some of them fatal, how come it is still Menendez-Ozcoidi L, Ortiz-Gomez JR, Olaguibel-Ribero JM, et al.:
in widespread clinical use? The search is ongoing for non- Allergy to low dose sugammadex. Anaesthesia 66:217, 2011.
depolarizing neuromuscular blockers with a succinylcho- Miller RD: Will succinylcholine ever disappear? Anesth Analg 98:
1674, 2004.
line-like onset-offset profile; to date, no acceptable substi- Mollerup HM, Gatke MR: Butyrylcholinesterase gene mutations in
tute has been found. Ultra-short-acting nondepolarizers patients with prolonged apnea after succinylcholine for electrocon-
have been developed but failed clinical trials because of vulsive therapy. Acta Anaesthesiol Scand 55:82, 2011.
toxicity or other safety concerns. Some of these new drugs Naguib M, Lien CA, Aker J, et al.: Posttetanic potentiation and fade in the
response to tetanic and train of four stimulation during succinylcholine-
await clinical trials in humans and may prove to be useful induced block. Anesth Analg 98:1686, 2004.
additions to our armamentarium. However, it is Rawicz M, Brandom BW, Wolf A, et al.: The place of suxamethonium
not easy to find a nondepolarizer with an onset of action in pediatric anesthesia. Pediatr Anesth 19:561, 2009.
CASE 21
Nondepolarizing Neuromuscular
Blockade
Barbara M. Dilos, DO • James B. Eisenkraft, MD
QUESTIONS
99
100
SECTION 4 Neuromuscular System
TABLE 21-1 Properties of Nondepolarizing Neuromuscular Blocking Drugs
ED95 Onset Time/ Elimination Cardiovascular Autonomic Intubating Dose
Drug (mg/kg) Clinical RI25–75 (min) Half-Life* (min) Route(s) of Elimination Effects Histamine Release Ganglion Block (mg/kg)
Atracurium 0.2 Slow/11–23 20 Nonenzymatic ester None Skin flushing None 0.5–0.6
hydrolysis Hypotension
Hoffman elimination Bronchospasm
Cisatracurium 0.05 Slow/11–23 20 Nonenzymatic ester None None None 0.15–0.2
hydrolysis
Hoffman elimination
Mivacurium 0.07 Slow/6–8 18 Hydrolysis by plasma None Yes None 0.2–0.25
cholinesterase
Pancuronium 0.07 Slow/24 145 Renal; some hepatic Tachycardia None None 0.08–0.12
Rocuronium 0.3 Rapid/10–15 60–75 Hepatic; some renal None None None 0.6–1; 1.2 (RSI)
d-Tubocurarine 0.5 Slow/25–35 80 Renal; minimal hepatic Hypotension Skin flushing Yes 0.5–0.6
Bradycardia
Vecuronium 0.05 Slow/10–15 62 Hepatic; some renal None None None 0.1–0.2
ED95, Mean effective dose producing 95% twitch height depression; RI25–75, time interval between recovery from 25%–75% twitch height; RSI, rapid-sequence induction.
*Time for plasma concentration to decrease by 50%.
21 Nondepolarizing Neuromuscular Blockade 101
SUGGESTED READINGS Paul M, Fokt RM, Kindler CH, et al.: Characterization of the inter-
Eger EI II, Weiskopf RB, Eisenkraft JB: Neuromuscular effects of inhaled actions between volatile anesthetics and neuromuscular blockers
anesthetics. p. 133. In The Pharmacology of Inhaled Anesthetics. at the muscle nicotinic acetylcholine receptor. Anesth Analg
Dannemiller Memorial Educational Foundation, San Antonio, 2002. 95:362, 2002.
Martyn J: Clinical pharmacology and drug therapy in the burned patient. Tempelhoff R, Modica PA, Jellish WS, et al.: Resistance to atracurium-
Anesthesiology 65:67, 1986. induced neuromuscular blockade in patients with intractable seizure
Martyn JA, Fagerlund MJ, Eriksson LI: Basic principles of neuromus- disorders treated with anticonvulsants. Anesth Analg 71:665,
cular transmission. Anaesthesia 64(Suppl 1):1, 2009. 1990.
Martyn JA, White DA, Gronert GA, et al.: Up-and-down regulation of Wright PM, McCarthy G, Szenohradszky J, et al.: Influence of chronic
skeletal muscle acetylcholine receptors: effects on neuromuscular phenytoin administration on the pharmacokinetics and pharmacody-
blockers. Anesthesiology 76:822, 1992. namics of vecuronium. Anesthesiology 100:626, 2004.
Naguib M, Flood P, McArdle JJ, et al.: Advances in neurobiology of the Wulf H, Ledowski T, Linstedt U, et al.: Neuromuscular blocking ef-
neuromuscular junction: implications for the anesthesiologist. Anes- fects of rocuronium during desflurane, isoflurane and sevoflurane
thesiology 96:202, 2002. anaesthesia. Can J Anaesth 45:526, 1998.
Ornstein E, Matteo RS, Schwartz AE, et al.: The effect of phenytoin on Yamauchi M, Takahashi H, Iwasaki H, et al.: Respiratory acidosis pro-
the magnitude and duration of neuromuscular block following atra- longs, while alkalosis shortens, the duration and recovery time of
curium and vecuronium. Anesthesiology 67:191, 1987. vecuronium in humans. J Clin Anesth 14:98, 2002.
CASE 22
Antagonism of Nondepolarizing
Neuromuscular Blockade
Barbara M. Dilos, DO • James B. Eisenkraft, MD
QUESTIONS
A 36-year-old woman underwent laparoscopic bilateral molecules gain greater access to nicotinic cholinergic
tubal ligation. She was otherwise in good general health. receptors at the motor end plates.
Tracheal intubation was facilitated with rocuronium, Pharmacologic agents may be used to increase the
0.6 mg/kg. No additional neuromuscular blocking drug amount of acetylcholine at the neuromuscular junction by
(NMBD) was administered. On completion of surgery, inhibiting the enzyme acetylcholinesterase. Inhibition of
train-of-four (TOF) monitoring demonstrated two twitches. acetylcholinesterase produces a competitive inhibition of
The decision was made to antagonize the residual neu- the NMBD at receptors. The neuromuscular block can be
romuscular blockade. partially or fully antagonized, depending on the relative
amounts of acetylcholine and NMBD molecules present.
1. Describe the principles underlying antagonism
of residual nondepolarizing neuromuscular 2. How is acetylcholinesterase inhibited?
blockade.
Acetylcholinesterase hydrolyzes acetylcholine at the neu-
Residual neuromuscular blockade can have serious con- romuscular junction. By inhibiting the action of acetyl-
sequences in the postoperative period. A study of patients cholinesterase, increased concentrations of acetylcholine
during the first 15 minutes after admission to the postan- accumulate at the neuromuscular junction. Acetylcholine
esthesia care unit found that 0.8% developed critical competes with NMBDs for nicotinic receptor sites at the
respiratory events. Mean TOF ratio was 0.62 in patients postjunctional membrane. Acetylcholinesterase inhibi-
who experienced these events compared with TOF ratios tion also results in presynaptic generation of an action
of 0.98 in patients who experienced no event. Complete potential that may spread retrograde up the axon and
recovery from neuromuscular blockade should be the cause other nerves in the same motor unit to discharge.
goal for every anesthetic. TOF monitoring is an excellent Acetylcholinesterase molecules possess an esteratic
way to assess neuromuscular blockade. Using a periph- and an anionic binding site. Anticholinesterases inacti-
eral nerve stimulator, one can assess residual blockade by vate the enzyme by reversibly binding to one or both of
the ratio of the fourth to first twitch amplitude. A TOF these sites. The stability of the bond determines the du-
ratio greater 0.9 should be achieved before tracheal ration of the inhibition. Edrophonium binds electrostati-
extubation. cally at the anionic site, forming a bond that is weak and
A competitive nondepolarizing neuromuscular block resulting in a relatively short duration of action. It also
can be terminated spontaneously or pharmacologically. has prejunctional effects, which promote the release of
Over time, spontaneous recovery occurs as the NMBD acetylcholine from the motor nerve terminal. Neostig-
diffuses away from receptor sites and is eliminated by mine and pyridostigmine form covalent bonds at the es-
metabolism or excretion. As the concentration of NMBD teratic site to form a carbamyl ester, which leads to a
in plasma and at effect sites decreases, acetylcholine more prolonged duration of effect.
103
104 SECTION 4 Neuromuscular System
Organophosphate compounds (e.g., parathion, mala- (i.e., when no twitches can be elicited), the duration to
thion) inhibit acetylcholinesterase by the formation of recovery is unknown, and attempts to antagonize the
irreversible bonds. These compounds are normally used block are likely to be unsuccessful.
as pesticides but have been used as chemical weapons Neostigmine appears to be a better antagonist than
because they are absorbed by ingestion, inhalation, and edrophonium when a profound neuromuscular block is
transdermally. Occasionally, a patient may present with a present, such as produced by long-acting nondepolar-
cholinergic crisis (see Chapter 24) because of organo- izing NMBDs. The degree of reversal depends directly
phosphate poisoning. on the dose of anticholinesterase administered. If spon-
taneous recovery of T1 is 50%, a full dose of anticho-
linesterase would not speed recovery significantly. A
3. Name clinically relevant acetylcholinesterase
smaller dose would be adequate and help protect from
inhibitors and their onsets of action. side effects. The recommended dose range for neostig-
Edrophonium, neostigmine, and pyridostigmine are the mine is 0.04 to 0.07 mg/kg and for edrophonium is 0.5
acetylcholinesterase inhibitors used clinically. They are to 1 mg/kg. A ceiling effect is observed so that addi-
all quaternary ammonium compounds; they do not pen- tional doses are ineffective. On a weight (mg) basis,
etrate the blood-brain barrier. Although in theory, these neostigmine is 5 times more potent than pyridostigmine
agents have the ability to affect cholinergic function in and about 12 times more potent than edrophonium.
the central nervous system, in practice, they do not reach Their durations of action range from 60 to 120 minutes
a high enough concentration to do so. However, physo- (Table 22-1).
stigmine is a tertiary ammonium compound that readily Neostigmine and pyridostigmine bind to anionic and
penetrates the blood-brain barrier. For this reason, it is esteratic sites of acetylcholinesterase molecules. This
not used for antagonism of neuromuscular blockade. binding accounts for their longer duration of action.
Edrophonium does not inhibit plasma (pseudo-) cholin- Edrophonium interacts with the anionic site of the mol-
esterase, whereas neostigmine does. ecule by hydrogen and electrostatic bonding, resulting in
The onsets of action of the anticholinesterase drugs a shorter duration of action. Edrophonium is excreted via
are as follows: the kidneys intact. In contrast, neostigmine is broken
• Edrophonium—1 to 2 minutes down to a carbamyl ester.
• Neostigmine—7 to 11 minutes
• Pyridostigmine—15 minutes 5. Why is it necessary to administer an anticholinergic
drug with an acetylcholinesterase inhibitor?
4. What are the usual doses and expected durations
Acetylcholine has both nicotinic and muscarinic ago-
of action for acetylcholinesterase inhibitors?
nist effects. Increasing acetylcholine concentrations at
Dose recommendations depend on the particular NMBD nicotinic receptors of the neuromuscular junction is
to be antagonized and the intensity of neuromuscular the goal for reversal, but many muscarinic effects are
blockade. The more intense the block, the longer the undesirable. These effects include profound bradycar-
time for adequate antagonism. When the spontaneous dia, junctional rhythm, asystole, salivation, increased
recovery of T1 is 25% or more or when four twitches are gastrointestinal motility, increased bronchopulmonary
present at a ratio of less than 0.3 to 0.4 to TOF stimula- secretions, and bronchospasm. An increased risk of
tion, a full antagonism dose is recommended. If only two postoperative nausea and vomiting has been impli-
twitches are present, recovery to a TOF ratio of 0.9 cated, but this is controversial.
would take much longer. To antagonize lesser degrees When an anticholinesterase drug is administered,
of blockade, smaller doses of anticholinesterase may be coadministration of an antimuscarinic agent, such as atro-
administered. If the anticholinesterase is given too early pine or glycopyrrolate, is necessary to prevent potentially
serious side effects. The time to onset of action is much a profound rocuronium or vecuronium block (i.e., with
shorter for atropine than for glycopyrrolate. Conse- no response to TOF stimulation) occurs within 2 to
quently, atropine is a better pairing with edrophonium, 3 minutes. Sugammadex appears to have few side effects,
which also has a more rapid onset of action than neostig- in contrast to neostigmine and edrophonium, and does
mine. However, atropine must be administered before not require the concomitant administration of an anti-
edrophonium, and edrophonium should be administered muscarinic. Although sugammadex has been used widely
only after the effects of atropine have been observed. This in Europe and elsewhere, at the time of this writing it is
timing of administration ensures the vagolytic effect of not approved for clinical use in the United States by the
atropine has taken place before the bradycardic effect of Food and Drug Administration because of concerns for
edrophonium. Glycopyrrolate has a slower onset and may allergic reactions.
be mixed with neostigmine because they possess similar
delays to onset. SUGGESTED READINGS
Beemer GH, Bjorksten AR, Dawson PJ, et al.: Determinants of the re-
6. What other class of drugs is under investigation versal time of competitive neuromuscular block by anticholinesterases.
Br J Anaesth 66:469, 1991.
for antagonism of nondepolarizing neuromuscular Caldwell JE, Miller RD: Clinical implications of sugammadex. Anaesthesia
blockade? 64(Suppl 1):66, 2009.
Cheng C, Sessler D, Apfel C: Does neostigmine administration produce
A novel approach to reversal of nondepolarizing block is a clinically significant increase in postoperative nausea and vomiting.
the use of sugammadex, a gamma cyclodextrin molecule Anesth Analg 101:1349, 2005.
designed specifically to bind steroidal nondepolarizing King MJ, Milazkiewicz R, Carli F, et al.: Influence of neostigmine on
postoperative vomiting. Br J Anaesth 61:403, 1988.
muscle relaxants. Administered intravenously, sugam- Kopman AF, Eikermann M: Antagonism of non-depolarising neuromus-
madex molecules encapsulate steroidal NMBD mole- cular blockade: current concepts. Anaesthesia 64(Suppl 1):22, 2009.
cules, rocuronium and vecuronium, to form a stable Murphy GS, Szokol JW, Marymount JH, et al.: Residual neuromuscular
complex that has no neuromuscular blocking properties. blockade and critical respiratory events in the post anesthesia care unit.
Rocuronium and vecuronium molecules dissociate from Anesth Analg 107:130, 2008.
Oslem S, White P, Tufanogullari B, et al.: Sugammadex reversal of
receptors at the motor end plates and diffuse down their rocuronium-induced neuromuscular blockade: a comparison with
concentration gradient to become bound to sugamma- neostigmine-glycopyrrolate and edrophonium-atropine. Anesth Analg
dex in the plasma. The time to complete recovery from 104:569, 2007.
CASE 23
QUESTIONS
1. Why is monitoring of neuromuscular blockade im- 4. Describe the clinically available devices used to
portant whenever a neuromuscular blocking drug monitor neuromuscular blockade.
is administered? 5. Describe patterns of stimulation used to monitor
2. What are the basic principles of neuromuscular neuromuscular blockade and implications of
blockade monitoring? evoked responses.
3. Why is a supramaximal stimulus used for 6. How can you evaluate this patient who has no re-
neuromuscular blockade monitoring? sponse to train-of-four stimulation?
A 50-year-old, healthy, 70-kg man (body mass index of a NMBD and recovery from relaxation becomes
24 kg/m2) is undergoing an inguinal hernia repair. He more predictable. Monitoring to ensure adequate re-
is tracheally intubated after administration of 70 mg covery from neuromuscular blockade is important to
of rocuronium (1 mg/kg) and is receiving sevoflurane in prevent respiratory failure after tracheal extubation,
oxygen/air and fentanyl. At 30 minutes into the procedure, which may occur as a problem in the postanesthesia
the surgeon complains that the patient is “tight,” and care unit.
an additional rocuronium dose of 20 mg (approximately
0.3 mg/kg) is administered. The surgeon announces 2. What are the basic principles of neuromuscular
5 minutes later that he is finished. You apply train-of-four blockade monitoring?
(TOF) stimulation over the ulnar nerve at the wrist, but no
twitch responses are elicited. Monitoring of neuromuscular transmission requires
supramaximal stimulation of a motor nerve and mea-
1. Why is monitoring of neuromuscular blockade surement of the response evoked in the innervated
important whenever a neuromuscular blocking muscle. NMBDs have no direct effect on muscle; if
stimulation is applied directly over a muscle, that
drug is administered?
muscle contracts despite complete blockade at the
Neuromuscular blocking drugs (NMBDs) are widely neuromuscular junction. It is important to stimulate
used to facilitate tracheal intubation and to provide and a motor nerve in a location where direct muscle
maintain optimal operating conditions. In the past, stimulation cannot occur and only the indirectly
neuromuscular blockade was commonly evaluated on evoked response (i.e., via the neuromuscular junc-
the basis of clinical criteria alone, such as a surgeon’s tion) is assessed.
assessment of inadequate relaxation, patient movement, It is essential to know which muscle to observe in re-
attempts at breathing “against the ventilator,” or obser- sponse to indirect stimulation. When the ulnar nerve is
vation of “curare clefts” in the capnograph tracing. stimulated, thumb adduction by the adductor pollicis
For certain procedures, excessive doses of an NMBD brevis muscle is the appropriate site to monitor. Finger
may be administered. Because there is considerable and wrist flexion should be ignored because they are
variability among patients’ sensitivities to NMBDs, likely due to direct stimulation if electrodes are placed
clinical criteria alone cannot be used to accurately asses over the forearm muscles.
depth of, or recovery from, neuromuscular blockade. During recovery from anesthesia, the most important
A quantitative and documentable method of assessment muscles are the muscles of respiration and airway patency,
is necessary. Monitoring neuromuscular blockade in but these muscles (e.g., diaphragm, laryngeal) cannot be
response to administration of a NMBD allows titration monitored during clinical anesthesia. The ulnar nerve–
of doses to the desired effect. Adequate relaxation can adductor pollicis brevis combination is easily monitored
be achieved without administering unnecessary doses and is used as a surrogate.
106
23 Monitoring the Neuromuscular Junction 107
3. Why is a supramaximal stimulus used for isometric contraction of the innervated muscle, com-
neuromuscular blockade monitoring? monly the adductor pollicis brevis. The mechanical force
developed is measured using a force transducer connected
Motor nerves consist of numerous nerve fibers, each of to the thumb. For accurate measurements, such as for
which innervates a motor unit in the muscle. Because the research purposes, it is necessary to preload the muscle
muscle’s total response is required to assess neuromuscular with 200–300 g of tension, and the force vector (i.e., the
blockade, all of the nerve fibers must be reliably stimulated. direction of thumb movement) must be perpendicular to
In this way, any decrement in muscle contraction is due to the force transducer. The force transducer is calibrated
neuromuscular junction blockade and not due to a failure in kg-force, and the output of the force transducer is
to stimulate all of the fibers in the motor nerve. displayed graphically or digitally on a monitor. In an un-
In a normal unparalyzed patient who has surface elec- paralyzed patient, delivery of supramaximal stimuli to the
trodes placed over the ulnar nerve, as the intensity (mA) nerve results in a maximal (100%) response in the muscle.
of nerve stimulation is gradually increased, the force of This response is considered to represent 100% and is
contraction of the muscle increases until all of the nerve used as a reference for subsequent evoked responses after
fibers are stimulated. Further increase in stimulus intensity the patient has received an NMBD.
does not result in further increase in evoked response. The Although a purpose-designed arm board with built-
stimulus producing a maximal muscle response is called in force transducer has been commercially available,
the maximal stimulus. Stimuli of greater intensity are MMG is not practical for routine clinical use. The force
termed supramaximal. During neuromuscular blockade transducer is bulky, the muscle must be preloaded with
monitoring, supramaximal stimuli (usually 120% of maxi- a specific tension, and the arm must be abducted and
mal stimulus current) are used to ensure that all nerve kept immobile so that there is no interference with
fibers are stimulated. The maximal (and supramaximal) movement of the thumb.
stimulus varies among individual patients, depending on
the amount of tissue between the skin and the nerve. The
Electromyography
negative stimulating electrode should always be placed
distal to the positive one because this configuration results Electromyography (EMG) records the compound muscle
in the greatest muscle response. action potential in response to peripheral motor nerve
stimulation. Stimulating electrodes are placed over the pe-
4. Describe the clinically available devices used ripheral motor nerve, and recording electrodes are placed
to monitor neuromuscular blockade. over the innervated muscle. The magnitude of the evoked
response is measured. Clinically, EMG is easier to use than
In principle, neuromuscular blockade monitoring requires MMG because muscle preloading and precise force vector
two devices: a peripheral nerve stimulator to deliver the su- measurements are unnecessary; both arms can be adducted
pramaximal stimulus and a device, which may be mechanical at the patient’s side. As a result, EMG has replaced MMG
or electrical, to measure the response evoked in the muscle. in neuromuscular studies conducted more recently. Inte-
grated EMG monitoring is commercially available only as
Peripheral Nerve Stimulators a modality in the Neuromuscular Transmission Module of
the GE S/5 monitoring system (GE Healthcare, Datex-
Stimulation of a nerve fiber is a function of the amount and Ohmeda S/5 NMT Module (Datex-Ohmeda Inc. P.O.Box
duration of current applied. Modern peripheral nerve stim- 7550, Madison, Wisconsin, 53707. USA)). Similar to
ulators are designed to deliver a constant current, despite MMG, the EMG response is first calibrated to 100% in an
changes in resistance that may develop over time between unparalyzed patient, and subsequent responses are dis-
the surface electrodes and the nerve. The current is deliv- played as a percentage of the initial response.
ered in square wave pulses of 200 !sec (0.2 msec) duration.
At this pulse width, motor nerves but not sensory nerves are
Accelerography
stimulated; this is because stimulation of sensory nerves re-
quires a longer pulse duration (approximately 1 msec). Accelerography is based on the principle that force is
Peripheral nerve stimulators are the devices most the product of mass times acceleration (F " ma). If mass
commonly used to facilitate assessment of neuromuscular is kept constant, force (of contraction) is directly propor-
blockade in clinical settings. With only a peripheral tional to acceleration. Accelerography uses a piezoelec-
nerve stimulator, the clinician must evaluate the force of tric transducer attached to the thumb (the mass of which
contraction by observing or palpating thumb adduction. remains constant) to determine the rate of angular
Such observations are difficult to quantify and are subject acceleration in response to nerve stimulation. The size of
to considerable interobserver variability. the acceleration output signal is displayed digitally and
The following devices may be used to quantify evoked graphically. Accelerography requires unobstructed thumb
response. movement, similar to MMG. This technology is com-
mercially available for clinical use and has been widely
Mechanomyography employed in clinical research studies. It provides a simple
and objective method of assessing neuromuscular block-
Historically, mechanomyography (MMG) has been the ade. It eliminates interobserver variability associated with
“gold standard” for objective monitoring of a muscle’s subjective clinical observation of evoked responses, on
evoked response. Stimulation of a motor nerve produces which peripheral nerve stimulators rely.
108 SECTION 4 Neuromuscular System
Kinemyography
Kinemyography (KMG) is clinically available as a modality
in the Neuromuscular Transmission Module of the GE S/5 a
monitoring system. KMG uses a piezoelectric strip incor-
porated into a flexible U-shaped (“boomerang”) device
that is placed between the thumb and index finger. The b
U-shaped device, mechanosensor, is designed to mimic a
MMG-like preload. Movement of the thumb produces a A B C
redistribution of electrical charge across the piezoelectric
membrane. The voltage produced by movement of the
thumb is measured, processed, and displayed digitally and 50 Hz 50 Hz 50 Hz
graphically on the monitor screen. Results have been
shown to correspond closely with MMG, making it a
reasonable option for clinical use. 5 seconds
FIGURE 23-1 ■ Tetanic stimulation. A, In the absence of a neuro-
5. Describe patterns of stimulation used to monitor muscular blocker, a 50-Hz tetanic train for 5 seconds produces a
muscular response of constant intensity. B, In the presence of
neuromuscular blockade and implications of increasing nondepolarizing neuromuscular block, there is de-
evoked responses. pression of the initial contraction but also fade with subsequent
pulses. The fade ratio is equal to the amplitude of the final con-
Several patterns of motor nerve stimulation are used to traction (the end of the tetanus) divided by the amplitude of the
monitor the neuromuscular junction. first contraction (the start of the tetanus) and is represented by
b/a. C, As nondepolarizing neuromuscular block increases, fade
increases, and if the block were deep enough, the response ul-
Single Twitch timately would disappear altogether. (Redrawn from Pollard BJ:
Neuromuscular imaging. Curr Anesth Crit Care 15:383, 2004.)
Single twitch is the simplest form of monitoring the neu-
romuscular junction. A single supramaximal stimulus is
applied for 0.2 msec. The size (“height”) of the twitch re- fade in muscle response). In the presence of incomplete
sponse remains at baseline until 75% of neuromuscular nondepolarizing neuromuscular blockade, the response is
junction receptors are occupied by NMBD and disappears not sustained (i.e., there is fade).
completely when 90%–95% of the receptors are occupied.
The single stimulus (twitch) is mostly used in research
Train of Four
where relative potencies of NMBDs can be measured and
rates of recovery can be quantified. NMBDs are compared As mentioned earlier, monitoring twitch response to single
by their ED95, which is the effective dose that produces a stimuli is impractical clinically because it requires a control
95% decrease in twitch height. twitch (Tc) measurement before the onset of neuromuscular
Before administration of NMBDs, a control twitch blockade. The answer to this problem is the TOF
response is required for later comparison, which makes pattern of stimulation. The motor nerve is stimulated with
this modality impractical for clinical use. Application of four successive supramaximal 0.2-msec stimuli delivered at
a single stimulus at a rate of 1/sec (1 Hz) results in no 2 Hz, and the ratio of the size of the fourth twitch to the first
decrement in twitch height in an unparalyzed patient. twitch (T4/T1 or fade ratio) is measured (Figure 23-2). It
In the presence of a depolarizing neuromuscular block, has been shown that the T4/T1 ratio is equivalent to the
the twitch response is uniformly smaller and increases
as recovery occurs. In the presence of an incomplete
nondepolarizing neuromuscular block, there is progres-
sive decrease (fade) in twitch height with each subse- a
quent stimulus. Return to the control twitch height
after administration of NMBDs does not mean that
100% of neuromuscular receptors are unoccupied; 75%
of neuromuscular junction receptors may still be occu-
pied because of the large margin of safety in normal
b
neuromuscular transmission.
Tetanic Stimulation
FIGURE 23-2 ■ Responses to a TOF stimulation pattern. The four
Tetanic stimulation (Figure 23-1) is usually applied at a stimuli are separated by 0.5 second each. The height of each bar
frequency of 50 Hz, (i.e., 50 stimuli/sec) for 5 seconds. In represents strength of muscular contraction. Initially, all four
unparalyzed patients, stimulation of a motor nerve at 50 Hz responses are equal. As nondepolarizing neuromuscular block-
results in sustained muscle contraction with a force greater ade increases, the fourth twitch is depressed earliest, and the
ratio b/a is known as a TOF ratio. As the block deepens, the four
than that achieved by a single stimulus. In the presence of responses decrease further, disappearing in the following order:
depolarizing neuromuscular blockade, tetanic stimulation fourth, third, second, first. (Redrawn from Pollard BJ: Neuromus-
produces sustained contraction of smaller force (i.e., no cular imaging. Curr Anesth Crit Care 15:383, 2004.
23 Monitoring the Neuromuscular Junction 109
T1/Tc ratio measured by MMG, and because TOF mea- stimulation is delivered for 5 seconds (producing fade),
surements do not require a control twitch measurement, followed by a hiatus in stimulation for 3 seconds, followed
TOF has become the modality of choice in clinical practice. by 20 single stimuli at 1 Hz; the responses to these
In the absence of nondepolarizing neuromuscular posttetanic stimuli are greater than the pretetanic ones
blockade, the TOF ratio is approximately 1. When 70%– (i.e., they are potentiated), and then gradually decrease in
75% of neuromuscular junction receptors are occupied by size (i.e., they fade). The degree and duration of the PTF
NMBD, the fourth response (T4) is lost. When 95% of depend on the degree of neuromuscular blockade.
neuromuscular junction receptors are occupied, all the Posttetanic count (PTC) is the application of the
twitches disappear. phenomenon of PTF to assess deeper levels of neuro-
TOF stimulation is very useful in assessing neuro- muscular blockade, when there is no response to stimu-
muscular blockade. A T4/T1 ratio greater than 0.9 is lation at 1 Hz, to TOF, or to 50 Hz. In this case, the
generally considered a good indicator of adequate: re- above-described sequence of stimulation is applied, and
spiratory muscle function, laryngeal muscle function the number of posttetanic twitch responses is counted
(i.e., airway patency and protection), vital capacity, and (Figure 23-4). The number of evoked twitch responses
maximum expiratory force. It also correlates with a is called the PTC and is related to the depth of neuro-
strong handgrip and ability to perform a 5-second head muscular blockade. Initially, there may be a PTC of 0 or
lift. When monitoring TOF by manual palpation, the 1 indicating profound neuromuscular blockade. The
degree of fade might be easily underestimated. PTC increases as recovery occurs and correlates with
the time to initial recovery of the twitch response to a
single stimulus or reappearance of the first twitch (T1)
Double-Burst Stimulation
in the TOF. If the PTC is zero, the time to recovery is
The accuracy of manual TOF assessment by clinicians is indeterminate.
poor, and it is frequently difficult to detect the presence of
fade. Double-burst stimulation (DBS) was suggested as a 6. How can you evaluate this patient who has
method to improve manual detection of fade. Instead of no response to train-of-four stimulation?
four stimuli (TOF), two bursts, each consisting of three
brief 50-Hz tetanic stimuli, are used. They are separated Ideally, neuromuscular monitoring will have been used
by an interval long enough to permit muscle relaxation, throughout the case with a control TOF at the beginning
usually 750 msec (Figure 23-3). The DBS is repeated ev- and intermittently thereafter; this ensures that the nerve
ery 12–15 seconds. Fade is more easily appreciated with stimulator is functioning. If the stimulator is applied only
DBS than with TOF because only two responses, one to at the end of the case and there appears to be no elicited
each burst, are compared. twitch response, the functionality of the nerve stimulator
should be checked. One way is to test it on oneself, using
a small current. Some peripheral nerve stimulators dis-
Posttetanic Facilitation and Posttetanic Count
play the current flowing (in mA), which ensures that the
Posttetanic facilitation (PTF) is characteristic of nonde- electrodes and contacts are adequate and that there is a
polarizing NMBDs. If a patient receives a nondepolariz- completed electrical circuit. A recorded current of zero
ing NMBD, the response to single stimuli (1 Hz) de-
creases, TOF ratio decreases, and there is fade in response
to 5 seconds of 50-Hz tetanic stimulation. If single stimuli
are applied (and evoke a small twitch response), then 50-Hz Response
Stimulus
Muscle 3 sec
Contraction 5 sec
Response
750 ms
Stimulus
Stimulus
1 Hz 50 Hz 1 Hz
from a stimulator equipped with a charged battery Eriksson LI, Lennmarken C, Staun P, et al.: Use of post-tetanic count
suggests problems such as desiccated skin electrodes or in assessment of a repetitive vecuronium-induced neuromuscular
block. Br J Anaesth 65:487, 1990.
broken wire between the stimulator and electrodes. Hemmerling TM, Le N: Brief review: Neuromuscular monitoring: an
If the peripheral nerve stimulator is working properly update for the clinician. Can J Anesth 54:58, 2007.
and there is no response to TOF or single twitch stimula- Kopman AF: Managing neuromuscular block: where are the guidelines?
tion, PTC can be used to assess neuromuscular blockade. If Anesth Analg 111:9, 2010.
Kopman AF: Perioperative monitoring of neuromuscular function.
the PTC is zero, neuromuscular blockade is profound and p. 261. In Reich DL, Kahn R, Mittnacht A, et al. (eds.): Monitoring
cannot be reversed at this time. The patient should be kept in Anesthesia and Perioperative Care. Cambridge University Press,
sedated, intubated, and ventilated until sufficient spontane- New York, 2011.
ous neuromuscular blockade recovery has occurred to Miller RD, Ward TA: Monitoring and pharmacologic reversal of a
allow for adequate antagonism of neuromuscular blockade. nondepolarizing neuromuscular blockade should be routine. Anesth
Analg 111:3, 2010.
Murphy GS, Brull SJ: Residual neuromuscular block: lessons un-
learned. Part I: definitions, incidence, and adverse physiologic effects
of residual neuromuscular block. Anesth Analg 111:120, 2010.
SUGGESTED READINGS Murphy GS, Brull SJ: Residual neuromuscular block: lessons unlearned.
Donati F: Neuromuscular monitoring: what evidence do we need to be Part II: methods to reduce the risk of residual weakness. Anesth Analg
convinced? Anesth Analg 111:6, 2010. 111:129, 2010.
Eriksson LI: Evidence-based practice and neuromuscular monitoring: Naguib M, Kopman AF, Lien CA, et al.: A survey of current management
it’s time for routine quantitative assessment. Anesthesiology 98:1037, of neuromuscular block in the United States and Europe. Anesth
2003. Analg 111:110, 2010.
CASE 24
Myasthenia Gravis
Jason H. Epstein, MD • James B. Eisenkraft, MD
QUESTIONS
A 38-year-old woman with a 5-year history of myasthenia fluctuating, painless weakness and easy fatigability of
gravis (MG) Osserman and Genkins grade IIB presented voluntary muscles. Weakness resolves with rest. Slow,
for transcervical thymectomy. Her medications were insidious onset is common, and the condition is associ-
pyridostigmine, 240 mg, azathioprine, 100 mg, and predni- ated with relapses and remissions. The incidence of MG is
sone, 15 mg per day in divided doses. She was also taking approximately 1 in 30,000 adults and 1 in 200,000 children
omeprazole 20 mg per day for reflux esophagitis. Spirome- and adolescents. These figures may underestimate the
try revealed a vital capacity of 60% predicted and forced true incidence because mild cases in elderly adults are
expiratory volume in 1 second/forced vital capacity of 80%. commonly misdiagnosed. Peak incidence occurs in the
After placement of standard monitors and while the patient third decade of life for women and fifth decade for men,
was breathing 100% oxygen, rapid-sequence induction with but any age may be affected.
cricoid pressure was performed using propofol, 2 mg/kg, In MG, antibodies are produced to the acetylcholine
and succinylcholine, 1.5 mg/kg. The trachea was intubated (nicotinic) receptor of the neuromuscular junction. Con-
uneventfully. Anesthesia was maintained with oxygen, air, sequently, patients with MG have 70% to 80% fewer
fentanyl, and desflurane as required. Ventilation was usable postsynaptic acetylcholine receptors at the end
controlled throughout the procedure. Neuromuscular plates of affected muscles, fewer folds in synaptic clefts,
monitoring with a peripheral nerve stimulator was initiated, and widened synaptic clefts. The amount of presynaptic
and cisatracurium, 0.05 mg/kg, was administered with acetylcholine released is normal or increased. In a person
resulting loss of twitch response to peripheral nerve with a normal number of acetylcholine receptors, only
stimulation. The surgery proceeded uneventfully and lasted 25% to 30% of the receptors are required for normal
2 hours. Anesthetic agents were discontinued, and the patient neuromuscular transmission; this is termed the “margin
demonstrated four equal twitch responses to train-of-four of safety” in neuromuscular transmission. In patients
(TOF) stimulation. Neostigmine, 0.06 mg/kg, and glyco- with MG, the margin of safety is decreased.
pyrrolate, 0.01 mg/kg, were administered. When the
patient was awake and responded to commands, her trachea 2. How is myasthenia gravis diagnosed, and how is
was extubated. Soon after extubation, the patient became it classified?
dyspneic.
The diagnosis of MG is suspected from the patient’s
history and confirmed by clinical, electrophysiologic,
1. What is myasthenia gravis?
immunologic, and pharmacologic testing. Although any
MG is an autoimmune disorder of the neuromuscular muscle group may be affected, the most common onset
junction, the function of which is routinely altered in is ocular, with ptosis or diplopia. If the disease remains
modern anesthesia practice. Typically, MG manifests as a localized to the eyes for 2 years, there is a low likelihood
111
112 SECTION 4 Neuromuscular System
TABLE 24-1 Clinical Classification of Myasthenia Gravis (after Osserman and Genkins*)
Grade Name Description Testing and Prognosis
I Ocular Involvement of ocular muscles only Electrophysiologic testing of
Diplopia and ptosis other musculature negative
IA Ocular ! peripheral Involvement of ocular muscles Electrophysiologic testing of
No clinical symptoms in peripheral other musculature positive
musculature
IIA Mild generalized Involvement of skeletal or bulbar Good response to drug
musculature therapy
No respiratory involvement
IIB Moderate generalized More severe involvement of skeletal Fair response to drug therapy
and bulbar muscles
Dysarthria, dysphagia, difficulty chewing
without respiratory involvement
III Acute fulminating Rapid onset of severe bulbar and Poor response to therapy
skeletal weakness with respiratory Low mortality rate
involvement
IV Late severe Severe MG developing "2 years Poor response to therapy
after onset of symptoms Poor prognosis
for most patients with MG; the exception is patients challenging in patients who are physically or psychologi-
with Osserman and Genkins class I MG. Response to cally dependent on them, and some authors argue that
thymectomy is best when the procedure is performed these drugs can be given without interfering significantly
within the first 3 years after diagnosis. Clinical outcome with perioperative management. Anticholinesterase dosage
is equivalent whether the procedure is performed via may be reduced during the relative immobility of hospital-
video-assisted thoracoscopy or via a median sternotomy. ization and surgery.
4. Explain why patients with myasthenia gravis 6. Describe an appropriate anesthetic technique
are resistant to succinylcholine but sensitive for patients with myasthenia gravis undergoing
to nondepolarizing muscle relaxants. transcervical thymectomy.
Acetylcholine receptors are each activated by two acetyl- Reports of successful anesthetic techniques for thymec-
choline molecules, which causes a small electrical current tomy in patients with MG include balanced anesthesia
across the membrane at the motor end plate. When the and total intravenous anesthesia (TIVA) techniques.
summation of small currents from multiple receptors Some authors advocate TIVA with thoracic epidural
reaches a threshold, the end plate depolarizes and muscle anesthesia to reduce the need for neuromuscular blocking
contraction occurs. Although only 20% of a normal num- agents and systemic opioids. All patients undergoing
ber of receptors are required for neuromuscular transmis- anesthesia should have American Society of Anesthesi-
sion, patients with MG can have 80% fewer receptors, and ologists standard monitors in place. When muscle relax-
any factor that even minimally interferes with neuromuscu- ants are to be administered, peripheral nerve stimulation
lar transmission may cause severe weakness. Small amounts and neuromuscular monitoring should also be performed,
of nondepolarizing neuromuscular relaxants may block preferably with a means to quantify responses objectively.
enough receptors to interfere with this transmission. After denitrogenation with 100% oxygen, induction of
Succinylcholine acts as an agonist at acetylcholine anesthesia is achieved with propofol, etomidate, or ket-
receptors and causes neuromuscular blockade by first amine. In elective cases, relaxation for tracheal intubation
depolarizing the motor end plate and then preventing is readily achieved with a potent inhaled anesthetic agent.
rapid repolarization. Because of the smaller number of Patients with MG are more sensitive to the neuromuscu-
receptors available in patients with MG, larger doses of lar depressant effects of these agents. Patients with MG
succinylcholine are required to activate sufficient recep- who were anesthetized with isoflurane at a 1.6 minimum
tors to cause depolarization. The ED95 dose (i.e., the alveolar concentration demonstrated a 30% to 50% de-
mean dose that produces a 95% decrease in the muscle’s crease in response (i.e., twitch height) to single stimuli,
response to supramaximal nerve stimulation) for succi- and a fade (TOF) ratio of 0.41. Less soluble inhaled
nylcholine in patients with MG is 2.6 times normal agents such as desflurane and sevoflurane produce similar
(normal being approximately 0.3 mg/kg). In addition to effects and are easily titrated.
exhibiting resistance to succinylcholine, patients with Patients who are unable to tolerate the cardiovascular
MG often have prolonged duration of action of the depression associated with potent inhaled agents may
drug. Both anticholinesterase drugs and plasmapheresis require balanced techniques with small incremental doses
may inhibit or decrease the amount of pseudocholines- of intermediate-acting nondepolarizing muscle relaxants.
terase, which is responsible for the metabolism of Because the sensitivity of any individual patient with MG
succinylcholine. may vary widely and because sensitivity to muscle relax-
ants is increased in the presence of potent inhaled anes-
5. How is a patient with myasthenia gravis optimized thetics, nondepolarizers should be titrated at one tenth
the usual dose. Vecuronium and rocuronium have been
for surgery?
safely used in patients with MG. Cisatracurium is an al-
Numerous anesthetic techniques are applicable to patients ternative choice that offers a short elimination half-life,
with MG undergoing thymectomy. No matter which tech- small volume of distribution, and high clearance by
nique is chosen, patients should be admitted in remission Hofmann elimination.
when possible. All other medical and emotional states are
best optimized before surgery. Patients with a history of 7. What are the considerations in a patient with
respiratory disease or bulbar involvement could benefit myasthenia gravis who requires a rapid-sequence
from pulmonary function testing. These patients should induction?
be informed of the potential for postoperative intubation
and ventilation and educated in the use of incentive Patients with MG who present for emergent surgery may
spirometers. Premedication is best used with caution and require rapid-sequence induction if they are at increased
avoided in patients with respiratory difficulty. risk for aspiration. As described earlier, patients with MG
Although steroids should be continued in the periopera- show resistance to the effects of succinylcholine; how-
tive period, recommendations for preoperative anticholin- ever, the standard intubating dose of 1 to 1.5 mg/kg
esterases are controversial. Withholding anticholinesterase represents 3.5 times the ED95 in patients without MG. A
medication may reduce or obviate the need for exogenous 1.5-mg/kg dose of succinylcholine has been successfully
neuromuscular blockade. Administration of preoperative used to facilitate intubation in a rapid-sequence fashion
anticholinesterase medication could prolong succinylcho- in patients with MG. Patients with MG frequently do
line effects and could antagonize nondepolarizing muscle not show fasciculation before paralysis with succinylcho-
relaxant effects. Withholding anticholinesterases may be line. Patients who have received recent anticholinesterase
114 SECTION 4 Neuromuscular System
medication or plasmapheresis may have a prolonged re- inspiratory force of #20 cm H2O may be observed when
sponse to succinylcholine because of delayed metabolism. 50% of receptors are still occupied by neuromuscular
Sugammadex is a cyclodextrin drug that is designed to blocking drugs. Patients can sustain a head lift for 5 seconds
bind rocuronium with great affinity, providing rapid and when 33% of receptors are occupied. Other, less sensitive
effective antagonism of deep rocuronium-induced neu- measures of strength include maintaining a tidal volume
romuscular blockade. Before the introduction of sugam- of 6 mL/kg, a TOF fade ratio greater than 0.9, and vital
madex, anticholinesterase drugs were the only option for capacity of 15 mL/kg (Table 24-2).
antagonism of residual neuromuscular blockade, which Patients with MG represent a special case because the
in patients with MG must be administered with caution above-mentioned criteria may not apply. The disease,
to avoid myasthenic or cholinergic crises. Sugammadex rather than residual neuromuscular blockade, may prevent
antagonized deep rocuronium-induced neuromuscular a patient with MG from reaching full strength. Because of
blockade within 210 seconds in patients with MG. Al- the variability of debilitation, preoperative measurements
though sugammadex offers potential advantages in the of strength are important for postoperative comparisons.
management of patients with MG, as of this writing, Before administration of an anesthetic drug that may in-
the Food and Drug Administration has not approved terfere with neuromuscular transmission, control EMG or
sugammadex for clinical use in the United States. TOF should be recorded. Response to tetanic stimulation
Another possible rapid-sequence induction technique may also be assessed after induction of anesthesia but
is to avoid neuromuscular blocking agents entirely. A before administration of drugs that interfere with neuro-
rapid-sequence intubation in a 14-year-old patient with muscular transmission.
MG and a full stomach using lidocaine, propofol, and It is important that a patient with MG have good muscle
remifentanil has been described. This technique allows function so as to be able to cough and clear secretions.
for a case to be managed without the potential adverse Patients with MG who demonstrate residual weakness on
effects of neuromuscular blocking agents. This technique emergence from anesthesia should not automatically be
seems attractive for use in patients with MG, but intubat- assumed to have residual blockade from a muscle relaxant.
ing conditions are frequently poor when neuromuscular Inhaled anesthetics, antibiotics, local anesthetics, anticon-
blocking agents are omitted. vulsants, and $-adrenergic blockers may interfere with
neuromuscular transmission (Box 24-1).
8. After emergence from anesthesia and before
extubation, how is adequacy of strength assessed? 9. What is a cholinergic crisis, and how is it
distinguished from a myasthenic crisis?
Various techniques are used to assess residual neuromus-
cular blockade. In normal patients, a sustained response Crisis is the acute onset of muscle weakness in a patient
to tetanic stimulation at 50 Hz for 5 seconds or a negative with MG. Cholinergic crisis arises from an excess of
FiO2, Fraction of inspired oxygen; pCO2, partial pressure of carbon dioxide; TOF, train-of-four.
*Negative inspiratory force is measured by inspiring against a gauge and indicator. The greater the
force generated, the more the indicator moves from its original set-point. The set-point is arbitrarily
labeled 0. Traditionally, the gauge has been calibrated with negative numbers. The more the indica-
tor is displaced from its 0 set-point, the more negative the reading. The important aspect is the
amount of indicator displacement. The greater the displacement, the more negative the reading.
Consequently, greater displacement is read as a larger absolute number. Because the numbers
are designated as negative numbers, confusion has arisen over their meaning. The greater the
absolute indicator displacement, the greater the force generated. A reading of #40 cm H2O
represents a greater inspiratory force than a reading of #20 cm H2O.
24 Myasthenia Gravis 115
acetylcholine at nicotinic and muscarinic receptor sites. dose greater than 750 mg/day, and preoperative vital
Usually occurring as a result of excess anticholinesterase capacity less than 2.9 L. These predictors were not found
administration, symptoms include weakness, wheezing, to be useful when applied to patients with MG having
increased secretions, fasciculations, nausea, vomiting, transcervical thymectomy at other centers or to patients
diarrhea, lacrimation, bradycardia, and hypotension. Re- with MG undergoing other types of surgery.
spiratory weakness may progress to respiratory failure, The incidence of postoperative respiratory failure is
whereas increased secretions and dysphagia predispose lower after transcervical rather than transsternal thymec-
to upper airway obstruction and aspiration pneumonitis. tomy. The risk of postoperative respiratory failure is more
Myasthenic crisis occurs when the amount of acetylcholine likely in some circumstances than others. For high-risk
available is insufficient to stimulate enough postsynaptic patients, preoperative plasma exchange and high-dose
receptors at the motor end plates, resulting in failure of perioperative steroid therapy, can help reduce the proba-
neuromuscular transmission. bility of respiratory failure.
Both cholinergic crisis and myasthenic crisis manifest
with muscle weakness, but because the appropriate treat- SUGGESTED READINGS
ment of one is the antithesis of the other, correct diagnosis Baraka A: Anesthesia and critical care of thymectomy for myasthenia
is critical. Two means of differentiating between both states gravis. Chest Surg Clin North Am 11:337, 2001.
are to check pupillary size and to perform an edrophonium Blichfeldt-Lauridsen L, Hansen BD: Anesthesia and myasthenia gravis.
challenge test. A patient in a cholinergic crisis has con- Acta Anaesthesiol Scand 56:17, 2012.
de Boer HD, van Egmond J, Driessen JJ, et al.: Sugammadex in patients
stricted pupils (miosis), whereas a patient in myasthenic with myasthenia gravis. Anaesthesia 65:653, 2010.
crisis has dilated pupils (mydriasis). In addition, a small dose Eisenkraft JB, Book WJ, Mann SM, et al.: Resistance to succinylcholine
of intravenous edrophonium (2 to 10 mg) improves strength in myasthenia gravis: a dose-response study. Anesthesiology 69:760,
in a patient in myasthenic crisis (relative dearth of acetyl- 1988.
choline), whereas a patient in cholinergic crisis (excess of Eisenkraft JB, Book WJ, Papatestas AE: Sensitivity to vecuronium in
myasthenia gravis: a dose-response study. Can J Anaesth 37:301, 1990.
acetylcholine) should show no change or an exacerbation Eskaros SM, Papadakos PJ, Lachmann B: Respiratory monitoring.
of symptoms. The muscarinic side effects of a cholinergic p. 1411. In Miller RD, Eriksson LI, Fleisher LA, et al. (eds.): Miller’s
crisis may be treated with atropine or glycopyrrolate. Anesthesia, 7th edition. Saunders, Philadelphia, 2010.
Grant PP, Jenkins LC: Prediction of the need for postoperative me-
chanical ventilation in myasthenia gravis: thymectomy compared to
10. Can the need for postoperative ventilation be other surgical procedures. Can Anaesth Soc J 29:112, 1982.
predicted preoperatively? Leventhal SR, Orkin FK, Hirsh RA: Prediction of the need for postop-
erative mechanical ventilation in myasthenia gravis. Anesthesiology
Patients with MG are at increased risk for prolonged post- 53:26, 1980.
operative ventilation. Attempts have been made to predict Mann R, Blobner M, Jelen-Esselborn S, et al.: Preanesthetic train-of-
four fade predicts the atracurium requirement of myasthenia gravis
preoperatively which patients are at greater risk for post- patients. Anesthesiology 93:346, 2000.
operative respiratory failure. In 24 patients undergoing Neustein SM, Eisenkraft JB, Cohen E: Anesthesia for thoracic surgery.
transsternal thymectomy under general anesthesia via an p. 1064. In Barash PG, Cullen BF, Stoelting RK, et al. (eds.): Clinical
endotracheal tube with nitrous oxide and either halothane Anesthesia, 6th edition. Lippincott Williams & Wilkins, Philadelphia,
2009.
or enflurane without muscle relaxants, positive predictors Politic GD, Tobias JD. Rapid sequence intubation without a neuromus-
included duration of MG greater than 6 years, history of cular blocking agent in a 14-year-old female patient with myasthenia
chronic respiratory disease aside from MG, pyridostigmine gravis. Paediatr Anaesth 17:285, 2007.
CASE 25
Malignant Hyperthermia
Joseph Sebeo, MD, PhD • James B. Eisenkraft, MD
QUESTIONS
A 12-year-old, 40-kg boy was scheduled for strabismus most cases reported in boys. MH can be described as a
corrective surgery of the right eye. He had no significant spectrum, ranging from the classic life-threatening reac-
past medical history and no family history of anesthetic tion to mild presentations.
problems or muscle or nerve disease. He had never
received general anesthesia before. Physical examination 2. What is the pathophysiology of malignant
was normal. The preoperative vital signs were blood
hyperthermia?
pressure 100/60 mm Hg, heart rate 92 beats per minute,
and axillary temperature 36.7° C. Because the patient was In the normal state, depolarization of skeletal muscle fiber
needle-phobic, an inhalation induction of anesthesia was membranes leads to calcium ion release from the sarcoplas-
achieved with sevoflurane 4.0 vol% in a mixture of mic reticulum (SR). After calcium diffusion into thin fila-
nitrous oxide and oxygen (fraction of inspired oxygen ments, calcium binds to calcium-regulatory sites on tropo-
0.4). After induction, an intravenous catheter was placed, nin, leading to normal excitation-contraction coupling. In
and rocuronium bromide, 20 mg, and fentanyl, 50 !g, MH, calcium is released from the SR at very high rates,
were administered. Direct laryngoscopy was performed, leading to a sustained hypermetabolic state and subsequent
and the trachea was intubated easily with a 6.0-mm loss of cellular integrity. This hypermetabolic state produces
cuffed tube. The patient’s heart rate suddenly increased increased lactate levels, high adenosine triphosphate (ATP)
60 minutes after intubation from 130 to 190 beats per consumption, increased carbon dioxide release, increased
minute. Over the next 10 minutes, the end-tidal carbon oxygen consumption, and increased muscle heat accumula-
dioxide (ETCO2) tension increased from 35 to 65 mm tion secondary to sustained muscle contractions. Later in
Hg, and the axillary temperature increased from 35° C to the clinical course, ATP production ceases, causing failure
38.9° C. An esophageal temperature probe showed a of intracellular membrane pumps. Cellular leakage of elec-
temperature of 39.5° C. trolytes follows, including potassium and calcium, enzymes
such as creatine phosphokinase, large amounts of metabolic
1. What is malignant hyperthermia? acids, and myoglobin. Fatal arrhythmias, end-organ dam-
age, and eventually death may ensue.
Malignant hyperthermia (MH) is a life-threatening famil- The ryanodine receptor has been implicated in the
ial hypermetabolic disorder of skeletal muscle that can be pathogenesis of MH. Ryanodine receptors are a group of
precipitated by specific anesthetic agents. MH was first high-conductance SR calcium channels in muscles and
reported in the 1960s and is characterized by tachycardia, endoplasmic reticulum in other cells. Mutations impair-
tachypnea, hyperthermia, generalized muscle rigidity, aci- ing function of ryanodine receptors occur in central core
dosis, and increasing ETCO2 levels. The incidence of disease, an autosomal dominant congenital myopathy,
MH is 1 in 15,000 anesthetics in children and 1 in and King-Denborough syndrome, a congenital myop-
50,000–100,000 anesthetics in adults. Children "15 years athy. Both conditions are associated with an increased
old account for #50% of all reported MH cases, with susceptibility to MH.
116
25 Malignant Hyperthermia 117
3. What are the clinical characteristics of malignant BOX 25-1 Differential Diagnosis of Suspected
hyperthermia? Malignant Hyperthermia Event
MH episodes are characterized by sinus tachycardia, mus- • Inadequate anesthesia/analgesia
cle contractures, arrhythmias, increased core temperature, • Insufficient ventilation/fresh gas flow
increased serum creatine kinase levels, myoglobinuria, and • Overwarming
eventually cardiac arrest. All of these changes combine • Exothermic reaction in absorber (sevoflurane $
with hypoxemia, hypercapnia, metabolic acidosis, respira- Baralyme)
tory acidosis, and hyperkalemia. Early recognition and • Anesthesia machine malfunction
treatment of MH are essential if an adverse outcome is to • Anaphylactic reaction
• Sepsis
be avoided. The earliest signs are usually masseter muscle
• Antimuscarinics
rigidity, tachypnea (if spontaneously breathing), tachycar- • Neuromuscular disorders
dia, and increasing ETCO2 (but not inspired carbon diox- • Neuroleptic malignant syndrome
ide). The sequence of clinical events during an episode of • Thyroid crisis
MH is summarized in Table 25-1. None of these signs are • Pheochromocytoma
specific for MH, and a broad differential diagnosis should • Carcinoid
always be considered (Box 25-1). • Cocaine toxicity
• Laparoscopic associated hypercarbia
4. Discuss masseter muscle rigidity during induction.
Children and adults can exhibit decreased mouth-opening second option is to convert to a nontriggering anesthetic
and increased jaw stiffness when succinylcholine is adminis- and proceed with surgery, monitoring carefully for any
tered after exposure to halogenated volatile anesthetics. signs of MH. In the case of emergency surgery that cannot
Masseter muscle rigidity (MMR) is the inability to open the be delayed, the only option is to convert to a nontriggering
jaw (trismus). The exact incidence of MMR after succinyl- anesthetic while maintaining a heightened vigilance for
choline administration is unknown but has been estimated MH. In all cases, the patient should be referred for further
to range from 1 in 1000 to 1 in 100,000 patients. MMR may evaluation of MH susceptibility.
be an early indicator of, but is not pathognomonic for, MH.
Differential diagnosis for MMR includes inadequate dose of 5. Explain the known triggering agents for malignant
succinylcholine, outdated succinylcholine, rapid succinylcho-
hyperthermia.
line hydrolysis, underlying myotonic dystrophy, trismus sec-
ondary to facial trauma, and MMR as an early sign of MH. All potent inhaled volatile anesthetics may trigger an
When MMR occurs, MH could ensue. Consequently, episode of MH, but they may not all be equal in this re-
all triggering agents should be discontinued, 100% oxygen spect; sevoflurane and isoflurane have been suggested to
should be delivered, monitoring should be continued for be more potent triggers than others. Succinylcholine is
evidence of other signs of MH, and an arterial blood gas also a potential trigger. These agents should be avoided
(ABG) should be drawn. Combined respiratory and meta- in patients with MH susceptibility. Although not directly
bolic acidosis indicates MH, and if present, the patient triggering a MH reaction, ketamine may lead to in-
should be treated appropriately. If the ABG does not show creased muscle tone, which confounds the diagnosis of
a combined respiratory and metabolic acidosis, and other MH. Use of ketamine is not contraindicated, but it may
signs of MH are absent, the anesthesiologist has two op- not be ideal in patients with a known history of MH.
tions. One is to postpone surgery, awaken the patient, and Anesthetic agents believed to be safe to use in a patient
continue monitoring in the postanesthesia care unit. The with MH susceptibility are listed in Box 25-2.
CPK, Creatine phosphokinase; DIC, disseminated intravascular coagulation; ETCO2, end tidal carbon dioxide; PVCs, premature ventricular
contraction.
118 SECTION 4 Neuromuscular System
7. How is a suspected case of malignant 8. What is the preparation for a known case of
hyperthermia treated? malignant hyperthermia?
Management of a suspected case of MH includes prompt Prompt management of MH is crucial to prevent an ad-
recognition and treatment as summarized in Table 25-2. verse outcome. An MH cart should be maintained and
Increasing ETCO2 is one of the earliest, most specific, immediately available. Activated charcoal filters placed in
25 Malignant Hyperthermia 119
Hyperkalemia
Hyperventilation
Insulin
Adult dose: insulin 10 units $ dextrose 50% 50 mL
Pediatric dose: insulin 0.1 unit/kg $ dextrose 50% 1 mL/kg
Sodium bicarbonate
Adult dose: 50 mEq/L over 5 minutes
Pediatric dose: 1–2 mEq/L
Calcium chloride (life-threatening hyperkalemia): 10 mg/kg
Arrhythmias
Usually resolves with treatment of acidosis and hyperkalemia
Standard drug therapy
Avoid calcium-channel blockers (hyperkalemia or cardiac arrest with dantrolene)
Acidosis
Hyperventilation
Sodium bicarbonate if pH "7.2
Myoglobinuria
Hydration to maintain urine output #2 mL/kg per hour
Diuretics: furosemide, mannitol
Urine alkalinization
ICU, Intensive care unit; MH, malignant hyperthermia, prn, pro re nata (as needed); TIVA, total intravenous anesthesia.
the inspiratory and expiratory limbs of the breathing dioxide absorber, and flushing the machine with oxygen
system have been shown to remove volatile anesthetics before inserting activated charcoal filters into the breath-
effectively from the anesthesia delivery system, and more ing system. Next, the circuit is flushed with the charcoal
recent studies have discussed their potential use in cases filters in place. The required flushing periods (to reach
of MH. Although no “safe” (i.e., nontriggering) concen- "5 ppm anesthetic concentrations) vary considerably
tration of potent inhaled anesthetics has been established among machines of different manufacturers. During
in humans, most studies aim for a level of "5 parts per anesthetic delivery, charcoal filters must remain in the
million (ppm) for a machine to be considered “clean.” breathing system, and fresh gas flow must be maintained
Preparation of the anesthesia workstation for a patient at #10 L per minute for the first 5 minutes and #2 L per
susceptible to MH includes removal of vaporizers, re- minute for the remainder of the case. As summarized in
placing the breathing system, substituting a new carbon Box 25-3, in addition to the standard American Society
120 SECTION 4 Neuromuscular System
BOX 25-3 Malignant Hyperthermia Cart raised hope in establishing noninvasive and more specific
procedures than the IVCT for MH diagnosis. However,
EQUIPMENT although genetic testing showed promise, because of the
• Syringes (60 mL % 5) to dilute dantrolene genetic and clinical variability of MH, the IVCT remains
• Irrigation tray the “gold standard” in the diagnosis of MH to date.
• Esophageal and bladder temperature probes
• Cold saline
• Ice packs
11. What is neuroleptic malignant syndrome?
• Central venous catheter kit Neuroleptic malignant syndrome (NMS) is a rare reac-
MEDICATIONS
tion to traditional (e.g., haloperidol, fluphenazine) and
nontraditional (e.g., quetiapine, risperidone) neuroleptics
• Dantrolene vials (36) and dopamine receptor antagonists (e.g., prochlorpera-
• Sterile water vials (100 mL)
• Sodium bicarbonate (2)
zine, metoclopramide). NMS is thought to result from an
• Dextrose 50% (2) acute dopaminergic blockade in the central nervous
• Furosemide (4) system. Clinical manifestations are very similar to MH
• Calcium chloride (2) and include hyperpyrexia, profuse sweating, and severe
• Insulin (1 refrigerated) muscle rigidity. NMS and MH are clinically similar but
• Lidocaine (1) pharmacologically distinct, with cross-reactivity between
triggering agents unlikely. The distinction between NMS
LABORATORY TEST SUPPLIES
and MH is made clinically based on history of exposure
• ABG kits (6) to a volatile anesthetic versus neuroleptic medications.
• Blood specimen tubes for: NMS is treated with dantrolene or bromocriptine, a do-
• Coagulation studies
• Myoglobin
pamine agonist.
• Creatine phosphokinase
• Complete blood count 12. What are some medicolegal issues in malignant
• Platelets hyperthermia?
Even with prompt diagnosis and appropriate management,
MH can be an unpredictable catastrophic reaction with a
of Anesthesiologists basic monitors, appropriate equip- high mortality rate. Departures from the standard of care
ment, drugs, and laboratory supplies must be available. may include administration of a MH trigger to a patient
with a known personal or family history of MH, failure to
9. What is the “gold standard” for diagnosing have appropriately stocked crash and MH carts available,
malignant hyperthermia? and substandard resuscitative response. Medicolegal impli-
cations of MH have made headlines when young, other-
The “gold standard” for MH diagnosis is the in vitro wise healthy patients died as a result of MH during office-
halothane-caffeine contracture test (IVCT) that was based procedures. In one case, the anesthesiologist was
developed in accordance with the European Group or reported to have failed to administer dantrolene in a timely
MHAUS and can define MH phenotypically. The IVCT manner; the lawsuit that ensued was eventually settled out
requires that fresh muscle be taken from the patient of court. It is imperative that all anesthesiology caregivers,
under local anesthesia. The muscle is exposed to halo- from office-based practitioners to practitioners in tertiary
thane and caffeine-containing solutions, and the force of care and academic institutions, have a MH cart readily
contraction is measured as the endpoint. Muscle from a available with an adequate supply (enough for 10 mg/kg in
patient with MH susceptibility shows an increased force the average adult) of unexpired dantrolene as well as resus-
of contraction. citation equipment.
When using a European MH group protocol, the A patient who has a history of MH should be strongly
IVCT has a sensitivity of 99% and specificity of 93.6%. encouraged to wear a MedicAlert or equivalent bracelet.
The MHAUS protocol has a sensitivity of 84% and Advice on managing a suspected case of MH is available
specificity of 78%. The IVCT is an expensive test, re- from the MHAUS 24-hour hotline (1-800-644-9737).
quires a surgical (muscle biopsy) procedure, is performed There is a MH registry on the MHAUS website (http://
only in specialized centers, and can be equivocal with the www.mhaus.org), and all cases of MH should be reported
mentioned rates of false-positive and false-negative to MHAUS.
results. This test should be used for susceptible patients
(e.g., with personal or family history of MH). In the case
SUGGESTED READINGS
of a patient who has just experienced a suspected MH
episode, the IVCT should be delayed for 6 months. Birgenheier N, Stoker R, Westenskow D, et al.: Activated charcoal effectively
removes inhaled anesthetics from modern anesthesia machines. Anesth
Analg 112:1363, 2011.
10. Is genetic testing available for malignant Brandom BW: Ambulatory surgery and malignant hyperthermia.
Curr Opin Anaesthesiol 22:744, 2009.
hyperthermia susceptibility? Brandom BW, Larach MG, Chen MS, et al.: Complications associated
with the administration of dantrolene 1987 to 2006: a report from the
A mutation of the ryanodine receptor gene (RYR1) in North American Malignant Hyperthermia Registry of the Malignant
skeletal muscle was discovered in the 1990s, and is Hyperthermia Association of the United States. Anesth Analg
responsible for a positive MH disposition. This discovery 112:1115, 2011.
25 Malignant Hyperthermia 121
Ellis FR: European Malignant Hyperpyrexia Group. Br J Anaesth Larach MG, Gronert GA, Allen GC, et al.: Clinical presentation, treatment,
56:1181, 1984. and complications of malignant hyperthermia in North America from
Glahn KP, Ellis FR, Halsall PJ, et al.: European Malignant Hyperthermia 1987 to 2006. Anesth Analg 110: 498, 2010.
Group: Recognizing and managing a malignant hyperthermia crisis: O’Flynn RP, Shutack JG, Rosenberg H, et al.: Masseter muscle rigidity
guidelines from the European Malignant Hyperthermia Group. Br J and malignant hyperthermia susceptibility in pediatric patients: an
Anaesth 105:417, 2010. update on management and diagnosis. Anesthesiology 80:1228, 1994.
Hirshey Dirksen SJ, Larach MG, Rosenberg H, et al.: Special article: Paladino TR: Malignant hyperthermia during general anesthesia:
future directions in malignant hyperthermia research and patient medicolegal considerations. Leg Med Annu 263, 1975.
care. Anesth Analg 113:1108, 2011. Strazis KP, Fox AW: Malignant hyperthermia: a review of published
Hopkins PM: Malignant hyperthermia: pharmacology of triggering. cases. Anesth Analg 77:297, 1993.
Br J Anaesth 107:48, 2011. Sudo RT, Carmo PL, Trachez MM, et al.: Effects of azumolene on
Keck PE Jr, Caroff SN, McElroy SL.: Neuroleptic malignant syndrome normal and malignant hyperthermia-susceptible skeletal muscle.
and malignant hyperthermia: end of a controversy? J Neuropsychiatry Basic Clin Pharmacol Toxicol 102:308, 2008.
Clin Neurosci 7:135, 1995. Sumitani M, Uchida K, Yasunaga H, et al.: Prevalence of malignant hyper-
Kim TW, Nemergut ME: Preparation of modern anesthesia workstations thermia and relationship with anesthetics in Japan: data from the diag-
for malignant hyperthermia-susceptible patients: a review of past and nosis procedure combination database. Anesthesiology 114:84, 2011.
present practice. Anesthesiology 114:205, 2011. Van der Spek AF, Reynolds PI, Fang WB, et al.: Changes in resistance
Larach MG, Dirksen SJ, Belani KG, et al.: Special article: creation of a to mouth opening induced by depolarizing and non-depolarizing
guide for the transfer of care of the malignant hyperthermia patient neuromuscular relaxants. Br J Anaesth 64:21, 1990.
from ambulatory surgery centers to receiving hospital facilities. Wappler F: Anesthesia for patients with a history of malignant hyper-
Anesth Analg 114:94, 2012. thermia. Curr Opin Anaesthesiol 23:417, 2010.
S ECTI O N 5
ENDOCRINE SYSTEM
122
CASE 26
Diabetes Mellitus
Jaime B. Hyman, MD
QUESTIONS
1. Describe the pathophysiology of type 1 and type 2 5. What is “tight glucose control,” and what are its
diabetes mellitus. advantages and disadvantages?
2. What are the end-organ effects of diabetes melli- 6. Describe and contrast diabetic ketoacidosis and
tus, and how do they affect the perioperative hyperglycemic hyperosmolar states.
course? 7. Outline the management of diabetic ketoacidosis
3. Discuss the oral medications and insulin prepara- and hyperglycemic hyperosmolar states.
tions available to treat diabetes mellitus and how 8. When should elective surgery be delayed because
they should be managed perioperatively. of hyperglycemia?
4. What impact does hyperglycemia have on periop-
erative morbidity and mortality?
A 62-year-old man with type 2 diabetes mellitus (DM) is DM commonly occurs in childhood and adolescence but
scheduled for a laparoscopic hemicolectomy. His medica- can occur at any age. Individuals with type 1 DM require
tions include metformin and glyburide. Preoperative exogenous insulin administration for survival. In the ab-
finger stick glucose value on the morning of surgery is sence of insulin administration, these individuals rapidly
360 mg/dL. become symptomatic from hyperglycemia. Carbohy-
drate, fat, and protein metabolism are dramatically dis-
turbed. Frequently, the first clinical presentation of a
1. Describe the pathophysiology of type 1 and type 2
type 1 diabetic is DKA. As a result of significantly im-
diabetes mellitus. paired glucose utilization, blood ketoacid concentration
DM is a metabolic disease arising from defects in insulin is elevated from increased lipolysis of fat and subsequent
secretion, insulin responsiveness, or both. Insulin is nor- conversion of fatty acids to ketoacids.
mally released from the endocrine pancreas, specifically Type 2 DM, which accounts for 90%–95% of the dis-
from pancreatic ! cells, in response to increases in blood ease burden, is caused by a combination of tissue insulin
glucose. Insulin receptors are present on cell membranes resistance and inadequate compensatory insulin secretory
of several tissue types. It is responsible for storing excess response. In contrast to type 1 diabetics, these patients
nutrients as glycogen in the liver, as fat in adipose tissue, typically do not require exogenous insulin administration
and as protein in muscle. These stored nutrients are to survive, at least initially. The risk of developing type 2
available during periods of fasting to maintain glucose DM increases with age, obesity, and inactivity. At earlier
delivery to the brain, muscle, and other organs. stages, it is asymptomatic and frequently goes undiag-
The diagnostic criteria for DM are listed in Box 26-1. nosed for years as hyperglycemia develops gradually.
Any of the listed criteria can establish the diagnosis of However, these patients are already at risk for developing
DM; it is not a requirement to meet all criteria. However, chronic microvascular and macrovascular complications
in the absence of hyperglycemia symptoms, the test is associated with DM. Table 26-1 outlines the major dif-
repeated before solidifying the diagnosis. In the acute ferences between type 1 and type 2 DM.
setting, hyperglycemia symptoms include polyuria, poly- Other rare causes of DM include genetic defects of
dipsia, weight loss, and blurred vision. The most extreme the pancreatic ! cells or genetic abnormalities in insulin
cases of acute hyperglycemia, diabetic ketoacidosis action. Diffuse injury to the pancreas from pancreatitis,
(DKA) and hyperglycemic hyperosmolar state (HHS), trauma, infection, cancer, or pancreatectomy can cause
can be life-threatening (see Questions 6 and 7). Uncon- diabetes, if extensive. Acromegaly, Cushing syndrome,
trolled chronic hyperglycemia is detrimental to multiple and pheochromocytoma can cause DM. Gestational
organ systems. DM, which affects 7% of all pregnancies, is glucose
Type 1 DM is caused by an absolute deficiency of insu- intolerance that is first recognized during pregnancy.
lin secretion; this accounts for only 5%–10% of cases. Insulin resistance usually resolves postpartum, but these
Classically, type 1 DM is caused by cell-mediated autoim- patients are at increased risk for developing type 2 DM
mune destruction of pancreatic ! cells. Immune-mediated later in life.
123
124 SECTION 5 Endocrine System
Type 1 Type 2
Cardiovascular Risk
Frequency 5%–10% 90%–95% Coronary artery disease is more prevalent in diabetics
and is often silent owing to neuropathy. DM is an inde-
Pathophysiology Autoimmune ! Increasing age, pendent risk factor for postoperative cardiac morbidity
cell destruction obesity, inactivity
and mortality and is included in the Revised Cardiac Risk
Defect Insulin deficiency Insulin resistance Index. Preoperative cardiac risk assessment is especially
Treatment Exogenous insu- Oral medications important in patients with DM.
lin required early in disease
Complications Propensity Propensity toward 3. Discuss the oral medications and insulin
toward DKA HHS preparations available to treat diabetes mellitus
DKA, Diabetic ketoacidosis; HHS, hyperglycemic hyperosmolar state. and how they should be managed perioperatively.
Oral agents used in the treatment of DM are outlined in
Table 26-2. Insulin preparations for subcutaneous use are
2. What are the end-organ effects of diabetes presented in Table 26-3.
mellitus, and how do they affect the perioperative Metformin, an oral hypoglycemic agent that is typi-
cally the first-line treatment for newly diagnosed type
course?
2 DM, warrants special mention because of the rare
DM affects nearly every organ system. Preoperative but potentially life-threatening side effect of lactic
evaluation should focus on systems that are most relevant acidosis associated with this drug. The perioperative
in the perioperative period. period may manifest with conditions leading to in-
creased risk for lactic acidosis, including impaired re-
nal or liver function, hemodynamic instability, and
Autonomic Dysfunction
decreased tissue perfusion. Metformin should be held
Damage to the nervous system from long-standing the morning of surgery, and use of metformin should
hyperglycemia can lead to autonomic dysfunction. be resumed only when renal function and circulatory
Patients with autonomic dysfunction are at greater risk status are stabilized postoperatively. Metformin is also
for intraoperative hypothermia from impaired periph- discontinued before and for 24–48 hours after the ad-
eral vasoconstriction. Similarly, these patients are sus- ministration of iodinated contrast material for radio-
ceptible to orthostatic hypotension, hemodynamic logic examination.
lability, and an increased risk of cardiovascular events. When administered as a solo agent, metformin does
They are prone to hypotension on induction of anes- not cause hypoglycemia. Other oral diabetic agents are
thesia, so doses should be adjusted accordingly. Ad- associated with hypoglycemia, particularly the sulfonyl-
vanced autonomic dysfunction may involve denervation ureas. These medications should be held the morning of
of vagal control and cardiac accelerator control of the surgery and throughout the perioperative period, as long
heart rate. Changes in heart rate normally seen with as the patient is fasting.
atropine or !-adrenergic blockers can be blunted in Type 1 and type 2 diabetics who are not adequately
patients with autonomic dysfunction. managed with oral agents typically receive basal-bolus
insulin maintenance regimens. Basal insulin is meant to
replace the patient’s baseline insulin that would be pro-
Gastroparesis
duced during fasting. The total daily dose of insulin is
Chronic hyperglycemia damages the gastrointestinal gan- usually divided into a 50% basal component and a 50%
glion cells, delaying gastric emptying and increasing the prandial component, either continuously via an insulin
risk of gastric aspiration during anesthesia. Diabetic pa- pump or by subcutaneous injection of a long-acting in-
tients suspected or known to have gastroparesis should be sulin once (insulin glargine) or twice (insulin detemir)
treated with full stomach precautions, so rapid-sequence daily plus short-acting boluses with food. Basal insulin
induction should be employed. Premedication with gastric can be continued in the perioperative period because it
26 Diabetes Mellitus 125
covers the fasting state. However, when type 2 diabetics usual dose on the morning of surgery. Insulin pumps
use long-acting insulins as their sole insulin, this is not can be continued intraoperatively, usually for proce-
meant to be basal dosing, and the dose should be re- dures lasting $2 hours, if secured away from the surgi-
duced perioperatively to avoid hypoglycemia. Interme- cal field.
diate-acting agents, such as NPH (neutral protamine In-hospital glycemic management is best achieved
Hagedorn) and insulin lispro protamine, display peaks with the use of insulin rather than oral diabetic
in activity (6 hours and 4–12 hours, respectively) that agents. In the perioperative period, frequent changes
can cause hypoglycemia during fasting. These agents in fasting status, unpredictable intestinal absorption
require dosing adjustments in the perioperative period. of medications, and rapidly changing clinical condi-
Patients are typically instructed to take half of their tions make the use of oral agents potentially less effec-
tive and unpredictable, and there is a risk for hypogly-
cemia. Correction of hyperglycemia in the perioperative
period can be accomplished with subcutaneous doses
TABLE 26-3 Insulin Preparations of ultra-rapid-acting insulin or regular insulin for am-
bulatory patients or patients in the postanesthesia care
Duration unit who will be admitted to a regular nursing floor.
Onset of Action Rough estimates for dosing are 1–4 units of insulin
Type (hours) Peak (hours) (hours) per 50 mg/dL decrease in glucose desired. Outside of
Insulin aspart, 5–15 min- 45–75 minutes 2–4 the immediate perioperative period, it is important to
lispro, utes include a basal insulin component meant to suppress
glusiline gluconeogenesis between meals. This is particularly
Regular 30 minutes 2–4 5–8 essential for type 1 diabetics, who without basal insu-
lin can rapidly develop DKA.
NPH (neutral 2 6 15 For critically ill patients, glycemic control is best
protamine
Hagedorn) achieved with intravenous insulin infusions. These pa-
tients can have unpredictable subcutaneous absorption of
Insulin lispro 2 4–12 18–24 insulin because of edema, hypotension, and peripheral
protamine
vasoconstriction. The same is true for patients undergo-
Insulin detemir 2 3–9 6–24 ing procedures where large fluid shifts or hemodynamic
Insulin glargine 2 No peak 18–26 lability are expected because skin perfusion can vary
greatly under these conditions.
126 SECTION 5 Endocrine System
4. What impact does hyperglycemia have on conditions unlikely to be generalizable to other ICU set-
tings, and parenteral nutrition for nearly all patients
perioperative morbidity and mortality? included in the study, which is known to cause hypergly-
Hyperglycemia is common in the perioperative period cemia and insulin resistance. After initial positive studies
both in diabetics and in nondiabetics. The neuroendo- advocated tight glycemic control, several professional
crine stress response to surgery causes release of coun- societies recommended strict glycemic control guide-
terregulatory hormones glucagon, epinephrine, and lines, but those original guidelines have subsequently
cortisol, which inhibit insulin secretion, increase insulin been called into question.
resistance, mobilize glycogen, and increase gluconeo- More recent trials have also questioned the benefits of
genesis. The severity of insulin resistance and resulting “tight glucose control” (as determined by glycosylated
hyperglycemia are directly related to the degree of sur- hemoglobin [HbA1c] levels) in outpatients with type 2
gical trauma. Hyperglycemia is especially common after DM, showing a higher risk of cardiovascular complica-
cardiac surgery and major abdominal surgery. It is also tions and mortality rate in tightly controlled groups.
more common for procedures lasting a long duration Hypoglycemia correlated with mortality in these studies.
and in open procedures more so than laparoscopic pro- Particularly concerning is that signs of hypoglycemia
cedures. Inhaled anesthetics contribute to perioperative may be masked in the perioperative period. Such signs in-
hyperglycemia by depressing insulin secretion in response clude blurred vision, confusion, diaphoresis, palpitations,
to increasing blood glucose levels. Perioperative steroid and weakness. Interrupted nutritional support during a
administration further exacerbates the propensity toward hospital stay without adjustment of insulin dosing can also
hyperglycemia. lead to hypoglycemia. Insulin is metabolized by the liver
Hyperglycemia in the perioperative period is associ- and kidney. Organ dysfunction can prolong the drug’s du-
ated with increased risk of infection secondary to im- ration of action, resulting in hypoglycemia. If improperly
paired leukocyte function—specifically, impaired che- dosed, insulin is a very dangerous medication. Overdoses
motaxis, phagocytosis, and intracellular bacterial killing. can lead to profound, life-threatening hypoglycemia.
It is also associated with impaired collagen synthesis and Conflicting evidence surrounding glucose control has
decreased nitric oxide production, reducing local perfu- led to a new paradigm in thinking about target glucose
sion and delaying wound healing. Vascular reactivity levels—that glycemic variability may be as important as
can be altered with increased levels of angiotensin II hyperglycemia when it comes to the detrimental effects
and enhanced systemic vascular resistance. Elevated of DM. Increased oxidative stress is seen with wide
glucose levels are also associated with renal injury, pul- swings in blood glucose. Oxidative stress from glycemic
monary complications, myocardial infarction, cerebro- variability is even more substantial than oxidative stress
vascular insult, longer hospital and intensive care unit associated with sustained hyperglycemia, which leads to
(ICU) stays, and increased mortality. These adverse free radical production. Free radicals are implicated in
outcomes are found to be more prevalent in patients causing vascular damage. Glucose fluctuations may also
without a previous diagnosis of DM who develop hy- trigger increases in cytokine expression and apoptosis.
perglycemia perioperatively than in patients with a Greater glucose variability has been associated with in-
known history of DM. creased mortality in surgical patients.
Studies aimed at delineating the precise goals for op-
5. What is “tight glucose control,” and what are its timum inpatient glucose management are ongoing, and
guidelines will likely continue to change. At this point,
advantages and disadvantages? the association between hyperglycemia and increased
Adverse outcomes associated with perioperative hyper- morbidity and mortality is strong, but the value of “tight
glycemia are well documented. The next practical ques- glucose control” has not been proven. The ideal blood
tion is whether interventions to decrease blood glucose glucose target and true efficacy of perioperative glycemic
levels in surgical patients improve outcomes. Several control remain to be clarified. Based on the balance of
studies evaluated the benefits of insulin therapy target- evidence to date, it is recommended by most professional
ing near-euglycemia (i.e., serum glucose 80–110 mg/dL) societies, including the American Association of Clinical
versus conventional management (i.e., serum glucose Endocrinologists and American Diabetes Association, to
$180–200 mg/dL). Early reports in critically ill patients target a blood glucose level of 140–180 mg/dL for most
advocated intensive glycemic control to reduce mortal- inpatients, while carefully monitoring for and treating
ity, bacteremia, acute kidney injury, blood transfusions, hypoglycemia should it arise.
critical illness neuropathy, duration of mechanical venti-
lation, and ICU stays. More recent trials and meta-
6. Describe and contrast diabetic ketoacidosis and
analyses failed to find reduced mortality or significant
improvement in other outcomes with “tight glucose hyperglycemic hyperosmolar states.
control” compared with more liberal glucose manage- DKA usually occurs in type 1 diabetics but can occur in
ment. Severe hypoglycemia is six times more common in type 2 diabetics. It is the result of decreased insulin
tightly controlled groups than conventionally managed levels that reduce glucose utilization and increase lipolysis
patients. Subsequent trials were halted early because of leading to the formation of fatty acids that are oxidized in
safety concerns for hypoglycemia in treatment groups. the liver to ketone bodies. Manifesting symptoms include
Criticisms of the initial studies include high ratios of dehydration, deep and rapid breathing (Kussmaul respira-
nurses and physicians to patients, which make study tion), fruity smelling breath, nausea and vomiting, and
26 Diabetes Mellitus 127
Thyroid Disease
Allan P. Reed, MD
QUESTIONS
1. How are thyroid hormones produced? 6. What are the complications of thyroid surgery?
2. Describe the classic presentation of 7. What are the intraoperative anesthetic consider-
thyrotoxicosis. ations for thyroid surgery?
3. How does thyroid storm differ from thyrotoxicosis? 8. How is regional anesthesia performed for thyroid
4. Describe the treatment of thyroid storm. surgery?
5. Describe aspects of the preoperative evaluation
for thyroid surgery.
phrenic nerve injury, and pneumothorax. Recurrent management is achieved in the usual manner. However,
laryngeal nerve injury can occur from stretching or tran- anticipated impossible mask ventilation or severe air-
secting the nerve. Bilateral injury can lead to respiratory way stenosis could indicate alternative airway manage-
distress. Controlled ventilation by anesthesia facemask is ment techniques. Examples include awake or asleep
usually sufficient to prevent hypoxia in the short-term. flexible fiberoptic intubation. Tracheal compression by
Reintubation or tracheostomy (or both) is required. a retrosternal goiter may make passage of the tracheal
Unilateral recurrent laryngeal nerve injury results in tube difficult. Armored tracheal tubes or smaller than
hoarseness, ineffective cough, and aspiration but not usual standard tracheal tubes may be necessary to pass
respiratory distress. through tortuous tracheas. In the United Kingdom,
Hypoparathyroidism can result from thyroidectomy supraglottic devices have been used, but there is a
when one or more parathyroids are removed. Parathy- risk of displacement and laryngospasm during gland
roid hormone helps maintain blood calcium levels. The manipulation.
absence of parathyroid hormone results in hypocalcemia, For most cases, standard induction and intubation
which produces muscle irritability. Chvostek (facial works well. Exaggerated hypotension may be seen
spasm) and Trousseau (carpal spasm) signs are classic on induction because of hypovolemia secondary to
bedside tests for hypocalcemia. Ionized calcium levels fever, diaphoresis, hypertension, and diarrhea. Treat-
obtained immediately are probably the best way to make ment includes fluid administration and direct-acting
the diagnosis. Hypocalcemia can result in laryngeal mus- vasopressors. Acute thyroid crisis during induction of
cle tetany, producing upper airway obstruction. The anesthesia can manifest with increased heart rate,
immediate treatment is airway management followed elevated blood pressure, and increasing end-tidal car-
by calcium replacement. Hypocalcemia usually occurs bon dioxide. This presentation mimics malignant
36 hours after surgery. hyperthermia. Malignant hyperthermia is associated
Tracheal compression can result from arterial bleed- with muscle rigidity and elevated creatine phosphoki-
ing. Blood lost under arterial pressure may dissect nase, whereas acute thyroid crisis is not.
through fascial planes and pool posterior to the trachea. No one anesthetic technique or agent has proved
The posterior tracheal wall is membranous, not carti- to be better than others. The goals of anesthetic manage-
laginous. Pressurized blood behind the trachea can push ment are to avoid hypertension and tachycardia. Mini-
the membrane into the tracheal lumen, producing nar- mum alveolar concentration does not increase in patients
rowing. Immediate treatment requires opening the with hyperthyroidism. Muscle relaxants are the best
surgical wound and evacuating the blood. If tracheal choice to prevent movement during tracheal manipula-
patency is not restored, intubation is in order. tion. However, they are contraindicated when recurrent
Phrenic nerve injury and pneumothorax both produce laryngeal nerve monitoring is employed. In these cases,
restrictive lung disease. Phrenic nerve palsy reduces dia- opioids, by depression of laryngeal reflexes, help prevent
phragmatic excursion, and pneumothorax reduces lung intraoperative patient movement and provide the added
volume. benefit of inhibiting coughing on emergence. Coughing
Other complications of thyroid surgery relate to the on emergence may predispose to bleeding from increased
extremes of thyroid function. Early on, thyroid storm is venous pressure. Graves disease is associated with myas-
a possibility, and later on hypothyroidism can manifest thenia gravis and other myopathies. Muscle relaxants
(Box 27-2). should be given judiciously in these patients.
Medications that stimulate the sympathetic nervous
7. What are the intraoperative anesthetic system should be avoided. Examples include ketamine,
pancuronium, epinephrine, and ephedrine. Anticholiner-
considerations for thyroid surgery?
gics, such as atropine, may increase the heart rate to a
Preoperative airway evaluation determines potential greater rate than under normal circumstances in these
methods for securing the airway. In most cases, airway patients. Glycopyrrolate may be used with caution.
Careful eye protection for patients with proptosis is
necessary to avoid complications from desiccation or
mechanical trauma. Carotid sinus manipulation may lead
BOX 27-2 Recognized Complications of to bradycardia, which should be treated with local anes-
Thyroid Surgery thetic infiltration or anticholinergics or both.
Tracheomalacia is diagnosed by digital palpitation of
COMPLICATIONS WITH THE POTENTIAL FOR a soft, thin tracheal segment after the thyroid gland
RESPIRATORY DISTRESS is removed. After extubation, airway obstruction from
• Recurrent laryngeal nerve palsy tracheal collapse may occur. If this happens, a tracheal
• Hypocalcemia tube or tracheostomy tube should be inserted beyond the
• Tracheal compression collapsed segment.
• Phrenic nerve injury At the end of the procedure, residual neuromuscular
• Pneumothorax
blockade is antagonized. In the past, it was routine to
COMPLICATIONS THAT DO NOT RESULT IN observe vocal cord motion during extubation. To facili-
RESPIRATORY DISTRESS tate this, deep extubation is followed by placement of a
• Hypothyroidism supraglottic device through which a fiberoptic scope is
• Thyroid storm inserted to observe vocal cord movement. However, this
practice is no longer routinely performed.
132 SECTION 5 Endocrine System
FIGURE 27-1 ■ Superficial cervical plexus block. (From Brown DL: Atlas of Regional Anesthesia, 4th ed. Saunders, Philadelphia, 2010. p. 181.)
After extubation and in the postanesthesia care unit, as- The deep cervical plexus block is intended to provide
sessment for respiratory distress or obstruction should be neck muscle relaxation. To perform a deep cervical
ongoing. Respiratory abnormalities may occur because of plexus block, local anesthesia is injected just above the
neck hematomas, recurrent laryngeal nerve injury, hypocal- anterior surface of the C4 transverse process. Approxi-
cemia, phrenic nerve injury, and pneumothorax. mately 10 mL of local anesthetic is injected with the
hope that it will spread along the paravertebral space.
8. How is regional anesthesia performed for thyroid Deep cervical plexus block is almost always complicated
by partial or full phrenic nerve block. For this reason,
surgery?
bilateral deep cervical plexus block is not recommended.
Local anesthesia for thyroidectomy is not a new concept; it Even unilateral block should be used cautiously for pa-
dates back to 1907. Regional anesthesia for thyroid surgery tients with poor pulmonary function. Other complica-
is frequently performed under cervical plexus block. The tions of deep cervical plexus block are intravascular in-
superficial cervical plexus receives contributions from cer- jection (vertebral artery), cervical epidural or subdural
vical nerve roots 1 through 4 (C1-4). It supplies sensory injection, cervical sympathectomy with Horner syn-
innervation to the lateral scalp (lesser occipital nerve), pinna drome, and recurrent laryngeal nerve involvement pro-
(greater auricular nerve), neck (transverse cervical nerve), ducing hoarseness. Horner syndrome includes ptosis,
and upper chest (supraclavicular nerve) (Figure 27-1). The myosis, and anhidrosis.
superficial cervical plexus courses subcutaneously at the
midlateral border of the sternocleidomastoid muscle. The
SUGGESTED READINGS
superficial cervical plexus block is a field block. Bupivacaine
or another long-lasting local anesthetic without epineph- Brown DL: Cervical plexus block. p. 177. In: Atlas of Regional Anesthesia,
4th edition. Saunders, Philadelphia, 2010.
rine is injected deep to and along the posterior border of Deutschman CS: Is chronic critical illness a state of endocrine dysfunc-
the sternocleidomastoid muscle. Approximately 5 to 10 mL tion? p. 246. In Deutschman CS, Neligan PJ (eds.): Evidenced Based
of local anesthetic is sufficient. Practice of Critical Care. Saunders, Philadelphia, 2010.
27 Thyroid Disease 133
Farling PA: Thyroid disease. Br J Anaesth 85:15, 2000. Suresh S, Jagannathan N: Somatic blockade of the head and neck.
Roizen MF, Fleisher LA: Anesthetic implications of concurrent disease. p. 405. In Cousins MJ, Carr DB, Horlocker TT, et al. (eds.):
p. 1086. In Miller RD, Eriksson LI, Fleisher LA, et al. (eds.): Miller’s Cousins and Bridenbaugh’s Neural Blockade in Clinical Anesthesia
anesthesia, 7th edition. Saunders, Philadelphia, 2010. and Pain Medicine, 4th edition. Lippincott Williams & Wilkins,
Sims CA: How do I diagnose and manage acute endocrine emergencies Philadelphia, 2009.
in the intensive care unit? p. 531. In Deutschman CS, Neligan PJ
(eds.): Evidenced Based Practice of Critical Care. Saunders,
Philadelphia, 2010.
CASE 28
Parathyroidectomy
Allan P. Reed, MD
QUESTIONS
1. Describe the physiology of calcium regulation. 6. How is parathyroid surgery performed under
2. What are the clinical features of hypercalcemia? regional anesthesia?
3. How is hypercalcemia treated? 7. What are the recognized complications of para-
4. How could hypercalcemia complicate anesthetic thyroid surgery?
care? 8. How is hypocalcemia treated?
5. Discuss a typical general anesthetic for parathyroid
surgery.
A 50-year-old woman presents for parathyroidectomy. Hypercalcemia affects the cardiovascular, renal, gas-
She has a history of hypertension, cholelithiasis, and trointestinal, hematologic, and central nervous systems.
nephrolithiasis. She denies seizures, syncope, palpitations, Calcium levels !13 mg/dL predispose to renal stones
and diaphoresis. She underwent general anesthesia for and other end-organ effects. Calcium concentrations
repair of a fractured femur without complications. Her !14 mg/dL are associated with uremia, coma, and cardiac
calcium concentration is 13 mg/dL. arrest. Table 28-1 summarizes the clinical presentation of
hypercalcemia.
1. Describe the physiology of calcium regulation.
3. How is hypercalcemia treated?
Extracellular calcium concentrations are regulated by
vitamin D and parathyroid hormone (PTH). Vitamin D The first step in treating hypercalcemia is to stop adminis-
increases calcium absorption from the gastrointestinal tract tration of calcium. Generally, this means eliminating
and augments the effects of PTH. PTH increases calcium calcium oral intake but could include intravenous adminis-
release from bone, increases calcium absorption from intes- tration. Simultaneous fluid administration with normal
tines, enhances vitamin D production, and decreases renal saline at 150 mL/hour and diuresis with furosemide are key
clearance of calcium. Under normal circumstances, PTH points. Thiazide diuretics are contraindicated because they
levels are inversely related to ionized calcium concentra- can increase calcium levels. This type of fluid management
tions. Calcitonin tends to decrease calcium levels. It is risks congestive heart failure, hypovolemic hypotension,
produced in the thyroid. hypokalemia, and hypomagnesemia. Dialysis may be
Calcium exists in two forms, bound and unbound. The needed for patients with preexisting heart failure or renal
bound portion is mostly attached to albumin. A small failure. Bisphosphonates such as pamidronate are reserved
percentage is complexed with anions such as citrate for life-threatening hypercalcemia. Salmon calcitonin,
and phosphate. The remainder is unbound. Unbound gallium nitrate, and glucocorticoids have also been used.
calcium is referred to as ionized or free calcium. Ionized
calcium is the physiologically important form. Alkalosis 4. How could hypercalcemia complicate anesthetic
decreases ionized calcium levels and predisposes to care?
clinically significant hypocalcemia.
Preoperative treatment for life-threatening hypercalcemia
involves intricate fluid management. Large volumes of
2. What are the clinical features of hypercalcemia?
infused fluids predispose to hypervolemia and heart fail-
Hypercalcemia occurs most commonly in association ure. Diuretic therapy risks hypokalemia. Hypercalcemia
with hyperparathyroidism from single benign parathy- complicates neuromuscular blockade in an unpredictable
roid adenomas. Other causes include malignant tumors, fashion. Consequently, muscle relaxants are best adminis-
immobility, thyroid toxicity, Paget disease, renal failure, tered in multiple small doses, with neuromuscular blockade
acquired immunodeficiency syndrome (AIDS), and monitoring. Osteoporosis predisposes to bone fractures
adrenal insufficiency. Parathyroid hyperplasia can be during positioning. Arrhythmias and conduction abnor-
related to pituitary adenomas and multiple endocrine malities may be present. Metabolic and respiratory acidosis
neoplasia (MEN). increase ionized calcium levels.
134
28 Parathyroidectomy 135
Perioperative Corticosteroid
Administration
Adel M. Bassily-Marcus, MD • Andrew B. Leibowitz, MD
QUESTIONS
1. Where are steroids naturally produced, and what 8. How long after discontinuation of steroids should
type of steroids are they? a patient be considered adrenally suppressed
2. What are the physiologic effects of and treated accordingly?
glucocorticosteroids? 9. What clinical scenarios frequently require steroid
3. What steroids are available for administration, and administration?
what are their equivalent doses? 10. How is adrenal reserve evaluated?
4. How much cortisol is normally produced, and what 11. If this patient develops septic shock from a bile
is Addison disease? leak in the postanesthesia care unit, should
5. What are Cushing syndrome and Cushing steroids be withheld or administered?
disease? 12. What is the duration of steroid treatment for criti-
6. Does this patient require “stress” dose steroids? cal illness related to corticosteroid insufficiency?
7. What is a stress dose of steroids; do you need to 13. If etomidate was used in this patient, is steroid
add mineralocorticoids? replacement warranted?
A 68-year-old man presented for laparoscopic cholecys- 3. What steroids are available for administration,
tectomy. He had been taking prednisone 10 mg per day and what are their equivalent doses?
for treatment of polymyalgia rheumatica. He had no
other relevant medical history. Dexamethasone (e.g., Decadron), methylprednisolone (e.g.,
Solu-Medrol), prednisone, and hydrocortisone (e.g., Solu-
1. Where are steroids naturally produced, and what Cortef [intravenous form], Cortef [oral form]) are the
four main steroids available for enteral or parenteral
type of steroids are they?
administration (not inhaled or topically applied). Their
The adrenal cortex produces three different classes of relative dose equivalents are:
steroids derived from the same basic cholesterol mole- • Dexamethasone 0.75
cule: glucocorticosteroids (cortisol), mineralocorticoids • Methylprednisolone 4
(aldosterone), and androgens (testosterone). The adrenal • Prednisone 5
medulla produces catecholamines via a different meta- • Hydrocortisone 20
bolic pathway, under different neurohumoral control, For example, a patient taking oral prednisone, 5 mg per
and derived from the amino acid tyrosine. day, who needs to be changed to an intravenous steroid of
identical potency would receive 20 mg of hydrocortisone
2. What are the physiologic effects of intravenously.
glucocorticosteroids?
4. How much cortisol is normally produced, and
Glucocorticosteroids are produced by the adrenal glands in what is Addison disease?
response to stimulation by adrenocorticotropic hormone
(ACTH). ACTH is secreted by the pituitary in response Under normal conditions, approximately 30 mg of corti-
to corticotropin-releasing hormone, which is produced in sol is produced daily. During periods of extreme stress
the hypothalamus. Glucocorticosteroids primarily affect (e.g., thoracic aortic surgery or septic shock), 300 mg
intermediary metabolism. They diffuse through cell mem- may be produced over the course of 24 hours.
branes and bind to specific glucocorticosteroid receptors, Addison disease results from chronic lack of endogenous
creating a complex that migrates to the nucleus and alters cortisol (and usually aldosterone) production. Clinical mani-
gene transcription. Resulting physiologic effects include festations include fatigue, weakness, anorexia, increased skin
an increase in blood glucose, mobilization of fatty acids, pigmentation, hypotension, hypoglycemia, hyponatremia,
catabolism, and antiinflammation. and hyperkalemia (Table 29-1). Most cases are idiopathic.
137
138 SECTION 5 Endocrine System
• Treat acute respiratory distress syndrome shock. In this investigation, patients in septic shock under-
• Manage vasogenic cerebral edema (e.g., brain tu- went a cosyntropin stimulation test. Patients were ran-
mors, spinal cord compression, acute pneumococcal domly assigned to receive either hydrocortisone, 50 mg
meningitis) by intravenous bolus every 6 hours, or a placebo. In the
hydrocortisone group, septic shock was reversed more
quickly than in the placebo group but with more episodes
10. How is adrenal reserve evaluated? of superinfection, including new sepsis and septic shock.
The most commonly performed outpatient test for adre- The study showed no difference in 28-day mortality for
nal reserve is a 24-hour urinary free cortisol collection. responders and nonresponders to the test whether they
For hospitalized patients, the ACTH stimulation test is received corticosteroids or placebo.
most commonly performed to determine the presence of Based primarily on this investigation, the Society of
adequate adrenal function. This screening test entails the Critical Care Medicine recommends hydrocortisone ad-
measurement of a baseline plasma cortisol, followed by a ministration only in the treatment of vasopressor-resistant
measurement at 30 minutes and 60 minutes after intrave- shock, defined as the need for increasingly higher doses of
nous administration of 250 !g of cosyntropin, an ACTH vasopressors or the need for a second vasopressor after
analogue. During periods of stress, the baseline plasma adequate fluid resuscitation. Although final conclusive evi-
cortisol level should exceed 20 mg/dL, and all patients dence is lacking, there is no utility at the present time in
should have an increase in plasma cortisol level of at least performing ACTH stimulation tests before administration
9 mg/dL above baseline with stimulation unless they of hydrocortisone in patients requiring vasopressors in the
have adrenal insufficiency. management of presumed septic shock.
In the patient in the present case, who was almost
11. If this patient develops septic shock from a bile certainly adrenally suppressed because of long-term ste-
roid administration, stress dose steroid administration
leak in the postanesthesia care unit, should
would generally be considered reasonable.
steroids be withheld or administered?
Although administration of steroids for patients who are 12. What is the duration of steroid treatment for
known to be adrenally suppressed is straightforward, steroid critical illness related to corticosteroid
administration in patients with septic shock has long been
debated. Steroid administration sometimes can improve insufficiency?
vascular responsiveness to catecholamine administration. The required duration of hydrocortisone replacement
Steroids are still administered in patients with vasopressor- therapy is unknown. In clinical trials, it has usually been
resistant septic shock, although clinical trials have generally 5 to 10 days and in practice usually depends on the clini-
revealed greater harm than benefit. cal response to therapy. If symptoms of hypotension or
In a study by Annane et al. (2002), patients with septic shock recur after discontinuation of steroids, the regimen
shock who received stress dose steroids and were proved to should be resumed at the prior dose and tapered slowly,
be adrenally insufficient based on cosyntropin (ACTH) if no other cause is found.
stimulation test had lower mortality rates compared with
patients who received placebo (53% vs. 63% at 28 days 13. If etomidate was used in this patient, is steroid
and 58% vs. 70% at the end of the intensive care unit stay)
(Box 29-1). A subsequent multicenter, randomized, dou- replacement warranted?
ble-blind, and placebo-controlled trial (CORTICUS) is Etomidate administration has been independently associ-
now the “gold standard.” This trial assessed whether “low” ated with poorer outcomes in critically ill patients. One
doses of corticosteroids improve survival from septic explanation is its preferential use in sicker patients, espe-
cially patients with severe sepsis who frequently already
have adrenal insufficiency. There is also some disagree-
ment concerning the need to administer steroids to pa-
BOX 29-1 Suggested Steroid Treatment in tients receiving etomidate. One large retrospective study
Septic Shock in patients with severe sepsis by Payen et al. (2012) found
no association between etomidate and changes in vaso-
PERFORM ACTH STIMULATION TEST pressor requirement, intensive care unit length of stay,
In patients requiring vasopressor therapy start: ventilator days, or hospital mortality. In exploring the
Hydrocortisone 50 mg intravenously every 6 hours effect of etomidate on outcome in patients with severe
Fludrocortisone 50 mg orally once daily (if enteral ac- sepsis, two randomized studies showed no outcome dif-
cess and absorption present) ference compared with ketamine or midazolam. Finally,
STIMULATION TEST RESULTS
in another randomized study, empiric steroid supplemen-
tation after etomidate administration did not change
Baseline cortisol level " 20 mg/dL, or outcome compared with placebo.
Rise from baseline level " 9 mg/dL
Continue therapy for 7 days
Baseline cortisol level # 20 mg/dL, or SUGGESTED READINGS
Rise from baseline level # 9 mg/dL Annane D, Sebille V, Charpentier C, et al.: Effect of treatment with low
Discontinue therapy doses of hydrocortisone and fludrocortisone on mortality in patient
with septic shock. JAMA 288:862, 2002.
140 SECTION 5 Endocrine System
Axelrod L: Perioperative management of patients treated with gluco- Payen JF, Dupuis C, Trouve-Buisson T, et al.: Corticosteroid after
corticoids. Endocrinol Metab Clin North Am 32:367, 2003. etomidate in critically ill patients: a randomized controlled trial. Crit
Cooper MS, Stewart P: Corticosteroid insufficiency in acutely ill Care Med 40:29, 2012.
patients. N Engl J Med 348:727, 2003. Sprung CL, Annane D, Keh D, et al.: Hydrocortisone therapy for pa-
Lamberts SWJ, Bruining HA, De Jong FH: Corticosteroid therapy in tients with septic shock. N Engl J Med 358:111, 2008.
severe illness. N Engl J Med 337:1285, 1997. Streck WF, Lockwood DH: Pituitary adrenal recovery following
Marik PE, Zaloga GP: Adrenal insufficiency in the critically ill: a new short-term suppression with corticosteroids. Am J Med 86:910,
look at an old problem. Chest 122:1784, 2002. 1979.
CASE 30
Pheochromocytoma
David B. Wax, MD
QUESTIONS
1. What is a pheochromocytoma? 4. What are intraoperative surgical and anesthetic
2. What are the signs and symptoms and diagnostic considerations?
criteria? 5. What are postoperative concerns and outcomes?
3. How is pheochromocytoma managed
preoperatively?
A 45-year-old, previously healthy woman was having in- catecholamine predominates. Norepinephrine secre-
creasingly frequent “panic attacks” accompanied by palpita- tion is most common and is usually sustained, with
tions, sweating, trembling, and headache. She was evaluated effects related to !-adrenergic stimulation. Epineph-
by her internist and was found to be moderately hyperten- rine release is less common and more often paroxysmal,
sive. This suggestive history prompted evaluation for possi- causing episodic effects related to "-adrenoreceptor
ble pheochromocytoma. Plasma metanephrine levels were stimulation. Dopamine release is least common and has
elevated, and subsequent imaging showed an adrenal mass. less specific signs and symptoms. Table 30-1 lists
She was started on doxazosin and referred to a surgeon. Her typical signs and symptoms as well as uncommon but
blood pressure improved, but other symptoms persisted. more severe end-organ manifestations of catecholamine
Atenolol was added to her medication regimen, and she was toxicity.
scheduled for laparoscopic adrenalectomy. Catecholamine release (and symptoms) from the
tumor may be provoked by postural changes, exercise,
anxiety, trauma, or pain. Foods and medications (e.g.,
1. What is a pheochromocytoma?
antidepressants, cold/flu medications, weight-loss medi-
A pheochromocytoma is a tumor of neuroendocrine tis- cations, cocaine, tobacco, alcohol) may also exacerbate
sue arising in the adrenal medulla from chromaffin cells symptoms by their effects on catecholamine metabolism.
that synthesize catecholamines. Neoplastic proliferation Pheochromocytoma may first manifest during anesthesia
of these cells can lead to release of one or more substances and surgery for another related tumor or unrelated
(norepinephrine, epinephrine, or dopamine) in varying condition or during pregnancy and may be confused
amounts and can cause catecholamine toxicity. Most with other conditions such as thyrotoxicosis, malignant
pheochromocytomas are solitary, benign, and sporadic, hyperthermia, or preeclampsia.
but they are occasionally multifocal, malignant, or part Diagnosis of pheochromocytoma is made by laboratory
of a syndrome (e.g., multiple endocrine neoplasias, von testing in patients with suggestive signs and symptoms.
Hippel–Lindau syndrome, neurofibromatosis, tuberous Elevated levels of metanephrine and normetanephrine
sclerosis, Sturge-Weber syndrome, ataxia-telangiectasia). measured in plasma (for patients with sustained signs and
They can also occur in pediatric and obstetric settings. symptoms) or 24-hour urine collection (for patients with
Similar tumors can arise in extraadrenal locations from paroxysmal signs and symptoms) confirm the diagnosis.
paraganglial cells of the autonomic nervous system (e.g., Absolute catecholamine concentrations may not always
in the organ of Zuckerkandl or carotid body) and in the correlate with the severity of signs and symptoms because
heart or pericardium. These paragangliomas are less of temporal variation, difference in the predominant cat-
likely to be functional compared with adrenal tumors. echolamine, and adrenoreceptor desensitization that may
Incidence of pheochromocytoma in the United States is occur with chronic exposure. Computed tomography,
approximately 1000 cases per year. magnetic resonance imaging, metaiodobenzylguanidine
scintiscan, or 18F-fluorodopa positron emission tomogra-
2. What are the signs and symptoms and diagnostic phy scanning can be used for tumor localization and
surgical planning. Before surgical intervention, echocar-
criteria?
diography may be performed to detect cardiomyopathy
Signs and symptoms of pheochromocytoma are related and monitor improvement after preoperative medical
to catecholamine excess and vary, depending on which therapy.
141
142 SECTION 5 Endocrine System
3. How is pheochromocytoma managed with a single agent, are intolerant of the aforementioned
preoperatively? agents, have only paroxysmal hypertension, or have
coronary vasospasm. Metyrosine, an inhibitor of cate-
The initial goal of preoperative medical therapy is to cholamine synthesis, may also be used preoperatively.
block the toxic effects of catecholamines to prevent and Long-acting medications may be discontinued 24 to
reverse end-organ damage. Table 30-2 presents agents 48 hours before surgery to help prevent postoperative
commonly used for this purpose. Therapy usually begins hypotension when the source of excess catecholamines is
by reversing !-adrenoreceptor-induced vasoconstric- removed.
tion. Phenoxybenzamine, a noncompetitive, nonselec- When blood pressure is normalized, consideration
tive, !-adrenoreceptor antagonist, is the traditional first- may be given to " Blockade. However, this treatment
line agent. Dosage is increased until blood pressure improves is necessary only for patients with predominantly
or intolerable side effects (e.g., postural hypotension, tachy- epinephrine-secreting tumors or patients who have
cardia, nasal congestion) develop. Selective, competitive, developed tachycardia from vasodilator therapy. " Blockers
!1-adrenoreceptor antagonists (e.g., prazosin, doxazosin, (especially nonselective ones) are not given until
terazosin) have also been used successfully. These agents ! blockade is achieved because "2 blockade can block
may cause less tachycardia than phenoxybenzamine, skeletal muscle vasodilation, which could exacerbate
and their shorter elimination times may be advanta- hypertension when combined with !1 agonism by nor-
geous in avoiding postoperative hypotension. Both epinephrine from the tumor. " Blockade could also
classes of !-blocking agents may cause postural hypo- potentially cause decompensation of catecholamine-
tension, which may be alleviated by salt and fluid induced cardiomyopathy. When indicated, "1-selective
supplementation. agents, such as atenolol or metoprolol, are typically
Calcium-channel blockers have also been used as a used. Mixed " and !1 antagonists, such as labetalol or
second agent in patients who have refractory hypertension carvedilol, may also be used, but they are not considered
b.i.d., Twice a day; IV, intravenously; p.o., per os (orally); q.d., once every day; q.i.d., four times a day; t.i.d., three times a day.
30 Pheochromocytoma 143
adequate as single-agent therapy because of the weak ! pancuronium, morphine, meperidine, ephedrine, meto-
effects and potential for causing worsening of hyper- clopramide, chlorpromazine, prochlorperazine, droperi-
tension owing to "2 blockade. dol) should be avoided, if possible. Aside from those
agents, most modern intravenous induction agents, opi-
4. What are intraoperative surgical and anesthetic oids, neuromuscular blockers, and inhaled agents can be
used safely; no agents are clearly superior to the others.
considerations?
Surgical manipulation and other events can trigger cat-
Surgical resection is the definitive treatment for pheo- echolamine release, resulting in acute hypertension and
chromocytoma. Surgery may be performed with open dysrhythmias. Medications must be immediately available
laparotomy technique or laparoscopic (with or without to treat such episodes. Short-acting agents may be prefer-
robotic assistance) technique. Surgical technique and able given the generally short-lived nature of the catechol-
patient positioning depend on tumor size, number, and amine surges. Various agents (see Table 30-2) can be used
location. For familial or bilateral adrenal tumors, partial depending on availability and practitioner preference. For
adrenalectomy may be attempted to avoid permanent supraventricular and ventricular dysrhythmias, " blockers
adrenal insufficiency. Regardless of technique, occlusion and lidocaine are usually effective. For hypotension, fluid
of the adrenal or other draining vein is desirable early in administration and direct-acting adrenergic agonists (e.g.,
the procedure to decrease catecholamine release into the phenylephrine, norepinephrine) can be used.
circulation during surgical manipulation of the tumor.
The intraoperative period may be complicated by 5. What are postoperative concerns and outcomes?
hemodynamic instability and blood loss. Large-bore
peripheral intravenous access and intraarterial blood Postoperative hypotension is common and, in addition to
pressure monitoring are advisable, and preoperative vol- the usual causes, may be due to persistent adrenergic
ume loading may be warranted. Central venous cannula- blockade from preoperative or intraoperative medications
tion may be considered for vasoactive infusions or volume that are still acting in the absence of opposing circulating
resuscitation but may not improve outcome compared catecholamines. Other causes of hypotension include
with peripheral-only access. Pulmonary artery catheter- downregulation of contralateral adrenal output or adrenal
ization is probably unnecessary other than in exceptional insufficiency after bilateral adrenalectomy. Alternatively,
cases of cardiovascular compromise. Similarly, intraopera- hypertension may persist because of residual tumor,
tive monitoring with transesophageal echocardiography is stored catecholamines, or chronic downregulation of
probably not warranted in all cases but may be helpful in adrenergic receptors. Hypoglycemia may result from
some circumstances. It is unknown whether using other rebound hyperinsulinism.
cardiac output monitoring technologies for goal-directed Major morbidity and mortality associated with pheo-
therapy improves outcomes in this setting. Thoracic epi- chromocytoma resection have decreased from 20% his-
dural catheterization for postoperative pain management torically to less than 5% more recently. These improve-
may improve analgesia after laparotomy. However, the ments in outcomes have been attributed to various
sympathetic blockade would not be expected to com- factors, including newer pharmacologic agents, better
pletely control intraoperative hypertension caused by tumor localization techniques, refined surgical tech-
circulating catecholamines released from the tumor and niques, closer attention to hemodynamics, and practitio-
may increase postoperative hypotension. ner experience.
Various stimuli have been implicated in provoking
catecholamine surges during the procedure, including
anesthesia induction, depolarizing neuromuscular block- SUGGESTED READINGS
ade, tracheal intubation, patient positioning, skin inci- Kinney MA, Narr BJ, Warner MA: Perioperative management
sion, and pneumoperitoneum. Succinylcholine-induced of pheochromocytoma. J Cardiothorac Vasc Anesth 16:359, 2002.
muscle fasciculation in the abdomen can cause tumor Lentschener C, Gaujoux S, Tesniere A, et al.: Point of controversy:
perioperative care of patients undergoing pheochromocytoma
compression and catecholamine release. Medications asso- removal—time for a reappraisal? Eur J Endocrinol 165:365, 2011.
ciated with histamine release or undesirable autonomic ef- Pacak K: Preoperative management of the pheochromocytoma
fects (e.g., ketamine, halothane, atracurium, tubocurarine, patient. J Clin Endocrinol Metab 92:4069, 2007.
CASE 31
Carcinoid Syndrome
Maria D. Castillo, MD
QUESTIONS
1. What are carcinoid tumors? 5. What are anesthetic concerns for patients with
2. Where do carcinoid tumors occur? carcinoid syndrome?
3. Describe the pathophysiology of carcinoid 6. How does somatostatin work?
syndrome. 7. Outline the perioperative management of patients
4. What is carcinoid crisis? with carcinoid tumors.
A 42-year-old woman presented with abdominal pain, tomography can be used to identify primary and metastatic
diarrhea, episodic facial flushing, and occasional wheez- tumors. In the absence of carcinoid syndrome, carcinoid
ing. On physical examination, a midsystolic heart murmur tumor may be diagnosed incidentally on chest or abdominal
was heard loudest along the left lower sternal border. x-ray. Carcinoid syndrome may also be diagnosed in
A mass was discovered in the ileocolic region during colo- patients undergoing unrelated surgery who present with
noscopy, and increased levels of 5-hydroxyindoleacetic carcinoid crisis in the perioperative period.
acid (5-HIAA) were found by 24-hour urine assay. The
patient was admitted for ileocolic resection with a pre-
2. Where do carcinoid tumors occur?
sumptive diagnosis of carcinoid syndrome.
Most carcinoid tumors occur in the gastrointestinal tract,
most commonly in the appendix, ileum, and rectum. They
1. What are carcinoid tumors?
may also occur in the bronchial tree, genitourinary tract,
Carcinoid tumors are slow-growing neoplasms of neu- thyroid, breast, pancreas, thymus, and liver. Because they
roendocrine tissue originating from enterochromaffin are slow-growing tumors, carcinoid tumors are usually
or Kulchitsky cells, with a reported incidence of 1 to 2 asymptomatic or produce vague, nonspecific symptoms
cases per 100,000 individuals. The term “carcinoid” such as abdominal pain. Over time, these tumors may
originally was used to describe a small bowel tumor cause intestinal obstruction or hemoptysis.
that was slow-growing but capable of metastatic spread. Metastatic disease occurs most commonly in the liver,
Carcinoid tumors can secrete an array of bioactive but carcinoid can spread to bone, mesenteric lymph
substances, including serotonin, histamine, prostaglan- nodes, myocardium, breasts, orbits of the eyes, adrenal
dins, vasoactive intestinal peptide, adrenocorticotropic glands, ovaries, spleen, pancreas, and lungs. Mesenteric
hormone, motilin, kallikreins, bradykinins, and tachy- metastases can cause intermittent bowel obstruction and
kinins (e.g., substance P, neuropeptide K, neurokinin A). abdominal pain.
Carcinoid tumors arising from the ileum or jejunum Traditional classification of carcinoid tumors is based on
appear as dense nests of cells with uniform size and the embryonic site of origin because it affects the clinical
nuclear appearance. Bronchogenic carcinoids may have presentation, the vasoactive substances that are secreted,
a typical carcinoid appearance or may resemble oat cell and overall survival. Foregut carcinoid tumors are located
carcinoma of the lung. in the thymus, esophagus, stomach, duodenum, pancreas,
Diagnosis of carcinoid tumors can be made by urine and gallbladder, bronchus, lung, and trachea. Foregut carcinoid
plasma assays of serotonin and its metabolite 5-HIAA; tumors may secrete adrenocorticotropic hormone and
however, 20% of patients with carcinoid syndrome may produce Cushing syndrome. Histamine release is more
have normal urinary 5-HIAA levels. Imaging techniques often associated with foregut carcinoid tumors, particularly
such as computed tomography scan, magnetic resonance tumors arising in the stomach. This histamine release may
imaging, endoscopy, endoscopic ultrasound, abdominal be due to the presence of histidine decarboxylase in normal
ultrasound, selective mesenteric angiography, and barium gastric mucosa. Midgut carcinoid tumors are found in the
small bowel radiography can help identify the primary jejunum, ileum, Meckel diverticulum, appendix, and colon.
tumor and, if possible, any metastases. Bronchoscopy can These tumors are more often associated with serotonin
be useful for locating a tumor in the bronchial tree. Local- release and classic carcinoid syndrome. Hindgut carcinoid
ization studies such as radiolabeled somatostatin analogue tumors are located in the rectum and are more likely
scintigraphy, bone scintigraphy, and positron emission to manifest with gastrointestinal bleeding. An alternative
144
31 Carcinoid Syndrome 145
classification system assigns the term “carcinoid tumor” from tryptophan via hydroxylation and decarboxyl-
only to midgut carcinoid tumors. Tumors arising from any ation, producing large amounts of serotonin may deplete
other site are referred to as neuroendocrine tumors of the the body’s tryptophan stores. Tryptophan is an essential
site of origin. amino acid necessary for the synthesis of proteins and
nicotinic acid. Hypoproteinemia, hypoalbuminemia,
3. Describe the pathophysiology of carcinoid decreased protein synthesis, decreased nicotinic acid
production, and the symptoms of pellagra may result.
syndrome.
Histamine release may cause bronchospasm and pos-
Although about 25% of carcinoid tumors actively secrete sibly produce flushing, although this remains unclear.
bioactive substances, less than 10% of patients develop Kallikreins are protease enzymes that generate kinins
classic carcinoid syndrome. Because the liver is very from kininogens on release into the bloodstream. Brady-
efficient at metabolizing these bioactive substances, the kinin release may cause profound vasomotor relaxation
syndrome occurs with primary tumors that are located in resulting in severe hypotension. Bradykinins can also
areas that do not drain into the portal system or with cause bronchospasm, particularly in asthmatics and in
hepatic, bone, gonadal, or pulmonary metastases that the presence of cardiac disease, and flushing, likely via
bypass hepatic metabolism. Although tumor size may not increased nitric oxide synthesis. Tachykinins, including
correlate with the clinical course of the patient, large neuropeptide K, neurokinin A, vasoactive intestinal pep-
liver tumors may secrete so much of these bioactive tide, and substance P, may cause flushing and longer term
substances that the liver’s ability to inactivate them may cardiac manifestations. Although the etiology is unclear,
be overwhelmed. Carcinoid syndrome may result when elevated levels of serotonin and tachykinins are likely
the active forms of neuropeptides and amine substances involved in the development of right-sided valvulitis and
are released into the systemic circulation. fibroblast proliferation. Tricuspid regurgitation is a com-
Signs and symptoms of classic carcinoid syndrome mon finding, but tricuspid stenosis, pulmonary insuffi-
include hypotension, hypertension, wheezing, diarrhea, ciency, and pulmonary stenosis may also develop. These
and episodic cutaneous flushing of the head, neck, trunk, valvular lesions may lead to right-sided heart failure, with
and upper extremities. Other possible manifestations edema, hepatomegaly, and fatigue on exertion. Left-sided
include abdominal pain, nausea, vomiting, telangiectasia, valvular lesions, including aortic and mitral insufficiency,
right-sided valvular disease, arrhythmias, pericardial ef- although less common, may occur. Fibrous tissue growth
fusion, and pellagra (dermatitis, diarrhea, and dementia) can interfere with electrical pathways, causing arrhythmias.
(Box 31-1). Dizziness and wheezing may occur with these Pericardial effusions, carcinoid plaques, and myocardial
episodes, which can be triggered by stress, exercise, or metastases are additional possible complications. Bronchial
ingestion of alcohol, coffee, or serotonin-rich foods such tumors may be associated with left-sided lesions, pulmo-
as bananas, avocados, plums, tomatoes, pineapples, kiwis, nary hypertension, and bronchospasm.
eggplant, plantains, or walnuts.
Serotonin can cause vasoconstriction or vasodila- 4. What is carcinoid crisis?
tion, which may manifest as hypertension or hypoten-
sion. Elevated serotonin levels can cause inotropic and Carcinoid crisis is a life-threatening form of carcinoid syn-
chronotropic responses in cardiac function; increased drome characterized by severe flushing with dramatic
gut motility, vomiting, bronchospasm, hyperglycemia, changes in blood pressure, cardiac arrhythmias, broncho-
and secretion of water, sodium, chloride, and potassium constriction, mental status changes, and circulatory col-
by the small intestine. Because serotonin is synthesized lapse. It results from the sudden release of excessive amounts
of tumor mediator substances (Box 31-2). Carcinoid crisis
can occur spontaneously, during induction of anesthesia,
during tracheal intubation, with physical manipulation of
BOX 31-1 Signs and Symptoms of Carcinoid the tumor, with chemical stimulation, with tumor necrosis
Syndrome from chemotherapy, and with hepatic artery ligation or
• Episodic cutaneous flushing
embolization.
• Hypertension
• Hypotension 5. What are anesthetic concerns for patients with
• Diarrhea carcinoid syndrome?
• Abdominal pain
• Bronchospasm The major perioperative goal is to prevent release of
• Nausea and vomiting bioactive mediators; this can be achieved by avoiding
• Delayed emergence from anesthesia triggering factors to prevent precipitating carcinoid
• Hepatomegaly crisis. A thorough history should be taken and a physical
• Hyperglycemia examination should be performed to determine the pres-
• Hypoalbuminemia and hypoproteinemia
• Gastrointestinal bleeding
ence and severity of signs and symptoms of carcinoid
• Pellagra syndrome, including flushing, diarrhea, wheezing, and
• Right heart failure heart murmur, and any triggers such as particular foods,
• Valvular disorders (tricuspid insufficiency, pulmonary caffeine, or alcohol. Laboratory tests including blood
stenosis) count, chemistry and liver function panels, blood glucose
concentration, and electrocardiogram (ECG) should
146 SECTION 5 Endocrine System
however, succinylcholine also has been used successfully that one of these vasoactive drugs becomes necessary, a
in reported cases. Anesthesia can be maintained using small dose can be administered and the response
infusions of propofol or remifentanil or inhalation anes- evaluated before further dosing.
thetics such as isoflurane, sevoflurane, or desflurane, or a Intraoperative hypertension can be treated with
combination of infusions and inhalation agents. Hypo- deepened anesthesia, opioids such as fentanyl or remi-
tension from inhalation anesthetic–induced peripheral fentanil, ! blockers such as esmolol, and octreotide.
vasodilation and myocardial depression can precipitate Nitroglycerin and sodium nitroprusside must be used
carcinoid crisis. Because serotonin can result in delayed with caution because resultant hypotension may trigger
emergence from anesthesia, shorter acting volatile agents mediator release.
with lower blood-gas solubility may be more desirable Patients with carcinoid tumor may present for hepatic
for these cases. Nitrous oxide also has been used safely in artery embolization rather than tumor resection. Although
patients with carcinoid syndrome. the liver receives 75% of its blood supply from the portal
Airway pressures should be monitored to detect the vein, most of the blood flow to the hepatic carcinoid tumor
onset of bronchospasm. Arterial blood gas measurements arrives via the hepatic artery, making embolization an ef-
can be used to help avoid hypercarbia and hypoxia fective means of tumor destruction while preserving he-
and manage hyperglycemia and electrolyte imbalances. patic function. With tumor destruction comes the possi-
Temperature should be monitored, and warming devices bility of massive tumor mediator release with resultant
such as forced air warming blankets and fluid warmers carcinoid crisis. Postoperatively, these patients may also
should be used to avoid hypothermia, another trigger of experience abdominal pain, nausea, vomiting, fever, and
mediator release. possible liver dysfunction.
Intraoperative hypotension should be treated with in- Because vasoactive mediators may remain in the circu-
travascular volume expansion and octreotide. If surgical lation for a period of time after tumor resection and be-
manipulation of tumor is coincident with hypotension, the cause of the possibility of some remaining undetected
manipulation should stop until blood pressure increases to metastases, careful postoperative hemodynamic monitor-
acceptable levels. Octreotide, 50 to 200 "g, can be given ing in an intensive care setting is prudent. Patients may
intravenously to treat severe hypotension and broncho- experience prolonged recovery from anesthesia because of
spasm, with doses repeated as necessary. Although octreo- elevated serotonin levels. Fluids and serum electrolytes
tide can be a lifesaving treatment, large doses may have should be closely monitored. Octreotide administration
been linked in at least one case to significant effects on the should be continued in the postoperative period. Adequate
cardiac conduction system, including bradycardia, Mobitz analgesia should be maintained, either with intravenous
type II atrioventricular block, and complete heart block. fentanyl or local anesthetic administered through the epi-
Other medications that may be useful in the management dural catheter. Vigilance should be maintained to avoid
of hemodynamic instability include rapid-onset, short- further triggers such as hypothermia, hypoxia, and hyper-
acting drugs such as esmolol, phenylephrine, and phentol- carbia. Ondansetron, a serotonin antagonist, is the anti-
amine. H1-Receptor and H2-receptor blockers may be emetic of choice because it may help attenuate symptoms
useful adjuvant therapies. Aprotinin, a kallikrein inhibitor, caused by serotonin excess.
has been effective in the treatment of hypotension refrac-
tory to octreotide. SUGGESTED READINGS
Other vasopressors that have been used safely include Cortinez FLI: Refractory hypotension during carcinoid resection
phenylephrine and vasopressin. Medications that cause surgery. Anaesthesia 55:505, 2000.
catecholamine release, such as ephedrine, should be Dierdorf SF: Carcinoid tumor and carcinoid syndrome. Curr Opin
avoided. Epinephrine, norepinephrine, and dopamine Anaesthesiol 16:343, 2003.
can make hypotension worse by further stimulating the Dilger JA, Rho EH, Que FG, et al.: Octreotide-induced bradycardia
and heart block during surgical resection of a carcinoid tumor.
release of vasoactive mediators. However, in cases of Anesth Analg 98:318, 2004.
carcinoid-related cardiac valvular surgery, vasopressors Farling PA, Durairaju AK: Remifentanil and anaesthesia for carcinoid
have been used successfully with octreotide. In the event syndrome. Br J Anaesth 92:893, 2004.
148 SECTION 5 Endocrine System
Kinney MA, Warner ME, Nagorney DM, et al.: Perianaesthetic Warner RR, Mani S, Profeta J, et al.: Octreotide treatment of carcinoid
risks and outcomes of abdominal surgery for metastatic carcinoid hypertensive crisis. Mt Sinai J Med 61:349, 1994.
tumours. Br J Anaesth 87:447, 2001. Zimmer C, Kienbaum P, Wiesemes R, et al.: Somatostatin does not
Levin MA, Flynn BC: Case report: primary ovarian carcinoid: a rare prevent serotonin release and flushing during chemoembolization of
tumor causing unexpected manifestations in a previously undiagnosed carcinoid liver metastases. Anesthesiology 98:1007, 2003.
woman. Anesth Analg 112:1158, 2011.
Mancuso K, Kaye AD, Boudreaux JP, et al.: Carcinoid syndrome and
perioperative anesthetic considerations. J Clin Anesth 23:329, 2011.
S EC TION 6
ABDOMEN
149
CASE 32
Full Stomach
Laurence M. Hausman, MD
QUESTIONS
1. What are the mechanisms a conscious person 6. How should the nasogastric tube be managed?
has to prevent regurgitation and pulmonary 7. What pharmacologic interventions can decrease
aspiration? the risk of aspiration?
2. Discuss the risk factors for regurgitation and 8. Why is cricoid pressure applied during rapid-
pulmonary aspiration during general anesthesia. sequence induction, and what are some of the
3. When can aspiration occur during the problems associated with applying cricoid
perioperative period? pressure?
4. Explain the problems associated with pulmonary 9. Describe the effects of commonly used anesthetic
aspiration. agents on lower esophageal sphincter tone.
5. If aspiration occurs, what are the usual course, 10. Outline an acceptable anesthetic plan for this
treatment, and prognosis? patient.
A 37-year-old woman with small bowel obstruction decreases. Reflux occurs when either the LES pressure
but otherwise in good general health presented to the decreases or the gastric pressure increases.
operating room for exploratory laparotomy, lysis of The angle where the esophagus meets the stomach also
adhesions, and possible bowel resection. Her past sur- protects against GERD. If the angle is oblique, high gastric
gical history was significant for cholecystectomy 3 years pressures are required to cause reflux. However, if the angle
ago, under general anesthesia, and cesarean delivery is small (as often occurs in patients with morbid obesity or
1 year ago with spinal anesthesia. Both procedures were a gravid uterus), reflux may occur at low gastric pressures.
without complication. She weighed 65 kg. In the pre- Another protective mechanism is the diaphragmatic
operative holding area, her vital signs were heart rate, crura that tighten at the lower esophagus to prevent reflux.
97 beats per minute, blood pressure, 130/65 mm Hg, and The upper esophageal sphincter (striated muscle that is
respiratory rate, 12 breaths per minute. She was found not under conscious control) is a third mechanism to pro-
to have acute abdominal tenderness, and she had a naso- tect against regurgitation. Virtually all commonly used
gastric tube in place. The tube was draining approxi- general anesthetics including muscle relaxants cause relax-
mately 25mL per hour of bilious fluid. Her hematocrit ation of this sphincter.
was 39%. Finally, there are intrinsic airway reflexes that protect
the airway against aspiration in the event of regurgita-
1. What are the mechanisms a conscious person tion. These include the cough reflex (a period of brief
has to prevent regurgitation and pulmonary inspiration followed by a forceful expiration), the expira-
tion reflex (expiration without inspiration), laryngospasm
aspiration?
and apnea (closure of both the false cords and the true
The lower esophageal sphincter (LES) is the primary cords), and spasmodic panting (rapid shallow breathing)
barrier to gastroesophageal reflux. The LES is 2 to 5 cm (Box 32-1).
long and moves upward with inspiration and downward
with exhalation. On swallowing, the esophagus under- 2. Discuss the risk factors for regurgitation and
goes peristaltic contractions to allow the passage of food,
pulmonary aspiration during general anesthesia.
and the LES relaxes. This sphincter traverses the dia-
phragm and has a resting pressure greater than gastric General anesthesia is associated with loss of protective
pressure. The difference in these pressures (LES pres- upper airway reflexes. A patient under general anesthesia
sure minus gastric pressure) is known as “barrier pres- who has regurgitation is at risk to aspirate the regurgi-
sure.” In normal subjects, an increase in abdominal tant. Any condition associated with an increase in intra-
pressure triggers an increase in lower esophageal pres- gastric volume, an increase in intragastric pressure, or a
sure, maintaining barrier pressure. Gastroesophageal decrease in LES tone may result in regurgitation and
reflux disease (GERD) occurs when the barrier pressure pulmonary aspiration (Box 32-2).
150
32 Full Stomach 151
against the diaphragm. Furthermore, the presence of a of volume can increase the intragastric pressure to
NGT has not been proven to limit the usefulness of cricoid 35 mm Hg. A force of 30 N (Newton) on the cricoid can
pressure. A third school of thought suggests withdrawing prevent regurgitation associated with 40 mm Hg of in-
the NGT to the midesophageal level (approximately 30 cm tragastric pressure. Older studies recommended 40 N of
from the nares) to allow for an increase in LES tone and a force. However, this much force is poorly tolerated, of-
decrease in overall esophageal pressure during induction, ten distorts laryngeal anatomy making intubation diffi-
decreasing not only the risk of regurgitation but also the cult, and predisposes to esophageal rupture. One solu-
risk of esophageal rupture. tion is to provide 20 N of force to a conscious patient.
This relatively small amount of force gives some protec-
7. What pharmacologic interventions can decrease tion against regurgitation; however, if intraesophageal
pressure increases too much, regurgitation will occur but
the risk of aspiration?
esophageal rupture will not. When the patient loses
Metoclopramide, a derivative of procainamide, facilitates consciousness, 30 N of force should be applied to the
gastric emptying by causing gastric peristalsis and relax- cricoid cartilage until the trachea is successfully intu-
ation at the pylorus. The effect of decreasing stomach bated. Cricoid pressure can increase the difficulty of
volume takes approximately 20 to 30 minutes. Metoclo- mask ventilation, if it is undertaken. Mask ventilation
pramide also increases LES tone within 1 to 3 minutes may be required in cases of difficult intubation.
of intravenous administration. Metoclopramide should Newer studies cast doubt on the effectiveness of cricoid
be avoided in cases of bowel obstruction. Because it is a pressure to prevent regurgitation and aspiration. Cricoid
dopaminergic antagonist, it should be avoided in pa- pressure may make visualization of the vocal cords during
tients with Parkinson disease or depression. It can also laryngoscopy more difficult by displacing the larynx later-
cause extrapyramidal side effects. The positive effects of ally, and it may completely occlude the airway. Cricoid
this drug are often inhibited by opioids that cause a pressure has also been shown to decrease LES tone and
delay in gastric emptying. may promote gastric reflux. However, literature both in
Cimetidine and ranitidine are competitive H2 blockers. favor and against the use of cricoid pressure during rapid-
They decrease basal gastric acid secretion that occurs in sequence induction is sparse. The standard of care as of
response to gastrin and food. Their onset of action is ap- this writing requires the use of cricoid pressure during
proximately 20 to 30 minutes when given intravenously. induction of anesthesia for patients at increased risk for
Sodium citrate is a nonparticulate antacid that in- aspiration.
creases gastric pH immediately on oral consumption. A
nonparticulate formulation is important because aspira- 9. Describe the effects of commonly used anesthetic
tion of particulate alkalis may also produce a chemical agents on lower esophageal sphincter tone.
pneumonitis.
Proton pump inhibitors (e.g., omeprazole, rabeprazole, Drugs that increase LES pressure and increase barrier
lansoprazole) block hydrogen and potassium adenosine pressure include the following:
triphosphatase enzyme systems at the secretory surface of • "-Adrenergic agonists
parietal cells in the stomach. These drugs decrease the • Antacids
volume and increase the pH of gastric secretions. • Antiemetics
Glycopyrrolate and atropine, both anticholinergics, in- • Cholinergics
crease gastric pH by inhibiting vagally mediated gastric • Edrophonium
acid production. Although glycopyrrolate also decreases • Histamines
LES tone, atropine does not. • Metoclopramide
• Metoprolol
8. Why is cricoid pressure applied during rapid- • Neostigmine
sequence induction, and what are some of the • Pancuronium
problems associated with applying cricoid • Succinylcholine
Drugs that decrease LES tone and decrease barrier
pressure?
pressure include the following:
The cricoid cartilage is the only complete cartilaginous • !-Adrenergic agonists
circular ring in the trachea. In 1961, Sellick reported that • Dopamine
posterior or rostral pressure applied to the cricoid carti- • Glycopyrrolate
lage would occlude the upper esophagus against the cer- • Inhalation agents
vical vertebrae and prevent regurgitation of gastric con- • Nitroglycerin
tents into the oropharynx, precluding aspiration of gastric • Opioids
contents. Theoretically, if gastroesophageal reflux should • Sodium nitroprusside
occur while cricoid pressure is applied, regurgitation into • Thiopental
the pharynx should not occur. However, cricoid pressure Drugs that have no effect on LES tone include the
is poorly tolerated in an awake patient and can cause the following:
patient to retch. Retching can increase intraesophageal • Cimetidine
pressure and predispose to esophageal rupture. • Propranolol
Maximum intragastric pressure is 25 mm Hg in • Ranitidine
starved supine patients. Gastric distention with 750 mL • Vecuronium
32 Full Stomach 153
Propofol lowers both esophageal and gastric pressure and this case, the most prudent approach would be awake
has no effect on barrier pressure. spontaneously breathing intubation, which is most of-
tenaccomplished with flexible fiberoptic equipment.
Awake intubation poses unique challenges in patients
10. Outline an acceptable anesthetic plan for this
with a full stomach. Awake instrumentation of the air-
patient. way requires profound airway anesthesia eliminating
Induction methods in patients with a full stomach vary protective coughing and gag reflexes. However, awake,
depending on several factors. One important factor is an unsedated patients know if they are going to vomit and
airway evaluation. The airway evaluation should always can turn their heads to the side. Under such circum-
include a thorough history of the patient’s prior airway stances, it is preferable to perform awake intubation
management problems. For patients with an acceptable rapidly and smoothly. Otherwise, bleeding, swelling,
airway evaluation, rapid-sequence induction with cricoid copious secretions, and vomiting can compromise the
pressure is indicated. Adequate time for preoxygenation process.
and denitrogenation is very important. The endpoint Inhalation induction by mask is contraindicated
for preoxygenation is an end-tidal oxygen value greater and should be performed only under exceptional cir-
than 90%. This concentration of oxygen is associated cumstances for patients who are at increased risk for
with denitrogenation of the functional residual capacity. aspiration.
Induction agents should be selected from agents with After the trachea has been intubated with a cuffed
rapid predictable onset times. Commonly used agents are tracheal tube, the anesthetic can be maintained in numer-
propofol, etomidate, and ketamine (sometimes a combina- ous ways including general anesthesia consisting of air,
tion of two or more is employed). Muscle relaxants should oxygen, an inhalation agent, opioid, and muscle relaxant
also have rapid onset times. Classically, the neuromuscular or total intravenous anesthesia. Even with a cuffed tra-
blocking agent used for rapid-sequence inductions has cheal tube in place, microaspiration may still occur
been succinylcholine. However, if succinylcholine is con- around the cuff. However, a cuffed tracheal tube provides
traindicated for any reason (e.g., hyperkalemia, burn, crush more protection than an uncuffed tube.
injury), rocuronium can be administered. Rocuronium is Extubation of the trachea is another period during
the only other neuromuscular blocking agent approved for which aspiration may occur. Before extubation, the patient
rapid-sequence induction. When administering rocuronium should be awake, alert, responsive, breathing spontane-
for rapid-sequence induction, the dose is doubled. The ously, and able to protect the airway.
disadvantage of using a nondepolarizing neuromuscular
blocking agent is that prolonged mask ventilation may SUGGESTED READINGS
be necessary if intubation is unsuccessful. If both mask Boet S, Duttchen K, Chan J, et al.: Cricoid pressure provides incomplete
ventilation and intubation are unsuccessful, a medical esophageal occlusion associated with lateral deviation: a magnetic
emergency may exist, which could require a surgical resonance imaging study. J Emerg Med 5:1, 2011.
Cotton BR, Smith G: The lower oesophageal sphincter and anaesthesia.
airway. Br J Anaesth 56:37, 1984.
Even in the face of a normal airway examination, in- Ehrenfeld JM, Cassedy EA, Forbes VE, et al.: Modified rapid sequence
tubation may be difficult. Often the only adjustments induction and intubation: a survey of United States current practice.
that need to be made are repositioning the patient’s head Anesth Analg 10:1, 2011.
El-Orbany M, Connolly LA: Rapid sequence induction and intubation:
into better sniffing position and changing the laryngo- current controversy. Anesth Analg 110:1318, 2010.
scope blade. If intubation is still unsuccessful, help from Holmes N, Martin D, Begley AM: Cricoid pressure: a review of the
anesthesia colleagues should be sought. At this point, it literature. J Periop Pract 21:234, 2011.
would be prudent to ventilate the patient gently through Metzner J, Posner KL, Lam MS, et al.: Closed claims analysis. Best
cricoid pressure, keeping peak airway pressures less than Pract Res Clin Anaesthesiol 25:263, 2011.
Nellipovitz DT, Crosby ET: No evidence for decreased incidence of
20 cm H2O; this would limit ventilation of the stomach. aspiration after rapid sequence induction. Can J Anesth 54:748, 2007.
Ventilation should be continued until the patient awak- Ng A, Smith G: Gastroesophageal reflux and aspiration of gastric con-
ens. If mask ventilation is difficult, ventilation through tents in anesthetic practice. Anesth Analg 93:494, 2001.
a supraglottic airway, such as a laryngeal mask airway, Olsson GL, Hallen B, Hambraeus-Jonzon K: Aspiration during anaesthesia:
a computer-aided study of 185 358 anaesthetics. Acta Anaesthesiol
is indicated. Gastric suctioning and tracheal intubation Scand 30:84, 1986.
are possible through many types of supraglottic airways. Smith KJ, Dobranowski J, Yip G, et al.: Cricoid pressure displaces the
Both mask ventilation and supraglottic airway placement esophagus: an observational study using magnetic resonance imaging.
can be impeded by cricoid pressure. Anesthesiology 99:60, 2003.
However, if the patient’s airway looks as though it Vanner RG, Pryle BJ: Regurgitation and oesophageal rupture with
cricoid pressure: a cadaver study. Anaesthesia 47:732, 1992.
may be difficult to manage by conventional means or if Warner MA, Warner ME, Weber JG: Clinical significance of pulmo-
the patient has a history of difficult airway manage- nary aspiration during the perioperative period. Anesthesiology
ment, rapid-sequence induction is contraindicated. In 78:56, 1993.
CASE 33
QUESTIONS
1. Describe liver cirrhosis and its systemic effects. 5. Why is avoidance of transfusion a reasonable
2. How do you evaluate a patient with severe liver request?
disease, and how does the liver disease affect the 6. How would you manage the fluids for this case
choice of anesthetic agents? and avoid transfusion?
3. What are the intraoperative considerations for 7. What are the concerns when using the Pringle
major hepatic resection in a noncirrhotic maneuver, and what are the concerns when using
patient? total caval isolation?
4. Is there a difference between right and left liver 8. How is postoperative pain best managed in
lobectomies? patients after hepatic resection?
A 62-year-old man with hypertension, hepatitis C, and outlines common problems related to chronic liver dis-
hepatocellular carcinoma presented for right liver partial ease that must be considered by the anesthesiologist.
lobectomy. The patient did not appear to have cirrhosis, and
laboratory studies were within normal limits. He underwent 2. How do you evaluate a patient with severe liver
an inguinal hernia repair under general anesthesia 13 years disease, and how does the liver disease affect the
ago without difficulty. General anesthesia was induced choice of anesthetic agents?
with propofol and fentanyl. Muscle relaxation was achieved
with vecuronium. General anesthesia was maintained with In addition to the usual directed history and physical
isoflurane and fentanyl. An intraarterial catheter and two examination of surgical patients, patients with cirrhosis
large-bore peripheral intravenous catheters were placed. of the liver require a thorough assessment regarding the
During the case, the surgeon asks you to limit severity of disease and recognition of the risk it entails.
fluid administration and avoid transfusion, if possible. The urgency of surgery dictates the time allowed to
Before resection of the tumor, the surgeon announces optimize coexisting medical problems. In acute hepatitis,
the “Pringle is on,” and the patient becomes hypoten- elective surgery is generally contraindicated, and emer-
sive and tachycardic. gency surgery carries a very high degree of risk. Common
signs and symptoms of liver disease should be sought to
1. Describe liver cirrhosis and its systemic effects. assess overall well-being. Jaundice, ascites, petechiae, and
ecchymoses are easy to assess quickly on first encountering
Cirrhosis of the liver affects approximately 3 million the patient. Figure 33-1 presents a rational approach to a
Americans and is the 12th leading cause of death in the patient with suspected liver disease.
United States. Chronic hepatitis refers to liver disease in A well-accepted method by which the severity of
which inflammation and necrosis are present for at least liver disease can be assessed is the Child-Pugh score
6 months and is most commonly due to hepatitis C virus (Table 33-2). Although the Child-Pugh score has been used
infection or alcohol abuse. The disease can be divided into for more than 30 years as a prognostic indicator for cir-
two major categories: cholestatic disease and hepatocellu- rhosis, it has several limitations, including two subjective
lar disease. Cholestatic diseases (e.g., primary biliary cir- variables of the five variables used, lack of a renal function
rhosis, primary sclerosing cholangitis) are uncommon correlate to survival, and overemphasis on measures of
causes of chronic hepatitis, whereas hepatocellular causes synthetic function (i.e., albumin and prothrombin time).
(e.g., infectious, autoimmune, steatohepatitis, or alcoholic) Child-Pugh scores are considered a good, although not
predominate and more often lead to hepatic resection or perfect, predictor of severity and subsequent mortality in
transplantation. these patients. The Model for End-Stage Liver Disease
Cirrhosis of the liver is a major challenge to the anes- (MELD) score is a more useful model for population com-
thesiologist because it leads to problems in nearly every parison and for use in transplant selection because it does
organ system. Most patients with long-standing liver not rely on subjective data. Instead, MELD scores involve
disease are functionally unwell and have poor nutritional nonempirically derived objective variables: bilirubin, creati-
status and exercise tolerance on presentation. Table 33-1 nine, international normalized ratio, and cause of cirrhosis.
154
33 Major Hepatic Resection 155
INR, International normalized ratio; NG, nasogastric; PT, prothrombin time; TEE, transesophageal echocardiography.
However, the MELD score is less useful in stratifying risk magnitude of the surgical procedure. Cirrhotic patients
in cirrhotic patients for nontransplant procedures. undergoing laparoscopic procedures tend to have better
Generally, severe liver disease portends a poor out- outcomes than patients undergoing laparotomy.
come because of increased morbidity and mortality from Although liver disease may affect the management of a
hepatic problems. Concurrent coexisting diseases in- patient’s anesthetic, minor operations generally have little
crease the risks. Class B or C patients are generally not effect on liver function. Perioperative liver damage is more
candidates for extensive hepatic resection. Because few likely dependent on the surgery than the anesthetic choice.
effective mechanical replacements exist for the failing Common issues with cirrhotic patients include the
liver (in contrast to the kidneys or heart), anesthesiolo- following:
gists must be able to assess severity adequately and care • Decreased doses or avoidance of premedicants
for patients with an appropriate level of intensity. Mor- (e.g., benzodiazepines) in the setting of even mild
bidity and mortality are also directly associated with the encephalopathy
156 SECTION 6 Abdomen
History
Examination
Laboratory studies if indicated
Asymptomatic biochemical
abnormalities
Acute liver disease Chronic liver disease
(No known underlying liver
disease)
Fulminant
Acute hepatitis Cirrhosis Non-cirrhotic
hepatic failure
FIGURE 33-1 ■ Preoperative assessment of a patient with liver disease. (Adapted from: Patel T. Surgery in the patient with liver disease.
Mayo Clin Proc 1999;74:593.)
• Presence of a full stomach owing to ascites and Conversely, low-extraction drugs (e.g., midazolam)
decreased gastric motility are influenced by protein binding allowing increased
• Endotracheal intubation to secure the airway (face- unbound drug to exert effects. Drug pharmacokinetics
masks and laryngeal mask airways should be avoided) in liver disease are complex. All medications given to
Abnormalities of protein binding, protein concentra- patients with diseased livers should be titrated to effect.
tion, volume status, volume of distribution, and me- Depending on the agent, alterations in protein anabo-
tabolism from hepatocyte derangement all have a signifi- lism by the liver as well as fluid shifts make dosing
cant impact on drug metabolism and pharmacokinetics of common anesthetic agents a challenge. In contrast
(Table 33-3). The severity of liver disease directly in- to the increased responsiveness to anesthetic agents,
fluences all of these variables and sensitivity to many patients with significant portal hypertension may have
anesthetic agents in the setting of encephalopathy. decreased responsiveness to catecholamines and either
Severe liver disease predictably alters the metabolism require increased doses or require nonadrenergic vaso-
of drugs with large extraction ratios (e.g., lidocaine) active drugs (e.g., vasopressin) for hemodynamic support
where clearance is dependent on hepatic blood flow. (see Table 33-3).
33 Major Hepatic Resection 157
TABLE 33-3 Effects of Chronic Liver Disease on Administration of Common Anesthetic Agents
Suggested Alterations in
Agents Drug Administration Description
Inhaled anesthetics
Nitrous oxide No change Encephalopathic patients may need less anesthetic overall,
Volatile anesthetics No change and overdose is easy. Volatile anesthetics at high doses can
induce hypotension and exacerbate disease state through
hypoperfusion. Sevoflurane, desflurane, and isoflurane
preserve hepatic blood flow and function well.
Induction agents
Propofol No change/decrease dose Intravenous anesthetics have a modest impact on hepatic blood
Etomidate No change flow and postoperative liver function when arterial blood
Ketamine No change pressure is maintained. Lower dose of propofol is sometimes
necessary if patient is hypovolemic or encephalopathic.
Opioids
Fentanyl No change Fentanyl is metabolized by the liver, but rapid redistribution
Remifentanil No change prevents significant alteration in elimination secondary to
Morphine, meperidine, Decrease dose/avoid liver disease. Remifentanil is metabolized by blood and
hydromorphone, altogether tissue esterases, and its elimination is unaltered. All other
sufentanil, alfentanil opioids are significantly affected by liver disease, leading to
accumulation and prolonged or profound effects.
Neuromuscular blockers
Succinylcholine No change Decreased cholinesterase levels may prolong effect of
succinylcholine. This is rarely the case.
Nondepolarizing No change: atracurium, Increased dosage for induction (increased volume of
agents cisatracurium distribution); decreased incremental or infusion doses
Decreased dose: vecuronium, for maintenance (decreased hepatic clearance).
rocuronium, mivacurium
Adjunctive agents
Benzodiazepines Decreased dose Decreased protein binding and increased free fractions of
midazolam and diazepam cause prolonged duration of action
and enhanced sedative effects.
Dexmedetomidine Decreased dose Primarily metabolized in the liver with minimal renal clearance.
expected to be greater than 1 L. An arterial line does not can exacerbate coagulopathy. An orogastric tube is usually
need to be placed before induction unless the patient’s placed, unless large or active varices are present. Positive
other comorbidities (e.g., cardiac disease, severe liver end expiratory pressure is avoided to limit back pressure in
disease) warrant it. the venous system, reducing congestion and bleeding.
Although the interactions between liver disease and The patient’s arms are abducted, and care must be taken
anesthetic agents are important to consider, noncir- to pad bony prominences for the purpose of reducing nerve
rhotic patients can often undergo a “straightforward” injury. Fluid management and blood product administration
anesthetic. Placement of spinal morphine or an epidural are discussed subsequently. Generally, normovolemia to
catheter is often used for postoperative analgesia (see slight hypovolemia is targeted, but the often requested “dry”
Q8). Anesthesia can be induced in the fashion most (e.g., hypovolemic) patient is rarely necessary to limit bleed-
suited to the particular patient (e.g., rapid sequence for ing. Throughout the case, “mugging” (i.e., compression) of
patients with large-volume ascites). General anesthesia the vena cava may occur as the liver is mobilized and re-
is usually maintained with inhalation agents rather tracted, acutely decreasing venous return and consequently
than intravenous agents because the slight decrease in leading to hypotension (often profound). Vasoactive sub-
hepatic blood flow seen with these agents is thought stances (e.g., phenylephrine, vasopressin) should be available
to limit bleeding. Rocuronium or vecuronium is often at all times to treat significant hypotensive episodes.
administered for muscle relaxation. In the presence Emergence from anesthesia generally involves the re-
of significant liver disease, cisatracurium is beneficial. sumption of spontaneous ventilation after fascial closure
Fentanyl, without spinal morphine, is given in higher so that titration of analgesics to a respiratory rate less than
doses because subcostal and upper abdominal incisions 20 breaths per minute can be accomplished. Antagonism
for open hepatectomy can be very painful (Figure 33-2). of neuromuscular blockade should be performed regard-
Doses of 8 to 15 $g/kg SD for the case generally suffice. less of when the last dose was administered to limit the
The use of patient warming devices, such as forced-air likelihood of postoperative respiratory events. Postopera-
warming blankets, is essential to avoid hypothermia, which tively, patients should be observed in the postanesthesia
care unit until transferred to a step-down unit where
invasive monitoring can be continued. Patients should
be monitored for respiratory depression (from residual
narcotics or splinting from painful incisions), rebleeding,
and acute liver failure.
maneuver effectively limits blood flowing into the liver There are two schools of thought with regard to how one
with the result that bleeding is principally a result of he- should approach neuraxial analgesia: epidural or single-shot
patic venous pressure, which itself is significantly reduced spinal opioid. The concern for potential changes in clotting
by maintaining low CVP and mean arterial pressure. The profiles after surgery is the primary reason epidural catheter
advantage of this approach is early vascular control before placement is avoided by some clinicians. Single-shot spinal
transection. The disadvantages are a tedious dissection opioid placement (usually morphine) is avoided by some
and the potential for injury to contralateral structures. clinicians because of the changes in postoperative drug me-
The time limit imposed by potential liver ischemia and tabolism that may lead to toxicity. Postoperative epidural
reperfusion injury, leading to liver insufficiency or hepatic analgesia has repeatedly been shown to be safe, although
failure postoperatively, means that a period of less than approximately 10% of patients have prolonged coagulation
45 minutes during surgery is optimal. Although the liver times. Analgesia from intrathecal morphine has been shown
has been shown to tolerate 1 hour of warm ischemia, some to be equivalent to epidural analgesia, but pruritus and
technical variations of the Pringle maneuver include inter- nausea occurred more frequently. One analgesic regimen
mittent vascular occlusion with cycles of approximately consists of 250 $g of intrathecal morphine administered at
15 minutes on and 5 minutes off. At either point in the the start of the case, limiting intravenous fentanyl to 3 to
Pringle maneuver (clamp on or clamp off), hypotensive 8 $g/kg over the course of the resection, and intravenous
episodes may occur. Hypotension during application of patient-controlled analgesia pump in the recovery period.
the clamp is due to decreased venous return that can be After the acute recovery period, all patients should be
successfully treated with boluses of phenylephrine or fluid nursed in a monitored setting (e.g., step-down unit) where
or both. Hypotension during release of the clamp is due respiratory depression can be detected expeditiously.
to reperfusion injury and release of ischemic mediators If epidural placement is desired, the American Society of
leading to vasodilation and cardiac depression (so-called Regional Anesthesia and Pain Medicine (ASRA) guidelines
stunning) from inflammatory mediator release. Judicious should be followed for epidural catheter removal, to avoid
use of vasopressors or inotropic agents (e.g., ephedrine) the risk of epidural hematoma. If intravenous agents are to
or both generally alleviates the derangements. Lactic be the sole analgesic strategy, the intraoperative adminis-
acidemia may also ensue following the Pringle maneuver tration of long-acting opioids such as methadone, mor-
and can be corrected by judicious fluid use. It may persist phine, or hydromorphone is advisable. Tracheal extubation
despite adequate resuscitation and should be followed in can be performed in most patients at the end of surgery, but
the immediate postoperative period as an early marker of respiratory depression must be watched for closely.
liver failure.
Total vascular isolation involves clamping of the up-
per and lower vena cava in addition to the porta hepatis. SUGGESTED READINGS
Although total vascular isolation was used in the past, it
Belghiti J, Regimbeau JM, Durand F, et al.: Resection of hepatocellular car-
is rarely necessary other than for the largest and most cinoma: a European experience on 328 cases. Hepatogastroenterology
complex lesions. Although the advantage of total caval 49:41, 2002.
isolation is markedly reduced blood loss at the liver Bossola M, Stockman J, Ben-Porat L, et al.: Influence of transfusions on
itself, the major disadvantages of lack of collateral flow perioperative and long-term outcome in patients following hepatic
resection for colorectal metastases. Ann Surg 241:381, 2005.
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obviate its use. Large blood losses during liver resection anatomical conditions]. J Chir 68:697, 1952.
are now rare, with median values of 200 to 500 mL. Gelman S: Venous function and central venous pressure: a physiologic
There is a strong emphasis on reduction of intraopera- story. Anesthesiology 108:735, 2008.
tive blood loss through a combination of anesthetic Giordano C, Deitte LA, Gravenstein N, et al.: What is the preferred
central venous pressure zero reference for hepatic resection? Anesth
techniques as described earlier and established surgical Analg 111:660, 2010.
techniques. For this reason, caval isolation is rarely em- Melendez JA, Arslan V, Fischer ME, et al.: Perioperative outcomes of
ployed. If it is planned, large-bore intravenous access major hepatic resections under low central venous pressure anesthesia:
beyond the “usual” for hepatic resections in the form blood loss, blood transfusion, and the risk of postoperative renal dys-
function. J Am Coll Surg 187:620, 1998.
of a central line (8.5F or 9F) is advisable for rapid fluid Patel T: Surgery in the patient with liver disease. Mayo Clin Proc
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the application of adjunctive hemostatic agents to the Pietri L, Siniscalchi A, Reggiani A, et al.: The use of intrathecal mor-
cut surface of the liver. These are purely adjunctive mea- phine for postoperative pain relief after liver resection: a comparison
sures and do not eliminate the need for good vascular with epidural analgesia. Anesth Analg 102:1157, 2006.
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control of bleeding. in viral hepatitis, hepatic disorders, and liver transplantation. Med Clin
North Am 84:1085, 2000.
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8. How is postoperative pain best managed in surgery. Surg Clin North Am 84:401, 2004.
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and hepatorenal syndrome in cirrhosis. Hepatology 42:439, 2005.
Management of postoperative pain in patients after liver Tripodi A, Mannucci PM: The coagulopathy of chronic liver disease.
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ously, a large incision means severe postoperative pain is Yamamoto J, Kosuge T, Takayama T, et al.: Perioperative blood transfusion
possible, and the location of the incision means that promotes recurrence of hepatocellular carcinoma after hepatectomy.
Surgery 115:303, 1994.
“splinting” may be common, leading to poor respiratory Ziser A, Plevak DJ, Wiesner RH, et al.: Morbidity and mortality in cir-
recovery. The “best” analgesic regimen after these proce- rhotic patients undergoing anesthesia and surgery. Anesthesiology
dures is still debated. 90:42, 1999.
CASE 34
QUESTIONS
1. Explain the natural history of aortic aneurysms. 5. How are patients undergoing aortic aneurysm
2. How is a patient with an aortic aneurysm evaluated surgery monitored?
preoperatively? 6. Explain the consequences of aortic cross-clamping.
3. Which medications are administered preoperatively? 7. Describe some options for postoperative analgesia.
4. Which anesthetic agents are used for aortic
aneurysm surgery?
A 71-year-old man with a 6-cm infrarenal aortic aneu- systems. The goal of preoperative evaluation is to de-
rysm presented for conventional aortic repair. His past tect coexisting diseases, assess the risk of adverse out-
medical history was significant for hypertension, stable comes, optimize the patient’s medical status, and devise an
angina, hypercholesterolemia, and smoking. anesthetic technique that minimizes complications. It is
not always possible to perform a complete preopera-
tive evaluation when surgery is required on an urgent
1. Explain the natural history of aortic aneurysms.
basis, so preoperative optimization of the patient is not
The natural history of all aneurysms is to expand in size. always feasible.
The tendency to rupture primarily depends on wall It is imperative to evaluate myocardial reserves before
stress. With increases in aneurysm diameters, the wall aortic surgery. Risk factors for myocardial ischemia include
stress increases as described by LaPlace law, increasing history of previous myocardial infarction, angina, conges-
the risk of rupture: tive heart failure, male gender, smoking, hypercholesterol-
emia, diabetes mellitus, and limited exercise tolerance.
pressure " radius Patients at low risk for myocardial ischemia may proceed
Wall stress !
2 " wall thickness to surgery without further evaluation; this represents
a very small subset of patients with aortic aneurysms. Pa-
The average growth rate of aortic aneurysms is 0.4 cm tients with a negative stress test within 2 years of surgery
per year. In a follow-up study of high-risk patients, the or who have had coronary artery bypass graft surgery
overall rupture rate was 3%, with a surgical mortality without postoperative symptoms probably do not require
(elective surgery for aneurysms !6 cm or symptomatic further work-up for myocardial ischemia. Although stress
aneurysms) of 4.9%. Approximately 34% of deaths were testing is probably most appropriate for patients with
due to causes unrelated to the aneurysm. The 5-year moderate risk, coronary angiography is recommended for
survival rate for untreated abdominal aortic aneurysms patients at high risk for myocardial ischemia.
greater than 6 cm was less than 10%, and the 5-year sur- There are two components to stress testing: “stress-
vival rate for untreated abdominal aortic aneurysms less ing” the myocardium and detection of myocardial is-
than 6 cm was 50%. Elevated diastolic blood pressure, chemia or infarction. “Stressing” is performed by either
aneurysm anteroposterior diameter greater than 5 cm, mechanical (e.g., exercise via treadmill or hand-crank)
and obstructive pulmonary disease were independent or pharmacologic means. Pharmacologic stress may
predictors of rupture. Predicted 5-year rupture rates involve drugs such as dobutamine that increase myo-
ranged from 2% when these risk factors were absent to cardial oxygen demand or drugs such as dipyridamole
100% when all three risk factors were present. that cause “myocardial steal.” Myocardial ischemia is
detected by electrocardiogram (ECG), nuclear studies,
2. How is a patient with an aortic aneurysm or echocardiography. Ischemic myocardium is charac-
terized by changes in ST segment elevations that occur
evaluated preoperatively?
with exercise. On nuclear studies, the absence of nu-
Nearly all patients presenting for aortic surgery have clear tracer uptake during stress and uptake of nuclear
coexisting medical conditions that can significantly affect tracers with rest is known as a reversible defect. Fixed
anesthetic management. Problems include diseases of the defects (i.e., absence of uptake during stress and rest) is
cardiovascular, pulmonary, renal, and central nervous consistent with old infarction. Ischemic myocardium
161
162 SECTION 6 Abdomen
hypotension with an associated increased rate of stroke A safe and reliable method of measuring acute
and greater mortality. If patients have significant risk of changes in blood pressure is required during aortic
CAD, "-adrenergic blockade should be carefully titrated surgery. Intraarterial monitoring accomplishes this
to heart rate and blood pressure. goal by providing continuous, beat-to-beat indication
of arterial pressure and waveform. An indwelling arte-
4. Which anesthetic agents are used for aortic rial catheter enables frequent sampling of arterial blood
for laboratory analyses.
aneurysm surgery?
Cannulation of a central vein is routinely performed
All patients presenting for emergency aortic surgery are for aortic surgery to measure filling pressures in the heart
treated as if they have a full stomach, whereas elective (using a central venous catheter or a pulmonary artery
cases must be considered individually. Avoiding hemody- catheter), provide a central route for drug administra-
namic aberrations during induction and tracheal intuba- tion, and enable rapid infusion of fluids. Central venous
tion are desirable. Various anesthetic agents can accom- access can be accomplished with a large-bore cannula
plish these goals, and the choice is a personal decision (“introducer”) in the right internal jugular vein or left
that depends on the clinical situation. High-dose opioid subclavian vein. Cannulation of the left internal jugular
techniques are still commonly employed for patients in vein may be associated with a greater incidence of
whom postoperative ventilatory support is anticipated; innominate vein perforation; because of the acute changes
however, normothermic, hemodynamically stable pa- in directions, catheterization of the pulmonary artery
tients may be considered for early extubation. Although is more difficult from the left internal jugular or right
no evidence-based practices favor one anesthetic tech- subclavian vein.
nique over another, it is probably most important to use Central venous pressure (CVP) does not give a di-
a technique that achieves the desired hemodynamic goal. rect indication of left heart filling pressure, but it may
Vasoactive medications, such as nitroprusside, nitroglyc- be used as an estimate of left-sided filling pressures in
erin, and esmolol, should be prepared preoperatively, patients with good left ventricular function. CVP has
including diluted amounts for bolus administration. been shown to correlate with left-sided filling pres-
sures during a change in volume status in patients with
5. How are patients undergoing aortic aneurysm CAD and ejection fractions greater than 40%. Other
studies have not shown a consistent relationship be-
surgery monitored?
tween CVP and pulmonary capillary wedge pressure.
Standard American Society of Anesthesiologists (ASA) Pulmonary artery catheterization should be strongly
monitors are placed for all patients presenting for sur- considered in patients with decreased ventricular func-
gery of the aorta. ECG with the ability to monitor limb tion, pulmonary hypertension, severe valvular disease,
and precordial leads (II and V5 at the minimum) is desir- or advanced systemic organ dysfunction. Monitoring of
able to detect myocardial ischemia and arrhythmias. right-sided pressures as the sole indication of volume
Foley catheterization is also prudent to assess volume status is probably not sufficient because of the inability
status and to provide early indication of renal malperfu- of the right heart pressures to reflect left heart preload.
sion. Because of the increased incidence of myocardial Pulmonary artery catheters may also be used to deter-
ischemia, coagulopathy, and wound infection, patients mine afterload, cardiac output by thermodilution, and
should remain normothermic perioperatively. oxygen delivery by measuring pulmonary artery oxygen
Anesthesia for aortic surgery is frequently complicated saturation. Although pulmonary artery catheters are
by marked sudden blood pressure lability. Shifts in intra- probably warranted in high-risk patients, no study
vascular volume, the effects of anesthetic agents, and has demonstrated better outcome with the use of this
surgical manipulations are the major causes. Sudden modality.
losses of significant amounts of blood may induce severe Transesophageal echocardiography (TEE) is a very
hypovolemia at almost any time. Changes in preload may useful monitoring tool during aortic surgery. Ventricular
be due to sudden and profound hemorrhage from inter- dysfunction and regional wall motion abnormalities may
costal artery back-bleeding, aortic disruptions, extensive be diagnosed. TEE produces images of the heart and
anastomotic suture leaks, and evaporative and third space great vessels, affording information such as regional wall
losses. Large-bore intravenous access is extremely im- motion abnormalities, indirect measurements of stroke
portant in aortic surgery. Aortic rupture can occur at volume and ejection fraction, valvular abnormalities, and
any time, and the ability to infuse intravenous fluids and aortic and pericardial pathology. Ventricular function
blood or blood products rapidly is necessary. One or two and intravascular volume status are probably the best
large-bore peripheral intravenous lines are recommended indications for using TEE during these procedures.
in addition to central venous access. A rapid infusion Competency in TEE is certified by the National Board
system with a fluid warmer should be immediately avail- of Echocardiography.
able. Blood salvaging techniques for autotransfusion are
recommended. The easiest blood salvaging technique 6. Explain the consequences of aortic
to employ is a centrifugal device that scavenges and cross-clamping.
washes erythrocytes. The disadvantages of this method
are delays in filling the centrifuge bowl; time consumed The most consistent hemodynamic response to acute
processing the blood; and lost plasma volume, proteins, aortic occlusion is an abrupt increase in afterload with a
coagulation factors, and platelets. resultant increase in proximal aortic pressure. During
164 SECTION 6 Abdomen
supraceliac aortic occlusion, there is an increase in pre- 7. Describe some options for postoperative analgesia.
load secondary to volume redistribution from veins distal
to the site of aortic occlusion. These increases in after- Intravenous opioid administration has the advantage
load, preload, and possibly contractility are associated of rapid uptake and attainment of therapeutic levels.
with enhanced myocardial oxygen demand and possibly However, this mode of administration is also associated
myocardial ischemia. Because of the expected increases in with rapid declines in drug concentration during which
preload from aortic occlusion, preload should be main- patients may experience pain. Although using larger
tained low before occlusion. Venodilators such as nitro- doses may increase the duration of analgesia, higher
glycerin, may be titrated to decrease preload further, doses may be associated with a greater number of adverse
and arterial dilators may be used to control increases in side effects. To minimize these side effects, small, fre-
afterload. During aortic occlusion, attention should be quent doses of opioids may be administered via a patient-
directed toward maintenance of preload, which may be controlled pump (i.e., patient-controlled analgesia). This
complicated by continued blood loss. technique allows greater comfort control during the hos-
Intraoperative hypotension may result from multiple pital course and may prevent overmedication. Although
causes. Hypovolemia, myocardial depression, and de- this technique is safe, respiratory depression may occur,
creases in afterload should be considered. One common so routine postoperative nursing care should include
etiology of hypotension is reperfusion. Unclamping careful monitoring of respiratory status.
hypotension may be caused by central hypovolemia An attractive alternative to the use of intravenous
secondary to blood pooling in reperfused tissues, opioids is epidural administration of analgesics. Local
hypoxia-mediated vasodilation, and accumulation of anesthetics, opioids, and other agents such as $2 ago-
vasoactive or myocardial-depressant metabolites such nists have been described as effective in significantly
as lactate. Treatment should be directed toward rapid decreasing the intensity of postoperative pain. Although
correction of hypovolemia, acidosis, and hypocalcemia this method can provide profound pain relief, it may be
and the judicious administration of vasoactive drugs. If associated with significant side effects. Local anesthetics
there is difficulty obtaining hemodynamic stability, the cause sympathetic blockade (with resultant decreases in
aorta can be temporarily reoccluded while resuscitation preload and afterload that may produce hypotension
continues. and tachycardia), motor blockade, and local anesthetic
Renal insufficiency may occur as a result of abdominal toxicity. Opioids may cause pruritus, nausea, vomiting,
aortic reconstruction. It is possible that pharmacologic urinary retention, or respiratory depression. These side
agents may provide renal protection during repair. Al- effects can usually be treated with conventional therapy
though mannitol may result in greater diuresis on post- (e.g., antihistamines, antiemetics) or specific opioid
operative day 1 and less subclinical glomerular and renal antagonists. Epidural opioids have the advantage of
tubular damage, it probably has no effect on postopera- specificity of action, without major hemodynamic
tive blood urea level, serum creatinine concentration, changes and motor blockade that are associated with
or creatinine clearance. There is little evidence of the local anesthetics.
effectiveness of furosemide as a renal protective agent. Preoperative epidural catheter insertion for postop-
Theoretically, the perioperative use of low doses erative analgesia is probably safe when perioperative
of dopamine may confer renal protection in high-risk anticoagulation is anticipated. Epidural anesthesia may
individuals. Low-dose dopamine (1 to 3 #g/kg/min) di- increase coronary blood flow, but there is contradic-
lates renal afferent arterioles and increases renal blood tory evidence on the effect of epidural anesthesia on
flow, independent of its cardiac effects. Dopamine infusion myocardial ischemia during noncardiac surgery. There
during aortic clamping results in a significant increase in have been multiple reports of attenuation in the stress
urine sodium output, potassium output, creatinine clear- response with perioperative and postoperative epidural
ance, and urine volume. The use of perioperative dopa- anesthesia and analgesia during vascular surgery. Sup-
mine during aortic surgery is associated with increases in plemental epidural anesthesia may significantly atten-
effective renal plasma flow and glomerular filtration rate uate catecholamine release during aortic occlusion and
and fractional excretion of sodium during the postopera- reperfusion. This reduction in the stress response by
tive period. However, studies have not demonstrated a epidural anesthesia or analgesia could decrease postop-
renal protective effect of low-dose dopamine use. It is erative hypercoagulability.
likely that renal dose dopamine administration during
the perioperative period confers no advantage over the
maintenance of euvolemia in most patients with vascular SUGGESTED READINGS
disease during infrarenal abdominal aortic aneurysm American Society of Anesthesiologists and the Society of Cardiovas-
repair. cular Anesthesiologists Task Force on Transesophageal Echocar-
diography: Practice guidelines for perioperative transesophageal
Fibrinolysis occurs with aortic cross-clamping. Vis- echocardiography. An updated report by the American Society of
ceral ischemia (which does not occur with infrarenal Anesthesiologists and the Society of Cardiovascular Anesthesiolo-
aortic clamping) may initiate fibrinolysis. Antifibrinol- gists Task Force on Transesophageal Echocardiography. Anesthesiol-
ytic agents should be strongly considered if supraceliac ogy 112:1084, 2010.
occlusion is anticipated. Aminocaproic acid, tranexamic American Society of Anesthesiologists Task Force on Pulmonary Artery
Catheterization: Practice guidelines for pulmonary artery catheteriza-
acid, and aprotinin all are effective in decreasing fibrino- tion: an updated report by the American Society of Anesthesiologists
lytic activity; however, aprotinin is no longer clinically Task Force on Pulmonary Artery Catheterization. Anesthesiology
available. 99:988, 2003.
34 Open Abdominal Aortic Repair 165
Bellomo R, Chapman M, Finfer S, et al.: Low-dose dopamine in patients College of Cardiology/American Heart Association Task Force on
with early renal dysfunction: a placebo-controlled randomised trial. Practice Guidelines (Writing Committee to Revise the 2002 Guide-
Australian and New Zealand Intensive Care Society (ANZICS) lines on Perioperative Cardiovascular Evaluation for Noncardiac
Clinical Trials Group. Lancet 356:2139, 2000. Surgery) Developed in Collaboration With the American Society of
Bernstein EF, Chan EL: Abdominal aortic aneurysm in high risk patients: Echocardiography, American Society of Nuclear Cardiology, Heart
outcome of selective management based on size and expansion rate. Rhythm Society, Society of Cardiovascular Anesthesiologists, Soci-
Ann Surg 200:255, 1984. ety for Cardiovascular Angiography and Interventions, Society for
Bois S, Couture P, Boudreault D, et al.: Epidural analgesia and intrave- Vascular Medicine and Biology, and Society for Vascular Surgery.
nous patient-controlled analgesia result in similar rates of postoperative J Am Coll Cardiol 50:1707, 2007.
myocardial ischemia after aortic surgery. Anesth Analg 85:1233, 1997. Frank SM, Fleisher LA, Breslow MJ, et al.: Perioperative maintenance
Devereaux PJ, Yang H, Guyatt GH, et al.: Rationale, design, and orga- of normothermia reduces the incidence of morbid cardiac events: a
nization of the Perioperative Ischemic Evaluation (POISE) trial: a randomized clinical trial. JAMA 277:1127, 1997.
randomized controlled trial of metoprolol versus placebo in patients Gelman S: The pathophysiology of aortic cross-clamping and unclamp-
undergoing noncardiac surgery. Am Heart J 152:223, 2006. ing. Anesthesiology 82:1026, 1995.
Fleischmann KE, Beckman JA, Buller CE, et al.: 2009 ACCF/AHA fo- Grines CL, Bonow RO, Casey DE Jr, et al.: Prevention of premature
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College of Cardiology Foundation/American Heart Association task artery stents: a science advisory from the American Heart Association,
force on practice guidelines. Circulation 120:2123, 2009. American College of Cardiology, Society for Cardiovascular Angiog-
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CASE 35
Endovascular Thoracic
Aortic Repair
Ronald A. Kahn, MD
QUESTIONS
1. What is the difference between conventional de- 6. What are the recognized potential complications
scending aortic reconstruction and endovascular of proximal graft deployment?
aortic repair? 7. What are the advantages of transesophageal
2. List the anatomic requirements and restrictions for echocardiography monitoring during aortic
endovascular aortic repair. thoracic endovascular repair?
3. What are the recognized surgical complications of 8. Explain the relationship between spinal cord is-
endovascular aortic aneurysm repair? chemia and endovascular thoracic aortic repair.
4. Discuss patient outcomes after thoracic endovas- 9. What is postimplantation syndrome?
cular aortic repairs compared with open repairs.
5. Which anesthetic technique is best for endovascular
aortic repair?
An 83-year-old man with a past medical history signifi- their established track record and low complication rate.
cant for coronary artery disease, congestive heart failure, Patients with severe medical comorbidities may be better
chronic obstructive pulmonary disease, hypertension, candidates for endovascular reconstruction.
and previous abdominal aortic aneurysm repair presented
with a 7-cm descending thoracic aortic aneurysm. The 2. List the anatomic requirements and restrictions
descending aortic aneurysm began 5 cm distal to the left
for endovascular aortic repair.
subclavian artery and extended for 30 cm. Because of the
patient’s concurrent medical conditions, an endovascular Not all patients with aortic pathology have suitable anat-
repair was planned. Several self-expanding endograft omy for endovascular repair. For EAR to be successful,
devices were used. the device must form a tight seal between graft and native
Anesthesia and surgery progressed without incident. artery. The proximal neck (i.e., proximal “landing zone”)
In the postanesthesia care unit, the patient became must be at least 15 mm in length, and the aneurysm neck
febrile and mildly hypotensive and developed oozing at diameter should be no larger than the largest endograft
the surgical sites. available. Similarly, the distal attachment site must be
nonaneurysmal and of sufficient length to accommodate
1. What is the difference between conventional a graft. No important aortic side branches, such as an ac-
descending aortic reconstruction and cessory renal artery or inferior mesenteric artery, can be
present in the aortic segment that is to be excluded. As
endovascular aortic repair?
a practical matter, excessive aneurysm neck tortuosity,
Endovascular aortic repair (EAR) is an alternative to con- severe calcification, aneurysmal necks !26 mm in diam-
ventional surgical repair of aortic pathology. Endovascular eter, and aneurysmal necks "10–15 mm in length may be
grafts are less invasive than conventional arterial recon- relative contraindications for EAR. Finally, there must
structions. Endovascular grafts are inserted through small be at least one large, straight iliac artery that can accom-
openings from remote arterial access sites and do not modate passage (i.e., act as a conduit) of the endograft
require large abdominal incisions. This technique obviates delivery system.
the need for extensive and prolonged aortic occlusion,
decreases blood loss, and avoids significant fluid shifts that 3. What are the recognized surgical complications of
occur with visceral manipulation, reducing the risk of
endovascular aortic aneurysm repair?
significant hemodynamic changes perioperatively.
Because long-term outcome studies of EAR are lacking, Although EAR is a less invasive technique compared with
younger patients with minimal or no medical comorbidi- open repair, it is nonetheless associated with significant
ties are frequently treated with open repairs because of perioperative complications. Iliac or aortic anatomy and
166
35 Endovascular Thoracic Aortic Repair 167
pathology may preclude insertion of endovascular sheaths (which was used in patients who underwent combined
(delivery systems). The possibility always exists of iatro- ascending aortic and arch surgery with endovascular
genic arterial rupture, which may necessitate emergent thoracic aortic aneurysm repair), large aneurysms or
resuscitation and immediate conversion to an open pro- large aneurysm neck diameters, and older patient age.
cedure, increasing the morbidity and mortality associated The major complications of the procedure were early
with the repair. death (9%), neurologic conditions (10%), and pulmo-
Injury to the aorta and end-organs may occur with nary conditions (12%). The 9% mortality was not
guidewire insertion and device manipulation via either much different from the reported 11% mortality asso-
embolization or obstruction. Distal embolization of aortic ciated with open repair. However, 16% of the patients
material to the bowel, lower extremities, or other organs is underwent emergency operations, and 60% of these
common. Although the endovascular device may obstruct patients were not candidates for open repair. Placed in
hypogastric artery flow, complications have not been re- context, the mortality rate is not unreasonable.
ported. Retrograde thromboembolism as a result of graft Dake et al. (1994) attributed this high incidence of
manipulation, injection of large volumes of contrast mate- stroke to catheter or sheath manipulations in the aortic
rial, vigorous flushing, or the passage of guidewires arch and ascending aorta, excessive anticoagulation, or
through a diseased aortic arch may result in cerebral possibly surgical manipulation of the carotid or subcla-
injury. Inadvertent guidewire placement into the heart vian arteries. In more recent studies, meta-analyses
has occurred with injury to the aortic valve or pericardial provide evidence that EAR is associated with a lower
tamponade with resultant hemodynamic collapse. incidence of early death, paraplegia, renal insufficiency,
Segmental or total renal injury may occur as a compli- transfusions, reoperation for bleeding, cardiac compli-
cation of EAR. Graft migration, renal artery dissection, cations, pneumonia, and length of stay compared with
and improper placement of the proximal portion of the open surgery. Both endovascular repair and open repair
endovascular device can occlude the renal arteries. Renal after ruptured thoracic aortic aneurysms were associ-
artery occlusion may lead to renal insufficiency and the ated with no differences in mortality or complications;
possibility of further procedures to correct the problem. however, uncomplicated discharge was more common
A significant amount of contrast material is used during after endovascular repair.
these procedures to define aortic anatomy, providing Long-term outcome has been better defined after
another possible mechanism for renal injury (Box 35-1). endovascular repair of infrarenal aortic aneurysms.
There is an initial earlier survival benefit after endovas-
4. Discuss patient outcomes after thoracic cular repair. With time, however, there is continued
endovascular aortic repairs compared with progression of the underlying aneurysmal disease with
need for continued surveillance and interventions after
open repairs.
EAR. Patients undergoing open repair have significantly
EAR may be a viable option for surgical treatment of greater rates of freedom from secondary interventions
thoracic aortic pathology. Dake et al. (1994) reported compared with patients undergoing EAR. After 2 years,
6-month, 1-year, and 2-year survival rates of 86%, there are no significant survival differences between
81%, and 73%, respectively, after endovascular tho- groups; these comparable survival rates continue for at
racic aortic aneurysm repair. Predictors of death least 6 years postoperatively.
included the following: patients who were not open
surgical candidates, the use of cardiopulmonary bypass 5. Which anesthetic technique is best
for endovascular aortic repair?
Different anesthetic techniques have been described for
BOX 35-1 Recognized Surgical Complications aortic stent graft placement including local anesthesia,
of Endovascular Aortic Repair regional anesthesia, and general anesthesia. Because early
procedures often required long surgical times, general
• Insertion of endovascular delivery system precluded anesthesia was usually administered to enhance patient
• Iliac artery anatomy or pathology
• Aortic anatomy or pathology
compliance. With increasing operator experience and
• Artery rupture with hypotension sophisticated devices, regional anesthetics (including epi-
• Embolization of aortic material dural, spinal, and continuous spinal anesthetics) and local
• Bowel anesthetics supplemented by sedation are more common.
• Lower extremities Choice of anesthetic technique depends on the planned
• Brain surgical interventions and the patient’s comorbid condi-
• Other organs tions. Operations that require percutaneous catheter
• Guidewire trauma placement with limited incisions are well tolerated under
• Aortic valve local anesthesia and sedation. Either regional or general
• Myocardial perforation with cardiac tamponade anesthesia is appropriate for extensive inguinal explora-
• Graft malposition
• Renal artery occlusion leading to renal impairment
tion and dissection or construction of a femoral artery-
• Occlusion of intercostal or anterior spinal cord artery to-femoral artery conduit. Surgical dissection into the
leading to paralysis retroperitoneum requires a higher level of regional anes-
• Postimplantation syndrome thesia or general anesthesia. Many of these procedures
take a long time to perform. Patients undergoing local
168 SECTION 6 Abdomen
anesthesia or regional anesthesia require intravenous are now obtainable. These images have previously been
sedation to treat agitation secondary to restlessness and unavailable by conventional transthoracic ultrasonogra-
discomfort from lying in one position for a prolonged phy. With the esophagus in close approximation to the
period. aorta, TEE has become an excellent tool for diagnosing
In a retrospective analysis of 91 patients undergoing pathology of the distal aortic arch, the descending tho-
EAR, local anesthesia was associated with reduced use racic aorta, and the proximal abdominal aorta. TEE can
of vasoactive agents, more favorable fluid balance, fewer provide instantaneous views of guidewires and endografts
intensive care unit admissions, and shorter hospital before deployment, in relation to normal and diseased
stays compared with regional or general anesthesia. In a thoracic aorta. Long-axis views are used to aid placement
prospective study of 239 patients undergoing EAR, no of the angiography catheter and delivery device. Higher
differences in all-cause mortality were observed among frequencies and transverse imaging plane views can help
different anesthetic techniques. However, local anesthe- identify the catheter tip and delivery system within the
sia was associated with a lower incidence of respiratory aorta.
complications compared with general anesthesia (0% ver- TEE has distinct advantages over perioperative angiog-
sus 5%; P " .01) and a lower incidence of renal failure raphy. TEE may provide exact vessel and lesion sizing and
compared with general or regional anesthesia (0% versus localization, which is difficult to obtain during single-
2% versus 1%; P " .02). Finally, in a larger multicenter plane angiography. Both endograft leakage (using Doppler
retrospective study of 5557 patients undergoing EAR, color flow imaging) and iatrogenic dissections may easily
the incidence of cardiac complications was significantly be diagnosed with TEE, in contrast to angiography. TEE
lower in both the local and the regional anesthesia can also be used to estimate endograft sizing and evaluate
groups compared with the general anesthesia group the endograft location. Large intercostal arteries have
(1.0% vs. 2.9% vs. 3.7%). Similarly, the incidence of been imaged, avoiding inadvertent obstruction by the
sepsis was significantly lower in the regional anesthesia aortic stent graft; however, consistent visualization of
group compared with the general anesthesia group intercostal arteries is not possible in all patients. After stent
(0.2% vs. 1.0%). Significant selection bias in these ret- graft placement, exclusion of flow from the aorta into the
rospective studies makes it difficult to extrapolate the aneurysm can be easily confirmed using color Doppler
results to clinical practice. flow imaging in most patients. Finally, because most of
these patients have severe concomitant cardiac disease,
6. What are the recognized potential complications perioperative TEE allows dynamic assessment of cardiac
function.
of proximal graft deployment?
Distal migration of the device occurring during proximal 8. Explain the relationship between spinal cord
endograft deployment may result in inadequate exclusion
ischemia and endovascular thoracic aortic repair.
of the aneurysmal sac with resultant endoleak. Older
styles of endovascular stent grafts employed large balloon The reported incidence of postoperative neurologic
angioplasty catheters to expand and secure the proximal injuries after endovascular thoracic aortic reconstruc-
stent attachment system to the underlying normal vessel tion is similar to open thoracic aortic repair. With
wall. These balloons have a large cross-sectional area, descending aortic reconstruction, intercostal arteries
predisposing to distal aortic migration as aortic blood that supply the anterior spinal cord may be sacrificed,
flow forces it forward. Device malposition secondary to resulting in spinal cord injury. Probable risk factors for
migration may result in either occlusion of major arterial paraplegia include the length of the thoracic endograft
branches or incomplete aneurysm exclusion. Induced and a history of previous abdominal aortic aneurysm
hypotension during device deployment has been success- repair. Evidence for the usefulness of cerebrospinal fluid
fully used to assist in proximal endovascular stent graft (CSF) drainage is extrapolated from the open thoracic
placement and may reduce the magnitude of migration. aortic repair literature. During thoracic aortic surgery,
Hypotension is induced using short-acting vasodilators when CSF pressure exceeds spinal venous pressure, a
or ventricular quiescence. Ventricular quiescence can be “critical closing pressure” is achieved, and the veins
achieved with adenosine or induced ventricular fibrilla- collapse independent of inflow pressure. Perioperative
tion. High-dose adenosine can produce sinoatrial and control of CSF pressure may reduce the incidence
atrioventricular node inhibition. Nevertheless, signifi- of spinal cord injury. Coselli et al. (2002) randomly as-
cant endovascular stent graft movement can occur as signed 145 patients undergoing thoracic abdominal
continued aortic blood flow forces it forward. Most aortic aneurysm repair with or without CSF drainage.
likely, no interventions are necessary for self-expanding Nine patients (13.0%) in the control group developed
devices. paraplegia or paraparesis compared with two patients
(2.6%) in the CSF drainage group. These data are sup-
7. What are the advantages of transesophageal ported by meta-analysis and retrospective analysis.
echocardiography monitoring during aortic Anecdotal evidence also exists for the reversal of spinal
cord symptoms by CSF drainage after endovascular
endovascular repair?
thoracic aortic repair. The use of prophylactic lumbar
With the rapid evolution of ultrasound technology and CSF drainage catheters and induced hypertension may
the advent of transesophageal echocardiography (TEE), be warranted in high-risk patients undergoing endo-
perioperative dynamic views of the cardiovascular system vascular thoracic aortic repair.
35 Endovascular Thoracic Aortic Repair 169
Transurethral Resection
of the Prostate
Laurence M. Hausman, MD • Daniel M. Gainsburg, MD, MS
QUESTIONS
1. What is TURP syndrome, and what is the 6. If a regional anesthetic is selected, what level of
treatment? anesthesia is required?
2. What other complications can occur during TURP? 7. The patient’s serum sodium level is 102 mEq/L
3. What types of irrigating fluids have been used for 1 hour and 15 minutes into the procedure; how
transurethral resection of the prostate? would you correct the sodium level to 135 mEq/L?
4. What toxicities are associated with glycine? 8. What surgical measures can minimize the
5. What are the anesthetic options for a patient incidence of TURP syndrome?
undergoing transurethral resection of the 9. What other minimally invasive surgical modalities
prostate? are available to treat benign prostatic hypertrophy?
A 74-year-old man with a past medical history of coro- Effects of TURP syndrome on the central nervous
nary artery disease with stable angina and hypertension system include headache, restlessness, agitation, confu-
was scheduled to undergo transurethral resection of sion, seizures, and eventually coma (Box 36-1). These
the prostate (TURP) for benign prostatic hypertrophy. findings are thought to be caused by cerebral edema, with
Current medications included metoprolol, 50 mg twice a a concomitant increase in intracerebral pressure. As the
day, and amlodipine, 10 mg once a day. The physical ex- neurologic condition worsens, the patient may develop
amination was unremarkable. Heart rate was 74 beats per decerebrate posturing, clonus, a positive Babinski sign,
minute, blood pressure was 160/75 mm Hg, and respira- brainstem herniation, and ultimately death. Ocular ex-
tory rate was 12 breaths per minute. The patient was amination often reveals bilateral dilated and sluggishly
177.5 cm tall and weighed 72 kg. reactive pupils and papilledema. Electroencephalography
often shows low-voltage activity. If coma occurs, it usu-
ally resolves within hours to days, but it can be perma-
1. What is TURP syndrome, and what is the treatment?
nent. The incidence of neurologic injury is more closely
TURP syndrome is a collection of signs and symptoms related to the rate of Na! decrease rather than the degree
that occur when excessive amounts of irrigating fluids are of hyponatremia.
absorbed through the opened prostatic venous sinusoids. Hyponatremia and fluid overload have deleterious con-
Absorption of fluids may result in water intoxication, sequences on the heart. The initial cardiovascular effects
hyponatremia, and hypoosmolality. Although most com- of fluid overload include hypertension and bradycardia.
monly associated with TURP, this syndrome may also However, serum Na! levels of 120 mEq/L are associated
occur with transurethral resection of bladder tumors, diag- with negative inotropic effects on the heart causing hypo-
nostic cystoscopy, percutaneous nephrolithotomy, and en- tension, pulmonary edema, and congestive heart failure.
doscopic gynecologic procedures. The incidence of TURP Serum Na! levels of less than 115 mEq/L are associated
syndrome is 0.78%–1.4%. The mortality rate in severe with electrocardiogram (ECG) changes, such as a widened
cases is 25%. The syndrome may be observed minutes QRS complex, ventricular ectopy, and T-wave inversion.
after resection starts up to 24 hours postoperatively. When serum Na! decreases to "100 mEq/L, respiratory
The decrease in serum sodium (Na!) levels during and cardiac arrest may occur (Box 36-2).
TURP ranges from 3.65–10 mEq/L. Several mechanisms If the patient develops signs and symptoms of TURP
for this decrease in Na! have been postulated. Hyponatre- syndrome, surgery should be concluded as soon as possi-
mia may be due to either simple dilution by the irrigating ble. Treatment should be directed at increasing the serum
solution or diffusion of Na! into the irrigating solution at Na! level and correcting volume overload by fluid restric-
the surgical site or into the periprostatic or retroperitoneal tion and administration of a loop diuretic, such as furose-
spaces. The degree of hyponatremia is related to the rate mide. In severe cases of hyponatremia, administration of
of absorption of the irrigating fluid and not to the absolute a hypertonic saline solution (3%–5% sodium chloride)
amount absorbed. may be necessary. Rapid correction of hyponatremia has
170
36 Transurethral Resection of the Prostate 171
BOX 36-1 Central Nervous System Effects of BOX 36-3 Complications of Transurethral
TURP Syndrome Resection of the Prostate
• Headache • Decerebrate posturing • Bladder perforation
• Restlessness • Clonus • Extraperitoneal or intraperitoneal
• Agitation • Babinski sign • Bleeding
• Confusion • Sluggishly reacting pupils • Related to size of gland and resection time
• Seizures • Papilledema • Coagulopathy
• Coma • Dilution of coagulation factors
• Primary fibrinolysis
• Disseminated intravascular coagulopathy
• Transient bacteremia and septicemia
BOX 36-2 Cardiovascular Effects of TURP • Toxicity of irrigating fluids
Syndrome • Hypervolemia
• Hyponatremia
• Na! "120 mEq/L • Na! "100 mEq/L • Hypothermia
• Hypotension • Respiratory arrest • Glycine toxicities
• Pulmonary edema • Cardiac arrest • Transient blindness
• Congestive heart failure • Hyperammonemia
• Na! "115 mEq/L • Nausea and vomiting
• Widened QRS complex • Coma
• Ventricular ectopy • Myocardial depression
• T-wave inversion • Electrocardiogram changes
been associated with cerebral edema and central pontine should be confirmed quickly by cystourethrography, and
myelinolysis. All other treatment is dictated by the pa- treatment should be with a suprapubic cystostomy.
tient’s symptoms. Supplemental oxygen should be consid-
ered, and the patient may require tracheal intubation and Bleeding
mechanical ventilation.
The prostate is a highly vascular organ. Because large
2. What other complications can occur during amounts of irrigation fluid are used, blood loss is difficult
to assess. Intraoperative blood loss corresponds to the size
transurethral resection of the prostate?
of the gland and resection time. Blood loss is generally
Approximately 7% of all patients undergoing TURP ex- considered to occur at a rate of 2–5 mL per minute of
perience a major complication. The 30-day mortality resection time and 20–50 mL/g of prostate tissue. Blood
rate has been estimated to be 0.2%–0.8%. This is a loss is linearly related to prostate size up to 35 g, at which
marked improvement over studies performed in the point blood loss tends to exceed the linear correlation.
1960s, which showed a mortality rate of approximately Patients with resection times of greater than 90 minutes
2.5%. Patients undergoing TURP are often elderly and or a prostate size of #60 g have been found to have a
have coexisting cardiopulmonary disorders making them significant increase in morbidity associated with bleeding.
more likely to experience complications. Because many
patients are on long-term diuretic therapy, they are often
Coagulopathy
dehydrated and present with electrolyte abnormalities
preoperatively. Other complications associated with this Subclinical coagulopathy occurs in approximately 6% of
procedure are described next (Box 36-3). patients undergoing TURP, whereas clinical coagulopathy
occurs approximately 1% of the time. This condition
Bladder Perforation seems to correlate with the mass of resected prostatic tis-
sue. It is a more likely event if the resected tissue is #35 g.
Bladder perforation occurs in approximately 1% of all Coagulopathy may be due to dilution of coagulation
TURP procedures. It may be caused by overdistention of factors and platelets.
the bladder with irrigating fluid or surgical instrumenta- Primary fibrinolysis has also been implicated as a cause of
tion. An early sign of bladder perforation is decreased coagulopathy. Plasminogen activator, which is responsible
return of irrigating fluid. The abdomen becomes dis- for converting plasminogen into plasmin, is released dur-
tended and often rigid. If the procedure is performed ing these procedures. The treatment of choice for primary
under regional anesthesia, patients may complain of fibrinolysis is aminocaproic acid.
pain or experience nausea and vomiting. Hypotension Secondary fibrinolysis may occur as a result of dis-
followed by hypertension is common. seminated intravascular coagulopathy (DIC). DIC is
Most perforations are extraperitoneal and benign in caused by systemic absorption of prostate tissue, which is
nature. This type of perforation causes pain in the perium- rich in thromboplastin. Consistent with this theory are
bilical region. However, pain in the upper abdomen or re- the low levels of plasminogen activator, platelets, and
ferred pain to the shoulder may be a sign of intraperitoneal fibrinogen that are commonly found in DIC and that
perforation, a potentially fatal complication. Diagnosis frequently accompany TURP. If DIC is suspected, the
172 SECTION 6 Abdomen
treatment is symptomatic. Fluid and blood products but absorption of distilled water caused hyponatremia and
are administered as needed. Heparin administration may hemolysis of red blood cells. This severe complication led
be beneficial. to the use of isoosmotic solutions such as saline or lactated
Ringers solution. However, because these solutions are
highly ionized, they caused dispersion of high-frequency
Transient Bacteremia and Septicemia
current from resectoscopes. The present generation of
The prostate, rich in pathogens, may cause postoperative irrigating fluids is electrically inert and isotonic. These
bacteremia via prostatic venous sinusoids. Indwelling uri- solutions include glycine and a mixture of sorbitol and
nary catheters enhance the risk. Approximately 6%–7% mannitol (Cytal), which are the most commonly used, as
of patients go on to develop sepsis. Treatment consists of well as glucose, mannitol, urea, and sorbitol.
antibiotics and supportive care.
4. What toxicities are associated with glycine?
Toxicity of Irrigating Fluids
Intravascular absorption of 1.5% glycine solution has been
The major toxicity of irrigation fluids used today is related implicated as a cause for many neurologic manifestations
to massive absorption causing fluid overload, hyponatre- associated with TURP, including transient blindness.
mia, and hypoosmolality. The incidence of hypoosmolality Glycine, a nonessential amino acid, readily crosses
and its associated neurologic sequelae has decreased since the blood-brain barrier. It has a distribution similar to
the use of nonelectrolyte isoosmotic irrigating solutions. $-aminobutyric acid, a naturally occurring inhibitory
However, fluid overload and hyponatremia still remain a neurotransmitter. Transient blindness may result from
problem. During TURP, 8 L of irrigating fluid may be inhibitory effects of glycine on the central nervous system
absorbed causing an average weight gain of about 2 kg. or a direct inhibitory effect on the retina. Glycine retinal
Some of this fluid (20%–30%) is absorbed directly into toxicity appears to be unrelated to its plasma concentration.
the vascular space. The remainder is absorbed into the Glycine is metabolized to ammonia, which may lead
periprostatic and the peritoneal space (interstitial space). to hyperammonemia in some patients. The mechanism
Several factors contribute to the rate of absorption of by which hyperammonemia develops is unclear. One
irrigating fluid, including prostate size, integrity of the postulated mechanism is that ammonia is converted to
prostatic capsule, and height of the irrigating fluid con- urea in the liver via the ornithine cycle, in a reaction re-
tainer. Greater amounts of irrigating fluid are absorbed quiring arginine. This mechanism of action is supported
when the prostate is large because of its richer blood by the fact that patients with arginine deficiency are more
supply and when the prostate capsule is violated. likely to develop hyperammonemia. Common signs and
Certain maneuvers can limit the amount of irrigating symptoms of ammonia toxicity include nausea and vom-
fluid absorbed. The first is to restrict the height of the iting. As the ammonia level increases to #500 mmol/L,
fluid container above the surgical field; this decreases coma may occur. Coma typically resolves when the am-
hydrostatic pressure driving fluid into sinuses. When the monia level decreases to "150 mmol/L. The cardiovas-
bag is #60 cm above the patient, absorption is greatly cular effects of glycine are myocardial depression and
enhanced. The second maneuver is to limit resection nonspecific ECG changes, such as T-wave depression.
times to "150 minutes because 10–30 mL of irrigation
fluid is absorbed per minute of resection. 5. What are the anesthetic options for a patient
Sorbitol and mannitol, both sugar alcohols, have been undergoing transurethral resection of the
associated with the development of lactic acidosis and hy-
prostate?
perglycemia. Specific effects of glycine are discussed later.
Regional anesthesia (Box 36-4) has long been considered
the anesthetic of choice for TURP. Regional anesthesia
Hypothermia
allows for monitoring of mental status changes, irritability,
Patients may develop hypothermia under either general and headache, the early signs of hyponatremia. If signs of
or neuraxial anesthesia. The hypothermia can be exacer- hyponatremia occur, serum Na! levels are checked and
bated by using room temperature irrigating fluids. Using treated expeditiously. Intraoperative irritability or combat-
warmed irrigating fluid decreases heat loss and shivering. iveness could result from hyponatremia. If caused by hy-
A theoretical concern exists that warming the irrigation ponatremia or hypoxia, deepening the sedation level could
fluids would cause vasodilation, increasing blood loss; be counterproductive.
however, this has not been shown to be a clinical prob-
lem. Because hypothermia may cause shivering, which
increases venous pressure, there may be increased blood
loss if the irrigating fluids are not warmed.
BOX 36-4 Benefits of Regional Anesthesia
3. What types of irrigating fluids have been used for • Early detection of TURP syndrome
transurethral resection of the prostate? • Detection of bladder perforation
• Decreased blood loss
The ideal irrigating fluid would be isotonic, electrically • Decreased incidence of deep vein thrombosis
inert, nontoxic, and transparent; however, this type of • Postoperative pain control
solution does not exist. Originally, distilled water was used,
36 Transurethral Resection of the Prostate 173
As discussed earlier, another potentially fatal compli- 7. The patient’s serum sodium level is 102 mEq/L
cation of TURP is bladder perforation. A T10 level of 1 hour and 15 minutes into the procedure;
sensory blockade would allow the patient to complain how would you correct the sodium level to
of abdominal or shoulder pain, which are symptoms of
135 mEq/L?
bladder perforation.
As with other pelvic procedures, regional anesthesia The Na! deficit must first be calculated using the following
has been shown to decrease blood loss and the incidence equation:
of deep vein thrombosis. The decrease in blood loss is
most likely secondary to the decrease in blood pressure Na!deficit mEq % TBW & (Na!desired ' Na!observed)
and in both central and peripheral venous pressure
associated with neuraxial anesthesia. Many different rea- TBW is total body water and constitutes 60% of lean body
sons have been postulated for the decreased incidence of weight in the average man and 50% of lean body weight in
deep vein thrombosis. One reason may be the increase in the average woman. In this example, the patient’s Na!
peripheral blood flow resulting from sympathetic block- deficit is:
ade. Other reasons include increased prothrombin time,
a measure of the extrinsic pathway of coagulation, and a 1425.6 mEq % (72 kg & 0.6) & (135 ' 102)
decrease in platelet count.
Another clear advantage of regional anesthesia is post- Hypertonic saline (3% sodium chloride) contains
operative pain control. Good postoperative pain control 513 mEq/L of Na!. The volume of hypertonic saline
also protects against sympathetic responses to pain, such required to replace a Na! deficit of 1425.6 mEq is 2.78 L.
as tachycardia and hypertension, which could increase the The maximum safe rate of increase in serum Na! is
likelihood of myocardial ischemia in susceptible patients. 0.5 mEq/L per hour. In this case, the serum Na! should
Comorbid conditions may necessitate general anesthe- be corrected over 66 hours. Thus, the hypertonic saline
sia. General anesthesia hides the early neurologic signs and should run at a rate of 1425.6/66 % 21.6 mL per hour.
symptoms associated with hyponatremia, hypoosmolality, In situations of significant hyponatremia associated with
or bladder perforation. When a general anesthetic is cho- seizures or progressive neurologic deterioration, it
sen, a smooth emergence is desirable. If the patient awak- may be necessary to correct the Na! deficit more rapidly
ens coughing and “bucking” on the endotracheal tube, (3 mEq/L per hour). This rapid correction should not
venous pressure increases, and bleeding may develop. exceed 2 hours and should be stopped if neurologic
symptoms resolve sooner.
6. If a regional anesthetic is selected, what level of
anesthesia is required? 8. What surgical measures can minimize the
incidence of TURP syndrome?
The level of anesthesia required depends on the anatomy
and sensory innervation of involved structures (Box 36-5). Several measures have been undertaken in an attempt to
The structures that need to be blocked are the bladder, minimize TURP syndrome. The primary goal is to re-
prostate, penis, and urethra. The dome of the bladder duce the volume of irrigating fluid that is absorbed during
receives its sensory innervation via T11-L2, whereas the resection; this may be achieved by one or a combination
neck of the bladder receives its sensory innervation via of methods:
S2-S4. The prostate receives its sensory innervation via • Decreasing hydrostatic pressure within the bladder and
T11-L2 and S2-S4. Finally, a sensory block of the penis prostatic venous pressure: Using reduced pressure
and scrotum requires blocking S2-S4. irrigation and lowering the fluid bag’s height (al-
Based on this anatomy, a block to the level of T10 is though there is some controversy concerning
usually sufficient for TURP. If a lower level is attained, whether the height of the bag is significant) decrease
bladder stretching from irrigation fluids would be un- hydrostatic pressure. Patient positioning on the
comfortable. Because a block at the level of S4 is also operating table also has an effect on irrigation ab-
required, spinal anesthesia is preferred over epidural sorption. Intravesical pressure needed to initiate
anesthesia. Epidural anesthesia sometimes results in absorption of irrigating fluid is lower in the Tren-
incomplete block of the sacral nerve roots. delenburg position compared with the horizontal
position. Trendelenburg position increases the risk
of TURP syndrome.
• Limiting operative time to "90 minutes: Operating
BOX 36-5 Sensory Innervation times longer than 90 minutes have been shown to
increase the incidence of TURP syndrome and in-
• T11-L2 traoperative bleeding.
• Bladder dome • Restricting TURP to prostate glands "45 g: Larger
• Prostate glands require longer resection times resulting
• S2-S4
• Bladder neck
in increased irrigant absorption and increased
• Prostate blood loss.
• Penis • Injecting intraprostatic vasopressin: Blood loss and amount
• Scrotum of irrigant fluid absorbed are reduced with vasopressin
injection.
174 SECTION 6 Abdomen
QUESTIONS
A 32-year-old man, weighing 396 lb (180 kg) and As noted earlier, in children, because of ongoing
standing 5 feet 7 inches (170 cm) tall, presented for growth and differences in distribution of fat and muscle
laparoscopic sleeve gastrectomy. He had a past medical that is age dependent and gender dependent, the calcu-
history of hypertension, diabetes mellitus, asthma, lated BMI is measured against other children of the
and gastroesophageal reflux disease. He used bilevel same age and gender (Figure 37-1). The calculated BMI
positive airway pressure (BiPAP) for obstructive sleep is plotted on growth charts from the U.S. Centers for
apnea (OSA) at night. Disease Control and Prevention that are based on age
and gender. A BMI percentile for age is determined.
The percentile determines the classification of obesity
1. How is body mass index defined?
(Table 37-3).
According to the World Health Organization, obesity is BMI calculations without taking into consideration
defined as abnormal or excessive fat accumulation that pres- body habitus may be misleading in certain patient popu-
ents a risk to health. Differences in weight among individuals lations. For example, in a muscular person, BMI may
are due only partly to variations in body fat. Total body suggest obesity but in fact reflects additional muscle
weight, although easy to obtain, is a limited measure of obe- mass. Also, in a person with degenerative loss of skeletal
sity. In 1832, Quetelet, a Belgian mathematician, defined the muscle mass, BMI may not account for the relative in-
relationship between weight and height and created the creased percentage in fat. Calculation of body fat per-
Quetelet index, which eventually became known as the body centage may help differentiate between obesity from
mass index (BMI), so named by Keys in 1972. excess body fat and increased muscle mass. Body fat
BMI is an index of weight-for-height that is com- percentage is calculated as follows:
monly used to classify obesity. It is defined as weight
in kilograms divided by the square of height in meters 1.2 (BMI) # 0.23 (age) $ 10.8 (sex) $ 5.4
(kg/m2). Although also applicable to children, age is an
additional factor. BMI values of !40 are commonly con- Sex is assigned a value of 1 for males and 0 for females.
sidered an indication for bariatric surgery. Patients with Men who have a body fat percentage "25% are classified
a BMI "35 and significant comorbidities (e.g., diabetes) as obese (Table 37-4). Our patient’s body fat percentage
are also candidates for bariatric surgery. Another indica- is 75.16%.
tion for bariatric surgery is a desire to become pregnant
in a nulliparous, obese woman. 2. What cardiopulmonary changes occur with
Although several classifications of obesity exist, the superobesity?
most widely accepted is from the World Health Organi-
zation and is based on BMI (Table 37-1). More recently, Superobesity affects multiple organ systems. Effects
with the increase of bariatric procedures, a slightly differ- on the respiratory system involve the upper and lower
ent classification has been introduced to the surgical airways and lung mechanics. Patients are prone to upper
literature (Table 37-2). The BMI of our patient is 62 airway obstruction, particularly during sleep. OSA, de-
(180 kg/1.7 m2), and he is classified as super-superobese. fined by the number of apnea and hypopnea events per
175
176 SECTION 6 Abdomen
TABLE 37-1 World Health Organization TABLE 37-2 Classification of Obesity Based
Classification of Obesity by on BMI in the Surgical Literature
Body Mass Index (BMI)
BMI (kg/m2) Classification
BMI (kg/m2) Classification 40–%50 Morbid obesity
%18.5 Underweight 50–%60 Superobesity
18.5–24.9 Normal !60 Super-superobesity
25–29.9 Overweight
30–34.9 Class I obesity
35–39.9 Class II obesity are decreased secondary to fat accumulation over the
!40 Class III obesity thorax and abdomen. The decrease in lung compliance
is also due to increased pulmonary blood flow secondary
to increased cardiac output and polycythemia seen in
hour of sleep, occurs in approximately 3%–7% of all men chronically hypoxemic patients.
and 2%–5% of all women (see Question 4 for details). A decrease in lung compliance leads to a decrease in
However, the prevalence of OSA is "50% higher in functional residual capacity (FRC), at the expense of expira-
obese individuals. Both chest wall and lung compliance tory reserve volume, vital capacity, and total lung capacity.
FIGURE 37-1 ■ An example of BMI-for-age for a 10-year-old boy and a 15-year-old boy who both have a BMI of 23. (From the Division
of Nutrition, Physical Activity, and Obesity, Centers for Disease Control and Prevention, Atlanta, GA.)
37 Super Morbid Obesity 177
TABLE 37-3 Classification of Obesity in the TABLE 37-5 Comorbidities Associated with
Pediatric Population by Body Mass Superobesity
Index Percentile
Cardiovascular Coronary artery disease
Percentile Classification Hypertension
Pulmonary hypertension
%5 Underweight Congestive heart failure
!5 Normal weight
!85 Overweight Respiratory Restrictive lung disease
!95 Obese Aspiration? Pneumonia? Asthma?
"99 Morbid obesity Obstructive sleep apnea
Obesity hypoventilation syndrome
Central nervous Cerebrovascular accidents
system Idiopathic intracranial hypertension
TABLE 37-4 Comparison of Status with Body Gastrointestinal Hiatal hernia
Fat Percentage Gastroesophageal reflux disease
Cholelithiasis
Description/Status Women (Fat %) Men (Fat %) Fatty infiltration of the liver
Normal fat 10–13 2–5 Endocrine Type 2 diabetes mellitus
Athletic 14–24 6–17 Polycystic ovarian syndrome
Average 25–31 18–24 Hematologic Deep vein thrombosis
Obese !32 !25 Pulmonary embolus
Musculoskeletal Osteoarthritis
Immunology h incidence of malignancies
Closing capacity is unchanged, but reduced FRC could Breast
result in normal tidal volumes occurring at lung volumes Ovarian
below closing capacity. Small airway closure, absorption Endometrial
atelectasis, ventilation/perfusion mismatch, and hypox- Esophageal
Colorectal
emia result. These changes are exacerbated during gen- Gallbladder
eral anesthesia and in the supine position. Stomach
Total blood volume is increased, but the total blood Pancreas
volume per total body weight measurement is decreased Liver
(i.e., 50 mL/kg). As weight increases, so does cardiac out- Prostate
put, with shunting to adipose tissue. The increase in cardiac
output is the result of left ventricular hypertrophy and in-
creased stroke volume. Ultimately, left ventricular hyper- are superobese have a 6-fold to 12-fold increase in all-cause
trophy, decreased left ventricular compliance, and impaired mortality rates.
filling (i.e., diastolic dysfunction) occur. The endpoint is
systolic dysfunction and left ventricular failure. 4. What is the pathophysiology of obstructive sleep
Right-sided heart changes are secondary to chronic apnea?
hypoxemia, particularly in patients with OSA. Chronic
hypoxemia and increased pulmonary blood volume lead to Although many patients with OSA are morbidly obese,
pulmonary hypertension, right ventricular hypertrophy, nonobese patients have OSA as well. OSA tends to occur
and ultimately right ventricular failure. in middle-aged and older adults (most prevalent at age 55).
Development of atherosclerosis is accelerated. How- Sedatives, hypnotics, alcohol, or muscle relaxants can
ever, it is difficult to detect the presence of coronary exacerbate OSA. Young patients with craniofacial abnor-
artery disease by history alone because obese patients malities can also have OSA.
tend to have sedentary lifestyles. A high index of suspi- Under normal circumstances, a breath is initiated by
cion and diagnostic testing are indicated. Hypertension contraction of the diaphragm and intercostal muscles,
and arrhythmias are frequent complications. increasing chest wall size. Negative pleural pressure is
created and transmitted from lower airways to the phar-
3. What comorbidities are associated ynx. The pharynx consists of mucosa and soft tissues
that lack bony attachments. When negative pressure is
with superobesity?
created in the pharynx, these tissues are drawn into the
Many comorbidities involving multiple organ systems lumen, as if the pharynx were imploding. This inward
occur in patients who are superobese (Table 37-5). The movement is opposed by constriction of the upper airway
death risk is increased. The relative risk for coronary heart dilator muscles, which maintain upper airway patency.
disease is 1.72 in patients with a BMI of 25–28.9 kg/m2 and Upper airway dilator muscles include the tensor palatine,
progressively increases with increasing BMI. Similar which brings the soft palate off the nasopharyngeal wall,
trends have been shown in the relationship between and the genioglossus, which advances the tongue off
obesity and stroke or congestive heart failure. Overall, the the oropharyngeal wall. However, during sleep, if the
estimated increase in cardiovascular mortality rate is four- inward movement of pharyngeal tissue is unopposed, up-
fold and the estimated increase in cancer-related mortality per airway obstruction results. Adequate compensation
rate is 2-fold in obese patients. The incidence of polycystic by airway dilator muscles is lost in obese patients, and
ovarian disease is also increased. As a group, people who upper airway obstruction results causing hypercarbia
178 SECTION 6 Abdomen
and hypoxia. The treatment for OSA consists of positive obesity (BMI "30 kg/m2), daytime hypoventilation
airway pressure, either continuous positive airway pressure (arterial carbon dioxide tension [PaCO2] "45 mm Hg,
(CPAP) or BiPAP, during sleep. arterial oxygen tension [PaO2] %70 mm Hg), and SDB
Hypoxic episodes during sleep lead to sympathetic in the absence of other causes of hypoventilation (e.g.,
discharge and arousal. When this cycle recurs several neuromuscular disease, metabolic abnormalities). The
times per night, restful sleep is interrupted, and patients presence of daytime hypercarbia differentiates OHS
experience daytime somnolence, irritability, impaired from OSA.
cognition, and reduced concentration. Recurring episodes Causes of daytime hypercarbia may include one or
of hypoxia eventually cause pulmonary hypertension, more of the following mechanisms:
right ventricular hypertrophy, and right-sided failure (cor • Abnormal respiratory mechanics secondary to obesity—
pulmonale). Reactive polycythemia commonly develops. more energy is needed to breathe effectively be-
cause obese patients experience restrictive airflow.
Restrictive air flow is due to excessive neck and
5. How is obstructive sleep apnea diagnosed?
airway tissue, decreased chest wall compliance
The first clinical indicator of OSA, loud snoring, is fre- secondary to substantial adipose tissue, impaired
quently reported by a sleeping partner. Definitive diagnosis diaphragmatic movement, and early respiratory
is obtained by sleep studies, which look for the incidence muscle fatigue.
of apnea and hypopnea. Apnea is defined as the total cessa- • Leptin resistance leading to central hypoventilation—
tion of gas flow through the airway for at least 10 seconds leptin is a hormone secreted by adipose tissue that
followed by arousal or 4% decrease in oxygen saturation, binds to leptin receptors in the brain increasing
despite attempts to breathe, or both. In patients with OSA, ventilation. In patients with OHS, leptin levels are
episodes of apnea occur at least five times per hour of sleep. greater than in patients with similar BMI but with-
Hypopnea is defined as a "50% reduction of gas flow out OHS. Over time, leptin resistance develops, and
through the airway for at least 10 seconds or decrease by levels increase without enhancing ventilation.
30% associated with arousal or a 4% decrease in oxygen • Inadequate compensation of acute hypercapnia—
saturation or both. In patients with OSA, hypopnea occurs hypercapnia during airway obstruction while
at least 15 times per hour of sleep. The severity of OSA is asleep is usually compensated by hyperventilation
based on the number of apnea-hypopnea events occurring on arousal and by renal excretion of bicarbonate.
during 1 hour (apnea-hypopnea index [AHI]). OSA is In patients with OHS, these compensatory mecha-
classified as follows: nisms are diminished, resulting in sustained elevation
• AHI 5–14: mild of PaCO2.
• AHI 15–30: moderate Treatment strategies for patients with OHS include
• AHI "30: severe positive airway pressure during sleep (e.g., CPAP or BiPAP),
supplemental oxygen, weight loss surgery, and respiratory
stimulants. Supplemental oxygen must be used judiciously.
6. How is STOP-bang useful in screening patients?
Although supplemental oxygen can improve oxygenation,
The STOP-Bang questionnaire is an 8-item tool it could decrease minute ventilation and exacerbate hyper-
(Table 37-6) used to identify patients with sleep-disordered capnia in the most severe cases. This effect is of particular
breathing (SDB). Each positive answer is assigned 1 point concern in postoperative patients who receive sedation
for a total of 8 points. Low risk for SDB is a score of &2, or opioids or both. Weight loss surgery is described in
and high risk for SDB is a score of !3. STOP-Bang is 87% Question 8.
sensitive for detecting moderate SDB and 70.4% sensitive Medroxyprogesterone is a respiratory stimulant. Stud-
for detecting severe SDB. ies have not shown a consistent benefit when this agent
was administered to patients with OHS. An association
with an increased risk of venous thromboembolism
7. What is obesity hypoventilation syndrome?
(VTE) limits its use in patients with OHS. Acetazol-
Obesity hypoventilation syndrome (OHS), commonly amide promotes renal excretions of bicarbonate inducing
referred to as Pickwickian syndrome, is characterized by a metabolic acidosis that increases ventilation.
A B
C D 100 cm
FIGURE 37-2 ■ Operative procedures for weight loss that are performed laparoscopically. A, Adjustable gastric band. B, Vertical sleeve
gastrectomy. C, Roux-en-Y gastric bypass. D, Duodenal switch operation. (From Miyano G, Garcia VF, Inge TH: Bariatric surgical proce-
dures in adolescence. In: Holcomb GW III, Murphy JP [eds.]: Ashcraft’s Pediatric Surgery, 5th edition. Saunders, Philadelphia, 2010.)
contraindicated, succinylcholine is the classic choice for pause at 40 cm H2O for 30 seconds) should be performed
muscle relaxation. In the event that the “cannot intubate, immediately after intubation and at least every half hour
cannot ventilate” situation is encountered, surgical access thereafter to improve oxygenation.
of the airway may be necessary.
Pneumoperitoneum
Positioning
Pneumoperitoneum significantly decreases static respi-
Positioning the patient may require removal of “ramping” ratory system compliance and increases respiratory
that was placed for intubation. The reverse Trendelen- resistance. These changes may not be associated with
burg position improves ventilation by increasing FRC and an alveolar-arterial oxygen tension difference, which is
pulmonary compliance. The legs are split into the “V” larger in superobese patients. During the pneumoperi-
position, and footpads are used to prevent the patient toneum phase, superobese patients have less efficient
from sliding off the bed. It is important to remember to ventilation (i.e., a 100-mL increase of ventilation reduces
release the footpads before adducting the legs. Shifting PaCO2 on average by 5.3 mm Hg in normal-weight
during surgery may have resulted in patient movement patients and by 3.6 mm Hg in obese patients). PaO2 is
down toward the footpads. Approximating the legs with- affected only by increased body weight.
out release of the footpads may cause untoward pressure
on the knees and hips resulting in injury. All pressure Infection and Venous Thromboembolism
points should be padded, and arms should be protected
from nerve injury. Obese patients, especially patients with diabetes, are prone
to infection and deep vein thrombosis. It is essential that
both appropriate antibiotic and venous thromboembolism
Anesthetic Agents
(VTE) prophylaxis are administered in a timely fashion.
An ideal anesthetic regimen has not been identified.
However, pharmacologic principles are important for Hemodynamic Monitoring
calculating the appropriate doses of medications adminis-
tered. The volume of distribution of lipophilic and polar Morbid obesity by itself is not an indication for invasive
drugs is altered because of increased absolute body water hemodynamic monitoring. As with other patients, coex-
content and lean body and adipose tissue mass. Whether isting diseases dictate the need for such devices. Inability
dosing is based on total body weight or ideal body weight to obtain reliable blood pressures by cuff is an acceptable
depends on the drug’s lipophilic profile (Box 37-1). reason to place an arterial catheter.
Maintenance of anesthesia can be accomplished with
inhalation agents (e.g., isoflurane, sevoflurane, desflu-
rane), total intravenous anesthesia (e.g., propofol), or a
12. How can extubation be performed safely?
combination of both. No one regimen is associated with a Superobese patients are especially vulnerable to complica-
faster emergence. Monitoring of neuromuscular blockade tions in the early postoperative period, particularly adverse
is important to guide dosing of neuromuscular blocking respiratory events. Although it is preferable to extubate the
drugs. trachea at the end of the procedure, it should occur only
when all extubation criteria are met. The most common
reason for failed extubation and the need for reintubation
Ventilatory Parameters
is inadequate antagonism of neuromuscular blockade.
Tidal volumes should be calculated based on ideal body Extubation should be performed with the patient in
weight, and respiratory rates should be increased. Low the sitting position to maximize respiratory mechanics.
levels of positive end expiratory pressure should be added Extubation criteria include the following:
(i.e., 5–10 cm H2O). Alveolar recruitment (i.e., inspiratory • Awake, alert, and following commands
• Tidal volume of 5 mL/kg (ideal body weight)
• Negative inspiratory force "40 cm H2O
BOX 37-1 Intravenous Drug Dosing • Head lift for 5 seconds
The anesthesiologist should be prepared for mask
TOTAL BODY WEIGHT ventilation or reintubation with emergency airway
Midazolam equipment available, as was for induction. At our institu-
Thiopental tion, two attending physicians (if available) are present at
Propofol (maintenance infusion) extubation for patients with a BMI of !60.
Fentanyl
Succinylcholine
Cisatracurium 13. What are postoperative considerations?
IDEAL BODY WEIGHT Ideally, extubated patients should be observed for several
Propofol (induction) minutes in the operating room. Once the patient is declared
Remifentanil stable, teamwork is needed to transfer superobese patients
Vecuronium safely from the operating table to a large bed. A mechanical
Rocuronium lift or Hovermat (HoverTech International, Bethlehem, PA)
may be necessary to move superobese patients safely.
182 SECTION 6 Abdomen
Robotic Prostatectomy
Daniel M. Gainsburg, MD, MS
QUESTIONS
1. What are the advantages of robotic-assisted lapa- during robotic-assisted laparoscopic radical
roscopic radical prostatectomy over traditional prostatectomy?
open radical prostatectomy? 6. What are the preanesthetic concerns in patients
2. Briefly describe the surgical procedure. presenting for robotic-assisted laparoscopic
3. What are the primary anesthetic concerns radical prostatectomy?
for robotic-assisted laparoscopic radical 7. Discuss the anesthetic technique for robotic-
prostatectomy? assisted laparoscopic radical prostatectomy.
4. Describe the cerebrovascular, respiratory, and 8. What are the concerns for positioning, ventilation,
hemodynamic effects of pneumoperitoneum in and fluid management of patients for robotic-
steep Trendelenburg position. assisted laparoscopic radical prostatectomy?
5. What are possible complications of pneumoperi-
toneum and steep Trendelenburg position
A 62-year-old, 77-kg man with prostate cancer presented tucked at the side, and head-to-toe drapes are placed.
for robotic-assisted laparoscopic radical prostatectomy Extensive draping limits the anesthesiologist’s view of the
(RALP). Past medical history included hypertension and patient and inhibits further examination of the patient.
hyperlipidemia. The procedure went smoothly with the All catheters, monitors, and patient protective devices
patient receiving 2500 mL of intravenous fluid and expe- have to be placed and secured before draping. At this
riencing a surgical blood loss of 50 mL. The patient’s point, carbon dioxide (CO2) pneumoperitoneum is initi-
trachea was extubated, and he was transferred to the ated, and the patient is placed in 30-degree to 45-degree
postanesthesia care unit (PACU). Shortly thereafter, he Trendelenburg position. During positioning, care is
was noted to have difficulty breathing and decreasing taken to prevent kinking or dislodging of the endotra-
oxygen saturation. It was decided to perform emergent cheal tube. The surgeon places additional ports in the
reintubation, and on direct laryngoscopy, the patient was abdomen, and the robotic arms are “docked” (attached)
noted to have severe laryngeal edema. to the ports. With the robot positioned over the patient
and its arms attached to the ports, the patient cannot be
1. What are the advantages of robotic-assisted moved. If cardiopulmonary resuscitation is required, the
laparoscopic radical prostatectomy over robot must first be detached and moved away.
The surgeon sits at the robot console. An assistant at the
traditional open radical prostatectomy?
patient’s side guides the robotic arms. Bladder neck, vas
RALP is gradually supplanting open and laparoscopic deferens, seminal vesicles, and prostate are dissected. As the
techniques for the surgical treatment of prostate cancer. prostate is dissected free, nerve-sparing is attempted when
RALP offers the advantages of better visualization and possible. When the prostate is freed up, it is placed else-
increased precision manipulation of delicate nerves and where in the abdominal cavity, and the surgeon completes
vessels. RALP also provides enhanced ability to preserve the vesicourethral anastomosis. Dissection of the pelvic
the integrity of neurovascular bundles and reduced median lymph nodes is performed followed by placement of a peri-
recovery times for urinary continence and sexual function vesical drain. With the robotic phase of surgery completed,
compared with open procedures. Other advantages are the robot is undocked and moved away from the patient.
decreased intraoperative bleeding, reduced transfusion The prostate is placed in a plastic specimen bag and
rates, less postoperative pain, shorter PACU stays, and removed from the patient through one of the port inci-
shortened hospital stays. sions. The patient is taken out of Trendelenburg position,
the remaining ports are removed, incisions are closed, the
patient’s legs are taken out of lithotomy position, and the
2. Briefly describe the surgical procedure.
patient is awakened. Depending on surgical experience and
In RALP, after induction of general anesthesia, the difficulty of the case, mean operative times range from
patient is placed in lithotomy position, arms are carefully 160–296 minutes with mean blood losses of 50–287 mL.
183
184 SECTION 6 Abdomen
3. What are the primary anesthetic concerns monitor rSO2, a reflection of the balance between cere-
for robotic-assisted laparoscopic radical bral oxygen supply and demand, is limited because it
prostatectomy? measures only rSO2 of the frontal cortex, not global
cerebral oxygenation. rSO2 was also found to increase
The primary anesthetic concerns for RALP are as follows: with increases in arterial carbon dioxide (PaCO2), but
• Physiologic effects of pneumoperitoneum in the because hypercapnia also causes an increase in cerebral
Trendelenburg position blood volume and eventually an increase in ICP, it
• Restricted access to the patient because of the massive is recommended that patients be maintained within
equipment placed over the patient normocapnic ranges.
• Prevention or treatment of complications second- Changes in respiratory homeostasis caused by pneu-
ary to inducing pneumoperitoneum and position- moperitoneum and steep Trendelenburg position are also
ing the patient in exaggerated lithotomy and steep significant. Pneumoperitoneum elevates intraabdominal
Trendelenburg pressure causing decreases in pulmonary compliance
and tidal volumes along with increases in peak and
4. Describe the cerebrovascular, respiratory, plateau airway pressures. The addition of steep Tren-
and hemodynamic effects of pneumoperitoneum delenburg position pushes abdominal contents against
in steep Trendelenburg position. the diaphragm. The resulting pressure reduces functional
reserve capacity, decreases pulmonary compliance, and
Significant cerebrovascular physiologic changes may predisposes to atelectasis. Further reductions in func-
occur with the use of pneumoperitoneum and the steep tional reserve capacity and pulmonary compliance are
Trendelenburg position (Box 38-1). Initiation of pneu- caused by increases in pulmonary blood volume and
moperitoneum increases intraabdominal pressure, which gravitational forces on mediastinal structures. To com-
results in increased intracranial pressure (ICP). Placing pensate for these effects, elevated peak airway pressures
patients in the Trendelenburg position also eventually are required to maintain a constant minute volume. With
increases ICP by elevating cerebral venous pressure, ascending peak inspiratory pressures, the risk of baro-
which hinders cerebral venous drainage and leads to trauma increases. This potential risk may be reduced
increases in cerebral blood volume and potentially cere- by decreasing tidal volume, increasing the respiratory
brospinal fluid volume. Cerebral perfusion does not rate, and tolerating a minimal level of hypercarbia.
appear to be compromised during RALP. Disastrous con- Another potential concern of the steep Trendelenburg
sequences nevertheless may occur secondary to excessive position is pulmonary interstitial edema, when much of
increases in ICP, especially in patients with cerebral the lung is below the left atrium.
ischemia and cerebrovascular disorders. Several observational studies have evaluated the
Regional cerebral oxygen saturation (rSO2) employ- hemodynamic effects of pneumoperitoneum in combi-
ing near-infrared spectroscopy cerebral oximetry has nation with the steep Trendelenburg position during
been used to evaluate cerebrovascular effects during RALP. In one large retrospective review comprising
RALP. Increases in rSO2 have been observed with the 1500 cases, mean arterial pressure, heart rate, and
use of pneumoperitoneum and the steep Trendelenburg cardiac output all were noted to be decreased. Prospec-
position suggesting that RALP does not induce cerebral tive studies with relatively small numbers of patients
ischemia. The use of near-infrared spectroscopy to observed increases in mean arterial pressure, central
venous pressure, and systemic vascular resistance with
only the initiation of pneumoperitoneum. These changes
are postulated to result from increased intraabdominal
BOX 38-1 Cerebrovascular, Respiratory, pressure compressing the aorta. Aortic compression
and Hemodynamic Effects of results in increased afterload and may be enhanced
Pneumoperitoneum in Steep further by humoral factors. Other studies found that
Trendelenburg Position central venous pressure did not change with insufflation
but increased only with the addition of the steep Tren-
CEREBROVASCULAR delenburg position.
g cerebral venous drainage nh CBV and h CSF Changes in heart rate and cardiac output have been
h intracranial pressure variably reported as increased, no change, or decreased.
Severe bradycardia, probably caused by vagal stimula-
RESPIRATORY tion during peritoneal distention, has occurred on
h peak and plateau airway pressures initiation of pneumoperitoneum in RALP cases. With
g pulmonary compliance the combination of pneumoperitoneum and steep Tren-
g functional residual capacity delenburg position, strain or workload on the heart,
HEMODYNAMIC as measured by right-sided and left-sided stroke work
index, is increased. The proposed mechanism for this
hg mean arterial pressure
phenomenon is increased filling pressures. In patients
hg or unchanged heart rate and cardiac output
h central venous pressure and systemic vascular resistance with sufficient cardiac reserve, these changes are prob-
h stroke work index ably well tolerated. Patients with compromised cardiac
function could develop heart failure from increased
CBV, Cerebral blood volume; CSF, cerebrospinal fluid. preload.
38 Robotic Prostatectomy 185
5. What are possible complications of disturbances may occur if these complications are not
pneumoperitoneum and steep Trendelenburg rapidly recognized.
position during robotic-assisted laparoscopic Another potentially life-threatening complication of
insufflation is venous gas embolism. Clinical presentation
radical prostatectomy?
depends on the size of the gas bubbles and speed of entry
Nonsurgical complications related to the use of CO2 into the circulation. This rare complication should be sus-
pneumoperitoneum and the steep Trendelenburg posi- pected whenever there is unexplained sudden cardiovas-
tion range from mild subcutaneous emphysema (SCE) to cular collapse with changes in the capnography tracing.
ischemic optic neuropathy (Box 38-2). Other potential During RALP, CO2 gas embolism has been associated with
complications include corneal abrasions, laryngeal edema, two distinct periods—initial insufflation of the peritoneum
brachial plexus injuries, and venous gas embolism. and dissection of the deep dorsal venous complex. In
CO2 SCE is a common complication of laparoscopic studies using transesophageal echocardiography, embolic
surgery resulting from extraperitoneal insufflation. Iden- events were detected only during transection of the deep
tified risk factors include maximum end-tidal CO2 of dorsal venous complex and were subclinical in their effects.
!50 mm Hg, six or more operative ports, operative time CO2 is generally used to achieve pneumoperitoneum
"200 minutes, and older patient age. CO2 insufflation for RALP and is extremely soluble in the presence of
pressure determines the extent of SCE, and when insuf- red blood cells. Consequently, gas embolism during
flation is stopped, SCE quickly resolves. Although SCE RALP tends to be less life-threatening than similar-sized
is thought to be relatively harmless, severe cases may air emboli.
cause substantial hypercarbia. In mild cases, the anesthe- If clinically significant gas emboli occur during RALP,
siologist might notice a fullness or swelling of the treatment consists of immediate desufflation of the abdo-
patient’s neck or chest after surgical drapes are removed. men, undocking and removing the robot to allow patient
A common finding is crepitus, the characteristic crack- access, maintaining steep Trendelenburg position, and
ling feel to the touch or sensation of air under the skin. In tilting the patient left side down. Tilting the patient as
severe cases, swelling of the neck could potentially inter- described reduces the amount of gas that could advance
fere with breathing after extubation; severely elevated through the right side of the heart and into the pulmonary
hypercarbia may cause an excessive increase in the work circulation. Additionally, hyperventilation of the patient
of breathing. The recommended approach is to keep the with 100% oxygen helps to correct hypoxemia, decrease
patient mechanically ventilated until severe crepitus and the size of the gas embolus if nitrous oxide was being
hypercarbia resolve. used, and increase CO2 excretion. If these maneuvers are
If high insufflation pressures are used, SCE may develop unsuccessful, aspiration of gas may be attempted through
in prefascial planes leading to life-threatening complica- a central venous catheter, but this is unlikely to be suc-
tions of pneumothorax, pneumomediastinum, and pneu- cessful. If required, cardiopulmonary resuscitation should
mopericardium. Significant respiratory and hemodynamic be initiated.
Care must be taken in positioning the patient for
RALP. As the operating table position changes from
supine/lithotomy to steep Trendelenburg position, the
BOX 38-2 Complications of patient could slide cephalad and possibly even off the
Pneumoperitoneum and Steep table. Several methods are used to prevent this cephalad
Trendelenburg Position during slide, but each has its drawbacks. Shoulder braces have
Robotic-Assisted Laparoscopic been shown to cause brachial plexus injuries by com-
Radical Prostatectomy pressing the upper trunk of the brachial plexus against
the first rib or depressing the humerus into the axilla
• CO2 SCE resulting in a stretch injury. Strapping the patient to the
• Crepitus operating table with chest straps in a crossover (“x”)
• Hypercarbia pattern has been observed to decrease pulmonary com-
• Pneumothorax pliance further in the steep Trendelenburg position with
• Pneumomediastinum
• Pneumopericardium
pneumoperitoneum. In the author’s institution, horse-
• Venous gas embolism shoe-shaped shoulder braces are carefully applied around
• Sudden cardiovascular collapse the patient’s acromioclavicular joints. This method pre-
• Changes in capnography tracing vents cephalad movement and brachial plexus injuries.
• Positioning Additionally, attention should be given to the pressure
• Sliding cephalad off the operating room table areas of the arms and legs to avoid ulnar neuropathy and
• Brachial plexus injuries lateral femoral cutaneous nerve injury.
• Peripheral nerve injuries Facial, pharyngeal, and laryngeal edema may also occur
• Facial, laryngeal, and pharyngeal edema with the combination of steep Trendelenburg position and
• Difficult extubation pneumoperitoneum. Increased amounts of intravenous
• May be difficult to reintubate
• Ocular injuries
fluid, reduced venous outflow from the patient’s head
• Corneal abrasions secondary to pneumoperitoneum, and use of the steep
• Ischemic optic neuropathy Trendelenburg position may lead to pharyngeal and laryn-
geal edema. Restricting fluid and limiting time in the
CO2, Carbon dioxide; SCE, subcutaneous emphysema. head-down position may help to avoid this complication.
186 SECTION 6 Abdomen
If facial or conjunctival edema is observed at the end artery disease but also may have renal abnormalities owing
of surgery, airway edema should be suspected. In this to prostatic hypertrophy.
instance, a cuff leak or breathe around test, although not Patients with known or suspected airway issues might
always reliable, can be performed before attempting extu- be at increased risk postoperatively because of possible
bation. In extreme cases of edema, consideration should be presence of airway edema. Preexisting peripheral neuro-
given to leaving the patient tracheally intubated and logic deficits should be noted and, if necessary, the con-
nursed in the upright position. If the patient develops scious patient should be placed in the lithotomy position
postextubation stridor or difficulty breathing, immediate prior to the induction of general anesthesia to verify free-
reintubation is required, although this may be difficult dom from neurologic exacerbation. Patients with glau-
because of airway edema. Extubation over an airway coma or other ocular diseases are currently at no known
exchange catheter and other means of rapidly obtaining an increased risk of ischemic optic neuropathy during RALP.
airway should be considered. Patients with significant cardiac disease require fur-
Ocular injuries range from common corneal abrasions ther evaluation. Depending on the severity of disease,
to rare cases of ischemic optic neuropathy. Corneal abra- echocardiogram, stress test, and perfusion studies might
sion during RALP has a reported incidence of 3%–13.5% be indicated. Special care must be taken in patients with
when using either eye or plastic tape. Causes range from drug-eluting stents because of the risk of stent thrombo-
chemosis (swelling or edema of the conjunctiva), exposure sis. Before discontinuing antiplatelet therapy, consulta-
keratopathy (excessive drying of the lower portion of the tion with a cardiologist is necessary. It is generally safe to
cornea owing to incomplete eyelid closure), or direct con- continue 81 mg of aspirin throughout the perioperative
tact trauma from equipment or the patient’s own fingers. period.
Symptoms are usually first reported by the patient while Higher peak airway pressures are often required to
in the PACU, tend to be of short duration, and are easily ventilate these patients. Although higher peak airway
treated. Recommended preventive measures include in- pressures are not a contraindication, care must be taken in
forming the patient concerning the risk of chemosis and patients with severe chronic obstructive pulmonary dis-
corneal abrasion, instruction to avoid eye touching in the ease. RALP is relatively contraindicated in patients with
PACU, restricting intravenous fluid during the case, and lung bullae or blebs because of the potential complication
the use of either eye patches or transparent occlusive of rupture.
dressings applied immediately after induction of general Obese patients (body mass index "30 kg/m2) present
anesthesia to protect the eyes. additional challenges because of higher incidence of
Ischemic optic neuropathy, an extremely rare and coronary artery disease, pulmonary dysfunction, and dia-
devastating complication of RALP, classically occurs in betes. Extra care should be undertaken when positioning
patients undergoing spine surgery in the prone position these patients for the steep Trendelenburg position to
with significant hypotension and blood loss. One case avoid neurologic injury and cephalad sliding.
of ischemic optic neuropathy during RALP has been
reported in the literature. The patient experienced hy- 7. Discuss the anesthetic technique for robotic-
potension, blood loss, significant fluid administration, assisted laparoscopic radical prostatectomy.
and blood transfusion and was in the Trendelenburg
position for a prolonged period of time. Intraocular The combination of pneumoperitoneum and steep Tren-
pressure has been observed to increase during RALP, delenburg position for RALP necessitates the choice of
with surgical duration and end-tidal CO2 being signifi- general endotracheal anesthesia with controlled ventila-
cant predictors. The steep Trendelenburg position is tion. Because of tracheal shortening during pneumoperito-
postulated to increase venous pressure in the head and neum, the endotracheal tube should be carefully positioned
neck leading to interstitial fluid accumulation from cap- to avoid endobronchial intubation. Although there is no
illary leak, decreased venous outflow, and decreased specific recommended anesthetic drug regimen, appropri-
perfusion of the optic nerve. Increased end-tidal CO2, ate choices should be based on the patient’s cardiovascular
which reflects increased PaCO2, may result in choroidal status and other comorbidities. For optimal pneumoperito-
vasodilation and elevated intraocular pressures. Injury neum to be achieved, complete muscle relaxation is essen-
to the optic nerve may be caused by several possible tial. Epidural analgesia for postoperative pain control is
mechanisms, such as venous infarction from decreased not recommended because postoperative discomfort is
venous outflow, ischemia caused by the small pial arter- substantially less in RALP compared with open proce-
ies supplying the nerve, and direct mechanical damage dures. Depending on the experience of the operative team
from elevated interstitial pressures. and the patient’s medical condition, additional monitoring
and intravenous fluid access may be required. If needed,
6. What are the preanesthetic concerns in patients these items should be placed before docking the robot
presenting for robotic-assisted laparoscopic because of limited patient access afterward.
radical prostatectomy?
8. What are the concerns for positioning, ventilation,
The mean age of men undergoing RALP is approximately and fluid management of patients for robotic-
60 years. A thorough preanesthetic evaluation should be assisted laparoscopic radical prostatectomy?
performed along with optimization of cardiovascular, re-
spiratory, metabolic, and other systems. This population Positioning is a significant concern in patients undergo-
of patients not only has an increased incidence of coronary ing RALP. One must ensure that the patient does not
38 Robotic Prostatectomy 187
slide cephalad or off the operating table when moved to Falabella A, Moore-Jeffries E, Sullivan MJ, et al.: Cardiac function during
the steep Trendelenburg position. Techniques that are steep Trendelenburg position and CO2 pneumoperitoneum for
robotic-assisted prostatectomy: a trans-oesophageal Doppler probe
commonly used to prevent this problem are chest bind- study. Int J Med Robotics Comput Assist Surg 3:312, 2007.
ing in a crossover (“x”) pattern, positioning on egg-crate Gainsburg DM, Wax D, Reich DL, et al.: Intraoperative management
foam or bean-bag mattress that is secured to the operat- of robotic-assisted versus open radical prostatectomy. JSLS 14:1–5,
ing table, or placing shoulder braces of various kinds. 2010.
Haas S, Haese A, Goetz AE, et al.: Haemodynamics and cardiac
The actual technique of positioning is usually one of function during robotic-assisted laparoscopic prostatectomy in steep
surgical preference; however, careful application to pre- Trendelenburg position. Int J Med Robotics Comput Assist Surg
vent injury is of utmost importance. 7:408, 2011.
As the intraabdominal pressure increases with insuffla- Halverson A, Buchanan R, Jacobs L, et al.: Evaluation of mechanism of
tion, so does the patient’s airway pressure. Ventilation may increased intracranial pressure with insufflation. Surg Endosc
12:266, 1998.
be difficult in patients with chronic obstructive or restric- Hong JY, Kim WO, Kil HK: Detection of subclinical CO2 embolism
tive pulmonary disease. Several different ventilation modes by transesophageal echocardiography during laparoscopic radical
may be tried for any one patient until best respiratory prostatectomy. Urology 75:581, 2010.
mechanics and gas exchange are achieved. Peak inspiratory Kalmar AF, Foubert L, Hendrickx JFA, et al.: Influence of steep
Trendelenburg position and CO2 pneumoperitoneum on cardiovas-
pressures greater than 50–60 cm H2O might result in cular, cerebrovascular, and respiratory homeostasis during robotic
barotrauma. prostatectomy. Br J Anaesth 104:433–439, 2010.
Minimal (#2000 mL) intravenous fluids should be Lestar M, Gunnarsson L, Lagerstrand L, et al.: Hemodynamic pertur-
infused to avoid excessive urine output obscuring the bations during robot-assisted laparoscopic radical prostatectomy in
operative field during vesicourethral anastomosis. Facial, 45° Trendelenburg position. Anesth Analg 113:1069, 2011.
Mavrocordatos P, Bissonnette B, Ravussin P: Effects of neck position
pharyngeal, and laryngeal edema might also be reduced and head elevation on intracranial pressure in anesthetized neuro-
by fluid restriction. The author’s recommendation is to logical patients. J Neurosurg Anesthesiol 12:10, 2000.
infuse intravenous fluid up to 800 mL until the surgeon Park EY, Koo BN, Min KT, et al.: The effect of pneumoperitoneum
completes the vesicourethral anastomosis and then pro- in the steep Trendelenburg position on cerebral oxygenation. Acta
Anaesthesiol Scand 53:895, 2009.
vide an additional 700–1200 mL of fluid to satisfy fluid Phong SVN, Koh LKD: Anaesthesia for robotic-assisted prostatec-
deficits by the end of surgery. tomy: considerations for laparoscopy in the Trendelenburg position.
Anaesth Intensive Care 35:281, 2007.
Piegeler T, Dreessen P, Schlapfer M, et al.: Impact of intraoperative
SUGGESTED READINGS fluid management on outcome in patients undergoing robotic-
assisted laparoscopic prostatectomy—a retrospective analysis. Eur J
Awad H, Santilli S, Ohr M, et al.: The effects of steep Trendelenburg Anaesth 28:6AP1, 2011.
positioning on intraocular pressure during robotic radical prostatec- Slustsky AS: ACCP consensus conference: mechanical ventilation.
tomy. Anesth Analg 109:473, 2009. Chest 104:1833, 1993.
Chang CH, Lee HK, Nam SH: The displacement of the tracheal tube Weber ED, Colyer MH, Lesser RL, et al.: Posterior ischemic optic neu-
during robot-assisted radical prostatectomy. Eur J Anaesthesiol ropathy after minimally invasive prostatectomy. J Neuroophthalmol
27:478, 2010. 27:285, 2007.
Danic MJ, Chow M, Alexander G, et al.: Anesthesia considerations for
robotic-assisted laparoscopic prostatectomy: a review of 1,500 cases.
J Robotic Surg 1:119, 2007.
CASE 39
QUESTIONS
1. What are the classifications of chronic kidney 5. Explain the relationship between acidemia and
disease? hyperkalemia.
2. How are patients selected for combined kidney- 6. Discuss the implications of fluid management in
pancreas transplantation? kidney-pancreas transplantation.
3. What are the major anesthetic concerns for 7. What is the role of transversus abdominis plane
kidney-pancreas transplantation? block for abdominal surgery?
4. How is insulin administration managed intraopera-
tively for patients with a continuous subcutaneous
insulin infusion?
A 44-year-old woman with type 1 diabetes mellitus as diaphoresis, headache, and abnormal mentation or
(DM), hypertension, hypothyroidism, and stage 5 chronic confusion, are indications for pancreas transplantation.
kidney disease (CKD) presented for cadaveric kidney- Kidney transplantation is indicated in patients with
pancreas transplantation. stages 4 and 5 CKD. In the United States at the present
time, the most common etiology for CKD and subsequent
1. What are the classifications of chronic kidney need for kidney transplantation is diabetic nephropathy.
When type 1 DM and CKD are present, as is the case in
disease?
50%–60% of patients, simultaneous pancreas-kidney
CKD is classified based on the presence of kidney damage (SPK) transplantation or pancreas transplantation after
and glomerular filtration rate (Table 39-1). Kidney damage kidney transplantation may be performed. The best results
is determined by either pathologic findings or abnormal with respect to graft survival appear to occur with SPK
markers found in blood, urine, or imaging. End-stage renal transplantation.
disease is termed stage 5 CKD. In 2010, "828 SPK transplantations were performed in
the United States. Although there have been "40 cases of
2. How are patients selected for combined kidney- living related pancreas-kidney transplantations performed,
most transplants are obtained from deceased donors.
pancreas transplantation?
The United Network of Organ Sharing is responsible for
Pancreas transplantation alone is indicated for patients cadaveric organ allocation. Organ matching is done based
with severe and difficult-to-control type 1 DM without on major blood group (ABO) compatibility followed by
evidence of renal dysfunction. In rare circumstances, it human leukocyte antigen (HLA) profiling of the recipient.
may be indicated in patients with DM secondary to A crossmatch is performed between the recipient and the
chronic pancreatitis or cystic fibrosis. Eligibility criteria, donor blood cells to determine if the recipient has antibod-
which can differ from institution to institution, include ies against donor antigens. HLA matching previously was a
age, human immunodeficiency virus (HIV) status, and high priority for organ matching; however, improved out-
body mass index. comes with newer immunosuppressant medications have
C peptide is generated during insulin biosynthesis diminished the importance of tissue typing.
and is released into the portal circulation along with
insulin. Measurement of C peptide levels can confirm 3. What are the major anesthetic concerns for
the absence or decreased production of insulin by the kidney-pancreas transplantation?
pancreas. C peptide levels !0.3–2 ng/mL are confirma-
tory evidence of the need for pancreatic transplanta- The anesthetic evaluation and management of patients
tion. Additionally, a history of intolerance to insulin undergoing SPK transplantation is directed at identifying
therapy and a history of recorded low glucose levels and optimizing organ dysfunction or metabolic abnormali-
without the expected symptoms of hypoglycemia, such ties that are associated with advanced DM and CKD. For a
188
39 Kidney and Pancreas Transplantation 189
Diabetes Uremia
• Coronary • Central
Disease Hyperventilation
• Glucose • Uremic Platelet
• Retinopathy Intolerance Dysfunction
• Nephropathy • Autonomic • Encephalopathy
• Ketoacidosis Dysfunction • Hypocalcemia
• Hyperglycemia • Sensory-motor • Hyperkalemia
• Hyperosmolar Neuropathy • Hypermagnesemia
hyperglycemic • Gastroparesis • Hyperphosphatemia
non-ketotic • Dyslipidemia • Hyperparathyroidism
syndrome • Hypertension • Osteodystrophy
• Acidemia • Pulmonary edema
• Vascular • Metabolic acidosis
Disease • Anemia
decrease postoperative pain but are unacceptable as pri- NS 0.45% if acidosis exists. Third space losses are re-
mary anesthetic plans. Epidural anesthesia could result in placed with crystalloid or colloid boluses or both to
splanchnic hypoperfusion and excessive crystalloid admin- maintain adequate end-organ perfusion pressures.
istration leading to swelling of the donor pancreas. Colloid
solutions may offer an advantage over crystalloid solutions 4. How is insulin administration managed
by reducing pancreatic swelling and may reduce graft intraoperatively for patients with a continuous
function complications. subcutaneous insulin infusion?
In addition to standard American Society of Anesthe-
siologists (ASA) monitors, invasive arterial pressure cath- These patients may present with varying levels of insulin
eters are recommended for closer observation of blood requirements; some may self-administer intermittent
pressure and for serial arterial blood gas (ABG) sampling. short-acting and long-acting insulin, whereas others may
Central venous catheters may be used for intravascular opt for continuous subcutaneous insulin infusion (CSII)
access, infusion of vasoactive medications, and trending therapy (also termed insulin pump). Institutions vary
central venous pressures. in regard to the perioperative management of patients
Intraoperatively, serial ABG samples allow for moni- with CSII therapy undergoing surgery. For surgeries not
toring of ventilation, oxygenation, acid-base status, elec- involving pancreas transplantation, particularly short
trolytes, hematocrit, and glucose. Glucose measurements ambulatory procedures, some institutions permit con-
can vary widely during the case, owing to methylpred- tinuation of the insulin pump, whereas others insist on
nisolone (hyperglycemia) and the newly anastomosed pump deactivation. However, for SPK transplantation,
pancreas (hypoglycemia). In brittle diabetics (diabetic discontinuing CSII affords the anesthesiologist improved
patients prone to glucose lability), glucose should be control of insulin requirements, which may abruptly
checked hourly, and after pancreatic anastomosis and change throughout surgery. Also, turning off CSII elimi-
release of the vascular clamp, it should be checked every nates the possibility of pump failure as a possible cause of
30 minutes. An important therapeutic goal is to maintain hyperglycemia. Additionally, when the pancreas is trans-
a physiologic pH, arterial oxygen (PaO2), arterial carbon planted and unclamping occurs, donor islet beta cells
dioxide (PaCO2), base deficit, sodium concentration, and begin to produce insulin, and glucose levels can decrease
potassium level. by 50 mg/dL per hour. Blood glucose levels in conjunc-
In addition to methylprednisolone, antithymocyte tion with C peptide levels serve as indicators of graft
globulin (ATG) or basiliximab is administered intraop- function. Hyperglycemia and low C peptide levels are
eratively to prevent acute organ rejection. ATG is a rab- signs of graft nonfunction, whereas euglycemia and normal
bit pasteurized gamma globulin that possesses side effects C peptide levels indicate adequate graft function. Most
including anaphylaxis and cytokine release syndrome. It practitioners administer both dextrose and insulin
is contraindicated in anyone with an allergy to rabbit throughout the procedure and into the postoperative
protein or a history of adverse reaction to ATG. Basilix- period, avoiding ketosis and decreasing neo–beta islet
imab is a murine/human monoclonal antibody that blocks cell activity. Some centers also use octreotide to decrease
activity of the interleukin 2-receptor alpha chain on the exocrine pancreas activity.
surface of activated T lymphocytes. It is associated with There are two strategies at the present time regarding
anaphylaxis. However, basiliximab is frequently used in insulin management after pancreas transplantation:
place of ATG because it has not been associated with • Complete replacement by exogenous insulin to meet
cytokine release syndrome. the body’s insulin requirements to “rest” the donor
Anecdotal evidence points to postoperative complica- beta islet cells for 3–4 days, followed by intermittent
tions in patients who have undergone renal transplanta- insulin dosing regimen.
tion, stemming from an acute combined metabolic and • PRN (pro re nata [as needed]) supplementation with
respiratory acidosis following tracheal extubation. For exogenous insulin, allowing for a quick measurement
this reason, we recommend checking an ABG 30 minutes of graft function while awaiting results of C peptide
before extubation and giving serious consideration to levels. After surgery, hyperglycemia commonly per-
continuing ventilatory support if the pH is !7.25 or the sists despite the production of endogenous insulin by
base deficit is "7 mEq/L. Other concerns regarding ex- the donor beta islet cells. This persistent hyperglyce-
tubation include fluid overload, hemodynamic instability, mia may be due to the insulin-resistant effects of
hyperkalemia, hypoxemia, and hypercarbia. Patients with immunosuppressive agents and the administration of
chronic obstructive pulmonary disease (COPD) and ob- high-dose glucocorticoids.
structive sleep apnea (OSA) are particularly vulnerable. Regardless of the presence or absence of CSII, extreme
Common postoperative fluid management consists of vigilance regarding glycemic management during the
5% dextrose 0.45% normal saline (NS) at 40 mL per perioperative period must be exercised. Glucose levels
hour and NS 0.45% for hourly urine output replace- should be determined hourly and then half-hourly im-
ment on a milliliter-for-milliliter basis. Patients under- mediately after unclamping the vascular supply to the
going renal transplantation may be oliguric, anuric, or pancreas. Glycemic management is best accomplished
polyuric. Hyperglycemia is an indication for removing with continuous insulin infusion intraoperatively that is
dextrose from intravenous solutions until serum glucose continued into the postoperative period. Dextrose solu-
levels are corrected. An insulin infusion is commonly tions should also be continued throughout the periopera-
continued throughout the initial perioperative period. tive period because ketosis has been reported to occur
Sodium bicarbonate (75 mEq) may be added to 1 L of even in patients who are euglycemic.
192 SECTION 6 Abdomen
5. Explain the relationship between acidemia 6. Discuss the implications of fluid management in
and hyperkalemia. kidney-pancreas transplantation.
Patients with renal failure and concomitant type 1 DM are The anesthesiologist’s role in SPK transplantation is to
at significant risk for developing acidemia and hyperkale- temper the desires of two medical specialties, the ne-
mia, particularly when there has been a lapse in hemodialy- phrologists who want the kidney “wet” and the pulmo-
sis. Because timing of dialysis and transplantation are diffi- nologists who want the lung “dry.” Depending on the
cult to coordinate, serum pH and potassium levels should be patient’s preoperative volume status, intraoperative
measured on the day of surgery. Abnormal values indicate fluid administration may be limited by concerns for
the need for hemodialysis before transplantation. volume overload on pulmonary and cardiovascular
Acidemia can occur secondary to ketoacidosis; admin- function, which may result in hypoxemia and impaired
istration of large amounts of chloride-containing crys- contractility. Conversely, volume restriction and deple-
talloids (see Question 6 for details); and retention of tion are associated with hypotension after anesthetic
sulfates, phosphates, and uric acid. A low pH can poten- induction, increased risk of delayed graft function, and
tiate the effects of sedative-hypnotics and opioids by end-organ hypoperfusion. This balancing act is com-
increasing the nonionized fraction, resulting in impaired plicated further by the wide selection of crystalloids
airway reflexes and respiratory depression. Monitoring and colloids available.
and management of acid-base status are necessary to Factors for selecting appropriate fluid replacement
prevent the sequelae of acidemia. By assessing serial include pH, potassium, and glucose content of various
ABG measurements, the anesthesiologist can make ap- intravenous solutions. In the setting of hyperkalemia,
propriate changes in minute ventilation to compensate it may be disadvantageous to administer PlasmaLyte
partially for a metabolic acidosis. However, after extuba- electrolyte solution or lactated Ringer’s solution be-
tion, the seriousness of respiratory depression becomes a cause both contain potassium (5 mEq/L and 4 mEq/L,
true challenge to the anesthesiologist; this is where com- respectively). As a result, sodium chloride 0.9% (NS)
bined effects of residual inhalation anesthetics, muscle is frequently used because it does not contain potas-
relaxants, opioids, and restricted diaphragmatic move- sium. However, NS has a pH of 5.0 and a chloride
ment owing to splinting can lead to rapid development content of 154 mEq/L and predisposes to hyperchlo-
of hypercarbia and acidemia. Patients with OSA and remic metabolic acidosis. At our institution, fluid man-
COPD are particularly vulnerable. Postoperative respi- agement (Table 39-3) during kidney transplantation is
ratory depression producing hypercarbia and acidosis is designed to limit acid-base imbalances. Typically,
concerning in the postanesthesia care unit (PACU). 2.5–5 L of fluid is administered during these opera-
Measures to improve respiratory function in the PACU tions. At minimum, hourly ABG measurements should
include raising the head of the bed 30 degrees, pain con- be obtained throughout surgery to monitor the pa-
trol (balanced to prevent hypoventilation from splinting tient’s acid-base status.
while avoiding respiratory depression), and continuous More recently, researchers have looked into the ef-
positive airway pressure for patients with OSA. fects of colloid solutions on pancreas transplantation.
Interconnected with acidemia is the life-threatening Early graft pancreatitis after reperfusion appears to be
metabolic disturbance of hyperkalemia. Extracellular acido- due to defects in the microcirculation, which may be
sis increases serum potassium levels by 0.5–0.8 mEq/L for caused by pancreatic swelling from aggressive crystal-
every decrease in pH of 0.1 unit; this occurs because as ex- loid administration. Other causes of impaired microcir-
cess extracellular hydrogen ion moves intracellularly along culation may be related to methods of organ preserva-
its concentration gradient, potassium moves out of the cell tion and medical management of the donor. Colloid
to maintain electrical neutrality. As potassium levels in- solutions may decrease the total crystalloid volume
crease, so does the likelihood of ECG changes, as follows: administered; however, the short-term and long-term
• 6 mEq/L—peaked T wave benefits of colloid solutions on graft function remain
• 7 mEq/L—prolonged PR interval unknown.
• 8–9 mEq/L—absent P waves and widened QRS The goals of fluid management should be aimed at
complex followed quickly by ventricular fibrillation optimizing cardiac performance to enable adequate blood
Intraoperative management of acute hyperkalemia is flow to transplanted tissues. Vasopressors are to be used
aimed at stabilizing cardiac membrane potentials and sparingly; however, they are indicated to maintain mean
promoting intracellular potassium shifts (Table 39-2). arterial pressure "65–70 mm Hg.
7. What is the role of transversus abdominis plane have decreased the incidence of complications by allowing
block for abdominal surgery? real-time visualization of the spread of local anesthetic in
the desired plane.
Transversus abdominis plane (TAP) block is traditionally The area is prepared and draped in a sterile fashion.
known as a landmark-guided block performed at the An ultrasound probe with sterile cover and sterile gel is
Petit triangle. The triangle landmarks include the iliac placed over the Petit triangle, at the midaxillary line in
crest inferiorly, the latissimus dorsi muscle medially, and a transverse plane to the lateral abdominal wall. After
the external oblique muscle laterally. TAP block was visualizing the various fascial planes and the perito-
originally described as a blind technique, performed based neum, the needle is directed in plane, crossing first the
on obtaining characteristic “pops” as one traverses through external oblique and then the internal oblique muscles.
fascial planes until the plane between the transversus Saline or local anesthetic, 2 mL, is injected in the plane
abdominis and the internal oblique muscles is identified between the internal oblique and transversus abdominis
(Figure 39-2). The dermatomal level covered by the block muscles. When proper needle placement is confirmed,
is from T10 to L1, which is from just above the umbilicus 20–30 mL of local anesthetic is administered. The vol-
to the superior iliac crest. SPK transplantations require ume, not the concentration, of local anesthetic used is
large midline incisions, often extending above the T10 the important factor. TAP blocks are “volume” blocks.
dermatome, whereas kidney transplantations are usually Bupivacaine 0.25%–0.5% or ropivacaine 0.5%–0.75%
performed with a diagonal incision in the left lower quad- provides longer duration of action. However, care
rant. Such distinction is significant because SPK would should be taken to prevent exceeding the maximum
require bilateral TAP blocks and these may not sufficiently recommended dose of the local anesthetic used. During
cover the surgical incision, whereas incisional pain from local anesthetic injection, the extent of spread should be
kidney transplantation alone is usually prevented with a monitored continuously by scanning cephalad, caudad,
unilateral TAP block. The blind approach has been com- medial, and lateral. Successful TAP blocks are associ-
plicated by inadvertent needle placement into the liver, ated with reduced postoperative morphine consumption
peritoneum, and bowel. Ultrasound-guided TAP blocks for 48 hours.
TA EO
IO
LS
PM
QL
ST
LD N
IL
MM
Skin
FIGURE 39-2 ■ Fascial planes of TAP block. EO, External oblique; IL, longissimus iliocostalis; IO, internal oblique; LD, latissimus dorsi; LS,
lumbar spine; MM, multifidus muscle; N, 50-mm blunt-tipped needle; PM, psoas major; QL, quadratus lumborum; ST, subcutaneous
tissue; TA, transversus abdominis. (From McDonnel JG, et al. The analgesic efficacy of transversus abdominis plane block after cesarean de-
livery: a randomized controlled trial. Anesth Analg 106:186, 2008.)
194 SECTION 6 Abdomen
SUGGESTED READINGS Koenhtop DE, Beebe DS, Belani KG: Perioperative anesthetic man-
agement of the kidney-pancreas transplant recipient. Curr Opin
Abdallah FW, Chan VW, Brull R: Transversus abdominis plane block: Anaesth 13:341, 2000.
a systematic review. Reg Anesth Pain Med 37:193, 2012. Nassar AA, Boyle ME, Seifert KM, et al.: Insulin pump therapy in patients
Freise CE, Narumi S, Stock PG, et al.: Simultaneous pancreas-kidney with diabetes undergoing surgery. Endocr Pract 18:49, 2012.
transplantation: an overview of indications, complications, and Schmied BM, Muller SA, Mehrabi A, et al.: Immunosuppressive stan-
outcomes. West J Med 170:11, 1999. dards in simultaneous kidney pancreas transplantation. Clin Trans-
Gruessner AC, Sutherland DE: Pancreas transplant outcomes for plant 20(Suppl 17):44, 2006.
United States (US) and non-US cases as reported to the United Yost CS, Niemann CU: Anesthesia for abdominal organ transplanta-
Network for Organ Sharing (UNOS) and the International tion. pp. 2155–2184. In Miller RD, Erikkson LI, Fleisher LA, et al.
Pancreas Transplant Registry as of June 2004. Clin Transplant (eds.): Miller’s Anesthesia, 7th edition. Churchill Livingstone,
19:433, 2005. Philadelphia, 2010.
S EC TION 7
195
CASE 40
QUESTIONS
1. How is normal intraocular pressure maintained? 4. What nonanesthetic pharmacologic agents can
decrease intraocular pressure?
2. What are anesthetic the considerations for repair
of open eye injuries? 5. How do you determine whether surgical repair of
an open eye injury is emergent or urgent?
3. Is succinylcholine contraindicated in open eye
injury?
A 5-year-old boy was shot with a BB gun at a family mydriatic drugs, increase IOP. Even arterial pulsations
barbecue. He is otherwise healthy and previously experi- cause measurable IOP changes.
enced an uncomplicated general anesthetic for bilateral
myringotomy and tube placement.
Choroidal Blood Volume
1. How is normal intraocular pressure maintained? Sudden increases in systemic blood pressure and CVP in-
crease choroidal blood volume, resulting in elevated IOP
Normal intraocular pressure (IOP) is 10–20 mm Hg with a because of the comparatively slow elimination process. Al-
difference of up to 5 mm Hg between the two eyes. Diurnal though choroidal vessels do not autoregulate, the factors
variation results in 2–3 mm Hg higher IOP each morning altering cerebral blood flow affect blood volume in the eye.
owing to mydriasis, supine position, and eyelid pressure Vasodilation occurs with hypercarbia, hypoxemia, and in-
during sleep. In addition, the supine position can increase creases in metabolic rate. Similar to cerebral blood flow,
IOP by 1–6 mm Hg. IOP is dependent on aqueous humor there is a linear relationship between arterial partial pressure
dynamics (most important factor), choroidal blood volume, of carbon dioxide (PaCO2) and blood flow. Hypoventila-
central venous pressure (CVP), and extraocular muscle tion, with the resulting elevation in PaCO2, increases IOP.
(EOM) tone.
Central Venous Pressure
Aqueous Humor Dynamics
Significant increases in CVP can temporarily inhibit the
The eye is divided into anterior and posterior chambers flow of aqueous humor through the Schlemm canal caus-
by the iris. The eye has 250 !L of aqueous humor; one ing an increase in IOP.
third of the aqueous humor is in the anterior chamber,
and two thirds is in the posterior chamber. Aqueous
Extraocular Muscle Tone
humor is necessary for proper light refraction, allowing
for vision. Additionally, it delivers oxygen and glucose EOMs differ from skeletal muscles. Compared with skel-
to the avascular lens and cornea. etal muscles, EOMs can rapidly and precisely control
Aqueous humor is produced by diffusion, filtration, contraction and relaxation and resist fatigue. Skeletal
and active secretion from choroidal capillaries in the muscles are innervated by a single axon to the midbelly
ciliary process located in the posterior chamber. It of each fiber. EOMs have single and multiple neuronal
flows from the posterior chamber, around the iris, and innervations allowing for focal contractions. Increased
into the anterior chamber. Elimination occurs through EOM tone increases IOP.
the space of Fontana and Schlemm canal at the irido-
corneal angle. Changes in intraocular fluid dynamics
2. What are the anesthetic considerations for repair
can cause significant alterations of IOP because the
globe is essentially noncompliant and surrounded by of open eye injuries?
the rigid orbit. Decreases in cross-sectional area of the The primary anesthetic goal for repair of open eye inju-
space of Fontana and Schlemm canal, as occur with ries is avoidance of sudden increases in IOP and the
196
40 Open Eye Injury and Intraocular Pressure 197
resultant extrusion of vitreous humor. Increases in IOP BOX 40-1 Anesthetic Considerations during
may be seen with increased venous and arterial pressure, Open Eye Surgery
coughing, bucking, Valsalva maneuver, increased PaCO2,
and the supine position. The following maneuvers can Aspiration precautions if “full stomach”
reduce or prevent increases in IOP: Elevate head of bed
• Reduce IOP Careful placement of anesthesia facemask
• Increase venous drainage by elevating the head Ensure optimal intubating conditions to avoid coughing and
• Prevent increases in IOP bucking
• Minimize preoperative sedation to avoid increases in Induction agents
PaCO2 secondary to sedation and hypoventilation Propofol decreases IOP
Ketamine
• Minimize hemodynamic response to laryngoscopy Studies vary as to whether it increases IOP
and intubation by ensuring deep anesthesia before Blepharospasm and nystagmus may interfere with
airway manipulation surgery
• Hyperventilate before intubation and during Increased incidence of PONV
surgery Etomidate
• Minimize bucking and coughing during laryngos- Decreases IOP
copy and intubation by providing adequate depth Myoclonus may cause injury to eye
of anesthesia and muscle relaxation Increased incidence of PONV
• Use anesthetic techniques designed to provide Neuromuscular blocking drugs
smooth emergence without coughing or bucking Succinylcholine
Probably does not increase IOP
while the endotracheal tube is still in place No evidence of vitreous extrusion
To allow for unobstructed access to the surgical field, Provides optimal intubation conditions in shortest
oral RAE tubes are popular choices for securing the air- time
way. Supraglottic airways, such as flexible laryngeal mask Nondepolarizing
airways, have also been used. Because airways are inac- Rocuronium only drug approved for rapid-sequence
cessible during eye surgery, care should be taken to se- induction
cure the artificial airway adequately. Prolonged mask ventilation may predispose to eye
Box 40-1 outlines considerations during various phases trauma from mask
of general anesthesia. Unprotected airway while awaiting for optimal intuba-
tion conditions
Laryngeal mask airway
3. Is succinylcholine contraindicated in open eye Not indicated if “full stomach”
injury? No access to airway
Does not protect against laryngospasm from light anes-
Most open globe surgeries are performed emergently thesia or aspiration
on patients subjected to trauma. All such patients are likely Maintenance
to be considered “full stomachs.” Because most of these Maintain deep anesthesia to decrease IOP
procedures are performed with general anesthesia, rapid- Neuromuscular blockade to ensure motionless field
sequence induction (RSI) to minimize aspiration risk is Hypocapnia
usually the induction technique of choice. Either succinyl- Hypoxia causes increased IOP by dilation of choroidal
choline or double-dose rocuronium is approved for RSI. circulation
Emergence
There are advantages and disadvantages related to both. Reversal agents have no effect on IOP
The use of succinylcholine has been a topic of consider- Smooth emergence (i.e., no coughing or bucking)
able debate for years. Traditional concerns focused on Prevention of PONV
a theoretic risk of intraocular contents extrusion after ad-
ministration of succinylcholine. After eye trauma, patients IOP, Intraocular pressure; PONV, postoperative nausea and vomiting.
reflexively press the eye with their hand and experience
blepharospasm, both of which predispose to vitreous loss
and extrusion. In other words, the damage is done before Although the exact mechanism is unknown, there
arriving in the operating room. To avoid succinylcholine are many proposed theories for IOP increases seen with
based on a theoretic concern that extrusion of intraocular succinylcholine administration. One theory suggests the
contents would occur fosters old teaching without scientific increase in IOP is caused by succinylcholine-induced tonic
evidence. Previous reports of extrusion of vitreous occurred contractions of the EOMs. However, this idea was ques-
during “light” anesthesia. The greater preponderance tioned by a study involving elective enucleation. After
of reports found no association between succinylcholine all EOMs were detached from the diseased eye, succinyl-
administration and vitreous expulsion. choline was administered, and IOP was measured. There
Succinylcholine administration increases IOP within was no difference in the IOP increase between eyes with
1 minute, and IOP peaks at 9 mm Hg within 6 minutes. detached EOMs and eyes with intact EOMs.
This peak pressure increase is significantly less than IOP Further research in this area suggests that the increase
elevations seen with crying, coughing, or bucking (e.g., in IOP may be a vascular event related to choroidal vascular
during suboptimal intubating conditions). It may be that dilation or decreased drainage as a result of elevated CVP.
the IOP increase seen with succinylcholine is of no clinical CVP elevation temporarily inhibits flow of aqueous humor
consequence if intubation conditions are optimized. through the Schlemm canal.
198 SECTION 7 Eye, Ear, Nose, and Throat
CVP, Central venous pressure; IOP, intraocular pressure; SVR, systemic vascular resistance.
Retinal Detachment
Patrick L. Sittler, MD
QUESTIONS
1. What are the different types of retinal detachment? 5. What are the different regional anesthesia options?
2. Briefly describe the different types of retinal 6. What are the considerations for general anesthesia?
detachment repairs. 7. What is the oculocardiac reflex, and how is it
3. Which patients are at risk for retinal detachment? treated?
4. What are the advantages and disadvantages of 8. What is the implication of injecting a “gas bubble”
general anesthesia versus regional anesthesia? into the eye?
A 36-year-old man presented for repair of right retinal de- 12-o’clock position, the patient would be required to re-
tachment. He had been hit in the eye with a baseball. The main in the upright position for 3–5 days.
patient was otherwise healthy, and he never had surgery. The purpose of the scleral buckle is to change the
internal contour of the globe by external manipulation.
1. What are the different types of retinal The inward displacement of the external tissue by the
scleral buckle closes the retinal disruption, preventing
detachment?
the passage of liquefied vitreous into the subretinal space.
There are three types of retinal detachments: rhegmatog- It is controversial whether or not draining the subretinal
enous, exudative, and tractional. Rhegmatogenous is the fluid should be done during the procedure. Proponents
most common type and is caused by disruption of the of draining the fluid believe that the decreased intraocu-
retina, allowing fluid to enter the subretinal space. Exuda- lar volume allows for the inward displacement by the
tive retinal detachment is rare and occurs when there is an scleral buckle without increasing intraocular pressure;
accumulation of fluid in the subretinal space without an this also allows the detached retina to rest on the scleral
obvious disruption of the retina. Tumors in the layers buckle, facilitating reattachment.
beneath the retina, such as choroidal melanoma, produce Vitrectomies involve removal of vitreous gel, relieving
exudative retinal detachment. The third type of retinal traction on the detached portion of the retina. Sometimes
detachment is a tractional detachment that occurs when the release of traction is insufficient to allow the retina to
fibrous or fibrovascular tissue caused by injury or inflam- reattach. After vitrectomy, vitreous gel is replaced with
mation pulls the retina away from subretinal layers. silicone oil or a “gas bubble” to restore normal pressure in
the eye. Depending on the size and location of the retinal
2. Briefly describe the different types of retinal detachment, pneumatic retinopexy may also be necessary.
detachment repairs.
3. Which patients are at risk for retinal
Methods employed for repair of retinal detachments detachment?
are scleral buckle, pneumatic retinopexy, or vitrectomy.
In some instances, more than one method is necessary. Several conditions predispose patients to retinal detach-
The endpoint of all of these procedures is to repair the ments. Among the ocular conditions associated with retinal
interruption of the retina, create an adhesion between detachments, high myopia (! 6.0 diopter) is associated
the retinal pigment epithelium and the retina, and pre- with almost a threefold increase in incidence. Retinal
vent recurrence of the detachment. detachment is a known complication of cataract surgery.
Surgical approaches vary depending on the method Cytomegalovirus retinitis, most often seen with acquired
selected. Although pneumatic retinopexy and vitrectomy immunodeficiency syndrome (AIDS), predisposes patients
are intraocular procedures, scleral buckles are extraocu- to retinal detachments. Ocular trauma is the cause of
lar. Pneumatic retinopexy involves injection of a “gas 10%–15% of retinal detachments and is the most common
bubble” into the vitreous cavity followed by cryopexy or cause in children. Another common cause of retinal
laser photocoagulation to seal the retinal detachment. detachment in children is retinopathy of prematurity.
After the procedure is completed, the patient is posi- Patients with a history of retinal detachment from intra-
tioned so that the “gas bubble” is abutting the repaired ocular pathology in one eye have a significant risk of retinal
retina. For example, if the retinal detachment is in the detachment in the other eye.
199
200 SECTION 7 Eye, Ear, Nose, and Throat
4. What are the advantages and disadvantages of and respiratory and cardiac arrest. The management of
LAST is described in Chapter 52.
general anesthesia versus regional anesthesia?
Advantages of general anesthesia include the following:
Selecting the appropriate anesthetic for any retinal sur- • Provision of ideal operating conditions such that the
gery should be specific to each patient, the underlying patient remains motionless for the duration of the
medical conditions, and the intended procedure. Discus- procedure
sion with the ophthalmologist regarding surgical needs • Anesthesia can continue for as long as needed in
and patient expectations also helps in deciding what type cases where surgery is prolonged
of anesthesia would be best suited. Disadvantages of general anesthesia include the fol-
There are several methods of providing adequate lowing:
operating conditions using regional anesthesia (retrobul- • Inaccessible airway, although it is secured
bar, peribulbar, sub-Tenon block) with or without seda- • Disruption of the surgical repair
tion. However, because some of these complex repairs may • Coughing or “bucking” during emergence and
take !2 hours and patients may be unable to tolerate lying extubation
motionless, it may be necessary to provide general anes- • Vomiting or retching in postoperative period
thesia to ensure patient safety, satisfaction, and the best • Increased time to surgical start
opportunity for a good surgical outcome (Table 41-1). • Increased time for emergence
Advantages of regional anesthesia include the fol- • Increased time spent in the postanesthesia care unit
lowing: (PACU)
• Shorter time in the operating room
• Shorter postoperative recovery times 5. What are the different regional anesthesia options?
• Reduced stress response
• Avoidance of undesirable side effects (e.g., nausea Regional anesthesia options are retrobulbar, peribulbar,
and vomiting) of general anesthesia and sub-Tenon block. Retrobulbar and peribulbar blocks
• Minimized risk of exacerbating cognitive dysfunc- are most commonly performed. Retrobulbar and peribul-
tion in patients with preexisting cognitive deficits bar blocks achieve anesthesia by a conduction block of the
Disadvantages of regional anesthesia include the intraorbital sensory divisions of the ophthalmic branch of
following: the trigeminal nerve. The difference between these blocks
• Unsecured and inaccessible airway is needle placement. Retrobulbar blocks are performed
• Uncooperative patient requiring escalating sedation posterior to the globe inside the cone comprising the extra-
that may result in respiratory depression ocular muscles. Peribulbar injections are performed out-
• Incomplete analgesia side this muscle cone and are dependent on spread of the
• Surgery outlasting analgesic duration local anesthetic. Sub-Tenon block is performed by making
• Ocular injury from patient movement a small entrance wound through the conjunctiva and Tenon
Regional techniques are not without risks. Minor risks capsule. A small amount of local anesthetic is injected intra-
include corneal abrasions and chemosis. More serious ocularly. The choice of block is based on personal prefer-
problems include permanent visual loss from perforation ence. All three blocks are effective.
of the globe especially in myopic patients, injury to the
optic nerve, and retrobulbar hemorrhage. Local anes- 6. What are the considerations for general anesthesia?
thetic systemic toxicity (LAST) occurs from either direct
vascular injection or spread of local anesthetic along the No specific general anesthetic has been shown to be more
dural sheath of the optic nerve into the cerebrospinal beneficial than others for retinal surgery. Nevertheless,
fluid. Manifestations of LAST may result in drowsiness, there are several issues to consider when planning the
temporary blindness of the contralateral eye, seizures, appropriate technique (Table 41-2).
Regional Anesthesia g Time in operating room Ocular injury from patient movement
g Stress response Unsecured, inaccessible airway
Faster recovery Incomplete analgesia
Avoid nausea and vomiting Surgery outlasts block analgesia
g Risk of cognitive dysfunction in susceptible patients
LMA, Laryngeal mask airway; N2O, nitrous oxide; PACU, postanesthesia care unit; PONV, postoperative nausea and vomiting;
RAE, Ring-Adair-Elwyn; TIVA, total intravenous anesthesia.
Airway
• Gasserian ganglion
To allow for unobstructed access to the surgical field, oral • Efferent limb—vagus nerve
Ring-Adair-Elwyn (RAE) tubes and flexible laryngeal The reflex is typically triggered preoperatively or in-
mask airways (LMAs) are popular choices for securing traoperatively. Preoperatively, pressure on extraocular
the airway. Because the airway is inaccessible during sur- muscles during retrobulbar or peribulbar block can pre-
gery, care should be taken to secure the artificial airway cipitate the reflex. Intraoperatively, pressure or traction
correctly and adequately. on the globe can produce the reflex. The most common
manifestation is severe bradycardia. However, cardiac
Nitrous Oxide dysrhythmias including junctional rhythm, ectopic atrial
rhythm, atrioventricular blockade, ventricular bigeminy,
In procedures where a “gas bubble” is to be injected, it multifocal premature ventricular contractions, wandering
is important to avoid using nitrous oxide (N2O). (See pacemaker, idioventricular rhythm, ventricular tachycar-
Question 8 for detailed explanation.) According to some dia, and asystole all have been described.
literature, N2O has been associated with postoperative The oculocardiac reflex is treated either prophylactically
nausea and vomiting (PONV). Avoiding N2O would be or symptomatically with an anticholinergic. Additionally,
recommended in patients at high risk for PONV and in surgical stimulation should cease until the arrhythmia has
cases that may result in disruption of the surgical inter- resolved.
vention from the physiologic consequences of increased
intraocular pressure from vomiting. 8. What is the implication of injecting a “gas
bubble” into the eye?
Emergence
N2O, because of its solubility, enters the “gas bubble”
Avoiding coughing or “bucking” during emergence and and causes an increase in volume; this results in an in-
extubation (or removal of the LMA) is important because crease in intraocular pressure and may compromise
it may result in disruption of the surgical repair. There are retinal circulation. N2O should be avoided in these
many different strategies to accomplish this; total intrave- cases. Because the “gas bubble” may remain in the
nous anesthesia (TIVA) with propofol may be of benefit. eye for 10–28 days, any subsequent general anesthetic
during this time period should not include N2O.
Nausea and Vomiting Patients are given an identification bracelet delineating
this information in the event they need surgery during
Avoiding PONV is important in these cases. PONV not this time.
only results in delayed PACU discharge and patient dis-
satisfaction, but, more importantly, vomiting or retching
may cause disruption of the surgical repair. Strategies
for reducing PONV include administering multimodal SUGGESTED READINGS
antiemetic therapy and TIVA with propofol.
Kreissig I: Surgical techniques for repair of primary retinal detachment,
part I: review of their development during the last 80 years. Folia Med
7. What is the oculocardiac reflex, and how is (Plovdiv) 51:5, 2009.
Kumar C, Dowd T: Ophthalmic regional anaesthesia. Curr Opin
it treated? Anesthesiol 21:632, 2008.
Moster MR, Azuara-Blanco A: Ocular anesthesia in the new millennium.
The oculocardiac reflex consists of the following: Ophthalmol Clin North Am 13:131, 2000.
• Afferent limb—ophthalmic division of the trigeminal Yanoff M, Duker J (eds.): Ophthalmology, 3rd edition. Mosby, St. Louis,
nerve 2008.
CASE 42
Tympanomastoidectomy
Cheryl K. Gooden, MD, FAAP
QUESTIONS
A 28-year-old woman with a history of chronic conductive 3. What are the intraoperative requirements
hearing loss presents for right tympanomastoidectomy. for tympanomastoidectomy?
Pertinent surgical anatomy is very small, necessitating
1. Why is tympanomastoidectomy performed?
magnification. Bleeding into the surgical field readily
When the eustachian tube malfunctions, a vacuum obscures the view through operating microscopes. Conse-
is created in the middle ear. This vacuum is usually quently, it is crucial to minimize intraoperative bleeding.
associated with chronic upper respiratory infections Because injury to the facial nerve is a major concern,
and allergies. The vacuum causes suction on the tym- facial nerve electromyography may be used during
panic membrane that is already weakened by recurrent tympanomastoidectomy. This monitoring necessitates a
infections. The result can be cholesteatoma, which is motionless patient in the absence of neuromuscular
an abnormal growth of primarily skin cells that occurs blocking agents.
behind a perforated tympanic membrane. Damage to During surgery, the head of the operating room table is
nearby bone surrounding the ear is a likely conse- turned 90–180 degrees away from the anesthesia machine.
quence of cholesteatoma. Associated symptoms include In addition, the patient’s head and neck are rotated to the
progressive hearing loss, dizziness, facial nerve damage, opposite side from the operative field. It is important to
and central nervous system infections with extension ensure the following:
into the brain. Tympanomastoidectomy is performed • Anesthetic circuit and monitoring cables are
to remove cholesteatoma and infected bone from the appropriately long
middle ear. • Neck is not hyperextended
Surgical treatment consists of an incision made behind • Dependent ear and eye are free of excessive pressure
the ear, opening the mastoid and exposing the middle ear.
Cholesteatoma or infected tissues or both are removed. 4. Are inhalation or intravenous anesthetic agents
The tympanic membrane is patched, and packing is preferred during tympanomastoidectomy?
placed in the external auditory canal.
The choice of inhalation anesthetic agents versus total in-
2. What the preoperative anesthesia considerations travenous anesthesia (TIVA) and whether one is more
advantageous than the other for middle ear surgery remain
are associated with tympanomastoidectomy?
controversial. Similar intraoperative hemodynamics can
Anesthesia assessment before tympanomastoidectomy be obtained with either intravenous or inhalation agents.
does not differ much from basic anesthesia assessment. The theoretic advantage of TIVA with propofol is the
Issues specific to middle ear disease should be addressed. possibility of less nausea and vomiting.
Decreased hearing acuity or use of hearing aids can make
communication challenging. Common manifestations of 5. Is nitrous oxide contraindicated during
middle ear–related disorders include nystagmus, vertigo, tympanomastoidectomy?
nausea, and vomiting. A history of motion sickness
or postoperative nausea and vomiting (PONV) is an It is probably best to avoid nitrous oxide (N2O) during
important issue to consider in the anesthetic plan. tympanomastoidectomy. N2O is 31 times more soluble in
202
42 Tympanomastoidectomy 203
blood (blood gas coefficient 0.47) than nitrogen (blood 7. What are the postanesthesia care unit concerns
gas coefficient 0.015). As a result, N2O diffuses into a
after tympanomastoidectomy?
closed air space (e.g., intestines, pneumothorax) more
rapidly than nitrogen diffuses out, causing expansion In the postanesthesia care unit (PACU), the most common
of the air space. Because the middle ear is a natural problems encountered after tympanomastoidectomy are
air space, middle ear pressure increases when N2O is nausea, vomiting, and vertigo. Although patients may
administered as part of the anesthetic technique; this is experience pain during recovery in the PACU, it tends to
particularly problematic in the presence of a blocked be less of an issue compared with PONV and vertigo.
eustachian tube. In this procedure, the tympanic mem- Most pain associated with tympanomastoidectomy occurs
brane graft may become dislodged by increased middle during the intraoperative phase as opposed to the recovery
ear pressure. Another consideration for avoiding N2O phase. Care in the PACU should be tailored to meet each
during tympanomastoidectomy is the loose association patient’s individual needs. Management may include hy-
between it and PONV and postdischarge nausea and dration, drug therapy, quiet, and avoiding rapid elevation
vomiting. of the head of the patient’s bed.
QUESTIONS
1. What are the predictors of difficult mask ventilation? cannot be intubated with a Macintosh blade; the
2. Discuss the risk factors for difficult intubation. patient has a good mask airway.
3. Are the risk factors for difficult intubation reliable 6. After induction of anesthesia, ventilation by
predictors of difficult intubation? facemask and intubation are impossible; what
4. How is an anticipated difficult intubation maneuvers may help?
approached? 7. How is successful tracheal intubation verified?
5. Describe the management options for a patient 8. After a difficult intubation, how is postoperative
who, after induction of anesthesia, unexpectedly extubation managed?
A 76-year-old man presents for endoscopic vocal cord duct cyst. Many of these problems cannot be detected by
injections. He underwent general anesthesia many years classic airway examination techniques. The presence of
ago without any known problems. The old records are any one factor is suggestive of difficult mask ventilation.
unavailable. He has limited translation of the temporo- The more factors present at the same time, the greater
mandibular joint. Otherwise, his airway examination is the likelihood of difficulty. Increased mandibulohyoid
within normal limits. distance has been associated with obstructive sleep apnea,
the pathophysiology of which may be related to difficult
1. What are the predictors of difficult mask mask ventilation.
Traditional facemask airway management is gener-
ventilation?
ally safe and effective. In the unusual instances when it
One of the most important predictors of a difficult airway is not, tracheal intubation remains the fallback option.
is a history of a difficult airway. The opposite is not al- Although this scheme works well in most cases, approxi-
ways true. A history of problem-free airway management mately 15% of difficult intubations are also difficult
is suggestive of future ease, but it is not a guarantee. mask airways.
Many factors that contribute to difficulty are progressive.
Examples of such problems include rheumatoid arthritis
and obesity. An airway history is recommended for all 2. Discuss the risk factors for difficult intubation.
patients. Review of prior anesthesia records is frequently Sniffing Position
helpful. They may describe previously encountered
problems, failed therapies, and successful solutions. The presence or absence of airway pathology does not
Difficult facemask ventilation occurs when a practi- influence the definition of difficult tracheal intubation. It
tioner cannot provide sufficient gas exchange because of occurs when multiple attempts at intubation are required.
inadequate mask seal, large volume leaks, or excessive Traditional laryngoscopy is performed to visualize the la-
resistance to the ingress or egress of gas; this occurs with ryngeal opening. The laryngoscopist is positioned outside
an incidence of 0.08%–5%. The wide range is probably the airway, above the patient’s head. To see the airway,
due to conflicting definitions of difficult mask airway. light must travel from the glottic opening to the laryngos-
Risk factors (Box 43-1) for difficult mask ventilation copist’s eye. This technique requires an uninterrupted
include a full beard, a massive jaw, edentulousness, skin linear path between the larynx and laryngoscopist because
sensitivity (burns, epidermolysis bullosa, fresh skin light generally travels in straight lines. Most manipula-
grafts), facial dressings, obesity, age !55 years, and a his- tions performed attempt to satisfy this criterion.
tory of snoring. Other criteria that suggest the possibility The airway contains three visual axes—the long axes
of difficult facemask ventilation include a large tongue, of the mouth, oropharynx, and larynx. In the neutral
heavy jaw muscles, a history of obstructive sleep apnea, position, these axes form acute and obtuse angles with
poor atlanto-occipital extension, some types of pharyngeal one another. Light cannot bend around these angles
pathology, facial burns, and facial deformities. Multiple under normal circumstances. To bring all three axes into
types of pharyngeal problems can produce difficult face- better alignment, Magill suggested the “sniffing the
mask ventilation, including lingual tonsil hypertrophy, morning air” position. True sniffing position requires
lingual tonsillar abscess, lingual thyroid, and thyroglossal both cervical flexion and atlanto-occipital extension.
204
43 The Difficult Airway 205
Tongue After filling the mandibular space with the tongue, ad-
ditional pressure on the laryngoscope blade lifts the man-
The tongue occupies space in the mouth and oropharynx. dible anteriorly. In this setting, mandibular displacement is
The base of the tongue resides close to the glottic aper- dependent on the TMJ. In addition to its hingelike motion,
ture. During traditional direct laryngoscopy, the base of the TMJ works in a gliding (translational) movement. The
the tongue falls posteriorly obstructing the line of sight gliding motion allows the mandible to slide anteriorly
into the glottis. Visualizing the larynx requires displacing across the maxilla. If the joint does not translate, the man-
the base of the tongue anteriorly so that the line of sight to dible cannot be displaced anteriorly, and the tongue cannot
the glottis is restored. The tongue is frequently displaced be moved out of the line of sight.
with a handheld rigid laryngoscope, to which Macintosh Recognizing the implications of tongue size to success-
and Miller blades are most commonly attached. Laryngo- ful laryngoscopy, Mallampati et al. in 1985 and Samsoon
scopes push the tongue anteriorly and in so doing, move it and Young in 1987 devised classification systems to pre-
from a posterior obstructing position to a new anterior dict difficult laryngoscopy using this concept. A difficult
nonobstructing position within the mandibular space. The laryngoscopy occurs when it is impossible to visualize any
mandibular space is the area between the two rami of the portion of the vocal cords. Mallampati and Samsoon rea-
mandible. Even with the tongue maximally displaced into soned that a large tongue could be identified on visual
the mandibular space, visualization of the larynx is some- inspection of the open mouth. Both classification systems
times inadequate. relate the size of the tongue to the oropharyngeal struc-
Usually, a normal-size tongue fits easily into a tures identified. A normal-size tongue allows for visualiza-
normal-size mandibular space, whereas a large tongue tion of certain oropharyngeal structures. As the tongue
would fit poorly. After filling the space, a large tongue size increases, some structures become hidden from view.
still occupies some of the oropharyngeal airway causing Consequently, both investigators proposed systems that
obstruction. For this reason, a large tongue (macroglos- reason backward from this premise.
sia) is a predictor of a difficult intubation. Similarly, a Application of the Mallampati or Samsoon classifica-
normal-size tongue fits poorly into a small mandibular tion system is easy and painless. The patient is seated in
space. Consequently, it occupies some of the oropha- the neutral position and asked to open the mouth wide and
ryngeal airway, obstructing the line of sight. For this protrude the tongue as much as possible without phona-
reason, a small mandible (micrognathia) is a predictor of tion. Phonation is discouraged because it raises the soft
difficult intubation. In essence, a tongue that is large palate and allows for visualization of additional structures.
compared with the size of the mouth, oropharynx, and The observer looks for specified anatomic landmarks: the
mandible takes up excessive space in the oropharynx fauces, pillars, uvula, and soft palate. The Mallampati clas-
and interferes with visualization. sification system uses three groups, and the Samsoon clas-
The base of the tongue resides so close to the larynx sification system uses four groups (Figure 43-1). Both
that inability to displace it adequately anteriorly creates systems suggest that as the tongue size increases, fewer
another problem. The base of the tongue hangs down over structures are visualized, and laryngoscopy becomes more
the larynx, and the glottis is hidden from view. The glottic difficult. Mallampati scores tend to be higher in pregnant
aperture is anatomically anterior to the base of the compared with nonpregnant patients.
tongue—hence the term “anterior larynx.” Under such Just as the size of the tongue can be estimated, so too
circumstances, the larynx is anterior to the base of the can the size of the mandible. This estimation is accom-
tongue and cannot be seen because the tongue hides it. plished by asking the patient to extend the head at the
Glottic and supraglottic masses that force the base of tongue atlanto-occipital joint and identifying the mandibular
posteriorly can create difficult intubations as well. Some of mentum and thyroid cartilage. The thyroid notch (Adam’s
the masses that may be encountered include lingual tonsils, apple) is the most superficial structure in the neck
epiglottic cysts, and thyroglossal duct cysts. and serves as a good landmark for the thyroid cartilage.
FIGURE 43-1 ■ Samsoon classification of pharyngeal structures. (From Samsoon GLT, Young JRB: Difficult tracheal intubation: a retrospective
study. Anaesthesia 42:487, 1987.)
43 The Difficult Airway 207
The vocal cords lie just caudad to the thyroid notch. The
TABLE 43-1 Predictors of Difficult Intubation
distance between the thyroid cartilage and mentum (thy-
romental distance) is measured in one of three ways. The
Factors That Suggest Difficult
measurement can be made with a set of spacers, a small Criteria Intubation
pocket ruler, or the observer’s fingers. The normal thyro-
mental distance is 6.5 cm. A thyromental distance !6 cm History History of difficult intubation
is predictive of an easy intubation. A thyromental dis- Length of upper Relatively long
tance "6 cm is suggestive of a difficult intubation. Rulers incisors
often are not present at the bedside. In the absence of a Interincisor distance #3 cm (#2 fingerbreadths)
ruler, practitioners can judge the thyromental distance
with their fingers. By knowing the width of one’s middle Overbite Maxillary incisors override
mandibular incisors
three fingers, which frequently approximates 6 cm, the
thyromental distance can be compared with the fingers’ TMJ translation Inability to extend mandibular
span. In this way, clinically relevant approximations can incisors anterior to maxillary
incisors
be taken into account when examining patients for the
purpose of predicting difficult intubation. The usefulness Mandibular space Small, indurated, encroached on
of predicting difficult intubation based on thyromental by mass
distance has been challenged. Data from Rocke et al. Cervical vertebral Cannot touch chin to chest or
(1992) and El-Ganzouri (1996) show that a decreased range of motion cannot extend neck
thyromental distance (receding mandible) offers a "7% Thyromental distance #6 cm (#3 fingerbreadths)
probability of predicting difficult intubation. Chou
Mallampati/Samsoon Mallampati III/Samsoon IV
(1993) and Brodsky et al. (2002) described patients whose classification Relatively large tongue
thyromental distances were !6.5 cm and who were dif- Uvula not visible
ficult intubations.
Neck Short, thick
Similar measurements and predictions have been
made using the hyoid bone and mandible as well as the Palate shape High arched or very narrow
sternum and mentum. Chou and Wu (2001) suggested
TMJ, Temporomandibular joint.
that a long mandibulohyoid distance predicts a large Adapted from American Society of Anesthesiologists Task Force on
hypopharyngeal tongue, which hides the glottis during Difficult Airway Management: Practice guidelines for management
laryngoscopy and produces a difficult intubation. They of the difficult airway. Anesthesiology 118:251, 2013.
reasoned that the tongue is hinged to the hyoid bone so
that a long hyomandibular length represents a caudad-
lying tongue. With the base of the tongue positioned
farther inferiorly, it occupies more space in the oropha-
ryngeal airway. Consequently, it obstructs the laryngos- 3. Are the risk factors for difficult intubation reliable
copist’s line of sight. The hyoid bone is more difficult
predictors of difficult intubation?
to feel than the thyroid cartilage and is often impossible
to locate. The sternum and mentum are generally easy to Although it makes intuitive sense to perform and is consis-
find, but the sternomental distance has not been sub- tent with best medical practices, airway evaluation frequently
stantiated as a good predictor of difficult intubation by falls short of its intended goal. Numerous rating systems
other investigators. based on recognized prediction criteria have been investi-
The ability to translate the TMJ is easily assessed gated. Most have recurrent problems.
before induction. The patient is asked to place the man- The first problem is nomenclature. A standardized
dibular incisors (bottom teeth) in front of the maxillary definition of a “difficult airway” did not exist until 1993.
incisors (upper teeth). Inability to perform this simple At that time, it was explained as a situation in which
task is usually from one of two sources. First, the TMJ a conventionally trained anesthesiologist experienced
may not glide, predicting a difficult intubation. Second, difficulty with mask ventilation, difficulty with tracheal
some patients find it difficult to coordinate the maneu- intubation, or both. For years, individual investigators
ver, in which case there is no implication for a difficult needed to establish their own definition of “difficult intu-
intubation. bation” each time studies were conducted. Consequently,
The upper lip bite test was proposed as a modification the endpoints of their work were not comparable with
of the TMJ displacement test. The upper lip bite test is other investigations in the field, making comparative anal-
performed by asking the patient to move the mandibular ysis of studies impossible. In 1993, the American Society
incisors as high on the upper lip as possible. The maneu- of Anesthesiologists (ASA) Committee on Practice Guide-
ver is similar to biting the lip. Contact of the teeth above lines for Management of the Difficult Airway offered
or on the vermilion border is thought to predict adequate a generally acceptable definition. The definition was
laryngoscopic views. Inability to contact the vermilion altered slightly 10 years later. In 2013, “difficult tracheal
border is thought to predict poor laryngoscopic views. intubation” referred to any intubation that required
Both the TMJ translation test and the upper lip bite test multiple attempts. This is a good clinical definition but
assess TMJ glide, which is an important consideration lacks the precision required for scientific investigation.
during laryngoscopy. Table 43-1 summarizes a quick, For example, some practitioners may perform a single
easy, bedside scheme for predicting difficult intubation. laryngoscopy and, based on the view obtained, elect to
208 SECTION 7 Eye, Ear, Nose, and Throat
forego further attempts at laryngoscopy. Such cases may entire patient population. For example, take a patient
be handled with a supraglottic airway device, regional population in which five patients are difficult to intubate.
anesthesia, or other techniques. This situation does not If a particular predictor of difficult intubation correctly
meet the definition of difficult intubation, when in fact it identifies all five patients, its sensitivity is 100%. If the
would have if one more attempt at intubation was per- test correctly identifies only two of the five patients, its
formed. The ASA definition serves as a good clinical sensitivity is 2/5 or 40%. Positive predictive value is the
understanding of difficult intubation but lacks the rigid, probability that difficult intubation patients identified
encompassing concerns required for scientific investiga- by the test are in fact difficult to intubate. If the test pre-
tion. “Failed intubation” is an easier term to understand. dicts that five patients will be difficult to intubate and
A failed intubation exists when laryngoscopists give up all five of those patients are difficult to intubate, its posi-
and admit that traditional intubation techniques would tive predictive value is 100%. If the test predicts that
not be successful. The endpoint is clear and occurs with 10 patients will be difficult to intubate but only 5 of them
an incidence of 1:280 in obstetric patients and 1:2230 in are difficult to intubate, its predictive value is 5/10 or
the general operating room population. 50%. As Yentis (2002, 2006) pointed out on more than
The second problem is identifying features that pre- one occasion, statistical tests such as sensitivity and posi-
dict difficult intubation; this is frequently accomplished tive predictive value applied to classic prediction criteria
by attempting to recognize characteristics found in pa- have yielded disappointing results.
tients who have proven to be difficult intubations. The In 1984, Cormack and Lehane described a grading
problem with such an approach is the lack of informa- system for comparing laryngoscopic views as follows:
tion about the same characteristics in patients who are Grade I—the entire glottic opening
easy intubations. As Turkan pointed out, we do not even Grade II—the posterior laryngeal aperture but not the
know the normal values for many prediction criteria. anterior portion
A better method is to apply multivariate analysis to Grade III—the epiglottis but not any part of the
patient populations in a prospective manner. In that larynx
way, a single factor can be compared for difficult and Grade IV—the soft palate but not the epiglottis
easy intubations. Various rating systems attempt to Early evidence indicated good correlation between
combine multiple predictors into a formula. To date, Mallampati/Samsoon classes and laryngoscopic grades. In
none has been satisfactory. other words, as the Mallampati/Samsoon classes increased
The third problem is validating the tests once they are in number, the prediction was that corresponding laryn-
promulgated. Validation tests performed on the same pa- goscopic grades would also increase in number for any
tient population used to identify them are misleading. This given patient. This concept formed the basis for using
is like counting the number of envelopes in a particular Mallampati/Samsoon classes to predict difficult intuba-
mailbox, predicting that all mailboxes contain that number tion. In 1992, Rocke et al. disproved that relationship.
of envelopes, and then validating the prediction by re- Rocke et al. investigated several classic predictors of dif-
counting the envelopes in that same mailbox. Validation ficult intubation and demonstrated that none of the ones
must be performed by counting the envelopes in multiple they studied was reliable predictors of difficult intubation
different mailboxes. In the same way, validation of difficult (Figure 43-2). More recently, Shiga and Langeron inde-
intubation predictors must be performed in multiple differ- pendently agreed. Classic prediction criteria essentially
ent patient populations. The experimental patient sample deal with surface anatomy. They screen for some factors
cannot be used to validate experimental results. Different that are associated with difficult intubation but fail to ad-
sample populations are needed for that. dress others. Some potential problems are hidden from
The fourth problem is the experimental methods. surface anatomy examinations. Subglottic, glottic, and
Individual practitioners differ, and clinical practice has supraglottic abnormalities, such as tracheal stenosis, lin-
shown that a particular patient who is difficult to intubate gual tonsil hypertrophy, or epiglottic prolapse into the
in the hands of one laryngoscopist may be successfully glottic opening, cannot be diagnosed by standard physical
intubated by another laryngoscopist. In this way, experi- examinations for predicting difficult intubation. Patho-
mental designs using more than one laryngoscopist physiologic factors such as mobile TMJ disks or disk frag-
introduce a source of variation, which detracts from ments can produce severely limited mouth opening after
attempts to control experimental conditions. Relying on induction of anesthesia, when none existed before. Precise
a single laryngoscopist obviates this problem but limits measurements of atlantoaxial motion sometimes fail to
the number of patients that can be enrolled into a single predict difficult intubation. These factors and others may
study. Another source of experimental error is observer be unrecognized by standard tests but complicate intuba-
variation. Observations performed by different experi- tion nonetheless. At the time of this writing, no single
menters are subject to variations and introduce another factor reliably predicts difficult intubation. The likelihood
source of erroneous data. The best way to prevent this of a difficult intubation increases when multiple predic-
problem is for all observations to be performed by a tors are present in a patient at the same time.
single experimenter. This too may limit the number of
patients enrolled in a single study. 4. How is an anticipated difficult intubation
Statistical tests for assessing the usefulness of criteria approached?
include sensitivity and positive predictive value. Sensitiv-
ity is the ratio of correctly identified difficult intubation Anticipated difficult intubations with proven or sus-
patients to all the difficult intubation patients within the pected difficult mask ventilation are best approached
43 The Difficult Airway 209
Class I (29.3%)
Class II (34.9%)
Class III (15.8%)
Class IV (3.7%)
I + SN (2.1%)
I + PI (0.2%)
I + RM (0.2%)
I + SN (5.7%)
II + PI (0.3%)
II + RM (0.4%)
III + SN (5.4%)
III + PI (0.07%)
III + RM (0.07%)
IV + SN (1.2%)
IV + PI (0.07%)
IV + RM (0.13%)
I + SN + PI (0%)
I + SN + RM (0.07%)
I + RM + PI (0%)
II + SN + PI (0.2%)
II + SN + RM (0.13%)
II + RM + PI (0%)
III + SN + PI (0.07%)
III + SN + RM (0%)
III + RM + PI (0%)
IV + SN + PI (0%)
IV + SN + RM (0%)
IV + RM + PI (0%)
I + SN + RM + PI (0%)
II + SN + RM + PI (0%)
III + SN + RM + PI (0%)
IV + SN + RM + PI (0%)
0 10 20 30 40 50 60 70 80 90 100
FIGURE 43-2 ■ Probability of experiencing a difficult intubation for combinations of risk factors and their observed incidence (percent-
ages). PI, Protruding maxillary incisors; RM, receding mandible; SN, short neck. (From Rocke DA, Murray WB, Rout CC, Gouws E: Rela-
tive risk analysis of factors associated with difficult intubation in obstetric anesthesia. Anesthesiology 77:67, 1992.)
with the patient awake and spontaneously breathing. Blind techniques, retraction blades, and fiberscopes are
Proper preparation of the airway before instrumentation commonly employed. Friable tumors, abscesses, and im-
is critical. Preparation begins approximately 1 hour be- pending obstructive airway tumors often require awake
fore arrival in the operating room. At that time, antisiala- tracheostomy.
gogues are administered as premedication. Their use is
intended to desiccate the mucosa before administration 5. Describe the management options for a patient
of topical local anesthetics. An intervening layer of secre- who, after induction of anesthesia, unexpectedly
tions acts as a physical barrier preventing contact be- cannot be intubated with a Macintosh blade; the
tween local anesthetic and mucosa. Without direct con-
patient has a good mask airway.
tact of the two, inadequate airway anesthesia results and
predisposes the patient to coughing, gagging, and with- Having induced general anesthesia in a patient and then
drawal. Copious secretions impair the view through flex- discovered a difficult intubation, it is imperative to main-
ible fiberoptic laryngoscopes. Depending on the degree tain oxygenation and ventilation. This is generally accom-
of preexisting airway compromise, preoperative sedation plished with a facemask and 100% oxygen. Successful
may be contraindicated. oxygenation during controlled ventilation and oxygen
After adequate antisialagogue effect, airway anesthesia desaturation during intubation attempts are monitored
is most easily achieved by nebulizing 4 mL of 4% lido- with pulse oximetry. During traditional laryngoscopy,
caine. Another equally effective option is to atomize the external posterior or lateral displacement of the larynx
same solution. Superior laryngeal nerve blocks and trans- may bring it into view. Improved sniffing position may be
tracheal nerve blocks are sometimes required. If the nasal helpful.
approach is planned, the risk of epistaxis can be mini- A multitude of retraction blades exist and vary in
mized with topical application of 0.5% phenylephrine, length and shape. They are used to displace the base of
4% cocaine, or 0.05% oxymetazoline (Afrin). In the ab- the tongue and epiglottis anterior to the line of sight.
sence of local nasal pathology, flexible fiberoptic nasotra- The most familiar types are the Macintosh and Miller
cheal intubation is generally less difficult than the oral blades. Difficulty with the Macintosh blade often arises
route. when its tip fails to elevate the hyoid bone, which
After achieving satisfactory airway anesthesia, most in- indirectly raises the epiglottis. Often, a straight blade
tubation techniques progress well to successful completion. elevates a floppy epiglottis when curved blades fail to
210 SECTION 7 Eye, Ear, Nose, and Throat
do so. Difficulty with the straight blade frequently arytenoid. To overcome this obstacle, the tracheal tube
comes from impacting on teeth. Upper airway edema or should be retracted 1–2 cm and rotated 90 degrees coun-
adipose tissue may sometimes encroach on the view of terclockwise. This maneuver brings the tip anteriorly,
traditional retraction laryngoscopes, which are open on away from the right arytenoid.
the right side. After exhausting one’s personal repertoire of tech-
Various stylets may be used. The hollow stylet, niques, simply repeating methods that have already failed
gummed elastic bougie, or similar devices should be seems to have little chance of success. Additional instru-
available in all anesthetizing locations. mentation leads to laryngeal and pharyngeal edema pre-
If a flexible fiberoptic laryngoscopy is not planned, disposing the patient to airway obstruction. Alternative
blind spontaneously breathing nasotracheal intubation options are listed in Box 43-2. Initial tracheostomy is indi-
is an alternative offering a good chance of success. cated for laryngeal fractures and for abscesses impinging
Vasoconstriction of the nasal mucosa, selection of a on the airway. The ASA Difficult Airway Algorithm serves
small nasal endotracheal tube (ETT) (6 mm), and gen- as a useful guideline (Figure 43-3).
erous lubrication of the tube’s distal portion are highly
recommended. If flexible fiberoptic intubation is 6. After induction of anesthesia, ventilation by
planned, the risk of epistaxis may dissuade one from facemask and intubation are impossible; what
the nasal approach. Epistaxis might seriously impair maneuvers may help?
mask ventilation and visualization by all means of
laryngoscopy. Inability to ventilate and intubate is a rare occurrence
Compared with various retraction blades and stylets, with a potentially tragic outcome. Several treatment op-
flexible fiberoptic laryngoscopy has established a long tions exist. Various oral and cricoid puncture methods
and impressive success record with difficult intubations. have been described to assist with such situations.
Flexible fiberoptic laryngoscopy is applicable to anesthe- Of the oral techniques, worldwide experience is
tized and awake patients. In an anesthetized patient, it greatest with laryngeal masks of various designs. The
can be performed with interrupted controlled ventilation laryngeal mask is a tube attached to a mask. The mask
by facemask, such as with traditional rigid laryngoscopy. has an inflatable balloon around its periphery. With the
Alternatively, it can be accomplished using simultaneous balloon deflated, the mask is advanced into the mouth
controlled ventilation via anesthesia facemasks equipped and through the airway until obstruction to passage is
with a self-sealing diaphragm. Flexible fiberoptic intuba- encountered. At this point, the mask should be posi-
tion in a paralyzed patient is generally more difficult than tioned cephalad to the esophagus and surrounding the
in a spontaneously breathing patient because the anterior larynx. The balloon is inflated in an attempt to create an
pharyngeal wall tends to collapse onto the posterior airtight chamber around the larynx. The tube exits from
pharyngeal wall, obstructing the view. Also, the larynx as- the mouth and is connected to an anesthesia breathing
sumes a more anterior position, hindering its identifica- circuit.
tion. Copious blood or secretions seriously impair vision Laryngeal masks are available in adult and pediatric
through a flexible fiberoptic laryngoscope (FFL). FFLs sizes. The mask works well in 90%–98% of cases. This
contain suction channels, but in contrast to suction chan- 2%–10% failure rate is far greater than the incidence of
nels in the pulmonologist’s bronchoscope, the channel in inability to ventilate and intubate. Nevertheless, the LM
the FFL is an inefficient one. Consequently, aspiration of has been successfully used for airway management in
blood and secretions is better accomplished with a stan- elective surgery as well as in cases of predicted and un-
dard large-bore suction device, such as the one normally anticipated difficult intubation. The laryngeal mask has
used for traditional rigid laryngoscopy. Passing oxygen been used to assist blind intubation and FFL-guided
through the working channel of the FFL tends to push intubation in patients whose larynges could not be visu-
blood and secretions out of the way, prevents fogging, alized by traditional rigid laryngoscopy.
and enhances the patient’s effective fraction of inspired If the inflatable balloon of the laryngeal mask is not
oxygen (Fio2). The sniffing position allows for further positioned properly, a large gas leak occurs around the
posterior displacement of the epiglottis, which could also mask, impairing ventilation. This leak is exacerbated by
obstruct the view. Consequently, cervical extension with
the head flat on the bed is preferable for flexible fiberop-
tic laryngoscopy. BOX 43-2 Options for Failed Traditional
Various aids to FFL insertion exist. Care must be Tracheal Intubation under General
taken to seat oral airways exactly in the midline to pre- Anesthesia
vent lateral displacement of the fiberscope, which adds
to the difficulty of intubation. In cases for which it is Continue anesthesia by facemask
especially important to do so, none of the presently Continue anesthesia with supraglottic device
available oral intubation airways adequately elevates the Regional anesthesia
base of the tongue. Insertion of the nasotracheal tube Awake spontaneous breathing (usually flexible fiberoptic intu-
bation)
before the fiberoptic scope risks epistaxis. Placing naso- Same day
tracheal tubes too far eliminates adequate space for ma- Several days later after resorption of airway edema
nipulating the scope between the nasotracheal tube and Tracheostomy
the larynx. Difficulty threading tracheal tubes into Cricothyroidotomy
the larynx may arise if the tube’s tip abuts the right
43 The Difficult Airway 211
FIGURE 43-3 ■ American Society of Anesthesiologists Difficult Airway Algorithm. This algorithm is intended as a practice guideline for
difficult airway management. Practitioners are free to deviate from this algorithm as the need arises for each individual situation.
(From American Society of Anesthesiologists Task Force on Difficult Airway Management: Practice guidelines for management of the difficult
airway—an updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology
118:251, 2013.)
212 SECTION 7 Eye, Ear, Nose, and Throat
FIGURE 43-5 ■ Cricothyroid puncture ventilation equipment (transtracheal ventilation). Most basic equipment adapts to common
gas outlets on anesthesia machines or resuscitation bags. It consists of a 14-gauge over-the-needle catheter with Luer-Lok adapter,
noncompressible oxygen tubing, standard 15-mm connector, and a source of pressurized oxygen. (Source of pressurized oxygen is
not shown.)
43 The Difficult Airway 213
and provides a step-down valve to reduce pressures to 8. After a difficult intubation, how is postoperative
approximately 20 psi.
With the patient in the supine position, the head is
extubation managed?
extended to expose the anterior neck. The thyroid carti- Extubation requires an estimate of postoperative air-
lage is palpated, and the finger is run inferiorly until a way edema. Repeated instrumentation during intuba-
depression (the cricothyroid membrane) is felt. Another tion and surgical manipulation independently and
dense substance (cricoid cartilage) is appreciated just additively contribute to tongue base and laryngeal
caudad to the depression. A 14-gauge needle is placed
through the skin perpendicular to all planes and ad-
vanced until the cricothyroid membrane is punctured.
Proper positioning within the trachea is confirmed by
freely aspirating air through the needle. The needle is
BOX 43-3 Methods to Verify Correct
removed, leaving the catheter positioned in the lumen of
Tracheal Tube Placement
the trachea. The device is attached to the intravenous
catheter, and 100% oxygen is administered under posi- MOST RELIABLE
tive pressure. Oxygen administration is most conve- Direct visualization of tracheal tube between the vocal
niently accomplished by attaching the 15-mm connector cords
to the anesthesia machine’s common gas outlet and con- Observation of carina via a flexible fiberoptic laryngo-
trolling the flow of oxygen with the oxygen flush valve. scope passed through the tracheal tube
Not all anesthesia machines that offer a common gas
outlet function well in this circumstance. Ventilation VERY RELIABLE
systems using pressure step-down valves interposed be- Expired carbon dioxide detection by colorimetry or
tween high-pressure oxygen sources, such as wall oxygen capnography
or oxygen tanks, can be attached to the same cricothyroid Esophageal detector device
puncture catheter. The higher the pressure generated, RELIABLE
the more likely the catheter will become dislodged, so a Auscultation of breath sounds
designated holder must be assigned to keep it in place. After Observation of chest expansion and contraction during
insufflation of oxygen through the 14-gauge catheter, exha- inspiration and exhalation
lation occurs through the natural airway. Consequently, it is Epigastric auscultation and observation for gastric disten-
important to ensure upper airway patency. If upper airway tion during respiration
obstruction exists, gas cannot escape, and subsequent Tactile confirmation by assistant as ETT is passed
breaths stack, which risks pneumothorax. Respiratory bag inflation and deflation during spontaneous
If ventilation and intubation are impaired by tissues respiration
encroaching on the airway, rigid bronchoscopy may Respiratory bag compliance and spontaneous refilling
provide for immediate lifesaving ventilation and oxy- Exhaled gas via the tracheal tube during chest compression
Condensation and evaporation of water during respirations
genation. Alternatively, emergency tracheostomy can Tracheal tube cuff palpation at the suprasternal notch
be performed. Emergency tracheostomy performed Endobronchial intubation
by the anesthesia care team has a high failure rate. Pulse oximetry
Emergency tracheostomy performed by surgeons has a Chest radiograph
high success rate.
214 SECTION 7 Eye, Ear, Nose, and Throat
Laser Laryngoscopy
Allan P. Reed, MD
QUESTIONS
1. Is postoperative voice quality worthy of consider- 7. How does laser light differ from natural light?
ation by the anesthesia care team? 8. What types of lasers are most frequently used for
2. What criteria are used to evaluate the airway? medical care?
3. Explain the special anesthesia requirements for laryn- 9. What are the hazards of laser laryngoscopy?
geal microsurgery. 10. How are laser airway fires treated?
4. Describe an anesthetic for laryngeal microsurgery. 11. Discuss the recognized postoperative problems
5. What ventilatory modes are employed for endo- that occur after laryngeal surgery.
scopic laryngeal surgery?
6. What are the special considerations for singers and
other patients who use their voices professionally?
A 50-year-old singer presents for laser laryngoscopy. She Consequently, anesthesia-related voice complications
has vocal fold polyps but otherwise is in good general that prevent them from speaking can have substantial
health. consequences and are worthy of our attention.
1. Is postoperative voice quality worthy of 2. What criteria are used to evaluate the airway?
consideration by the anesthesia care team? Anesthesia societies in multiple countries recommend
The anesthesia care team generally focuses on major airway evaluation focusing on history and physical ex-
life-threatening issues. Preoperative and postoperative amination of surface landmarks. However, these recom-
hoarseness is a secondary concern. However, in the mendations ignore many sources of airway problems.
minds of patients who use their voices professionally, The location and size of pathologic airway lesions can
voice problems assume great importance. Phonosur- have significant effects on airway management. For
gery is dedicated to restoring voice quality. Singers, esophageal pathologies, such as obstructing lesions, and
actors, teachers, clergy, lawyers, politicians, and many gastrointestinal bleeding, the potential for aspiration
others use their voices professionally. These patients should be explored. Inspiratory stridor suggests airway
strive for the best quality sounds possible. Singers in stenosis approximately 4 mm in diameter. However, the
particular are anxious about laryngeal instrumentation, absence of stridor does not always indicate a normal-size
especially tracheal intubation. They are acutely aware airway, and stridor may be absent despite a very stenosed
of instances in which patients could not sing after ei- airway. Exhausted patients may not generate enough
ther brief or prolonged intubation. Intubation injuries airflow to produce stridor, even in the face of significant
to vocal folds are usually due to anatomic disruptions stenosis. Voice changes such as hoarseness are nonspe-
or neuromotor injury. Examples of anatomic disrup- cific and frequently result from small, nonobstructive le-
tions include vocal fold tears, intubation granuloma, sions or potentially from mediastinal lesions. Dysphagia
arytenoid dislocation, and vocal fold edema. Prolonged suggests the possibility of supraglottic obstruction.
intubation can be complicated by laryngeal stenosis, Inability to lie flat, the need to sit upright, and frequent
intubation grooves, or cricoarytenoid arthrodesis and position changes to breathe are symptoms of severe air-
granulomas. Neuromotor injuries include vocal fold way obstruction.
paralysis or paresis secondary to recurrent laryngeal Supraglottic and glottic masses are evaluated by
nerve compression from a high-riding endotracheal nasopharyngoscopy in an awake, spontaneously breath-
tube (ETT) cuff. Postintubation vocal fold paralysis is ing patient. Subglottic and tracheal problems are in-
uncommon given the numbers of procedures per- vestigated with chest x-rays, computed tomography, or
formed under general anesthesia. magnetic resonance imaging. These problems often
Some patients whose voices are unintelligible desire manifest with inspiratory and expiratory stridor. Ide-
to restore speech for communication. For these pa- ally, airway imaging should be reviewed and discussed
tients, a hoarse or soft voice is better than no voice at all. with the surgeon. Previous anesthesia records could
215
216 SECTION 7 Eye, Ear, Nose and Throat
reveal prior problems with mask ventilation, laryngos- and obscure the glottis during laryngoscopy. Classically,
copy, bleeding, or extubation. patients with epiglottitis receive general anesthesia fol-
lowed by laryngoscopy and intubation. Nevertheless,
some supraglottic lesions may indicate the need for
3. Explain the special anesthesia requirements for
awake intubation.
laryngeal microsurgery. Laryngeal lesions, such as large vocal cord polyps and
During laryngeal microsurgery procedures, surgeons and papillomas, have the potential to create partial airway
anesthesiologists occupy the same space at the same time. obstruction after induction of general anesthesia. They
They must share the airway. The mouth and pharynx rarely result in total airway obstruction but can make
provide relatively little room for rigid suspension laryn- mask (or other supraglottic airway) ventilation difficult.
goscopes and other tools, surgical visualization, and sur- Contrary to classic teaching, obstruction is frequently
gical manipulation. Millimeters of space can determine worse in anesthetized spontaneously breathing patients
success or failure. Anesthesia equipment must take up as than in anesthetized patients receiving positive pressure
little room as possible. A small ETT or jet ventilation is ventilation by facemask. Spontaneous ventilation is nega-
generally used. tive pressure ventilation. As the diaphragm and intercos-
Airway surgery involves profound stimulation, requir- tal muscles contract, intrathoracic pressure is reduced.
ing deep anesthesia for relatively brief periods. At the Reduced intrathoracic pressure falls below barometric
conclusion of surgery, stimulation quickly decreases to pressure and is frequently referred to as negative pres-
almost nothing, while patients remain deeply anesthe- sure. Negative pressure is transmitted to the upper air-
tized. The goals for emergence are rapid awakening way, where it tends to draw pharyngeal tissues into the
without coughing or bucking. Coughing or bucking airway. It is as if soft tissues are imploding into the upper
abrades laryngeal incisions as vocal folds are forced airway. Pharyngeal dilator muscles normally work to
against indwelling ETTs or the adjacent vocal fold. maintain airway patency, but general anesthesia reduces
Coughing and bucking also can result in dislodgment of muscle tone, allowing soft tissues to collapse inward.
sutures and hemorrhage. Many patients are placed on Positive pressure ventilation tends to stent the airway
voice rest postoperatively to prevent incision trauma that open, and consequently it is more effective in these cases.
can impair healing. An opioid-based anesthetic with If spontaneous ventilation is maintained, assisted ventila-
short-acting agents is desirable. An opioid-based anes- tion with positive pressure and oral or nasopharyngeal
thetic provides laryngeal sensory depression, allowing for airways could be beneficial.
smooth emergence. Spontaneous ventilation is useful to evaluate airway
Airway surgery is associated with the highest risk for dynamics. Tracheomalacia is a prime example. In this
postextubation airway compromise. It is of paramount case, inhalation induction is performed with sevoflurane
importance to confirm adequate return of strength be- and 100% oxygen. When a sufficient depth of anesthesia
fore extubation. It is the author’s preference to extubate is achieved, laryngoscopy to view the trachea during in-
awake patients as opposed to deeply anesthetized or spiration and expiration can proceed.
heavily sedated patients. Strong muscle tone is required Subglottic lesions do not inhibit laryngeal visualization
for airway dilator muscles to maintain upper airway pa- but can prevent advancing an ETT beyond the larynx and
tency. Conscious efforts to maintain an open airway into the trachea. If subglottic lesions are present, a variety
contribute to successful extubation. of small ETTs and a jet ventilation system should be avail-
able. Small-diameter ETTs are required to allow for opti-
mal surgical visualization and manipulation. For adult
4. Describe an anesthetic for laryngeal
patients, 5.5 mm internal diameter (ID) ETTs generally
microsurgery. satisfy this requirement and allow for adequate gas ex-
Phonomicrosurgery usually requires general anesthesia. change. Controversy exists over the use of such small
Surgical access to the airway and aerodigestive tracts is ETTs in large adults. Adequate minute ventilation deliv-
improved by using small ETTs and adequate muscle re- ered through small ETTs is accompanied by high read-
laxation. In the absence of muscle relaxation, deep planes ings on inspiratory pressure monitors. This is generally of
of anesthesia are required. Suspension laryngoscopy is little clinical importance because small ETTs act as resis-
highly stimulating and tends to produce hypertension tors. There is a substantial decrease in pressure across a
and tachycardia. Sufficient anesthetic depth and agents small ETT. Actual intratracheal pressures approximate
that effectively blunt sympathetic stimulation, such as pressures seen with larger ETTs. Consequently, the risk
remifentanil or !-adrenergic blockers, or both, are com- of barotrauma is not substantially greater using small
monly used. Most of these procedures are of short dura- ETTs than it is with large ones. A common technique to
tion, so judicious use of muscle relaxants and short-acting reduce inspiratory pressures is to adjust the inspiratory-
anesthetic agents is helpful. The operating room table to-expiratory (I:E) ratio from 1:2 to 1:1; this provides
is generally turned 90 or 180 degrees from its usual posi- more time for inspiration, reducing the inspiratory pres-
tion. Respiratory circuits and cables need to be suffi- sure required to achieve adequate tidal volumes. Alterna-
ciently long to extend the additional distance. Laser tive modes of ventilation, such as pressure-controlled
surgery is associated with its own special risks and is dis- volume guaranteed, are also applicable.
cussed later. For nonobstructing airway lesions, standard tech-
Mobile supraglottic lesions can obstruct gas flow niques of induction, maintenance, and ventilation work
through the larynx during positive pressure ventilation well. It is common practice to administer topical local
44 Laser Laryngoscopy 217
anesthetic to the larynx and trachea during laryngoscopy. BOX 44-1 Laryngeal Microsurgery
This practice is intended to reduce postoperative cough-
ing and laryngospasm. Also, in the absence of muscle GENERAL CONSIDERATIONS
relaxants, anesthetized vocal folds help to provide vocal • Operating room table turned 90 or 180 degrees
cord immobility. Lidocaine 2% or 4% solutions are com- • Expandable breathing circuit
monly used for laryngotracheal anesthesia. • Adequate length of monitoring cables
Vocal fold immobility is crucial for laryngeal surgery. • Small ETT (5.5 mm ID)
Immobility is frequently achieved with muscle relaxants, • Ventilation
but alternatives exist. For most short cases, reduced doses • I:E ratio of 1:1 to decrease peak airway pressure may
of commonly available intermediate-acting nondepolar- be required
izing neuromuscular blockers are appropriate. Loading • Consider jet ventilation
doses of muscle relaxants should be avoided. Neuromus- • Blunt sympathetic stimulation
• Deep plane of anesthesia
cular monitoring is required to determine the need for • Opioids
antagonism of the motor block and to determine suffi- • !-adrenergic blockers
cient return of strength for tracheal extubation. Airway • Vocal cord immobility
surgery is associated with a relatively high risk of postex- • Reduced doses of intermediate-acting muscle relaxants
tubation respiratory distress. Adequate muscle strength • Opioids
can reduce this risk. • Deep plane of anesthesia
An alternative to muscle relaxants is a deep plane of • Emergence
anesthesia; this is typically accomplished with total in- • Avoid coughing and bucking
travenous anesthesia using high-dose remifentanil (e.g., CONSIDERATIONS BY PATHOLOGY
"0.2 #g/kg/min) or balanced anesthesia with remifen-
• Airway dynamics (e.g., tracheomalacia)
tanil and volatile anesthetics. Relatively high doses of • Maintain spontaneous ventilation for diagnostic
remifentanil render vocal cord movement unlikely. purposes
Avoiding muscle relaxants precludes anaphylaxis and • Laryngeal lesions
residual neuromuscular blockade secondary to their • Less obstruction with positive pressure ventilation
use. High-dose opioids dampen the sympathetic re- • Potentially difficult facemask or supraglottic airway
sponse to laryngoscopy and intubation; however, they ventilation
predispose to vocal cord adduction, which can impair • Subglottic lesions
mask ventilation and predispose to vocal cord trauma • May be difficult to pass tracheal tube
during intubation. • Consider jet ventilation
Anesthesia emergence can be accompanied by cough-
ing and straining, both of which are potentially harmful
after upper airway surgery. Forceful vocal cord adduction
with or without an ETT in place exacerbates surgical tis-
sue damage. The result is impaired healing, with vocal
cord scarring and permanent adverse voice changes. TABLE 44-1 Advantages and Disadvantages of
Consequently, laryngeal topical anesthesia during airway Closed versus Open Anesthesia
manipulation and emergence from anesthesia and ade- Systems
quate opioid plasma levels are employed. Remifentanil
offers intense analgesia and short duration of action, Advantages Disadvantages
making it an excellent opioid choice. Alternatively, deep Closed Familiar to all anes- Limits surgical
extubation can be considered to help reduce coughing on systems thesiologists visibility
emergence. However, deep extubation risks aspiration of Best protection Interferes
blood and debris that frequently accompanies airway against with surgical
aspiration manipulation
surgery. High-dose opioids allow patients to awaken
PPV possible Risks ETT-related
comfortably with the ETT in place, after which extuba- Minimal OR laryngeal
tion can occur when they are able to protect their own pollution trauma
airways (Box 44-1). Risk of fire
during laser
surgery
5. What ventilatory modes are employed
Open Maximum surgical Requires special
for endoscopic laryngeal surgery? systems visibility knowledge,
Ventilatory techniques for laryngeal surgery are highly Maximum surgical training, and
manipulation equipment
sophisticated. They are categorized as closed and open g risk of ETT-related No aspiration
systems, and each one is associated with advantages and tracheal trauma protection
disadvantages (Table 44-1). Closed systems offer several g risk of fire during Cannot provide
advantages; they are familiar to the anesthesia care team, laser surgery PPV
protect best against aspiration, allow positive pressure
ventilation, and minimize operating room pollution. ETT, Endotracheal tube; OR, operating room; PPV, positive pressure
ventilation.
However, they also have certain disadvantages. They limit
surgical visibility, interfere with surgical manipulations,
218 SECTION 7 Eye, Ear, Nose and Throat
risk ETT-related laryngeal damage, and predispose to directly into the trachea. A major advantage of subglottic jet
fire during laser applications depending on the type of ventilation over proximal jet ventilation is vocal cord im-
ETT used. mobility. Disadvantages of subglottic compared with proxi-
Open systems maximize laryngeal visualization, reduce mal jet ventilation include slight obstruction of the surgical
the risk of ETT trauma, and minimize the risk of laser field and barotrauma.
fires. Some types of open system ventilation require special Both proximal and subglottic techniques provide
knowledge, training, and equipment. Also, open systems adequate oxygenation and ventilation. Sanders’ manual
fail to protect against aspiration. Selection of open versus ventilator valves are applicable to normal respiratory
closed systems is based on the location, size, mobility, and rates. High-frequency jet ventilators are set to deliver
vascularity of the lesion. Certain operations may require approximately 110 breaths per minute. High-frequency
changing from one method to another. For example, a jet ventilation provides for continuous gas flow out of the
closed system with an ETT could be changed to an open airway, which tends to carry away small amounts of blood
system intraoperatively for a lesion that is rendered inac- and debris as well as reducing peak and mean airway
cessible by the ETT. A jet ventilation system may be pressures, which could minimize ventilator-related hypo-
changed to a closed system with an ETT for excessive tension. Ventilator rate, percent inspiratory time, and
blood or debris that could cause aspiration pneumonia. driving pressure affect arterial carbon dioxide tension
Open techniques of ventilation include spontaneous (PaCO2). Continuous positive airway pressure and frac-
ventilation, apneic oxygenation, and jet ventilation. Dur- tion of inspired oxygen (FiO2) contribute to oxygenation.
ing spontaneous ventilation, anesthesia maintenance is Jet ventilation requires airway patency for air entrain-
achieved with potent inhalation agents via facemask, na- ment and gas egress. Upper airway obstruction that does
sopharyngeal airway, or laryngoscope or bronchoscope not allow escape of gas from the lungs predisposes to
side port. Disadvantages of spontaneous ventilation with pneumothorax and pneumomediastinum. Airway patency
potent anesthetic gases include coughing, bucking, ap- can be achieved with chin lift, jaw thrust, or placement of
nea, laryngospasm, vocal cord movement, hemodynamic a laryngoscope.
fluctuations, inability to protect against aspiration, and The Venturi principle draws large volumes of gas into
operating room pollution with anesthetic gases. Intrave- the lungs, augmenting the small oxygen pulses delivered
nous agents help to overcome some of these problems. directly by high-frequency jet ventilation. Adequacy of
Remifentanil and propofol are frequently used adjuncts. oxygenation is monitored by pulse oximetry. Ventilation
Apneic oxygenation is applicable to foreign body re- is monitored noninvasively by capnometry. Open systems
moval as well as nonobstructing glottic and subglottic are amenable to qualitative measurement of end-tidal
lesions. Surgical manipulation occurs during apneic peri- carbon dioxide (ETCO2), which demonstrates that venti-
ods. Oxygenation can be provided by anesthesia facemask lation is occurring. Quantitative measurement of ETCO2
or ETT. This technique works best in patients with from open systems is of little clinical value. Chest wall
normal functional residual capacity. One administers undulations and breath sounds are clinical evidence of
100% oxygen in an attempt to reach an end-tidal oxygen ventilation.
concentration of "90%. Apneic periods and surgical
manipulation are allowed to proceed until oxygen satura- 6. What are the special considerations for singers
tions by pulse oximetry (SpO2) decrease to the low 90s. and other patients who use their voices
Anesthesia is maintained with intravenous agents or professionally?
potent inhaled anesthetics or both. Time for surgical
manipulation is limited by oxyhemoglobin desaturation. Most patients experiencing postoperative voice changes
Jet ventilation requires administration of 100% oxy- find it annoying. Patients who use their voices profes-
gen under approximately 20 pounds/square inch (psi) sionally find it devastating. Scrupulous attention to detail
pressure, via a catheter or blunt needle. Jet ventilation and superior skills are required in these patients. Induc-
systems do not accommodate potent inhaled anesthesia tion of anesthesia must provide optimal intubating con-
vaporizers. Consequently, total intravenous anesthesia is ditions. The requirements are deep anesthesia and pro-
required. Remifentanil, 0.05–0.2 #g/kg/min, and propo- found muscle relaxation. The combination of both deep
fol, 50–100 #g/kg/min, are commonly employed. anesthesia and profound muscle relaxation allows the
Supraglottic (proximal) jet ventilation is performed by glottic opening to fall posteriorly for ease of visualization
fixing a jet needle to a suspension laryngoscope or rigid and provides vocal cord abduction. Vocal cord abduction
bronchoscope. The jet needle is aimed at the larynx so moves the cords away from the glottic midline, reducing
that oxygen enters the trachea. Advantages of supraglot- the risk for trauma during ETT passage. Adducted vocal
tic jet ventilation include an unobstructed surgical view cords are subject to laceration and hematoma formation
and limited risk of laser fires. The risk of laser fire is lim- as the ETT is inserted. The ETT should be passed
ited by eliminating polyvinyl chloride (PVC) ETTs and through the posterior glottis, between both vocal cords
by diluting delivered oxygen jets with room air. Room air without touching either one. Stylets are avoided if pos-
entrainment is explained by the Venturi principle. Poten- sible. Intubation over fiberscopes risks contact with vocal
tial problems include poor oxygenation; gastric insuffla- cords during ETT advancement. Blind intubation is
tion; aspiration of blood, smoke, and debris; vocal cord similarly discouraged. When inserting the laryngoscope
movement; and barotrauma. blade, it is best to look for the glottis from a proximal to
Subglottic jet ventilation involves placing a 2–3 mm di- distal direction to avoid arytenoid injury from the laryn-
ameter jetting catheter into the trachea. Oxygen is delivered goscope blade. Emergence should be free from coughing
44 Laser Laryngoscopy 219
and bucking. At extubation, the ETT cuff is completely smoke. The smoke could contain carcinogens and viral
deflated, and the tube is removed during inspiration. particles. When released into the atmosphere, these con-
For brief procedures, 5.5 mm ID ETTs provide mini- taminants contact exposed skin of patients and operating
mal laryngeal trauma, good gas exchange, and excellent room personnel. They could also be inhaled by individu-
surgical visualization. For longer operations, 6.0 mm ID als in the room. Total body draping for patients and
and 6.5 mm ID ETTs work well for most adults. special masks that resist laser plume contaminants for
Supraglottic devices, such as laryngeal masks, avoid personnel should be used. Smoke evacuators are also
tracheal intubation and its inherent risks. However, they helpful. Perforation of the esophagus can occur during
are not without potential problems. Supraglottic devices laryngeal surgery. Inappropriate energy transfer has the
do not protect against aspiration, expose laryngeal mucosa potential to injure patients and operating room staff.
to desiccation from dry anesthetic gases, and have been Examples include ignition of an ETT or surgical drapes.
associated with arytenoid dislocation and nerve damage. These hazards are minimized by aiming the beam before
activating it.
The potential for eye damage can be reduced by tap-
7. How does laser light differ from natural light?
ing the eyelids shut and covering them with moist gauze,
The acronym “laser” stands for light amplification by metallic eye shields, or both. Wet towels are placed
stimulated emission of radiation. Laser light is a single around the patient’s head, face, and neck to decrease the
frequency of radiation emitted in parallel beams. Its spot risk of fire from an errant laser beam. Wraparound gog-
size does not vary over distance. Natural light diverges as gles are used to protect patients and personnel from eye
distance from its source increases. Laser light is mono- damage. Clear plastic or glass goggles block CO2 lasers,
chromatic. Natural light is composed of a spectrum of but specific colored goggles are required for other types
wavelengths representing many colors. of lasers, such as Nd:YAG and argon lasers.
Lasers place anesthesia equipment at risk for damage.
Lasers have ignited ETTs. PVC ETTs are readily pene-
8. What types of lasers are most frequently used
trated by lasers. When penetration occurs, flames are
for medical care? created, and PVC degrades to toxic substances. Flames
Carbon dioxide (CO2) lasers are most commonly used for are directed toward the lungs, resulting in tracheal dam-
laryngoscopy. The laser energy is absorbed by water with age and pulmonary burns. When these conditions are
a spread of only a few cell layers. CO2 lasers create pre- duplicated in a laboratory, flames exiting the ETT are
cise vaporization with little peripheral damage. CO2 laser reminiscent of a blowtorch. Metal ETTs reduce the haz-
light is invisible, so an aiming beam of helium-neon is ard but are laser resistant, not laser proof. The cuffs on
used to demonstrate where the laser is pointed. metal ETTs are highly susceptible to fire from laser dam-
Neodymium:yttrium-aluminum-garnet (Nd:YAG) lasers age. For this reason, cuffs are filled with water. The hope
are used for thermocoagulation of hemorrhagic lesions. is that a small fire would be extinguished by water escap-
They are used for respiratory tumors and gastrointestinal ing from the perforated cuff. Packing the ETT cuff with
tract varices. Ruby and argon lasers are absorbed by pig- saline-soaked gauze helps to reduce the risk of perfora-
mented cells such as hemoglobin. tion and fires. Box 44-2 lists the components of a typical
anesthetic for laser laryngoscopy.
9. What are the hazards of laser laryngoscopy?
10. How are laser airway fires treated?
The most well-known hazard of laser laryngoscopy is
airway fire. Anesthetic management is designed to mini- Precautions to minimize the risk of airway laser fires do not
mize the potential for fire. Gas mixtures are formulated prevent all of them. Surgeons are most likely to identify the
to reduce the probability of combustion, while simulta-
neously providing adequate oxygenation. Oxygen and
nitrous oxide (N2O) individually support combustion. BOX 44-2 Components of a Typical
FiO2 is supplied at 30% and increased only if required to Anesthetic for Laser Laryngoscopy
improve oxyhemoglobin saturation. N2O is avoided dur-
ing laser laryngoscopy. ETT cuffs that form a poor seal GAS MIXTURE
or that are deflated by laser beams leak inspired gases Avoid nitrous oxide
into the larynx. Delivered high oxygen concentrations or Use lowest FiO2 patient will tolerate (goal 30%)
N2O migrates to the larynx, so fire is a risk with contin- Preferable mixtures are air/oxygen or helium/oxygen
ued laser use. Many laser ETTs are equipped with two
cuffs. If the upper cuff is unintentionally deflated, the TOTAL INTRAVENOUS ANESTHESIA
lower cuff should still provide an airtight seal. Propofol infusion
Additional problems related to lasers include atmo- Remifentanil infusion
spheric contamination, perforation of unintended adja- VENTILATION SYSTEMS
cent tissues, inappropriate energy transfer, and embolic Closed circle system
events (usually occurring during gynecologic proce- Low-frequency (handheld) jet ventilation system
dures). Atmospheric contamination is the most com- High-frequency jet ventilation system
monly occurring complication of laser surgery. Laser
light vaporizes intracellular water and emits a plume of FiO2, fraction of inspired oxygen.
220 SECTION 7 Eye, Ear, Nose and Throat
fire first. As soon as the fire is recognized, oxygen admin- One sign of upper airway obstruction is stridor. Stri-
istration should be stopped, and a burning ETT or cot- dor is usually a high-pitched inspiratory noise emanating
tonoid should be removed. Oxygen administration is in- from the airway. It can result from partial obstruction or
terrupted first to prevent additional airway damage from near-complete obstruction. Treatment options are 100%
a flame that is drawn into the uppermost portions of the oxygen by facemask, sitting position, and steroids. Some
airway as the burning object is removed. If tissues con- patients may benefit from nebulized racemic epineph-
tinue to burn, water should be poured down the airway rine. For selected patients, heliox, a helium/oxygen mix-
to extinguish the fire. An easily accessible bowl or bottle ture, can improve gas flow through a narrowed airway.
of water should be kept on the operating room nurse’s Stridorous noise can diminish because the airway diam-
table for this purpose. When the fire has been extin- eter is improving or because it is getting worse and less
guished, oxygenation can be resumed by facemask or a gas is passing through it.
new ETT. Examination of the airway is then performed.
Prophylactic tracheal intubation against future airway
edema and resulting obstruction is probably prudent but
may be difficult. If pulmonary burns are anticipated, tra- SUGGESTED READINGS
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Gaitini LA, Fradis M, Vaida SJ, et al.: Pneumomediastinum due to
the best choice. It is possible that tracheal reintubation Venturi jet ventilation used during microlaryngeal surgery in a previ-
would be more difficult after instrumentation and fire. ously neck-irradiated patient. Ann Otol Rhinol Laryngol 109:519,
Sometimes it may be best to leave the original ETT in 2000.
place if it is functioning well. Tracheostomy may be nec- Hunsaker DH: Anesthesia for microlaryngeal surgery: the case for
subglottic jet ventilation. Laryngoscope 104:1, 1994.
essary. When airway control is confirmed, bronchoscopy Jaquet Y, Monnier P, Van Melle G, et al.: Complications of different
and laryngoscopy for diagnosis of airway burns should be ventilation strategies in endoscopic laryngeal. Anesthesiology 104:52,
performed. Evidence of inhalation or smoke damage may 2006.
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tive pressure mechanical ventilation. breoptic nasotracheal intubation. Acta Anaesthesiol Scand 44:511,
2000.
Maktabi MA, Smith RB, Todd MM: Is routine endotracheal intubation
11. Discuss the recognized postoperative problems as safe as we think or wish? Anesthesiology 99:247, 2003.
Mencke T, Echternach M, Kleinsschidt S, et al.: Laryngeal morbidity
that occur after laryngeal surgery. and quality of tracheal intubation. Anesthesiology 98:1049, 2003.
Mevorach DL: The management and treatment of recurrent postop-
Laryngeal surgery is frequently accompanied by postop- erative laryngospasm. Anesth Analg 83:1110, 1996.
erative upper airway problems. After tracheal extubation, Postma GN, McGuirt WF Sr, Butler SG, et al.: Laryngopharyngeal
blood, secretions, debris, or pain in the distribution of the abnormalities in hospitalized patients with dysphagia. Laryngoscope
superior laryngeal nerve can produce laryngospasm. It can 117:1720, 2007.
result in partial or total airway obstruction. Attempts to Santos PM, Afrassiabi A, Weymuller EA Jr: Risk factors associated with
prolonged intubation and laryngeal injury. Otolaryngol Head Neck
prevent laryngospasm include topical local anesthesia, Surg 111:453, 1994.
intravenous lidocaine, and adequate analgesia. Treatment Simpson CB, Amin MR, Postam GN: Topical anesthesia of the airway
includes suctioning the airway, administration of 100% and esophagus. Ear Nose Throat J 83:2, 2004.
oxygen by facemask, positive pressure to splint the airway Stenqvist O, Sonander H, Nilsson K: Small endotracheal tubes—ventilator
and intratracheal pressures during ventilation. Br J Anaesth 51:375,
open, and small doses of succinylcholine (10–20 mg). 1979.
Alternatively, induction agents such as propofol may Tanaka A, Isono S, Ishikawa T, et al.: Laryngeal resistance before and
help. Other causes of postextubation stridor include after minor surgery. Anesthesiology 99:252, 2003.
laryngomalacia, tracheomalacia, vocal cord paralysis, Vila J, Bosque MD, Garcia M, et al.: Endoscopic evolution of laryngeal
airway edema, hematoma, soft tissue obstruction, and re- injuries caused by translaryngeal intubation. Eur Arch Otorhinolar-
yngol 254:S97, 1997.
tained foreign body (e.g., cottonoid, throat pack). Fiber- Werkhaven JA: Microlaryngoscopy-airway management with anaes-
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CASE 45
QUESTIONS
1. What is functional endoscopic sinus surgery? 7. Explain the risks and benefits of deliberate
2. To what are complications associated with hypotension.
functional endoscopic sinus surgery attributed? 8. Describe the various techniques and medications
3. List anesthetic considerations and goals. used to improve the quality of the surgical field by
4. What information should be obtained during the both surgeons and anesthesiologists.
preoperative assessment? 9. What techniques are available to decrease
5. Describe Samter’s triad and the anesthetic postoperative pain and minimize recovery time
implications. after functional endoscopic sinus surgery?
6. Explain the concept of “controlled” or “deliberate”
hypotensive anesthetic technique.
A 25-year-old woman with chronic sinusitis presents for procedures, including skull base surgery, transsphenoidal
functional endoscopic sinus surgery (FESS). She has a his- pituitary tumor resection, and treatment of vascular
tory of asthma, nasal polyps, and recurrent sinus infections malformations.
that are unresponsive to multiple treatments with steroids
and antibiotics. She reports a severe allergy to aspirin and 2. To what are complications associated with
is anxious about postoperative pain. After induction of
functional endoscopic sinus surgery attributed?
general anesthesia, her blood pressure monitor reads
70/40 mm Hg. The surgeon complains of increased bleed- FESS generally is a low-risk procedure and carries with
ing in the field and asks to decrease the blood pressure it a large safety profile. However, many catastrophic
further to improve visualization. complications, including death, have been reported in
patients undergoing FESS. These complications include
1. What is functional endoscopic sinus surgery? massive hemorrhage, direct brain injury, blindness from
ocular and optic nerve damage, anosmia (impaired sense
FESS is a nasal endoscopic technique that allows visualiza- of smell), cerebrospinal fluid leak, and intracranial infec-
tion of the paranasal sinuses and nasal cavity without a skin tion. These complications are listed in Table 45-1, and
incision. Described in the late 1970s by Messerklinger and they are categorized into three major groups: orbital,
Stamberger, FESS has become increasingly popular in the intracranial, and nasal. These complications have been
last 30 years and is now one of the most commonly per- attributed to the location of the paranasal sinuses and
formed ambulatory surgical procedures in otolaryngology. nasal cavity within the skull and their close proximity to
Combined with its low risk of major complications and numerous major and significant anatomic structures,
high success rate, it is the mainstay in the surgical treat- such as the internal carotid arteries, orbits, optic nerves,
ment of sinusitis; nasal polyps; epistaxis; and bacterial, and intracranial cavity (Figure 45-1).
fungal, recurrent, acute, and chronic sinus problems. Because of the limited field of view through endoscopes,
Across gender, ethnicity, and age groups, chronic sinusitis the risk of major complications is thought to increase when
affects approximately 35 million Americans annually and uncontrolled or excessive intraoperative bleeding into the
accounts for 11.6 million physician visits each year. surgical field impairs visualization of important anatomic
Chronic sinusitis has been shown to have a dramatic effect structures. Intraoperative bleeding and poor surgical condi-
on quality of life, comparable with that seen in conditions tions not only increase complications but also can prolong
such as coronary artery disease and asthma. More recently, total surgical time and lead to incomplete resection of tissue
functional sinus endoscopy has expanded to provide a rela- or tumors, which may require reoperations. Numerous fac-
tively low-morbidity approach to various other surgical tors related to the patient’s comorbidities and medications,
221
222 SECTION 7 Eye, Ear, Nose and Throat
FIGURE 45-1 ■ Proximity of sinuses and surgical field to critical structures, including the brain and orbit. (From Standring S [ed.]: Gray’s
Anatomy: The Anatomical Basis of Clinical Practice, 40th edition. Churchill Livingstone, Philadelphia, 2009.)
the type of procedure performed, and the anesthetic tech- operative times. Active infections, extensive sinusitis, and
nique can contribute to a poorly visualized surgical field large tumors may be associated with increased blood loss.
secondary to excessive intraoperative bleeding. In addition, the applications of FESS as a surgical tech-
nique are constantly broadening, including skull base
surgery. Providing a secure airway and motionless surgical
3. List anesthetic considerations and goals.
field via general anesthesia is likely to be preferred for
In highly motivated patients with minimal or limited sino- most procedures.
nasal disease, simple sinus surgery can be performed with For reasons stated earlier, facilitation of a “bloodless”
infiltration of local anesthetic, nerve blocks, and vasocon- surgical field should be a principal concern. Other im-
strictors alone or with monitored anesthesia care. In such portant anesthetic considerations and goals for FESS are
instances, excellent communication between all parties listed in Table 45-2. These include airway protection
involved (i.e., surgeon, anesthesiologist, and patient) is and prevention of aspiration of blood and tissue, patient
necessary to create optimal surgical conditions. However, immobility, and emergence from anesthesia without
monitored anesthesia care should be used with caution in bucking on extubation. Coughing or straining can in-
patients who may be uncooperative (e.g., children, devel- crease postoperative bleeding. In addition, because FESS
opmentally disabled adults), possess potentially difficult is often performed as an outpatient ambulatory proce-
airways (e.g., patients with obstructive sleep apnea, obesity, dure, a rapid recovery profile is highly desired. Avoiding
airway pathology), have a risk of aspiration (e.g., patients postoperative nausea and vomiting (PONV) (postopera-
with gastroesophageal reflux disease), or require longer tive retching can also promote postoperative bleeding)
45 Functional Endoscopic Sinus Surgery 223
while providing sufficient postoperative analgesia is also may not tolerate the tachycardia and hypertension as-
desirable. sociated with increased circulating catecholamines.
Cocaine and epinephrine should be used with caution
4. What information should be obtained during the in these patients. Antiplatelet or anticoagulation ther-
apy should be discontinued before surgery in concor-
preoperative assessment?
dance with current practice guidelines, particularly in
Anesthesiologists caring for patients undergoing FESS the setting of coronary stents. As of 2010, patients
must constantly negotiate between the patient’s various with drug-eluting stents taking clopidogrel and aspi-
comorbidities and the risks incurred by optimizing the rin should avoid elective surgery and cessation of an-
surgical field (i.e., reduced intraoperative bleeding) via tiplatelet therapy until at least 1 year after placement
induced physiologic derangements (i.e., reduction in of the stent, and resumption of these medications
cardiac output [CO] and hypotension). A thorough yet should be coordinated carefully with the patient’s
directed evaluation done in accordance with current cardiologist. The American College of Cardiology/
American Society of Anesthesiologists (ASA) practice American Heart Association (ACC/AHA) further rec-
advisory guidelines on preanesthetic evaluation should be ommended that, if possible, aspirin should be contin-
performed in all patients undergoing FESS. ued into the perioperative period even after 1 year has
“Controlled hypotension” is not without risk, and passed since placement of a drug-eluting stent. It is
patients with significant cardiac or vascular disease, in- important that the perioperative management of anti-
cluding valvular pathology, congestive heart failure, and coagulation therapy in these patients is discussed be-
atherosclerotic disease may not tolerate significant de- tween the surgeon, the anesthesiologist, and the pa-
creases in mean arterial pressure (MAP). Significant end- tient’s cardiologist before the day of surgery. Helpful
organ damage can result. Assessment of physiologic re- preoperative studies include prothrombin time, acti-
serve and tolerance of “deliberate hypotension” can be vated thromboplastin time, platelet count, and complete
obtained with a history focusing on exercise tolerance blood count.
and symptoms with physical exertion. Complaints of
dyspnea, chest pain, palpitations, or dizziness with climb- 5. Describe Samter’s triad and the anesthetic
ing two or more flights of stairs (i.e., !4 metabolic implications.
equivalents or METS) or occasionally during rest may
indicate the need for further cardiovascular testing, such Patients undergoing FESS tend to share certain comorbidi-
as an electrocardiogram (ECG), echocardiogram, stress ties that may be of particular concern to anesthesiologists
test, or coronary angiography. (Table 45-3). Preoperative diagnoses and indications for
Local vasoconstrictors such as cocaine or epineph- FESS include nasal polyps, chronic sinusitis, recurrent sinus
rine are commonly applied in FESS. Patients with infections, benign and malignant tumors, and management
significant coronary artery disease or cardiac arrhythmias of previous surgical procedures (e.g., cerebrospinal fluid
leak, scar tissue formation). The coexistence of asthma or The degree of deliberate or controlled hypotension must
reactive airways disease and nasal polyposis in patients is be individualized to each patient and should be tailored
roughly 20%–30%. Samter’s triad, or aspirin-exacerbated until the desired effect is obtained (i.e., dry or bloodless
respiratory disease, is the combination of reactive airways surgical field) as opposed to a predetermined value. The
disease, chronic rhinitis and nasal polyps, and sensitivity benefit of achieving a “bloodless field” must always be
to aspirin. The disease is produced by an abnormality in counterbalanced by the necessity to provide adequate
the arachidonic acid cascade resulting in overproduction oxygen delivery to tissues by maintaining acceptable
of leukotrienes. Aspirin blocks the production of prosta- cerebral and coronary blood flow.
glandins and shifts the cascade toward the production of MAP is defined as the product of systemic vascular
leukotrienes, precipitating allergylike effects, such as bron- resistance (SVR) and CO, as follows:
chospasm, urticaria, or anaphylaxis. Other nonsteroidal
MAP # SVR $ CO
antiinflammatory drugs (NSAIDs), such as ketorolac or
ibuprofen, similarly block prostaglandin formation and A reduction in SVR, CO, or both can be implemented
should be avoided in these patients, although acetamino- to achieve a lower MAP. However, more recent
phen is generally considered safe. evidence has suggested that interventions that aim
Patients with a history of poorly controlled asthma or at reducing CO have been demonstrated to be more
reactive airways disease commonly present for FESS. effective in improving surgical conditions in FESS
These patients should be seen and medically optimized compared with interventions reducing SVR. Reduction
before surgery as indicated by history and symptoms. Pre- of SVR is often achieved through the use of vasodilating
operative use of oral or inhaled "2-adrenergic agonists agents, such as calcium channel blockers, nitrates,
(e.g., albuterol), anticholinergics (e.g., ipratropium bro- hydralazine, or potent inhaled anesthetics. In addition,
mide), antileukotrienes (e.g., montelukast), corticoste- drugs such as labetalol or phentolamine provide block-
roids, and antibiotics may be necessary. Achieving con- ade of %-adrenergic receptors, with significant SVR
trolled hypotension through the use of intraoperative reduction. However, improvement of operating condi-
"-adrenergic blockers, including "1-selective agents (e.g., tions via a reduction of SVR is seldom seen unless
metoprolol, esmolol), should be approached with caution profound hypotension is experienced (MAP &50 mm
because of increased likelihood of bronchospasm. Hg), and there is evidence to suggest that excessive
Long-term steroid use is also prevalent among vasodilation may exacerbate bleeding and promote
patients undergoing FESS. Although routine use of increased capillary blood flow.
steroids for treatment of chronic sinusitis is controver- As stated earlier, a reduction in CO effectively de-
sial, preoperative steroids have been shown to improve creases MAP. CO depends on several physiologic param-
surgical conditions in patients with rhinosinusitis and eters, including preload, afterload, contractility, heart
polyposis owing to their antiinflammatory and anti- rate, and rhythm. Pharmacologic blockade of "-adrener-
edema effects. In addition, perioperative use of steroids gic receptors through the use of metoprolol, labetalol,
is particularly advantageous because steroids have effec- and esmolol decreases heart rate and contractility.
tive antiemetic properties. Adrenal or pituitary insuffi- Numerous studies have shown a significant correlation
ciency may be a concern in these patients; however, as between bradycardia and improved surgical conditions.
long as patients receive their usual daily maintenance In addition, studies in which "-adrenergic blockade was
dose preoperatively or are administered equivalent in- the primary technique in CO reduction demonstrated
travenous doses during the intraoperative period, it achievement of optimal surgical conditions at a higher
generally does not pose a problem. MAP (!65 mm Hg). Short-acting "-adrenergic block-
ade via an esmolol infusion was found to provide superior
6. Explain the concept of “controlled” or surgical conditions compared with sodium nitroprusside,
a vasodilating agent, which required a much lower MAP
“deliberate” hypotensive anesthetic technique.
of 50–54 mm Hg to achieve optimal surgical conditions.
Assuming normal platelet function and barring any frank This finding suggests that “deliberate hypotension,” or a
coagulopathy, intraoperative bleeding in FESS primarily simple reduction in systemic blood pressure, is not the
depends on the extensive vascularity of nasal and sinus contributing factor in reduction of intraoperative bleed-
mucosa. Intraoperative bleeding is also a function of ing, but rather a “deliberately decreased CO” via a reduc-
the intensity of blood flow through the major vessels tion in heart rate and contractility.
and capillaries within the nasal cavity. This intensity is
influenced greatly by the relationship between MAP and 7. Explain the risks and benefits of deliberate
regional or central venous pressures. “Controlled” hypo- hypotension.
tension is an anesthetic technique aimed at “deliberately”
significantly decreasing the MAP and has long been As previously stated, inducing hypotension is not without
advocated to aid in the reduction of blood loss and risk. The use of "-adrenergic blockers in perioperative care is
improve visualization in sinus surgery. controversial. Current studies on routine use of perioperative
It is generally accepted that one can safely achieve a 30% "-adrenergic blockade show an increased risk of morbidity
decrease from baseline MAP or an absolute value of 50 mm and mortality in patients not requiring these agents periop-
Hg in healthy patients with ASA class I status. However, eratively. Patients who were at high risk of cardiovascular
deliberate hypotension itself cannot be defined by an exact complications and who were not receiving "-adrenergic
number, percentage, or blood pressure measurement. blockers preoperatively were observed to be at higher risk for
45 Functional Endoscopic Sinus Surgery 225
adverse outcomes postoperatively. In patients with a drugs are associated with significant risks secondary to
low risk of cardiovascular complications, the effects of systemic absorption. Reported serious adverse conse-
"-adrenergic blockade during the perioperative period quences include bradycardia, unstable tachyarrhyth-
on morbidity and mortality have yet to be studied. A mias, hypertensive crisis, myocardial infarction, stroke,
significant number of patients presenting for FESS have and cardiogenic shock. The use of these medications
associated reactive airways disease, and "-adrenergic should be limited or avoided completely in patients with
blockade is contraindicated in these patients. Regardless significant cardiac disease. Hypertension related to
of the use of "-adrenergic blockade or vasodilatory agents, phenylephrine and epinephrine is usually short-lived
deliberate reduction of CO is not without problems. Sig- and generally dissipates spontaneously. Specific treat-
nificant ischemia causing organ failure as a result of con- ment is not required. When hypertension from phenyl-
trolled hypotension is estimated at 0.6%. As previously ephrine and epinephrine persists, "-adrenergic block-
stated, the benefits of a bloodless surgical field may be at ade as sole treatment can create or exacerbate unopposed
odds with the risks incurred by significantly decreasing %-agonist activity and greatly increase afterload on the
tissue perfusion and limiting oxygen delivery to vital heart. Direct vasodilators, mixed " and % antagonists, or
organs. “Controlled” hypotension may be especially chal- pure % antagonists are the appropriate pharmacologic
lenging in certain patient populations (e.g., patients with therapies in this instance.
known cardiovascular disease, patients with valvular pa-
thology such as aortic stenosis and carotid disease). Imple- Positioning
mentation of such a technique should be judiciously tai-
lored to each patient’s specific needs and limitations. Positioning of the patient and surgical field can have a
considerable impact on the reduction of intraoperative
8. Describe the various techniques and medications bleeding in FESS. Placing the patient in reverse Tren-
used to improve the quality of the surgical field by delenburg position has been advocated as a technique to
reduce blood loss and improve surgical conditions in
both surgeons and anesthesiologists.
FESS. Elevation of the head by at least 15 degrees creates
An important anesthetic goal for FESS, regardless of tech- enough venous pooling in the lower extremities to reduce
nique, is to minimize intraoperative bleeding. Even small venous sinus congestion and edema. However, because
amounts of blood in the surgical field can significantly blood pressure measurements are commonly taken at the
compromise visibility because of the limited space of the level of the heart, they would overestimate the blood
nose and sinus. A bloodless field through deliberate hypo- pressure at the level of the brain and circle of Willis,
tension is not always feasible. When successful, a bloodless which would be lower because of the effect of gravity on
surgical field improves surgical visibility, minimizes surgi- blood flow. This decrease in blood pressure at the level of
cal time, and reduces surgical risk. Although the cause the head is aggravated further when a deliberate hypoten-
of significant intraoperative bleeding is multifactorial, a sive technique is employed. Lastly, because the surgical
variety of effective techniques can be implemented during field remains above the level of the heart, this position
the perioperative period that reduce bleeding and carries a small but significant risk of venous air embolism,
inflammation. and such cases have been reported in FESS.
9. What techniques are available to decrease index finger of the nondominant hand is placed over the
postoperative pain and minimize recovery time infraorbital foramen (Figure 45-2). A 25-gauge 11⁄2-inch
after functional endoscopic sinus surgery? long needle is positioned through the ipsilateral nares.
The needle is advanced toward the finger marking the
Postoperative pain after FESS ranges from mild to moder- foramen, and 2 mL of 0.5%–0.75% bupivacaine is injected
ate. Often a multimodal approach is implemented. The after negative aspiration. This technique should be avoided
use of remifentanil offers no sustained postoperative anal- in patients with pathology (e.g., neoplasms, arteriovenous
gesia because it is rapidly metabolized. Nonselective malformations) involving the anterior nasal cavity or nasal
NSAIDs, such as ketorolac, are commonly avoided in vestibule.
FESS because of an association between nasal polyps, as- The pterygopalatine ganglion or sphenopalatine gan-
pirin sensitivity, and reactive airways disease. Additionally, glion supplies the lacrimal gland, paranasal sinuses, mu-
inhibition of thromboxane A2 by nonselective NSAIDs cosa of the nasal cavity and pharynx, gingiva, and mucous
can impair platelet aggregation. Current evidence shows membrane of the hard palate. The ganglion is blocked
equivalence in pain relief among local anesthetics, selective via the greater palatine foramen approach. Placing the
cyclooxygenase (COX)-2 or COX-3 NSAIDs, and opioids patient supine and extending the neck, the greater pala-
when used separately in FESS. The general approach is tine foramen is identified medially to the gum line of the
to use nerve blocks with long-acting local anesthetics such first or second molar on the posterior portion of the hard
as bupivacaine before surgery, nonopioid analgesics such palate. A curved blade laryngoscope is useful in providing
as acetaminophen or selective COX-2 inhibitors intraop- adequate exposure and illumination after endotracheal
eratively or immediately postoperatively, and longer acting intubation. A 25-gauge 11⁄2-inch long needle is bent at
opioids such as fentanyl for rescue treatments in the 1.5 cm and advanced through the foramen at an angle of
postanesthesia care unit (PACU). 45 degrees at a superior and slightly posterior trajectory.
Roughly 1.5–2.0 mL of lidocaine with 1:100,000 epineph-
Postoperative Regional Anesthesia for rine is injected after demonstrating negative aspiration.
Functional Endoscopic Sinus Surgery The use of epinephrine minimizes systemic absorption
in this highly vascular region. This technique has been
The maxillary division of the trigeminal nerve (V2) pro- associated with complications such as intravascular injec-
vides the major sensory innervation to the midface, includ- tion, intraorbital and optic nerve injury, and transient
ing the lower eyelid, upper lip, maxillary sinus, nasal cavity, diplopia. In a published double-blind randomized study,
and soft and hard palate. Specifically, the infraorbital nerve our group determined that patients who receive both
and sphenopalatine ganglion, branches of the maxillary blocks require less opioid analgesia in the PACU and are
nerve, are targeted for local anesthesia blockade for FESS. discharged home 40 minutes earlier on average compared
The infraorbital nerve provides sensation to the cheek, with patients who did not receive the blocks.
upper lip, eyelid, and lateral aspect of the nose. The Otolaryngologists are using intraoperative computed
nerve exits the infraorbital foramen approximately 1 cm tomography image (CT) guidance with increasing fre-
below the inferior orbital ridge along a vertical line from quency during FESS. Infiltration of local anesthesia during
the medial limbus of the eye. The infraorbital notch can infraorbital nerve blocks can interfere with the guidance
be easily palpated rolling one’s fingertip over the inferior system registration by deforming facial skin depth and
orbital rim. This block can be performed via intraoral or facial topography that is required for proper calibration
transnasal approaches. For the transnasal technique, the and patient identification (Figure 45-3).
FIGURE 45-2 ■ A, Transnasal approach to infraorbital nerve block. B, Relevant anatomy showing the distribution of anesthesia from
the block.
228 SECTION 7 Eye, Ear, Nose and Throat
FIGURE 45-3 ■ A, Topography before infraorbital nerve block placement. B, Subsequent derangement of facial topography from local
injection.
BLOOD
229
CASE 46
Transfusion Reaction
Barry J. Segal, MD
QUESTIONS
A 67-year-old woman with a fractured right femur (TRALI), heat-induced hemolyzed RBCs, and transfusion-
presents for intramedullary nailing under spinal anes- associated circulatory overload (TACO).
thesia. After 45 minutes, she loses 1200 mL of blood Delayed reactions occur after 24 hours and often
and receives 1 unit of designated donor red blood cells 3 days to months after transfusion. Types of delayed
(RBCs). Within minutes of initiating transfusion, the reactions include delayed extravascular hemolytic, allo-
patient is shivering and complains of chills, nausea, and immunization, graft-versus-host disease (GVHD), and
difficulty breathing. Her heart rate increases from infectious (viral, parasitic, and bacterial).
84 beats per minute to 128 beats per minute, ST segments
are depressed, and the blood pressure decreases from 3. Can all blood products cause transfusion
124/72 mm Hg to 82/46 mm Hg. The urine in the
urometer has turned from clear to pink.
reactions?
All blood products can cause transfusion reactions. The
type of transfusion reaction depends on the blood prod-
1. Is this a transfusion reaction?
uct administered. Only incompatible RBC transfusions
The immediacy of presentation as well as the scope of cause intravascular or extravascular hemolytic transfusion
signs and symptoms indicates that this is an acute hemo- reactions. Allergic reactions, which are probably the
lytic transfusion reaction. This type of reaction is the most common transfusion reactions (1%–3% of all trans-
most severe immediate transfusion reaction and occurs fusions), can occur with RBC, plasma, or platelet transfu-
infrequently. Prior data suggested that acute reactions sions. Allergic reactions usually result from preformed
manifest with an incidence of 1:10,000–1:50,000 units antibodies to plasma proteins. IgE may mediate allergic
of blood products administered. Newer data suggest a reactions, and anaphylaxis may occur. Febrile reactions
frequency of approximately 1:250,000–1:500,000. may be produced by stored leukocytes producing in-
A Canadian hemovigilance study found 11 cases of creased interleukin (IL)-1 (endogenous pyrogen) or anti-
acute hemolytic transfusions out of 138,605 RBC units IgA antibodies produced by individuals who are deficient
given in 2000. Death rates were 25% when !1000 mL in IgA or an IgA subclass. IL-6, IL-1#, and tumor necro-
was transfused and 44% when "1000 mL of incompatible sis factor (TNF)-$, also endogenous pyrogens, have been
ABO blood was given. found to increase in stored platelet concentrates.
2. Are all transfusion reactions immediate? 4. What are the etiologies and presentations
of transfusion reactions?
Immediate transfusion reactions occur within the first
24 hours of administration of blood components. Types Immediate Transfusion Reactions
of immediate transfusion reactions include acute intra- Acute Intravascular Hemolytic Transfusion
vascular hemolytic transfusion reaction (AIHTR) and Reaction
acute extravascular hemolytic transfusion reaction, allergic
transfusion reactions (mild, anaphylactic, anaphylactoid), AIHTR usually occurs intravascularly. Destruction of
febrile nonhemolytic transfusion reaction (FNHTR), donor and occasionally recipient RBCs releases free hemo-
hypotensive transfusion reaction, bacteria-contaminated globin and stroma of destroyed erythrocytes, elaborates
or septic transfusion, transfusion-related lung injury cytokines and chemokines, activates complement, reduces
230
46 Transfusion Reaction 231
oxygen carrying capacity, and causes electrolyte imbalances. commonly associated with Rh group incompatibility.
This reaction can have devastating results. Morbidity and Complement either is not activated or attaches only
mortality vary with the amount of blood transfused and the to C3b receptors, without activation to C3a or C5a
type and amount of antigen and antibody transfused. receptors. There is no intravascular RBC destruction.
The most common cause of AIHTR is ABO incom- Extravascular removal of opsonized RBCs occurs either
patibility. High IgM (anti-A, anti-B) antibody titers in by the spleen (C3b) or liver (IgG). The direct antibody
the recipient attach to donor erythrocyte antigen. Anti- test (DAT) becomes positive (as it does with AIHTR)
body-coated donor RBCs are referred to as opsonized from alloantibodies binding to incompatible erythro-
RBCs. Destruction of these cells and activation of cytes. The hematocrit and haptoglobin levels decrease
complement lead to acute intravascular hemolysis. slowly, but hemoglobinemia or hemoglobinuria is rare.
Although ABO antibodies are most often implicated in A low-grade fever may be produced by cytokine release
fatal reactions, antibodies to Rh, Duffy, Kell, Lewis, and or IL-1 production.
Kidd can be just as devastating. In an O-positive individ-
ual (with anti-A and anti-B antibodies), the most common Febrile Nonhemolytic Transfusion Reaction
antibody is anti-A. Anti-Rh is usually an IgG-mediated
reaction that does not generally activate complement. FNHTR, the most common type of transfusion reac-
The number of antigenic sites on the RBC varies, with tion, is related to the presence of donor leukocytes in
many more ABO antigens (2–8 % 105) per cell, in contrast transfused blood products (particularly RBCs and
to lesser antigens, such as Kell (3–6 % 103 per cell). The platelets). Typically, there is a 1° C (usually !2° C)
higher the number of antigens present, the greater the increase in temperature. Febrile reactions "2° C are
likelihood of complement activation. usually associated with transfusion of bacterial con-
Attachment of IgM begins a cascade of events leading to taminated blood products.
complement activation; cytokine, chemokine (TNF-$, IL-1, FNHTR can occur immediately or several hours after
IL-6), and kinin production; thrombin generation; tissue transfusion (usually within 4 hours) and usually resolves
factor elaboration; and platelet activation. IgM-induced within 48 hours. Chills, subjective feelings of cold,
complement activation as well as sometimes IgG-induced or rigors often accompany the febrile reaction. These
complement activation, leads to anaphylotoxin production symptoms may be present in the absence of increased
composed of complement fragments C3a, C4a, and C5a. temperature. Other conditions that produce this constel-
Activation of complement components 3, 4, and 5 (particu- lation of symptoms include AIHTR, acute extravascular
larly C3 and C5) produces cell lysis, degranulation of mast hemolytic transfusion reaction, anaphylactic reactions,
cells, histamine release, smooth muscle contraction, cyto- anaphylactoid reactions, and TRALI. Other symptoms
toxic oxygen free radical production, and chemotaxis of include headache, myalgias, nausea, and nonproductive
leukocytes. cough.
Opsonized RBCs are phagocytized, in particular by mac- FNHTR is mediated by recipient alloantibodies
rophages and less so by monocytes. These cells degranulate, against donor leukocytes. These leukocytes release cyto-
releasing histamine, serotonin, proinflammatory cytokines kines, and platelets release proinflammatory cytokines
and chemokines (including TNF-$ and kallikrein), and ac- (IL-1, IL-6, IL-8, and TNF-$), all of which act on the
tivated bradykinin. This process causes hypotension and hypothalamus producing febrile reactions.
capillary leak, producing direct and reflex tachycardia, renal Prestorage leukoreduction of RBC and platelet units
dysfunction, and often respiratory distress. TNF-$, which has markedly reduced the incidence of FNHTR. Before
is produced during hemolysis, also leads to endothelial the practice of prestorage leukoreduction, temperature
tissue factor release and extrinsic followed by intrinsic elevation occurred in 43%–75% of transfusions. Patients
coagulation cascade activation, thrombin generation, experiencing a previous febrile reaction have a 12.5%
and platelet activation; this contributes to disseminated chance of having another and should be given leukocyte-
intravascular coagulopathy (DIC) seen with AIHTR. depleted units.
Free hemoglobin binds to endothelial nitric oxide, pre-
venting the action of endothelial relaxing factor and leads Allergic Transfusion Reaction
to renovascular vasoconstriction. Norepinephrine release,
owing to hypotension induced by bradykinin, serotonin, Allergic transfusion reactions occur in about 1% of all
and histamine, leads to further vasoconstriction. Destroyed transfusions. Manifestations range from the most common
red cell stroma induces further vasoconstriction and clogs mild reaction (e.g., urticaria, pruritus, swelling, rash) to
microtubules. IL-1, IL-1 receptor antagonist, and IL-6 the relatively rare anaphylactoid and anaphylactic reac-
activation of genes also occurs, leading to RBC autoanti- tions. Allergic reactions are due to release of histamine
body and alloantibody production, which may have a part when donor plasma proteins attach to preformed IgE
in delayed hemolytic transfusion reaction (DHTR) and the or IgG antibodies on mast cells in sensitized individuals.
degree to which extravascular hemolysis occurs. Histamine may also be infused from stored blood prod-
ucts. Allergic reactions are more likely to occur with fresh
frozen plasma transfusions. However, a reaction can occur
Acute Extravascular Hemolytic Transfusion
with RBC and platelet transfusions because there is plasma
Reaction
in these blood products as well.
Acute extravascular hemolytic transfusion reaction gen- Anaphylactic reactions consist of bronchospasm, severe
erally involves non-ABO antigen groups. They are most hypotension, tachycardia, urticaria, and possibly laryngeal
232 SECTION 8 Blood
edema. Awake patients may also complain of dyspnea, storage. Staphylococcus aureus, Staphylococcus epidermidis,
chest pain, nausea, and vomiting. This reaction occurs Streptococcus species, and gram-negative organisms
most commonly in IgA-deficient individuals, who are can contaminate blood components. Salmonella has been
sensitized by exposure to “foreign” IgA proteins from pre- reported as a contaminant in platelets.
vious transfusions or pregnancy, or individuals lacking in Transfused bacteria or endotoxins or both can lead to
other plasma proteins, such as haptoglobin. Anaphylactoid sepsis, with release of proinflammatory cytokines and
reactions usually occur with a larger volume of transfusion, interleukins (IL-1, TNF-$) as well as complement acti-
are less severe, and are often proportionate to the volume vation; this produces the clinical picture of sepsis. Inter-
infused. leukin and cytokine interaction with endothelial smooth
muscle locally produces nitric oxide, which leads to the
refractory hypotension of sepsis. Sudden development of
Hypotensive Transfusion Reaction
hypotension and rigors in awake patients or hypotension
A hypotensive transfusion reaction, in which the systolic and DIC symptoms in anesthetized patients suggests a
or diastolic blood pressure decreases at least 30 mm Hg bacteria-contaminated transfusion. The incidence of
within the first few minutes of a blood transfusion, may septic transfusions has decreased by the routine use
be the result of contact activation (intrinsic coagulation of bacterial monitoring systems, some of which detect
pathway) and generation of bradykinin and other kinins. oxygen consumption of blood components.
Septic transfusions, anaphylaxis, TRALI, and acute he-
molytic transfusion reactions may also manifest in this Transfusion-Related Lung Injury
manner. Awake patients may experience facial flushing,
nausea, abdominal pain, shock, and respiratory distress. The incidence of TRALI is 1:1000–1:4500 transfu-
Bradykinin acts on kinin receptors of blood vessel sions. Although uncommon, TRALI is the leading
endothelium leading to hypotension and edema forma- cause of transfusion morbidity and accounts for 47% of
tion from intracellular fluid leaking. Because angiotensin- transfusion-related deaths. It can occur with a transfu-
converting enzyme breaks down bradykinin, this reaction sion of any blood-derived product, although more
is most often seen in patients taking angiotensin- commonly with platelets and plasma. There is a higher
converting enzyme inhibitors. Contact activation can incidence with blood component transfusion donated
occur with the use of blood warmers, with the use of from multiparous women (because of their exposure to
some leukoreduction filters, and from prostate glandular fetal blood) or from individuals who received multiple
kininogen. transfusions in the past. Despite supportive measures
and aggressive ventilatory support, there is a 5%–10%
mortality rate.
Bacteria-Contaminated or Septic Transfusion
TRALI is any noncardiogenic pulmonary edema oc-
Because of improved viral contamination detection, most curring within 6 hours of a transfusion. It is associated
infectious transfusion reactions are caused by bacterial with chills, hypoxemia, and fever. Bilateral pulmonary
contamination of transfused blood products. Individuals infiltrates are seen on chest x-ray, and severe pulmonary
may present with mild fever or frank sepsis leading to insufficiency may develop similar to adult respiratory
hypotension, respiratory distress, acute kidney failure, distress syndrome. In mild cases, there is dyspnea, with
DIC, and circulatory collapse. Septic transfusions are spontaneous resolution of symptoms. Most patients
usually associated with an increase of "2° C in tempera- (approximately 70%) require intubation and mechanical
ture. Absence of hemoglobinemia (and hemoglobinuria) ventilation. The lung injury is usually transient, with re-
distinguishes this reaction from AIHTR. turn of preevent oxygenation levels within 72–96 hours,
Blood product contamination may occur from asymp- although occasionally this may take a week to resolve.
tomatic donors who later develop infection; transmission of Under general anesthesia, it may be difficult to differen-
donor skin flora into the collection system; contamination tiate TRALI from acute hemolytic reaction, hypotensive
of collection bags, which then contaminate phlebotomists; reaction, anaphylactic reaction, septic transfusion, and
and bacterial contamination of water baths used to thaw transfusion-associated circulatory overload.
blood component units. Blood donations are declined from TRALI probably occurs as a two-step process. In
individuals with temperatures "37.5° C, or who present many cases, it develops in patients with preexisting
with infectious symptoms such as upper respiratory symp- conditions (e.g., recent surgery, malignancy, infec-
toms and diarrhea. tions). These preexisting conditions cause neutrophil
There is a higher incidence of transmitted bacterial priming, allowing them to marginate and sequester
infections from platelets that are stored at room tem- along the pulmonary vasculature. The second step
perature (22° C) than RBCs (stored between 1° C and 6° occurs when transfused blood activates these primed
C). The longer the storage time ("5 days), the greater leukocytes and cytotoxic granules are released. Cyto-
the risk of bacterial infection. Although the U.S. Food toxic substances disrupt endothelium resulting in inter-
and Drug Administration limits platelet storage to 5 days, stitial and alveolar edema. The mechanism involves
platelets are still the most common cause of transfusion- transfused lipids, granulocytes, major antibodies, or
transmitted bacterial infections. Sepsis may occur from platelet-derived proinflammatory mediators (CD40)
any contaminated blood component transfusion. reacting with sequestered recipient leukocytes. How-
Some bacteria, such as Pseudomonas, Enterobacter, and ever, TRALI can also occur with fresh frozen plasma
Yersinia, can grow at the low temperatures used for RBC transfusions that have no cellular components.
46 Transfusion Reaction 233
Transfusion-Associated Circulatory Overload the next time crossmatching is performed. When the
recipient is reexposed to the RBC antigen, a secondary
Rapid administration of blood products may result in immune response is triggered, and antibody levels
TACO. Individuals at particular risk are patients with increase with a more rapid and larger reaction than
preexisting cardiac disease or renal insufficiency. TACO occurred during the first exposure, lysing donor RBCs;
may manifest as congestive heart failure with dyspnea, this usually occurs in the spleen and reticuloendothelial
oxygen desaturation, circulatory overload, jugular venous system, and it results in a less severe reaction and is
distention, increasing central vascular pressures (central self-limiting. This response most commonly occurs
venous pressure, pulmonary capillary wedge pressure), in the Rh group. The most common presentation is
and tachycardia. a low-grade temperature, increasing bilirubin, and
In a nonbleeding patient, transfusion rates should be unexplained decreasing hemoglobin. A newly positive
limited to 2–3 mL/kg/hour and less in patients with car- DAT is diagnostic.
diovascular compromise. TACO may easily occur with
rapid transfusion devices, when active bleeding has
Graft-versus-Host Disease
stopped and aggressive transfusion continues.
GVHD may occur 8–10 days after transfusion, although
Other Acute Transfusion Reactions it is more commonly seen with bone marrow transplan-
tation. It more commonly occurs in immunocompro-
Hyperkalemia. Rapid transfusion with multiple units mised patients, in whom unopposed donor lymphocytes
of older RBCs can lead to intravascular hyperkalemia. attack recipient tissues. It can be seen in organ trans-
This condition usually occurs when administered blood plant recipients and neonates who had a blood exchange
is near the end of its expiration date, and large volumes transfusion. It can also occur in immunocompetent re-
have been transfused. A review of U.S. combat patients cipients who are transfused blood from first-degree rela-
in Iraq demonstrated that 7 units of RBCs were needed tives. The mechanism of GVHD is that both the donor
to increase potassium (K&) concentrations transiently to and the recipient have similar human leukocyte antigen
"5.5 mEq/L. As storage time increases, there is a linear haplotypes. The recipient does not reject the donor
increase of K& concentration in the supernatant. RBCs lymphocytes, but the donor recognizes the recipient as
have a K& concentration of 2 mEq/L, which increases having foreign cells and initiates an immune response.
to 45 mEq/L over 42 days of storage, using citrate- Irradiation is the only effective method to reduce the
phosphate-dextrose (CPD) preservative. Sodium-adenine- incidence of GVHD.
glucose-mannitol is used in Canada and Great Britain. Bone marrow is frequently involved resulting in
CPD or CPD with adenine is commonly used in the aplasia. Involvement of the liver and skin is often
United States. unrecognized. Patients frequently die from bleeding
Other factors predisposing to hyperkalemia include diatheses and infections within several weeks.
hypovolemia, small patient size, amount of blood trans-
fused, and prior irradiation of transfused blood. The in-
Delayed Acquired Transfusion-Transmitted
crease in K& appears to be transient and is often normal
Infection
several hours after transfusion. Techniques to limit the
increase of K& include use of in-line K& scavenging filters, Delayed acquired transfusion-transmitted infections
RBC washing (by the blood bank or more expeditiously include the hepatitis viruses B and C, cytomegalovirus,
with a cell saver), infusing through larger bore intravenous and human immunodeficiency virus (HIV). Modern
catheters, and insulin-dextrose treatment. screening techniques employed by blood banks have
significantly reduced the incidence of these transfu-
Citrate Toxicity. Massive transfusions have been associ- sion-transmitted infections. At the present time, the
ated with transient increases in citrate levels. Citrate American Association of Blood Banks reports the risk
is normally metabolized in the liver. Large volumes of of acquiring hepatitis B virus is 1:137,000 transfusions;
RBCs, reduced liver perfusion or function, and hypo- hepatitis C virus, 1:1,1000,000 transfusions; and HIV,
thermia impair citrate metabolism leading to increased 1:1,900,000 transfusions.
citrate levels. Citrate binds calcium and magnesium lead-
ing to hypocalcemia and hypomagnesemia, which can
5. How are different transfusion-related reactions
impair cardiac function and produce coagulopathy.
managed?
Delayed Transfusion Reactions Immediate recognition and treatment of transfusion
Delayed Hemolytic Transfusion Reaction reactions provide for the best results. Awake patients
describe myriad symptoms, including chills, fever, rigors,
DHTR usually occurs 3–10 days after transfusion and headache, back and flank pain, chest pain and spasms,
is usually mild. It occurs more commonly extravascu- lightheadedness, heart racing, dyspnea, itching, and a
larly but can occur intravascularly as well. DHTR is feeling of impending doom. In an anesthetized patient, a
usually due to an amnestic antigen-antibody response. transfusion reaction may manifest as hypotension, shock,
The recipient, after exposure to RBC antigen (previ- decreased oxygen saturation, bronchospasm, urticaria,
ous transfusion or pregnancy), develops antibodies coagulopathy, increased bleeding, venipuncture oozing,
whose levels decrease over time and are undetectable and hemoglobinuria.
234 SECTION 8 Blood
Management of an acute transfusion reaction is directed Broad-spectrum antibiotics administered for septic
at removing the cause and assessing airway, breathing, and transfusions have met with equivocal results. Pressor
circulation. The transfusion is stopped immediately, and support is often required. Febrile reactions are treated
the unit of blood is removed. Whether the intravenous with acetaminophen or nonsteroidal antiinflammatory
tubing should also be removed has been debated. The drugs or both and supportive care.
theoretical benefit of removing the intravenous tubing is
that any further blood product contained within the tubing 6. Can transfusion reactions be prevented?
would be prevented from reaching the patient. However,
this manipulation may result in loss of intravenous access, The incidence of transfusion reactions can be mark-
which could be devastating in a hypotensive patient requiring edly reduced but probably not eliminated. The most
emergent care. important preventive measures are proper patient and
During this time, airway patency is established, adequate correct blood sample identification. Restriction of
oxygenation and ventilation are ensured, and hemody- blood donations from multiparous women, disqualifying
namic support is provided. In an awake patient, supple- individuals with a history of transfusion-related reac-
mental oxygen should be provided. If oxygen desaturation tions, eliminating designated donors, and safe blood
or a shock state develops (as with AIHTR, allergic trans- banking techniques all contribute to safe transfusion
fusion reaction, TRALI, or TACO), tracheal intubation practices.
and ventilation with positive end expiratory pressure The choice of transfused blood and blood products
should be instituted to maintain oxygenation. In the oper- could decrease the incidence of adverse transfusion reac-
ating room with an anesthetized and already intubated tions. Leukoreduction may decrease incidences of febrile
patient, administered oxygen should be increased to reactions, nonhemolytic transfusion reactions, and perhaps
100%. An increased amount of positive end expiratory TRALI. Irradiation of blood components can decrease the
pressure to maintain alveolar stability and recruitment incidence of GVHD reactions. Allergic reaction can be
and increased minute ventilation may be required. These limited by transfusing saline washed cells, whereas anaphy-
maneuvers may be especially helpful for TRALI and lactic reactions can be limited by transfusing washed RBCs,
associated adult respiratory distress syndrome. Some frozen deglycerolized RBCs, or RBCs from IgA-deficient
data suggest that steroid use may be beneficial in TRALI. donors.
Diuretics are indicated for patients with TACO but not Single donor platelet apheresis is probably safer than
for patients with TRALI. multiple donor units with respect to transfusion reactions
Pressor support may be required. Phenylephrine, nor- and infections. The risk of TRALI, allergic reactions,
epinephrine, or epinephrine (particularly for anaphylactic and volume overload or TACO is greater with fresh fro-
or anaphylactoid reactions) is generally used. Vasopressin zen plasma transfusion than cryoprecipitate. However,
and occasionally methylene blue infusions may be neces- the chance of infection is higher with cryoprecipitate
sary in refractory hypotension, particularly in hypotensive because 10 donors are required rather than 4 donors,
transfusion reactions. which are used in plasma.
A health care worker should be designated to:
• Confirm the unit’s identification information against
the patient’s name band to rule out clerical errors. SUGGESTED READINGS
• Send a blood sample from the patient to the blood Choate JD, Maitta RW, Tormey CA, et al.: Transfusion reactions to blood
bank along with the removed blood component unit and cell therapy products. In Hoffman R, Benz EJ Jr, Silberstein LE,
for retyping and crossmatching (compatibility testing) et al. (eds): Hematology: Basic Principles and Practice, 6th edition.
Saunders, Philadelphia, 2013.
as well as for a DAT. Davenport RD: Pathophysiology of hemolytic transfusion reactions.
• Send blood samples to the laboratory for complete Semin Hematol 42:165, 2005.
blood count, coagulation profile, free hemoglobin Domen RE: Adverse reactions associated with autologous blood transfu-
levels, haptoglobin concentrations, electrolytes, blood sion: evaluation and incidence at a large academic hospital. Transfusion
38:296, 1998.
urea nitrogen, and creatinine. An arterial blood gas Gilliss B, Looney M: Experimental models of transfusion-related acute
should be analyzed as well. A urine sample is sent to lung injury. Transfus Med Rev 25:1, 2011.
detect the presence of hemoglobin. National Healthcare Safety Network (NHSN): Biovigilance Compo-
• Obtain cultures from the blood component unit if nent. Centers for Disease Control and Prevention, Atlanta, GA,
bacteria contamination is suspected. 2011.
Roback JD, Grossman BJ, Harris T, et al. (eds): Technical Manual,
If hemoglobinemia or hemoglobinuria is present, 17th edition. American Association of Blood Banks, Bethesda, MD,
treatment to protect renal function should be instituted. 2011. Shirey RS, King KE, Ness PM: Hemolytic transfusion reactions:
This treatment includes fluid administration to increase acute and delayed. p. 668. In Hillyer CD, Silberstein LE, Ness PM, et al.
urine output, diuretics (e.g., furosemide, mannitol), and (eds): Blood Banking and Transfusion Medicine, 2nd edition.
Churchill Livingstone, Philadelphia, 2007.
urine alkalinization by infusion of sodium bicarbonate Stramer SL, Hollinger FB, Kleinman S, et al.: Emerging infectious dis-
(add 75 mEq of sodium bicarbonate to 1 L of 0.5 normal ease agents and their potential threat to transfusion safety. Transfusion
saline and infuse at 125 mL/hour). 49(Suppl 2):1, 2009.
Allergic reactions are treated with diphenhydramine, Tinegate H, Birchall J, Gray A, et al.: Guideline on the investigation
25 to 50 mg, and famotidine, 20 mg intravenously. The and management of acute transfusion reactions. Prepared by the
BCSH Blood Transfusion Task Force. Br J Haematol 159:143, 2012.
combination of histamine H1 and H2 blockers is more Vraets A, Lin Y, Callum JL: Transfusion-associated hyperkalemia.
effective than H1 blocker therapy alone. Epinephrine is Transfus Med Rev 25:184, 2011.
the mainstay therapy for anaphylactic reactions.
CASE 47
Perioperative Coagulopathies
Edward R. Mathney, MD
QUESTIONS
1. Which patients require preoperative coagulation 4. How are perioperative coagulopathies diagnosed?
evaluation? 5. How are perioperative coagulopathies treated?
2. What laboratory tests are performed to diagnose
preoperative coagulopathies?
3. What are the most common perioperative
coagulopathies?
A 56-year-old man with hepatitis C cirrhosis and hepato- then be designed. An argument can be made for obtain-
cellular carcinoma involving segments II and III presents ing preoperative coagulation studies in the absence of
for left hepatectomy. Preoperative laboratory tests show a bleeding history if the scheduled procedure is associ-
hemoglobin concentration, 9.8 g/dL; platelet count, 102 ! ated with a catastrophic (e.g., intracranial surgery) or
109/L; prothrombin time (PT), 16 seconds (normal PT high (e.g., hepatic resection) risk of bleeding. Preop-
range, 11–15 seconds); international normalized ratio (INR), erative coagulation studies also may be indicated in
1.3; and partial thromboplastin time (PTT), 49 seconds situations where the patient cannot provide a history
(normal PTT range, 25–39 seconds). (e.g., unconscious patient) and is undergoing a high-
risk procedure. However, preoperative coagulation
abnormalities may not reflect the etiology of intraop-
1. Which patients require preoperative coagulation
erative coagulopathies.
evaluation?
The goal of preoperative coagulation evaluation is to 2. What laboratory tests are performed to diagnose
optimize patient safety by identifying prothrombotic and
antithrombotic tendencies that may influence the periop-
preoperative coagulopathies?
erative course. The more recent paradigm shift toward PTT was originally developed to monitor heparin effects
evidence-based approaches to preoperative evaluation on the intrinsic coagulation cascade (Figure 47-1). PTT
and testing includes coagulation. Increased evidence has is sensitive to changes in factors I, II, V, VIII, IX, X, XI,
exposed the shortcomings of routine laboratory testing and XII; heparin; fibrinogen degradation products; ac-
and point-of-care (POC) devices for monitoring coagula- quired or congenital factor inhibitors; hypothermia;
tion in goal-directed management of intraoperative and hypofibrinogenemia. PT was developed to monitor
coagulopathies is becoming more common. vitamin K antagonist medications (specifically warfa-
“Routine” preoperative coagulation studies are not rin) and their effects on the extrinsic coagulation cas-
useful. Platelet count, PT, and PTT are rarely abnor- cade. PT is sensitive to changes in factors I, II, V, VII,
mal in patients without a clinical indication for such and X. To overcome interlaboratory variation in PT
tests (e.g., excessive bleeding after dental procedures). caused by different reagents, INR was introduced. Dif-
Abnormalities in these screening tests rarely affect intra- ferent pretest variables can affect PT and PTT results.
operative blood loss but may lead to further unnecessary Automated PT/PTT instruments can be affected by
testing and increased exposure to blood products. Instead elevated hematocrit ("55%), which prolongs clotting
of routine laboratory testing, all preoperative coagula- time; plasma turbidity owing to lipemia (in nonfasting
tion evaluations should begin with a personal and family patients), hemolysis, or elevated bilirubin. The time
standardized bleeding history, medication history, and between specimen collection and PTT testing (i.e.,
physical examination, with the goal of identifying pa- "4 hours) can lead to a falsely prolonged clotting time
tients in need of further investigation (Table 47-1). because of factor VIII lability.
When asked about medications, some patients neglect to Platelets are critical for hemostasis. Tissue injury ex-
mention homeopathic and natural remedies that may poses extracellular matrix proteins to which platelets
affect coagulation. adhere using von Willebrand factor (vWF) as a bridge.
When adverse factors are identified, further investi- Platelets are then “activated,” releasing fibrinogen, fac-
gation should be performed to define the specific co- tor V, factor VIII, vWF, adenosine diphosphate, adenos-
agulopathy. A perioperative management strategy can ine triphosphate, calcium, serotonin, histamine, and
235
236 SECTION 8 Blood
epinephrine, all of which recruit and activate additional associated with adequate hemostasis. Although there
platelets as well as activate plasma-mediated coagula- are no absolute guidelines, platelet transfusion should
tion. Exposed platelet glycoprotein (GP) IIb/IIIa recep- be considered if the platelet count is $10 ! 103/#L or
tors provide binding sites for fibrin cross-linking. $50 ! 103/#L in a patient with bleeding or a perioperative
Platelet abnormalities can be either quantitative or patient. The decision to transfuse platelets must be
qualitative. Quantitative platelet abnormalities are de- weighed against the risk of viral or bacterial infection,
tected by platelet counts most commonly performed by transfusion-related acute lung injury (TRALI), stroke,
automated machines but may require manual counts and death.
when platelet values are abnormally low. Hemodilution Despite a normal platelet count, qualitative platelet
and ethylenediamine tetraacetic acid (EDTA)–induced abnormalities may exist (e.g., uremia, von Willebrand
platelet clumping are common causes of falsely low plate- disease [vWD], antiplatelet therapy). Platelet function
let counts. Generally, platelet counts "100 ! 103/#L are analyzers can detect qualitative platelet abnormalities
47 Perioperative Coagulopathies 237
FIGURE 47-1 ■ Coagulation cascade. (From Porwit A, et al. [eds]: Bone Marrow Pathology. Churchill Livingstone, Philadelphia, 2011.)
Intrinsic pathway factor deficiency Normal PT, h PTT Specific plasma-derived factor
(e.g., hemophilia) concentrates, PCC, rFVIIa, FFP,
cryoprecipitate, fibrinogen
Factor VII deficiency Normal PT, h PTT concentrate
Dabigatran Hemodialysis
Rivaroxaban PCC
Congenital or Congenital (e.g., von Willebrand Decreased platelet Consider transfusion if platelet count
acquired disease, Bernard-Soulier syndrome, function (possibly $50 ! 103/#L or if platelet dysfunc-
platelet Glanzmann thrombasthenia) with normal platelet tion is suspected
dysfunction Antiplatelet medications count)
CPB Thrombocytopenia
ECMO
ACT, activated clotting time; CPB, cardiopulmonary bypass; DDAVP, desmopressin; ECMO, extracorporeal membrane oxygenation; FEIBA,
factor eight inhibitory bypass activity; FFP, fresh frozen plasma; IVIG, intravenous immunoglobulin; PCC, prothrombin complex concentrate;
PT, prothrombin time; PTT, partial thromboplastin time; rFVIIa, recombinant factor VIIa; FVII, factor VII; FDP, fibrin degredation products.
47 Perioperative Coagulopathies 239
allowing for targeting treatment to deficient compo- from the thromboelastography result. The residual
nents. Use of POC devices for goal-directed therapy maximal amplitude measurement reflects fibrinogen
has been shown to reduce blood product administra- activity only, enabling determination of platelet con-
tion in cardiac, liver, trauma, and obstetric surgery. tribution to total clot strength. The platelet mapping
Several institutions have developed transfusion algo- assay modification allows for identification of platelet-
rithms based on POC measurements with some reported inhibiting drugs.
success. Rotational thromboelastometry (ROTEM; Tem Inno-
Thromboelastography (TEG; Haemonetics, Brain- vations GmbH, Munich, Germany) is another viscoelastic
tree, MA) measures viscoelasticity of whole blood from monitor of coagulation that has more widespread use in
initiation of fibrin formation to maximal platelet clot Europe but has been approved by the U.S. Food and Drug
strength and through fibrinolysis (Figure 47-2). A blood Administration for use in the United States since 2011
sample is placed in a cuvette that is rotated slowly to ac- (Figure 47-4). A blood sample is placed in a cuvette, and
tivate clotting. The following five values represent differ- instead of the cuvette rotating (as in thromboelastogra-
ent mechanisms of clot formation: phy), the sensor shaft placed in the cuvette rotates. Rota-
• r value—time to initial fibrin formation tional thromboelastometry provides information similar to
• Increased values imply factor deficiency or inhibitor thromboelastography on coagulation in a sample of whole
• K value—time from the end of R time to an ampli- blood. The following parameters are measured:
tude of 20 mm • Clotting time—time from the start of the reaction
• Reflects clot kinetics to an amplitude of 2 mm
• Affected by any variable that would slow clot • Reflects defects in plasma-mediated coagulation
formation (e.g., factor deficiency, heparin) (e.g., factor deficiency, heparin)
• ' angle—tangent of the curve made as K is reached • Clot formation time—time from an amplitude of
(20 mm) 2–20 mm
• Reflects the kinetics of fibrin production and • Involves fibrin polymerization and clot stabilization
cross-linking • Affected by platelet function and to some degree
• Affected by any variable that would slow clot fibrinogen and coagulation factors
formation (e.g., factor deficiency, heparin) • Maximum clot firmness—maximal amplitude of the
• MA (Maximal Amplitude) tracing
• Indication of clot strength • Reflects platelet count, platelet function, and
• Depends on both platelet number and function as fibrinogen concentration
well as adequate fibrinogen levels • Maximum lysis—percent reduction in clot firmness
• Lysis of the developed clot—measured at both • Identifies hyperfibrinolysis
30 minutes and 60 minutes Modifications to rotational thromboelastometry allow
• Reflects degree of fibrinolysis identification of the pathologic mechanism of intraopera-
• If abnormal, implies excess plasminogen activity tive coagulopathy (Table 47-3).
Figure 47-3 depicts thromboelastography results seen Platelet POC tests have not had as much success in
with different coagulation abnormalities. goal-directed management of hemostasis as viscoelastic
Different additives can be used with thromboelas- measures of coagulation. The platelet function analyzer
tography measurements to improve diagnostic capa- (PFA-100; Siemens Healthcare Diagnostics, Deerfield,
bilities. The addition of heparinase identifies abnor- IL) measures in vitro bleeding time by using a vacuum to
mal coagulation secondary to excessive heparin activity. perfuse blood through an aperture in the presence of
If excessive fibrinolysis is detected, antifibrinolytics platelet activating compounds. Further studies have
can be added to assess efficacy of treatment. c7E3 Fab shown that the platelet function analyzer requires plate-
(ReoPro), a monoclonal antibody that binds to plate- let counts "100 ! 103/#L and a hematocrit "30%. It
let GP IIb/IIIa receptors, eliminates platelet activity has a high negative predictive value and a low positive
30 min
αº
MA A30
20 mm
r K
Thrombosis Fibrinolysis
FIGURE 47-2 ■ Thromboelastography (see text for explanation). (From Deakin C: Clinical Notes for the FRCA. Churchill Livingstone, Philadelphia,
2011.)
47 Perioperative Coagulopathies 241
Normal
R;K;MA;Angle = Normal
Anticoagulants/hemophilia
Factor deficiency
R;K = Prolonged
MA;Angle = Deceased
Platelet Blockers
Thrombocytopenia/
Thrombocytopathy
R ~ Normal; K = Prolonged;
MA = Decreased
Hypercoagulation
R;K = Decrease;
MA;Angle = Increased
D.I.C
Stage 1
Hypercoagulable state with
secondary fibrinolysis
Stage 2
Hypercoagulable state
FIGURE 47-3 ■ Normal and abnormal thromboelastography results. (From Deakin C: Clinical Notes for the FRCA. Churchill Livingstone,
Philadelphia, 2011.)
! - angle (°)
60
40
40 → Clot Quality
60
CT=Clotting Time (sec)
10 20 30 40 50
Min
FIGURE 47-4 ■ Rotational thromboelastometry. (From Armstrong S, Fernando R, Ashpole K, et al.: Assessment of coagulation in the
obstetric population using ROTEM thromboelastometry. Int J Obstet Anesth 20:293, 2011.)
242 SECTION 8 Blood
predictive value for etiology of inadequate hemostasis, ($1.6). Mildly abnormal coagulation studies are unreli-
diminishing its utility in transfusion algorithms. Platelet- able predictors of perioperative blood loss. FFP is only
works (Helena Laboratories, Beaumont, TX) compares partially effective in correcting coagulopathy associated
platelet counts in a control sample with counts after with warfarin use and liver disease.
platelet activation and aggregation, giving a percentage In the setting of massive transfusion, FFP is inade-
of reactive platelets. Plateletworks has been shown to quate to increase plasma fibrinogen levels, necessitating
correlate with standard methods of laboratory platelet cryoprecipitate administration. An estimated 30 mL/kg
counts and can detect GP IIb/IIIa receptor inhibition of FFP is needed to increase plasma fibrinogen by 1
and platelet dysfunction related to CPB. g/L, whereas 15 mL (1 unit)/10 kg of cryoprecipitate
increases plasma fibrinogen by 0.5 g/L. More recently,
the first fibrinogen concentrate became available in the
5. How are perioperative coagulopathies treated?
United States, but it is approved by the U.S. Food and
Treatment of perioperative coagulopathies involves re- Drug Administration only for afibrinogenemia and
storing the deficient components of coagulation and hypofibrinogenemia. Current evidence is shifting to-
eliminating the cause. PRBCs are transfused to increase ward the need for higher fibrinogen levels to provide
oxygen-carrying capacity but may also play a role in sufficient fibrin clot polymerization. All current recom-
promoting hemostasis because red blood cell (RBC) mendations suggest fibrinogen levels "1 g/L, with
mass leads to margination of platelets near vessel walls some European guidelines recommending "1.5–2 g/L,
and sites of vascular injury. In addition, RBCs release in the setting of perioperative bleeding. It has been sug-
adenosine diphosphate under shear stress, which aids in gested that high fibrinogen levels ("3 g/L) may even
activation of platelets. compensate for thrombocytopenia.
FFP contains all the components of coagulation found Prothrombin complex concentrate (PCC) contains
in patients’ plasma, including factors, anticoagulants, and factors II, IX, and X (and VII in Europe) at levels 25 times
natural antifibrinolytics. Evolving evidence suggests that those seen in FFP. PCC eliminates disadvantages of FFP
early intervention with FFP during massive transfusion administration such as volume overload, hemodilution,
and higher FFP-to-RBC transfusion ratios (%1:1) may infection, and the need for crossmatching. PCC is recom-
lead to a mortality benefit. Currently, there are no guide- mended to antagonize the effects of warfarin and can treat
lines to standardize the optimal FFP-to-RBC ratio. The specific factor deficiencies. Evidence for use in dilutional
risk of viral transmission, TRALI, and volume overload coagulopathy and massive transfusion is equivocal. Its use
must be weighed against the benefits of plasma transfu- must be weighed against the risk of thrombosis in the
sion. In the presence of factor inhibitors (e.g., acquired presence of diluted antithrombin. Factor eight inhibitor
hemophilia, heparin, direct thrombin inhibitor, or factor bypass activity (FEIBA), containing factors II, IX, X, and
Xa inhibitor), FFP is ineffective to treat or prevent bleed- activated VII, is useful in patients with hemophilia A or B
ing because the inhibitor acts against the factors in FFP with inhibitors.
as well. Large volumes of FFP (15–30 mL/kg) are neces- Recombinant activated factor VII (rFVIIa) is thought
sary to achieve adequate factor concentrations when to bind to tissue factor at the site of vascular injury and
there is a deficiency and ongoing losses. FFP is not effec- amplify thrombin generation. As with PCC, evidence for
tive in correcting mildly elevated PT, PTT, and INR rFVIIa use in hemodilution is equivocal, and it is likely
47 Perioperative Coagulopathies 243
efficacious only with adequate fibrinogen levels. The the benefits of antifibrinolytic therapy when considering
theoretical risk of thrombotic complications must be administration of these medications.
weighed against the risk of ongoing hemorrhage. There Successful treatment of perioperative coagulopathies
are numerous reports of rFVIIa effectiveness as an off- depends on diagnosing the deficiency and treating with the
label use during life-threatening hemorrhage that is un- appropriate replacement component. Continual monitor-
responsive to conventional management. ing and assessment are important because changing coagu-
Platelet transfusion is usually considered when the lopathies may require different management strategies.
count becomes $50 ! 103/#L, although considering
margination in vivo and release of sequestered platelets,
the threshold for transfusion is unclear. If platelet dys- SUGGESTED READINGS
function is suspected, transfusion may restore functional Kamal A, Tefferi A, Pruthi R: How to interpret and pursue an abnormal
prothrombin time, partial thromboplastin time, and bleeding time in
platelets to the circulation. adults. Mayo Clin Proc 82:864, 2007.
Desmopressin (DDAVP), a V-2 receptor agonist, Kozek-Langenecker SA: Perioperative coagulation monitoring. Best
stimulates vWF release from endothelial cells and in- Pract Res Clin Anaesthesiol 24:27, 2010.
creases available factor VIII. Outside of hemophilia A Levi M, van der Poll T: Disseminated intravascular coagulation: a re-
(factor VIII deficiency) and vWD, DDAVP is thought to view for the internist. Intern Emerg Med 8:23, 2013.
Levy JH, Faraoni D, Spring JL, et al.: Managing new oral anticoagulants
increase platelet adhesion to vessel walls and promote a in the perioperative and intensive care unit setting. Anesthesiology
state of heightened coagulability and fibrin formation. It 118:1466, 2013.
has been shown to decrease perioperative blood loss, but Seicean A, Schiltz NK, Seicean S, et al.: Use and utility of preoperative
it may not reduce perioperative transfusion of PRBCs. hemostatic screening and patient history in adult neurosurgical patients.
J Neurosurg 116:1097, 2012.
Usefulness may be limited in critically ill patients already Slaughter TF: Coagulation. In Miller RD, Eriksson LI, Fleisher LA, et
receiving exogenous vasopressin. al. (eds): Miller’s Anesthesia, 7th edition. Churchill Livingstone,
As previously stated, several situations may favor Philadelphia, 2009.
fibrinolysis, and the efficacy of antifibrinolytics (e.g., Sniecinski RM, Karkouti K, Levy JH: Managing clotting: a North
&-aminocaproic acid and tranexamic acid) for reducing American perspective. Curr Opin Anaesthesiol 25:74, 2012.
Tinmouth A: Evidence for a rational use of frozen plasma for the treat-
blood loss and PRBC transfusion requirements has been ment and prevention of bleeding. Transfus Apher Sci 46:293, 2012.
shown in trauma, cardiac, orthopedic, and hepatic sur- Warner DS: Pathophysiology and treatment of coagulopathy in massive
gery. Risk of thrombotic events must be weighed against hemorrhage and hemodilution. Anesthesiology 113:1205, 2010.
CASE 48
Blood Replacement
Mark Gettes, MD
QUESTIONS
A 70-year-old, 70-kg man is scheduled for revision total Under normal conditions (e.g., absence of pulmonary
hip prosthesis. He has a history of hypertension con- disease, normal Hb, physiologic shunt of 2%–3%), arterial
trolled on medical therapy, and type 2 diabetes mellitus. oxyhemoglobin saturation is approximately 97%, and
He is otherwise in good health. The starting hemoglobin the partial pressure of dissolved oxygen is approximately
(Hb) and hematocrit (Hct) are 13 g/dL and 40%, respec- 100 mm Hg. CaO2 can then be calculated as follows:
tively. He predonated 2 units of his own blood
and states that he wishes only his own blood to be used CaO2 ! (15 g/dL " 1.34 " 0.97)
during surgery. # (100 mm Hg " 0.0031)
CaO2 ! 19.5 # 0.31
1. How is oxygen transported? CaO2 ! 20 mL O2/100 mL blood
A major function of the circulation is to carry oxygen to This calculation demonstrates that the amount of oxygen
tissues for use in metabolism. Oxygen delivery ( DO2 ), or dissolved in plasma (0.31 mL/100 mL blood) is negligible
oxygen transport, is the product of two factors: blood compared with the amount carried by Hb (19.5 mL/
flow, or cardiac output (CO), and the amount of oxygen 100 mL blood).
carried in the blood, or arterial oxygen content (CaO2): Because oxyhemoglobin binding factor (1.34) and SaO2
DO2 ! CO " CaO2
(0.97) are constant under normal conditions, CaO2 varies
almost linearly with Hb concentration. Under abnormal
As oxygen content of blood decreases, DO2 can be conditions, such as obesity and term pregnancy, rapid falls
maintained by a proportionate increase in CO. in SaO2 during induction of anesthesia result in immediate
Oxygen in blood exist in two forms. It is bound by Hb decreases in CaO2. The compensatory tachycardia may or
and dissolved in plasma. The oxygen content of 100 mL may not be sufficient to maintain normal DO2 .
of blood is described by the following equation:
CaO2 ! (Hb " 1.34 " SaO2) # (PaO2 " 0.0031) 2. Describe the compensatory mechanisms for blood
loss.
where CaO2 is arterial oxygen content in milliliters of
oxygen per 100 mL of blood, SaO2 is percent of arterial Blood loss results in diminished intravascular volume and
Hb saturated with oxygen, and PaO2 is partial pressure of reduced oxygen-carrying capacity secondary to loss of
arterial oxygen. Hb. As intravascular volume decreases, compensatory
244
48 Blood Replacement 245
vasoconstriction and tachycardia occur in an attempt to pre- TRICC (Transfusion Requirements in Critical Care) trial
serve CO. Continuing volume loss results in decreased CO, found no significant difference in outcomes in patients
reducing DO2 to tissues. Restoration of intravascular vol- assigned to a transfusion trigger of Hb 7 g/dL as opposed
ume by infusion of either colloid solution in a 1:1 ratio to to Hb 10 g/dL. Certain complications (i.e., myocardial
blood loss or crystalloid solution in a 3:1 ratio allows normal- infarction, congestive heart failure) were higher in the
ization of CO and maintenance of hemodynamic stability. Hb 10 g/dL group. Similarly, a study comparing transfu-
Several mechanisms are available to respond to loss of sion thresholds in patients with cardiac risk factors
oxygen-carrying capacity. First, CO may increase with undergoing surgery for hip fracture found no significant
restoration of intravascular volume, maintaining or increas- improvements in outcomes when using a transfusion
ing DO2 . Second, at the tissue level, oxygen extraction threshold of Hb 8 g/dL as opposed to Hb 10 g/dL.
may increase. Normal mixed venous oxygen saturation is The safest blood transfusion is no transfusion. However,
approximately 75%; this indicates that only 25% of avail- if “no blood transfusion” is not an option, potential compli-
able oxygen is being extracted. A substantial reserve of cations of blood transfusion can be decreased by using the
oxygen is available to the tissues, which can be used simply patient’s own blood, rather than blood from a donor.
by increasing the amount extracted. As of this writing, the current practice guidelines of the
American Society of Anesthesiologists (ASA) for periopera-
3. What is the minimum acceptable hemoglobin tive blood transfusion reflect the consensus that previously
recommended thresholds of Hb 10 g/dL were unnecessar-
concentration (transfusion trigger)?
ily high. The precise transfusion trigger has yet to be deter-
If blood loss continues during surgery, even if intravascu- mined. The ASA practice guidelines state that “red blood
lar volume is maintained, oxygen-carrying capacity even- cells should usually be administered when the hemoglobin
tually falls too low to meet metabolic demands, and red level is less than 6 g/dL and . . . are usually unnecessary
cell transfusion is required. The minimum safe level of when the level is more than 10 g/dL.” The guidelines also
Hb, or transfusion trigger, is a question on which much support the use of preadmission blood collection, acute
attention has been focused. In the mid-twentieth century, normovolemic hemodilution, and intraoperative red blood
advances in the science of transfusion medicine and the cell recovery in situations where autologous blood is
greater safety of blood banking led to routine transfusion required or preferred.
of patients to maintain an arbitrary Hb level of $10 g/dL
or Hct $30%. However, fueled largely by awareness 4. List potential sources of autologous blood.
of the role of blood transfusion in the transmission of
acquired immunodeficiency syndrome (AIDS), recogni- Physician awareness of the dangers associated with ho-
tion of morbidity associated with blood transfusion grew. mologous blood transfusions as well as increased pressure
Increasingly, attempts have been made to determine from the public to avoid transfusions has led to an increased
scientifically the transfusion trigger—the Hb threshold use of autologous blood sources. These sources are the
at which red cell transfusion is warranted. following:
From animal models and from experience with other- • Preoperative autologous blood donation
wise healthy Jehovah’s Witnesses, it is known that survival • Acute isovolemic hemodilution (AIHD)
is possible with a Hct of 5%–6% (Hb 2 g/dL) if normo- • Intraoperative cell salvage
volemia is maintained. Experience with other chronically • Postoperative cell salvage
anemic patients, such as patients with renal failure, showed Each of the above-listed autologous blood sources has a
that Hct values in the low 20s are routinely tolerated. From role to play in avoidance of homologous transfusion.
these data, it is apparent that previously recommended
transfusion triggers of Hb 10 g/dL and a Hct of 30% are
5. Explain acute isovolemic hemodilution.
unnecessarily restrictive.
Attempts to determine the transfusion trigger have AIHD is a procedure in which whole blood is removed
focused in particular on patients with risk factors for car- perioperatively, while intravascular volume is maintained
diac disease. Maximal stress on DO2 occurs in the heart, by simultaneous infusion of crystalloid or colloid solu-
with 70% of available oxygen extracted, as opposed to tions. The blood, which is withdrawn into standard blood
25% for the body as a whole. If CaO2 decreases, the re- bags containing anticoagulant, is available for transfusion
serve for increased extraction is low, and the only available to the patient either during surgery or in the postoperative
compensatory mechanism is to increase coronary blood period. In this way, autologous whole blood containing red
flow. In patients with coronary artery disease, ability to cells, clotting factors, and platelets is available. The advan-
increase coronary blood flow may be compromised, and tages of AIHD are summarized in Box 48-1.
the critical Hct level—the transfusion trigger—may be
much higher. Similarly, patients with significant valvular 6. Outline the physiologic response to acute
heart disease or poor ventricular function as well as isovolemic hemodilution.
patients in whom CaO2 is limited by pulmonary disease
or who are in hypermetabolic states with large oxygen To understand how AIHD may be safely accomplished, it
extractions may have high transfusion triggers. is necessary to understand the physiologic response to its
Although not defining a precise transfusion trigger, use. As previously discussed, DO2 is the product of CO
several studies concur that the previous transfusion trigger and CaO2. As whole blood is withdrawn for isovolemic
of Hb 10 g/dL or Hct 30% was unnecessarily high. The hemodilution, red cells are removed from the circulation
246 SECTION 8 Blood
BOX 48-4 Selection of Patients for Acute containing either heparin or citrate. The suction
Isovolemic Hemodilution pressures used in cell salvage systems are low ((100
mm Hg) to avoid hemolysis of collected blood. The
• Indications blood is passed through a filter to remove debris and
• Anticipated blood loss $1000 mL stored in a canister until a sufficient volume is present
• Starting hematocrit $36% for further processing.
• Contraindications Concentration: The mixture of blood, anticoagulant,
• Anemia and irrigating solution collected by the suction is
• Coronary artery disease passed into a centrifuge bowl, where the heavier red
• Left ventricular dysfunction cells are retained and the lighter elements are spun
• Valvular heart disease
• Renal disease
off and discarded.
• Pulmonary disease Washing: A large volume of saline is passed through the
• Carotid stenosis centrifuge bowl, further removing noncellular ele-
ments and debris, leaving red cells suspended in saline.
Reinfusion: The red cell/saline mixture is pumped from
the centrifuge into a standard plastic infusion bag,
wide variety of cases, including major urologic surgery, which is available for transfusion back to the patient.
orthopedics, gynecologic surgery, plastic and reconstruc- Modern cell salvage devices can process and return a
tive surgery, neurosurgery (brain and tumor resection), unit of blood every 3 minutes in the face of rapid bleeding.
and cardiothoracic surgery. Reduction in homologous
blood usage has been reported to range from 18%–90%. 10. Outline the characteristics of blood obtained
Age per se is not a contraindication to hemodilution, and
use of AIHD has been described in both elderly and
by cell salvage.
pediatric patients. Salvaged autologous blood differs from banked blood
Because the major compensatory mechanism for hemo- and other sources of autologous blood in many ways.
dilution is increased blood flow, isovolemic hemodilution is Salvaged autologous blood is basically a suspension of red
contraindicated in patients whose ability to increase either cells in saline. The Hct of salvaged blood may vary de-
systemic or coronary blood flow might be compromised. pending on the amount of blood collected from the field
AIHD is contraindicated in patients with anemia, carotid but is typically in the 50%–60% range. Once processed,
artery stenosis, coronary artery disease, left ventricular salvaged blood contains essentially no clotting factors or
dysfunction, and aortic or mitral valve stenosis. Because platelets. If large volumes of salvaged blood are used to
of the fluid shifts involved, AIHD is contraindicated in replace surgical blood loss, dilutional thrombocytopenia
patients with renal or pulmonary disease. and low levels of clotting factors may result. Salvaged
Significant preexisting myocardial or brain disease blood does not exhibit the storage lesion that is present
represents a contraindication to isovolemic hemodilution in banked blood (Table 48-1). The 2,3-diphosphoglycer-
because myocardial ischemia and cerebral hypoxia are its ate level of salvaged blood is normal, and it does not
major associated complications. Coagulopathies emanat- exhibit the low pH, elevated potassium, and microaggre-
ing from reduced factor levels may be exacerbated by gate formation found in banked blood. Chromium-
dilutional effects. labeling studies have shown that salvaged red cells have
normal survival times after they are reinfused. Indices
9. What is intraoperative cell salvage, and how do of red cell viability, such as resistance to osmotic stress,
are superior in salvaged blood compared with banked
modern cell salvage devices work?
blood.
Intraoperative cell salvage is a procedure in which blood
lost during surgery is collected and made available for 11. Discuss the indications and benefits
transfusion back to the same patient. Modern cell-saving
devices function by a four-step process, as follows: of intraoperative cell salvage.
Collection: Blood is suctioned from the surgical field and Intraoperative cell salvage has been used in various surgical
mixed in the suction tubing with an anticoagulant settings, and its ability to reduce homologous blood use is
the perioperative period. A surgical blood loss of BOX 48-6 Preoperative Autologous Blood
&1000 mL should be anticipated. The surgical blood Donation
schedule serves as a guide to whether or not transfu-
sion is likely. Patients should not be encouraged to INDICATIONS
donate blood for procedures in which there is little • Blood loss $1000 mL
chance of significant blood loss.
Criteria for donation of autologous blood are less PATIENT CRITERIA
stringent than the criteria for volunteer donation. Autolo- • Hb 11 g/dL
gous donors need at least a predonation Hb of 11 g/dL or • Hct 33%
Hct of 33%. Age is not a criterion for predonation. • Age is not a criterion
In patients weighing $50 kg, 450 mL of whole blood is CONTRAINDICATIONS
donated at each visit. In patients weighing (50 kg, the
volume of blood removed is proportional to weight, using • Bacteremia
• Lack of intravenous access
the following formula: • Cardiac disease
Volume of the blood donated in mL/450 mL • Unstable angina
! donor weight (kg)/50 kg • Aortic stenosis
• Left main coronary artery disease
PABD requires a suitable interval between the deci-
sion to undertake surgery and the date of the operation. NOT CONTRAINDICATIONS
The storage life of blood is 35 days. Consequently, there • HIV
is no point in donating blood $5 weeks preoperatively. • HBsAg
A unit of blood may be banked every 3 days, depending • History of malignancy
on the donor’s Hct, but donations are usually made every
HB, Hemoglobin; HBsAG, hepatitis B surface antigen; Hct, hematocrit;
7 days. Units can be donated up to 3 days preoperatively. HIV, human immunodeficiency virus.
In the event that surgery is postponed, blood may be
frozen to prevent outdating if necessary.
In rare cases where collection of large numbers of
15. What are the disadvantages and risks of
autologous units is required, blood may be frozen and
stored over long periods. Patients should be started on preoperative autologous blood donation?
oral iron therapy when the decision to predonate blood Some risks associated with blood transfusions (i.e., ABO
is made. Use of recombinant erythropoietin to increase incompatibility owing to clinical or administrative error,
the amount of blood available for predonation and to bacterial contamination) are not eliminated by PABD.
decrease the interval between donations has been de- For this reason, it is generally argued that the criteria for
scribed and may be beneficial in patients who are anemic, transfusing a unit of autologous blood (i.e., transfusion
in patients who require large numbers of autologous trigger) should be the same as for a homologous unit.
units, or in situations where the presurgical intervals are Other experts believe that because the risks associated
short. Erythropoietin therapy as described is expensive with autologous blood are decreased relative to homolo-
and remains experimental as of this writing. gous blood, the risk-to-benefit ratio is altered, and the
There are several contraindications to PABD. Because criteria for transfusion of autologous blood should be
microorganisms may proliferate during blood storage, liberalized.
septicemia is an absolute contraindication to predonation. Paradoxically, use of PABD can result in a lower Hct
Lack of intravenous access may also prohibit predonation. at discharge. A reduced Hct occurs because many pa-
Patients who are positive for HIV or hepatitis B surface tients who predonate blood do not have adequate time in
antigen (HBsAg) may predonate blood. Such units must the interval before surgery to regenerate fully the amount
be labeled and segregated to protect other patients who of blood they donated. These patients are essentially
might erroneously receive the units as well as workers hemodiluted at the time of surgery. If they do not receive
handling the units. Retransfusing this blood requires a a blood transfusion (because of low intraoperative blood
special order from the patient’s physician. loss), their discharge Hct will be lower than if they had
As in other aspects of transfusion medicine, patients not predonated.
with cardiac disease represent a gray area in terms of Similarly, in an era of cost-effectiveness analysis, the
risk. Most centers exclude patients with unstable use of PABD has been challenged. In certain surgical
angina, aortic stenosis, or left main coronary artery settings (e.g., total joint replacement), the use of PABD
disease but accept donors with stable coronary artery decreases by approximately 70% the likelihood that a
disease. Some investigators have advocated monitoring patient will require homologous transfusion. In other
(blood pressure, electrocardiography [ECG], pulse, settings (e.g., hysterectomy), fewer patients require
and oxygen saturation), simultaneous fluid administra- transfusion, and a higher percentage of the units
tion, and physician supervision of high-risk patients collected by PABD are discarded. Factors that increase
making autologous donations. Future studies are the cost-effectiveness of PABD include appropriate case
needed to define precisely the risk in these patients. selection (i.e., cases where there is a high likelihood that
In contrast to homologous blood donation, a history the units will be transfused) and providing a long enough
of malignancy is not a contraindication for PABD time interval between donation and surgery to allow regen-
(Box 48-6). erative erythropoiesis to occur. The use of erythropoietin
250 SECTION 8 Blood
is a mandatory part of informed consent for any opera- syndrome, and spongiform encephalopathies on the
tion in which blood transfusion is likely. safety of the blood supply is of concern to both the public
AIHD has the advantage of low cost and is a point-of-care and the medical community. Spurred by such factors, the
intervention. It obviates the need for planning weeks in popularity of so-called bloodless surgery programs, de-
advance and eliminates the risk of administrative error asso- signed to reduce or minimize exposure to homologous
ciated with stored blood. It is of comparable efficiency and blood, has increased, and such programs are offered by
costs less than PABD or cell salvage. However, the amount approximately 100 centers in the United States.
of red blood cells saved by AIHD is quite small and usually A comprehensive program to decrease homologous
clinically insignificant. For AIHD to be clinically useful, blood exposure uses all of the techniques discussed in this
both low Hct and large surgical blood losses must be safely chapter. Additional factors contributing to decreased
tolerated. Numerous authors have raised concerns about the blood loss include careful surgical techniques; mainte-
iatrogenic introduction of risk in patients with previously nance of normothermia; use of regional anesthesia; and,
unappreciated cardiac disease from moderate or profound in select patients, use of hypotensive general anesthesia.
hemodilution. Because of such concerns, the use of AIHD is When combined with an appropriate transfusion trigger,
probably of limited benefit to older patients. Its use is prob- these techniques all contribute to minimizing patient
ably least controversial and of greatest benefit in pediatric or exposure to homologous blood.
young adult patients with a low likelihood of unappreciated
cardiac disease, who are not anemic, and who are having
surgeries with large anticipated blood loss. SUGGESTED READINGS
Intraoperative cell salvage is a widely used and highly
American Society of Anesthesiologists: Practice guidelines for peri-
effective method of reducing exposure of patients to operative blood transfusion and adjuvant therapies. Anesthesiol
homologous blood, and this procedure can rapidly pro- 105:1, 2006.
vide autologous blood for return in cases involving large Brecher ME, Goodnough LT: The rise and fall of preoperative
amounts of bleeding. Its use has been criticized largely autologous blood donation. Transfusion 41:1459, 2001.
Gillon J: Controversies in transfusion medicine—acute normovolemic
on the grounds of cost-effectiveness, with the break- hemodilution in elective major surgery: con. Transfusion 34:270, 1994.
even point at 2 units of blood. However, expenses can Goodnough LT: Risks of blood transfusion. Crit Care Med 31:S678,
be limited by initially setting up only the collection 2003.
(suction) part of the apparatus. Later, after confirming Goodnough LT: The role of recombinant growth factor in transfusion
that sufficient blood has been collected, the more costly medicine. Br J Anaesth 70:80, 1993.
Klinberg IW: Autotransfusion and blood conservation in urologic oncology.
remainder of the system can be installed. In this way, Semin Surg Oncol 5:286, 1989.
unnecessary costs associated with cell salvage can be Murray DF, Gress E, Weinstein SL: Coagulation after reinfusion of
decreased. Although theoretical concern exists about autologous scavenged red blood cells. Anesth Analg 75:125, 1992.
using cell salvage in cases of malignancy and bactere- Pomper GJ, Wu YY, Snydre EL: Risks of transfusion-transmitted
infections: 2003. Curr Opin Hematol 10:412, 2003.
mia, clinical studies and experience have not shown an Rossi EC, Simon TL, Moss GS (eds.): Principles of transfusion medicine,
increase in either metastatic tumor spread or infection 2nd edition. Lippincott, Williams & Wilkins, Philadelphia, 1995.
rates. Intraoperative cell salvage is an essential part of Shan H, Zhang P: Viral attacks on the blood supply: the impact of severe
blood conservation programs. acute respiratory syndrome in Beijing. Transfusion 44:467, 2004.
Advances over the past decade have greatly decreased Shander A: Surgery without blood. Crit Care Med 31:S708, 2003.
Simpson P: Perioperative blood loss and its reduction: the role of the
the likelihood of transmission of viral diseases such as anaesthetist. Br J Anaesth 69:498, 1992.
HIV and hepatitis C via blood transfusion. Nonetheless, Stehling LC, Zauder HL: Acute normovolemic hemodilution. Transfusion
avoidance of blood transfusion remains a significant pub- 31:857, 1991.
lic concern and has been identified as one of the most Toy PT, Strauss RG, Stehling LC, et al.: Predeposited autologous
blood for elective surgery: a national multicenter study. N Engl J
important factors in a patient’s decision as to where to Med 316:517, 1987.
seek medical care. The potential impact of emerging Williamson KR, Taswell HF: Intraoperative blood salvage: a review.
diseases such as West Nile virus, severe acute respiratory Transfusion 31:663, 1991.
CASE 49
QUESTIONS
A 13-year-old girl with idiopathic scoliosis was scheduled • Adolescent idiopathic scoliosis occurs between age
for posterior spinal fusion with instrumentation. The 10 years and skeletal maturity and is more commonly
patient’s past medical history was otherwise unremark- seen in girls.
able. She had no prior surgical history. The patient was a There are many causes and associated conditions in
Jehovah’s Witness. which scoliosis may occur (Box 49-1).
2. How is scoliosis classified? 4. What will a Jehovah’s Witness refuse and accept
in terms of blood transfusions?
Idiopathic scoliosis is the most common form of scoliosis.
There may be a genetic component, but, as the name The policy of the Watchtower Bible and Tract Society
implies, its cause is unknown. Idiopathic scoliosis can be (WTS) with regard to blood is based on Jehovah’s Witnesses
divided into three different types: infantile, juvenile, and (JW) elders’ interpretation of biblical passages. The JW el-
adolescent. ders determined that blood transfusions violate God’s law.
• Infantile idiopathic scoliosis is diagnosed between JWs believe that blood removed from the body must be
birth and up to 3 years of age and has a higher inci- discarded. Many JWs refuse blood transfusions of whole
dence among boys. Most of these curves resolve blood and its primary components including red blood cells,
spontaneously without treatment. The curves of white blood cells, platelets, and plasma. Fractions obtained
infantile idiopathic scoliosis are thought to be sec- from primary blood components are potentially acceptable
ondary to molding in utero. to JWs (Figure 49-2).
• Juvenile idiopathic scoliosis is diagnosed between JWs do not participate in preoperative autologous
the ages of 3 and 10 years and is more evenly distrib- blood donation. JWs embrace the use of nonblood alter-
uted between boys and girls. natives. Intraoperative acute normovolemic hemodilution
252
49 The Jehovah’s Witness Patient 253
FIGURE 49-2 ■ Blood components acceptable to Jehovah’s Witnesses. (Reprinted with permission from
Bodnaruk ZM, Wong CH, Thomas MJ. Meeting the clinical challenge of care for Jehovah’s Witnesses.
Transfus Med Rev 2004;18:105–16.)
7. Describe the preoperative evaluation of patients Cardiovascular impairment is seen in patients with
with scoliosis. scoliosis. Mitral valve prolapse is the most common
cardiovascular abnormality associated with scoliosis.
Preoperative evaluation begins with a history and phys- Severe restrictive lung disease may cause changes in
ical examination. It should include the etiology and pulmonary vasculature leading to pulmonary hyperten-
implications for anesthetic management. Factors for sion. Pulmonary hypertension can produce right ven-
consideration involve the degree of spinal curvature, tricular failure or cor pulmonale. Clinical findings of
cardiopulmonary impairment, and coexisting disease. cor pulmonale include an S4 heart sound, jugular venous
Box 49-2 lists studies that may be performed as part of distention, hepatomegaly, pedal edema, and a left para-
the preoperative evaluation. Some or all of these tests sternal lift.
are ordered depending on the severity of scoliosis.
Pulmonary function tests can play a major role in 8. What are the intraoperative anesthetic
determining anesthetic management for patients un-
considerations for posterior spinal fusion surgery?
dergoing posterior spinal fusion surgery. Restrictive
lung disease is the most commonly encountered pul- If a wake-up test is planned, this unusual procedure must
monary abnormality observed with scoliosis. A vital be explained to patients during the preoperative interview.
capacity of #30% of predicted value forecasts the need In most patients, preoperative sedation is acceptable.
for postoperative ventilation. Pulmonary function tests However, some patients with scoliosis have significant re-
can determine if obstructive disease is responsive to spiratory dysfunction contraindicating preoperative seda-
bronchodilators. tion. Further impairment of an already tenuous respiratory
system can cause hypoxemia, hypercarbia, and acidosis.
Either inhalation for pediatric patients or intravenous
induction is acceptable. If somatosensory evoked poten-
BOX 49-2 Preoperative Evaluation for tial and motor evoked potential monitoring are planned,
Patients with Scoliosis isoflurane, sevoflurane, or desflurane should be main-
tained at !0.5 minimum alveolar concentration. The
• Etiology and implications of scoliosis preferred anesthetic technique for cases involving evoked
• Cobb angle potential monitoring is infusion of a hypnotic agent
• Hematocrit and platelet count such as propofol and an opioid such as remifentanil.
• Blood type and crossmatching Neuromuscular blocking agents are avoided if motor
• PT/PTT, INR evoked potentials are used. (See Chapter 18 for further
• Chest radiograph details.)
• Electrocardiogram
• Pulmonary function tests (in the presence of restrictive or
In addition to the standard intraoperative monitors,
obstructive lung disease) an arterial catheter and a urinary catheter should be
• Spirometry (FVC, FEV1, FEV1/FVC) placed. The arterial catheter allows for measuring arte-
• Lung volumes (TLC, FRC, RV, FRC/TLC, RV/TLC) rial blood pressure on a beat-to-beat basis and facilitates
• Arterial blood gas (in the presence of severe pulmonary blood sampling. For most of these cases, placement of
disease) a central venous catheter is not warranted and is left to
• Assessment for cardiovascular impairment the discretion of the anesthesiologist. Transesophageal
• Coexisting disease echocardiography may be necessary in the presence of
severe cardiopulmonary disease.
FEV1, Forced expiratory volume in 1 second; FRC, functional residual
capacity; FVC, forced vital capacity; INR, international normalized Turning and positioning the patient prone require
ratio; PT, prothrombin time; PTT, partial thromboplastin time; RV, extreme care. It is important to avoid pressure on the
residual volume; TLC, total lung capacity. eyes. Retinal artery occlusion and blindness have been
49 The Jehovah’s Witness Patient 255
reported after back surgery performed with the patient in overall reduction in surgical blood loss is minimal. Acute
the prone position. It is also necessary to avoid pressure normovolemic hemodilution and antifibrinolytic ther-
necrosis of the ears, nose, and forehead. The head should apy are less commonly employed.
be in proper alignment and positioned so that easy in- A detailed review of techniques to minimize blood
spection of the face can be achieved. The chest, abdo- loss is beyond the scope of this chapter. Table 49-1 sum-
men, and pelvic areas should rest on parallel bolsters marizes medications that contribute to achieving induced
or other devices that avoid pressure on the axillae, breasts, hypotension. Mean arterial pressure should be maintained
and genitalia. The arms should rest at the sides with "50 mm Hg to provide adequate spinal cord perfusion and
the elbows flexed and the shoulders abducted no greater cerebral blood flow. Generally, a mean arterial pressure of
than 90 degrees to avoid stretching the brachial plexus. 50–60 mm Hg is ideal. In addition, arterial blood gases
A considerable decrease in body temperature can occur should be monitored during the procedure. Contraindica-
during spinal surgery if large body surface areas are tions to the use of controlled hypotension include preexist-
exposed. Precautions should be taken to avoid intraop- ing major end-organ dysfunction, hemoglobinopathies,
erative hypothermia. These include forced-air warming polycythemia, and elevated intracranial pressure.
blankets, intravenous fluid warming systems, and adjust-
ment of ambient temperatures. 9. What is the wake-up test?
Significant blood loss is common during this surgery.
Several techniques have been designed to minimize The wake-up test is aptly named. Patients are awakened
blood loss and the need for homologous blood transfu- intraoperatively to test motor tracts. After completion of
sion (Box 49-3). More specifically, intraoperative tech- the test, surgical anesthesia is deepened. Awareness under
niques are cell salvage, controlled hypotension, surgical anesthesia is upsetting for many patients. When wake-up
technique, and local infiltration with an epinephrine- tests are planned, they should be discussed before induc-
containing solution. The last-mentioned method helps tion. Many patients later report amnesia for the test.
to reduce bleeding at the site of infiltration, but the Most patients who remember the episode do not report
discomfort.
The wake-up test is used to assess anterior spinal cord
BOX 49-3 Strategies for Avoiding (motor) pathways. It does not investigate posterior spinal
Homologous Blood Transfusions cord (sensory) pathways. The wake-up test is performed
intraoperatively after spine instrumentation. Adequate
• Preoperative erythropoietin notice should be given to the anesthesiologist by the sur-
• Acute normovolemic hemodilution geon so as to coordinate the timing of “lightening the
• Pharmacologic therapy (e.g., tranexamic acid, aminoca-
anesthesia” to an appropriate level so that the patient can
proic acid)
• Intraoperative cell salvage with retransfusion follow commands. The wake-up test can present a chal-
• Anesthetic technique (controlled hypotension) lenge for the anesthesiologist with regard to the balance
• Surgical technique that must be maintained between the patient performing
some level of activity but without excessive movement.
The wake-up test begins by assessing the level of the patients, extubation may be delayed, and the factors
patient’s comprehension by asking the patient to squeeze leading to postoperative intubation can be the same as
the anesthesiologist’s hand. If the response is acceptable, factors associated with any general anesthetic. Addition-
the patient is asked to move the feet. If the patient is ally, factors more specifically related to patients with
unable to move the feet, spinal distraction must be scoliosis include possible underlying pulmonary dys-
decreased, and the test is repeated. Excessive distraction function, persistent muscle weakness, and issues related
can compromise spinal cord blood flow leading to is- to any coexisting diseases.
chemia and may result in postoperative paraplegia. After Postoperative anesthetic concerns focus on known
completion of the wake-up test, anesthesia is deepened complications after posterior spinal fusion surgery, and
with return to general anesthesia. these include bleeding, pneumothorax, atelectasis, respi-
The wake-up test has limitations. It evaluates the ratory distress, and neurologic deficit. Another area of
patient’s motor function at only one point in time. It has concern in postoperative anesthetic care is pain manage-
no bearing on the time following the performance of the ment. Pain in the initial postoperative period can be
test, when spinal cord injury remains a possibility. The managed by intravenous patient-controlled analgesia
wake-up test is not appropriate for young children or with opioids. In young children or cognitively impaired
cognitively impaired patients. Excessive patient move- patients, a continuous intravenous opioid infusion is sug-
ment may promote self-extubation, bleeding, air em- gested. Most patients are cared for in an intensive care
bolus, or disruption of the spinal instrumentation. unit after scoliosis repair.
At the present time, neurophysiologic monitoring
is used in almost all spine surgeries, and the wake-up
SUGGESTED READINGS
test is rarely used. Somatosensory evoked potential and
motor evoked potential monitoring offer the advantage Benson K: The Jehovah’s Witness patient: considerations for the anes-
thesiologist. Anesth Analg 69:647, 1989.
of continuous assessment throughout surgery. Bodnaruk Z, Wong C, Thomas M: Meeting the clinical challenge of
care for Jehovah’s Witnesses. Tranfus Med Rev 18:106, 2004.
Galloway G, Zamel K: Neurophysiologic intraoperative monitoring in
10. What are the postoperative anesthetic concerns pediatrics. Pediatr Neurol 44:161, 2011.
after scoliosis repair? Lin ES, Kaye AD, Baluch AR: Preanesthetic assessment of the Jehovah’s
Witness patient. Oschner J 12:61, 2012.
In most patients, the goal at the end of scoliosis repair is Tobias J: Strategies for minimizing blood loss in orthopedic surgery.
to awaken and extubate in the operating room. In some Semin Hematol 41(Suppl 1):145, 2004.
CASE 50
QUESTIONS
1. Which patient populations are at risk for sickle cell 5. Should every patient with sickle cell disease
trait and sickle cell disease? have a hemoglobin of 10 g/dL in the perioperative
2. What is the underlying genetic abnormality re- period?
sponsible for sickle cell disease, and how does 6. What are the postoperative concerns for patients
this lead to sickling? with sickle cell disease?
3. Describe the presentations of sickle cell disease. 7. Is regional anesthesia safer than general anes-
4. What are the perioperative considerations for thesia for patients with sickle cell disease; should
patients with sickle cell disease? tourniquets be avoided?
A 10-year-old boy of Mediterranean descent with sickle gene) is called sickle cell trait. This genetic makeup of
cell disease (SCD) that was diagnosed during his first year sickle cell trait may confer protection to individuals exposed
of life presented to the operating room for laparoscopic to the malaria-causing parasite Plasmodium falciparum.
cholecystectomy. At age 8 years, he was hospitalized for The homozygous genotype HbSS (i.e., two abnormal
3 days with vasoocclusive painful crisis. He currently takes beta-globin chains) results in SCD, with the potential for
no medication and had no previous surgeries. hemolysis and its resultant complications. The manifes-
tations of SCD result from deoxygenation of HbS, which
1. Which patient populations are at risk for sickle leads to hemoglobin instability and decreased molecular
cell trait and sickle cell disease? solubility. With prolonged deoxygenation, irreversible
polymerization of intracellular insoluble HbSS strands
Sickle cell trait results from asymptomatic heterozygous (gelation) begin to form; this activates sickling, a process
carriers of the abnormal hemoglobin S (HbS) gene. It of cell membrane distortion and cell deformability, giv-
occurs in 10%–30% of people in equatorial Africa as well ing red blood cells the microscopic appearance referred
as Mediterranean areas such as Sicily, southern Italy, to as sickle cells. The sickle shape of red blood cells
northern Greece, Turkey, Saudi Arabia, southwest Asia, makes for slower and difficult, or impossible, propaga-
and central India. Malaria is endemic in these areas. It has tion through blood vessels. A multifactorial process
been postulated that HbS may be protective against ma- of red blood cell clumping, hemolysis, reduced cell life
laria. However, descendants of people from these areas are span, sludging of vasculature, endothelial damage, vascular
more likely to have sickle cell disease (SCD). About 8% of obstruction or occlusion, and an inflammatory response
African Americans have sickle cell trait, whereas 0.3%–1.3% eventually leads to some of the clinical conditions
of African Americans have SCD. discussed in Question 3. The baseline hemoglobin of
patients with SCD is usually 5–9 g/dL owing to chronic
2. What is the underlying genetic abnormality hemolysis.
responsible for sickle cell disease, and how
does this lead to sickling? 3. Describe the presentations of sickle cell disease.
SCD is a heterogeneous, inherited disorder of the beta- • Acute vasoocclusive (pain) crisis, the most common
hemoglobin chain. It is a multisystem disorder that may presentation, manifests as skeletal bone pain from
manifest during childhood or adulthood, with marked occlusion by sickled cells of the vasculature resulting
variability in onset and severity. in inflammatory mediator release and subsequent
Normally, hemoglobin A (HbA), which makes up most increased intramedullary pressure and nociceptor
normal adult hemoglobin (96%–98%), is composed of two stimulation. Pain can occur at an early age (6 months)
alpha-globin and two beta-globin chains. However, HbS in the hands and feet (i.e., hand-foot syndrome) and
possesses one abnormal beta-globin chain because of a at later ages in the long bones (e.g., ribs, spine, hips.)
single valine substitution for glutamic acid at the sixth posi- More than three pain episodes per year indicate
tion of the beta-globin chain. The heterozygous carrier severe disease and risk of early death. Aggressive
state HbAS (i.e., one abnormal and one normal beta-globin management of these patients includes analgesics
257
258 SECTION 8 Blood
(e.g., patient-controlled analgesia), hydration, warmth, cholelithiasis, stroke, cranial nerve neuropathies, sickle
rest, reassurance, antibiotics, and possibly steroids. retinopathy, impaired growth, pregnancy complications,
• Acute chest syndrome (ACS) is a medical emergency in bone marrow infarcts, cardiomegaly, hematuria, renal in-
which the patient presents with chest pain, hypox- farcts, renal failure, or priapism. Autoinfarction of the
emia, and respiratory distress. ACS is the leading spleen renders these patients functionally hyposplenic or
cause of death and hospitalization in patients with asplenic and susceptible to infections with encapsulated
SCD. Treatment consists of oxygen, continuous bacterial organisms (e.g., Streptococcus pneumoniae, Neisse-
positive airway pressure or mechanical ventilation, ria meningitidis, Haemophilus influenzae). Patients with
antibiotics, bronchodilators, hydration, and possibly SCD are placed on prophylactic antibiotics.
steroids. Pulmonary infarcts and pulmonary fibrosis
are potential complications. 4. What are the perioperative considerations
• Hemolytic crisis (or aplastic crisis), although rare, for patients with sickle cell disease?
occurs when there is rapid red blood cell death and
massive suppression of normal erythropoiesis. An Preoperative assessment includes obtaining a history of
infection is often implicated (e.g., parvovirus B19, sickle cell manifestations in the past, hospitalizations,
Epstein-Barr virus). If treated appropriately, this transfusions, transfusion reactions, and a thorough re-
crisis can be self-limited with bone marrow activity view of all organ systems. A medication history should
returning in 10 days. be obtained as well, focusing on analgesic usage, steroids,
• Splenic sequestration crisis typically occurs during bronchodilators, and antibiotics. Baseline vital signs
childhood and is the result of the spleen sequester- include oxygen saturation on room air, especially for
ing a massive amount of red blood cells. It may be patients with a history of ACS. The history and physical
a minor or major event. Transfusion and elective examination dictate whether further testing, such as pul-
splenectomy may be necessary. monary function tests, echocardiogram, arterial blood
Because SCD is a multisystem disease (Table 50-1), these gas, renal function studies, and neurologic imaging is
patients can present with liver dysfunction, jaundice, indicated.
In most situations, there is little clinical benefit in
obtaining HbS levels, although an updated and recent
assessment by the patient’s hematologist should be
TABLE 50-1 Clinical Manifestations of Sickle
obtained in anticipation of surgery. Communication
Cell Disease
among the hematologist, primary care physician, sur-
Organ System Manifestation geon, and anesthesiologist is vital to establish continuity
of care. A baseline hemoglobin and type and screen are
Central nervous Acute pain warranted. Blood should be available based on the risk of
Stroke
Cranial nerve neuropathy surgery and baseline laboratory studies. Transfusion to
Peripheral neuropathy correct anemia may be necessary before surgery.
Children with SCD have a much higher risk of peri-
Ophthalmologic Sickle retinopathy
operative morbidity and mortality. Intravascular sickling
Pulmonary Infarct and sludging are potentiated in the perioperative period
Pneumonia because there is an increased risk for pain, hypothermia,
Acute chest syndrome
hypoxemia, acidosis, poor perfusion, dehydration, and
Cardiac Pulmonary hypertension anemia. These risk factors should be avoided and aggres-
Cardiomegaly sively treated in the perioperative period. The perioperative
Cardiomyopathy
Coronary syndrome goals to prevent sickling are listed in Box 50-1.
Surgical interventions are common in patients with
Hepatobiliary Cholelithiasis SCD because these patients have chronic or acute sys-
Liver dysfunction
tem dysfunctions. Frequent surgeries in patients with
Renal Hematuria SCD include cholecystectomy (elevated bilirubin
Isosthenuria levels secondary to chronic hemolysis leads to an in-
Infarct
Papillary necrosis creased incidence of cholelithiasis), splenectomy (hyper-
Renal tubular acidosis splenism, splenic sequestration of sickle cells, splenic
Renal medullary carcinoma infarction), orthopedic procedures (infections, avascular
Genitourinary Priapism necrosis), and otolaryngologic procedures. Depending
on patient factors and surgical risk, the frequency
Immunologic Infection of postoperative complications in patients with SCD
Splenic sequestration crisis
Splenic autoinfarction may be 52%.
Susceptibility to encapsulated
bacterial infections 5. Should every patient with sickle cell disease
Musculoskeletal Aseptic necrosis have a hemoglobin of 10 g/dL in the perioperative
Bone infarct period?
Hematologic Hemolytic anemia
Jaundice Transfusion in the perioperative period is controversial.
The benefits of transfusion include correcting anemia
50 Sickle Cell Disease 259
BOX 50-1 Perioperative Goals to Prevent HbS to !30%. Coordination with the patient’s health
Sickling care team is essential in these cases.
ORTHOPEDICS
260
CASE 51
QUESTIONS
1. What are the preoperative anesthetic considerations 4. Summarize the current guidelines on neuraxial anes-
for a patient with coronary artery drug-eluting stents thesia for an anticoagulated patient in terms of com-
currently taking antiplatelet medications? monly used agents, herbal agents, and new agents.
2. Is there evidence for bridging therapy to 5. What anesthetic technique would you plan for
decrease the risk of stent thrombosis resulting this patient; what are the established benefits of
from premature discontinuation of thienopyridine regional anesthesia in terms of major postoperative
therapy? outcomes?
3. What are the risks and benefits of early hip 6. Discuss the options for postoperative pain manage-
surgery in this patient; is this considered elective ment, and explain the role of continuous lumbar
surgery; would you proceed with this case? plexus and femoral blockade.
An 85-year-old woman presented for left hip arthroplasty management of patients with coronary artery stents (See
after a fall sustained 2 days previously. She has osteoar- Chapter 2 for further details). The most critical preopera-
thritis with severe hip pain and had planned to have a tive evaluation of these patients involves the type, timing,
total hip replacement in the future. She has coronary number, and location of the stents. A cardiology consulta-
artery disease for which she required two drug-eluting tion and echocardiography may be considered to assess
stents 6 months ago. Current medications are metopro- myocardial perfusion and ventricular function and to plan
lol, 50 mg, simvastatin, 20 mg, aspirin, 325 mg, and for perioperative coronary stent management. Current
clopidogrel, 75 mg. recommendations from this practice alert are summarized
as follows:
1. What are the preoperative anesthetic considerations • Delay elective noncardiac procedures for which
for a patient with coronary artery drug-eluting there is a significant bleeding risk for the following
stents currently taking antiplatelet medications? time frames:
• Bare metal stents—minimum of 1 month (usually
Elderly patients presenting for orthopedic procedures chosen over drug-eluting stents if urgent surgery
have a high prevalence of cardiopulmonary comorbidi- is imminent or planned ahead of time)
ties. These patients are at considerable risk for adverse • Drug-eluting stents—12 months
perioperative events including myocardial infarction • For all procedures (including urgent or emergent),
(MI), acute stent thrombosis, and death. The evaluation continue aspirin therapy throughout perioperative
and optimization of all cardiac risks are paramount to period.
patient survival. • Beyond this time frame, discontinue clopidogrel for
Percutaneous coronary intervention with balloon an- 7 days or ticlopidine for 14 days before surgery and
gioplasty and placement of stents within obstructed coro- restart therapy as soon as postsurgical hemostasis is
nary vessels has emerged as an effective and widespread adequate.
treatment for symptomatic coronary artery disease. After
initial implantation, the foreign body nature of stent struts 2. Is there evidence for bridging therapy to decrease
can serve as a nidus for thrombi formation. Dual antiplate- the risk of stent thrombosis resulting from premature
let therapy with aspirin and a thienopyridine derivative
discontinuation of thienopyridine therapy?
(e.g., clopidogrel) is administered to decrease the risk of
stent thrombosis. After a period of time, stent struts are In 2007, several organizations including the American
incorporated into coronary artery endothelium, and the Heart Association (AHA) and American College of
risk of thrombosis is significantly reduced. Nevertheless, Cardiology (ACC) convened and authored two publica-
patients at risk for stent thrombosis requiring elective, tions on premature discontinuation of antiplatelet ther-
urgent, or lifesaving surgery can present at any time. apy. The AHA/ACC guidelines emphasized the increased
In 2009, the American Society of Anesthesiologists risk of life-threatening stent thrombosis and acute MI
(ASA) published a practice alert to address perioperative in the perioperative period as a result of premature
261
262 SECTION 9 Orthopedics
discontinuation of thienopyridine therapy. The AHA/ reduction in mortality is calculated after adjusting for a
ACC concluded that there are no clear benefits to using myriad of perioperative confounding factors. Other benefits
any anticoagulants, including warfarin or heparin, or any of early hip surgery include decreased incidences of pneu-
antithrombotics as bridging therapy to decrease the inci- monia and pressure ulcers and improved quality of life for
dence of stent thrombosis. patients who would otherwise be bed bound. Overall, these
benefits make a strong and convincing argument that early
3. What are the risks and benefits of early hip surgical intervention reduces mortality, and hip fracture sur-
surgery in this patient; is this considered elective gery should not be classified as a purely elective procedure.
As mentioned, the best approach to explain the risks
surgery; would you proceed with this case?
and benefits is to have an informed dialogue with the
As with many difficult clinical decisions, informed dia- patient. On one hand, performing surgery after acute
logue between the patient and the perioperative care discontinuation of clopidogrel puts the patient at risk for
team regarding risks and benefits of surgery is essential the opposing problems of stent thrombosis (incidence
to ensure optimal management. In this scenario, the and mortality approximately 15%) and increased risk of
major risks of proceeding with surgery are adverse peri- bleeding. As mentioned, the dearth of large prospective
operative cardiac events from premature discontinuation clinical studies makes it nearly impossible to quantify
of clopidogrel and increased surgical hemorrhage from these individual risks. On the other hand, deferring sur-
prolonged platelet inhibition. This clinical dilemma is a gery puts the patient at significant risk for mortality
double-edged sword. According to the 2007 AHA/ACC (37%), developing pneumonia and pressure ulcers while
advisory, early discontinuation of antiplatelet therapy in bed bound, and an overall decrease in quality of life. The
patients with drug-eluting stents is associated with a urgent and complex nature of this clinical dilemma calls
25%–29% incidence of stent thrombosis. These data for a critical perioperative evaluation on an individual
come from two large cohort observational studies on basis with an interdisciplinary approach that uses all
medical patients presenting for percutaneous coronary pertinent medical information.
intervention after acute MI. The reasons for early cessa-
tion of therapy in these studies were primarily related to 4. Summarize the current guidelines on neuraxial
poor patient adherence. Although it may be unfair to anesthesia for an anticoagulated patient in
extrapolate these findings for the perioperative popula- terms of commonly used agents, herbal agents,
tion, clear evidence for guidance is lacking. Two fre- and new agents.
quently quoted studies in the surgical population, with
only 40 patients and 47 patients in each group, estab- Table 51-1 summarizes evidenced-based guidelines pub-
lished the incidence of stent thrombosis as 15%–17% lished by the American Society of Regional Anesthesia
(approximately 7 patients in each study). Both retrospec- and Pain Medicine (ASRA) in 2010. The authors note
tive studies involved withholding aspirin, ticlopidine, or that “variances from recommendations contained in this
both agents prematurely within 2 weeks after bare metal document may be acceptable based on the judgment of
stent placement in patients proceeding with noncardiac the responsible anesthesiologist.”
surgery. The antiplatelet agents were stopped at least Several recurring themes are applicable to the general
5 days before surgery in one study, whereas the other management of anticoagulated patients receiving neur-
study continued these agents up to 2 days and even on axial anesthesia, as follows:
the day of surgery. In both studies, six of the seven • Review the patient’s medical history to ensure that
patients with stent thrombosis died, resulting in an 86% there are no concomitant anticoagulants that would
case-fatality rate in patients who developed stent throm- increase the risk of spinal hematoma.
bosis. Of the 20 patients who continued antiplatelet • During neuraxial anesthesia and analgesia in high-
therapy throughout the perioperative period, only 1 died risk patients receiving anticoagulants (e.g., spinal,
after surgery. The authors explain that the stressful, pro- placing or removing epidural catheters, placing or
coagulant, and proinflammatory nature of surgery may removing deep blocks or catheters), intensive neu-
exacerbate stent thrombosis further in this setting. No rologic monitoring and vigilant nursing checks
randomized trials have studied bleeding risk in this surgi- should be established (less than every 2 hours), and
cal population. The increased risk of hemorrhage is in- neuraxial solutions to minimize sensory and motor
ferred from studies involving patients with drug-eluting blockade should be used. (This is emphasized by the
stents taking clopidogrel undergoing cardiac surgery. word MONITOR in Table 51-1.)
Given these catastrophic cardiac and possible bleeding • Low-molecular-weight heparin subcutaneous dosing
risks, it seems reasonable to postpone surgery. However, for perioperative thromboprophylaxis in hip replace-
the decision to delay hip surgery in an elderly patient is not ment is as follows:
always straightforward. First, the 30-day and 1-year mor- • Twice-daily dosing: 30 mg every 12 hours, first
tality rates in the elderly population with hip fractures are dose within 12–24 hours after surgery
5%–10% and 12%–37%, respectively. In two separate • Once-daily dosing: 40 mg once, first dose within
large meta-analyses, Simunovic et al. (2010) and Shiga et al. 9–15 hours before surgery
(2008) demonstrated 19%–40% risk reduction in mortality • Examples of high-dose low-molecular-weight
if hip surgery was performed !72 hours after fracture. heparin:
These meta-analyses were based on numerous clinical trials • Enoxaparin, 1 mg/kg every 12 hours, 1.5 mg/kg
with a cumulative number of patients up to 250,000. Risk daily
51 Total Hip Replacement 263
TABLE 51-1 The 2010 American Society of Regional Anesthesia and Pain Medicine
Recommendations for Neuraxial Anesthesia and Concomitant Anticoagulation Therapy
Wait Time between Last Needle
Wait Time between Anticoag- Puncture or Catheter Removal to
Drug Key ASRA Guidelines ulant and Needle Insertion Initiating Anticoagulation
Thienopyridine Actual risk unknown due to Clopidogrel—7 days Restart as soon as adequate
derivatives lack of clinical trials Ticlopidine—14 days surgical hemostasis is achieved
Prasugrel—5–7 days
Warfarin* Check INR if first dose Initiating therapy: INR !1.5 or No wait time necessary because
given "24 hours or more first dose given within warfarin takes "24 hours to reach
than one dose given 48 hours peak effect
preoperatively Discontinuation of long-term
therapy: 5 days with
normal INR
Heparin Safe with 5000 units SQ BID 2–4 hours after heparin is 1–2 hours
"10,000 units daily or stopped
TID dosing: Proceed but For IV or TID dosing, consider
MONITOR† MONITOR† after needle
On heparin for " 4 days insertion
obtain platelet count owing
to risk of heparin-induced
thrombocytopenia
LMWH (i.e., enoxa- No evidence for routine 12 hours for prophylactic dose 24 hours after bloody or
parin, dalteparin, checking of anti-Xa level 24 hours for higher doses difficult placement
tinzaparin) Female, elderly, renal impair- (e.g., bridging therapy, BID: first dose 24 hours; remove
ment, and concomitant DVT treatment, postopera- catheters at 22 hours after
anticoagulants associated tive prophylaxis) surgery
with increased risks of Daily dosing: "8 hours after
spinal hematoma surgery and then second dose
24 hours afterward
Remove catheter "12 hours after
last dose but 2 hours before
next dose
NSAIDs Single agent: no added risk No contraindication No contraindication
Glycoprotein IIb/IIIa Contraindicated within Abciximab—24–48 hours Unclear
antagonists 4 weeks of surgery
Risk with neuraxial anesthesia Eptifibatide and tirofiban—
unknown 4–8 hours
Thrombin inhibitors: No antidote or reversal Unknown timing from Insufficient evidence about safety
argatroban, desi- Avoid neuraxial techniques published guidelines European experience: 2–4 hours
rudin, lepirudin, Most recent ASRA expert
bivalirudin; dabig- recommendation:
atran (oral)‡ dabigatran—5–7 days
European experience:
8–10 hours
Factor Xa inhibitor: Unknown risk; proceed if Unknown 2 hours in the trial
fondaparinux; Ri- atraumatic, first-pass
varoxaban (oral)§ needle insertion§
European experience: Fondaparinux in Germany:
fondaparinux—36–42 hours 6–12 hours
Fibrinolytics/ Never proceed “except highly No data; avoid needle if No data on safety and timing
thrombolytics unusual circumstances” possible Avoid agents after needle if possible
Wait at least 10 days if neurax-
ial blockade must proceed
Herbal medications Garlic, ginkgo biloba, and No interference as single No interference as single agent
ginseng all increase agent
bleeding, but clinical
studies are lacking
ASRA, American Society of Regional Anesthesia and Pain Medicine; BID, twice a day; DVT, deep vein thrombosis; INR, international normalized ratio; IV,
intravenous; LMWH, low-molecular-weight heparin; NSAIDs, nonsteroidal antiinflammatory drugs; SQ, subcutaneously; TID, three times a day.
*See section International Normalized Ratio
†
MONITOR # Intensive neurologic monitoring, vigilant nursing checks (at least every 2 hours), neuraxial solutions to minimize sensory and motor
blockade.
‡
See section Dabigatran
§
See section Factor Xa Inhibitors
264 SECTION 9 Orthopedics
procedure-specific meta-analyses and randomized con- being unilateral and often obviating the need for uri-
trolled trials have failed to report conclusive or significant nary catheter placement; performance of this block is
clinical outcomes. Nevertheless, thoracic epidural analgesia described in Chapter 53. In the 2010 ASRA guidelines,
has been shown to reduce the incidence of MI and the risk lumbar plexus block was classified as a deep regional
of postoperative pneumonia and respiratory failure after block and subjected to the same precautions as neur-
major vascular and orthopedic procedures. Other notewor- axial anesthesia. Aggressive postoperative prophylaxis
thy advantages of high-quality epidural analgesia include a for deep vein thrombosis with enoxaparin in patients
decrease in postoperative ileus, a decrease in overall pain undergoing orthopedic procedures precludes the use
scores at rest and during activity through postoperative of an indwelling catheter for postoperative pain con-
day 4, and increase in overall patient satisfaction. trol. In this patient, in whom antiplatelet therapy is
Epidural analgesia is not the only regional technique required perioperatively, there is a minimal role for this
shown to have a role in improving postoperative out- technique.
comes. A 2006 meta-analysis comparing continuous peri- Femoral nerve blockade has been shown to be as effica-
neural analgesia with mixed systemic opioids showed cious as lumber plexus block for postoperative pain control
that perineural techniques have superior pain control for and has the advantage of not being considered a deep
48–72 hours, wider applicability in ambulatory surgery, block. A disadvantage of this block is the incidence of mo-
and significant reductions in both the length of hospital tor weakness interfering with ambulation and physical
stay and adverse effects (e.g., nausea, pruritus, sedation) therapy. Appropriate neurologic monitoring, patient and
for major orthopedic procedures. nursing education, and fall precautions should be estab-
Planning the anesthetic should involve careful consid- lished. Adjunct analgesic medications are still required
eration on balancing the risk of neuraxial hemorrhage with this modality.
with proven advantages of regional pain management in
terms of major postoperative outcomes.
SUGGESTED READINGS
6. Discuss the options for postoperative pain
American Society of Anesthesiologists Committee on Standards and
management, and explain the role of continuous Practice Parameters: Practice alert for the perioperative management
lumbar plexus and femoral blockade. of patients with coronary artery stents: a report by the American
Society of Anesthesiologists Committee on Standards and Practice
If general anesthesia is chosen for this patient’s intraop- Parameters. Anesthesiology 110:22, 2009.
erative management, a multimodal postoperative analge- Fleisher LA, Beckman JA, Brown KA, et al.: ACC/AHA 2007. Guide-
sia regimen should be considered to optimize outcomes. lines on Perioperative Cardiovascular Evaluation and Care for Non-
Regional techniques provide adequate pain control, which cardiac Surgery: Executive Summary: a report of the American
College of Cardiology/American Heart Association Task Force on
decreases cardiovascular risks postoperatively. In addition, Practice Guidelines (Writing Committee to Revise the 2002 Guide-
blunting severe pain allows for physical therapy necessary lines on Perioperative Cardiovascular Evaluation for Noncardiac
for optimal range of motion. The mainstay of postopera- Surgery): developed in collaboration with the American Society of
tive pain management is intravenous patient-controlled Echocardiography, American Society of Nuclear Cardiology, Heart
Rhythm Society, Society of Cardiovascular Anesthesiologists, Soci-
analgesia with fentanyl, morphine, or hydromorphone. ety for Cardiovascular Angiography and Interventions, Society for
However, as discussed earlier, systemic opioids are infe- Vascular Medicine and Biology, and Society for Vascular Surgery.
rior to regional techniques (especially epidural analgesia) Circulation 116:1971, 2007.
in terms of desired outcomes. Grines CL, Bonow RO, Casey DE Jr, et al.: American Heart Associa-
Medications that can be administered for multimodal tion; American College of Cardiology; Society for Cardiovascular
Angiography and Interventions; American College of Surgeons;
analgesia include acetaminophen, nonsteroidal antiinflam- American Dental Association; American College of Physicians: Pre-
matory drugs (NSAIDs), $-aminobutyric acid (GABA) vention of premature discontinuation of dual antiplatelet therapy in
analogues, N-methyl-d-aspartate (NMDA) receptor antag- patients with coronary artery stents: a science advisory from the
onists (e.g., ketamine, methadone), long-acting neuraxial American Heart Association, American College of Cardiology, Soci-
ety for Cardiovascular Angiography and Interventions, American
opioids, and peripheral regional blockade. In 2010, the College of Surgeons, and American Dental Association, with repre-
Food and Drug Administration approved the use of intrave- sentation from the American College of Physicians. Circulation
nous acetaminophen in the United States. Intravenous acet- 115:813, 2007.
aminophen has been shown to be efficacious in reducing Horlocker TT, Wedel DJ, Rowlingson JC, et al.: Regional anesthesia in the
pain scores after major orthopedic procedures, but its use patient receiving antithrombotic or thrombolytic therapy: American
Society of Regional Anesthesia and Pain Medicine Evidence-Based
is limited by cost, clinical experience, and its contraindica- Guidelines (Third Edition). Reg Anesth Pain Med 35:64, 2010.
tion in patients with liver dysfunction. In this patient Ilfeld BM, Mariano ER, Madison SJ, et al.: Continuous femoral
taking clopidogrel, NSAIDs, neuraxial opioids, and versus posterior lumbar plexus nerve blocks for analgesia after
placement of a neuraxial catheter are contraindicated. hip arthroplasty: a randomized, controlled study. Anesth Analg
113:897, 2011.
GABAergic agents and NMDA receptor antagonists are Liu SS, Wu CL: Effect of postoperative analgesia on major postopera-
useful adjuncts and should be considered in this patient. tive complications: a systematic update of the evidence. Anesth Analg
However, controversial efficacy and adverse effects limit 104:689, 2007.
the widespread use of these agents in clinical practice. Shiga T, Wajima Z, Ohe Y: Is operative delay associated with increased
Traditionally, unilateral lumbar plexus blockade involv- mortality of hip fracture patients? Systematic review, meta-analysis,
and meta-regression. Can J Anaesth 55:146, 2008.
ing a single injection or placement of an indwelling cath- Simunovic N, Devereaux PJ, Sprague S, et al.: Effect of early surgery
eter has demonstrated comparable analgesia with epidural after hip fracture on mortality and complications: systematic review
techniques. This technique also offers the advantage of and meta-analysis. Can Med Assoc J 182:1609, 2010.
CASE 52
QUESTIONS
1. Describe the anatomic structure of the brachial 4. How does one perform a supraclavicular nerve
plexus. block?
2. What are the terminal branches of the brachial 5. What role does ultrasound have in placement of a
plexus, and what do they innervate? brachial plexus nerve block?
3. How does surgical site affect the anatomic 6. How is local anesthesia systemic toxicity diagnosed?
approach to the brachial plexus; what are possible 7. How is local anesthesia systemic toxicity treated?
and expected effects of each of these blocks?
A 53-year-old, 60-kg woman with a left olecranon fracture After passing the first rib and continuing underneath the
presented for open reduction and internal fixation. Her clavicle, these divisions merge again to form three cords,
past medical history was significant for hypertension and which are named relative to their position to the axillary
mild exertional dyspnea. She had a negative nuclear stress artery: posterior (C5-T1), lateral (C5-C7), and medial
test 1 month before surgery, and her estimated ejection (C8-T1). The posterior cord is formed from the union of
fraction was 65%. Placement of a continuous supraclavicu- the posterior divisions of all three trunks and contains in-
lar brachial plexus block was performed using an ultra- nervation from all the nerve roots that compose the bra-
sound-guided technique, with an 18-gauge 50-mm Tuohy chial plexus. The lateral cord is composed of the anterior
needle via an in-plane approach in a medial-to-lateral di- divisions of the superior and middle trunks. The medial
rection. A 20-gauge catheter was inserted to a distance cord is a continuation of the anterior division from the in-
5 cm beyond the end of the needle, and 40 mL of 2% lido- ferior trunk. These cords divide into various nerve branches
caine was injected through the catheter. General anesthesia that innervate the upper extremity (Figure 52-1).
was induced to provide patient comfort while in the lateral
decubitus position, and the airway was secured with a 2. What are the terminal branches of the brachial
No. 4 laryngeal mask airway. A bolus of 20 mL of 0.375% plexus, and what do they innervate?
bupivacaine was administered via the catheter 2 hours into
the procedure, and the patient became hemodynamically The five major terminal branches of the brachial plexus
unstable. Ventricular fibrillation was seen on the electro- are the musculocutaneous, axillary, radial, median, and
cardiogram (ECG). ulnar nerves. Nerves that originate from the brachial
plexus and their sensory and motor innervations are
1. Describe the anatomic structure of the brachial listed in Table 52-1.
plexus.
3. How does surgical site affect the anatomic
Ventral rami of C5-T1 form the brachial plexus. The approach to the brachial plexus; what are possible
brachial plexus supplies motor and sensory innervation to and expected effects of each of these blocks?
the upper extremity with the exception of the trapezius
muscle and cutaneous innervation to the axilla. These The brachial plexus comprises C5-T1 nerve roots that
two areas are innervated by the ventral rami of C3 and are surrounded by prevertebral fascia. Prevertebral fascia
C4 and the intercostobrachial nerve. extends from the spine into the upper extremity. These
C5-T1 nerve roots pass posterior to the vertebral nerves divide and exit the plexus at varying points. If a
artery as they exit from the transverse processes. Shortly block is performed after a nerve has already exited the
thereafter, the nerve roots of C5 and C6 combine to form plexus, that nerve is spared. Anesthesia of the brachial
the superior trunk of the brachial plexus. The root of C7 plexus can be provided by interscalene, supraclavicular,
forms the middle trunk, and the roots of C8 and T1 form infraclavicular, or axillary approaches. Generally, a block
the inferior trunk. These three trunks pass between the that is placed anatomically distal to the spinal cord pro-
anterior and middle scalene muscles. As the three trunks vides better distal coverage of the upper extremity at the
pass over the first rib, they divide into the anterior and expense of proximal coverage.
posterior divisions of the brachial plexus, which supply The most proximal block is an interscalene nerve
ventral and dorsal innervations to the upper extremity. block. It is performed at the level of C6, between the
266
52 Brachial Plexus Anesthesia 267
FIGURE 52-1 ■ Anatomy of the brachial plexus. (From Neumann D: Shoulder complex. In: Kinesiology of the Musculoskeletal System:
Foundations for Rehabilitation, 2nd edition, Mosby, St. Louis, 2010.)
anterior and middle scalene muscles. The interscalene for surgical anesthesia of the medial hand (ulnar distribu-
block is best suited for surgery of the shoulder, upper tion). Complications of an interscalene nerve block in-
arm, and elbow and for postoperative pain relief of distal clude unilateral phrenic nerve palsy. The incidence of
clavicle surgery. The interscalene approach often does unilateral phrenic nerve palsy reaches almost 100% when
not cover the C8 and T1 nerve roots, which are crucial the nerve block is performed with a nerve stimulator
268 SECTION 9 Orthopedics
TABLE 52-2 Side Effects and Coverage Areas of Brachial Plexus Blocks
Very Likely or
Placement Definite Side Effect Possible Side Effect Coverage Area
Interscalene Ipsilateral phrenic Vertebral artery puncture Shoulder to elbow
nerve palsy* Subarachnoid puncture
Horner syndrome Recurrent laryngeal nerve block
Ptosis Neuronal injury
Miosis
Anhidrosis
Nasal congestion
Supraclavicular Ipsilateral phrenic Ipsilateral pneumothorax Distal 2⁄3 of arm including hand
nerve palsy* Subclavian artery puncture*
Horner syndrome
Recurrent laryngeal nerve block
Neuronal injury
Infraclavicular Ipsilateral pneumothorax Distal arm just above
Axillary artery puncture elbow including hand
Horner syndrome†
Ipsilateral phrenic nerve palsy†
Neuronal injury
Axillary Axillary artery puncture Forearm and hand
Hematoma Musculocutaneous nerve must
Neuronal injury be blocked separately for
lateral forearm coverage
*
Can be reduced with the use of ultrasound guidance.
†
Much less likely than in interscalene block.
technique, although this can be reduced under ultra- An infraclavicular nerve block is performed just supe-
sound guidance. This block also often results in a unilat- rior and medial to the coracoid process, approximately
eral Horner syndrome (ptosis, miosis, anhidrosis) and 3 cm below the clavicle. At this anatomic location, the
nasal congestion of the ipsilateral nares. Other possible brachial plexus has become the medial, posterior, and lateral
side effects that occur rarely include vertebral artery cords bundled closely around the axillary artery. This block
puncture, subarachnoid puncture, epidural block, and is ideally suited for surgery of the distal arm, elbow, wrist,
recurrent laryngeal nerve block (Table 52-2). and hand. The supraclavicular and infraclavicular locations
A supraclavicular nerve block is performed along the are similar in terms of block distribution. However, the in-
superior border of the clavicle just lateral to the subclavian fraclavicular block has minimal effect on respiratory func-
artery. At this level, the nerve roots seen at the interscalene tion and very low incidence of Horner syndrome compared
approach have combined to form the superior, middle, and with the supraclavicular block, especially if the latter is
inferior trunks. Bundling into trunks at this location allows achieved under a nerve stimulator technique.
for excellent coverage of the upper extremity. A supracla- An axillary block is the most distal block of the bra-
vicular block provides complete surgical anesthesia of the chial plexus and can be performed via ultrasound-guided,
distal two thirds of the arm through to the hand, including nerve stimulator, and transarterial techniques. At this
coverage where a tourniquet is usually applied, and is con- anatomic point, the nerves have reached their terminal
sidered the “spinal of the upper extremity.” Complications branches (i.e., musculocutaneous, radial, median, and
include ipsilateral hemidiaphragm paralysis (phrenic nerve ulnar nerves). Performing a block at this level provides
palsy), which has an incidence of 50% when the block is excellent surgical anesthesia of the hand and forearm.
performed under nerve stimulator guidance. More recent However, the exit of the musculocutaneous nerve from
studies have shown that the incidence of phrenic nerve the brachial plexus is variable and often occurs proximal
palsy is substantially reduced when a supraclavicular nerve to this point, so consideration must be given to blocking
block is performed under ultrasound guidance, even when the musculocutaneous nerve separately. Specifically, the
the same volume of local anesthetic is used. The different musculocutaneous nerve can be anesthetized by inject-
incidences of phrenic nerve palsy could be related to dif- ing 5 mL of local anesthetic into the belly of the coraco-
ferent needle paths and insertion points between the two brachialis muscle. If a tourniquet is required, T2 must
techniques. Given the potential for hemidiaphragmatic also be anesthetized separately; this can be accomplished
paralysis, particularly with the nerve stimulator technique, by performing a ring block with 5 mL of local anesthetic
supraclavicular approaches and interscalene techniques at the same level the axillary block was placed. Side ef-
should be avoided in patients with poor underlying respi- fects of axillary nerve blocks are limited. Axillary artery
ratory function. Other rare side effects include Horner puncture may occur and may be intentional depending
syndrome from stellate ganglion blockade and hoarseness on block technique and intravascular local anesthetic
from recurrent laryngeal nerve blockade. injection.
52 Brachial Plexus Anesthesia 269
4. How does one perform a supraclavicular ners are using this modality in lieu of nerve stimulators.
nerve block? Potential benefits of ultrasound for peripheral nerve
blocks include decreased time to block performance and
Supraclavicular nerve blocks can be performed via two dif- decreased overall complication rate, particularly in rela-
ferent techniques: the plumb-bob technique with simulta- tion to vascular puncture.
neous nerve stimulator, or ultrasound guidance, with direct Various studies have been performed to compare
visualization. For nerve stimulator techniques, patients are nerve stimulator and ultrasound-guided techniques for
positioned supine. ECG, pulse oximetry, and blood pressure brachial plexus nerve blocks. Most of these studies found
monitors are placed, and midazolam can be administered that ultrasound guidance leads to faster onset of sensory
for mild to moderate sedation and anxiolysis. The patient’s block and increased block success. Many studies also
head is turned to the contralateral side to which the block showed decreased block performance time, decreased
will be placed. The area from the lower neck lateral to the incidence of vascular puncture, and decreased number of
acromion process and inferior to just below the clavicle is needle passes. However, some studies did not clarify
prepared in sterile fashion. The lateralmost insertion of whether ultrasound scanning before performing the
the sternocleidomastoid muscle on the clavicle is identified, block was included in this performance time, leaving
immediately superior to the edge of the clavicle. A 22-gauge some controversy surrounding this claim. The increased
2-inch insulated needle is inserted perpendicular to the vascular puncture rate and increased number of needle
ground while connected to a nerve stimulator delivering 1 passes in the nerve stimulator groups did not increase the
mA of current. If flexion or extension of the digits is seen, rate of complications or affect patient satisfaction.
the nerve stimulator current is turned down to 0.4–0.5 mA. In terms of complications, evidence suggests that
If movement is still seen and negative aspiration rules out hemidiaphragmatic paresis can be avoided when per-
intravascular location of the needle tip, 40 mL of local anes- forming a supraclavicular block with ultrasound guidance
thetic is injected in 5-mL aliquots, after ensuring negative as opposed to nerve stimulator technique even when
aspiration between injections. If no muscle twitch is elicited, identical local anesthetic injections are made. Similarly,
the needle is redirected in small steps in the cephalad direc- studies suggest that using smaller volumes of local anes-
tion up to a 30-degree angle, at which point the same steps thetic can decrease hemidiaphragmatic paresis associated
can be undertaken in the caudad direction. Care must be with interscalene nerve block. Smaller local anesthetic
taken to avoid subclavian artery injection. volumes are possible when ultrasound-guided techniques
In an ultrasound-guided technique, the patient is pre- are used. One complication that is not avoided by an
pared in similar fashion. Ultrasound is used to identify the ultrasound-guided technique is nerve injury. Multiple
internal jugular vein and carotid artery. By continuously studies have demonstrated no difference in the rate of
scanning laterally from this position and just superior to nerve injury whether a block is performed by nerve
the clavicle, the next major vessel along this trajectory, the stimulator technique or ultrasound-guided technique.
subclavian artery, can be identified. The brachial plexus Finally, multiple studies have demonstrated that resi-
can be seen just lateral to the artery. Using an in-plane dents perform ultrasound-guided blocks faster and with
approach, the 50-mm needle is inserted at a 30-degree greater success compared with nerve stimulator tech-
angle from the lateral-to-medial direction. When insert- niques. Increasing availability and decreasing cost of
ing a catheter, one performs the block from a medial-to- portable ultrasound machines have resulted in increased
lateral direction, threading the catheter away from the interest for this technique and have contributed to a
subclavian artery. In either scenario, gentle aspiration resurgence in the use of regional anesthesia.
before injecting local anesthetic and at injection of every
5 mL thereafter is essential to avoid intravascular injec- 6. How is local anesthesia systemic toxicity
tion. Typically, 30–40 mL of local anesthetic is used.
diagnosed?
If the block is primarily for postoperative analgesia,
0.25% bupivacaine can be used for the entire volume. Local anesthesia systemic toxicity (LAST) is a syndrome
However, if the block is to be used in lieu of general an- resulting from intravascular accumulation of local anes-
esthesia and requires a quicker onset, at least half of the thetic. This accumulation occurs via direct intravascular
volume should be either 1.5% mepivacaine or 1.5%–2% injection of local anesthetics or from the absorption of
lidocaine. Alkalization of mepivacaine allows for a faster large deposits of local anesthetic as administered during
onset, so 2 mL of sodium bicarbonate is added per 20 mL a nerve block. In a review of 93 cases of LAST from
of mepivacaine. A block for short procedures with mini- 1979–2009, patients with preexisting cardiac and neuro-
mal postoperative pain could be performed solely with logic disease seem to be at higher risk of developing
mepivacaine or lidocaine. cardiac and neurologic symptoms.
Initial signs of systemic toxicity in an awake patient
5. What role does ultrasound have in placement include central nervous system (CNS) complaints of tin-
of a brachial plexus nerve block? nitus, metallic taste, circumoral numbness, and psycho-
motor agitation. These symptoms can progress quickly
Classically, peripheral nerve blocks were performed using to loss of consciousness, seizure, and respiratory arrest.
approximate anatomic landmarks, with nerve stimulators The aforementioned review showed that 89% of cases
that would yield paresthesias and muscular contraction included CNS involvement as presenting symptoms,
when placed in close proximity to the target nerve. With although neurologic and cardiac signs and symptoms can
increasing access to portable ultrasound, more practitio- be concurrent, particularly with intravascular injection.
270 SECTION 9 Orthopedics
QUESTIONS
1. Describe the sensory innervation of the lower for continuous infusion via the femoral nerve
extremity. catheter?
2. Which nerves are affected during anterior cruci- 7. What are the differences between a femoral
ate ligament surgery? nerve, 3-in-1, fascia iliaca, and lumbar plexus
3. What are the anesthetic options for anterior blocks?
cruciate ligament surgery? 8. How would you manage severe posterior knee
4. What is the benefit of placing a femoral nerve pain occurring postoperatively?
catheter? 9. What are the regional anesthetic options for
5. How are femoral nerve blocks performed, and how open reduction internal fixation (ORIF) of a fifth
are femoral catheters placed? metatarsal fracture?
6. Which local anesthetic would you choose for a
femoral nerve block; what solution would you use
A 29-year-old man presented for arthroscopic-assisted terminal branches of the common fibular nerve include
repair of a torn right knee anterior cruciate ligament the deep and superficial fibular nerves. The union of
(ACL). The patient was discharged home after adequate branches from the common fibular and tibial nerves
analgesia was achieved with both a femoral nerve catheter forms the sural nerve. Sensory innervation of the sacral
and a sciatic block. He returned to the emergency depart- plexus is shown in Table 53-2.
ment the following evening after falling when he got up to
use the bathroom. An x-ray showed a fracture of the left 2. Which nerves are affected during anterior
fifth metatarsal. An open reduction and internal fixation cruciate ligament surgery?
(ORIF) of the fifth metatarsal is planned.
Postoperative pain after ACL repair originates from skin
1. Describe the sensory innervation of the lower incisions, tibial periosteum at the bone tunnel site, in-
flammation and swelling within the knee joint, and the
extremity.
tendon harvest site (if an autograft is used). The nerves
Innervation of the lower extremity is derived from nerves involved are the following:
of the lumbar and sacral plexuses, sometimes collectively • Femoral nerve: skin incisions adjacent to the patellar
referred to as the lumbosacral plexuses (Figure 53-1). The tendon
lumbar plexus, which lies between the psoas major and • Tibial nerve: tibial periosteum
quadratus lumborum fascias, is derived from the ventral • Branches of femoral, obturator, sciatic nerves: internal
rami of L1 to L4, with some contribution from T12, and knee joint
branches into the iliohypogastric, ilioinguinal, genito- • Autograft harvest:
femoral, lateral femoral cutaneous (also known as the • Femoral nerve: patellar tendon
lateral cutaneous nerve of the thigh), obturator, and femo- • Obturator nerve: gracilis tendon
ral nerves. The saphenous nerve is the largest terminal • Tibial nerve: semitendinosus tendon
branch of the femoral nerve. Sensory innervation of the
lumbar plexus is shown in Table 53-1. 3. What are the anesthetic options for anterior
The sacral plexus is derived from the ventral rami of cruciate ligament surgery?
L4 to S4 and gives off the superior and inferior gluteal
nerves, the posterior cutaneous nerve of the thigh, the ACL surgery may be successfully performed under gen-
pudendal nerve, and the sciatic nerve. The sciatic nerve eral anesthesia, neuraxial anesthesia, or peripheral nerve
is composed of two nerves, tibial and common fibular block. Although general anesthesia provides excellent
(formerly known as peroneal), bound together by a operating conditions during surgery, it does not provide
common sheath. The terminal branches of the tibial postoperative analgesia. Postoperative pain relief can be
nerve include the medial and lateral plantar nerves. The accomplished with either intravenous analgesic agents
271
272 SECTION 9 Orthopedics
FIGURE 53-1 ■ Extension of nerves from the lumbosacral plexus. Sciatic nerve (divides in midthigh—tibial division and peroneal
division), femoral nerve, and obturator nerve. (From Miller MD, Chhabra AB, Hurwitz SR, et al., editors. Orthopaedic surgical approaches.
Philadelphia: Saunders; 2008. p. 434.)
or femoral or lumbar plexus blocks or catheters placed catheter provides the potential for an extended period
perioperatively. of postoperative analgesia, it is inappropriate for am-
Spinal or epidural neuraxial anesthesia provides bulatory procedures. For optimal postoperative pain
adequate analgesia for the procedure but limited post- control, a single-shot spinal technique should be com-
operative pain relief. Although placement of an epidural bined with a femoral nerve catheter. The femoral nerve
53 Lower Extremity Anesthesia 273
catheter provides extended postoperative analgesia 5. How are femoral nerve blocks performed,
without motor weakness in the nonoperative leg. and how are femoral catheters placed?
Peripheral nerve blocks alone can provide anesthesia,
with or without the addition of sedation. They can also For all blocks described in this case, the following steps are
provide postoperative pain relief, either by continuous local standard. Physiologic monitors are placed and sedation is
anesthetic infusion via a catheter or by administration of a administered, if appropriate. After the clinician dons a
long-acting local anesthetic in the original block. Depend- mask, washes hands, and puts on sterile gloves, a sterile
ing on the surgical plan, options include sciatic nerve block preparation of the skin is performed with chlorhexidine.
combined with either a lumbar plexus or fascia iliaca block. Subcutaneous infiltration with local anesthetic is achieved
before inserting the block needle. When appropriate
4. What is the benefit of placing a femoral needle placement is confirmed and after negative aspira-
tion for blood is confirmed, local anesthetic is injected in
nerve catheter?
small aliquots. Aspiration for blood should be repeated
Continuous peripheral nerve blocks have been shown to between each aliquot injection.
decrease pain, sleep disturbances, opioid use, and opioid- Multiple techniques have been described for per-
related side effects. They also improve overall patient forming femoral nerve blocks, all of which are placed in
satisfaction after moderately painful orthopedic surgeries the supine position. Differences in the techniques are as
in both the upper and the lower extremity. Femoral nerve follows:
catheters after ACL repair specifically have been shown to • Paresthesia technique: The femoral arterial pulse is
provide superior analgesia compared with intraarticular palpated and marked 1–2 cm caudad to an imaginary
or patellar tendon wound infusions, intravenous agents line corresponding to the inguinal ligament. Ap-
alone, or placebo. In studies involving total knee replace- proximately 1 cm lateral to this mark, a needle is
ment, femoral nerve catheters have been found to reduce inserted at a 90-degree angle to the skin and ad-
pain with movement, which can aid in achieving recovery vanced until paresthesias are evoked in the femoral
milestones expected during physical therapy. nerve distribution (see Table 53-1). After appropriate
274 SECTION 9 Orthopedics
needle placement is determined, 20 mL of local take longer to insert compared with nonstimulating cath-
anesthetic is injected. eters, and block success is not improved.
• Nerve stimulator technique: A stimulating needle is
advanced in an identical fashion to the paresthesia 6. Which local anesthetic would you choose
technique or at the level of the femoral crease but for a femoral nerve block; what solution
always lateral to the femoral arterial pulse. The would you use for continuous infusion via
stimulating needle is initially set to deliver 1 mA of the femoral nerve catheter?
current at a frequency of 2 Hz and then reduced to
0.2–0.4 mA once quadriceps stimulation is achieved, The desired block density and duration of postoperative
as evidenced by a “patellar snap” (visible or palpable analgesia dictate the choice of local anesthetic. For the
contraction of the quadriceps muscle), usually at initial bolus injection of local anesthetic, a long-acting
a depth of 2–3 cm. If the quadriceps response is local anesthetic such as bupivacaine or ropivacaine may be
retained as current is reduced, placement is appro- appropriate to establish lasting analgesia. A shorter-acting
priate, and local anesthetic is injected. A sartorius local anesthetic, such as lidocaine or mepivacaine, can also
muscle twitch (transverse contraction across the be appropriate and would be preferred by some because
thigh) is not considered an adequate response. If a these agents have less cardiotoxicity. If the nerve block
sartorius muscle twitch is elicited, the stimulating is the sole anesthetic, a higher concentration, such as
needle is redirected laterally until a true quadriceps 0.5% bupivacaine or 0.75%–1% ropivacaine, is required
response is appreciated. to achieve surgical anesthesia. If used as an adjunct to
• Ultrasound-guided technique: The ultrasound probe general or spinal anesthesia, a lower concentration, such
is placed in the femoral crease producing an axial as 0.25% bupivacaine or 0.5% ropivacaine, is adequate.
view. In this view, the femoral vein, artery, and For a continuous postoperative infusion via catheter,
nerve can be identified medial to lateral. The nerve a long-acting local anesthetic is preferred because it
may be approached with either an in-plane or out- provides continued analgesia even after the catheter is re-
of-plane view. In the in-plane view, the block needle moved. Typically, 0.1% –0.2% bupivacaine or 0.1%–0.3%
is advanced from lateral to medial with the goal of ropivacaine is infused at 5–10 mL per hour.
placing the tip just lateral to the femoral nerve.
When appropriate positioning is achieved, 10–20 mL 7. What are the differences between a femoral
of local anesthetic is injected under direct visualiza- nerve, 3-in-1, fascia iliaca, and lumbar plexus
tion. In the out-of-plane view, the block needle is blocks?
placed adjacent to the ultrasound probe, directly
over the femoral nerve, and advanced until its tip As previously described, femoral nerve blocks are per-
is visualized at the desired injection site (just lateral formed with the intent of anesthetizing a single nerve.
to the nerve); under direct visualization, local anes- Three-in-one blocks are performed with the intent of
thetic is injected. spreading local anesthetic around three major nerves of
The paresthesia technique is rarely used because both the lumbar plexus, the femoral, obturator, and lateral
nerve stimulator–guided and ultrasound-guided techniques femoral cutaneous nerves, as they pass in a common plane
are more successful. Nerve stimulator and ultrasound- beneath the fascia iliaca. Performance of a three-in-one
guided techniques are equally efficacious. An advantage of block is nearly identical to performance of a femoral
the ultrasound-guided technique is the ability to observe block, but a larger volume of local anesthetic, 25–30 mL,
local anesthetic spread and make adjustments midway is needed. Pressure is applied 2–4 cm below the injection
through performance of the technique, if necessary. The site during injection to promote proximal flow toward the
ultrasound-guided technique may also provide protection plexus. Even with perfect technique, the block often does
against intravascular injection of local anesthetic. not adequately anesthetize all three nerves. The femoral
A continuous nerve block catheter can be placed and lateral femoral cutaneous nerves are reliably blocked;
using any of the above-described techniques. To facilitate however, obturator nerve block is not guaranteed, with
passage of the catheter, a larger bore hollow needle is in- reported success rates ranging from 4%–78%.
serted at an acute angle to the skin. After injection of local The fascia iliaca block is performed lateral to the site
anesthetic, a catheter is threaded through the needle into where a femoral or three-in-one block is performed.
the space created by the local anesthetic bolus. After Needle entry is 1 cm below the inguinal ligament, two
threading the catheter 5–10 cm past the needle tip, the thirds the distance from the pubic tubercle to the ante-
needle is carefully withdrawn over the catheter, which is rior superior iliac spine. Using either the “two pop”
secured with a sterile dressing. An alternative method is to technique or ultrasound guidance, the needle is advanced
inject saline instead of local anesthetic to “open the space” first through the fascia lata and then the fascia iliaca. Lo-
so that the catheter can be easily threaded. Local anesthetic cal anesthetic is injected in the plane below the fascia
is injected through the catheter to ensure that anesthesia iliaca. The technique for fascia iliaca block relies on the
and analgesia occur, minimizing “secondary block failure.” anatomic proximity of the lateral femoral cutaneous and
There are two types of catheters, stimulating or non- femoral nerves below the fascia iliaca. The obturator
stimulating. The advantage of the stimulating catheter is nerve may be blocked with this technique, but as with the
that its position can be confirmed by eliciting the appro- three-in-one block, it is not reliably anesthetized.
priate muscle responses. Although some practitioners The lumbar plexus block is the only block that reliably
prefer stimulating catheters, they are more costly and anesthetizes the femoral, lateral femoral cutaneous, and
53 Lower Extremity Anesthesia 275
obturator nerves. It also blocks the genitofemoral, ilioin- should generate gluteal twitches and with further advance-
guinal, and iliohypogastric nerves. It is a deeper, more ment, usually 5–8 cm, twitches of the hamstring muscles,
difficult block to perform and carries a higher risk of calf, or foot to indicate sciatic nerve stimulation. If these
local anesthetic systemic toxicity. The block is performed twitches are preserved when the current is decreased to
with the patient in the lateral position with the operative 0.2–0.5 mA, 15–20 mL of local anesthetic is injected.
side up. Approaching posteriorly, the needle is inserted With the ultrasound-guided technique, the nerve is
3–4 cm lateral to the midline, at the level of the iliac crest. visualized deep to the gluteus maximus muscle and super-
A nerve stimulator may be used to elicit first paravertebral ficial and lateral to the ischial bone. For better anatomic
muscle twitches and then quadriceps muscle twitches. identification, color Doppler may be used to locate the
When the quadriceps muscle twitches are maintained as pudendal vessels adjacent to the ischial spine and the in-
the current is decreased to 0.5–1 mA, the needle is in the ferior gluteal artery adjacent to the sciatic nerve. The
appropriate position, and 25–30 mL of local anesthetic is sciatic nerve is imaged in the transverse or short-axis
injected. For ultrasound-guided blocks, a curved 2- to view. The block needle is advanced using either an in-
5-MHz ultrasound probe is used to approximate the depth plane or out-of-plane technique through the gluteus
of the plexus by localizing the psoas muscle. The lumbar maximus to the level of the sciatic nerve. At this point,
plexus lies within the posterior one third of the psoas nerve stimulation may be used to verify correct needle
muscle bulk (Table 53-3). placement further. Ideally, local anesthetic spread should
For all of these nerve blocks, the choice of local anes- be visualized circumferential to the nerve.
thetic would be determined by desired block density and The anterior approach to the sciatic nerve block is
duration of analgesia. more difficult and usually reserved for patients who can-
not tolerate the posterior approach position. This option
8. How would you manage severe posterior blocks the sciatic nerve further distally as it passes the
lesser trochanter. The articular branches to the hip and
knee pain occurring postoperatively?
the posterior cutaneous nerve are not included. Although
The posterior knee joint is innervated by branches of the this approach would be adequate for surgery or pain at the
sciatic nerve that are not covered by a femoral nerve cathe- level of the knee or below, it would not adequately anes-
ter. Replacing or administering a bolus of local anesthetic in thetize the thigh for tourniquet placement.
a patient with a femoral catheter would not treat this pain. Needle insertion for the anterior approach to the sci-
Available options include intravenous opioids and sciatic atic nerve is 4–5 cm distal to the femoral arterial pulse on
nerve block. Either single-shot or continuous sciatic block a line drawn perpendicular to the femoral crease. A stimu-
provides pain relief without further sedation and retains the lating needle is inserted perpendicular to the skin and
advantages conferred by the femoral nerve catheter. advanced until twitches of the calf, foot, or toes are
Sciatic nerve block is performed via either a poste- achieved, usually at a depth of 10–12 cm. If these twitches
rior or an anterior approach. The posterior approach is are maintained with the current reduced to 0.2–0.5 mA,
accomplished in the semiprone Sims position with the 20 mL of local anesthetic may be injected.
operative side up and the knee and hip flexed. Either a
nerve stimulation or ultrasound-guided technique may 9. What are the regional anesthetic options
be used. With the nerve stimulation technique, a line for open reduction internal fixation (ORIF)
is drawn between the greater trochanter and posterior of a fifth metatarsal fracture?
superior iliac spine. The needle is inserted perpendicular
to the skin 4 cm inferior to the midpoint of this line. The This patient’s fall illustrates an important point regarding
needle is advanced with a current of 1.5 mA. Stimulation patient safety after femoral nerve block. Patients with
TABLE 53-3 Comparison of Femoral, Three-in-One, Fascia Iliaca, and Lumbar Plexus Blocks
Nerve Block Site of Block Needle Insertion Nerves Blocked Amount of Local Anesthetic
Femoral At or just below femoral crease, lateral Femoral 10–20 mL
to femoral artery
Three-in-one At or just below femoral crease, lateral Femoral 25–30 mL
to femoral artery, with pressure Lateral femoral cutaneous
applied inferior to injection site ! Obturator
Fascia iliaca 1 cm below inguinal ligament, 2⁄3 the Femoral 30–40 mL
distance from pubic tubercle to Lateral femoral cutaneous
anterior superior iliac spine ! Obturator
Lumbar plexus 3–4 cm lateral to spinous process at Femoral 25–30 mL
level of iliac crest Lateral femoral cutaneous
Obturator
Genitofemoral
Ilioinguinal
Iliohypogastric
276 SECTION 9 Orthopedics
femoral nerve catheters or even single-shot blocks must be Stimulation of the sciatic nerve is confirmed by move-
warned that they are at risk for falls because of weakened ment of the foot that persists when the stimulating
quadriceps muscles or unintentional injury to the anesthe- current is reduced to 0.2–0.5 mA; this usually occurs
tized leg. Patients should be instructed to wear a knee at a depth of 3–5 cm. At this point, 30–40 mL of local
immobilizer and to use crutches when ambulating. anesthetic is injected.
There are several regional anesthetic options for Using the ultrasound-guided technique, an ultra-
ORIF of the fifth metatarsal. The following nerves sound probe is placed laterally across the popliteal
must be blocked to ensure adequate anesthesia for this crease, producing an axial view of the popliteal fossa.
procedure: First, the popliteal artery is identified. Just superficial
• Sural (lateral aspect of the foot) and lateral to it (sometimes referred to as “high and
• Superficial fibular (dorsal aspect of the foot) outside”) is the tibial nerve. More superficial to that is
• Plantar branches of the tibial nerve (plantar surface the common fibular nerve. At this site, the nerves are
of the foot) usually separate, requiring scanning proximally to iden-
A spinal block and combined spinal-epidural anes- tify the point of bifurcation, often 7–10 cm proximal to
thetic are options. However, these techniques block a the popliteal crease. If the point of bifurcation is pro-
much greater area than necessary for the surgery and hibitively high, the tibial and common fibular nerves
carry the usual risk of hypotension and delay in mobiliza- may be blocked separately. The block needle is inserted
tion after surgery. using either an in-plane or out-of-plane technique.
A popliteal block would be an appropriate choice for When the needle tip is positioned adjacent to the
this procedure. This technique anesthetizes the sciatic desired nerve, 30–40 mL of local anesthetic is injected.
nerve at the level of the popliteal fossa, where the common Repositioning of the needle may be required midway
fibular and tibial nerves separate, anesthetizing both nerves through the procedure to ensure circumferential spread
and all their branches, including the sural, superficial of the local anesthetic.
fibular, and plantar nerves. The popliteal block may be An ankle block may also be performed for this proce-
performed using nerve stimulation or ultrasound-guided dure. An ankle block is composed of five separate nerve
techniques. blocks, two of them deep (posterior tibial and deep fibu-
A popliteal block is usually performed in the prone lar nerves) and three of them superficial (saphenous,
position unless patient-related issues (e.g., pain or patient sural, and superficial fibular nerves). Although all five
condition) preclude use of this position, in which case the nerve blocks of the ankle block are described here, not
block may be performed in the lateral position. Using all are necessary for reduction of the fifth metatarsal.
nerve stimulation, the biceps femoris tendon (laterally), Block of the deep fibular and saphenous nerves is
the semitendinosus tendon (medially), and the popliteal unnecessary for this particular procedure. For each
crease are identified. The needle is inserted halfway nerve blocked, approximately 6 mL of local anesthetic is
between the two tendons, 7 cm proximal to the popliteal injected. This block is usually performed without ultra-
crease. The nerve stimulator is initially set to deliver a sound guidance or nerve stimulator guidance; its efficacy
current of 1.5 mA. There should be no local muscle relies entirely on accurate identification of landmarks
twitches above the knee if needle placement is correct. (Table 53-4).
SUGGESTED READINGS Neal JM, Brull R, Chan VW, et al.: The ASRA evidence-based
medicine assessment of ultrasound-guided regional anesthesia
Bigeleisen P, Orebaugh S, Moayeri N, et al.: Ultrasound-Guided and pain medicine: executive summary. Reg Anesth Pain Med
Regional Anesthesia and Pain Medicine. Lippincott Williams & 35(2 Suppl):S1, 2010.
Wilkins, Philadelphia, 2009.
Gray AT: Atlas of Ultrasound-Guided Regional Anesthesia. Saunders,
Philadelphia, 2010. Web Resources
Hadzic A, Vloka JD: Peripheral Nerve Blocks—Principles and Practice. www.asra.com Accessed: January 23, 2013.
McGraw-Hill, New York, 2004. www.nysora.com Accessed: January 23, 2013.
Murray JM, Derbyshire S, Shields MO: Lower limb blocks. Anaesthesia www.ultrasoundblock.com Accessed: January 23, 2013.
65:57, 2010.
S ECTI O N 10
OBSTETRICS
278
CASE 54
QUESTIONS
1. What options are available to the mother for labor 7. Describe the elements of placental drug transfer.
analgesia? 8. What techniques can be used for pain relief after
2. What are the advantages and disadvantages of cesarean delivery?
various neuraxial anesthetic techniques for labor 9. What is the differential diagnosis of postpartum
and delivery? hemorrhage?
3. What is a “walking epidural”? 10. Explain the risk factors, presentation, and treatment
4. Describe neuraxial anesthetic techniques that can of uterine atony.
be employed for cesarean delivery. 11. Describe the presentation and treatment of
5. Outline treatment for postdural puncture headache. retained placenta.
6. What are the advantages and disadvantages of
general anesthesia for cesarean delivery?
A 27-year-old woman presented to the delivery suite in contraction. Although this technique provides moderately
labor after an uncomplicated pregnancy. A lumbar epidu- good analgesia, it is not commonly used because of the
ral catheter was placed at the L4-L5 interspace to facilitate risk of maternal aspiration with deep levels of anesthesia.
analgesia. After an adequate trial of labor, the obstetrician Epidural and combined spinal-epidural (CSE) neuraxial
elected to perform a cesarean delivery for cephalopelvic anesthesia techniques have become popular modalities for
disproportion. A T4 level of anesthesia was achieved via labor analgesia because of their safety and efficacy profile.
the epidural catheter, and the cesarean delivery was initi-
ated. Immediately after delivery of the infant, maternal 2. What are the advantages and disadvantages
hemorrhage ensued. of various neuraxial anesthetic techniques
for labor and delivery?
1. What options are available to the mother for labor
Rational use of neuraxial anesthesia necessitates an un-
analgesia?
derstanding of the pain pathways involved during labor.
Many techniques have been used to reduce the perception Labor is traditionally divided into three distinct stages
of pain during labor. In addition to systemic medications, (Table 54-1):
inhalation agents, neuraxial anesthesia, hypnosis, psycho- • First stage begins with the onset of regular contrac-
prophylaxis, acupuncture, and transcutaneous electrical tions and ends with complete cervical dilation.
nerve stimulation have been used. • Second stage begins when the cervix is completely
Systemic opioids can be used to attenuate labor pains; dilated and ends with delivery of the fetus.
however, they do not completely eliminate the pain. The • Third stage begins after delivery of the fetus and
opioids meperidine, morphine, fentanyl, and the ago- concludes with delivery of the placenta.
nist-antagonist butorphanol have been used. Opioids The first stage of labor is associated with uterine
can be administered as an intravenous bolus or with and cervical pain mediated by spinal segments T10-L1
intravenous patient-controlled analgesia. The choice (Figure 54-1). Local anesthetics administered to the epi-
of opioid varies by institution and local experience. dural, spinal, or caudal spaces readily anesthetize these
Remifentanil can also be used with intravenous patient- pain pathways. In addition, subarachnoid opioids and
controlled analgesia. The advantage of remifentanil is paracervical blocks can be used for pain relief during
that its onset and duration of action are shorter than the first stage of labor. Caudal anesthesia is rarely used
those of other opioids. However, it is also very potent, because of the risk of inadvertent fetal scalp penetration
and close maternal respiratory monitoring, preferably and the associated high fetal levels of local anesthetic.
with pulse oximetry, is required. The second stage of labor is associated with perineal
Inhalation analgesia during labor is another option. and vaginal distention mediated by spinal segments S2-S4.
The goal is to achieve analgesia without depressing airway Epidural, spinal, and caudal anesthetics are also effective
reflexes. Typically, the mother, using a hand-held device, during the second stage of labor. In addition, pudendal
self-administers nitrous oxide at the beginning of each nerve blocks can be used for second-stage analgesia.
279
280 SECTION 10 Obstetrics
There are several advantages to the CSE technique. monitored for 30–60 minutes after induction of analgesia
The primary advantage is the rapid (3–5 minutes) onset of and reassessed at least every 30 minutes thereafter. Be-
analgesia. There is also less motor blockade, and there cause even small doses of subarachnoid and epidural local
may be less hypotension because the spinal component is anesthetics can produce motor deficits, motor function
primarily with an opioid. Most concerns associated with should be assessed. This assessment is accomplished by
CSE are only theoretical. There is no increased risk of asking the parturient to perform a modified deep knee
subarachnoid catheter migration of the epidural catheter. bend or step up and down on a stool. She must have an
Metallic particles are not produced as a result of passing escort at all times.
one needle through another. The incidence of postdural
puncture headache (PDPH) is not increased by the inten- 4. Describe neuraxial anesthetic techniques that
tional dural puncture. Fetal bradycardia in association can be employed for cesarean delivery.
with a hypertonic uterus may occur immediately or
shortly after administration of the spinal medication. Neuraxial anesthetic techniques include spinal, epidural,
There does not appear to be any difference in the inci- and CSE anesthesia. During neuraxial anesthesia, the
dence of fetal heart rate decelerations or emergent cesar- mother remains awake during the delivery, significantly
ean delivery after labor epidural or spinal anesthesia. One decreasing the risk of maternal aspiration associated with
proposed theory for increased uterine tone after CSE is general anesthesia. Neuraxial anesthesia also minimizes
related to the rapid decrease in maternal catecholamines the potential for depression of the neonate from maternal
associated with the rapid onset of pain relief. The de- drug administration. Because neuraxial anesthesia is safer
crease in circulating "-adrenergic agonists results in a than general anesthesia for both the mother and the
predominance of #-adrenergic activity, which causes uter- fetus, it should be used for all elective cesarean deliveries
ine contractions. If this should occur, treatment is with unless there are specific contraindications.
subcutaneous terbutaline or intravenous nitroglycerin. Few absolute contraindications exist to neuraxial anes-
thesia. Absolute contraindications include infection at the
injection site, severe hypovolemia, increased intracranial
3. What is a “walking epidural”?
pressure, patient refusal, and coagulation abnormalities.
The term “walking epidural” has become popular, espe- Relative contraindications include neurologic disease such
cially in the lay community. This term refers to any as multiple sclerosis, history of back surgery or back pain,
epidural or spinal technique that allows the parturient to and systemic infection (Box 54-1).
ambulate during labor. Some initial retrospective data Spinal anesthesia provides reliable and rapid anesthe-
suggested that ambulating or the upright position is sia. In certain urgent situations, spinal anesthesia can be
associated with a shorter first stage of labor, less pain in used in place of general anesthesia. Disadvantages of
early labor, and decreased analgesia requirements. How- spinal anesthesia include a potential for hypotension,
ever, prospective and randomized studies have not been inability to control the spread of anesthesia, limited dura-
able to document any medical benefit of ambulating, in tion, and possibility of PDPH.
terms of either duration of labor or mode of delivery. Continuous epidural anesthesia allows for multiple
Even if the patient does not want to ambulate, using repeat doses of local anesthetic, which offers better con-
a technique that produces minimal motor blockade trol over anesthetic spread, mitigates against precipitous
improves maternal satisfaction. Minimal motor block decreases in blood pressure, and allows almost unlimited
may also improve obstetric outcome in terms of mode of duration of anesthesia. Epidural anesthesia can be used
delivery. The incidence of operative vaginal delivery may for both labor and cesarean delivery. Compared with
be lower when dilute local anesthetics are used. Both spinal anesthesia, the major disadvantages of epidural
epidural analgesia using dilute local anesthetic and opioid anesthesia are the time required to place a needle or
solutions and a CSE technique can achieve this goal. catheter and the potential for local anesthetic toxicity.
However, several precautions should be taken before al- The CSE technique can also be used for cesarean deliv-
lowing a parturient to walk after receiving epidural or ery. It has the advantages of a spinal: The anesthetic is reli-
CSE analgesia. First, it should be determined whether able with quick onset. It has the advantages of an epidural:
she is a candidate for intermittent fetal heart rate moni- The resultant block can be prolonged with repeated doses
toring. Blood pressure and fetal heart rate should be (Box 54-2).
282 SECTION 10 Obstetrics
BOX 54-1 Advantages and Contraindications 5. Outline treatment for postdural puncture
to Neuraxial Anesthesia for headache.
Cesarean Delivery
PDPH can occur any time the dura is punctured. Persis-
ADVANTAGES tent cerebrospinal fluid leak decreases the amount of liquid
• Decreased risk of maternal aspiration available to cushion the brain. In the absence of an ade-
• Minimizes neonatal depression from maternal drug ad- quate fluid buffer, the brain shifts within the calvaria, plac-
ministration ing tension on pain-sensitive blood vessels. Risk factors for
PDPH include increasing size of needle, type of needle
ABSOLUTE CONTRAINDICATIONS (risk is lower with pencil-point needles), bevel positioned
• Infection at site perpendicular to dural fibers (for non–pencil-point nee-
• Severe hypovolemia dles), female gender, pregnancy, and increasing number of
• Increased intracranial pressure attempts.
• Patient refusal PDPHs are classically located over the occipital or
• Coagulation abnormalities
frontal regions. They are frequently accompanied by neck
RELATIVE CONTRAINDICATIONS tension, tinnitus, diplopia, photophobia, nausea, and
• Neurologic disease (e.g., multiple sclerosis) vomiting. An important diagnostic feature of a PDPH is
• History of back surgery exacerbation with postural changes—worse in the sitting
• History of back pain or erect position and better in the supine position.
• Systemic infection Treatment is divided into noninvasive and invasive
measures. Noninvasive therapy includes analgesics, hydra-
tion, and caffeine. Invasive therapy involves placing an
epidural blood patch; this is accomplished by sterilely in-
jecting 20 mL of autologous blood into the epidural space.
The overall success rate is 70%–75%. A second blood
patch is occasionally needed. Prophylactic blood patching,
BOX 54-2 Suggested Technique for injecting blood through an existing epidural catheter after
Performing Neuraxial Anesthesia labor and before its removal, has been considered, but
for Cesarean Delivery more recent data suggest it is not beneficial.
1. Check anesthesia machine. Prepare resuscitative equip- 6. What are the advantages and disadvantages
ment and drugs including endotracheal tubes of different
sizes, laryngoscopes, airways, suction, induction agent
of general anesthesia for cesarean delivery?
(propofol, etomidate, or ketamine), succinylcholine, The major advantages of general anesthesia over neurax-
ephedrine, and phenylephrine. ial anesthesia are the shorter preoperative preparatory
2. Transport to the operating room with left uterine time and the absence of a sympathectomy. The disadvan-
displacement.
3. Administer a nonparticulate antacid by mouth.
tages of general anesthesia include the need to intubate
4. Place standard American Society of Anesthesiologists the trachea, possibility of maternal aspiration, and neona-
monitors including blood pressure cuff, electrocardio- tal depression. In addition, general anesthesia precludes
gram, and pulse oximeter. Administer oxygen via nasal immediate maternal bonding.
cannula or facemask. Tracheal intubation can be more difficult in the partu-
5. Epidural: After placing an epidural catheter, administer rient than in the general population. Airway difficulty is
3 mL of 2% lidocaine as a test dose. Wait 5 minutes, the leading cause of maternal morbidity and mortality.
observing for signs of either intravascular or subarach- Care must be taken both at the initiation of general
noid injection. After confirming catheter position, inject anesthesia and when the mother awakens because airway
2% lidocaine with epinephrine 1:200,000, 3% chloro- catastrophes can occur at that point as well.
procaine, or 0.5% bupivacaine in aliquots of 5 mL, no
more frequently than every 5 minutes until a T4 level
Aspiration pneumonia is an important cause of morbid-
of anesthesia is achieved. After delivery of the infant, ity and mortality in the parturient undergoing general
administer preservative-free morphine sulfate 3–4 mg anesthesia, and general anesthesia should be reserved for
for postoperative analgesia. emergent situations. Before induction of general anesthe-
6. Spinal: Use a small-gauge pencil-point spinal needle. sia, a careful evaluation of the airway should be performed,
Administer 1.5 mL of 0.75% hyperbaric bupivacaine and a nonparticulate antacid should be administered. Ant-
with preservative-free morphine sulfate 0.1–0.25 mg for acids increase gastric pH resulting in a decreased incidence
postoperative analgesia and severity of pneumonitis should aspiration occur. Defas-
7. Monitor vital signs every 1–2 minutes for the first ciculating doses of nondepolarizing muscle relaxants are
15 minutes and then every 5 minutes thereafter, avoided before induction because they may produce weak-
if stable.
8. If hypotension occurs, administer 250–500 mL boluses
ness predisposing to aspiration and may delay the onset
of crystalloid and ephedrine in 5-mg or phenylephrine time of succinylcholine.
in 50-!g increments, until blood pressure returns to After preoxygenation, induction of anesthesia can pro-
normal. ceed with essentially any of the available induction agents
and application of cricoid pressure. Propofol is often chosen
54 Labor and Delivery 283
for patients who are hemodynamically stable, whereas ket- 7. Describe the elements of placental drug transfer.
amine or etomidate is frequently selected when there is
hemodynamic instability or severe bronchospasm. Placental drug transfer occurs by diffusion. Fick equation
Muscle relaxation for endotracheal intubation is describes the factors governing transfer of drugs across
achieved with succinylcholine because it provides the most the placenta.
rapid onset among relaxants currently available. Duration
Qd % Kd • A • [Pd(m) & Pd(f )]/b
of action of succinylcholine may be prolonged because of
decreased levels of pseudocholinesterase compared with where:
the nonpregnant state. The extended duration of action Qd % quantity of drug transferred per unit time
generally does not exceed 15 minutes and is clinically Kd % diffusion constant for the drug
insignificant. Muscle relaxants do not cross the placenta A % surface area of the placenta
because they are highly ionized and have a large molecular Pd(m) % mean drug concentration of maternal blood
weight. in the intervillous space
Anesthesia is maintained with 50% nitrous oxide in Pd(f) % mean drug concentration of fetal blood in the
oxygen and any of the potent inhaled agents. Nitrous oxide intervillous space
does cross the placenta, but it does not cause significant b % thickness of the placenta.
fetal depression owing to fetal tissue uptake if the induction Factors over which the anesthesiologist has control
to delivery time is $20 minutes. Sub-minimum alveolar are limited to the specific drug administered and the
concentrations of potent inhaled anesthetic agents admin- amount used. Other factors, such as the surface area and
istered before delivery protect from maternal recall without thickness of the placenta, are not under the control of the
causing fetal depression or uterine relaxation. After delivery anesthesiologist. To minimize the amount of drug reach-
of the fetus, nitrous oxide concentrations are increased, and ing the placenta, the quantity of maternally administered
opioids are administered to supplement the anesthetic. drug needs to be reduced.
Extubation of the trachea follows classic full stomach Diffusion constants, which vary from one drug
precautions. Residual muscle relaxation is antagonized to another, are determined by four main properties:
with an anticholinesterase and vagolytic agents, and the molecular weight, lipid solubility, protein binding, and
patient must be fully awake (Box 54-3). electrical charge. Placental transfer of drug is facili-
tated by a molecular weight of $500, high lipid solubil-
ity, minimal maternal protein binding, and a low de-
gree of ionization. Fentanyl, a nonionized, highly
lipid-soluble molecule with a low molecular weight,
BOX 54-3 Suggested Method of Performing easily crosses the placenta. In contrast, succinylcholine,
General Anesthesia for Cesarean a highly ionized molecule, does not readily cross the
Delivery placenta.
1. Check anesthesia machine. Prepare resuscitative equip-
ment and drugs including endotracheal tubes of different 8. What techniques can be used for pain relief
sizes, laryngoscopes, airways, suction, induction agent after cesarean delivery?
(propofol, etomidate, or ketamine), succinylcholine,
ephedrine, and phenylephrine. Intravenous, intramuscular, and neuraxial opioids can
2. Transport to the operating room with left uterine be administered for pain relief after cesarean delivery.
displacement. Women who receive epidural morphine sulfate complain
3. Administer a nonparticulate antacid by mouth. of less pain than women who receive intravenous or in-
4. Place standard American Society of Anesthesiologists tramuscular morphine sulfate. Morphine sulfate in either
monitors including blood pressure cuff, electrocardio- the subarachnoid or the epidural space provides analgesia
gram, pulse oximeter, and end-tidal carbon dioxide. for up to 24 hours. The dose of epidural morphine is
5. After denitrogenation with 100% oxygen for 3–5 minutes, 3–4 mg, and the dose of subarachnoid morphine is
induce anesthesia with propofol 1–2 mg/kg, etomidate
0.2–0.3 mg/kg, or ketamine 1–2 mg/kg followed by
0.1–0.25 mg.
succinylcholine 100 mg, and apply cricoid pressure. Do
not use a defasciculating dose of a nondepolarizing 9. What is the differential diagnosis of postpartum
agent. hemorrhage?
6. Maintain anesthesia with 50% nitrous oxide in oxygen
and sub-minimum alveolar concentrations of potent The most common cause of postpartum hemorrhage
inhaled anesthetics until the infant is delivered. is uterine atony, which occurs in 2%–5% of all deliv-
7. After delivery of the infant, administer fentanyl 100 !g eries. Other causes of postpartum hemorrhage in-
and increase nitrous oxide concentration to 70%. Keep clude retained placenta, placenta accreta, cervical and
concentration of halogenated agents $0.5 minimum vaginal lacerations, inverted uterus, and conditions
alveolar concentration to avoid uterine relaxation.
8. At completion of procedure, administer neostigmine
associated with coagulopathy such as amniotic fluid
0.07 mg/kg and glycopyrrolate 0.01 mg/kg to antagonize embolism and preeclampsia. Treatment of postpar-
residual neuromuscular blockade. tum hemorrhage depends on the etiology. Coagu-
9. Extubate trachea when the patient is fully awake. lopathies often respond to treating the underlying
cause (Box 54-4).
284 SECTION 10 Obstetrics
Preeclampsia
Yaakov Beilin, MD
QUESTIONS
from altered immunity such as graft-versus-host reaction. result in hypertension and edema. Thromboplastin can
It is also possible that placental prostaglandin imbalance initiate coagulopathies such as disseminated intravascular
between thromboxane and prostacyclin leads to pre- coagulation (DIC).
eclampsia. In a normal pregnancy, prostacyclin and throm-
boxane are produced in equal amounts by the placenta. 4. Describe the pathophysiology of preeclampsia.
In a pregnancy complicated by preeclampsia, there is a
relative increase in thromboxane production. Thrombox- The hallmark of preeclampsia is vasospasm that occurs
ane causes increased vasoconstriction, platelet aggrega- secondary to increased circulating levels of renin, aldo-
tion, and uterine activity and a simultaneous decrease in sterone, angiotensin, and catecholamines. Aldosterone
uteroplacental blood flow. These effects are observed in also causes sodium and water retention, which leads to
preeclampsia. generalized edema. Because almost every organ system is
Uteroplacental ischemia leads to the production of affected in a parturient with preeclampsia, it is best to
substances similar to renin and thromboplastin. Renin take a systematic approach when discussing the changes
causes release of angiotensin and aldosterone, which seen in preeclampsia (Box 55-2).
Central Nervous System thromboplastin time can also be elevated. Fibrinogen levels
can decrease, and frank DIC can occur.
The central nervous system effects of preeclampsia in-
clude cerebral edema and cerebral vasospasm. Intracra-
Uteroplacental System
nial pressure increases in some cases, but cerebral blood
flow and oxygen consumption remain normal. Clinical Intervillous blood flow is decreased twofold to threefold
findings related to central nervous system changes in- and is a major contributing factor of fetal morbidity
clude headache, hyperreflexia, blurred vision, vertigo, and mortality. The incidence of premature labor is in-
blindness, seizures, and coma. Cerebral hemorrhage is creased because of placental hypoperfusion. Because of
the leading cause of death in patients with preeclampsia. decreased uteroplacental blood flow, the placenta is often
small and shows signs of premature aging. The uterus is
Pulmonary System also hyperactive and markedly sensitive to oxytocin.
A parturient with preeclampsia is at an increased risk for
Tracheal intubation may be difficult secondary to laryn- placental abruption.
geal and upper airway edema. Increased secretions and
airway congestion predispose the mother to upper airway
5. What is the obstetric management of preeclampsia?
infections. Pulmonary capillary leak into the interstitium
accounts for intrapulmonary shunting and a deteriorating Obstetric management of a patient with preeclampsia is
alveolar-arterial (A-a) oxygen gradient. aimed at controlling the disease and preventing progres-
sion to eclampsia. The patient should be on complete bed
Cardiovascular System rest with left uterine displacement. Serial determinations
of blood pressure, weight gain, renal and coagulation func-
Generalized vasoconstriction produces hypertension, im- tion, and central nervous system irritability should be done.
paired tissue perfusion, and cellular hypoxia. Translocated Oral fluid and sodium intake should not be restricted. The
fluid from the vascular compartment to the interstitium routine use of diuretics to control edema is no longer
leads to generalized edema, hypovolemia, and hemocon- recommended. Fetal well-being should be monitored via
centration. An inverse relationship exists between the in- a nonstress test, oxytocin challenge, or biophysical profile.
travascular volume and the degree of hypertension. He- Delivery of the fetus and placenta is considered the defini-
moconcentration leads to increased blood viscosity, which tive treatment of preeclampsia and should be done for
exacerbates tissue hypoxia further. Although hematocrit either fetal or maternal reasons. Fetal indications include
is typically elevated, a relative anemia usually exists, and evidence of fetal distress or cessation of fetal maturation.
blood loss is poorly tolerated. Vasospasm leads to an in- Maternal indications include worsening preeclampsia.
crease in systemic vascular resistance, which increases
cardiac work. The already hyperdynamic cardiovascular 6. How is preeclampsia prevented from degenerating
system becomes stressed further, and cardiac output in-
into eclampsia?
creases. Over time, left ventricular hypertrophy occurs
leading to left ventricular dysfunction. Magnesium sulfate (MgSO4), a central nervous system
depressant and anticonvulsant, is the first-line drug for
Renal System the prevention of eclampsia. One of the many sites of
action of MgSO4 is at the myoneural junction. The de-
Renal blood flow is reduced leading to a decrease in the crease in hyperreflexia seen with the administration of
glomerular filtration rate and creatinine clearance. Almost MgSO4 is due to the inhibition of acetylcholine release at
all renal function tests are impaired. An increasing uric the neuromuscular junction, decreased sensitivity of the
acid level correlates with the severity of disease. Damaged motor end plate to acetylcholine, and decreased excit-
glomeruli allow for renal loss of proteins. ability of the muscle membrane. MgSO4 is also a mild
vasodilator and decreases uterine hyperactivity, which
Hepatic System results in an increase in uterine blood flow. It also causes
vasodilation at the renal and liver beds improving their
Vasospasm leads to hepatic periportal hemorrhages and function (Box 55-3).
hepatocellular damage. Swelling of the liver capsule from
subcapsular hematomas may produce abdominal pain.
Hepatic rupture has been reported in severe cases. Elevated BOX 55-3 Magnesium Sulfate Properties
liver enzymes occur with deteriorating hepatic function.
• Central nervous system depressant
• Anticonvulsant
Hematologic System • Myoneural junction
Coagulation abnormalities also occur. The most common • Inhibits release of acetylcholine
• Decreases acetylcholine sensitivity of motor end plate
finding is thrombocytopenia, which can occur with or
• Decreases excitability of muscle membrane
without other coagulopathies. A syndrome of hemolysis, • Mild vasodilator
elevated liver function tests, and low platelet count • Decreases uterine hyperactivity
(HELLP) has been described. A qualitative platelet abnor- • Crosses placenta
mality also frequently is present even without a quantitative • Toxicity treated with calcium administration
problem. Prothrombin time, thrombin time, and partial
288 SECTION 10 Obstetrics
The range of therapeutic levels of magnesium is used initially and the response noted before increasing
4–8 mEq/L. Above this level, magnesium has both the dose.
maternal and neonatal side effects. Magnesium can lead The most frequently used antihypertensive agent is
to electrocardiogram (ECG) changes and ultimately hydralazine, which not only decreases blood pressure but
cardiac and respiratory arrest. However, these severe also increases renal and uteroplacental blood flow. The
side effects do not occur until after the loss of deep ten- tachycardia that occurs with the use of hydralazine can be
don reflexes (Table 55-2). Cardiac and respiratory side treated with a # blocker. Hydralazine is not the agent of
effects may be avoided by monitoring serum magnesium choice in the acute situation because it takes 10–20 minutes
levels and deep tendon reflexes. Because of its actions before an effect is seen.
at the neuromuscular junction, magnesium increases Nitroprusside, a potent arterial vasodilator, is often
the sensitivity of the mother to both depolarizing and used when immediate control of blood pressure is
nondepolarizing muscle relaxants. required. It is administered by infusion making it easy
Because magnesium crosses the placenta, the neonate to titrate to effect. However, nitroprusside crosses the
can also exhibit signs of magnesium toxicity. Signs of placenta, and cyanide toxicity has been described in the
magnesium toxicity in the newborn include respiratory neonate after prolonged infusion in the mother. Trimeth-
depression, apnea, and decreased muscle tone. Magne- aphan, a ganglionic blocker, has also been used with good
sium toxicity in the newborn and the mother can be success in the emergent situation.
reversed with the administration of calcium. Nitroglycerin, a venous dilator, is useful when tight
MgSO4 is administered intravenously with a loading control of blood pressure is required for prolonged
dose of 2–4 g over 15 minutes followed by an infusion of periods. Nitroglycerin is not as potent as nitroprusside,
1–3 g per hour. MgSO4 is primarily excreted by the kid- but it is easy to titrate and has minimal effect on the
neys. Renal function must be carefully monitored, and fetus.
the magnesium dose is decreased accordingly when renal Propranolol, diazoxide, and methyldopa are generally
insufficiency is present. not used in patients with preeclampsia because of their
adverse side effects (Table 55-3).
7. How is preeclampsia-related hypertension
managed? 8. What are the potential consequences of epidural
analgesia in a patient with preeclampsia?
Control of hypertension in a parturient with preeclampsia
is imperative because acute elevations of blood pressure Epidural anesthesia can be beneficial for a patient with
can lead to cerebral hemorrhage, the leading cause of preeclampsia. Decreasing or eliminating the sensation of
mortality. The patient’s blood pressure should be neither pain reduces hyperventilation, decreases catecholamine
acutely decreased nor decreased to levels considered nor- release, decreases anxiety, and increases uteroplacental
mal for other parturients because a low blood pressure blood flow. A neuraxial anesthetic also obviates the need
could compromise uteroplacental blood flow. Although for a general anesthetic in case of cesarean delivery with
MgSO4 causes vasodilation, it does not treat hypertension its inherent risk of aspiration. However, before inserting
adequately, and an alternative antihypertensive drug is the epidural catheter, the blood pressure must be con-
usually needed. Also, as in any patient with hypertension, trolled, the intravascular volume must be repleted, and
responses to both antihypertensive and pressor agents are the coagulation profile must be normal.
exaggerated. Reduced doses of these agents should be The diastolic blood pressure should be $110 mm Hg
before beginning a neuraxial anesthetic. Frequent blood
pressure measurements are needed during the anesthetic.
An arterial line may be necessary if the blood pressure is
labile.
TABLE 55-2 Effects of Magnesium at Different A parturient with hypertensive disease may be fluid-
Plasma Levels depleted. Urine output is monitored to guide fluid
administration. If urine output is diminished, a fluid
Magnesium Plasma challenge of 500–1000 mL of an isotonic crystalloid
Levels (mEq/L) Systemic Effects should be given depending on the clinical scenario. If
1.5–2 Normal plasma levels urine output does not increase, central venous pres-
sure monitoring or transthoracic echocardiography
4–8 Therapeutic range
should be considered.
5–10 ECG changes—prolonged P–R Platelet consumption is a component of preeclampsia
interval, widened QRS that can lead to coagulation factor consumption and
10 Decreased deep tendon reflexes DIC. A platelet count and coagulation profile must be
Respiratory depression checked before administering the anesthetic. Generally,
15 Respiratory arrest the platelet count decreases before other indices of
Sinoatrial and atrioventricular coagulation are prolonged. It is acceptable to check the
conduction defects platelet count first and, if it is $100,000 mm%3, then to
25 Cardiac arrest check the prothrombin time, partial thromboplastin
time, and fibrinogen. Because preeclampsia is a dynamic
55 Preeclampsia 289
process, the coagulation parameters should be checked is needed. A neuromuscular monitor should be used to
close to the time of administering the block. guide subsequent doses of muscle relaxants. An array of
laryngoscopes, endotracheal tubes, laryngeal mask air-
9. What are the anesthetic options for cesarean ways, and videolaryngoscopes should be available to deal
with a potentially difficult airway.
delivery for a patient with preeclampsia?
After the blood pressure is controlled and the fluid 10. Outline the anticipated postpartum problems
status and coagulation parameters are normalized, associated with preeclampsia.
cesarean delivery can be safely performed under epidu-
ral, spinal, or general anesthesia. The benefit of neur- Although delivery of the fetus and placenta are consid-
axial anesthesia is avoidance of airway manipulation ered the definitive treatment for preeclampsia, it can
in a patient at risk for pulmonary aspiration. Also, a take hours to days for the symptoms to resolve com-
parturient with preeclampsia is exquisitely sensitive to pletely. The patient is still at risk for convulsions. The
blood pressure increases during laryngoscopy. Blood blood pressure should be monitored and the MgSO4
pressure is generally well maintained during both infusion should be continued for at least 24 hours after
spinal and epidural anesthesia; this author routinely delivery.
uses spinal anesthesia.
General anesthesia is often required for an emergency
cesarean delivery. Even in the presence of fetal distress, SUGGESTED READINGS
time should be taken to control the blood pressure ade-
Aya AG, Mangin R, Vialles N, et al.: Patients with severe preeclampsia
quately before induction because laryngoscopy may cause experience less hypotension during spinal anesthesia for elective cesar-
a significant increase in blood pressure, which can lead ean delivery than healthy parturients: a prospective cohort comparison.
to cerebral hemorrhage. After preoxygenation, a rapid- Anesth Analg 97:867, 2003.
sequence induction with cricoid pressure is performed. If Beer AE: Possible immunologic bases of preeclampsia/eclampsia.
the patient is receiving MgSO4, succinylcholine and non- Semin Perinatol 2:39, 1978.
Cotton DB, Gonik B, Dorman K, et al.: Cardiovascular alterations in
depolarizing muscle relaxants may have a prolonged du- severe pregnancy-induced hypertension: relationship of central venous
ration of action. However, the dose of succinylcholine pressure to pulmonary capillary wedge pressure. Am J Obstet Gynecol
should not be reduced because a fast onset of paralysis 151:762, 1985.
290 SECTION 10 Obstetrics
Duckitt K, Harrington D: Risk factors for pre-eclampsia at antenatal Visalyaputra S, Rodanant O, Somboonviboon W, et al.: Spinal versus
booking: systematic review of controlled studies. BMJ 330:565, 2005. epidural anesthesia for cesarean delivery in severe preeclampsia: a
Jouppila P, Jouppila R, Hollmen A, et al.: Lumbar epidural analgesia to prospective randomized, multicenter study. Anesth Analg 101:862,
improve intervillous blood flow during labor in severe preeclampsia. 2005.
Obstet Gynecol 59:158, 1982. Wallace DH, Leveno KJ, Cunningham FG, et al.: Randomized com-
Lucas MJ, Leveno KJ, Cunningham FG: A comparison of magnesium parison of general and regional anesthesia for cesarean delivery in
sulfate with phenytoin for the prevention of eclampsia. N Engl J Med pregnancies complicated by severe preeclampsia. Obstet Gynecol
333:201, 1995. 86:193, 1995.
CASE 56
Abruptio Placentae
and Placenta Previa
Howard H. Bernstein, MD • Yaakov Beilin, MD
QUESTIONS
1. What are the major causes of third-trimester 9. The obstetrician notes 3 hours into labor a signifi-
bleeding? cant increase in vaginal bleeding and a decrease
2. What is abruptio placentae, and what are the risk in maternal blood pressure to 80/40 mm Hg with a
factors for this condition? pulse of 120 beats per minute. Fetal tachycardia
3. What are the manifesting signs and symptoms with late decelerations and absent variability are
of abruptio placentae, and how is the diagnosis noted on the fetal heart rate monitor. Assuming the
made? patient has not yet received an epidural for regional
analgesia, how would you anesthetize this patient
4. Describe the obstetric management of abruptio for an emergency cesarean delivery?
placentae.
10. What is placenta previa?
5. Describe the effects of pregnancy on coagulation.
11. Describe the clinical presentation of placenta
6. What is disseminated intravascular coagulopathy, previa, and explain how the diagnosis is made.
and how is it managed?
12. Discuss the obstetric management of placenta previa.
7. How is fetal distress diagnosed?
13. How would you anesthetize a patient with placenta
8. The patient is given a trial of labor, and the previa for cesarean delivery?
obstetrician requests a consultation for labor
analgesia. What are your concerns, and how 14. How would you manage massive obstetric
would you proceed? hemorrhage?
A 25-year-old woman at 37 weeks gestation presents 2. What is abruptio placentae, and what are the risk
to the labor floor complaining of abdominal pain
factors for this condition?
accompanied by vaginal bleeding. Her blood pressure
on admission is 110/60 mm Hg with a pulse of 90 beats Abruptio placentae refers to premature separation of the
per minute. She is contracting every 5 minutes and her placenta (i.e., before delivery of the fetus). It occurs in
cervix is 3 cm dilated. Fetal heart rate (FHR) monitor- about 1 in 100 to 1 in 150 deliveries and carries a perina-
ing demonstrates a category I tracing. tal mortality rate of approximately 20%. The incidence
of abruption increases with age and is more common in
1. What are the major causes of third-trimester African American women. Abruption is associated with
bleeding? chronic or pregnancy-induced hypertension, multiparity,
cigarette smoking, and cocaine abuse. In women who
A “bloody show” is the most common cause of bleed- have experienced a prior abruption, the risk of recurrence
ing during the third trimester. This bleeding occurs is 10 times higher than that of the general population.
during labor and is due to effacement and dilation
of the cervix. Placental problems are responsible for 3. What are the manifesting signs and symptoms
most pathologic bleeding in the third trimester, and of abruptio placentae, and how is the diagnosis
placental abruption and placenta previa are the most
made?
common placental problems. Cervical bleeding sec-
ondary to polyps and carcinoma is much less common. Classically, abruptio placentae is described as painful bleed-
Vasa previa, umbilical cord vessels traveling within the ing. The patient may experience a sudden “tearing” pain in
placental membranes and covering the cervical the abdomen, followed by the onset of vaginal bleeding and
os, is a rare cause of third-trimester bleeding. Other labor pains. A tumultuous labor pattern follows, with fre-
rare causes of third-trimester bleeding are maternal quent contractions and an increase in base tone of the uterus.
coagulopathy, owing to preeclampsia, and intrauterine The patient may state that it feels as though the contraction
fetal demise (Box 56-1). never ends. The amount of vaginal bleeding is variable and
291
292 SECTION 10 Obstetrics
7. How is fetal distress diagnosed? PT, Prothrombin time; PTT, partial thromboplastin time.
210
180
150
120
90
60
30
12:50
100
12
10 75
8
50
6
4
25
2
0 kPa UA 0 mml
FIGURE 56-1 ■ Fetal heart rate tracing demonstrating good variability.
294 SECTION 10 Obstetrics
210
180
150
120
90
60
30
NBP 149/
100
12
10 75
8
50
6
4
25
2
0 kPa UA 0 mmHg
210 210
180 180
150 150
120 120
90 90
60 60
30 30
149 NBP
12 100 12 100
10 75 10 75
8 8
6 50 6 50
4 25 4 25
2 2
0 kPa UA 0 mmHg 0 kPa UA 0 mmHg
FIGURE 56-3 ■ Fetal heart rate tracing demonstrating a late deceleration.
of oxygen (pO2) resulting in vagal-mediated slowing of the administering oxygen to the mother, improving left
FHR. In interpreting the significance of a late deceleration, uterine displacement, and increasing maternal blood
FHR variability must be assessed. In the presence of mod- pressure with either fluids or vasopressors.
erate variability, significant neonatal cerebral hypoxia has
not yet occurred, and a good neonatal outcome can be ex- 8. The patient is given a trial of labor, and the
pected. If late decelerations occur with minimal or absent obstetrician requests a consultation for labor
FHR variability, the tracing is more ominous. analgesia. What are your concerns, and how
would you proceed?
Variable Decelerations
Painful vaginal bleeding is consistent with placental
Variable decelerations reach nadir in !30 seconds. The abruption. Before a regional anesthetic is initiated, the
nadir of a variable deceleration is not related to the peak patient’s intravascular volume, blood count, and coagula-
of the contraction. Variable decelerations are unrelated to tion status require careful evaluation. Initial laboratory
the time of onset of the uterine contraction (Figure 56-4). evaluation should include hemoglobin, hematocrit, plate-
Variable decelerations are due to vagal-mediated reflexes let count, PT and PTT, fibrinogen level, and fibrin split
stimulated by umbilical cord compression. Variable decel- products to evaluate the degree of hemorrhage and
erations are considered severe if they last $30 seconds to rule out DIC. Volume repletion should proceed with
with a nadir FHR of %60 beats per minute. Mild to mod- crystalloid, colloid, or packed red blood cells, as indi-
erate variable decelerations are rarely associated with fetal cated. If significant hemorrhage has not occurred and
hypoxia. However, severe and recurrent decelerations there is no laboratory evidence of DIC, epidural analge-
may lead to the development of fetal hypoxia and acidosis. sia may be instituted.
In that case, the FHR tracing also demonstrates loss of
variability.
9. The obstetrician notes 3 hours into labor a
In addition to FHR monitoring, fetal scalp stimulation, significant increase in vaginal bleeding and a
by digital examination, or fetal acoustic stimulation may decrease in maternal blood pressure to 80/40 mm
be used to assess fetal well-being. The presence of FHR Hg with a pulse of 120 beats per minute; fetal
acceleration after scalp stimulation is associated with a fetal tachycardia with late decelerations and absent
pH $7.20. Intrapartum fetal pulse oximetry is a new tech- variability are noted on the fetal heart rate
nology that may offer advantages over traditional monitor- monitor. Assuming the patient has not yet
ing techniques, but it is currently not widely used. received an epidural for regional analgesia, how
When a nonreassuring FHR tracing is identified, in would you anesthetize this patient for an
utero fetal resuscitation should commence. Correctable
emergency cesarean delivery?
causes include maternal hypotension, hyperstimulation
of the uterus by oxytocin (Pitocin), and umbilical cord To decide on an anesthetic plan, both maternal and
compression. Fetal well-being may be enhanced by fetal conditions must be evaluated. In this case, both
296 SECTION 10 Obstetrics
90 90 90
60 60 60
30 30 30
M !!!, P !!!
NBP 167/ 83 M123 P 74
12:50
100 100
12 12
75 10 75 10
8 8
50 50
6 6
25 4 25 4
2 2
UA 0 mmHg 0 kPa UA 0 mmHg 0 kPa
FIGURE 56-4 ■ Fetal heart rate tracing demonstrating variable decelerations.
The previa may be marginal, partial, or complete. with placenta previa have an uneventful prenatal
With a complete placenta previa, the placenta covers course. Because the placenta covers the cervical os,
the entire cervical os, preventing vaginal delivery of the cesarean delivery is needed. In the absence of maternal
fetus. Incomplete coverage of the cervical os is referred hemorrhage, a regional anesthetic, spinal or epidural,
to as a partial placenta previa. A marginal previa is a may be performed in the usual fashion. Adequate
partial placenta previa with minimal placental coverage intravenous access should be obtained before place-
of the cervix. A low-lying placenta is one that implants ment of the spinal anesthetic and the patient should
in the lower uterine segment but does not cover the have crossmatched blood available in case unexpected
internal cervical os. hemorrhage occurs. The anesthesia team must be
prepared to convert to general anesthesia in the event
significant hemorrhage and maternal hemodynamic
11. Describe the clinical presentation of placenta
instability develop.
previa, and explain how the diagnosis is made. In the presence of significant hemorrhage, regional
Bleeding from a placenta previa is not associated with anesthesia is contraindicated, and a general anesthetic
abdominal pain and may be sudden in onset. The amount should be performed. Adequate intravenous access should
of bleeding may range from very mild and intermittent to be obtained before induction, and appropriate monitoring
profuse and life-threatening. (e.g., intraarterial catheter) should be placed. Induction
Diagnosis is usually made by ultrasound evaluation of anesthesia would follow the same guidelines as for a
of the position of the placenta relative to the internal placental abruption.
cervical os. If the diagnosis cannot be made by ultra-
sound, a vaginal examination is performed in the operating 14. How would you manage massive obstetric
room (Table 56-2). The patient is brought to the operating
room and prepared for emergency induction of general hemorrhage?
anesthesia and cesarean delivery in the event of profuse Management of massive obstetric hemorrhage is based on
hemorrhage after vaginal examination. This is referred to principles established to manage hemorrhage secondary
as a “double setup.” to trauma. To date, there are no controlled trials of the
management of obstetric hemorrhage.
As soon as abnormal bleeding is diagnosed, additional
12. Discuss the obstetric management of placenta
large-bore (i.e., #16-gauge) intravenous catheters should
previa. be placed. In addition, it is frequently useful to place an
Management of placenta previa depends on the amount arterial catheter for both ease of sampling blood and
of blood lost, the presence or absence of further bleeding, beat-to-beat blood pressure monitoring. It is easier to
the type of previa, and the gestational age of the fetus. place venous and arterial catheters before the onset of
If bleeding has stopped and both the mother and the hemorrhagic shock. These lines can always be removed if
fetus are stable, a conservative approach is elected. Bed the emergency is more easily handled than expected.
rest with fetal monitoring is prescribed to allow further The management of massive hemorrhage requires a
maturation of the fetus. Additional bleeding episodes or multidisciplinary approach. Blood bank personnel should
signs of fetal distress indicate the need for an immediate be informed that an obstetric massive hemorrhage is
cesarean delivery. occurring so that appropriate personnel can be assigned
to prepare blood and blood products. In addition, early
surgical consultation should be obtained to assist the
13. How would you anesthetize a patient with
obstetricians. At many institutions, the surgeon would
placenta previa for cesarean delivery? be a gynecologic oncologist, but if one is unavailable,
As with a placental abruption, both the fetal and the a general surgeon should be called. If a coagulopathy
maternal conditions must be evaluated. Most women develops, a hematologist may also be consulted.
Based on data from the trauma literature, massive
transfusion protocols have been developed. It has been
TABLE 56-2 Placenta Previa versus Abruptio found that transfusion of equal numbers of equivalent
Placentae units of blood, FFP, and platelets results in a greater
survival rate. Massive transfusion protocol should be
Placenta Previa Abruptio Placentae
initiated when any of the following has occurred:
Pain Painless bleeding Painful bleeding • Estimated blood loss of one blood volume
Blood Bright red Port wine • Development of sustained hypotension or acidemia
(pH %7.1 or base deficit $&6)
Clotting Yes No • Development of coagulopathy or thrombocytopenia
Blood loss Obvious Concealed behind or both
the placenta Packed red blood cells (PRBCs) and FFP are trans-
DIC Rare Possibility fused in a ratio of 1:1. Single-donor apheresis platelets
should be administered when 4–6 units of PRBCs and
Diagnosis Confirmed by Clinical and
ultrasound ultrasound FFP have been administered. One unit of single-donor
apheresis platelets is equivalent to 6 units of pooled
DIC, Disseminated intravascular coagulation. platelets.
298 SECTION 10 Obstetrics
QUESTIONS
A 32-year-old woman who was 17 weeks pregnant pre- occur during the gestational period and what impact
sented to the emergency department complaining of they have on the administration of anesthesia. Fetal
abdominal pain, nausea, and vomiting. After physical concerns include the possible teratogenic effects of an-
examination, a presumptive diagnosis of appendicitis was esthetic agents, avoidance of intrauterine fetal asphyxia,
made, and an emergency appendectomy was scheduled. and prevention of premature labor.
1. What is the incidence of nonobstetric surgery in 3. Describe the physiologic changes during
pregnant patients? pregnancy and the impact they have on
anesthesia.
The incidence of nonobstetric surgery during pregnancy
is 0.3%–2%. There are approximately 4 million deliveries Respiratory System
per year in the United States, which means that 80,000
pregnant women require surgery annually. This figure As a result of increased progesterone levels during the
may be an underestimate because it does not account for first trimester, minute ventilation is increased by al-
surgery performed before clinical recognition of preg- most 50% and remains at this level for the remainder
nancy. Appendectomy is the most common nonobstetric of the pregnancy. The increase in minute ventilation
operation performed during pregnancy. However, almost leads to a decrease in arterial carbon dioxide tension
every type of surgical procedure has been successfully (PaCO2) to approximately 30 mm Hg. Arterial pH re-
performed in pregnant patients, including open heart mains unchanged because of a compensatory increase
procedures with cardiopulmonary bypass, neurosurgical in renal excretion of bicarbonate ions. At term, alveolar
procedures requiring hypotensive techniques and hypo- ventilation is increased by 70% because anatomic dead
thermia, and liver transplantation. space does not change significantly during pregnancy.
After the fifth month of pregnancy, the functional re-
2. What are the anesthetic concerns in a pregnant sidual capacity, expiratory reserve volume, and residual
volume all are decreased by about 20% because of the
patient?
gravid uterus pushing on the diaphragm. Vital capacity
Anesthetizing a pregnant patient is one of the only is not appreciably changed from prepregnancy levels.
times an anesthesiologist must consider two patients
simultaneously. Maternal considerations result from the Anesthetic Implications
physiologic changes of pregnancy that affect almost
every organ system (Table 57-1). To provide safe anes- Increased alveolar ventilation and decreased functional
thesia to a pregnant patient, one must not only under- residual capacity lead to a more rapid uptake and excre-
stand the physiologic changes but also know when they tion of inhaled anesthetics. The decrease in functional
299
300 SECTION 10 Obstetrics
BUN, Blood urea nitrogen; HCO3!, bicarbonate; MAC, minimum alveolar concentration; PaCO2, arterial carbon dioxide tension; PaO2, arte-
rial oxygen tension.
residual capacity in conjunction with increases in cardiac related to an increase in heart rate (15%). Cardiac output
output, metabolic rate, and oxygen consumption make increases slightly further during the second trimester, and
the pregnant patient more susceptible to arterial hypox- this increase lasts throughout the pregnancy.
emia during periods of apnea or airway obstruction. Blood pressure normally decreases during pregnancy
Edema, weight gain, and increase in breast size may because of a 15% decrease in systemic vascular resistance.
make tracheal intubation technically difficult. An array of Near term, 10%–15% of patients have a dramatic reduc-
laryngoscope blades and handles and other emergency tion in blood pressure in the supine position, often associ-
airway management equipment should be available. Capil- ated with diaphoresis, nausea, vomiting, pallor, and changes
lary engorgement of the mucosal lining of the upper air- in cerebration. This condition is known as supine hypoten-
way accompanies pregnancy. Extreme care is mandated sive syndrome and is caused by compression of the inferior
during manipulation of the airway, and a smaller than nor- vena cava and aorta by the gravid uterus. Other manifesta-
mal tracheal tube needs to be used. The use of a nasal tions of the syndrome are decreases in renal and uteropla-
airway and nasotracheal intubation should be avoided. cental blood flow from compression of the aorta.
Intravascular volume is increased by 35% during
Cardiovascular System pregnancy. Because plasma volume increases by a greater
percentage than red blood cell volume (45% and 20%),
Cardiac output is increased by 30%–40% during the first there is a relative anemia during pregnancy. Neverthe-
trimester. This increase in cardiac output is primarily re- less, a hemoglobin concentration !11 g/dL is considered
lated to an increase in stroke volume (30%) and secondarily abnormal.
57 Anesthesia for Nonobstetric Surgery during Pregnancy 301
Nitrous oxide is a known teratogen in mammals and could not be linked to either the specific anesthetic
rapidly crosses the human placenta. The proposed agents or the anesthetic technique. Most operations
mechanism is that nitrous oxide oxidizes vitamin B12, (54%) were performed under general anesthesia, and ni-
which cannot function as a cofactor for the enzyme me- trous oxide was used in 98% of the general anesthetics.
thionine synthetase. Methionine synthetase is needed The increased risk to the fetus may be due to the condi-
for the formation of thymidine, a subunit of DNA. tion that necessitated surgery in the first place, with the
However, pretreatment of rats exposed to nitrous oxide highest rate occurring with gynecologic procedures.
with folinic acid, which bypasses the methionine synthe- These data are very important because they clearly dem-
tase step in DNA synthesis, does not prevent congenital onstrate that anesthetic agents are not teratogenic and
abnormalities. In addition, suppression of methionine that the greatest risk is premature labor with the delivery
synthetase occurs at low concentrations of nitrous of a low-birth-weight infant. The data suggest that the
oxide—concentrations found to be safe in animal studies. anesthetic agents are not responsible for the major com-
Despite these theoretical concerns, nitrous oxide has not plication of surgery: premature labor and early delivery
been found to be associated with congenital abnormalities of the fetus.
in humans. The FDA has not given nitrous oxide a cate-
gory classification because it is a medical gas and not 5. What precautions should be taken to avoid
directly regulated by the FDA. intrauterine fetal asphyxia?
Numerous epidemiologic studies have been performed
to determine the health hazards, including birth defects Intrauterine fetal asphyxia is avoided by maintaining
and spontaneous abortions, of pregnant women with normal maternal arterial oxygen tension (PaO2), PaCO2,
long-term exposure to anesthetic gases. All the studies and uterine blood flow. Maternal hypoxemia may lead
found similar results. The authors of the largest study, to fetal hypoxemia and fetal demise. General anesthesia
sponsored by the American Society of Anesthesiologists is a particular risk to pregnant patients because manage-
(ASA) (1974), sent questionnaires to 73,496 individuals ment of the airway can be difficult, and the rate of he-
who may have been exposed to anesthetic gases to gather moglobin oxygen desaturation is increased owing to the
information about the extent of their exposure and re- decreased functional residual capacity and increased
productive outcome. The study population included the oxygen consumption. However, care also must be taken
entire membership of the ASA, the American Association during a regional anesthetic because a high segmental
of Nurse Anesthetists, the Association of Operating level of anesthesia during a major conduction block, a
Room Nurses, and the Association of Operating Room toxic local anesthetic reaction, or oversedation can also
Technicians. The investigators found that operating lead to a hypoxic event. High inspired oxygen tension
room personnel had an increased risk of spontaneous does not adversely affect the fetus even if 100% oxygen
abortions and congenital abnormalities. They recom- is administered.
mended that a means to scavenge trace anesthetic gases Maternal hypercapnia and hypocapnia can be detri-
should be mandatory in all operating rooms, which is the mental to the fetus. Severe hypocapnia produced by
current standard. However, all these studies were later criti- excessive positive pressure ventilation may increase
cized for their lack of a control group, low response rate to mean intrathoracic pressure, decrease venous return,
questionnaires, recall bias, and statistical inaccuracies. and lead to a decrease in uterine blood flow. In addition,
There have also been several retrospective studies of maternal alkalosis, as produced by hyperventilation,
pregnant patients who had undergone surgery to deter- decreases uterine blood flow by direct vasoconstriction
mine whether there is an association between anesthesia and decreases oxygen delivery by shifting the maternal
and surgery and congenital defects, spontaneous abor- oxyhemoglobin dissociation curve to the left. Severe
tions, or fetal demise. All studies found similar results. hypercapnia is detrimental because it is associated with
In the largest study, Mazze and Kallen (1989) linked the fetal acidosis and myocardial depression.
data from three Swedish health registries: the Medical Both drugs and anesthetic procedures affect uterine
Birth Registry, the Registry of Congenital Malforma- blood flow. Placental blood flow is directly propor-
tions, and the Hospital Discharge Registry for the 9-year tional to the net perfusion pressure across the intervil-
period 1973–1981. They examined the data for four ad- lous space and inversely proportional to the resistance.
verse outcomes including congenital defects, stillborn Perfusion pressure is decreased by hypotension, which
infants, infants born alive but who died within 7 days, and may be due to the use of an epidural or spinal anes-
infants with a birth weight !1500 g and !2500 g. They thetic, aortocaval compression in the supine position,
found 5405 of 720,000 women had undergone surgery or hemorrhage. Vasoconstriction secondary to the use
during their pregnancy. In their data set, most proce- of #-adrenergic drugs, decreased PaCO2, or increased
dures were performed during the first trimester (41.6%), catecholamines (e.g., occurs during pain, apprehension,
and the incidence decreased during the second (34.8%) or light anesthesia) increases vascular resistance and
and third (23.5%) trimesters. There was no increase in decreases uteroplacental blood flow.
infants with congenital abnormalities or stillborn births
among patients who underwent surgery while pregnant 6. How is preterm labor prevented?
during any trimester. However, the number of infants
born with a birth weight !1500 g and !2500 g and the Premature labor, preterm delivery, and delivery of an
number of infants who died within 7 days of birth were infant !1500 g are the most significant risks to the fetus.
greater in patients who underwent surgery while preg- Medications that have #-adrenergic agonist properties
nant; this was true during all three trimesters. These risks (e.g., ketamine and phenylephrine) can increase uterine
304 SECTION 10 Obstetrics
Thrombocytopenia in Pregnancy
Yaakov Beilin, MD
QUESTIONS
1. What is the concern when placing an epidural 11. Are there any cases of epidural hematoma in a
catheter if the platelet count is low? parturient with thrombocytopenia?
2. Who is at risk for developing an epidural hematoma? 12. What is the evidence that initiating an epidural
3. What is considered a low platelet count from the anesthetic in a patient with a low platelet count
perspective of epidural catheter placement, and may be safe?
why is there controversy regarding choosing a 13. How do you evaluate a patient who has a low
lowest “safe” platelet count? platelet count?
4. What is the expected platelet count during 14. What are practical recommendations regarding
pregnancy? neuraxial anesthesia in a parturient who presents
5. Describe coagulation and the role platelets play with a low platelet count?
in the process. 15. What is low-molecular-weight heparin, and how
6. What are causes of thrombocytopenia during does it compare with and differ from standard
pregnancy? heparin?
7. What tests are available to evaluate platelet 16. Why do some pregnant women take low-molecular-
function? weight heparin?
8. Describe the thromboelastogram and its 17. What has been the anesthetic experience with
limitations. low-molecular-weight heparin and neuraxial
9. Describe the platelet function analyzer and its anesthesia?
limitations. 18. What are the unique recommendations for anesthetiz-
10. What is the overall risk of epidural hematoma? ing a parturient taking low-molecular-weight heparin?
A 22-year-old woman presented to the labor and delivery A patient with a clinically active coagulopathy is consid-
suite at 40 weeks’ gestation with mild uterine contractions. ered to have an absolute contraindication to regional
The obstetricians decided to augment labor with oxytocin anesthesia. However, many gray areas exist, and this is
and requested an epidural anesthetic for labor analgesia. especially true in patients with thrombocytopenia.
The patient’s past medical history was significant for mis-
carriage during a previous pregnancy. Until 2 weeks ago, 3. What is considered a low platelet count from the
she had been receiving enoxaparin (Lovenox) injections, perspective of epidural catheter placement, and
30 mg twice a day. Her laboratory data were within normal why is there controversy regarding choosing a
limits except for a platelet count of 76,000 mm!3. lowest “safe” platelet count?
1. What is the concern when placing an epidural An epidural hematoma is a potentially catastrophic com-
plication, which can lead to permanent paralysis. It is
catheter if the platelet count is low?
prudent to practice in a conservative manner and refrain
The concern when placing an epidural catheter in the from epidural anesthesia if the patient is at increased risk
face of a low platelet count is that if either the needle or of developing this complication. In 1988, Cousins and
the catheter punctured a blood vessel, the blood would Bromage recommended against epidural anesthesia if the
not clot, leading to an epidural hematoma. platelet count is "100,000 mm!3. However, this recom-
mendation has been widely disputed. Thrombocytopenia
2. Who is at risk for developing an epidural is the most common hematologic disorder during preg-
nancy. Choosing an absolute platelet count below which it
hematoma?
is considered too dangerous to place a neuraxial anesthetic
Anyone who receives a spinal or epidural anesthetic is may dictate the use of general anesthesia, which carries its
at risk for developing an epidural hematoma. Epidural own risks in a parturient. A review of pregnancy-related
hematoma is an extremely rare event and is generally as- deaths found that fatality rates for parturients adminis-
sociated with patients who have disorders of hemostasis. tered general anesthesia for cesarean delivery were much
306
58 Thrombocytopenia in Pregnancy 307
Platelet count decreases by approximately 20% during ITP, Idiopathic thrombocytopenic purpura
normal pregnancy; most platelet counts remain #150,000
mm!3. However, approximately 7% of all parturients
present with a platelet count "150,000 mm!3, and
0.5%–1% present with a platelet count "100,000 mm!3. both platelet quantity and quality must be assessed. Tests
of platelet function have been criticized for being diffi-
5. Describe coagulation and the role that platelets cult to perform, lacking reproducibility, and being of
questionable clinical relevance. The ideal test would be
play in the process.
easy to perform, would be inexpensive, and would not
Clotting can be thought of as occurring in two phases: pri- require specialized equipment, with results that could be
mary and secondary hemostasis. Primary hemostasis is the reproduced and correlate with outcome. Bedside tests of
creation of the initial platelet plug, and secondary hemosta- coagulation include the thromboelastogram (Thrombe-
sis is the creation of the stable fibrin clot. Platelets play an lastograph; Haemoscope Corporation, Skokie, IL) and
important role in both processes. Generally, blood vessels the platelet function analyzer (PFA-100; Dade Behring,
prevent platelet adhesion by releasing a potent vasodilator, Newark, DE).
prostacyclin. After vessel wall injury, prostacyclin levels de-
crease, and platelets adhere to the vessel wall. Adhesion 8. Describe the thromboelastogram and its
leads to activation and degranulation with release of adenos- limitations.
ine diphosphate (ADP), serotonin, and thromboxane, which
leads to platelet aggregation. Further aggregation leads to The thromboelastogram measures all phases of coagula-
formation of a platelet plug. This plug is unstable and re- tion and fibrinolysis by using "1 mL of a whole blood
quires fibrin formation (secondary hemostasis), which oc- sample to measure the shear elasticity of clotting blood.
curs by activation of the intrinsic or extrinsic coagulation Blood is placed in a cylindrical cup that oscillates. A pin
system. Platelets provide the phospholipid membrane on is suspended in the blood by a torsion wire and is moni-
which the coagulation cascade occurs. Platelet abnormali- tored for motion. The torque of the rotating cup affects
ties can be qualitative or quantitative and are the most com- the pin only after fibrin-platelet bonding has linked the
mon hematologic disorders during pregnancy. cup and pin together. The strength of the developing clot
affects the magnitude of the pin motion such that strong
6. What are the causes of thrombocytopenia during clots move the pin directly in phase with the cup and
weak clots do not. The resulting profile is a measure of
pregnancy?
the time it takes for the first fibrin strand to form, the
Most cases (99%) of thrombocytopenia during pregnancy kinetics of the clot, strength of the clot, and breakdown
are related to one of three causes: hypertensive disorders of the clot (Figure 58-1). The maximum amplitude (MA)
such as preeclampsia, gestational thrombocytopenia, or has been found to correlate best with platelet function.
idiopathic thrombocytopenic purpura (ITP). When eval- Orlikowski et al. (1996) measured platelet counts,
uating a parturient with thrombocytopenia, there are thromboelastogram parameters, and bleeding times in
two specific issues to consider. The first concern is healthy pregnant women and in women with preeclamp-
whether the disorder is static or dynamic (Table 58-1). sia. They found that the MA remains normal (53 mm)
If the disorder is static, as occurs during gestational until the platelet count decreases to "54,000 mm!3 (95%
thrombocytopenia or ITP, the platelet count is usually confidence limit, 40,000–75,000 mm!3). Based on their
stable. If the disorder is dynamic, as occurs during pre- study, they suggested that a platelet count of 75,000 mm!3
eclampsia, the platelet count may change rapidly, and it is should be associated with adequate hemostasis. However,
important to obtain serial platelet counts. The second there is no clinical evidence that a normal MA correlates
issue is whether platelet function is normal or abnormal. with safe epidural anesthesia.
Platelet function is typically normal in gestational throm-
bocytopenia and ITP and may be abnormal in preeclampsia. 9. Describe the platelet function analyzer and its
limitations.
7. What tests are available to evaluate platelet
The platelet function analyzer is specific for platelet
function?
function, the primary hematologic disorder of parturi-
A patient who presents with a platelet disorder is diffi- ents. The machine simulates the in vivo hemostatic
cult to evaluate with standard laboratory tests because mechanism of platelet function by accelerating citrated
308 SECTION 10 Obstetrics
Normal TEG
2 hours
MA time
RK
R Maximum Amplitude
Draw amplitude
Start
Angle
FIGURE 58-1 ■ Thromboelastogram (TEG). R is time until the onset of clotting. K is time until the tracing amplitude reaches 20 mm.
The angle between the tangent line drawn from the curve to the split point and the horizontal line of the tracing is measured in
degrees. MA is the maximum amplitude, a measure of clotting strength. MA correlates best with platelet function.
whole blood through a 150-mm aperture in a collagen seizure in the postanesthesia care unit 1 hour after the
membrane. The collagen membrane is coated with one of procedure. There was no seizure activity in her lower
two platelet activators: epinephrine or ADP. The car- extremities, and a computed tomography scan revealed
tridges are named for the platelet activator that coats an epidural collection. A laminectomy was performed
them, CEPI or CADP. The time taken for the aperture to 6 hours after epidural catheter placement, at which time
close is called the closure time. Reference range for the 4 mL of blood was drained from the epidural space. The
CEPI cartridge is 78–199 seconds and for the CADP car- patient experienced a complete recovery. It is unlikely
tridge is 55–137 seconds. This machine can be used as a 4 mL of blood was sufficient to cause her symptoms, and
screening tool for patients who present with unknown it is more likely the symptoms were related to residual
coagulopathies and is sensitive for the detection of von local anesthetic, but this cannot be proven.
Willebrand disease. Studies in parturients have focused on
defining the expected closure time in pregnancy and if 12. What is the evidence that initiating an epidural
there is a closure time that correlates with significant anesthetic in a patient with a low platelet count
thrombocytopenia. Similar to the limitations of the throm-
boelastogram, there are no clinical studies defining specific
may be safe?
closure times that correlate with epidural hematoma. The safety of initiating epidural anesthesia with a platelet
count "100,000 mm!3 is supported by three retrospec-
tive studies. In the largest study, Beilin et al. (1997)
10. What is the overall risk of epidural hematoma? reviewed the medical records of 15,919 consecutive
The overall risk of spinal or epidural hematoma after parturients during a 3-year period. Among 80 women
neuraxial anesthesia is 1:150,000–250,000. Vandermeulen who presented with a platelet count "100,000 mm!3, 30
et al. (1994) reviewed the literature and found 61 cases of received an epidural anesthetic without sequelae. The
anesthesia-related epidural hematoma. Most cases (68%) lowest platelet count in the study was 69,000 mm!3.
occurred in patients with coagulopathies, and 75% of all These 30 women had certain characteristics in common.
patients with hematoma had an epidural rather than a The platelet count did not decrease around the time of
spinal anesthetic. Of patients who received an epidural epidural catheter placement, and there was no clinical
anesthetic, 88% had an epidural catheter inserted, and evidence of bleeding. In that study, five women were
almost 50% of those patients developed an epidural denied an epidural anesthetic because of a decreasing
hematoma after catheter removal. platelet count, and two women were denied an epidural
anesthetic because of evidence of bruising.
11. Are there any cases of epidural hematoma in a
parturient with thrombocytopenia? 13. How do you evaluate a patient who has a low
There is one case in the literature of a woman with pre- platelet count?
eclampsia with a platelet count of 71,000 mm!3 who A routine platelet count is unnecessary in an otherwise
received an epidural catheter for cesarean delivery and healthy parturient and should be drawn based on patient
developed an epidural hematoma. The epidural catheter history, physical examination, and clinical signs. If the
was placed without complication. The patient had a platelet count is found to be low, it is important to confirm
58 Thrombocytopenia in Pregnancy 309
the result with a manual count. Automated counters can be 5000–30,000. Heparin acts as an anticoagulant by binding
unreliable, especially at lower platelet levels. The patient to antithrombin III and potentiates the inhibition of fac-
history and physical examination are key components tors IIa (thrombin), IXa, Xa, XIa, and XIIa. A specific
when deciding whether to proceed with regional anesthe- pentasaccharide sequence on the heparin chain has a
sia in parturients with thrombocytopenia. Consultation high-affinity binding site for antithrombin III; only about
with a hematologist, preferably before labor, can also help 30% of the heparin molecule has this sequence. To cata-
with assessing the etiology of thrombocytopenia and de- lyze inhibition of factor Xa, only the pentasaccharide
termining whether the platelets are functioning adequately. binding sequence is necessary. However, to catalyze inhi-
If there is a history of easy bruising or if the patient has bition of factor IIa, a heparin molecule must contain both
petechiae or ecchymosis, regional anesthesia should not be this high-affinity pentasaccharide sequence and an addi-
offered. If the patient has no bleeding history, our general tional chain of at least 13 sugars. UH is highly sulfated
practice is to obtain at least one additional platelet count and negatively charged. As a result, it has a great affinity
as close in time to epidural catheter placement as possible for plasma and vascular matrix proteins and has "30%
to ensure that it is not decreasing further. This additional bioavailability. Low-molecular-weight heparin (LMWH)
platelet count is especially important for disease processes is produced by chemical or enzymatic depolymerization
that are dynamic, such as preeclampsia. We do not obtain of standard heparin, which produces shorter polysaccha-
any bedside tests of platelet function, and we do not ride chains of 13–22 sugars and a molecular weight of
have any absolute platelet count cutoff. A patient with a 4000–6000. LMWH has the same anti-Xa activity as stan-
stable platelet count of 50,000 mm!3, as seen in ITP, is dard heparin with less anti-IIa (thrombin) activity. The
probably at lower risk than a patient with a platelet count concentration of LMWH is referred to in international
of 75,000 mm!3 that is rapidly decreasing, as seen in standards and expressed as anti-Xa units per millimeter.
preeclampsia. Generally, I place an epidural catheter in The reduced molecular size leads to lower binding of
women with stable platelet counts of approximately plasma and endothelial cell proteins; this results in #90%
75,000 mm!3. Other physicians are comfortable with bioavailability after subcutaneous injection, a longer
lower platelet counts, especially in women with ITP. plasma half-life (4–6 hours vs. 0.5–1 hour for standard
There is no absolute cutoff, and the risks of epidural heparin), and a predictable and reproducible dose re-
placement versus general anesthesia have to be individual- sponse. Laboratory monitoring is not required. The peak
ized. Informed consent must be obtained. LMWH anti-Xa activity occurs 3–4 hours after subcuta-
neous injection, and anti-Xa levels are approximately 50%
14. What are practical recommendations regarding of peak levels at 12 hours. LMWH excretion is almost
solely via the kidneys. Protamine sulfate is able to neutral-
neuraxial anesthesia in a parturient who
ize 100% of anti-IIa activity but only 60%–70% of anti-
presents with a low platelet count? Xa activity and is not effective at neutralizing LMWH
If the decision is made to proceed with neuraxial anesthe- effects.
sia, a subarachnoid block using a small-caliber spinal
needle is preferable to epidural anesthesia. This block is 16. Why do some pregnant women take
not always possible, especially for women in labor who
require repeated doses of local anesthetic. low-molecular-weight heparin?
Epidural anesthetics should be placed using a midline Pregnancy induces a state of hypercoagulability, but
technique. The lowest concentration of local anesthetic thromboembolic complications are rare. However,
necessary to produce analgesia while preserving motor some parturients require anticoagulant medication dur-
function is recommended. Patients should be examined ing the antepartum period, such as patients with disor-
every 1–2 hours for motor block, and these examinations ders of hemostasis, mechanical heart prostheses, or at
should continue until after the anesthetic has worn off high risk for venous thromboembolism. Additionally,
and the catheter has been removed. In this way, if the anticoagulant medication is used in women with a history
patient develops a motor block out of proportion to of fetal loss related to thrombophilia and hypercoagula-
what one would expect or if the anesthetic has a pro- ble syndromes, such as antithrombin III deficiency,
longed duration of action, the patient can be immedi- antiphospholipid syndrome, and protein C or S deficiency.
ately assessed with magnetic resonance imaging for the Warfarin causes abnormal fetal development and con-
development of an epidural hematoma. Immediate eval- genital malformations during the first trimester, such as
uation is necessary because an emergent laminectomy nasal hypoplasia and skeletal dysplasias. It also in-
and decompression must be performed within 6–12 hours creases the risk of maternal and fetal hemorrhage when
to preserve function. If patients develop a coagulopathy given during the peripartum period. Heparin and
with an indwelling epidural catheter, the catheter should LMWH do not cross the placenta, are not teratogenic,
be removed only after the coagulation parameters are and are unlikely to cause fetal hemorrhage. LMWH
corrected. has gained widespread use in pregnancy and has certain
advantages over UH. UH and LMWH have similar
15. What is low-molecular-weight heparin, and how hemorrhagic complication rates and antithrombotic
efficacy. However, LMWH, in contrast to UH, does
does it compare with and differ from standard
not require laboratory monitoring because the re-
heparin? sponse is predictable. Also, there is less risk of serious
Standard unfractionated heparin (UH) is a mixture of complications with LMWH, such as heparin-induced
linear polysaccharide chains, with a molecular weight of thrombocytopenia and osteoporosis.
310 SECTION 10 Obstetrics
17. What has been the anesthetic experience with needle placement or administration of antiplatelet or
low-molecular-weight heparin and neuraxial anticoagulant medication. None of the patients was
pregnant.
anesthesia?
The release of LMWH for general use in the United 18. What are the unique recommendations
States in May 1993 sparked a new challenge for anes-
for anesthetizing a parturient taking
thesiologists. Previously, spinal or epidural hematoma
was a rare occurrence, reportedly "1 in 150,000– low-molecular-weight heparin?
220,000. Enoxaparin, the first LMWH to be approved Neuraxial anesthesia can be safely administered to a patient
by the U.S. Food and Drug Administration (FDA), had receiving LMWH if certain guidelines and precautions are
been used for many years in Europe. However, the met. The American Society of Regional Anesthesia and
approved dosing schedule of enoxaparin was 30 mg Pain Medicine (ASRA) convened a consensus conference
(3000 units) every 12 hours in the United States as on neuraxial anesthesia in 1998. The committee recon-
opposed to 40 mg (4000 units) once daily in Europe. vened for a second consensus conference in 2002 and a
Within 1 year of its introduction in the United States, third meeting in 2009. Following these meetings, recom-
two cases of epidural hematoma were voluntarily re- mendations regarding the administration of neuraxial
ported through the MedWatch system. The warning anesthesia to patients receiving anticoagulation therapy
section of the drug label was revised, and a letter from were developed. These recommendations are summa-
the manufacturer was issued to practitioners to alert rized in Box 58-1.
them to the risk of spinal hematoma in patients under-
going neuraxial anesthesia while receiving LMWH.
Despite these warnings, 40 cases of perioperative neur-
axial hematoma in patients on LMWH were voluntarily SUGGESTED READINGS
reported between May 1993 and November 1997. A American Society of Anesthesiologists Task Force on Obstetric Anesthe-
FDA Health Advisory was issued in December 1997. sia: Practice guidelines for obstetric anesthesia: an updated report by
the American Society of Anesthesiologists Task Force on Obstetric
The actual risk of spinal or epidural hematoma in Anesthesia. Anesthesiology 106:843, 2007.
patients receiving LMWH while undergoing neuraxial Beilin Y, Bodian CA, Haddad EM, et al.: Practice patterns of anesthe-
anesthesia is difficult to estimate. There are likely addi- siologists regarding situations in obstetric anesthesia where clinical
tional, unreported cases. The reported incidences of spinal management is controversial. Anesth Analg 83:735, 1996.
Beilin Y, Zahn J, Comerford M: Safe epidural analgesia in thirty partu-
or epidural hematoma in patients receiving LMWH may rients with platelet counts between 69,000 and 98,000 mm–3. Anesth
be approximately 1 in 3000 for continuous epidural anes- Analg 85:385, 1997.
thesia and 1 in 40,000 for spinal anesthesia. Of the 40 cases Cosmi B, Hirsh J: Low molecular weight heparins. Curr Opin Cardiol
of spinal or epidural hematoma associated with LMWH in 9:612, 1994.
conjunction with neuraxial anesthesia, 2 patients received Cousins MJ, Bromage PR: Epidural neural blockade. p. 335. In Cousins
MJ, Bridenbaugh PO (eds): Neural Blockade in Clinical Anesthesia
epidural steroid injections; 6 underwent spinal anesthe- and Management of Pain, 2nd edition. Lippincott, Philadelphia, 1988.
sia, 1 of which was continuous spinal anesthesia; 23 had Douglas MJ. Platelets: the parturient and regional anesthesia. Int
continuous epidural anesthesia; 6 underwent unspeci- J Obstet Anesth 10:113, 2001.
fied techniques; and 3 had general anesthesia after Hawkins JL, Chang J, Palmer SK, et al.: Anesthesia-related maternal
mortality in the United States: 1979-2002. Obstet Gynecol 117:69,
attempted or failed neuraxial anesthesia. Also, some 2011.
patients had additional risk factors for the develop- Heit JA. Low-molecular-weight heparin: biochemistry, pharmacology,
ment of spinal or epidural hematoma, such as difficult and concurrent drug precautions. Reg Anesth Pain Med 23:135, 1998.
58 Thrombocytopenia in Pregnancy 311
Horlocker TT, Heit JA: Low molecular weight heparin: biochemistry, Orlikowski CE, Rocke DA, Murray WB, et al.: Thromboelastography
pharmacology, perioperative prophylaxis regimens, and guidelines changes in pre-eclampsia and eclampsia. Br J Anaesth 77:157, 1996.
for regional anesthetic management. Anesth Analg 85:874, 1997. Scott DB, Hibbard BM: Serious non-fatal complications associated
Horlocker TT, Wedel DJ, Rowlingson JC, et al.: Regional anesthesia in the with extradural block in obstetric practice. Br J Anaesth 64:537,
patient receiving antithrombotic or thrombolytic therapy: American 1990.
Society of Regional Anesthesia and Pain Medicine Evidence-Based Vandermeulen EP, Van Aken H, Vermylen J: Anticoagulants and spinal-
Guidelines (Third Edition). Reg Anesth Pain Med 35:64, 2010. epidural anesthesia. Anesth Analg 79:1165, 1994.
Lind SE: The bleeding time does not predict surgical bleeding. Blood Yuen TS, Kua JS, Tan IK: Spinal haematoma following epidural anaes-
77:2547, 1991. thesia in a patient with eclampsia. Anaesthesia 54:350, 1999.
S ECTI O N 11
PEDIATRICS
312
CASE 59
QUESTIONS
1. What are the differences between gastroschisis 3. How would you manage this neonate
and omphalocele? intraoperatively?
2. What are the preoperative concerns for these 4. What is the surgical treatment for gastroschisis
two defects? and omphalocele?
A 2-day-old, 3-kg neonate, born at 36 weeks’ gestation, abdominal wall layers. The abdominal wall defect, which
was brought to the operating room for surgical repair of is commonly located to the right of the umbilicus, per-
an abdominal wall defect. The defect was at the base of mits abdominal viscera to herniate. The degree of her-
the umbilicus and had a membranous covering. niation outside the peritoneal cavity varies from slight to
major. There is no membranous covering of the intes-
1. What are the differences between gastroschisis tines in gastroschisis resulting in loss of extracellular fluid
and omphalocele? and risk of infection. The intestines are edematous,
dilated, inflamed, and functionally abnormal. Gut malro-
Gastroschisis and omphalocele differ in their embryo- tation and volvulus are associated with gastroschisis.
logic origin, location, and associated congenital anoma- Gastroschisis is a neonatal emergency that requires im-
lies. Fetal ultrasonography during the first trimester can mediate or urgent surgical intervention. Risk factors for
distinguish the two defects from each other. Specificity gastroschisis include maternal age "20 years, maternal
for identifying gastroschisis and omphalocele by ultra- cigarette smoking, maternal illicit drug use, and maternal
sound is 95%, but sensitivity is only 60%–75%. Maternal use of over-the-counter vasoactive drugs. Although no
alpha fetoprotein (AFP) levels may suggest a diagnosis of congenital anomalies are associated with gastroschisis,
omphalocele or gastroschisis. High levels of AFP ob- intestinal abnormalities such as malrotation, volvulus,
tained during amniocentesis are associated not only with and atresia can occur (Table 59-1).
neural tube defects but also with abdominal wall defects.
At 5–10 weeks of gestational age, the midgut is extruded 2. What are the preoperative concerns for these
into the extraembryonic coelom. By 10 weeks of gestational
two defects?
age, the midgut normally returns to the abdominal cavity.
Omphalocele results from failure of intestinal contents Management of neonates with these defects preoperatively
to migrate from the yolk sac into the abdominal cavity. focuses on reducing fluid losses and preventing infection,
Amnion covers the omphalocele and protects the abdomi- hypothermia, and trauma to the viscera. A warm moist-
nal contents from infection and loss of intracellular fluid. ened sterile dressing should be applied to the exposed
The bowel is morphologically and usually functionally viscera, and a sterile clear plastic bag should envelope the
normal. Omphalocele is located at the base of the umbilical lower body of the infant to minimize temperature and
cord and includes not only the intestines but also often fluid losses.
parts of the liver and other organs. Omphalocele has a high Neonates with abdominal wall defects are assessed for
association with congenital anomalies such as cardiac, associated congenital anomalies, particularly cardiac and
craniofacial, and urologic defects and chromosomal ab- urologic problems. For preterm infants, respiratory abnor-
normalities. Omphalocele associated with macroglossia, malities should be ascertained. Adequate intravenous
organomegaly, hypoglycemia, and mental retardation is access is established for fluid resuscitation. An arterial
known as Beckwith-Wiedemann syndrome. Omphalocele is catheter may be necessary for frequent blood sampling, and
also associated with advanced maternal age. Most mothers a central venous catheter may be used to aid in fluid man-
of infants with omphalocele are !30 years of age. agement. Significant electrolyte imbalances and fluid
In contrast to omphalocele, gastroschisis develops deficits should be corrected preoperatively. Neonates with
later in fetal life, after the intestines have returned to the gastroschisis may require multiple boluses of 20 mL/kg of
abdominal cavity, and has a higher incidence of prematu- balanced salt solution to replace evaporative and third space
rity. Gastroschisis develops from occlusion of the ompha- losses. Albumin is occasionally required for intravascular
lomesenteric artery, resulting in ischemia and atrophy of volume expansion.
313
314 SECTION 11 Pediatrics
QUESTIONS
A full-term, 3-kg infant born vaginally was noted to be remaining cases occur through the esophageal hiatus
cyanotic despite being given blow-by 100% oxygen and (Table 60-1).
adequate respiratory effort. On closer inspection, the Lung development is impaired by the presence of
infant was observed to have a scaphoid abdomen. On abdominal contents in the pleural cavity during fetal
physical examination, there were no breath sounds on the growth. The degree of impairment of lung development
left, and the heart sounds were shifted to the right. The is determined by both the amount of abdominal contents
trachea was intubated, and the neonate was brought to in the pleural cavity and the time of migration. The
the neonatal intensive care unit (NICU) for further greater the amount of abdominal contents in the pleural
evaluation and management. cavity and the earlier the migration, the greater the
degree of pulmonary hypoplasia that is present at birth.
1. Describe the embryology and pathophysiology Not only is the ipsilateral lung affected, but also there are
developmental changes in the contralateral lung. These
of congenital diaphragmatic hernia.
changes include the following:
The incidence of congenital diaphragmatic hernia (CDH) • Decreased number of bronchi and alveoli
is 1 in 2000 to 1 in 5000 live births. There may be • Smaller pulmonary artery
associated congenital anomalies of the central nervous, • Inappropriately muscularized pulmonary arteries
gastrointestinal, genitourinary, and cardiovascular sys- • Decreased cross-sectional area of pulmonary artery
tems. Chromosomal anomalies also may be present. In branches
the fetus, during the first month of life, there is a single The physiologic changes that occur secondary to devel-
pleuroperitoneal cavity. During the second month, the opmental changes in the lung are an increase in pulmonary
pleuroperitoneal membrane begins to form, separating vascular resistance (PVR) and persistent pulmonary hyper-
the pleural and peritoneal cavities. The last portion of tension. Decreased pulmonary blood flow and right-to-left
this membrane to form is the posterolateral portion; the shunting through the foramen ovale and ductus arteriosus
right side closes before the left side. The fetal gut is contribute to progressive hypoxia and acidosis. These
outside the pleuroperitoneal cavity in the yolk sac during physiologic changes can be divided into two components:
the first month of fetal life and returns to the peritoneal (1) irreversible (owing to pulmonary hypoplasia and abnor-
cavity during the second month of development. If the mal vasculature) and (2) reversible (owing to vasoconstric-
gut returns before full closure of the pleuroperitoneal tion of abnormal muscularized arteries). The greater the
membrane, any or all portions of the gut may migrate up irreversible component, the poorer the prognosis. To date,
into the pleural cavity. There are three sites where there is no method available to determine accurately which
migration of the gut may occur: component is predominant.
• Posterolateral (foramen of Bochdalek) Although compression of the lung by abdominal con-
• Anteromedial (foramen of Morgagni) tents in the pleural cavity is detrimental, it does not
• Esophageal hiatus contribute significantly to hypoxia and acidosis. CDH is
The most common site of migration (80%) is through no longer considered a surgical emergency. The initial
the posterolateral portion, the left side more commonly management of these neonates is directed at improving
than the right. Approximately 1% of diaphragmatic her- oxygenation and ventilation. Surgery should be consid-
nias occur through the anteromedial portion, and the ered only after stabilization of the neonate’s condition.
316
60 Congenital Diaphragmatic Hernia 317
TABLE 60-1 Types of Diaphragmatic Hernia distention of the abdominal organs in the thorax,
which would further impair oxygenation and ventila-
tion (Box 60-2). The trachea should be intubated, and
Type Location Frequency
inflation pressures should be limited to !40 cm H2O to
Foramen of Bochdalek Posteromedial 80% avoid causing a pneumothorax. A pneumothorax is most
Foramen of Morgagni Anteromedial 1% likely to occur in the contralateral lung, which is where
most of the gas exchange occurs. An orogastric tube
Esophageal hiatus 19%
should be inserted to assist in deflation of the stomach. If
transfer to the NICU is delayed, an arterial and intrave-
In a stable neonate, surgery is usually scheduled in the nous catheter should be inserted to guide therapy and to
next 24–48 hours. administer pharmacologic agents. If possible, the arterial
catheter should be placed in the right radial artery so that
2. What are the clinical features of congenital preductal oxygenation is measured.
Measures both to prevent further increases in PVR and
diaphragmatic hernia?
to promote a decrease in PVR, increasing pulmonary
The manifesting symptom of CDH is respiratory dis- blood flow, should be instituted. These measures include
tress, with tachypnea and cyanosis, in the neonatal increased oxygenation, hypocarbia, alkalosis, avoidance of
period (Box 60-1). On visual inspection, the abdomen sympathetic stimulation, and normothermia (Box 60-3).
may appear scaphoid and the thorax barrel-shaped. On Pharmacologic vasodilator therapy may be necessary.
physical examination, breath sounds are absent on the Tolazoline is most commonly used for this purpose.
affected side (most commonly the left side), and the car- However, systemic hypotension may be associated with
diac impulse is shifted to the opposite side of the defect its use, and volume replacement and pharmacologic sup-
(most commonly the right side). Bowel sounds on the port of the systemic blood pressure may be necessary.
affected side are an uncommon finding. Fluid replacement should be performed judiciously to
The onset of respiratory symptoms correlates well avoid volume overload and pulmonary edema. Inhaled
with the degree of lung hypoplasia and with prognosis. nitric oxide, a specific pulmonary vasodilator, has been
The earlier the symptoms manifest, the greater the de- used in these patients with variable results. The benefit of
gree of lung hypoplasia is present. Neonates presenting nitric oxide is that systemic hypotension is avoided. If
in the first hour of life have the highest mortality. these measures do not improve the neonate’s condition,
extracorporeal membrane oxygenation (ECMO) may be
3. How is congenital diaphragmatic hernia used. ECMO provides the neonate with adequate gas
exchange while allowing the lungs to rest and mature.
diagnosed?
The diagnosis of CDH may be made prenatally or postna- 5. What is permissive hypercapnia?
tally. With the increased use of ultrasonography in the
prenatal period, prenatal diagnosis of CDH is more com- Permissive hypercapnia is an alternative modality in the
mon. Findings consistent with a diagnosis of CDH are treatment of neonates with CDH. Conventional ventila-
polyhydramnios, visualization of the fetal stomach in the tory management resulted in pulmonary barotrauma
thorax, and shift of the mediastinum away from the side of secondary to high inspiratory pressures needed to achieve
the hernia. A poor prognosis can be anticipated if the liver adequate ventilation and oxygenation. In permissive
is seen in the thorax and there is a low lung-to-head ratio. hypercapnia, the arterial carbon dioxide tension (PaCO2)
Postnatally, the diagnosis should be considered if the
above-described clinical features are present. Definitive
diagnosis is made by chest radiograph showing abdominal
contents in the thoracic cavity.
BOX 60-2 Delivery Room Management
is allowed to increase, while maintaining adequate cause intestinal distention, which could compromise
oxygenation and acid-base balance. The benefit of this the neonate and impede abdominal closure. However,
technique is that lower peak inspiratory pressures are depending on the neonate’s cardiovascular stability, inha-
used resulting in less pulmonary barotrauma. The goal lation agents may not be tolerated well. In most cases, an
during permissive hypercapnia is to maintain a preductal oxygen–opioid–muscle relaxant combination would be
oxygen saturation of "90%. Acid-base balance is main- optimal.
tained with either bicarbonate or tris(hydroxymethyl)
aminomethane (THAM). With this technique, PVR 7. What problems may occur intraoperatively
may not be maximally lowered, but it may allow for and postoperatively?
sufficient pulmonary blood flow to achieve adequate
oxygenation. If the above-mentioned goals are unattain- Meticulous attention should be paid to adequate oxygen-
able, conventional treatment modalities for reducing ation and ventilation of these neonates. There is an
PVR should be instituted. increased risk for pneumothorax, especially on the contra-
lateral side. If this should occur, it would be life-threatening.
6. What are the anesthetic considerations for Use of ventilation pressures "40 cm H2O should be
avoided so as not to cause a pneumothorax. No attempt
neonates with congenital diaphragmatic hernia?
should be made to inflate the contralateral lung manually
Surgery may be scheduled after the patient is stabilized. because of this potentially life-threatening risk. A diagno-
Most surgeons prefer a transabdominal approach. The sis of pneumothorax should be considered when any
abdominal organs are reduced, and the diaphragm is re- abrupt change in the neonate’s condition occurs during
paired either primarily or with a synthetic patch. In most surgery. When in doubt of the diagnosis, a needle should
cases, the abdominal wall can be closed primarily, but in be inserted into the contralateral chest. This maneuver
some instances a Silastic pouch may be created. both diagnoses the presence of a pneumothorax and treats
In the last decade, thoracoscopic repair has gained pneumothorax. A chest tube should be placed after the
increasing popularity. However, this method of repair diagnosis is made.
is associated with a longer duration of surgery and a Postoperatively, these neonates may continue to require
higher rate of recurrence. Insufflation of carbon dioxide oxygen and ventilatory support. Pulmonary hypertension
to 3 mm Hg was sufficient to reduce the intrathoracic may persist, and there may be continued clinical deteriora-
viscera into the abdomen. No clinically significant in- tion despite surgical correction. This deterioration is
crease in PaCO2 occurred. due to the severe pulmonary hypoplasia that existed pre-
Anesthetic management of patients (Box 60-4) in- operatively and the change in pulmonary mechanics after
cludes continuation of preoperative measures to improve surgery.
oxygenation and ventilation and to promote a decrease in
PVR. To reduce excessive ventilator pressures, small tidal 8. Describe the techniques for fetal surgery.
volumes and rapid respiratory rates may be necessary. If
permissive hypercapnia was employed, these measures Two techniques for fetal correction of CDH have been
should be continued intraoperatively. Pharmacologic in- described. The first technique is surgical correction of
fusions should be continued. Arterial blood gases should the diaphragmatic defect and reduction of the abdominal
be monitored frequently, and any changes in ventilation, contents into the abdominal cavity. This technique
oxygenation, and acid-base balance should be treated cannot be performed if the liver is in the thoracic cavity
expeditiously. It is important to avoid hypoxia and acido- because it would result in compromised flow through
sis, which would lead to an increase in PVR that would the umbilical vein. The second technique is tracheal
be very difficult to reverse. Measures to prevent hypo- occlusion, which has been shown to result in lung devel-
thermia are also important in the management of these opment. However, this technique has been fraught with
patients. problems and is not widely used.
All anesthetic agents may be used in these neonates
with the exception of nitrous oxide. Nitrous oxide may
SUGGESTED READINGS
Brett C, Davis PJ: Anesthesia for general surgery in the neonate.
pp. 567-574. In Davis PJ, Cladis FP, Motoyama EK (eds.): Smith’s
BOX 60-4 Anesthetic Management Aneshtesia for Infants and Children, 8th edition. Mosby, Philadelphia,
2011.
• Prevent increases in PVR Lansdale N, Alam S, Losty AP, et al.: Neonatal endosurgical congenital
• Adequate oxygenation diaphragmatic hernia repair: a systematic review and meta-analysis.
Ann Surg 252:20, 2010.
• Hyperventilation Roberts JD Jr, Romanelli TM, Todres ID: Neonatal emergencies. p. 757.
• Alkalosis In Cote CJ, Lerman J, Todres ID (eds.): A practice of anesthesia for
• Maintain normothermia infants and children, 4th edition. Saunders, Philadelphia, 2009.
• Continue pharmacologic infusions Sluiter I, van de Ven CP, Wijnen RMH, et al.: Congenital diaphrag-
• Avoid nitrous oxide matic hernia: still a moving target. Semin Fetal Neonatal Med
16:139, 2011.
CASE 61
Tracheoesophageal Fistula
Michael Chietero, MD
QUESTIONS
A 1-day-old, 3.3-kg neonate presented to the operating presence of a fistula between the trachea and distal esopha-
room for repair of tracheoesophageal fistula (TEF). The gus (Gross types C and D). Absence of air in the stomach
patient was born at 38 weeks gestation by normal vaginal occurs with cases of EA without a distal fistula (Gross types
delivery. A and B). The “H”-type fistula (TEF without atresia, Gross
type E) usually manifests later in life, most commonly
with choking during feedings and recurrent pneumonitis.
1. What is a tracheoesophageal fistula?
TEF is a congenital malformation involving esophageal 3. What are the preoperative concerns in patients
atresia (EA) combined with a fistula connecting the esoph- with tracheoesophageal fistula?
agus to the trachea. These abnormalities can occur in vari-
ous combinations. The most common classification system There is a 30%–50% incidence of associated anomalies
of TEFs is Gross’ classification (Figure 61-1). Table 61-1 in infants with EA and TEF. Particular combinations
describes the various types of TEF and their approximate have been described, termed VATER association or,
incidence. The most common type, EA with a distal fistula more exactly, VACTERL association (Table 61-2).
(Gross type C), accounts for approximately 80% of cases. The approximate incidence of associated anomalies is
The incidence of EA and TEF is approximately 1 in shown in Table 61-3. The prevalence of congenital heart
3000 births. Embryologically, the trachea and esophagus disease often necessitates an electrocardiogram (ECG) and
both originate from the ventral diverticulum of the primi- echocardiogram preoperatively. In addition, because renal
tive foregut. They normally become separated by the esoph- anomalies can also occur, evaluation of renal function
agotracheal septum. Because the trachea is situated anterior should be documented. Finally, because of the potential
to the esophagus, the fistula is located on the posterior as- for vertebral malformations, a lumbar ultrasound may be
pect of the trachea and usually just proximal to the carina. indicated if a sacral dimple is present. A lumbar ultrasound
is especially indicated if a thoracic epidural catheter placed
2. What is the typical presentation of a patient via the caudal route is planned for postoperative analgesia.
Pulmonary complications can have important implica-
with a tracheoesophageal fistula?
tions for the anesthesiologist. Atelectasis from gastric dis-
In contrast to other congenital anomalies, it is difficult to tention and aspiration from regurgitation are common
diagnose TEF in utero. Polyhydramnios is often present pulmonary complications; both lead to reduced pulmonary
because EA prevents the fetus from swallowing amniotic compliance and ventilation/perfusion ( V ˙ /Q)
˙ mismatching.
fluid. At delivery, an orogastric tube cannot be passed Preoperative management of patients with TEF primarily
into the stomach. Typically, the orogastric tube passes involves preventing pulmonary complications until surgery
only to a distance of approximately 10 cm from the gums. is performed. Management includes the following:
In most cases, the diagnosis is initially suspected at the • Cessation of feeding
first feeding, when the neonate presents with coughing, • Positioning the infant slightly head up (30 degrees)
choking, and cyanosis (the “three Cs”). Excessive saliva- to minimize regurgitation of gastric contents through
tion and respiratory distress can also occur. the fistula
Confirmation of the diagnosis is made radiographically • Intermittent suctioning of the proximal esophageal
when a radiopaque orogastric catheter is seen curled in pouch catheter
the proximal esophageal pouch. The presence of air in There is also an increased incidence of prematurity
the stomach and intestines on radiography signifies the in patients with TEF, especially in patients who have
319
320 SECTION 11 Pediatrics
Pyloric Stenosis
Francine S. Yudkowitz, MD, FAAP
QUESTIONS
1. What is pyloric stenosis? 5. What is the surgical treatment for pyloric stenosis?
2. What is the clinical presentation of pyloric stenosis? 6. What are the anesthetic considerations for patients
3. How is the diagnosis made? with pyloric stenosis?
4. What metabolic derangements are associated
with pyloric stenosis, and how are they treated?
A 4-week-old infant presented for pyloromyotomy. The sodium is excreted along with the bicarbonate, urinary
patient had a 3-day history of nonbilious, projectile sodium concentrations cannot be relied on as an indi-
vomiting. rect measure of the volume status. Chloride is reab-
sorbed in exchange for bicarbonate leading to minimal
urinary chloride concentrations.
1. What is pyloric stenosis?
As the infant becomes more dehydrated, the renal
Pyloric stenosis is caused by circular muscular hypertro- response is aimed at maintaining intravascular volume.
phy at the pylorus. It produces gastric outlet obstruction. Aldosterone is secreted, which results in conservation
Pyloric stenosis usually manifests between 2 and 6 weeks of sodium and loss of potassium. In the distal tubule,
of age but can manifest earlier. There is a higher incidence sodium is conserved at the expense of hydrogen, and an
in male infants. acidic urine is excreted.
The degree of dehydration should be assessed to guide
2. What is the clinical presentation of pyloric fluid resuscitation. Sodium chloride is the isotonic fluid
of choice for resuscitation. It may be necessary to correct
stenosis?
hypovolemia rapidly with 10–20 mL/kg of normal saline
Symptoms may begin with regurgitation, which progresses if the patient is exhibiting signs of shock. Glucose should
to nonbilious, projectile vomiting. Jaundice may occur in be administered as well. These infants may have depleted
5% of infants secondary to hepatic gluconyltransferase glycogen stores in the liver leading to the development of
deficiency. Jaundice usually resolves after treatment. hypoglycemia if glucose is not provided.
Hypovolemia, electrolyte imbalance, and acid-base
derangements should be corrected before surgical
3. How is the diagnosis made?
intervention. The presence of normal plasma chloride
On physical examination, an olive-like mass can be levels suggests that there is adequate fluid and electro-
palpated in the epigastrium just right of the midline. lyte resuscitation.
The diagnosis can be confirmed either by ultrasound
or by barium swallow. However, barium swallow adds 5. What is the surgical treatment for pyloric
to the risk of aspiration pneumonitis in the periopera- stenosis?
tive period.
The surgical treatment of pyloric stenosis is laparo-
4. What metabolic derangements are associated scopic pyloromyotomy, in which the circular muscles of
the pylorus are spread apart. Occasionally, duodenal
with pyloric stenosis, and how are they treated?
perforation may occur, which is easily sutured closed.
Vomiting from pyloric stenosis usually leads to hypovo- This complication may slightly delay the start of oral
lemia and a hypochloremic, hypokalemic metabolic feeds after surgery.
alkalosis. Because the vomitus consists only of gastric
contents, hydrogen, sodium, potassium, and chloride 6. What are the anesthetic considerations for
ions are lost. Initially, the renal response is to maintain patients with pyloric stenosis?
acid-base balance. Alkaline urine is excreted because the
bicarbonate load presented to the kidneys exceeds the Pyloric stenosis is a medical and not a surgical emergency.
absorption capability of the proximal tubules. Because Before the start of anesthesia, hypovolemia, electrolyte
322
62 Pyloric Stenosis 323
imbalances, and acid-base derangements should be com- postoperatively. In addition, opioids may increase the risk
pletely corrected. Before induction, the stomach should for postoperative apnea that may occur secondary to
be suctioned with a large-bore (14F) orogastric tube while changes in cerebrospinal fluid pH and hyperventilation.
placing the infant in supine, right lateral, and left lateral Glucose infusion should be administered during the pro-
positions to decrease the risk of regurgitation and aspira- cedure to avoid hypoglycemia. Extubation should be
tion. If a smaller sized orogastric or nasogastric tube is done only when the infant is awake and protective airway
already present, it should be replaced. reflexes are reestablished.
Although inhalation induction has been described for Depending on the postconceptual age of the infant,
these patients, most anesthesiologists would consider apnea monitoring may be necessary postoperatively.
them as having a “full stomach.” Consequently, either a
rapid-sequence induction with cricoid pressure or an
awake intubation would be indicated. Although awake SUGGESTED READINGS
intubation is a viable option, it is associated with oxygen
Cook-Sather SD, Tulloch HV, Cnaan A, et al.: A comparison of awake
desaturation, bradycardia, longer time to intubation, and versus paralyzed tracheal intubation for infants with pyloric stenosis.
reduced first attempt success rates. It does not provide Anesth Analg 86:945, 1998.
any advantage over a rapid-sequence induction. Mainte- Hammer G, Hall S, Davis PJ: Anesthesia for general abdominal, thoracic,
nance of anesthesia can be accomplished either by inhala- urologic, and bariatric surgery. p. 690. In Davis PJ, Cladis FP,
tion or by a balanced technique. Muscle relaxants are not Motoyama EK (eds.): Smith’s Anesthesia for Infants and Children, 8th
edition. Mosby, Philadelphia, pp. 750-751, 2011.
necessary. The use of opioids may not be necessary be- Roberts JD Jr, Romanelli TM, Todres ID: Neonatal emergencies.
cause the surgeon usually infiltrates the surgical wound p. 761. In Cote CJ, Lerman J, Todres ID (eds.): A Practice Of Anesthe-
with local anesthetic, which provides adequate analgesia sia for Infants and Children, 4th edition. Saunders, Philadelphia, 2009.
CASE 63
QUESTIONS
1. What is the incidence of congenital heart disease? 6. What are common intracardiac lesions with right-
2. What is the differential diagnosis for a systolic to-left shunting and reduced pulmonary blood flow?
murmur? 7. What are the anesthetic considerations for right-
3. What are the general anesthetic considerations to-left shunting lesions with reduced pulmonary
for common congenital cardiac lesions? blood flow?
4. What are common intracardiac lesions with 8. What surgical options are available for congenital
left-to-right shunting? heart disease?
5. What are the anesthetic considerations for 9. Describe the surgical repair and sequelae of spe-
left-to-right shunting lesions? cific congenital cardiac lesions.
A 5-week-old infant was scheduled for bilateral inguinal 3. What are the general anesthetic considerations
herniorrhaphy. On preoperative evaluation, the infant for common congenital cardiac lesions?
was noted to be tachypneic and tachycardic. A IV/VI
Extracardiac Defects
systolic murmur was heard at the left sternal border.
Associated extracardiac defects are present in 5–50% of
1. What is the incidence of congenital heart children with CHD. In 17–18%, the defect is part of
a syndrome or chromosomal anomaly. Genitourinary
disease? tract anomalies are among the most common lesions
The incidence of congenital heart disease (CHD) is ap- and are present in 4–15% of patients with CHD. Major
proximately 6 to 8 in 1000 live births. It is the most com- chromosomal anomalies with associated cardiac lesions
mon congenital malformation. The incidence of CHD has of anesthetic significance are Down (trisomy 21), Turner,
increased as a result of improvements in diagnostic testing, Noonan, and DiGeorge syndromes.
increased awareness, and improved medical treatments of
critically ill infants. Approximately 40,000 children are
Prevention of Air Embolism
born each year with CHD in the United States. The most
common CHD lesions manifest with a systolic murmur All patients with shunt lesions (i.e., communication be-
(Table 63-1). The main consequences of significant CHD tween the pulmonary and systemic circulation), regardless
are congestive heart failure and cyanosis. of the presence or absence of pulmonary outflow obstruc-
tion or usual shunting pattern, are at risk for air emboli to
2. What is the differential diagnosis for a systolic the systemic circulation. Shunts are often bidirectional,
and owing to the earlier relaxation of the left ventricle
murmur? compared with the right ventricle, a left-to-right shunt
Systolic murmurs can be either innocent or pathologic. may transiently reverse during this portion of the cardiac
Innocent murmurs are soft flow murmurs without cycle. On sudden obstruction to right ventricular output
physiologic consequences. Pathologic murmurs are secondary to air embolism, a left-to-right shunt converts
loud, pansystolic or late systolic, and are associated to a right-to-left shunt pattern. The following precautions
with cardiac anomalies. The most common lesions should be followed whenever caring for a patient with a
associated with a systolic murmur in young infants are shunt lesion:
ventricular septal defect (VSD) and patent ductus arte- • Intravenous (IV) tubing should be meticulously
riosus (PDA). These infants have signs of mild conges- debubbled and then rechecked after warming the
tive heart failure (i.e., tachypnea and tachycardia) and operating room. Warming could allow nitrogen
should undergo a cardiology evaluation before surgery. to come out of solution in the IV fluid, forming
Transthoracic echocardiography is presently the fast- additional hazardous bubbles.
est, most accurate, and least invasive diagnostic tool to • All IV lines should be connected while free flowing.
establish an exact anatomic diagnosis in most patients • All syringes should be cleared of air, and before in-
with CHD. jecting into an IV line, a small amount of fluid should
324
63 Congenital Heart Disease 325
Note: Antibiotics should be given 30-60 minutes before procedure start. If dose was not given, may
administer up to 2 hours after the procedure finished.
Modifed from Wilson W, Taubert KA, Gewitz M, et al.: Prevention of Infective Endocarditis: Guidelines
From the American Heart Association: A Guideline From the American Heart Association Rheumatic
Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the
Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia,
and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation
116:1736-1754, 2007.
326 SECTION 11 Pediatrics
4. What are common intracardiac lesions Before the development of pulmonary vascular disease,
the volume of the shunt may be manipulated by changing
with left-to-right shunting? PVR or SVR or both. High oxygen concentrations, hy-
Common intracardiac lesions with left-to-right shunt- perventilation, and alkalosis lead to pulmonary vasodila-
ing include all forms of atrial septal defects (ASDs), tion and may cause massive increases in left-to-right
VSDs, PDA, and other large aortopulmonary connec- shunting. With the limited cardiac output of the small
tions. The magnitude and direction of the shunt depend infant, this increase in left-to-right shunting can lead
on the difference between the outflow resistances of the to severe systemic underperfusion and cardiovascular
two connections and the size of the defect. Exceptions collapse. Similarly, an increase in afterload leads to an
are communications between the left ventricle and increase in left-to-right shunting, as long as PVR is less
right atrium where obligatory shunting of blood occurs than SVR. Most patients with large shunts receive anti-
owing to the large pressure difference that exists between congestive medications (e.g., digoxin, furosemide) and an
these two cardiac chambers. afterload-reducing agent (e.g., angiotensin-converting
enzyme inhibitor) before cardiac surgery or if managed
Atrial Septal Defects medically only.
In the following conditions, anatomic repair is attempted because they may indicate an underlying residual defect
but results in residual defects or requires use of prosthetic and may be the harbinger of sudden death. Ventricular
materials: premature beats can be seen with right ventriculotomy
• TOF or resection, elevated intracavitary pressure (as seen with
• Atrioventricular (AV) canal defect valvular stenosis), and cardiomyopathies with diastolic
• Obstructive valvular lesions dysfunction. Cardiomyopathies with diastolic dysfunc-
• Lesions requiring insertion of a conduit between the tion can be seen after surgery with suboptimal myocardial
ventricle and respective artery (usually the right preservation or when pressure and volume overload
ventricle and pulmonary artery) of the ventricle were present for a long time before
• Valve replacement corrective surgery, particularly if associated with an
In patients in whom anatomic repair is not feasible, increased hematocrit.
palliative repair is attempted to try to establish normal Occasionally, the stress of anesthesia and surgery may
cardiovascular physiology. Included in this group is unmask an underlying rhythm disturbance. New ventricu-
the initial repair of TGA by the Mustard or Senning lar extrasystoles observed during anesthesia in a patient
operation. In this procedure, blood flow is redirected with previous TOF repair should be brought to the cardi-
at the atrial level (i.e., atrial switch) where pulmonary ologist’s attention so that appropriate follow-up can occur.
venous blood is directed to the aorta and systemic venous TOF repair has the highest association of ventricular ar-
blood is directed to the pulmonary artery. Also included rhythmias and sudden death in the long-term after repair,
in this group are cardiac malformations that result particularly in patients operated on later in life and in
in only one functional ventricle that supports the earlier series. To prevent this complication, an implantable
pulmonic and systemic circulation. This heterogeneous cardioverter-defibrillator may be required.
group of lesions requires several staged surgical inter-
ventions until the final Fontan operation, which results
in separation of the two circulations but without a 9. Describe the surgical repair and sequelae of
pulmonary ventricle. specific congenital cardiac lesions.
One of the most common sequelae after surgery for Atrial Septal Defects
CHD is arrhythmia (Box 63-3). Supraventricular arrhyth-
mias are the most common arrhythmias and can be life- Secundum ASD is associated with a 30% incidence of
threatening under certain conditions (e.g., atrial flutter mitral valve prolapse. Patients need to be followed for the
after Fontan operation). They are particularly common development of mitral regurgitation, which occurs in
after repairs with extensive atrial suture lines or elevated 5–10% of patients, or ventricular arrhythmias. Early and
atrial pressures or both. Atrial arrhythmias may be either late atrial arrhythmias occur after ASD repair, particu-
tachycardias or bradycardias. These arrhythmias are often larly if the patient was $20 years old at the time of repair,
refractory to medical therapy and may require ablation or in which case it could be present even before surgery.
pacemaker insertion. After Senning or Mustard procedure Development of paroxysmal or chronic atrial fibrillation
for TGA, only 20–40% of patients are in sinus rhythm requires anticoagulation therapy to prevent systemic em-
5–10 years following surgery. After the Fontan procedure bolization. The risk of late development (i.e., 25–30 years
performed with direct atrial-to-pulmonary artery anasto- after repair) of atrial flutter or fibrillation is 4% if repair
moses, there is at least a 30% incidence of atrial arrhyth- is done before age 10 years and 58% if repair is done after
mias. Newer Fontan surgical approaches, either lateral age 40 years. The presence of a large left-to-right shunt
tunnel or extracardiac conduits, attempt to diminish the before surgery is an additional risk factor for the develop-
incidence of late arrhythmias. Atrial arrhythmias also are ment of late atrial arrhythmias. The most commonly
seen in 5–10% of patients after repair of a secundum ASD, observed arrhythmias after repair of sinus venosus
particularly following repair at an older age. Supraven- defects are sinus node dysfunction and sick sinus
tricular arrhythmias are associated with a 2–8% incidence syndrome, which occur in at least 10% of patients.
of sudden death.
Ventricular arrhythmias, although less common in Ventricular Septal Defect
the postoperative period, are frequently more significant
The incidence of residual VSD after surgery is !5%.
Patients with subarterial VSD may have aortic insuffi-
BOX 63-3 Arrhythmias after Congenital ciency, which is an indication to close even a small
Heart Disease Procedures defect. In 3% of cases, regurgitation is progressive.
After VSD repair, many patients (30–65%) have a right
• Atrial arrhythmias bundle-branch block (RBBB) on electrocardiogram
• Senning or Mustard procedure (ECG). Previously, when a right ventriculotomy was
• Fontan commonly performed, serious ventricular arrhythmias
• Secundum ASD were seen in at least 34% of patients, with a 1–2%
• Ventricular arrhythmias
• Right ventriculotomy
incidence of sudden death. Complete heart block is one
• Right ventricular resection of the risk factors of VSD closure, but with improved
• Elevated intracavitary pressure surgical techniques the incidence is !2%. Complete
• Cardiomyopathies with diastolic dysfunction heart block is also seen after device closure of a peri-
membranous VSD where it can develop late and cause
330 SECTION 11 Pediatrics
sudden death. It is also a late sequela of patients who regurgitation. Although the cleft mitral valve is compe-
exhibit bifascicular block after surgery (i.e., RBBB and tent in most patients, 10–15% of patients have mitral
left anterior hemiblock). Most patients whose defects valve regurgitation at the time of initial surgery. Because
are closed before age 2 years have normal cardiovascu- of the abnormality of the mitral valve, long-term mitral
lar function. However, they have a greater risk for insufficiency remains a serious problem after repair of
arrhythmias compared with the normal population. primum ASDs and complete canals. In $60% of patients
Patients operated on later in life may have persistence followed long-term after repair of partial AV septal de-
of depressed myocardial reserve and progressive pulmo- fects, evidence of mitral regurgitation is found that may
nary hypertension. require eventual mitral valve replacement. After repair
of complete AV septal defect in infancy, the incidence of
mitral regurgitation requiring reintervention is approxi-
Coarctation of the Aorta
mately 7%. First-degree heart block is seen in 50% of
In 50% of patients with coarctation of the aorta, other patients after repair. Malignant tachyarrhythmias may
associated cardiac lesions are present. Bicuspid aortic develop as patients age.
valve is seen in 85% of patients, and 3–10% have berry
aneurysms of the circle of Willis. Coarctation of the Tetralogy of Fallot
aorta occurs in 35% of patients with Turner syndrome.
The technique of repair of coarctation of the aorta Older TOF repairs have resulted in right ventricular dys-
has changed over the years. The preferred technique at function secondary to pulmonary insufficiency and a high
the present time is resection of the coarcted aorta and incidence of arrhythmias from extensive right ventricu-
end-to-end anastomosis. Older repairs included patch lotomies. Incomplete relief of right ventricular outflow
aortoplasty, subclavian flap aortoplasty, and interposition obstruction, demonstrated by a right-ventricle-to-left
graft. Patch aortoplasty has been abandoned because it is ventricle systolic pressure ratio $0.5, is an independent
associated with a high incidence of aortic aneurysm for- predictor of late mortality after repair. Repair at an older
mation that expands rapidly and has led to aortic rupture age is also associated with higher long-term mortality, as
and death. Subclavian flap aortoplasty is still used occa- is the presence of a large outflow patch. Most patients
sionally. Blood pressure measurements in the left arm are symptom-free after repair. However, in the survivors
may be unreliable after this procedure. Bridging grafts of the earlier repairs, there is a 6% incidence of sudden
are occasionally used in older patients with repeated death, or 0.3% per patient year, and at least 10% inci-
coarctations. Repair in infancy is associated with a dence of inducible ventricular tachycardia requiring
15–20% incidence of repeat coarctation, which can be implantation of a cardioverter-defibrillator. Nearly
managed effectively with balloon angioplasty. Balloon one third of patients at late follow-up have atrial tachy-
angioplasty is not effective for primary coarctation in cardias, which can also cause sudden death. Most patients
the newborn. However, it can be performed in older have a RBBB on ECG.
patients, in whom a stent can be placed in the dilated The presence of ventricular ectopy must be thor-
coarctation site to maintain the diameter. A long-term oughly evaluated preoperatively. The presence of resid-
sequela of balloon angioplasty is the development of an ual lesions, VSD, or right ventricular hypertension
aortic aneurysm at the angioplasty site (2–14%). should be identified before any procedure. Sympathetic
Patients with repaired coarctation of the aorta are at stress in the setting of right ventricular hypertension and
risk for development of late hypertension in the absence an old ventriculotomy scar increase the propensity for
of repeat coarctation. Age at repair is the strongest pre- ventricular dysrhythmias. Patients with significant pul-
dictor for this complication. Repair after age of 5 years monary insufficiency may not tolerate rapid fluid shifts.
has a 75% incidence of systolic hypertension at 25-year Vascular access may be difficult in patients with multiple
follow-up. Long-term survivors have an accelerated risk previous cardiovascular procedures. Patients with residual
of coronary artery disease, myocardial infarction, and shunts are at risk for paradoxical emboli.
premature death. In addition, because of the high inci-
dence of bicuspid aortic valve, 7–10% of patients develop Transposition of the Great Arteries
aortic valvular disease requiring aortic valve replacement.
In the perioperative period, patients who are normoten- TGA represents 5–7% of all congenital cardiac defects
sive at rest may develop significant hypertension with and is the most common cause of cyanotic CHD in new-
minimal stimulation; this may be due to underlying hy- borns. In TGA, the aorta arises from the right ventricle
pertensive disease or unrecognized repeat coarctation. and the pulmonary artery from the left, creating two
parallel circulations. Survival past the neonatal period is
impossible unless some mixing between the circulations
Atrioventricular Septal Defects
occurs, through a PDA, ASD, or VSD. If insufficient
AV septal defects are the most common cardiac defect mixing is present, these critically ill and severely cyanotic
associated with Down syndrome. The complete form infants must undergo emergent balloon atrioseptostomy
results in severe CHF and pulmonary hypertension. The to create an ASD and allow for better mixing. Before
defect is usually repaired in infancy because of symptoms surgical interventions, 90% of patients died within the
and to prevent development of obstructive pulmonary first year of life. Surgical interventions are aimed at
vascular disease. Primum ASDs manifest similar to se- improving mixing, redirecting flow of systemic venous
cundum ASD, unless associated with significant mitral or pulmonary venous return to pulmonary artery or
63 Congenital Heart Disease 331
aorta, or anatomically correcting the problem. The ini- Single Ventricle and the Fontan Operation
tial physiologic repair for this condition was “switching”
the blood return at the atrial level with the help of an A multitude of complex congenital cardiac lesions have
intraatrial baffle, the Mustard and Senning procedures. only one functional ventricle to support the pulmonary
This repair resulted in the right ventricle becoming the and systemic circulation or can be repaired only by con-
systemic ventricle and extensive suture lines in the atria. verting them to single-ventricle physiology. Common
There is now $40-year follow-up available for these lesions that are “repaired” in this way include tricuspid
patients. The 20-year survival rate is 80%, but late mor- atresia, double inlet left or right ventricle, hypoplastic
bidity is common. Sinus rhythm is present in !20% of left heart syndrome (HLHS), and pulmonary atresia with
patients, and $10% of patients have developed right intact septum and hypoplastic right ventricle. In infancy,
ventricular failure requiring either transplantation or these patients undergo a procedure to balance pulmonary
conversion to an arterial switch. The intraatrial baffle blood flow between the systemic circulation and the
leads to systemic venous obstruction in 10–20% of pa- pulmonary circulation. This procedure involves either
tients, which may not be clinically apparent except for the creation of an aortopulmonary shunt for pulmonary
mild facial swelling. Monitoring of the CVP may be quite perfusion or banding of the pulmonary artery to restrict
misleading under these circumstances and may cause excessive flow. In HLHS, the aorta is reconstructed dur-
superior vena cava (SVC) syndrome. Both the Mustard ing the same procedure (i.e., Norwood stage 1).
and the Senning procedures resulted in obstruction of the A hybrid approach has been advocated to avoid
right pulmonary vein owing to baffle shrinkage in 5–10% either a shunting procedure or a Norwood stage 1 in
of patients, frequently requiring reoperation because the newborn period. For ductus dependent lesions re-
of unilateral pulmonary venous hypertension. However, quiring an aortopulmonary shunt, a stent is inserted in
the most serious long-term complication is the severe the ductus in the catheterization laboratory, avoiding
arrhythmias that follow both procedures. Sinus node dys- a surgical procedure. For HLHS, bilateral pulmonary
function or atrial flutter (25%) can result in sudden death. artery banding is performed via median sternotomy,
Late right ventricular dysfunction leads to ventricular and a stent is inserted in the ductus in an antegrade
tachycardia. Patients may be receiving multiple antiar- direction. At about 6 months of age, to relieve the
rhythmic drugs and may require pacemaker implantation volume load on the single ventricle, the venous return
to prevent complications from this therapy. Pacemakers from the upper extremity is diverted directly into
are necessary in patients with sick sinus syndrome. the lung by anastomosis of the SVC to the pulmonary
Tachyarrhythmias are presently treated with radiofre- artery (bidirectional Glenn operation). The pulmonary
quency ablation, if possible, but may require an implantable valve is occluded or the pulmonary band is left in situ
antitachycardia device. After the Mustard procedure, 50% (pulsatile Glenn operation). The PDA or aortopulmo-
of patients have a pacemaker by age 30 years. nary shunt is ligated. Aortic arch reconstruction is
Because of the disappointing long-term results of the performed during the same surgery after a neonatal
atrial switch procedures, anatomic correction at the arte- hybrid procedure.
rial level has been the preferred approach since the mid- All patients remain cyanotic after these procedures.
1980s. It involves transection of both great vessels with Because all blood mixes in the single ventricle, with bal-
relocation of the aorta above the pulmonary valve and the anced flow to the systemic and pulmonary vascular bed
left ventricle and relocation of the pulmonary artery above and normal cardiac output, oxygen saturation is between
the aortic valve and the right ventricle. The coronary 80% and 85%. In the final stage procedure (Fontan),
arteries are disconnected and relocated to the neoaorta. complete separation of the two circulations is achieved by
Long-term follow-up of $30 years is now available. There diversion of the inferior vena cava (IVC) blood to the
is a significant reduction in arrhythmias, better systemic pulmonary artery. There have been several modifications
ventricular function, and better exercise tolerance. In the of this procedure over the years. At the present time, the
initial series, supravalvular pulmonary stenosis occurred in IVC is channeled either through an intraatrial lateral
$10% of patients requiring dilation or reoperation. With baffle or via an extracardiac conduit to the pulmonary
modifications in the surgical technique, this complication artery. Because pulmonary blood flow and cardiac output
has become rare. Aortic insufficiency, which may eventu- depend on a pressure gradient between the CVP and
ally require aortic valve replacement, occurs in long-term the mean pulmonary or intrathoracic pressure, PVR has
survivors. In addition, 1–3% of patients have asymptom- to be low and myocardial function relatively normal to
atic occlusion of one coronary artery on follow-up coro- avoid excessively high CVP. Patients have limited poten-
nary angiography. Patients after atrial switch procedures tial to increase cardiac output because of limited flow
may have limited cardiac reserve. They also may have dif- across the venous channels. A fenestration is created
ficult central access problems. The course of central lines between the IVC channel and the right atrium to allow
on the chest film appears quite abnormal because the cath- decompression of high venous pressure. Because the fen-
eter traverses from the SVC along the baffle into the estration creates a right-to-left shunt, cardiac output is
mitral valve, left ventricle, and pulmonary artery. After the maintained at the expense of full oxygenation.
arterial switch procedure, patients should be evaluated for These patients are at risk for several long-term problems,
supravalvular stenosis and may be at risk for development as follows:
of myocardial ischemia secondary to coronary stenosis. • Persistently elevated CVP leads to protein-losing
These patients are otherwise similar to a person with a enteropathy in 5–13% of patients $10 years old.
structurally normal heart. • Persistent pleural effusions.
332 SECTION 11 Pediatrics
• Atrial suture lines and atrial distention lead to a • Maintenance of adequate preload and sinus rhythm
high incidence of atrial tachyarrhythmias. Atrial is important.
flutter occurs in 40–50% of patients 15 years after • Cardiodepressant drugs should be avoided.
the procedure. • Spontaneous ventilation should be maintained if
• If the single ventricle is a right ventricle, ventricular possible to minimize increases in intrathoracic
function deteriorates progressively. pressure.
• Abnormal cardiac function is present in 50% of • Controlled ventilation should be adjusted to keep
patients 10 years after the repair. positive intrathoracic pressure to a minimum.
• The 15-year survival rate is 60–73%. • CVP catheters should be used only when absolutely
• Spontaneous thrombosis requiring long-term indicated because of the risk of thrombosis and
low-dose anticoagulation. obstruction to venous return.
• Afterload-reducing agents are required to protect myo- • Neuraxial anesthesia should be carefully titrated to
cardial function and to maintain low left atrial pressure. allow for adjustment for acute decreases in preload
• Sinus rhythm is important to maintain cardiac output. and afterload.
• Reduced exercise tolerance is present. • Endocarditis prophylaxis is indicated in the presence
Key considerations for anesthetic management are the of a shunt or with a fenestration.
following: • Paradoxical emboli are a risk in the presence of a
• A thorough preoperative cardiac evaluation should fenestration or baffle leak.
be performed including echocardiography to assess The surgical repair and sequelae of specific congenital
function of the AV valve and ventricle. heart lesions are summarized in Box 63-4.
SUGGESTED READINGS Wilson W, Taubert KA, Gewitz M, et al.; American Heart Association
Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee;
Diaz LK: Anesthesia for non-cardiac surgery and magnetic imaging. American Heart Association Council on Cardiovascular Disease in
p. 546. In Andropuolos DB (ed.): Anesthesia for Congenital Heart the Young; American Heart Association Council on Clinical Cardiol-
Disease. Wiley-Blackwell, Oxford, 2010. ogy; American Heart Association Council on Cardiovascular Surgery
Greeley WJ, Berkowitz DH, Nathan AT: Anesthesia for pediatric cardiac and Anesthesia; Quality of Care and Outcomes Research Interdisci-
surgery. In Miller RD, Eriksson LI, Fleisher LA, et al. (eds.): Miller’s plinary Working Group: Prevention of infective endocarditis: guide-
Anesthesia, 7th edition. Churchill Livingstone, Philadelphia, 2009. lines from the American Heart Association: a guideline from the
Miller-Hance WC: Anesthesia for non-cardiac surgery in children with American Heart Association Rheumatic Fever, Endocarditis, and
congenital heart disease. p. 465. In Coté CJ, Lerman J, Todres ID (eds.): Kawasaki Disease Committee, Council on Cardiovascular Disease
A Practice of Anesthesia for Infants and Children. Saunders, Philadelphia, in the Young, and the Council on Clinical Cardiology, Council on
2009. Cardiovascular Surgery and Anesthesia, and the Quality of Care and
Odegard KC, DiNardo JA, Laussen PC: Anesthesia for congenital Outcomes Research Interdisciplinary Working Group. Circulation
heart disease. p. 588. In Gregory GA, Andropoulos DB (eds.): 116:1736, 2007.
Gregory’s Pediatric Anesthesia, 5th edition. Wiley-Blackwell, West
Sussex, 2012.
CASE 64
Preterm Infant
Scott D. Lipson, MD
QUESTIONS
1. How does prematurity affect survival, and how is 5. What intraoperative monitors and temperature-
it classified? regulating measures should be used for this
2. What unique developmental considerations must former preterm neonate?
be taken into account when caring for preterm or 6. What are the goals for oxygen administration
term neonates? intraoperatively?
3. What specific medical problems affect preterm 7. Is this patient a candidate for discharge to home
neonates? immediately after surgery?
4. What pharmacologic differences must be considered 8. Would a regional anesthetic allow for this patient
in preterm and term neonates? to be discharged home earlier?
A 20-week-old infant who was born at 25 weeks gestational 2. What unique developmental considerations must
age presented for right inguinal hernia repair before dis- be taken into account when caring for preterm or
charge home from the neonatal intensive care unit (NICU). term neonates?
Circulation
1. How does prematurity affect survival,
and how is it classified? After delivery, the neonatal circulation undergoes nu-
merous changes as it transitions from fetal circulation to
There are !500,000 preterm births in the United States adult-type circulation over the first days to weeks of life
each year, accounting for !1 in every 8 births. The rate of (Table 64-1). Pulmonary vascular resistance (PVR) de-
premature birth in the United States has increased !35% creases rapidly on the first day of life, and pulmonary
since the 1980s. This increase is due in large part blood flow increases. Pressure on the left side of the heart
to greater numbers of fertility treatments, resulting in increases with an increase in pulmonary venous return
increasing numbers of multiple births and an older maternal and systemic vascular resistance. These changes, along
population, both of which can lead to premature deliver- with higher oxygen levels, promote functional closure of
ies. Survival rate for preterm infants born at 23 weeks two in utero connections between the right and left sides
gestational age is 11%–33%; survival for infants born at of the circulation. Mechanical closure continues over
25 weeks gestational age is 55%–75%. Morbidity among weeks to months. During this transitional period, the
survivors of both of these groups is still around 50%. circulation can alternate between fetal and adult because
NICU care has also improved over this period, which shunts can reopen under certain conditions. Close atten-
means preterm infants are surviving longer. Because pre- tion must be paid to changes in hemodynamics during
term infants are at increased risk for numerous congenital anesthesia and surgical stress because they can induce
and acquired complications, many need anesthetic care circulatory changes that can trigger shunt reopening.
either in the operating room (OR) or in off-site locations. Numerous factors can increase the risk of prolonged
Newborns are classified by gestational age as follows: transitional circulation, including prematurity, elevated
PVR, acidosis, hypothermia, meconium aspiration, and
Full-term infant 38–42 weeks congenital heart disease (CHD).
Postterm infant !42 weeks
Preterm infant "37 weeks Cardiovascular
Micropremature infant "26 weeks (or weight
Myocardium in infants is stiff and poorly compliant sec-
"800 g)
ondary to poorly developed contractile cellular mass
Extremely low gestational 23–27 weeks compared with older children. Stroke volume is relatively
age newborn (ELGAN) fixed making the increased cardiac output predominately
rate dependent. Because the infant heart normally func-
Preterm infants weighing "1000 g are classified further tions at the top of the Frank-Starling curve, changes in
as extremely low birth weight. volume or afterload are poorly tolerated. Preoperative
334
64 Preterm Infant 335
GFR, Glomerular filtration rate; PVR, pulmonary vascular resistance; VA /FRC, alveolar ventilation-to-functional residual capacity ratio.
Pulmonary
fasting and other perioperative fluid deficits must be
accounted for. Lung development continues in utero much later than
The neonate has a poorly developed sympathetic other organs. The lungs cannot function on their own
nervous system, which is unable to compensate for ex utero until 34–36 week gestational age, when lung
periods of stress with changes in heart rate, preload, or volume, surface area for gas exchange, and surfactant pro-
afterload. Infants are considered “vagotonic” because duction to help keep small airways open all have developed
of the imbalance between the immature sympathetic adequately. Alveolar maturation continues postnatally,
and developed parasympathetic systems. Infants often increasing in size and number, for approximately 8 years.
respond initially with bradycardia when they become The relatively small number and size of neonatal alveoli lead
hypoxic or stimulated, such as during laryngoscopy. to reduced lung compliance and small airways prone to clo-
Neonatal sarcoplasmic reticulum has reduced calcium sure. In contrast, the cartilaginous neonatal rib cage makes
storage ability, making the heart susceptible to cardiac the chest wall highly compliant. As a result, the ribs provide
depression from changes in calcium levels or from the less support to maintain open alveoli. The work of breathing
depressant effects of anesthetic agents. is increased with the subsequent breath to reexpand these
336 SECTION 11 Pediatrics
closed airways. These factors cause a higher closing volume, is delayed in premature infants. GFR is approximately
with small airway closure during normal tidal volume. 40% of adult values in neonates and even lower in
Minute ventilation (or alveolar ventilation) is higher preterm infants, with GFR values proportional to gesta-
than in adults secondary to an increased respiratory rate tional age. This decreased GFR results in decreased cre-
because tidal volume on a per kilogram basis is the same atinine clearance; immature diluting and concentrating
as in adults. The alveolar ventilation-to-functional re- ability; and impaired sodium, glucose, and bicarbonate
sidual capacity ratio is higher because of the increased management in neonates. These problems are worse in
alveolar ventilation (5:1 vs. 1.5:1 in adults). Additionally, preterm infants. Decreased GFR impairs excretion of
oxygen consumption is increased twofold to threefold. saline, excessive water, and medications. Renal function
These factors, limited oxygen stores and increased oxy- approaches adult values around 2 years of age.
gen demand, lead to rapid oxyhemoglobin desaturation
during periods of apnea or airway obstruction. Liver
The diaphragm and intercostal muscles are composed
of two types of muscle fibers. Type I fibers are fatigue- The liver builds up its glycogen stores primarily in the
resistant, and type II fibers are fatigue-prone and less last trimester of fetal life; this means preterm infants
energy efficient. The neonate has a decreased amount of have missed much and ELGANs have missed nearly all
type I fibers, resulting in an increased work of breathing of their intrauterine glycogen storage time. Although
and early fatigue if airway obstruction occurs. Under term infants are susceptible to hypoglycemia, this is
general anesthesia, there is a further increase in chest especially a concern in preterm neonates. Glucose he-
wall compliance because of muscle relaxation. At end mostasis management is imperative in the perioperative
expiration, the lungs reach a lower volume. Conse- setting. Maintenance glucose requirement for preterm
quently, it takes more work to open airways during infants is 8–10 mg/kg per minute, whereas in full-term
the next breath. For this reason, tracheal intubation is neonates it is 5–8 mg/kg per minute.
indicated during general anesthesia. The liver is the primary site for drug metabolism, which
The respiratory drive to hypoxia or hypercarbia is not is slower in neonates, owing in part to relatively lower he-
yet developed. Both stimuli induce respiratory depres- patic blood flow. Decreased metabolism in this population
sion and breath holding. is secondary to deficiencies of many of the enzymes re-
quired for oxidation, reduction, hydrolysis, and conjuga-
tion of medications. Many enzymes still need to be exposed
Pediatric Airway
to toxins or drugs, which serve to stimulate and induce
The neonatal airway has numerous anatomic differences further development of these enzymatic pathways.
that must be accounted for. Infants have a proportionally
larger head and tongue with a shorter trachea and neck Gastrointestinal
than adults. The large tongue may make mask ventilation
difficult and necessitate use of an oral airway to relieve There is an increased incidence of gastroesophageal reflux
airway obstruction. The neonate’s upper airway is suscep- in infants until age 4–5 months, with the rate particularly
tible to closure, especially if the head is flexed when lying high in preterm infants, secondary to decreased lower
supine owing to the relatively large occiput. Use of a shoul- esophageal sphincter tone.
der roll may help open the airway and improve visualiza-
tion of the glottic region. The larynx is located more Thermoregulation
cephalad (C4 vs. adult level of C5) with an epiglottis that is
short, omega-shaped, and angled over the glottic opening. Heat loss to the environment is particularly high in the
The larynx in a preterm infant is even more cephalad, lo- neonatal period because of thin skin, poor fat stores,
cated at the C3 level. These differences make straight la- and a high surface-to-weight ratio. Fully developed
ryngoscope blades especially useful in the neonatal period. epidermis is present only after 32 weeks gestational age,
The narrowest portion of the airway is the cricoid cartilage, making preterm newborn skin a large source of heat and
necessitating performance of a leak test around a cuffed or water loss. Evaporative loss of water can be 5–6 mL/kg
uncuffed endotracheal tube, with an ideal leak "30 cm per hour. Cold is poorly tolerated because it increases
H2O but greater than peak airway pressures. The anterior oxygen consumption and leads to metabolic acidosis.
attachment of the vocal cords in infants is more caudad In contrast to adults, neonates are unable to preserve
than the posterior attachment, in contrast to the adult vocal or generate heat by peripheral vasoconstriction and
cords that are perpendicular to the tracheal axis. When shivering. Neonates produce heat by nonshivering ther-
placing the tracheal tube, it often becomes hung up at the mogenesis that occurs predominately in brown fat that
anterior commissure. This situation is particularly prob- is rich in mitochondria. Brown fat is located between
lematic when performing nasal intubations. When placing the scapulae, in the axillae and mediastinum, and around
the tracheal tube, every effort should be made to introduce the adrenal glands. Increased sympathetic output results
it through the posterior aspect of the vocal cords. in an increase in circulating norepinephrine and thyroid-
stimulating hormone that uncouples oxidative phos-
phorylation in brown fat, generating heat. Approxi-
Kidneys
mately 25% of the cardiac output is diverted to brown
Glomerular filtration rate (GFR) and tubular function fat resulting in direct warming of the blood. This pro-
reach maturation around 5 months of age, although this cess uses vital energy stores in neonates and takes a high
64 Preterm Infant 337
caloric toll. Circulating norepinephrine increases PVR. Preoperative understanding of the cardiac anatomy
Neonates left exposed to room air can lose 150 kcal per and physiology in infants with CHD is critical to man-
minute. Anesthetic agents negatively affect nonshiver- aging intraoperative hemodynamics. Equally impor-
ing thermogenesis. tant is awareness of the presence of right-to-left shunts
that allow entrained air to bypass the lungs and enter
the cerebral and coronary circulations. Debubbling
Hematologic Development
of intravenous tubing and careful injection of medica-
In utero, the predominant hemoglobin is fetal hemoglobin tions to avoid introducing air into the intravenous line
(HbF), which is characterized by high affinity for oxygen. are important measures to avoid this catastrophic
HbF is 50% saturated with oxygen (P50) at 19 mm Hg. event.
The P50 of adult hemoglobin (HbA) is 27 mm Hg. In
utero, HbF efficiently delivers oxygen to the relatively Lung Disease
hypoxic tissues. However, ex utero, when tissue oxygen
levels increase, HbF delivers oxygen less efficiently Infant respiratory distress syndrome (IRDS), formerly
than HbA. Transfusion thresholds are higher in infants known as hyaline membrane disease, occurs in preterm
who have predominantly HbF compared with infants infants secondary to immature surfactant production and
whose hemoglobin has converted to HbA. A preterm impaired structural support of lung tissue. IRDS is the
infant who received blood transfusions in the NICU number one cause of mortality in preterm newborns.
would have predominantly HbA depending on the total The incidence of IRDS is inversely related to gestational
amount transfused. Transfusion thresholds should be age, with about 50% of newborns of 26–28 weeks gesta-
considered based on the HbA profile. tional age affected compared with approximately 25% of
Normal hemoglobin values at birth are as follows: newborns of 30 weeks gestational age affected. IRDS
manifests shortly after birth as progressive respiratory
failure with tachypnea, increased work of breathing,
Full-term newborn 14–20 g/dL grunting, tachycardia, cyanosis, and hypercarbia. It is
Preterm newborn, 32–36 weeks 13–14 g/dL commonly treated with ventilatory support, progressing
gestational age as needed from continuous positive airway pressure
Preterm newborn, 28–32 weeks 12–13 g/dL to endotracheal intubation with exogenous surfactant
gestational age administration and to high-frequency oscillatory ventila-
tion and extracorporeal membrane oxygenation in extreme
circumstances.
Physiologic anemia occurs at 9–12 weeks in full-term Before 34–36 weeks of gestational age, many preterm
infants, with a nadir of 9–11 g/dL, and at 4–8 weeks in neonates often need some degree of respiratory sup-
preterm infants, with a nadir of 7–9 g/dL. After 12 weeks, port, whether or not they are classified with IRDS.
hemoglobin levels normalize around 12 g/dL for the first However, these life-sustaining measures often disrupt
2 years, although preterm infants may take 1 year to lung development and may lead to bronchopulmonary
reach this level. Oxygen delivery is not compromised dysplasia (BPD) and chronic lung disease. In mild cases,
during these hemoglobin level changes because during disruption of alveolar and vascular growth is seen. In
the transition from HbF to HbA, the oxygen-hemoglo- more extreme cases, inflammation and scarring of the
bin dissociation curve shifts to the right. Additionally, lungs with alveolar septal injury and interstitial fibrosis
2,3-diphosphoglycerate levels increase, which shifts the occurs. Intubation and supplemental oxygen may be
oxyhemoglobin curve to the right, allowing better off- needed; however, attempts to limit the use of both have
loading of oxygen to tissues. been shown to decrease the severity of BPD. Continu-
ous positive airway pressure may be used instead of in-
tubation, when appropriate. Anesthetic care of preterm
3. What specific medical problems affect preterm neonates usually necessitates intubation and mechanical
neonates? ventilation. Lung protective ventilation strategies used
in the NICU should be used during anesthetic care
Cardiovascular
when appropriate. These strategies include a target
Preterm neonates are more likely to have CHD, the peak inspiratory pressure of 14–18 cm H2O and tidal
combination of which increases morbidity in this sub- volumes of 4–6 mL/kg with slightly higher respiratory
set of infants. Preterm neonates are at particular risk rates than normal to achieve normal minute ventilation.
for patent ductus arteriosus (PDA), which occurs in Positive end expiratory pressure of 4–5 cm H2O should
!50% of ELGANs. The degree of shunting through also be used.
the PDA is a function of size, fluid status, and gradient Many preterm neonates are poor candidates for tra-
between the PVR and systemic vascular resistance. cheal extubation in the OR, especially if they are at risk
Significant left-to-right shunting puts these newborns for postoperative apnea. Leaving the tracheal tube in
at risk for congestive heart failure and pulmonary place should also be considered if the infant is going
edema. Subsequent systemic hypoperfusion increases directly from the OR to a distant NICU. Because of the
the risk of gastrointestinal ischemia causing necrotizing detrimental effects of prolonged mechanical ventilation
enterocolitis, intraventricular hemorrhage (IVH), and in these patients, the anesthetic should be tailored to
renal insufficiency. allow for early tracheal extubation when in the NICU.
338 SECTION 11 Pediatrics
infants should be admitted and monitored with the The duration of surgical anesthesia from spinal tech-
same guidelines as ex-preterm neonates who are niques is approximately 60 minutes in neonates because
"60 weeks PCA. of their larger cerebrospinal fluid volume per kilogram
The only parameter that consistently relates to post- and a more rapid cerebrospinal fluid turnover. The dura-
operative apnea episodes is hemoglobin "10 g/dL. A tion may vary slightly depending on the local anesthetic
preoperative hematocrit should be obtained if the deci- administered. Because of the relatively short duration,
sion to delay surgery would be based on hemoglobin spinal anesthesia should be considered only in cases in
level. Caffeine administered intravenously may decrease which the surgeon can complete the procedure in this
the incidence of postoperative apnea, but it does not time frame. To maximize the time the surgeon has to
preclude the need to admit infants at risk for apnea perform the procedure, the surgeon should be present at
monitoring. the time of block and immediately ready to operate.
Adenotonsillectomy
Francine S. Yudkowitz, MD, FAAP
QUESTIONS
1. What are the indications for adenotonsillectomy? 5. Describe the intraoperative management for
2. What is the pathophysiology of obstructive sleep adenotonsillectomy.
apnea, and how is it diagnosed? 6. What are the anticipated postoperative problems?
3. What should be included in the preoperative eval- 7. Which patients should be admitted postoperatively?
uation for adenotonsillectomy? 8. How is a patient with postadenotonsillectomy
4. Is premedication recommended for this child? bleeding managed?
A 3-year-old girl with obstructive sleep apnea presented and exacerbates upper airway obstruction. Patients with
for adenotonsillectomy (AT). She had a 3-day history of neuromuscular or craniofacial disorders are at increased
a runny nose and a productive cough. risk for OSA, especially if tonsillar hypertrophy coexists.
Airway obstruction results in hypoxia and hypercarbia
that trigger the brainstem arousal reflex causing in-
1. What are the indications for adenotonsillectomy?
creased pharyngeal tone. When pharyngeal dilator mus-
The most common indication for adenotonsillectomy cles contract, soft tissues are moved out of the airway
(AT) in pediatric patients is sleep-disordered breathing. lumen, and airway patency is improved. This series of
Obstructive sleep apnea (OSA) is an extreme form events occurs many times during sleep, disrupting the
of sleep-disordered breathing. Other indications include normal sleep cycle. Symptoms consist of snoring, breath-
recurrent pharyngitis, peritonsillar abscess, dysphagia, ing pauses, gasping, and use of accessory respiratory
asymmetric tonsillar hypertrophy, halitosis, and post- muscles. Enuresis and excessive sweating may also occur.
transplant lymphoproliferative disorder. Indications for If the sleep cycle is significantly disturbed, daytime som-
adenoidectomy without tonsillectomy are adenoidal nolence is present as well.
hypertrophy, chronic sinusitis, adenoiditis, and recurrent Chronic hypoxia and hypercarbia lead to pulmonary
otitis media. vasoconstriction and pulmonary hypertension. Right
atrial enlargement, right ventricular hypertrophy, and
2. What is the pathophysiology of obstructive sleep ultimately right-sided heart failure (cor pulmonale) de-
velop if OSA is not treated early (Figure 65-1). Polycy-
apnea, and how is it diagnosed?
themia may occur in response to chronic hypoxia.
Respiration involves chest wall expansion and dia- The “gold standard” for the diagnosis of OSA is poly-
phragm descension, both of which create negative intra- somnography. Polysomnography is an overnight sleep
pleural pressure. This negative pressure is distributed study during which electroencephalogram, electromyo-
throughout the lower and upper airway. Negative pres- gram, electrocardiogram (ECG), pulse oximetry, airflow,
sure in the pharynx tends to draw soft tissues inward, and thoracic and abdominal movements are monitored.
predisposing to upper airway obstruction. During sleep, The number of obstructed breaths, percentage of de-
airway patency is maintained despite a decrease in pha- creased airflow, and degree of oxygen desaturation are
ryngeal muscle tone. This situation may be altered in used to determine whether obstructive apnea or hypop-
the presence of neuromuscular hypotonia or craniofa- nea is present. Obstructive apnea is defined as !90%
cial abnormalities or when alcohol or sedatives are decrease in airflow despite respiratory effort. Obstructive
taken (Box 65-1). Tonsillar hypertrophy exacerbates up- hypopnea is defined as !50% decrease in airflow despite
per airway obstruction in two ways. First, it encroaches respiratory effort and a !3% decrease in oxygen satura-
on the airway, narrowing its cross-sectional area. Sec- tion. The apnea-hypopnea index determines the severity
ond, when the cross-sectional area is reduced suffi- of OSA. Severe OSA is defined as an apnea-hypopnea
ciently, airflow through the stenosed pharynx increases, index score !10 and oxygen desaturation nadir "80%.
which produces reduced pressure inside the pharynx by In the absence of a polysomnography study, the parent’s
the Bernoulli effect. The additional decrease in pharyn- description of the symptoms or home sleep video is used
geal pressure draws soft tissues farther into the airway to determine the need for AT.
341
342 SECTION 11 Pediatrics
Pulmonary hypertension
7. Which patients should be admitted type and cross, platelet count, and coagulation studies.
postoperatively? Emergent surgery cannot be delayed waiting for the
results because the bleeding will not stop until surgical
Patients at increased risk for postoperative respiratory control is obtained.
complications are frequently admitted overnight for ap- In the operating room, the following items should be
nea monitoring, including the following: prepared:
• "3 years old • Multiple laryngoscope blades
• Craniofacial abnormalities • Styletted endotracheal tubes
• Neuromuscular abnormalities • Two large-bore suctions
Depending on your institution, apnea monitoring may • Alternative airway devices
require admission to an intensive care unit. Patients who • Tracheostomy equipment
do not meet PACU discharge criteria must be admitted Induction of general anesthesia should not proceed
as well; these include the following: without an attending surgeon present and ready to per-
• Continued need for supplemental oxygen form a surgical airway, if necessary. Full stomach precau-
• Poor oral intake tions are taken with these patients (i.e., rapid sequence
• Continued vomiting induction with cricoid pressure). An awake fiberoptic
• Exhibit airway obstruction in the PACU intubation for an identified difficult airway may be im-
possible in an agitated child or if there is blood in the
8. How is a patient with postadenotonsillectomy airway. A mask inhalation induction may be performed if
bleeding managed? there is concern about the airway. The patient is placed
in the right lateral decubitus position with the head
Bleeding after AT occurs either in the first 24 hours or, down. This position may decrease the risk of aspiration
more commonly, 5–10 days postoperatively when the because blood pools in the oral pharynx.
eschar falls off. The preoperative evaluation of these The choice of induction agent depends on the he-
patients should be directed at assessment of the airway modynamic stability and volume status of the patient.
and volume status (Box 65-3). A complete assessment Administering a 20-mL/kg bolus of isotonic fluid be-
of the airway may be impossible in an agitated child, fore induction may prevent hypotension. Etomidate or
but visual inspection of the external airway and details ketamine in reduced doses may be administered if vol-
of airway management during the previous AT are ume status is still a concern. Alternatively, propofol
helpful. may be used in a decreased dose. Either succinylcholine
Assessment of the volume status and fluid resuscita- or rocuronium may be administered. However, if the
tion must be performed expeditiously. The amount of procedure is short, the duration of action of rocuronium
blood loss may not be evident because much of the exceeds the surgical time. Succinylcholine, with its
blood may have been swallowed. Heart rate and blood short duration of action, may be preferable if a difficult
pressure help guide fluid management. If intravenous airway is anticipated.
access cannot be accomplished rapidly, intraosseous ac- Hemoglobin and hematocrit levels should guide
cess should be obtained. If shock is present, a bolus of blood transfusions. Coagulation factors are replaced if
non–glucose-containing isotonic fluid (20 mL/kg) is a coagulopathy is detected by laboratory testing or is
administered over 5–10 minutes and repeated as needed suspected.
if hypotension persists. Blood is drawn for hemoglobin,
SUGGESTED READINGS
Cardwell M, Siviter G, Smith A: Non-steroidal anti-inflammatory drugs
and perioperative bleeding in paediatric tonsillectomy. Cochrane Data-
base Syst Rev (18):CD003591, 2005.
BOX 65-3 Preoperative Evaluation for Guffin TN, Har-el G, Sanders A, et al.: Acute postobstructive pulmo-
Postadenotonsillectomy Bleeding nary edema. Otolaryngol Head Neck Surg 112:235, 1995.
Schwengel DA, Sterni LM, Tunkel DE, et al.: Perioperative manage-
• Airway assessment ment of children with obstructive sleep apnea. Anesth Analg 109:60,
2009.
• Anatomy—visual inspection
Tait AR, Melviya S: Anesthesia for the child with an upper respiratory
• Previous anesthetic tract infection: still a dilemma. Anesth Analg 100:59, 2005.
• Volume status Williams PJ, Bailey PM: Comparison of the reinforced laryngeal mask
• Heart rate and blood pressure airway and tracheal intubation for adenotonsillectomy. Can J Anaesth
• Intravenous or intraosseous access 40:1171, 1993.
• Non–glucose-containing isotonic fluid Wilson MN, Long LS, Ved S, et al.: Younger paediatric adenotonsillar
• Blood transfusion (based on hemoglobin and hematocrit) surgical patients exhibit more complications at mouth gag insertion
with LMA use. Int J Pediatr Otorhinolaryngol 73:1173, 2009.
CASE 66
QUESTIONS
1. What is foreign body aspiration, and how does 4. How is a patient with foreign body aspiration
it occur? managed intraoperatively?
2. How does a patient with foreign body aspiration 5. What are the postoperative concerns in a patient
typically present? who has aspirated a foreign body?
3. What are the preoperative concerns in a patient
with foreign body aspiration?
An 18-month-old boy was brought to the pediatric emer- infants or abdominal thrusts in children. More often,
gency department by his parents. Two hours previously, airway obstruction is incomplete, and these patients typi-
he had gagged and choked while eating dinner. Since cally present to the emergency department.
then, he has been agitated and coughing intermittently. On physical examination, the child may appear agi-
tated. Agitation could be due to hypoxemia. Tachypnea
1. What is foreign body aspiration, and how does it and tachycardia are often present. Coughing, unilateral
decreased breath sounds, and wheezing are the classic
occur?
signs. There should be a high suspicion for foreign body
Foreign body aspiration, the lodging of a substance in the aspiration in any child in this age range who presents
trachea or bronchus, is a very serious condition and can be to the emergency department with new-onset wheezing,
a life-threatening emergency because there is a potential especially if unilateral. If the child shows significant respi-
for complete airway obstruction. Foreign body aspiration ratory compromise, rapid transport to the operating room
occurs most commonly in children 1–3 years old because is indicated. In stable children with a questionable diagno-
they often put foreign substances in their mouths, lack sis, chest x-rays may be helpful. Although most foreign
molars to chew their food adequately, and often run or bodies are not radiopaque, indirect findings such as hyper-
play with objects in their mouths. Peanuts, seeds, and inflation of the obstructed lung secondary to air trapping
other food particles are the most common foreign bodies or atelectasis secondary to decreased ventilation may be
aspirated (Figure 66-1). Less frequently, other objects suggestive of the diagnosis. Hyperinflation is best visual-
such as plastic game pieces and small batteries are aspi- ized in an expiratory film but may be difficult to obtain in
rated. In addition, certain aspirated objects may cause younger age groups.
intense irritation and edema (e.g., peanuts from the oil The presentation of a patient with foreign body inges-
component) or corrosion and necrosis (e.g., batteries) to tion is slightly different. Coughing and choking can occur
the airway mucosa. initially because of laryngeal irritation, followed by refusal
Foreign bodies can also be ingested into the hypo- to feed, increased salivation, discomfort with swallowing,
pharynx, esophagus, and stomach. Although often not as and vomiting. In contrast to airway foreign bodies, these
urgent or life-threatening, these cases can still present a foreign bodies are often radiopaque, and a chest x-ray is
significant challenge. These children are typically older frequently helpful to confirm the diagnosis, revealing type
(1–6 years old), and the foreign bodies are usually coins, and location. These cases are typically not as urgent, with
bones, or plastic game pieces. the exception of ingestion of potentially toxic objects,
such as batteries, or potentially traumatic objects, such as
2. How does a patient with foreign body aspiration open safety pins (Figure 66-2).
typically present?
3. What are the preoperative concerns in a patient
There is often a history of choking, gagging, coughing, with foreign body aspiration?
or wheezing occurring when the child is eating or when
playing with small objects. A period of cyanosis may be Patients should be thoroughly evaluated before coming to
noted by the parents. A foreign body large enough to the operating room, especially noting their preoperative
obstruct the trachea completely requires immediate respiratory status and oxygen saturation. The type of for-
treatment with back blows and chest compressions in eign body aspirated (i.e., food particle or inanimate object),
345
346 SECTION 11 Pediatrics
the foreign body into the trachea. The result could be BOX 66-1 Intraoperative Concerns
complete airway obstruction or relocation into the con-
tralateral, unaffected main stem bronchus. Organic food FOREIGN BODY ASPIRATION
particles (especially peanuts) often fragment when grasped • Spontaneous or controlled ventilation, at discretion of
with the forceps, and multiple passes must be performed anesthesiologist and surgeon
to remove it completely. After the foreign body is re- • Sharing of airway with surgeon without endotracheal
moved, the surgeon takes another look to evacuate any tube in place
viscous secretions and to assess whether any residual com- • Corticosteroids to reduce airway edema
ponents remain and the degree of resultant edema. This • Avoid nitrous oxide
inspection helps guide postoperative management. If • Deep inhalation anesthesia or TIVA, especially during
significant airway edema is present, a decision may be foreign body removal
• Potential for complete airway obstruction
made to keep the patient’s trachea intubated and admit the • Potential for airway compromise even after foreign
patient to the intensive care unit (ICU) postoperatively. body removed
Foreign body ingestion in the gastrointestinal tract is
removed via esophagogastroduodenoscopy with a flexible FOREIGN BODY INGESTION
fiberoptic endoscope, usually performed by a gastroenter- • Aspiration risk
ologist. The concern with an ingested foreign body is • Cautious cricoid pressure, if necessary
obstruction, trauma, or perforation of the gastrointestinal • Intubation to protect airway
tract. General inhalation anesthesia or TIVA with endo- • Risk of trauma to gastrointestinal tract
tracheal intubation is required because there is a risk of
complete airway obstruction if the foreign body is lost
into the trachea or hypopharynx during removal. If the
patient has recently eaten, the procedure should be delayed may be beneficial. If airway trauma and edema are severe,
for an appropriate amount of time. If the child is dyspneic the patient can remain intubated and sent to an ICU.
and the procedure cannot be delayed, a rapid-sequence Complications after foreign body aspiration are rare,
induction should be performed to decrease the risk of but they do occur. Complications include laryngeal,
pulmonary aspiration. Cricoid pressure should be used tracheal, or bronchial trauma; pneumothorax; and pneu-
cautiously, if at all, for foreign bodies in the hypopharynx monia. Failure to remove the foreign body by bronchos-
because it may irritate the upper airway, dislodge the copy occurs in a small percentage of cases, necessitating
foreign body into the trachea, or cause trauma to the either repeat rigid bronchoscopy or rarely mediastinos-
esophagus. Complications resulting from the removal of copy or thoracotomy.
an ingested foreign body include trauma or perforation
of the gastrointestinal tract (Box 66-1).
QUESTIONS
A 4-year-old boy with an intracranial mass presented for convert ferromagnetic objects into missiles that can lead
magnetic resonance imaging (MRI) of the brain. Past to injury or lethal outcomes to patients or personnel.
medical history was significant for Down syndrome Care must be taken to avoid the use of or to have in one’s
(trisomy 21) and seizure disorder. Surgical history included possession objects such as pens, scissors, clamps, stetho-
tonsillectomy and adenoidectomy under general anesthesia scopes, nonlithium batteries, ferromagnetic compressed
at age 2 years without complications. gas cylinders, and other objects that are ferromagnetic.
Before bringing any piece of equipment into the MRI
1. What is magnetic resonance imaging? suite, it should be checked to ensure that it is MRI-
compatible.
MRI incorporates the use of static and gradient magnetic Patients with implanted ferromagnetic devices or ob-
fields with radiofrequency (RF) pulses to produce im- jects, which include pacemakers, tissue expanders with
ages of the body. Magnetic field strengths range from metallic ports, implantable cardioverter defibrillators,
0.15–3.0 tesla (T). The tesla is a measure of magnetic implantable infusion pumps, cochlear implants, and cer-
field strength (1 T ! 10,000 gauss). Image quality depends tain types of intracranial aneurysm clips, are generally
on the strength of the magnetic field. excluded from MRI studies. The magnetic fields of MRI
Hydrogen is the element most commonly used in MRI scanners can potentially affect the function and safety of
because it is the most abundant element in human tissue these devices. Newer aneurysm clips contain nonferrous
and it can be magnetized. Atoms, such as hydrogen, with material and are not considered to be problematic. How-
an unpaired number of protons or neutrons respond to ever, a thorough investigation of the type of aneurysm
and align themselves within the magnetic field of the MRI clip is required before proceeding with an MRI study.
scanner. Metallic-based substances such as eye makeup or tattoos
After placement of the patient within the cylindrical can produce local skin irritation during MRI scanning
bore of the magnet, a steady state is established in which (Box 67-1). Metals that are known to be safe include
hydrogen atoms are in alignment. RF pulses are intro- stainless steel, titanium, alloys, and nickel. Plastic equip-
duced and deflect the orientation of the atoms. When the ment is preferred for use in proximity to MRI magnets.
RF pulses are eliminated, the hydrogen atoms return to
their original position of alignment. As these atoms estab- 3. What are the specific problems encountered
lish a resting state, the energy emitted is used to produce a with physiologic monitors and equipment
resulting image.
in the magnetic resonance imaging suite?
2. What are the magnetic field problems associated The use of conventional electrocardiogram (ECG) mon-
with the magnetic resonance imaging? itors in the MRI suite can distort the image because wire
leads act as antennas. Additionally, ECG monitors may
MRI magnets exert a substantial pull on ferromagnetic be unable to distinguish myocardial electrical potentials
objects. The major concern is that the magnet could from background static magnetic field and RF pulses.
348
67 MRI and the Down Syndrome Child 349
6. Describe the preanesthetic evaluation of children positions. The atlas-dens interval is often used to quantify
with Down syndrome. movement of the atlantoaxial joint. The atlas-dens interval
is measured from the posterior margin of the anterior arch
The preanesthetic evaluation of children with Down of the first cervical spine to the anterior margin of the
syndrome should include a complete history and physical dens. The normal atlas-dens interval for children is
examination. The anesthetic assessment focuses particu- #4.5 mm.
larly on the organ systems most commonly involved The current recommendation is that screening for
in Down syndrome. A detailed systematic approach is atlantoaxial instability should be performed at 3–5 years
necessary to prepare for potential intraoperative events. of age. Follow-up cervical radiographs at 3-year intervals
Further evaluation of these patients depends on the extent are no longer recommended. Obtaining a good history
of organ system involvement. and neurologic assessment are key factors. When a child
Atlantoaxial instability is present in 10–20% of children with Down syndrome presents for general anesthesia, all
with Down syndrome and is a major source of concern in precautions must be taken to maintain the cervical spine
the perianesthetic period. Several neurologic deficits may in neutral position.
be associated with atlantoaxial instability (Box 67-3).
Screening for atlantoaxial instability includes lateral cervical 7. What anesthetic alternatives are available
spine radiographs in the flexed, extended, and neutral for children with Down syndrome undergoing
magnetic resonance imaging?
BOX 67-3 Neurologic Deficits Associated Premedication for a child with Down syndrome may be
with Atlantoaxial Instability necessary to facilitate induction of anesthesia. Oral or
intranasal midazolam may be considered for premedica-
• Gait abnormalities
tion. Intramuscular ketamine has also been used success-
• Neck pain
• Torticollis fully. However, ketamine is relatively contraindicated for
• Mild extremity weakness the patient in this case because of his seizure disorder.
• Hyperreflexia Parental presence during induction of anesthesia is quite
• Spasticity helpful. However, parental presence should not be viewed
as a substitute for premedication.
67 MRI and the Down Syndrome Child 351
If the airway examination appears normal, either an children after discharge from the facility. In addition,
inhalation or intravenous induction can be performed. instructions must be given to parents to contact the facil-
An endotracheal tube and laryngeal mask airway used ity immediately if they observe any untoward reaction in
with general anesthesia are good options. Sedation with their children.
a propofol or dexmedetomidine infusion may also be
considered. The choice of anesthetic technique for
a child with Down syndrome involves similar decision
making as with any patient. SUGGESTED READINGS
Gooden C, Dilos B: Anesthesia for magnetic resonance imaging. Int
Anesthesiol Clin 41:29, 2003.
8. What are the postanesthetic concerns for children Mason K, Lerman J: Dexmedetomidine in children: current knowledge
with Down syndrome after magnetic resonance and future applications. Anesth Analg 113:1129, 2011.
imaging? Menon D, Peden C, Hall A, et al.: Magnetic resonance for the anaesthetist.
Part I. Physical principles, applications and safety aspects. Anaesthesia
Postanesthetic concerns after MRI are the same as after an 47:240, 1992.
Mitchell V, Howard R, Facer E: Down’s syndrome and anesthesia. Pediatr
anesthetic in the operating room. The child with Down Anesth 5:379, 1995.
syndrome should be observed in either a postanesthesia Patteson S, Chesney J: Anesthetic management for magnetic resonance
care unit or a recovery area at the MRI location equipped imaging: problems and solutions. Anesth Analg 74:121, 1992.
with appropriate monitors and nursing personnel. The Peden C, Menon D, Hall A, et al.: Magnetic resonance for the anaesthetist.
child can be discharged as soon as criteria defined by the Part II. Anaesthesia and monitoring in MR units. Anaesthesia 47:508,
1992.
facility have been met. Because many MRI examinations Williams J, Somerville G, Miner M, et al.: Atlanto-axial subluxation
are performed on an outpatient basis, parents should be and trisomy 21: another perioperative complication. Anesthesiology
informed about what to expect and observe in their 67:253, 1987.
S ECTI O N 12
PAIN
352
CASE 68
QUESTIONS
A 28-year-old woman with osteosarcoma presented for recommend a baseline electrocardiogram for all patients
excision of a mediastinal mass under general anesthesia. started on methadone treatment and ongoing cardiac
She underwent left hemipelvectomy approximately 2 years evaluation, especially for patients with multiple comor-
ago. There was no other significant medical history. Her bidities or who are treated with drug classes known to
symptoms consisted of allodynia over her left lower ex- prolong Q–T intervals. Numerous case reports exist of
tremity with radicular symptoms in an S1 distribution life-threatening arrhythmias associated with the use of
and somatic pain in the left pelvis and hip area. Her current methadone.
medications included methadone, 10 mg orally every Breakthrough cancer pain can be treated with any
4 hours, and hydromorphone, 8 mg every 2–3 hours for short-acting opioid such as hydromorphone or oxyco-
breakthrough pain. Additionally, she stated she “needed” to done depending on the individual genetic profile of
take hydromorphone and oxycodone, which she obtained opioid receptors and CYP450 metabolism. One of the
from her sister, who had back pain. biggest challenges in treating cancer breakthrough pain
is the ability to ensure fast and effective analgesia. Most
1. Is this an appropriate analgesic regimen before opioids, such as morphine and hydromorphone, achieve
surgery? an onset of action within 15–20 minutes when adminis-
tered orally. Almost complete plasma metabolism occurs
Using long-acting and short-acting opioids for break- within 3 hours. In cases where a more rapid onset of
through cancer pain has been the mainstay of therapy for analgesia is sought, administration of faster lipophilic
chronic malignant pain for !4 decades. This concept agents, such as fentanyl via the buccal or transmucosal
began with the World Health Organization “analgesic route, should be considered.
ladder” for treating moderate-to-severe pain associated
with malignancies. Methadone pharmacokinetics allows 2. What is the difference between tolerance,
for two or three times daily dosing to provide analgesia; physical dependence, addiction, and
however, its metabolic half-life is 72–96 hours with a
pseudoaddiction?
bioavailability of almost 98%, and this has to be taken
into account when dosing methadone more than three or Tolerance is a clinical and biomolecular phenomenon
four times daily. Dosing methadone every 4 hours, as in characterized by diminished clinical effect after repeated
this patient, not only predisposes to toxic effects such as exposure to a medication. Rapid escalation of doses
respiratory depression but also has the potential for rapid could represent an indication of drug-aberrant behavior.
development of tolerance and hyperalgesia. More recent Tolerance to analgesic effects of specific doses can occur
guidelines published in the Annals of Internal Medicine later in treatment, but tolerance to side effects of opioids
353
354 SECTION 12 Pain
occurs much sooner (e.g., nausea, vomiting, sedation, con- preemptive analgesia by NSAIDs and cyclooxygenase-2
stipation). Cross-tolerance refers to tolerance resulting inhibitors. Inhibition of presynaptic glutamate secretion in
from use of another opioid with similar pharmacologic the substantia gelatinosa via inhibition of Ca""-gated
action. Use of long-term opioids can also induce a central channels was the proposed mechanism of gabapentinoids.
sensitization syndrome characterized by hyperalgesia. This patient would benefit from a single dose of gaba-
Physical dependence can occur after long-term analge- pentin (600–1200 mg) given before incision and oral or
sia with opioids. Abrupt cessation produces a withdrawal intravenous (650–1000 mg) acetaminophen. Ketorolac or
syndrome characterized by hypertension, tachycardia, celecoxib used before surgical procedures with antici-
insomnia, dysphoria, hallucinations, and a subjective pated high blood volume loss poses certain challenges,
“craving for drug.” such as increased intraoperative blood loss and acute
In contrast, addiction is a psychobiologic syndrome kidney injury. They should be used as a last alternative
associated with impaired control over substances (i.e., after discussion with the surgeon.
compulsive use despite harm or craving). Addiction appears
to be influenced by genetic, social, and environmental 4. What are the clinical implications of inadequate
factors and is sometimes difficult to distinguish from postoperative analgesia?
other forms of abuse, such as self-medication to alleviate
stress, to alleviate depression, or to facilitate sleep. Inadequate postoperative analgesia can predispose patients
A common entity, which is present in this clinical sce- to various complications, some with potentially ominous
nario, is pseudoaddiction, the “need” to increase the consequences (Table 68-1). Pain increases secretion of
doses of opioids for adequate analgesia without any par- adrenergic mediators (e.g., epinephrine, norepinephrine)
ticular linkage to a clear addictive behavior. However, an from the medullo-suprarenal gland and presynaptic
addictive personality trait cannot be excluded. sympathetic afferents. Adrenergic responses cause intense
vasoconstriction and sustained tachycardia, which can
3. What is preemptive analgesia; could it be result in increased myocardial oxygen consumption; this
may lead to cardiac dysrhythmias, coronary vasoconstric-
considered for this patient?
tion, and poor peripheral and central perfusion. Libera-
The concept of preemptive analgesia was developed, al- tion of catecholamines produces enhanced cortisol levels
though never entirely proved, approximately 20 years followed by a decreased inflammatory response through
ago. Administration of certain medications that reduce elevated cytokine and prostaglandin levels. Additionally,
peripheral or central nociception was associated with there is an increase in basal glucose levels with decreased
markedly reduced use of postoperative opioids. These pancreatic insulin secretion that ultimately leads to poor
medications included gabapentinoids (e.g., gabapentin, wound healing. Stress associated with inadequately
pregabalin), cyclooxygenase-2 inhibitors (e.g., celecoxib, treated acute pain can produce hypercoagulability and
rofecoxib), and nonsteroidal antiinflammatory drugs impaired activity of both innate and adaptive immunity.
(NSAIDs) (e.g., ibuprofen, ketorolac). Consequences of these complications may include venous
Inhibition of prostaglandins and inflammatory cyto- thromboembolic disease and increased risk of postopera-
kines in the periphery was the proposed mechanism of tive infections. Unmanaged, acute postoperative pain can
delay mobilization, which can also increase the risk of but is intimately associated with chronic persistent post-
venous thromboembolic disease, produce joint stiffness, operative pain syndrome.
delay rehabilitation, and prolong hospitalization. Although mechanisms are complex, they involve
Decreased inspiratory efforts secondary to “splinting” N-methyl-d-aspartate (NMDA) receptors that regulate
of the intercostal and abdominal muscles leads to a the amount of mediators secreted and open channels in
decrease in tidal volume and inspiratory reserve capacity. postsynaptic membranes. This particular receptor is be-
Pulmonary vasoconstriction results in an increase in the lieved to be mainly responsible for the “central sensitization”
total pulmonary dead space. The end result is atelectasis mechanism, and it could explain why serially maintained
and increased bronchial secretions predisposing these impulses from the periphery keep the postsynaptic chan-
patients to tracheobronchial and pulmonary infections. nels open for long periods. This theory is consistent with
Decreased motility of the gastrointestinal tract leads the observation that NMDA antagonists, such as metha-
to increased transit time (ileus), and the adrenergic re- done and ketamine, reduce postoperative pain, especially
sponse may lead to mucosal ischemia. Urinary retention in patients who have tolerance of or are dependent on high
and sphincter constriction results in inability to void, doses of preoperative opioids.
which promotes urinary tract infections.
Aside from negative impacts on various organ systems, 6. Which agents could be used intraoperatively to
inadequate postoperative pain control increases stress diminish postoperative opioid use?
and anxiety levels in patients and families. The increased
stress and anxiety levels result in overall negative experi- In a patient who has tolerance to or is addicted to opioids,
ences, which are reflected in poorer outcomes and lower a multimodal analgesic approach can be accomplished
pain satisfaction scores. with various agents. Analgesia can begin preoperatively
or intraoperatively. Agents used include primarily anti-
5. How is pain classified, and what is central inflammatory and NMDA antagonists. Intravenous ac-
etaminophen, in doses of 650–1000 mg, has been shown
sensitization?
to decrease opioid use during major orthopedic surgery.
Nociception is a complex process. It involves multiple Although there are no reports showing that intravenous
mechanisms of transduction and translation of chemical acetaminophen poses a risk to increasing liver trans-
reactions that occur in the periphery after injury. From aminases, caution should be exercised in patients with
there, impulses are transmitted through various channels previous liver injury or transplantation. Ketorolac, a
via specific fibers and ultimately integrated at central direct prostaglandin inhibitor, has been studied in thora-
levels (thalamus and cortex). After injury, various media- coabdominal surgery. Ketorolac, in therapeutic doses of
tors, such as prostaglandins, cytokines, and interleukins, 30 mg, is the analgesic equivalent of 10 mg of morphine
are liberated from activated mast cells and platelets. This administered intravenously. However, this dose can re-
group of substances, commonly known as “inflammatory sult in inhibition of platelet aggregation and potentially
soup,” generates chemical transmissions via neuronal acute tubular necrosis leading to renal failure. Most tho-
sodium influx in dorsal root ganglia afferent fibers, com- racic surgeons do not use it until 24 hours after incision.
prising mostly A-delta and C fibers. It has never been proved that reducing the ketorolac
Pain is classified as either somatic, the most common dose to 15 mg reduces the risk for these complications.
cause of acute postoperative pain syndromes, or visceral, Doses exceeding 45 mg or 60 mg do not offer better
depending on its source (Table 68-2). Both types of pain analgesic outcomes compared with other major opioids.
can be subdivided further into either neuropathic, often Ketamine and methadone, both NMDA receptor an-
described as “shooting” (e.g., intercostal neuritis after tagonists, have been extensively studied for the treatment
thoracotomy), or nonneuropathic, which is sympathetic- of chronic malignant and nonmalignant pain, including
mediated or non–sympathetic-mediated. Sympathetic- sympathetically mediated pain syndromes. Although be-
mediated pain can be discerned easily among other syn- lieved to be useful for addicted individuals, methadone
dromes by the presence of allodynia (i.e., pain secondary has emerged more recently as a long-acting opioid used
to nonnoxious stimuli), hyperesthesia (i.e., increased for intraoperative analgesia in doses of 5 mg or 10 mg
sensitivity to nonnoxious stimuli), and hyperalgesia (i.e., administered intravenously. Owing to its unique pharma-
increased pain secondary to noxious stimuli). This type of cokinetics, with a bioavailability of !95%, methadone
pain does not follow a dermatomal pattern of transmission achieves an analgesic level comparable with 10 mg of
morphine within the first 60 minutes. Its NMDA activity local anesthetics is reduced preload, which predisposes to
coupled with long-standing mu receptor agonism sec- hypotension. This side effect is generally corrected by ad-
ondary to its beta-elimination half-life probably creates ministration of fluids or vasoconstrictive agents or both.
diminished glutamate excitatory activity in the dorsal Additionally, for certain patient groups, clonidine, a direct
horn that is responsible for less opioid use. Methadone #2-adrenergic receptor agonist, can be added to the
can easily be continued throughout the postoperative epidural infusion in doses of 0.5–1 $g/mL. Addition of
period in total doses of 5 mg or 10 mg daily, divided clonidine decreases the amount of postoperative opioids
into two doses (e.g., 2.5 mg or 5 mg twice a day). Because required but increases sedation and vasodilation. The ad-
of its “unpredictable” half-life, methadone is rarely pre- vantages of neuraxial techniques are listed in Box 68-1.
scribed more often than two or three times daily. Although parenteral analgesia remains a feasible mode
Ketamine, mainly used as an anesthetic induction of treatment, opioid doses for tolerant patients would be
agent, has been popular among anesthesiologists for a much higher with a very narrow therapeutic window; this
long time. Several more recent studies employed ket- creates a situation where adverse effects, such as decreased
amine as an induction agent, maintenance agent, or both sensorium and respiratory depression, are more likely to
for both spine and thoracoabdominal surgery. Ketamine, occur. Patients with opioid tolerance or pseudoaddiction
when infused during surgery in doses of 0.3–0.5 mg/kg who receive only parenteral opioids very often require
per hour and continued throughout the first 24–48 hours benzodiazepines to decrease their anxiety levels and mus-
postoperatively, was clearly associated with less opioid cle relaxants to counteract “tense” thoracic and abdominal
use. However, these patients need to be monitored post- walls that can exacerbate postoperative pain. These agents
operatively in an intermediate monitored care unit for have the propensity to increase and “tip over” the overall
side effects such as tachycardia, hypertension, dysphoria, respiratory depressant effects of parenteral opioids.
and hallucinations. Ketamine may be contraindicated for Despite the many advantages of neuraxial analgesia,
patients with cardiovascular disease because of tachycardia there are also associated risks, such as hematoma and
and hypertension. Dysphoria and hallucinations can be infection. In some published studies, the incidence of
prevented by administration of benzodiazepines (e.g., neuraxial hematoma in the epidural space was reported
diazepam or lorazepam) in divided doses. as 1:150,000 compared with 1:220,000 in the intrathecal
space. Guidelines for the performance of neuraxial tech-
7. What are the advantages of neuraxial versus niques in patients receiving anticoagulation must be
strictly followed (see Chapter 51 for full details). Finally,
parenteral opioid analgesia for this patient?
placing these catheters in various anatomic locations
Some studies show that analgesia achieved by neuraxial require specialized expertise.
opioids is not superior to analgesia produced by parenteral
opioids in the postoperative period. However, most studies 8. What is patient-controlled analgesia?
show that neuraxial opioids (Table 68-3) decrease the total
amount of opioids administered, resulting in decreased Patient-controlled analgesia (PCA) involves administra-
pain scores, respiratory depression, nausea, pruritus, and tion of opioids via a pump that the patient controls.
constipation. For example, the dose of morphine used in A continuous basal rate may or may not be set in addition
the epidural and intrathecal space is approximately one to a bolus, of which the dose and timing frequency
tenth to one hundredth of the dose administered via the (usually 6–10 minutes) are determined by clinicians.
parenteral route. Another advantage of the neuraxial route
is the ability to administer intermediate-acting or long-
acting local anesthetics (e.g., bupivacaine or ropivacaine)
in addition to opioids. Inclusion of local anesthetics has BOX 68-1 Advantages of Neuraxial Analgesia
been shown to enhance the analgesia achieved and decrease
the use of opioids via both the neuraxial route and the • Efficacious levels of analgesia
parenteral route. One of the main side effects of neuraxial • Decreased “splinting” improving overall respiratory effort
• Decreased incidence of atelectasis and infection
• Vasodilation by local anesthetics
• Afterload reduction
TABLE 68-3 Advantages of Neuraxial versus • Decreased myocardial workload decreasing risk for
Parenteral Opioids adverse cardiac events
• Increased unopposed vagal output to gastrointestinal
Neuraxial Parenteral
muscular layer
• Promotes gastric emptying time
Less total opioid No special techniques • Increased intestinal transit
consumption needed • Intestinal mucosa vasodilation
Use of local anesthetics Easy titration • Decreased opioid use
and clonidine with Lack of neuraxial hematoma • Bladder emptying time decreases
opioid-sparing effect and infections
• Promotes proper micturition
Decreases infection rates No effects on anastomoses
Decreases opioid-induced (vagal output) • Decreased bladder urinary retention
side effects Cost-effective • Decreased urinary tract infections
Improved satisfaction Similar satisfaction scores (?) • Enhancement of fibrinolytic-to-coagulation ratio
rates (?) • Decreased incidence of thromboembolic events
68 Acute Postoperative Pain 357
Patients control analgesia by pressing a button that deliv- solubility, cross the dura mater much faster than less
ers a preset dose. The risk of overdosing is limited lipid-soluble opioids, such as morphine or hydromor-
by predetermined dose and timing frequency. Before phone. Because of their higher lipid solubility, a greater
initiating PCA, it is advisable to attain a plasma concen- proportion of fentanyl and sufentanil transfers into epi-
tration commensurate with the desired analgesic level. dural vessels. Studies have shown that the higher the
The most commonly used opioids and suggested dosing gradient of fentanyl across the dural layer, the quicker the
schedules employed in clinical practice for postoperative onset, and less opioid can achieve initial high plasma
pain are listed in Table 68-4. The choice of opioid is concentrations.
determined by pharmacokinetics (e.g., lipophilic profile), In contrast to highly lipid-soluble molecules, the less
side effects, practitioner’s familiarity, availability, and cost. soluble ones, such as morphine or hydromorphone, have
For example, owing to its histamine release, morphine the tendency to “linger” in the epidural space before
might not be the first choice in patients with obstructive crossing the dura mater. This “lingering” accounts for
lung disease (e.g., asthma, emphysema). Hydromorphone their delayed mu receptor agonism in the substantia
may be the first choice in patients with tolerance to other gelatinosa (i.e., the onset of morphine’s analgesic effect is
opioids because it exhibits a stronger affinity to spinal and 30–60 minutes after administration). The rate of intra-
supraspinal mu opioid receptors with potentially less side vascular absorption is also delayed and is primarily
effects such as nausea and vomiting. dependent on the opioid dose and the complexity of the
Whether patients benefit from instituting a basal rate epidural vasculature. Another important mechanism of
in the immediate postoperative period is still debated. action for these drugs is cephalad migration in the epidu-
Initial studies documented decreased pain scores and ral and intrathecal spaces. The consequence is “delayed”
diminished opioid use when minimal basal rates were used supraspinal analgesia and delayed onset of adverse effects,
postoperatively. However, subsequent research showed a in particular, respiratory depression. For morphine, the
threefold increase in the incidence of somnolence, respi- response to this migration can occur 12–18 hours after
ratory depression, nausea, and vomiting when basal rates administration. As a result, these patients should be
were provided; this can be attributed to the waxing and monitored for respiratory depression for at least 24 hours
waning character of surgical pain in the first 24 hours. with continuous pulse oximetry. Hydromorphone has
Common medications, such as benzodiazepines and anti- similar pharmacokinetic properties to morphine, and
histamines, may contribute to the higher incidence of monitoring requirements are similar.
somnolence and respiratory depression. This situation is Intrathecal opioids behave similarly to epidural opi-
of particular concern in a patient with obstructive sleep oids but with much smaller doses. For example, the dose
apnea, who has a greater susceptibility to respiratory de- of morphine in the intrathecal space is 10 times smaller
pression from opioids, especially when combined with than via the epidural route (1:10), whereas for hydromor-
other sedatives. There are many patients in whom the phone, the ratio decreases to 1:5. For lipid-soluble drugs,
diagnosis of obstructive sleep apnea is unknown, which the ratio is 1:4 for fentanyl and 1:5 for sufentanil.
makes using a basal rate even more problematic. If a basal For opioid-tolerant patients, hydromorphone, for its
rate is used, additional monitoring for the first 24 hours strong mu receptor agonism, or fentanyl, for its quick
is warranted. onset of action, may be the best option for epidural admin-
istration. Usually, solutions administered via the epidural
9. What are the differences between major opioids route have either 10–15 $g/mL of hydromorphone or
used for neuraxial analgesia; what is the main 2–5 $g/mL of fentanyl. Local anesthetics and other
mechanism by which opioids produce analgesia adjuncts (e.g., clonidine) are commonly added to opioid
infusions, not to attain a superior analgesic effect but
in the epidural space?
rather to decrease the dose of opioid needed. Bupivacaine
Neuraxial opioids activate mu receptors in the substantia 0.0625%–0.125%, with or without clonidine 0.5–1 $g/mL,
gelatinosa of the spinal cord dorsal horn. Epidural opi- is the most commonly used adjuvant.
oids have to transfer through the dura mater, the rate of
which depends on its lipophilicity. The onset of analgesia 10. Compare the different local anesthetics used in
is directly related to the lipophilicity and dose of opioid the neuraxial space, and identify the main
administered. Fentanyl and sufentanil, with higher lipid
mechanism of action.
Local anesthetics are usually added to epidural opioid in-
fusions to achieve a higher dermatomal level of analgesia
TABLE 68-4 Routine Adult Patient-Controlled and anesthesia and to decrease the opioid dose, while
Analgesia Opioid Dosing achieving similar analgesia. Local anesthetics are catego-
rized into short-acting, intermediate-acting, and long-
Basal Rate Bolus Dose Lock-Out acting. Their principle mechanism of action involves
Drug (mg/hour) (mg) (minutes) direct inhibition of Na"-gated channels along the neu-
rilemma layer and decreased signal output to the cen-
Fentanyl 0.01–0.015 0.01–0.02 6–10
tral nervous system by increasing the threshold for
Hydromorphone 0.1–0.2 0.1–0.3 6–10 membrane depolarization. The action is more intense
Morphine 1 0.4–1.8 6–10 as the concentration of local anesthetic increases and
depends on the amount of myelin present on the outer
358 SECTION 12 Pain
membrane of nerve fibers. Small myelinated A-delta and 11. What are the alternative postoperative analgesic
unmyelinated C fibers, which are primarily responsible
for nociception, are inhibited before the large myelinated
modalities for this patient?
A fibers. Patients, such as the patient in this case, who are already on
Effects of local anesthetics are related to their pKa (i.e., high-dose opioids preoperatively, are ideal candidates for
the physiologic pH at which 50% of molecules are in a multimodal analgesia in the postoperative period. Gabapen-
nonionized state) and lipid solubility. Because only the tinoids (e.g., gabapentin, pregabalin) and NSAIDs (e.g.,
nonionized molecules can cross the neuronal membrane, ketorolac) reduce the amount of opioids required. The start-
inhibition of Na" channels depends on the amount of ing dose for gabapentin is 300 mg three times a day. In older
nonionized form available at a given pH. The pKa of all patients or patients with renal impairment, the dose should
local anesthetics is higher than physiologic pH to varying be decreased to 100 mg two or three times a day. Doses can
degrees. At physiologic pH (7.4), a greater proportion of be increased every 48–72 hours up to 600–800 mg three
the local anesthetic molecules exists in the ionized form times a day. For pregabalin, a starting total dose of 50 mg per
that cannot penetrate the neuronal membrane. When day divided into two doses might prove efficacious. For
comparing the time to onset of action of various local routine postoperative care, gabapentin should not exceed
anesthetics, agents with a lower pKa (i.e., closer to physi- 1200 mg in divided doses, and pregabalin should not exceed
ologic pH) have a greater proportion of nonionized 150 mg in divided doses. These medications should not be
molecules and a shorter time to onset of action. By adding stopped abruptly because of the risk for seizures. When
sodium bicarbonate to the local anesthetic solution, in- severe surgical pain has abated, these medications should be
creasing pH, the time to onset of action can be shortened weaned over the course of 2 weeks.
further (Table 68-5). Bupivacaine and ropivacaine have NSAIDs provide analgesia through peripheral and
the same pKa but different onset times and durations of potentially central prostaglandin inhibition. Doses of
action. The variance in lipophilicity helps to explain 15–30 mg of ketorolac every 6 hours have the ability to
these variations. maintain adequate analgesia with minimum effects on
Lipid solubility determines the speed of onset of local renal parenchyma or gastric mucosa. Doses !30 mg have
anesthetics in a similar fashion to opioid-induced analgesia. not been shown to be more efficacious and have the
The greater the lipid solubility, the faster the molecules propensity of inducing acute tubular necrosis in the renal
inhibit depolarization in the primary afferents and effer- medulla. Because of the potential risk of hematoma, most
ents in the dorsal horn. thoracic and colorectal surgeons would agree to start
Reuptake of local anesthetics by the epidural and ketorolac no sooner than 24 hours after surgical incision.
subdural vessels contributes to the rate of removal and Intravenous acetaminophen, a centrally mediated anti-
ultimate metabolism. Local anesthetics are metabolized inflammatory medication, has captured the interest of
either by liver cytochrome microenzymes (e.g., bupiva- clinicians involved in spine and colorectal surgeries.
caine, ropivacaine, lidocaine) or by plasma esterases Although its mechanism of action remains largely unknown,
(e.g., chloroprocaine, procaine, cocaine). it has shown promise when used in conjunction with smaller
doses of opioids in the immediate perioperative period.
In patients ! 50 kg, the dose of intravenous acetaminophen
is either 650 mg every four hours or 1000 mg every 6 hours.
These doses are efficacious in decreasing postoperative pain
TABLE 68-5 Physicochemical Properties of scores while also decreasing opioid use. The main concern
Local Anesthetics with the use of intravenous acetaminophen is the risk of
liver toxicity. When appropriate dosing, as approved by the
Onset Half-Life U.S. Food and Drug Administration (FDA), was fol-
Anesthetics pKa (hours) (hours)
lowed, liver toxicity was not clinically significant. The
Amides cost of intravenous acetaminophen is greater than the cost
Bupivacaine 8.1 0.3–0.5 3.5 saving in reduced opioid dosing. However, the greater
Etidocaine 7.7 0.3–0.5 2.6 cost may be offset by the reduced rate of adverse events,
particularly respiratory depression, which occurs with
Lidocaine 7.9 0.1–0.3 1.6
greater opioid use.
Mepivacaine 7.6 0.1–0.3 1.9
Ropivacaine 8.1 0.1–0.3 1.9 12. What are the short-term and long-term goals of
analgesia for this patient?
Esters
Chlorprocaine* 8.7 0.01–0.1 0.11 Short-term goals are aimed at providing optimal peri-
Procaine* 8.9 0.1–0.3 0.14
operative analgesia in addition to proper and routine
postoperative care. For complicated patients such as
*Chlorprocaine and procaine have a pKa !8 but a short onset time this one, consultation with a pain management specialist
and duration of action. This would seem to be unexpected. is indicated. A multimodal analgesic regimen might include
Chlorprocaine and procaine are used in much higher concentra- the following agents:
tions than most other local anesthetics. Consequently, the
number of molecules of local anesthetic is much higher in
• Methadone in doses of 2.5 mg three times a day
these solutions compared with other commonly used drugs • Hydromorphone or morphine via PCA pump
such as bupivacaine. • Gabapentin 300 mg three times a day
68 Acute Postoperative Pain 359
• Nortriptyline 10 mg at night Chang AK, Bijur PE, Baccelieri A: Efficacy and safety profile of a single
• Intravenous acetaminophen 1000 mg every 6 hours dose of hydromorphone compared with morphine in older adults
with acute, severe pain: a prospective, randomized, double-blind
• Ketorolac 30 mg every 6 hours clinical trial. Am J Geriatr Pharmacother 7:1, 2009.
Long-term goals should take into consideration risks De Oliveira GS Jr, Agarwal D, Benzon HT: Perioperative single dose
of tolerance and addiction. An open dialogue among ketorolac to prevent postoperative pain: a meta-analysis of randomized
clinicians, the patient, and family members regarding trials. Anesth Analg 114:424, 2012.
long-term treatment plans should be ongoing. Pain man- Gottschalk A, Cohen SP, Yang S, et al.: Preventing and treating pain
after thoracic surgery. Anesthesiology 104:594, 2006.
agement specialists in conjunction with a counselor or Gottschalk A, Durieux ME, Nemergut EC: Intraoperative methadone
psychologist may be needed to address this patient’s an- improves postoperative pain control in patients undergoing complex
algesic issues. spine surgery. Anesth Analg 112:218, 2011.
After the acute pain phase is over, interventional Hagle ME, Lehr VT, Brubakken K: Respiratory depression in adult
patients with intravenous patient-controlled analgesia. Orthop Nurs
options, such as neurolytic blocks with alcohol or phenol 23:18, 2004.
and radiofrequency ablation of somatic or sympathetic Horlocker TT, Wedel DJ, Rowlingson JC: Regional anesthesia in the
nerve fibers, should be considered. A new modality of patient receiving antithrombotic or thrombolytic therapy: American
treatment involving neuromodulation, via spinal cord Society of Regional Anesthesia and Pain Medicine Evidence-Based
stimulation or intrathecal therapy, has been used for these Guidelines (Third Edition). Reg Anesth Pain Med 35:64, 2010.
Korkmaz Dilmen O, Tunali Y, Cakmakkaya OS: Efficacy of intravenous
patients, especially for palliative purposes. Considering paracetamol, metamizol and lornoxicam on postoperative pain and
that the dosage of opioid used in the intrathecal space is morphine consumption after lumbar disc surgery. Eur J Anaesthesiol
significantly smaller than the dosage via the parenteral 27:428, 2010.
route, this modality would facilitate decreasing the total Liu SS, Bae JJ, Bieltz M, et al.: A prospective survey of patient-
controlled epidural analgesia with bupivacaine and clonidine after
daily amount of opioid usage, minimizing side effects. An total hip replacement: a pre- and postchange comparison with bupi-
additional benefit of this method is the ability to add a vacaine and hydromorphone in 1,000 patients. Anesth Analg 113:
local anesthetic, such as bupivacaine or ropivacaine, along 1213, 2011.
with other adjuvants, such as clonidine. A more recently Loftus RW, Yeager MP, Clark JA, et al.: Intraoperative ketamine reduces
added breakthrough bolus device as part of the intrathecal perioperative opiate consumption in opiate-dependent patients with
chronic back pain undergoing back surgery. Anesthesiology 113:
pump allows the patient to administer additional boluses 639, 2010.
during breakthrough pain. This added feature makes this Parikh HG, Dash SK, Upasani CB: Study of the effect of oral gabapentin
modality an ideal tool for palliative treatment when all used as preemptive analgesia to attenuate post-operative pain in
other analgesic regimens have been futile. patients undergoing abdominal surgery under general anesthesia.
Saudi J Anaesth 4:137, 2010.
Sinatra R: Causes and consequences of inadequate management of
acute pain. Pain Med 11:1859, 2010.
SUGGESTED READINGS Sinatra RS, Jahr JS, Reynolds L, et al.: Intravenous acetaminophen for
Bang EC, Lee HS, Kang YI, et al.: Onset of labor epidural analgesia pain after major orthopedic surgery: an expanded analysis. Pain Pract
with ropivacaine and a varying dose of fentanyl: a randomized 12:357, 2012.
controlled trial. Int J Obstet Anesth 21:45, 2012. Sinnott CJ, Garfield JM, Thalhammer JG, et al.: Addition of sodium
Boussofara M, Mtaallah MH, Bracco D, et al.: Co-analgesic effect of bicarbonate to lidocaine decreases the duration of peripheral nerve
ketorolac after thoracic surgery. Tunis Med 84:427, 2006. block in the rat. Anesthesiology 93:1045, 2000.
Brogan SE, Winter NB: Patient-controlled intrathecal analgesia for the Urban MK, Ya Deau JT, Wukovits B, et al.: Ketamine as an adjunct to
management of breakthrough cancer pain: a retrospective review and postoperative pain management in opioid tolerant patients after
commentary. Pain Med 12:1758, 2011. spinal fusions: a prospective randomized trial. HSS J 4:62, 2008.
CASE 69
QUESTIONS
1. What is the incidence of low back pain? 7. What are the signs and symptoms of sacroiliac
2. What is the differential diagnosis of low back disease, and how is it treated?
pain? 8. What are the facet joints, and how does pathology
3. Discuss the evaluation of a patient with low back of facet joints manifest?
pain. 9. What is the mechanism of action of epidural
4. What is the classic presentation of a patient with steroid injections?
a herniated nucleus pulposus? 10. What are the pathogenesis, diagnosis, and
5. Differentiate the clinical presentation of a patient treatment of internal disk disruption?
with a herniated nucleus pulposus from a patient 11. What oral medications are prescribed for low
with spinal stenosis. back pain?
6. What are the pathogenesis and treatment of 12. What is failed back syndrome, and how is it
myofascial syndrome (trigger points)? managed?
A 42-year-old man presented to a pain management spe- theory, the pain should be reversible with local anesthetic
cialist with low back and leg pain that began after lifting blockade of the structure. The most common cause of
a heavy object. The pain started in the middle of his low back pain is believed to be myofascial pain, or mus-
lower back and radiated down the back of his right leg cular in origin. Other common causes of low back pain
into the sole of his right foot. The pain was not relieved include internal disk disruption (IDD), sacroiliac (SI)
with acetaminophen and bed rest. Magnetic resonance joint pain, and pain from facet joint arthropathy. Lumbar
imaging (MRI) of the lumbar spine showed a herniated stenosis, which causes narrowing of the spinal canal, is a
disk at the L5-S1 level with impingement of the S1 nerve common cause of low back pain, especially in elderly
root. The patient was otherwise in excellent health. patients, as is lumbar degenerative disk disease and spon-
dylosis. Less frequent skeletal causes include metabolic
(osteoporosis), neoplastic (primary or metastatic), infec-
1. What is the incidence of low back pain?
tious (osteomyelitis, epidural abscess), traumatic (frac-
Low back pain with or without radiculopathy (pain or tures), and congenital (scoliosis) conditions. Rheumatoid
abnormal neurologic function caused by pressure on or and other types of inflammatory arthritis can also cause
irritation of a spinal nerve) is the second most common low back pain.
reason patients visit a physician and accounts for 3% of A herniated disk (herniated nucleus pulposus) usually
all hospital discharges. During their lifetime, 80% of the causes pain or other neurologic dysfunction down the leg.
U.S. population experience low back pain, and it has Back pain and leg pain of neurologic origin may also
been estimated that at any time approximately 15% of originate from irritation of nerves by spinal osteophytes;
Americans have low back pain. Back pain affects patients tumors in the pelvis or near the spinal column; or diseases
of all ages; elderly adults have more severe pain and pain of the neuraxis, such as inflammation (herpes zoster) or
of longer duration. neoplasms (intradural or epidural tumors).
Because of the large differential diagnosis, a thorough
2. What is the differential diagnosis of low investigation and evaluation is necessary to determine the
cause of lower back pain. Although it is easy to rule out
back pain?
many factors that may cause pain, the exact etiology of
Low back pain can be caused by a multitude of patho- pain often is difficult to determine, especially when dealing
logic processes. Although most cases of low back pain are with nonradicular pain.
of muscular or spinal origin, many intraabdominal and
lower thoracic pathologies can refer pain to the low back. 3. Discuss the evaluation of a patient with
Examples include pancreatic cancer, lower lobe pneumo- low back pain.
nia, and aortic aneurysms.
For a structure in the spine to cause pain, it must be Low back pain must be evaluated and managed the same
innervated, subject to possible injury or irritation, and in way as any other presenting complaint. Although most
360
69 Low Back Pain 361
cases of low back pain resolve with conservative treatment, posterior facet joints, osteophytes from osteoarthritis,
back pain lasting !1 month requires a complete clinical hypertrophy of the ligamentum flavum, and bulging of
evaluation, consisting of a full history, physical examina- the disk anulus. These structures may impinge on nerve
tion, and interpretation of laboratory data. The history roots or the cauda equina and produce typical radicular
should concentrate on the characteristics and location of pain, although patients with spinal stenosis may also
the pain and a review of modifying factors. Associated fac- present with nonradicular low back pain. Patients with
tors, such as leg weakness or changes in bladder or bowel spinal stenosis may experience neurogenic claudication,
function, need to be elicited. A full medical and surgical which is leg pain while walking that is relieved by sitting
history and complete review of systems are required. and resting. Neurogenic claudication differs from vascu-
While performing a physical examination that concen- lar claudication in that the sitting position relieves the
trates on the lower back and lower extremities, a differen- pain in the former condition, and cessation of walking
tial diagnosis of the cause of pain should be obtained. relieves the pain in the latter condition.
Before any intervention on the spine, lumbosacral MRI or Pain from spinal stenosis differs from the pain of a
computed tomography (CT) scan should be obtained to herniated disk in that flexion of the lumbar spine relieves
rule in a diagnosis and to rule out rarer sources of pain, spinal stenosis pain. Disk disease pain is typically relieved
such as a malignancy or epidural abscess. by reclining and may be increased with flexion of the
lumbar spine. Another difference between spinal stenosis
4. What is the classic presentation of a patient with and disk disease is that pain and neurologic deficits can
extend over several dermatomes with spinal stenosis be-
a herniated nucleus pulposus?
cause of the diffuse nature of the disease. A herniated
The average age of patients presenting with a herniated nucleus pulposus usually manifests as a localized disease
disk is 30–50 years. Although pain from a herniated nu- of a limited dermatomal distribution. Spinal stenosis is
cleus pulposus (herniated disk) may start after trauma, characterized by chronic, mild discomfort that progresses
such as lifting a heavy object, it also can occur without over time. Conversely, the hallmark of disk disease is the
any obvious inciting event. Depending on the nerve root acute and severe onset of radicular pain (Table 69-1).
involved, the dermatomal distribution of pain may be in CT scan or MRI ultimately makes the definitive diag-
the back of the leg (lower lumbar disks) or in the groin or nosis. As noted under Question 4, it is important that
anterior thigh (upper lumbar to midlumbar disks). The the findings on these scans are correlated with clinical
pain and occasionally accompanying neurologic dysfunc- symptoms.
tion may be caused by mechanical compression of nerve
roots or more likely by chemical inflammation from sub- 6. What are the pathogenesis and treatment of
stances released from degenerating intervertebral disks myofascial syndrome (trigger points)?
(e.g., phospholipase A, bradykinin, histamine). The pain
is usually aggravated by bending, coughing, or sneezing Myofascial trigger points can be found in !50% of the
and is improved with resting and lying down. Rarely, population. Acute muscle strain or chronic repetitive
bowel or bladder dysfunction can occur. CT scan or MRI motion leads to tissue damage and the release of calcium
is invaluable in confirming the diagnosis. However, im- from the sarcoplasmic reticulum, causing a localized,
aging must be correlated with clinical symptoms, because sustained contracture of the muscle fibers. Myofascial
positive findings on imaging may not be related to the syndrome manifests as discrete, well-localized, point pain
present symptoms. Approximately 30% of asymptomatic and tenderness over these areas. A taut muscular band is
adults have abnormalities on lumbar MRI. often palpated causing a painful reaction (jump sign)
Physical examination demonstrates increased pain when when pressure is applied.
tension is applied to the lumbosacral plexus. Tests such as Multiple treatment modalities exist. More common
the bowstring sign (radicular pain elicited by popliteal pres- treatments include spray and stretch technique (with
sure with the hip flexed and knee extended) and the ethyl chloride), trigger point injections with local anes-
Lasègue test (radicular pain secondary to foot dorsiflexion thetic (with or without steroids), massage therapy, trans-
with the leg extended) are indicative of nerve irritation. cutaneous electrical nerve stimulation, and acupuncture.
Sensory deficits may manifest over the dermatomal
distribution of the involved nerve. Reflex testing of L4
radiculopathy may show a decreased response to the knee TABLE 69-1 Spinal Stenosis versus Herniated
reflex, whereas S1 radiculopathy may show a decrease in Disk
the Achilles reflex. Motor deficits over the respective
nerve root may also occur; for example, L5 radiculopathy Spinal Stenosis Herniated Nucleus Pulposus
may cause weakness of dorsiflexion of the foot.
Pain relieved with flexion Pain relieved by reclining
of spine
5. Differentiate the clinical presentation of a patient Pain increased with flexion
with a herniated nucleus pulposus from a patient Pain and neurologic Limited dermatome
with spinal stenosis. deficits over several distribution
dermatomes
Spinal stenosis, which is primarily seen in older patients,
Chronic mild discomfort Acute and severe onset
is caused by narrowing of the central spinal canal or progressing with time
the lateral neuroforamen by a combination of enlarging
362 SECTION 12 Pain
Although used by some practitioners, the efficacy of has significant but incomplete pain relief, the injection can
botulinum toxin for the treatment of myofascial pain has be repeated in 3–4 weeks. If no relief is obtained, another
not been firmly established in clinical trials. route of epidural steroid administration should be consid-
ered. The three most commonly performed approaches to
7. What are the signs and symptoms of sacroiliac the epidural space are transforaminal, caudal, and inter-
laminar. Standard of practice dictates that no matter what
disease, and how is it treated?
approach is chosen, it should be performed under fluoro-
The SI joint may be responsible for almost 20% of cases scopic guidance with the use of contrast dye. Contrast-
of chronic, nonradicular back pain. The SI joint is a sy- enhanced fluoroscopy ensures proper needle placement
novial joint bordered by multiple strong ligaments. Strain and that the injectant reaches the proper target and greatly
and degeneration cause pain and restricted motion. Pain eliminates the risk of intravascular injection.
from the SI joint is concentrated over the joint but may More recent studies of the efficacy of ESIs have shown
radiate into the ipsilateral buttock and posterior thigh. benefits of transforaminal ESIs in the treatment of ra-
Tenderness to palpation may be elicited over the joint, dicular pain, including decreased pain, increased func-
although this is not universal. A positive Faber test (uni- tion, and decreased need for surgery. Caudal ESIs have
lateral low back pain with a combination of flexion, ab- shown efficacy in the treatment of both radicular and
duction, and external rotation of the hip) is suggestive of nonradicular pain from lumbar stenosis and degenerative
SI joint pain. disk disease. Older studies looking at the efficacy of inter-
SI disease is treated by fluoroscopy-guided steroid in- laminar ESIs produced variable conclusions; however,
jections into and around the joint. Although the relief many of these studies had design flaws.
from this treatment may be long-lasting, it is often tran- Better response to ESIs generally is shown in younger
sient. The exact innervation of the SI joint is debatable and patients and patients with pain of "6 months’ duration.
not completely understood, and long-lasting relief from Large series have supported the relative safety of this pro-
techniques such as radiofrequency lesioning has been vari- cedure. Recognized but rare complications of ESIs include
able. Physiotherapy and appropriate use of medications dural puncture, salt and water retention, congestive heart
may help with the pain. failure, hyperglycemia, epidural abscess, and hemorrhage.
Transforaminal approaches risk radicular artery injection
8. What are the facet joints, and how does pathology of a particulate steroid compound, which could produce
anterior spinal artery infarction and paralysis.
of facet joints manifest?
Facet joint arthropathy is a common cause of back pain 10. What are the pathogenesis, diagnosis, and
in younger and older patients. Facet joints are paired
joints at each vertebral level and are true synovial joints. treatment of internal disk disruption?
Synovitis and articular degeneration cause local tender- IDD is a common cause of axial (nonradicular) low back
ness over the involved joint with referred pain into the pain. IDD may begin as a vertebral end plate fracture
buttock and posterolateral leg, which usually, but not caused by chronic repetitive motion or acute strain lead-
always, worsens with extension of the spine. ing to annular tears of varying degrees. Nerve endings
Painful manifestations of facet disease, sacroiliitis, and may grow into the inner annulus (which is normally non-
lumbosacral radiculopathy often mimic each other. A diag- innervated) and can become sensitized by chemicals leak-
nosis of facet joint disease may be made by history, physical ing from the nucleus pulposus via the tears. Clinically,
examination, and interpretation of radiographs. However, IDD manifests as bandlike axial back pain. Lumbosacral
the only way to confirm the diagnosis is with blockade of MRI may be helpful in making the diagnosis, but a pro-
medial branch nerves, which innervate the joint. When a vocative diskogram correlating radiologic and clinical
diagnosis is confirmed, radiofrequency lesioning of the findings may be more specific and sensitive.
nerves is considered the best treatment for long-lasting Oral analgesics and physical therapy are first-line
relief. Injecting local anesthetic and steroids directly into treatments for IDD. The role of interventional therapy
the facet joint may provide long-lasting relief. for IDD is questionable, and there is no widely accepted
therapy for it. ESIs have been used, but there is little
9. What is the mechanism of action of epidural evidence showing efficacy. Intradiscal electrothermoco-
agulation (IDET) has been championed by many inter-
steroid injections?
ventional pain specialists, but its efficacy has not been
Radicular pain is caused by nerve inflammation from proved in large-scale studies. In IDET, a flexible probe
chemical irritation and less commonly from direct im- is percutaneously introduced into the disk annulus, and
pingement of the nerve. Steroids injected into the epidural heating occurs. Several theories have been proposed re-
space produce antiinflammatory effects on the nerve roots garding the mechanism of action of IDET. It may inter-
of a more concentrated nature compared with oral steroids. rupt the nerve supply to the disk, denature the chemical
A series of epidural steroid injections (ESIs) may be per- mediators of sensitization, coagulate the collagen in the
formed depending on the patient’s response; the traditional disk to close the tear, or coagulate the nociceptors.
“cookbook” formula of up to three injections performed Alternative techniques that produce a radiofrequency
every 2 weeks is no longer standard practice. A typical ESI lesion, instead of a heat lesion, to the annulus are avail-
contains 80 mg of methylprednisolone, 12–18 mg of beta- able. If instability is present along with IDD, spinal
methasone, or 40–80 mg of triamcinolone. If the patient fusion may be necessary.
69 Low Back Pain 363
11. What oral medications are prescribed for low inhibitory spinal cord pain nerve pathways. TCAs have
analgesic properties independent of their antidepressant
back pain? activity. Other effects of TCAs that can be used in pain
Oral analgesics and physical therapy should be the corner- management include sedation (fostering a good night’s
stone of treatment in most cases of low back pain. Nonste- sleep), potentiation of opioid analgesia, and mood elevation.
roidal antiinflammatory drugs (NSAIDs) are frequently Muscle relaxants (e.g., cyclobenzaprine, 5–10 mg;
used to relieve low back pain. They serve a dual purpose, metaxalone, 800 mg; or tizanidine, 2–4 mg, all adminis-
acting as both an antiinflammatory agent and an analgesic. tered three to four times daily) can be used short-term
Prostaglandins sensitize nociceptors to painful stimuli and when there is a component of pain from muscle spasm.
potentiate the algesic effect of bradykinins. By inhibiting The most common side effect of this class of medica-
the enzyme cyclooxygenase, NSAIDs inhibit prostaglan- tions is sedation. An extended-release formulation of
din synthesis, reduce inflammation, and provide analgesia. cyclobenzaprine is now available and can be adminis-
Side effects of NSAIDs include gastric irritation, renal tered in doses of 15–30 mg at bedtime to decrease the
dysfunction, platelet inhibition, hypertension, increased pain from muscle spasm and to promote a good night’s
risk of myocardial infarction, hepatic dysfunction, and tin- sleep (Table 69-2).
nitus. Commonly used NSAIDs include diclofenac, 75 mg Although opioids are often used and are considered
twice daily; meloxicam, 7.5 mg twice daily; and etodolac, acceptable by most practitioners for short-term therapy
200–400 mg three times a day (maximum 1000 mg/day). of acute back pain, the use of long-acting opioid agents
Cyclooxygenase-2 specific inhibitors (celecoxib, 200 mg for chronic pain is very controversial. Some studies point
daily) provide analgesia and antiinflammatory actions out their safety and benefits, including analgesia and
and decrease the detrimental side effects of NSAIDs improved functioning, whereas other studies point out
such as gastric ulceration and bleeding. the various side effects associated with opioid use, such as
In recent years, anticonvulsant agents (gabapentin, nausea and constipation, tolerance with the need for
pregabalin) have been used in the treatment of low back escalating doses, addiction, respiratory depression, pruri-
pain when there is a neuropathic component to the tus, hyperalgesia, and euphoria or dysphoria. In addition,
pain. The exact mechanism of the analgesic property of deficiency in immune and endocrine function may occur
this class of drugs has not been specifically determined, with prolonged use of opioids. The individual practitio-
although decreased calcium influx leading to decreased ner must decide about the use of long-term opioids in
neurotransmitter release has been postulated. A useful each patient. If opioids are used, guidelines for their use,
side effect of this class of medications is sedation, so such as those published by the American Society of Inter-
a larger dose is often administered at night to help ventional Pain Physicians, should be followed.
patients sleep. These medications are started at a low
dose (e.g., gabapentin, 100–300 mg three times daily, or
12. What is failed back syndrome, and how is it
pregabalin, 25 mg three times daily) and are titrated to
effect. Side effects include sedation, dizziness, and managed?
weight gain, especially at higher doses. Failed back syndrome (FBS) is a syndrome in which pain
Less frequently, tricyclic antidepressants (TCAs) are persists, usually with decreased functioning, after lumbar
used as analgesic agents. TCAs, such as amitriptyline and surgery. The incidence of FBS is 15%–30%. The etiol-
nortriptyline, decrease the reuptake of serotonin and nor- ogy of FBS includes complications (scarring) from the
epinephrine, which are neurotransmitters in the descending surgery, performing the “wrong surgery” (i.e., incorrect
bid, Twice a day; hs, at bedtime; MI, myocardial infarction; NSAIDs, nonsteroidal antiinflammatory drugs; qd, once a day; qid, four times a
day; tid, three times a day.
*
Start at low dose and titrate up to desired effect.
†
Given before bedtime to help decrease pain from muscle spasm and improve sleep.
364 SECTION 12 Pain
Postherpetic Neuralgia
Yury Khelemsky, MD
QUESTIONS
An 82-year-old woman presented to the pain management patients may experience radicular pain without a preced-
office with severe right chest wall pain. The pain started ing rash. Allodynia, defined as pain resulting from a nor-
5 months ago, before an outbreak of vesicular rashes in the mally nonpainful stimulus, such as light touch, is nearly
same distribution; however, the pain persisted after the universal in patients with PHN. Areas of diminished or
lesions resolved. The pain radiated from the posterior to absent sensation to pain, touch, temperature, and vibra-
anterior thorax and was stabbing and burning in nature. tion may also be present. PHN is associated with signifi-
cant psychosocial dysfunction and decreased quality of
life, especially in elderly patients.
1. What is postherpetic neuralgia?
Postherpetic neuralgia (PHN) is a chronic pain syn- 4. What are the risk factors for development
drome that develops after an acute outbreak of varicella- of postherpetic neuralgia?
zoster virus, also known as shingles. In acute herpes
zoster, reactivation of dormant virus in a cranial or dorsal Advanced age, greater rash severity, intensity of acute pain,
root ganglion leads to pain and a characteristic rash in the deep pain at initial presentation, female gender, ophthal-
distribution of one or more dermatomes. Typically, the mic location, anxiety and depression, and allodynia have
pain associated with acute herpes zoster resolves after been described as predictors for the development of PHN.
approximately 1 month; however, approximately 10% of
patients develop persistent pain, which if present after 5. Can postherpetic neuralgia be prevented?
4 months from rash onset is classified as PHN.
Several strategies have been employed to prevent PHN,
2. What is the pathophysiology of postherpetic including vaccination, antiviral agents, tricyclic antide-
pressants, gabapentinoids, neuraxial blockade, and periph-
neuralgia?
eral nerve blocks. Shingles cannot be transmitted between
Pain during the acute episode of herpetic neuralgia is individuals. However, varicella-zoster virus can be spread
likely secondary to inflammation produced as viral par- from a person with active shingles (blisters) to a person
ticles move along nerves and damage affected neural who has never had chickenpox, resulting in the develop-
structures. Sustained activity of primary afferent neurons ment of chickenpox but not shingles. Vaccination is the
supplying the dorsal horn may induce long-term poten- most effective preventive intervention, decreasing the in-
tiation of stimuli, known as central sensitization. Central cidence of PHN by 66.5%. Initiation of antiviral medica-
sensitization along with neuronal degeneration is a likely tions, all of which have similar efficacy, within 72 hours of
pathophysiologic mechanism of PHN. Ongoing viral rash onset can decrease the severity of acute pain and the
replication does not appear to be responsible for PHN. duration of PHN. Administration of amitriptyline, a tricy-
clic antidepressant, within 48 hours of the onset of rash
3. What are the clinical manifestations of and continuing for 2 months can decrease the incidence of
PHN. In an uncontrolled study, gabapentin was found to
postherpetic neuralgia?
be effective in preventing PHN when used in conjunction
Patients with PHN typically present with sharp or burn- with an antiviral agent. It is unclear if epidural or intrathe-
ing pain over the distribution of thoracic, cervical, or tri- cal injection of local anesthetic or glucocorticoid or both,
geminal nerves, in the area of the resolved rash. Rarely, prevents PHN because studies on this topic have had
365
366 SECTION 12 Pain
QUESTIONS
1. Define complex regional pain syndrome type 1 and 5. How is complex regional pain syndrome diagnosed?
type 2. 6. What nerve blocks can be used for diagnosis and
2. What are the pathophysiologic theories regarding treatment of complex regional pain syndrome?
the etiology of complex regional pain syndrome? 7. What other modalities can be used to treat complex
3. Delineate the different stages of complex regional regional pain syndrome?
pain syndrome.
4. What are the signs and symptoms of complex
regional pain syndrome?
A 39-year-old secretary was healthy until 1 year ago The clinical heterogeneity of CRPS is indicative of patient-
when she tripped and fell onto her right arm while at to-patient variability in the activation of these pathways
work. She awoke 10 days later with severe burning pain after noxious stimuli.
from the palm to the midforearm. The arm began to Even minor tissue trauma can be sufficient to amplify
swell and intermittently turned pale and red. When the signaling in traumatized tissue and result in long-term
patient presented, the arm was exquisitely tender to peripheral sensitization. However, the way in which the
touch and the patient was unable to wear long-sleeved immune system and nervous system interact, particu-
shirts. She was unable to use the arm and had become larly in bones, muscle, and connective tissue, is not fully
depressed. understood.
Vasomotor dysfunction is common in CRPS. The
1. Define complex regional pain syndrome type 1 affected limb is usually warmer than the healthy limb
and type 2. early on and cooler than the healthy limb later on. This
shift in temperature suggests that the activity in vasocon-
Complex regional pain syndrome (CRPS) is a disease strictor neurons changes over time in CRPS.
process that consists of continuous pain, often burning in The central nervous system undergoes functional and
nature, usually consequent to an injury or a noxious structural changes in people with persistent pain, and
stimulus. CRPS usually manifests with varying degrees of these changes are thought to be especially important in
autonomic and trophic changes along with sensory and people with CRPS. A potentially important mechanism is
motor dysfunction. hyperalgesic priming. According to this theory, a tran-
CRPS type 1 was previously known as reflex sympa- sient insult triggers long-lasting changes in primary
thetic dystrophy, and CRPS type 2 was previously known afferent nociceptors that cause them to become hyper-
as causalgia. The nomenclature has been changed to responsive to future mild insults that would not normally
dispel some of the old theories regarding the possible provoke pain.
etiologies for these diseases. Other theories include the existence of ephapses, or
CRPS types 1 and 2 have similar signs and symptoms. neurologic short circuits between the somatic and sym-
In CRPS type 2, a history is commonly elicited describing pathetic nervous systems, possibly caused by trauma. It
a macroscopic nerve injury, such as a traumatic amputa- is unclear whether these connections are actual struc-
tion, whereas with CRPS type 1, the inciting event may tural connections or “chemical” connections caused by
be a minor injury or may never be determined. the release of neurotransmitters. These ephapses could
explain the clinical findings in CRPS. Stimuli that are
2. What are the pathophysiologic theories regarding usually mediated by the autonomic nervous system, such
the etiology of complex regional pain syndrome? as responses to emotion, temperature, and weather, are
rerouted through the somatic nervous system and cause
Understanding of CRPS has increased substantially over pain. Stimuli that are usually mediated by the somatic
the past decade. Three major pathophysiologic pathways nervous system, such as light touch, are rerouted through
have been identified: aberrant inflammatory mechanisms, the autonomic nervous system and cause an uncoordi-
vasomotor dysfunction, and maladaptive neuroplasticity. nated sympathetic response.
367
368 SECTION 12 Pain
3. Delineate the different stages of complex regional 4. What are the signs and symptoms of complex
pain syndrome. regional pain syndrome?
CRPS is usually described in three different stages Patients with CRPS type 1 usually present with a history of
(Table 71-1). very minor trauma, or patients may have no recollection
of an injury. In contrast, the initial history for CRPS type 2
consists of a major injury with macroscopic nerve damage.
Stage 1: Acute or Hyperemic Stage
Rarely, cerebrovascular accidents or myocardial infarctions
Stage 1 occurs within days to weeks of the initial injury may be complicated by CRPS. The most common symptom
and is characterized by a predominance of severe burn- of CRPS is burning pain. Although CRPS usually occurs in
ing or lancinating pain. It is notable for signs of sympa- an extremity, it can occur anywhere in the body, including
thetic blockade; the area affected is red, warm, and dry. the face or major joints, such as the knee or shoulder.
Hyperesthesia—an exaggerated response to stimuli—and Because of its atypical presentation, the diagnosis of CRPS
allodynia—a painful response to nonpainful stimuli—are in a joint is very difficult, and the clinician must have a high
prominent symptoms of this stage. Treatments instituted degree of suspicion when other pathologies have been ruled
in stage 1 have the best prognosis for a cure. out. Because this syndrome derives from sympathetic inner-
vation, affected areas can encompass nondermatomal distri-
butions. Neurologic abnormalities such as allodynia and
Stage 2: Dystrophic Stage
hyperesthesia are common with CRPS but can occur with
Stage 2 occurs weeks to months after the initial insult. somatic neuropathies as well. Depending on the stage of the
The signs and symptoms of this stage are consistent with disease, varying degrees of color, temperature, sweating, and
sympathetic hyperexcitability. The area involved is pale trophic changes may be present. Less common manifesta-
or cyanotic and cool. Burning pain associated with tions include motor and sensory dysfunction.
hyperesthesia and allodynia is very common. Although
treatments in this stage can be successful, the longer the 5. How is complex regional pain syndrome
duration of the symptoms, the poorer the prognosis. diagnosed?
The diagnosis of CRPS is a clinical one, made by history
Stage 3: Atrophic Stage
and physical examination. Diagnosis of CRPS is based
Stage 3 occurs months to years after the initial injury. either on the Orlando criteria, endorsed by the Interna-
Atrophy of the tissues in the involved area occurs because tional Association for the Study of Pain, or on a modified
of prolonged vasoconstriction caused by increased sym- version called the Budapest criteria, summarized as follows:
pathetic discharge over time. Burning and hyperesthesia a. Continuing pain, disproportionate to any inciting
become less prominent, and trophic changes predomi- event
nate. The skin in the area becomes smooth and glassy, b. Must report at least one symptom in three of the
and the hair begins to fall out. The nails become brittle, categories in “d” below
and muscles become atrophic. The bones in the area c. Must report one sign in two or more of the catego-
show a classic patchy demineralization on radiography ries in “d” below
known as Sudek atrophy of the bone. The prognosis for d. No other diagnostic criteria can explain the signs
pain relief and functionality is very poor at this point. and symptoms better
Frequently, patients do not experience all three stages of i. Sensory: hyperesthesia or allodynia
the syndrome. Stages may be skipped, or the progression ii. Vasomotor: temperature asymmetry, skin color
may be halted with appropriate therapy. changes, or skin color asymmetry
iii. Sudomotor or edema: edema, sweating changes, A good indicator of a successful sympathetic block to the
or sweating asymmetry lower extremity is either vasodilation or increased tem-
iv. Motor or trophic: decreased range of motion, perature in the leg. Complications that can occur include
motor dysfunction (weakness, tremor, or dysto- inguinal neuralgia, a selective nerve root block, intravascu-
nia), or trophic changes (hair, nails, or skin) lar injection, spinal or epidural anesthesia, renal trauma,
The most commonly used diagnostic test involves and intradiscal injection.
blocking the sympathetic innervation to the affected area
and noting any improvement in the clinical symptoms. 7. What other modalities can be used to treat
complex regional pain syndrome?
6. What nerve blocks can be used for diagnosis
Physical therapy to prevent trophic changes associated
and treatment of complex regional pain syndrome?
with CRPS is of the utmost importance in conjunction
The two most common sympathetic nerve blocks used with other treatment modalities. The key to successful
for both diagnosis and treatment of CRPS are stellate therapy seems to be predominately dependent on treat-
ganglion and lumbar sympathetic blocks. The stellate ing the syndrome as early as possible. Psychotherapy is
ganglion is created by a fusion of the inferior cervical sometimes a productive adjunct to treatment.
sympathetic ganglion and the first thoracic sympathetic The purposes of medications used to treat CRPS are
ganglion. Anatomically, it is located near the transverse to provide patient comfort to facilitate physical therapy,
process of C7 or T1 and has axons that arise from sym- reduce pain, and decrease neuronal discharge. As a result
pathetic cell bodies from the T1 through T5 spinal cord of the continued poor understanding of the etiology of
levels. Axons that pass through the stellate ganglion sup- CRPS, medication management has proved to be chal-
ply sympathetic innervation to the head, neck, and upper lenging. However, medications should be selected with
extremities. the goals of decreasing inflammation, ectopic firing of
Although the ganglion sits at C7 to T1, traditionally, nerves, and sympathetic outflow. Pharmacologic thera-
a stellate ganglion block is performed at the level of the pies with calcitonin, bisphosphonates, free radical scav-
transverse process of C6, where Chaissagnac tubercle is engers, steroids, and gabapentin have been studied with
located. Benefits of performing the injection at this level only bisphosphonate treatment showing improvement.
include a lower risk of pneumothorax and a decreased Oral sympatholytics, such as beta blockers, decrease the
incidence of intravascular injection. The vertebral artery effects of sympathetic discharge but can cause systemic
lies anterior to transverse process at C7 and dives poste- side effects, especially related to the cardiovascular sys-
riorly at C6 in most patients. Although for years the tem. Tricyclic antidepressants and antiarrhythmic agents
procedure was performed using only anatomic land- have also been described as therapies for CRPS. The use
marks, at the present time, most are performed under of opioids in the treatment of CRPS is controversial
fluoroscopic guidance at either the C6 or the C7 level. because of the risk of addiction and abuse.
Fluoroscopic guidance and the use of contrast dye have Intravenous regional blocks can be performed along
allowed the procedure to be performed with greater with or in lieu of sympathetic nerve blocks. Seven
safety at C7, increasing the likelihood of a successful randomized controlled trials comparing intravenous
block. A good indication of a successful sympathetic regional blocks with placebo are available at the present.
block to the head and neck region is the development Mixed somatic and sympathetic blocks such as epidurals
of Horner sign (ptosis, miosis, and anhydrosis). A good or spinals can be used but lack diagnostic specificity.
indicator of a successful sympathetic block to the upper Spinal cord stimulation has shown statistically better
extremity is either vasodilation or increased temperature results for refractory CRPS at 2 years; however, there
in the arm. Complications of a stellate ganglion block were no statistical differences in any measured variables
include hoarseness, intravascular (vertebral artery) injec- over 5 years.
tion causing seizures, pneumothorax, bradycardia, dia-
phragmatic paralysis, intrathecal or epidural injection,
arm weakness, bleeding, and infection. SUGGESTED READINGS
Lumbar sympathetic blocks are indicated for CRPS Marinus J, Moseley GL, Birklein F, et al.: Clinical features and patho-
involving the lower extremities. These blocks should be physiology of complex regional pain syndrome. Lancet Neurol 10:
performed under fluoroscopic guidance with contrast dye 637, 2011.
Stokes LT, Goebel A: Complex regional pain syndrome in adults:
to confirm proper needle placement. The needle is concise guidelines. Clin Med 11:596, 2011.
placed anterolateral to the body of the lumbar vertebra Tran DQ, Duong S, Bertini P, et al.: Treatment of complex regional pain
at the L2, L3, or L4 level, most commonly at the L3 level. syndrome: a review of the evidence. Can J Anaesth 57:149, 2010.
CASE 72
QUESTIONS
1. What is the incidence of cancer pain? 7. What is breakthrough pain, and how is it treated?
2. What is the prevalence of cancer pain by organ 8. Describe the anatomy of the celiac plexus.
system? 9. What are the indications for performing a celiac
3. What are the different causes of pain in patients plexus block?
with cancer? 10. How is a celiac plexus block performed, and what
4. What is the WHO ladder? complications can occur?
5. What guidelines can be followed in devising a long- 11. What are the differences between alcohol and
term analgesic regimen for treating cancer pain? phenol neurolysis?
6. What are the advantages of set-dose extended- 12. When would one use intrathecal versus epidural
release opioid management? analgesia for cancer pain management?
A 57-year-old man presented to the pain management side effects, and radiation complications. Syndromes unre-
specialist complaining of epigastric pain radiating to the lated to cancer cause 10% of pain in oncology patients.
back. His sclerae were mildly icteric. Magnetic resonance Patients with cancer may also have common non–cancer-
imaging (MRI) showed a mass at the head of the pancreas. related pain syndromes, such as lower back pain and
headaches.
1. What is the incidence of cancer pain?
4. What is the WHO ladder?
The number of new cases of cancer in the United States
is almost 2 million per year. Of these, approximately 50% The World Health Organization (WHO) devised a proto-
of patients with intermediate-stage cancers and 75% col (Box 72-1) for treating pain using a tiered approach.
of patients with advanced-stage cancers have pain. The This protocol allows for the use of less potent medications
incidence of cancer pain is approximately 1 million cases initially (first tier), followed by increasingly more potent
per year. medications (second and third tiers) which are added in
a stepwise approach until the patient is comfortable.
2. What is the prevalence of cancer pain by organ According to the WHO, about 85% of cancer patients
can be kept comfortable using this protocol.
system?
In the WHO ladder, first-tier medications include non-
Different organ systems are variably associated with can- opioid analgesics such as nonsteroidal antiinflammatory
cer pain. Pancreatic cancer is the most common type of drugs (NSAIDs), antidepressants, and anticonvulsants.
cancer associated with pain. Bone cancer is the second Second-tier medications include “weak opioids,” which
most common malignancy producing pain. Both cancers have ceiling dosages owing to their combination with acet-
cause pain in !80% of cases. Breast, lung, and colon aminophen or NSAIDs. Third-tier analgesics include all
cancers are associated with pain in !70% of cases. sole opioid preparations, both short-acting and extended-
Lymphomas and leukemias produce pain in about 60% release preparations. Despite the addition of large doses
of patients. of opioids in the third tier, the nonopioid medications from
tier 1 should be continued, taking advantage of their differ-
3. What are the different causes of pain in patients ent mechanism of action in treating pain. A good knowl-
edge of opioid equipotency conversions is necessary to be
with cancer?
able to change from one opioid to another.
There are multiple causes of cancer pain. In approximately The WHO ladder can be further extrapolated clini-
65% of cases, pain is caused by direct invasion, involve- cally to include invasive techniques. Oral analgesics are
ment of nerves or the neuraxis, obstruction of a viscus, or tried first, followed by intravenous opioids, analgesia via
metastasis to distant tissues. Anticancer treatments are tunneled epidural catheters, implantable analgesic devices
responsible for 25% of cancer pain. Treatment-related pain (e.g., intrathecal infusion pumps), and finally neuroabla-
is due to surgery, diagnostic procedures, chemotherapy tive procedures.
370
72 Cancer Pain Management 371
Patches
Continuous-release fentanyl patch (Duragesic; Janssen 72 100 "g/hour # morphine
Pharmaceuticals, Titusville, NJ) 3 mg/hour IV
Buprenorphine transdermal patch (Butrans; Purdue Pharma 1 week 5 "g/hour # morphine
LP, Stamford, CT) 30 mg/day po
7. What is breakthrough pain, and how is it treated? 9. What are the indications for performing a celiac
Breakthrough pain is a transient exacerbation of pain on
plexus block?
the background of stable pain in a patient receiving There are three main indications for blockade of the
long-term opioid therapy. Breakthrough pain occurs in celiac plexus:
about 64% of patients with cancer with a median of four • To treat pain from intraabdominal organs (inner-
pain episodes per day with an onset of $3 minutes and a vated by the celiac plexus), especially secondary to
duration of about 30 minutes. The breakthrough pain malignancy, which is the most common reason for
can be due to end of dosing intervals of long-term pain performing celiac plexus blocks (this block can also
medications, incident pain, nonvolitional precipitants be used for nonmalignant pain)
(coughing, sneezing, flatulence), or can be idiopathic. • To increase blood flow to the splanchnic vessels in
Breakthrough pain is mainly treated with fast-onset, abdominal angina
short-duration analgesics. A new class of breakthrough • To increase peristalsis in the gastrointestinal tract in
analgesics is available (Table 72-2) for acute cancer pain dysmotility syndromes, such as with diabetes mellitus
known as rapid-onset opioids. Fentanyl (high lipophilic- or scleroderma
ity) is the analgesic of choice for these medications. Their
onset time is approximately 5–15 minutes, and the phar- 10. How is a celiac plexus block performed,
macokinetic profile mirrors the time frame associated
with acute pain. Risk Evaluation and Mitigation Strate-
and what complications can occur?
gies (REMS) are now required to be implemented by Celiac plexus blocks are performed with either fluoros-
manufacturers of rapid-onset opioids. The purpose of the copy or computed tomography (CT) scan. The patient is
REMS is to try to decrease the risk of misuse and abuse placed in the prone position unless he or she cannot toler-
of these rapid-onset opioids. The strategies emphasize ate it because of ascites or other intraabdominal processes.
the distribution of educational tools regarding the proper The plexus lies anterior to the aorta and posterior to the
clinical use of the rapid-onset opioids to practitioners, vena cava. Needles are placed from each side of the body
pharmacists, and patients. Knowledge of the risks versus to lie anterior to the body of L1 bilaterally. Dye injection
benefits must be documented by all of these parties to be confirms needle placement in the retroperitoneum. A
able to be involved with the prescribing of this class of maximum of 40 mL of either local anesthetic for diagnos-
medications. tic blocks (usually 0.25% bupivacaine) or neurolytic agent
(see Question 11) for therapeutic blocks is injected.
Complications that can occur with celiac plexus block-
8. Describe the anatomy of the celiac plexus. ade include hypotension; injury to adjacent viscera (e.g.,
The celiac plexus is part of the sympathetic nervous kidneys, pancreas, pleura, lungs, aorta, intestines); lower
system and is made up of the celiac, superior mesen- extremity dysesthesias or motor dysfunction; intravascular
teric, and aorticorenal ganglia. Nerve fibers that tra- injections; retroperitoneal hematomas; and intrathecal,
verse the celiac plexus arise from cell bodies from T5 epidural, intrapsoas, or intraosseous injections (Box 72-2).
through T12 and leave the spinal cord without synaps-
ing in the paravertebral ganglia. These sympathetic
fibers form the greater, lesser, and least splanchnic BOX 72-2 Complications of Celiac Plexus
nerves and coalesce around the celiac artery at ap- Block
proximately the L1 level. Here they synapse with post-
ganglionic fibers that supply the intraabdominal organs • Hypotension
below the diaphragm up to the splenic flexure of the • Trauma to kidneys, pancreas, pleura, lungs, aorta, intestines
• Lower extremity dysesthesias or motor dysfunction
large intestine. These include the stomach, small and • Intravascular injection
large intestines, pancreas, hepatobiliary system, kid- • Retroperitoneal hematoma
neys, adrenals, spleen, and omentum. The celiac plexus • Epidural, intrathecal, intradiscal, intraosseous, intrapsoas
contains visceral afferent and efferent fibers and some injection
parasympathetic fibers.
72 Cancer Pain Management 373
TABLE 72-3 Differences between Alcohol and Phenol for Neurolytic Blocks
Alcohol Phenol
Mechanism of action Extraction of neuronal cholesterol, Coagulation of neuronal proteins
phospholipids, and cerebrosides
Precipitation of lipoprotein and mucoproteins
Injection Painful Local anesthetic effect (?)
Subarachnoid Hypobaric Hyperbaric
Potency Greater (?) Less (?)
Duration Longer acting Shorter acting
Perivascular injection Safe May cause blood vessel wall necrosis
As is the case with any invasive procedure, sterile tech- 12. When would one use intrathecal versus epidural
nique is imperative to avoid infection, especially in a
patient with cancer who may be immunosuppressed.
analgesia for cancer pain management?
Both epidural and intrathecal analgesia systems allow for
the delivery of a wide variety of opioids, local anesthetics,
11. What are the differences between alcohol
and adjuvants (e.g., clonidine, baclofen) directly into the
and phenol neurolysis? central nervous system. Epidural and intrathecal analge-
Neurolysis can be accomplished with several modalities sia systems allow for smaller dosing compared with oral
including alcohol or phenol (Table 72-3). Alcohol for and intravenous administration and potentially fewer side
neurolysis is usually used in concentrations of 50%–70%. effects. In particular, the use of local anesthetics enables
It produces neurolysis by extracting cholesterol, phos- denser analgesia and a possible opioid-sparing effect.
pholipids, and cerebrosides and causing precipitation Permanent intrathecal analgesia reservoirs are more ex-
of lipoproteins and mucoproteins; this results in damage pensive to place than externalized epidural infusion systems
to both the Schwann cell and the axon. Clinically, alcohol but are less expensive to maintain in the long-term. If the
is painful on injection and is hypobaric if used for intra- patient’s life expectancy is !3–4 months, the intrathecal an-
thecal neurolysis. Relative to phenol, alcohol may be algesia system with an internal pump is financially preferable.
more potent with a longer duration of action.
The primary neurolytic effect of phenol is via coagula-
SUGGESTED READINGS
tion of proteins. It also causes nonselective damage to
neural tissue. Phenol might have a secondary local anes- De Leon-Casasola OA (ed): Cancer pain. Saunders, Philadelphia, 2006.
Gordon DB, et al: American Pain Society recommendations for improv-
thetic effect. Intrathecally, phenol is hyperbaric. Phenol ing the quality of acute and cancer pain management. Arch Intern
has a great affinity for vascular tissue, and injury to Med 165:1574, 2005.
adjacent blood vessels must be considered when it is used. Portenoy RK: Treatment of cancer pain. Lancet 377:2236, 2011.
For this reason, many pain specialists prefer alcohol to Ripamonti CI, Bandieri E, Roila F: Management of cancer pain:
ESMO Clinical Practice Guidelines. Ann Oncol 22(Suppl 6):69,
phenol for celiac plexus blocks. Radiofrequency lesion- 2011.
ing, cryoablation, and glycerol are other modalities used Yan BM, Myers RP: Neurolytic celiac plexus block for control in unre-
for neurolysis. sectable pancreatic cancer. Am J Gastroenterol 102:430, 2007.
S ECTI O N 13
AMBULATORY ANESTHESIA
374
CASE 73
Ambulatory Surgery
Laurence M. Hausman, MD • James N. Koppel, MD
QUE STIONS
1. Are there advantages to performing surgery on 17. Describe the intravenous regional anesthetic
an ambulatory basis? technique (Bier block) for surgery on the
2. Which patients are considered acceptable extremities.
candidates for ambulatory surgery? 18. What sedatives can be administered to
3. Are there patients who should never have supplement a regional anesthetic?
surgery on an ambulatory basis? 19. What complications of nerve block anesthesia
4. Are diabetic patients suitable candidates for are of special concern to ambulatory surgery
ambulatory surgery? patients?
5. What types of surgical procedures are 20. Do all ambulatory surgery patients require
appropriate for ambulatory surgery? tracheal intubation?
6. What is the appropriate fasting time before am- 21. What is the role of propofol in ambulatory surgery?
bulatory surgery that necessitates an anesthetic? 22. What is total intravenous anesthesia, and what
7. Should drugs be administered to empty the are its advantages and disadvantages?
stomach or change gastric acidity or volume 23. Define the term “moderate sedation”; when is it
before administering an anesthetic? used, and what advantages does it offer over
8. How are patients evaluated before an ambulatory general anesthesia?
anesthetic? 24. Can succinylcholine myalgias be avoided?
9. Which preoperative laboratory studies should be 25. Can a relative overdose of benzodiazepine be
obtained before surgery? safely treated with an antagonist?
10. Should an internist evaluate each patient before 26. Do newer volatile agents offer advantages over
ambulatory surgery? older agents?
11. Is an anxiolytic premedication advisable before 27. What are the etiologies of nausea and vomiting,
ambulatory surgery, and what agents are and what measures can be taken to decrease the
appropriate? incidence and severity of nausea and vomiting?
12. What are the reasons for last-minute cancellation 28. How is postoperative pain best controlled in
or postponement of surgery? ambulatory surgery patients?
13. What is the ideal anesthetic for an ambulatory 29. What discharge criteria must be met before a
surgical procedure? patient may leave the ambulatory surgery center?
14. What are the relative or absolute contraindications 30. What are the causes of unexpected hospitalization
to general anesthesia in the ambulatory setting? after ambulatory surgery?
15. What are the advantages and disadvantages of 31. When may patients operate a motor vehicle after
performing regional anesthesia in ambulatory receiving general anesthesia?
surgery patients? 32. What is the role of aftercare centers for ambula-
16. What are the advantages and disadvantages of tory surgery patients?
nerve block techniques for ambulatory surgery 33. Are quality assurance and continuous quality
patients? improvement possible for ambulatory surgery?
A 38-year-old woman is scheduled for diagnostic pelvic protamine Hagedorn (NPH) and 6 units of regular insu-
laparoscopy at 3 o’clock in the afternoon as an ambulatory lin every morning and 10 units of NPH and 3 units of
procedure. She arrives at the ambulatory surgery center regular insulin every night.
(ASC) 1 hour before scheduled surgery, accompanied by
her 11-year-old son, and appears to be extremely appre- 1. Are there advantages to performing surgery on an
hensive. Prior medical history is significant for asymp-
ambulatory basis?
tomatic gastroesophageal reflux disease; long-standing
stable asthma that has been successfully treated with in- There are multiple advantages to performing surgery on
haled sympathomimetics and steroids; and type 1 diabetes an ambulatory basis. First, patients return more quickly
mellitus, currently controlled with 25 units of neutral to the familiar home environment; this can be very
375
376 SECTION 13 Ambulatory Anesthesia
important for both pediatric and geriatric surgical 3. Are there patients who should never have surgery
patients. A reduction in nosocomial infections has also
on an ambulatory basis?
been noted. Medication errors related to faulty prescrib-
ing or dispensing of drugs is decreased in ambulatory Ex-preterm infants who are !55–60 weeks postconceptual
surgery. age should not have ambulatory surgery. These infants
Overall costs for ambulatory procedures are usually are at risk for postoperative apnea and bradycardia for the
reduced. Cost savings are due to decreased laboratory test- next 12 hours (and may last up to 48 hours) after sedation
ing, fewer medical consultations, and reduced numbers of and general anesthesia. In-hospital monitoring of ex-pre-
pharmaceuticals dispensed. The significant expense of term infants is recommended postoperatively. For similar
both the inpatient hospitalization and the hospital facility reasons, term infants !44 weeks postconceptual age should
fee is avoided. have surgery performed as inpatients. Postoperative respira-
Other, less tangible advantages include ease of sched- tory monitoring is mandatory for at least 12–18 hours. If
uling procedures and an improved sense of patient pri- possible, surgery and diagnostic procedures requiring seda-
vacy because most ASCs are staffed by a small consistent tion or general anesthesia should be postponed until the
group of personnel. child passes the unsafe period.
2. Which patients are considered acceptable 4. Are diabetic patients suitable candidates for
candidates for ambulatory surgery? ambulatory surgery?
Acceptable candidates for ambulatory surgery generally Diabetic patients may present a major challenge for the
have relatively stable medical conditions. However, anesthesiologist when scheduled for ambulatory surgery.
many centers now accept American Society of Anesthe- Because of the critical nature of glucose homeostasis, it
siologists (ASA) physical statuses III and IV patients for may be advisable to handle exceptionally brittle diabetics
selected, relatively noninvasive surgical procedures and on an inpatient basis. Preoperatively, diabetic patients
diagnostic studies. Generally, less invasive surgery is must be carefully assessed for the presence of end-organ
performed on patients who are less healthy, whereas damage. Cardiovascular disease, autonomic and renal
more invasive surgery is performed on ASA physical insufficiency, and gastroparesis may lead to potential
status I or II patients. Patients with cardiovascular dis- problems in the perioperative period.
ease have an increased risk of perioperative complica- It is preferable to schedule surgery for patients with type
tions and may not be suitable candidates for invasive 1 diabetes as the first or second case of the day. The major
ambulatory procedures. Patients with severe physical concerns are to avoid the extremes of plasma glucose, both
or mental handicaps are often excluded from consider- hypoglycemia and hyperglycemia, and acidosis. Delays in
ation as candidates for ambulatory surgery. Patients or insulin administration may lead to ketoacidosis despite the
caregivers must be able to comprehend and comply fasting state. For this reason, it is recommended that pa-
with postoperative instructions for successful ambula- tients receive insulin along with a continuous infusion of
tory surgery. dextrose on arrival at the ASC. Insulin may be administered
Ambulatory surgery is well suited for pediatric by either the subcutaneous or the intravenous route. The
patients. Generally, ambulatory surgical procedures advantage of administering a continuous infusion of regular
performed on children are shorter in duration, less insulin versus one third to one half of the usual long-acting
extensive, and less invasive than most procedures per- insulin dose subcutaneously has not been demonstrated.
formed on adults. Additional benefits to pediatric pa- Another option for early-morning surgical procedures is to
tients include less disruption of the child’s normal administer the usual long-acting insulin dose subcutane-
feeding schedule and decreased separation time from ously immediately after surgery and shift the time of all
parents. Exposure to the unfamiliar and frightening meals and future insulin injections by the same offset.
hospital milieu can be reduced to the bare minimum. Patients receiving oral hypoglycemic agents must be
Additionally, because recovery times are short for pro- carefully monitored in the perioperative period by finger-
cedures such as myringotomy and tubes, circumcision, stick or blood glucose determinations. The half-life of
and inguinal herniorrhaphy, early discharge from the some oral agents (e.g., chlorpropamide) may be 60 hours.
facility is feasible. Patients with type 2 diabetes mellitus rarely develop keto-
Preoperative communication and collaboration be- acidosis. However, these patients can experience hyperos-
tween anesthesiologists and surgeons are essential in the molar, nonketotic coma when significant hyperglycemia
event of a questionable or problem patient. The surgeon and dehydration occur.
who is to perform the procedure, the patient, and the Before discharge, it is critical that diabetic patients are
family must be agreeable to the concept of ambulatory capable of eating. They also should be relatively free of
surgery. However, reimbursement schedules created by nausea that might lead to emesis and inability to maintain
insurance carriers often convince the occasional skeptic adequate caloric intake.
because costs associated with hospitalization for proce-
dures that can be readily performed on an ambulatory 5. What types of surgical procedures are appropriate
basis usually are not covered. Overwhelming and incon-
for ambulatory surgery?
trovertible evidence of medical necessity for inpatient
care must be presented to obtain authorization for post- Initially, ambulatory surgery procedures were limited to
operative hospitalization. 11⁄2 hours. The concern was for lengthy postanesthesia
73 Ambulatory Surgery 377
recovery time that would extend beyond the facility’s outpatients. The ASA fasting guidelines recommend
hours of operation. However, newer anesthetic agents 8 hours for solids, 6 hours for light meals (i.e., toast and
allow for safe discharges on a timely basis even after long tea), 4 hours for breast milk, and 2 hours for clear liquids.
procedures performed with general anesthesia. Ingestion of 8 oz. of orange juice without pulp or coffee
The types of surgical procedures that may be per- without milk has not been shown to increase gastric
formed on an ambulatory basis depend on whether an volume. Both resting gastric volume and acidity may be
ASC is truly a freestanding unit (i.e., geographically de- reduced, which may decrease further the incidence
tached from a hospital) or is located within a hospital or and potentially devastating sequelae of intraoperative
directly contiguous to an inpatient facility. Hospital-based aspiration.
units often accept patients with a greater severity of base- Other benefits result from decreasing the fasting time
line illness and may perform more complex surgical pro- in patients preoperatively. Patients allowed to drink clear
cedures for many reasons. In the event of unexpected fluids are more content while waiting for surgical proce-
massive surgical hemorrhage, availability of immediate dures that either were delayed or were scheduled later in
blood bank support is crucial and available in hospitals. the day. Thirst is relieved, and hunger may be dimin-
However, when the need for blood may be anticipated ished. Ingestion of glucose-containing solutions may also
preoperatively, freestanding ASCs can arrange for blood prevent relative degrees of hypoglycemia. Medications
products to be available, and transfusions may be admin- required for the maintenance of homeostasis, such as
istered if the need arises. Patients may also be asked to blood pressure and cardiac drugs, can be taken orally up
donate one or more units of autologous blood, which may to 1 hour before surgery with 1 oz. of water.
be kept available for intraoperative or postoperative use. Fasting guidelines should not be made on a case-
Procedures in which blood might be administered include by-case basis but rather should be reflected in facility-
extensive liposuction or reduction mammoplasty. Radiol- wide or institution-wide guidelines.
ogy services, subspecialty consultative services, and the
relative ease of hospital transfer for overnight admission 7. Should drugs be administered to empty the
allow performance of more involved and invasive proce- stomach or change gastric acidity or volume
dures in hospital-based ASCs. before administering an anesthetic?
Ideal procedures for ambulatory surgery result in rela-
tively minor postoperative physiologic changes including Studies regarding differences in resting gastric volume
fluid shifts and blood loss. Commonly performed surger- between inpatients and ambulatory patients have yielded
ies include procedures from all surgical disciplines and conflicting results. No evidence supports the notion that
subspecialties. A few examples include cataract extraction; every patient must receive liquid nonparticulate antacids
breast surgery; plastic surgery; gynecologic procedures (0.3 molar sodium citrate, 30 mL) before induction of
such as dilation and curettage, hysteroscopy, termination anesthesia. A soluble (nonparticulate) antacid is substi-
of pregnancy, and laparoscopy; arthroscopy; and inguinal tuted for the conventional nonabsorbable antacid con-
and umbilical herniorrhaphies. The common denomina- taining aluminum, magnesium, or calcium hydroxide to
tor of all these procedures is that they are associated with avoid severe chemical pneumonitis that may result from
only mild to moderate degrees of postoperative pain, aspiration of these particulate substances. Other pharma-
which may be readily controlled by oral analgesic agents. cologic agents include H2-receptor blockers (e.g., raniti-
In the early days of ambulatory surgery, a tonsillectomy dine, famotidine), which inhibit gastric acid production
was an example of a procedure that was considered to re- and decrease gastric volume. Mental confusion has been
quire overnight in-hospital observation. Today, tonsillec- reported after intravenous administration of cimetidine in
tomy is being performed on an ambulatory basis in many geriatric patients. Ranitidine is more potent and specific
centers, although the period of postoperative observation is and has a longer duration of action than cimetidine.
increased compared with other ambulatory surgeries. After Metoclopramide increases tone in the lower esophageal
tonsillectomy, nausea and vomiting are the most common sphincter and facilitates gastric emptying. However, it
complications causing morbidity. Early bleeding, if it does not guarantee a stomach free of gastric contents.
occurs, usually becomes evident within the first 6 hours. It Metoclopramide, in conjunction with an H2 receptor
is acceptable to discharge individuals to home who are blocker, may be more efficacious than one drug by itself.
otherwise in good health, reside within a reasonable dis- However, routine use of these drugs in patients without
tance from the facility, are accompanied by a responsible specific risk factors is not currently recommended. Addi-
adult, and have successfully tolerated oral intake without tionally, although nonparticulate antacids work immedi-
nausea and vomiting. It is especially important that ately, these intravenous drugs take 30 minutes to several
adequate fluid repletion is accomplished before discharge hours for full effect.
because early attempts at fluid intake by mouth after tonsil- Diabetes mellitus with evidence of autonomic dys-
lectomy may be unsuccessful as a result of pharyngeal pain. function or gastric atony (gastroparesis), documented
symptomatic hiatal hernia, untreated gastroesophageal
6. What is the appropriate fasting time before reflux, pregnancy in active labor, significant obesity,
ambulatory surgery that necessitates acute abdomen, and current opioid use or abuse are con-
ditions that appear to increase the incidence of gastric
an anesthetic?
regurgitation and aspiration during induction or emer-
The preoperative fasting period prescribed for patient gence from general anesthesia or during heavy sedation.
who will receive anesthesia is identical for inpatients and Prophylaxis in these situations is recommended. There
378 SECTION 13 Ambulatory Anesthesia
is no advantage to administration of triple prophylaxis from the operating room. It is less than optimal to con-
with H2-receptor antagonists, soluble antacids, and duct a preanesthesia interview and examination with the
metoclopramide. If prophylaxis with an H2 blocker is patient stripped of clothing and strapped to the operating
employed, it should be given the evening before as well room table. Additionally, with the surgeon and nurses
as on the morning of surgery. Another effective regimen waiting and instrumentation prepared, the pressure on
combines metoclopramide on the morning of surgery the anesthesiologist to proceed with anesthesia may be
and a nonparticulate antacid immediately before surgery. intense.
Despite administration of pharmacologic agents and The anesthesiologist should not fail to question patients
imposition of fasting, significant amounts of acidic gas- firmly regarding the use of illicit and nonprescription
tric contents may remain. Aspiration of gastric material is drugs. In one patient population, 25% of subjects tested
a relatively rare occurrence. If a patient is observed to positive for commonly abused substances in their urine.
aspirate and if symptoms of coughing, wheezing, or Depending on the drug involved, modifications in patient
hypoxemia while breathing room air do not develop management, including cancellation of surgery, might be
within 2 hours, significant respiratory sequelae are well advised. Additionally, users of illicit drugs may have
unlikely. Reliable and otherwise healthy ambulatory diminished capability or interest in complying with postop-
patients can probably be discharged after several hours erative instructions.
of observation in the postanesthesia care unit (PACU).
They must be instructed to contact their physician at the 9. Which preoperative laboratory studies should be
onset of symptoms.
obtained before surgery?
8. How are patients evaluated before an ambulatory For an ambulatory surgery unit that is affiliated with
or attached to a hospital, clinical laboratory testing guide-
anesthetic?
lines should be identical to the related institution. It has
Ideally, on the day before surgery, the patient would have been well established that “shotgun,” nonselective screen-
a private conference with the anesthesiologist who will be ing batteries of laboratory, radiographic, and other studies
caring for him or her. Rapport and trust could be estab- yield an extraordinarily low rate of abnormal findings,
lished, a history could be obtained, and physical assess- few of which may have a significant impact on patient
ment could be conducted. Appropriate laboratory tests management. Patients scheduled for surgery should
would be ordered, and additional consultations, if neces- have preoperative testing ordered selectively, based on
sary, could be requested. Finally, information from old the results of their history and physical examination.
medical records could be obtained. Indiscriminate testing can have potentially serious and
To avoid an additional trip for the patient and family, deleterious consequences. To explain abnormal results,
some facilities substitute a screening telephone interview additional studies may be required. Some invasive studies
for a personal interview conducted by either a nurse or an have inherent dangers. Abnormalities often are simply
anesthesiologist several days before surgery. Pertinent ignored, creating a potential medicolegal liability. Indis-
medical history can be elicited, general and specific in- criminate screening often reveals abnormalities that are
structions can be given, and reassurance can be offered irrelevant to either the surgery or the choice of anesthetic
to the patient. In this scenario, laboratory studies and agent or technique. Some centers use handheld comput-
additional components of the medical record, including ers to obtain patient histories. Branching lines of ques-
an electrocardiogram (ECG) and radiographs, if neces- tioning dependent on previous answers allow extensive
sary, are performed immediately before surgery. Previ- information gathering. At the conclusion of the interac-
ously established criteria and patient comorbidities tive interview, computers can provide detailed printouts
determine the tests that must be obtained. On the day of of significant findings and suggest indicated preoperative
surgery, the anesthesiologist must review all information testing. Many facilities do not require preoperative testing
with the patient, conduct the appropriate examination, in otherwise healthy men and women !40–50 years old
and obtain informed consent. who are undergoing superficial surgical procedures.
The surgeon must assume a large degree of responsi-
bility for the patient’s preoperative preparation. Surgeons 10. Should an internist evaluate each patient before
are often the only physician to see patients before the day
of surgery. Beside conducting a thorough history and ambulatory surgery?
physical examination, the surgeon may also request med- The same rules and standards regarding preoperative
ical consultation when appropriate. To aid in the screen- evaluation of patients apply for surgery scheduled on
ing process, surgeons may selectively order laboratory both an inpatient and an ambulatory basis. An internist
and other examinations according to written guidelines or medical subspecialist should be consulted whenever
established by the medical facility. However, a mecha- the stability of a patient’s medical condition is question-
nism should be in place for free communication between able. Although the magnitude of physiologic perturbations
the surgeon’s office and the facility so that appropriate associated with some ambulatory surgery procedures may
action may be taken when abnormal laboratory values or be minor, there is nothing minor about the administra-
other reports are received. tion of an anesthetic. A complete written history and
The anesthesiologist’s preoperative interview should physical examination are required as part of the medi-
be conducted in a relaxed, unhurried, and comprehensive cal record before administration of anesthesia and
manner both chronologically and geographically apart commencement of surgery. This history and physical
73 Ambulatory Surgery 379
examination may be performed by the surgeon if the distress both the patient and the surgeon and make for
patient has no comorbidities that would necessitate input inefficient use of available operating room time. Addi-
from an internist or medical specialist. tional questioning may reveal either new symptoms or
significant history that was not previously elicited. Phys-
11. Is an anxiolytic premedication advisable before ical findings apparent on a last-minute assessment by the
anesthesiologist may preclude the safe administration of
ambulatory surgery, and what agents are
an anesthetic. Examples include an acute upper respira-
appropriate? tory tract infection or an exacerbation of bronchospastic
Because the goal of anesthesia for ambulatory surgery is pulmonary disease. Finally, patients may arrive late to
to permit early discharge to home, there was concern that the facility or without a responsible escort to accompany
the administration of short-acting anxiolytic or analgesic them home.
premedication might delay recovery from anesthesia and
prolong time in the PACU with a resultant delay in 13. What is the ideal anesthetic for an ambulatory
patient discharge. Many patients experience anxiety in the
immediate preoperative period, and pharmacologic man- surgical procedure?
agement is quite acceptable. The administration of either No single anesthetic is ideal for every procedure. How-
diazepam, 5–10 mg orally, 1–2 hours before surgery or ever, the goal of the anesthetic is to allow for patient
midazolam, 1–2 mg intravenously, after an intravenous discharge shortly after completion of the procedure. An
catheter is placed before surgery can ameliorate distress if ideal general anesthetic agent would have rapid onset,
deemed desirable. The amnestic effect of intravenous permit quick return to baseline levels of lucidity and
midazolam is powerful, and patients may not remember equilibrium, and provide freedom from deleterious car-
having seen their surgeon if it is administered before diovascular and respiratory effects. It would provide in-
meeting the surgeon. Midazolam can also be given orally, traoperative amnesia, analgesia, and muscle relaxation
although much larger doses (0.5–1 mg/kg) are required and possess antiemetic properties. This ideal single agent
because of first-pass hepatic degradation. Opioid pre- does not exist at the present time (Table 73-1). In an
medication may contribute to the incidence of postopera- attempt to avoid some of the unpleasant side effects
tive nausea and vomiting (PONV). Preoperative oral associated with general anesthesia, regional anesthetic
doses of clonidine, a centrally acting "2-adrenergic ago- techniques, including field blocks, intravenous regional
nist, have been used to provide sedation, reduce anesthetic block (i.e., Bier block), various approaches to the brachial
requirements, and decrease episodes of hypertension and plexus, ankle block, and spinal and epidural anesthesia,
tachycardia during intubation and maintenance of general have been offered to patients as an alternative to general
anesthesia. Side effects include dry mouth, hypotension, anesthesia.
and postoperative sedation.
Relaxation techniques can be taught preoperatively 14. What are the relative or absolute contraindications
to patients and may aid in reduction of anxiety levels.
Instruction of these techniques is time-consuming and to general anesthesia in the ambulatory setting?
requires substantial patient motivation. They are usually Sometimes general anesthesia should be avoided, if pos-
reserved for select patients with extreme phobias. The sible. For example, patients with severe, poorly con-
effects of longer acting anesthetics and the surgical proce- trolled asthma or documented bullous emphysema should
dure itself contribute more significantly to the recovery not receive general anesthesia. In these cases, lesser con-
time and delayed discharge. Although time to discharge, cern should be given to the possibility of a postdural
a gross measurement, may remain unaffected, tasks that puncture headache (PDPH) if more serious sequelae are
require fine coordination and speedy reaction times likely to result during or after administration of a general
may still be deleteriously affected by the anesthetic anesthetic. However, such cases are the exception rather
(i.e., both premedication and intraoperative anesthetic than the rule, and in most instances, the final choice of
techniques). anesthesia should remain with the patient, guided by the
anesthesiologist. Additionally, when patients arrive for
extremely minor surgery without an escort, a local anes-
12. What are the reasons for last-minute
thetic injection alone without sedation might suffice for
cancellation or postponement of surgery? anesthesia. This type of anesthesia might allow the
The incidence of last-minute postponement or cancella- patient to return home unaccompanied. It sometimes
tion of ambulatory procedures often exceeds the cancel- becomes necessary to supplement local anesthesia with
lation rate for inpatient procedures. Multiple factors intravenous sedation, and an escort would be mandatory
contribute to this problem. Repeat physical examination under these circumstances.
by the surgeon may reveal the disappearance of pathol-
ogy. Patients may forget and ingest either solid food or 15. What are the advantages and disadvantages of
liquids before arrival at the medical facility. Abnormal performing regional anesthesia in ambulatory
test results that were not available or not previously
reviewed may be discovered. Communication between surgery patients?
the surgeon and anesthesiologist regarding laboratory Regional anesthesia offers several advantages for patients
abnormalities helps to reduce the incidence of last- undergoing ambulatory surgery. If little or no intraopera-
minute cancellation of surgery, consequences of which tive sedation is required, little or none of the “hangover”
380 SECTION 13 Ambulatory Anesthesia
effect will be present throughout the postoperative Postoperative headache is postulated to result from star-
period. Patients who express fear about losing conscious- vation and dehydration.
ness or the loss of control associated with general anesthe- Spinal anesthesia provided by tetracaine and bupivacaine
sia may prefer regional techniques. Some patients have a has been associated with PACU stays lasting 6–8 hours.
strong desire to remain awake to view arthroscopic sur- This must be considered before performing regional anes-
gery as it is performed. thesia, especially if the procedure is performed later in the
However, spinal or epidural anesthesia has potential day. Another disadvantage of spinal anesthesia for ambula-
disadvantages. There had been concern regarding the tory patients is the potential for persistent autonomic block-
apparent increased incidence of PDPH in patients who ade lasting 1–2 hours after restoration of motor function.
ambulate postoperatively. Experience has shown that the This autonomic blockade can result in inability to urinate
incidence of PDPH is equal among patients who are and urinary bladder catheterization. Increasing duration of
nonambulatory and ambulatory, but that the onset may sympathetic blockade correlates with increased incidence of
be delayed in patients who remain recumbent for a lon- urinary retention.
ger period of time. If spinal anesthesia is chosen, the use
of conventional smaller gauge needles and newer designs 16. What are the advantages and disadvantages of
(e.g., Greene, Sprotte, Whitacre) that include modifica- nerve block techniques for ambulatory surgery
tions at the tip appear to reduce markedly the incidence
of PDPH. Pencil-point Greene, conical Sprotte, and patients?
side port Whitacre needles split rather than cut dural There are numerous advantages of nerve block tech-
fibers, which may reduce cerebrospinal fluid leak and niques for surgery. They can provide profound analgesia
ameliorate PDPH. Reducing the incidence of PDPH to into the postoperative period, which may allow early re-
approximately 1%–2% or less would be an ideal goal. turn home. However, rapid return to presurgical levels of
Technical failure rates of the various needles must also mental alertness and acuity can be achieved only if judi-
be figured into the overall equation. cious amounts of sedative drugs are administered during
Patients must be informed of the potential for both performance of the block and surgery. Patients may
PDPH because ambulatory patients expect to resume experience a decreased incidence of nausea in the early
their normal activities shortly after surgery. Additional postoperative period if smaller amounts of intravenous
recommendations to reduce the incidence of headache opioids are required or can be avoided entirely; this may
include aligning the bevel edge of conventional needles also allow earlier alimentation and speedier return to
parallel to the longitudinal axis of the body and the normal functioning.
dural fibers. This represents an attempt to prevent cut- There are a few disadvantages to performing nerve
ting dural fibers and allows for separating them intact. blocks in patients undergoing ambulatory surgery. Prep-
Avoiding multiple dural punctures also is helpful. aration and performance of a block anesthetic may re-
Maintenance of adequate hydration intraoperatively quire more time than the induction of general anesthesia.
and postoperatively and avoidance of straining or lift- In some instances, the performance of regional blocks
ing are recommended. Patients presenting with persis- and establishment of surgical anesthesia may take longer
tent PDPH may require an epidural blood patch for than the proposed operation. Brachial plexus and other
relief. It is especially important to follow up patients nerve blocks have a known failure rate, and incomplete or
with a telephone call at 24–48 hours after surgery to inadequate anesthesia delays the onset of surgery further.
inquire about the presence of any problems. Conserva- Some patients cannot tolerate any sensation whatsoever
tive treatment of PDPHs in ambulatory patients in- and may require inordinately large amounts of sedative
cludes traditional mild analgesics, fluids, and bed rest. drugs throughout the procedure. Increased use of seda-
An epidural blood patch should be considered early if tives might easily negate some of the advantages of
the headache is perceived by the patient to be extraor- selecting a regional approach.
dinarily severe or incapacitating or the patient must Patients who have not been seen by an anesthesiolo-
return to work immediately or care for children. gist before the actual day of surgery and arrive with
To avoid PDPH in younger patients, an epidural anes- the expectation of receiving general anesthesia may be
thetic may be offered if regional techniques are requested unprepared to accept another technique. The surgeon’s
or medically indicated. Epidural anesthesia requires preference also influences the receptiveness of patients
greater technical expertise and may be slightly more to regional techniques. A surgeon who prefers the use
time-consuming to perform compared with spinal anes- of major conduction anesthesia or nerve blocks often
thesia. Insertion of a catheter into the epidural space informs patients of the benefits and availability of these
allows additional incremental doses of anesthetic to be techniques during preoperative discussions.
added if surgical time is unexpectedly lengthened. Addi-
tionally, shorter acting local anesthetics facilitate coordi- 17. Describe the intravenous regional anesthetic
nating block recovery and procedure completion. How- technique (Bier block) for surgery on the
ever, the incidence of PDPH after unintended dural
puncture with larger gauge epidural needles is signifi- extremities.
cantly higher. The reported incidence of headache after The intravenous regional anesthetic, Bier block, is an
general anesthesia in ambulatory patients exceeds the easily performed and extremely predictable method for
incidence of headache after regional anesthesia, although providing anesthesia of the extremities. It is best reserved
it is usually much less incapacitating and is self-limited. for procedures on the upper extremity below the elbow,
382 SECTION 13 Ambulatory Anesthesia
although it can provide anesthesia for surgery on the to provide adjunctive analgesia during an inadequate
distal lower extremity as well. The technique of intrave- block. It can be administered by intravenous bolus or
nous regional block requires little technical skill other by continuous infusion. Bolus doses of 0.5 #g/kg may
than the placement of an additional intravenous catheter be administered with repeat doses titrated to desired
in the hand or foot of the extremity to be anesthetized. effect. For a continuous infusion, the dose ranges from
The block has a rapid onset, and the success rate 0.02–0.3 #g/kg/minute. Side effects common to all
approaches 100% in most hands. Only minor patient drugs in the opioid class include nausea, vomiting, and
discomfort occurs during performance of the block. After significant respiratory depression. Because remifentanil
the arm is exsanguinated by wrapping it in an Esmarch has no redistribution and is quickly eliminated by
(elastic) bandage, a tourniquet is inflated to 100 mm Hg plasma esterases, it does not provide postoperative an-
over systolic pressure, and the elastic bandage is then algesia. Alternatively, fentanyl administered in intrave-
removed. Through the previously placed intravenous nous bolus doses of 25–50 #g can be employed to
catheter, 50 mL of 0.5% preservative-free lidocaine is provide adjunctive analgesia. In contrast to remifent-
injected. Surgical anesthesia is achieved within approxi- anil, fentanyl provides postoperative analgesia because
mately 10 minutes. it is redistributed and has an elimination half-life of
Because infused local anesthetic may enter the sys- 180 minutes.
temic circulation, anesthesiologists must remain vigilant Propofol also can be used to provide sedation. It can
for development of subtle central nervous system (CNS) be administered by either bolus dose (10–20 mg) or con-
changes. Frank seizures may occur if the tourniquet fails tinuous infusion (0.05–0.1 mg/kg/minute) and titrated to
shortly after the drug is injected. the desired hypnotic effect. Inherent antinausea and an-
Usually, little or no intraoperative sedation or adjunc- tiemetic properties of propofol provide an advantage in
tive analgesia is required. On release of the tourniquet, the ambulatory setting.
anesthesia rapidly dissipates. The Bier block is recom-
mended when postoperative surgical pain is apt to be 19. What complications of nerve block anesthesia
minimal. It is ideal for procedures such as ganglion cyst are of special concern to ambulatory surgery
excision, trigger finger repair, removal of foreign bodies,
and carpal tunnel release.
patients?
The potential for pneumothorax must be considered
when performing supraclavicular, infraclavicular, and
18. What sedatives can be administered to
interscalene approaches to the brachial plexus. In this
supplement a regional anesthetic? regard, the axillary approach is much safer. Pneumotho-
The best anxiolytic may be a solid relationship between rax may necessitate placement of a chest tube or pro-
the anesthesiologist and patient. However, excellent rap- longed observation. The occurrence of CNS toxicity
port may be difficult to establish within the confines of a ranging from tinnitus to frank seizures secondary to an
fast-paced ASC. It has been shown that a preoperative intravascular injection during attempted block may lead
visit with the anesthesiologist immediately before sur- to postponement or cancellation of the procedure. Intra-
gery may serve as a powerful anxiolytic. lipid solution should always be on hand to treat local
In the pharmacologic realm, intravenous midazolam anesthetic–induced cardiotoxicity.
provides excellent sedative and anxiolytic properties
(Table 73-1). It is water-soluble, nonirritating to veins, 20. Do all ambulatory surgery patients require
painless on administration, provides superb amnesia
with rapid onset, and well accepted by patients. Diaze- tracheal intubation?
pam can cause significant discomfort on intravenous in- Whether ambulatory patients have increased gastric
fusion as well as thrombophlebitis in a significant num- volumes compared with inpatients is questionable. The
ber of cases. Intravenous diazepam has been virtually small incidence of documented aspiration among previ-
eliminated from the practice of anesthesia. Midazolam ously healthy individuals presenting for elective surgery
has a much shorter elimination half-life of 1–4 hours does not indicate routine tracheal intubation for every
compared with diazepam and provides a significantly patient. Tracheal intubation should be reserved for
shorter time to recovery. Midazolam is best titrated ev- patients with known risk factors that predispose to aspi-
ery 2 minutes in increments of 1–2 mg because its onset ration. If the surgical procedure requires that the airway
is rapid, and effects may be profound. Sedation after must be shared with the surgeon or if an airway cannot
small to moderate intravenous doses usually lasts ap- be easily or safely maintained using a supraglottic device,
proximately 20–30 minutes. The profound amnestic tracheal intubation should be performed.
properties may interfere with assimilating and following The laryngeal mask airway (LMA), approved by the
instructions. Some patients who receive midazolam be- U.S. Food and Drug Administration (FDA) for use in
come completely disoriented, uncooperative, or even 1991, has proved its value in both the inpatient and am-
combative. This situation may necessitate increasing bulatory surgery settings. It is presently manufactured in
the depth of sedation, pharmacologic reversal, or con- many sizes and is appropriate for adult patients as well as
version to a general anesthetic. neonates. After induction of general anesthesia, the LMA
Remifentanil is an excellent addition for a patient is inserted blindly into the pharynx after the patient is
who requires a short-acting opioid either to provide placed into the sniffing position with extension of the
analgesia during the performance of a painful block or head. Deep anesthesia is necessary for placement of the
73 Ambulatory Surgery 383
device. After inflation of the cuff, formation of a low- remifentanil, can be administered along with an infusion
pressure seal allows both positive pressure and spontane- of propofol. Additional bolus doses of propofol can be
ous ventilation. After recovery of normal reflexes and infused to deepen the level of anesthesia rapidly. Another
when the patient is able to respond to commands and major advantage of propofol appears to be a significantly
open the mouth, the device can be gently removed from diminished incidence of PONV. Propofol’s inherent
the oral pharynx. antiemetic properties allow earlier discharge of patients.
When properly placed, the LMA can free the anesthe- When used for both induction and maintenance of anes-
siologist’s hands for other tasks, including record keep- thesia in cases lasting approximately 1 hour, faster recov-
ing, monitoring adjustments, and other responsibilities. ery time is noted compared with a thiopental induction
The incidence of sore throat after LMA use is less than followed by maintenance with isoflurane and nitrous
that associated with tracheal intubation. Because muscle oxide. Patients anesthetized with propofol appear to
relaxants are not required for LMA insertion, postopera- awaken with a positive mood, and they regain equilib-
tive myalgias associated with succinylcholine can be rium including the ability to ambulate early. The require-
avoided. Additionally, ocular and oral trauma associated ment for pain medication in the postoperative period
with conventional facemasks and oral airways may be appears to be reduced, which may be related to an overall
avoided. Edentulous patients, characteristically more dif- feeling of well-being.
ficult to ventilate by facemask, can be managed well with Two disadvantages of propofol include the lack of
this device. Because LMAs do not interfere with laryn- analgesic properties and pain on injection. Regarding
geal function and glottic closure, an effective cough is the former, combining propofol with an opioid, such as
possible with this airway in place. remifentanil or fentanyl, provides analgesia. Discomfort
Aspiration of gastric contents has been reported associated with administration can be avoided by infu-
during LMA use. LMAs do not guarantee airway pro- sion into large veins and pretreatment with intravenous
tection. Elective insertion of LMAs is contraindicated lidocaine. Injecting lidocaine, 10–25 mg intravenously,
in patients who are at increased risk for aspiration. before administering propofol or adding lidocaine to the
However, LMAs are indicated in urgent or emergent propofol solution ameliorates or eliminates the discom-
situations when airway management proves to be diffi- fort in most patients. Addition of lidocaine to propofol
cult. Contraindications include oral pathology, low frequently produces clumping of the solution. There
pulmonary compliance, inadequate mouth opening, is concern that small clumps could act as pulmonary
and increased risk of aspiration. emboli.
Infectious hazards are associated with propofol use.
Propofol is composed of soybean oil and egg lecithins,
21. What is the role of propofol in ambulatory
which serve as an excellent culture medium for bacterial
surgery? growth. It is important to draw up the drug in an aseptic
Propofol may be used to provide sedation during re- fashion shortly before it is administered. Additionally, it
gional anesthesia, to induce general anesthesia, and to is imperative to discard the syringe after single patient
maintain general anesthesia. Propofol is a water-insolu- use. Repeated use of the same syringe throughout the day
ble, highly protein bound, lipophilic compound. It is for multiple patients has been associated with clusters of
rapidly redistributed, and hepatic and extrahepatic clear- bacterial septicemia.
ance (pulmonary) permit rapid recovery of cognitive
function. It provides reduced postoperative sedation and 22. What is total intravenous anesthesia, and what
drowsiness compared with traditionally employed ultra-
short-acting barbiturates. Depressant effects on the CNS are its advantages and disadvantages?
are dose dependent and range from mild sedation to TIVA is a technique in which bolus doses or continuous
unconsciousness. Neither retrograde nor antegrade am- infusions of intravenous anesthetic drugs are administered
nesia is associated with this drug. For induction of anes- for induction and maintenance of anesthesia (Box 73-1).
thesia, propofol can be administered as a bolus dose The various components of general anesthesia—hypnosis,
(2–2.5 mg/kg slowly), and its effect can be maintained via amnesia, analgesia, muscle relaxation—can be provided
continuous intravenous infusion (0.1–0.15 mg/kg/minute). individually and controlled by varying the rates of infu-
Dosages are reduced in debilitated and elderly patients. sion, influencing serum concentrations. The depth of an-
For sedation during regional anesthesia, incremental esthesia can be controlled in a similar manner to dialing in
doses of 10–20 mg (0.3 mg/kg) may be administered, or desired concentrations on a vaporizer.
an infusion can be started. There is a known relationship TIVA avoids the use of all gases with the exception
between propofol serum drug levels and therapeutic ef- of oxygen, compressed air, or helium. Contamination
fects. For propofol, the target concentration is 3–6 #g/mL of the operating room suite that invariably occurs
to provide surgical anesthesia. when using volatile agents, despite the use of scaven-
When administered as the sole agent, propofol may ger systems, may be eliminated entirely. Because non-
not provide amnesia 100% of the time, and intraopera- flammable gases may be employed, the technique is
tive awareness has been reported. It is often used in con- applicable to laser surgery. For procedures on the up-
junction with nitrous oxide, a volatile anesthetic, or per airway, TIVA is perfect for use with jet ventilation.
midazolam. Propofol has no muscle relaxant or analgesic Additionally, intravenous anesthesia does not depend
properties. For total intravenous anesthesia (TIVA), a on normal pulmonary function for wash-in or washout
continuous infusion of a short-acting opioid, such as of active agents.
384 SECTION 13 Ambulatory Anesthesia
Refinement of computer-assisted infusion systems 23. Define the term “moderate sedation”; when is it
allows anesthesiologists to achieve therapeutic blood
used, and what advantages does it offer over
concentrations of various anesthetic and sedative drugs.
Episodes of “light” anesthesia can be treated with bolus general anesthesia?
doses or increased infusion rates. Additional benefits Moderate sedation, previously known as conscious seda-
include rapid awakening at the conclusion of surgery tion, is a state of decreased consciousness, airway patency,
and reduced PONV in patients who receive propofol. intact gag reflexes, and ability to respond to verbal instruc-
Because few facilities are equipped to measure blood tions. When properly executed, moderate sedation pro-
concentration of intravenous anesthetics, a potential dis- vides anxiolysis, amnesia, safety, and comfort. Moderate
advantage of TIVA includes awareness during surgery. sedation is a valuable adjunct to properly placed local anes-
Alternatively, processed electroencephalography (EEG) thetic or regional anesthetic. Because interference with
is used to judge depth of CNS depression. The reliability short-term memory occurs, the patient experiences a mark-
of EEG is controversial. Each monitor uses a proprietary edly distorted perception of time. The anesthesiologist can
algorithm to analyze EEG data creating a linear score of increase a patient’s tolerance and acceptance of the discom-
0–100. A score of 0 usually denotes complete EEG sup- forts associated with an ongoing procedure by providing
pression, whereas a score of 100 usually correlates with encouragement and a sense of well-being and security. The
the awake unsedated state. Each monitor has its own goal is to allow the patient, anesthesiologist, and surgeon to
range of numbers that correlate with depth of anesthesia. communicate throughout the operative procedure.
These monitors are of questionable value. Moderate sedation is achieved by titration of intrave-
Traditionally, when a patient became hypertensive or nous agents administered by intermittent bolus injection
tachycardic intraoperatively, anesthesiologists would or continuous infusion. Because moderate sedation is
usually deepen the anesthetic. However, this change in part of a continuum, it is possible for moderate sedation
vital signs can be attributed to several causes. The most to progress to deep sedation or even general anesthesia.
common of these causes are “light” anesthesia, pain, and Propofol, midazolam, and remifentanil have pharmacoki-
essential hypertension. Increased heart rate and elevated netic properties that achieve these goals. These character-
blood pressure that are concomitant with a higher CNS istics include rapid onset, easy titration, and a relatively
monitor score are most likely due to “light” anesthesia. short duration of action, which allow for early recovery.
The appropriate response would be to deepen the anes- Benzodiazepines and opioids are combined frequently.
thesia with a bolus of propofol. If the monitor score This combination predisposes to respiratory depression
remains within the range for general anesthesia, the re- including apnea. Hypoxemia or apneic episodes have
sponse to increased heart rate and elevated blood pressure been demonstrated frequently when benzodiazepines and
would be to give an opioid for pain. The choice of opioid opioids are used together compared with either drug
would be either an ultra-short-acting opioid (e.g., remi- used alone. Supplemental oxygen should be provided via
fentanil) for a short-lived painful stimulus (e.g., esopha- mask or nasal cannula, and respiration should be carefully
goscopy) or a longer acting opioid (e.g., fentanyl) for a monitored.
persistent painful stimulus (e.g., incision). Present standards of care require monitoring heart
Whether or not it is cost-effective to use CNS moni- rate, blood pressure, respirations (via end-tidal carbon
tors on all patients has been heatedly debated in the dioxide), oxygen saturation, temperature, and ECG.
anesthesia community. Nasal cannulas are now available with a separate tube
73 Ambulatory Surgery 385
that can be attached to the sampling probe from a Although desflurane and isoflurane have similar mus-
capnograph, allowing for end-tidal carbon dioxide mon- cle relaxing properties, higher levels of desflurane can be
itoring. This monitoring is particularly useful during administered without concern about delayed emergence.
procedures where the anesthesiologist may be physically Times to ambulation and discharge with desflurane are
separated from the airway. similar to propofol, although patients anesthetized with
Although a patient may appear awake and fully recov- desflurane appear to be less sedated in the early postop-
ered at the end of surgery using this technique, vigilance erative period. However, nausea and vomiting were less
for respiratory depression must be maintained through- frequent with propofol.
out the postoperative period. In the PACU, hypercarbia Sevoflurane is odorless. It does not predispose to
or respiratory arrest may occur if the patient is left coughing and breath-holding on rapid inhalation induc-
unstimulated. tion. Its solubility in blood approaches that of nitrous
oxide. Fires have been reported when sevoflurane is used
in the presence of desiccated soda lime. Both sevoflurane
24. Can succinylcholine myalgias be avoided? and desflurane can provide sufficient muscle relaxation to
Disadvantages of succinylcholine include postoperative allow tracheal intubation. Both can trigger malignant
myalgias and the potential for malignant hyperthermia. hyperthermia.
Myalgias, which occur five times more commonly after
ambulatory surgery than after inpatient procedures, 27. What are the etiologies of nausea and vomiting,
sometimes may far outlast the discomforts associated and what measures can be taken to decrease the
with surgery. Muscle pains may vary in intensity from
mild to incapacitating and often develop on the first post- incidence and severity of nausea and vomiting?
operative day. There is no guaranteed way to eliminate PONV remains a significant problem in patients who
the succinylcholine myalgias. However, pretreatment receive either general anesthesia or intravenous seda-
with 1 mg of a nondepolarizing neuromuscular blocker, tion. PONV is among the most commonly reported
such as vecuronium, may ameliorate fasciculations and complications associated with ambulatory surgery, and
associated myalgias. hospitalization following an ambulatory procedure is
often attributable to it. Persistent and severe retching or
vomiting can disrupt surgical repairs and increase bleed-
25. Can a relative overdose of benzodiazepine be
ing. PONV can lead to dehydration and electrolyte im-
safely treated with an antagonist? balances. Some degree of nausea or frank vomiting can
Flumazenil is an intravenously administered competitive be expected to occur in 10%–40% of patients who have
benzodiazepine receptor antagonist at specific benzodi- not received antiemetic prophylaxis. The incidence of
azepine binding sites in the CNS. It can be titrated to PONV depends on the type of surgical procedure per-
obtain the desired degree of benzodiazepine antagonism formed and the anesthetic administered. It has been
as evidenced by patient arousal. Midazolam has varying demonstrated that patients undergoing laparoscopy have
effects at different dosages. At small doses, it is anxiolytic. a 35% incidence of nausea and vomiting; manipulation
Increasing the dose administered increases the amount of of abdominal viscera, retained intraperitoneal carbon
sedation encountered. Larger doses induce hypnosis dioxide, and use of electrocautery are potential causes.
(sleep). Careful titration of flumazenil may allow partial Symptoms occur regardless of whether a general anes-
antagonism of excessive benzodiazepine effect. thetic or epidural technique is employed. Arthroscopic
When contemplating the use of any reversal agent in surgical procedures are associated with a much lower
the setting of ambulatory surgery, it is important to re- incidence of symptoms than laparoscopic surgeries or
member that the duration of action of both flumazenil and ovum retrievals.
naloxone (to reverse opioids) is short-lived. Additional The cause of PONV is multifactorial (Box 73-2). Obe-
patient observation before PACU discharge is required sity, sudden movement or changes in patient position, his-
whenever these agents have been administered. tory of motion sickness, postoperative hypotension, female
gender, days 4 and 5 of the menstrual cycle, pain, opioid
administration, anesthetic technique used, and site of
26. Do newer volatile agents offer advantages over
surgery all contribute to these symptoms. They are often
older agents? disquieting and sometimes incapacitating. Physical mea-
Two volatile anesthetic agents, desflurane and sevoflu- sures and pharmacologic agents have been employed in
rane, both ethers, have been extensively used in clinical attempts to reduce the incidence of PONV. Examples
practice. Desflurane is a clear nonflammable liquid that is include intraoperative gastric suctioning to remove stom-
extremely insoluble and requires a specially designed, ach contents and limiting positive pressure during mask
heated vaporizer for administration. The gas has an odor ventilation to reduce the potential for gastric dilation.
and is an airway irritant. It can produce coughing, Multiple studies have both implicated and exonerated
breath-holding, and laryngospasm; its use as an inhala- nitrous oxide. It is unlikely that this gas plays a major role in
tion induction agent is precluded. Its major advantage is influencing the presence or absence of nausea in the postop-
low blood and tissue solubility, which allows for fast erative period. However, induction agents do influence the
emergence compared with currently available volatile incidence of postoperative symptoms. Etomidate and ket-
agents. Low solubility properties also allow rapid titra- amine are associated with a much higher incidence of these
tion of anesthetic depth. symptoms compared with thiopental. General anesthesia
386 SECTION 13 Ambulatory Anesthesia
BOX 73-2 Factors Associated with TABLE 73-2 Prophylaxis and Treatment
Postoperative Nausea and Vomiting of Postoperative Nausea and
Vomiting
ASSOCIATED CONDITIONS
• Obesity Dosage and Route
• Pregnancy Class and Drug of Administration
• History of motion sickness Droperidol 0.0625-0.125 mg IV
• History of previous postoperative vomiting
• Recent ingestion of food Phenothiazines 5–10 mg/70 kg IV/IM
• Anxiety Prochlorperazine
• Female gender Steroid 4–10 mg IV in adults
• Day 4–5 of menstrual cycle Dexamethasone 150 #g/kg
• Diabetes mellitus
Serotonin antagonists 1–4 mg/40–80 kg IV in adults;
• Age (uncommon !3 years of age) Ondansetron 0.1 mg/kg in children
SURGICAL PROCEDURE Sympathomimetics 10–25 mg/70 kg IV/IM
• Strabismus correction Ephedrine
• Laparoscopy Anticholinergics Releases 1.5 mg over
• Dilation and curettage Scopolamine patch 3 days transdermally
• Orchiopexy
• Varicocelectomy IM, Intramuscularly; IV, intravenously.
• Ear surgery
ANESTHESIA-RELATED
form is approved by the FDA for prophylaxis and treat-
• Etomidate and ketamine & thiobarbiturates & propofol
ment of PONV associated with general anesthesia. An
• Opioid/N2O/relaxant & than volatile anesthetic & propofol
• Intraoperative and postoperative opioids oral formulation is also available. It has been demon-
• Positive-pressure mask ventilation forcing air into the strated that a combination of agents, perhaps in conjunc-
gastrointestinal tract tion with propofol, may be most efficacious in the
• Anticholinesterases prophylaxis of PONV. Prophylactic administration of
dexamethasone, 4–10 mg intravenously, at the beginning
MISCELLANEOUS of the procedure in conjunction with ondansetron has
• Blood entering gastrointestinal tract during surgery also been shown to be efficacious in preventing PONV.
• Uncontrolled pain Droperidol has long been used as an antiemetic. Its
• Rapid changes in positioning or during rapid transport on use fell out of favor after a “black box” warning from the
stretcher
FDA was issued. Concern arose over the potential for
• Early ambulation and oral intake
• Systemic hypotension arrhythmias in patients with prolonged QT intervals.
• Vasovagal episode However, it can still be used as long as continuous ECG
monitoring is employed.
N2O, Nitrous oxide. Transdermal scopolamine, proven earlier to prevent
motion sickness, has been studied for the prevention of
induced and maintained with propofol is associated with the PONV. Although effective in reducing symptoms when
least number of episodes of PONV. applied before surgery, significant side effects, including
Adequate hydration must be ensured during the opera- dry mouth, sedation, dysphoria, and urinary retention,
tive period and maintained in the PACU. To avoid epi- may occur. It is often reserved for preoperative use in
sodes of PONV, it is recommended to hydrate intraop- patients who have a strong history of motion sickness. In
eratively with at least 15–20 mL/kg of crystalloid solutions pediatric patients, the incidence of visual disturbances
and to avoid pushing oral fluids and food postoperatively. and hallucinations after application of the patch is in-
Intravenous fluid repletion allows oral fluids to be offered creased. Some clinicians have placed the patch before
sparingly. Solids should be withheld until the patient ex- PACU discharge in patients whose nausea has not com-
presses hunger. In addition, postponing early ambulation pletely resolved. However, the patch should be avoided
may help to reduce symptoms. in elderly patients, pregnant patients, patients who are
Many drugs are helpful in the prevention of PONV lactating, and patients with glaucoma.
(Table 73-2). Most authors recommend treating patients Ephedrine has been used in the treatment of PONV
with a multimodal approach. This would require using in the PACU. Hypotension or documented postural
different drugs from different pharmacologic groups. hypotension in the postoperative period is often due to
Popular drugs in the anesthesiologist’s armamentarium intravascular volume deficits and should be ruled out.
against PONV are the serotonin receptor antagonists, Treatment consists of crystalloid infusion to correct he-
ondansetron and granisetron. They do not appear to modynamic instability. Ephedrine has been shown to be
affect awakening from general anesthesia and have no useful in patients whose symptoms are causally related to
extrapyramidal effects or sedative qualities. Ondansetron assuming the upright position. Ephedrine, 0.5 mg/kg
appears to offer improved control over nausea and vomit- given intramuscularly, has been used in patients under-
ing. The effective dose is 2–4 mg intravenously and has a going laparoscopy with some success. Patients who re-
duration of action of up to 24 hours. The intravenous ceived ephedrine also had lower sedation scores, and no
73 Ambulatory Surgery 387
differences in mean arterial blood pressure were noted. Ketorolac, a NSAID, has been administered orally, in-
It may be indicated in otherwise healthy patients who tramuscularly, and intravenously in an attempt to prevent
have a history of motion sickness or in patients who ex- and relieve pain and reduce opioid requirements. The
perience dizziness, nausea, or vomiting when attempting drug itself is free of opioid-related side effects, including
to ambulate in the postoperative period. sedation, respiratory depression, and vomiting. Some cli-
Many surgical centers have abandoned the routine nicians are hesitant to employ this class of drugs because
administration of prophylactic antiemetics to every of their potential for bleeding. When administered orally,
patient. However, the authors recommend antiemetics gastric irritation may be encountered. Cyclooxygenase-2
for specific surgical procedures, such as strabismus re- inhibitors minimize the potential for postoperative bleed-
pair or laparoscopic surgery, that are associated with ing and the risk of gastrointestinal complications and are
high incidences of PONV. becoming popular as a nonopioid adjuvant for treating
Sometimes simply relieving postoperative pain may al- postoperative pain.
leviate nausea. The use of acupuncture has been reported
in some studies to be effective, but its use is not wide- 29. What discharge criteria must be met before a
spread. A propofol-based anesthetic is associated with
fewer emetic symptoms, earlier ability to tolerate oral
patient may leave the ambulatory surgery center?
alimentation, and shorter stays in the PACU compared Patients who have received a peripheral nerve block (e.g.,
with induction with a thiobarbiturate and maintenance ankle block, brachial plexus block) may be discharged
with isoflurane. Despite careful anesthetic management despite the persistence of residual anesthesia or paresthe-
including propofol and prophylactic medication, PONV sias. The effected limb should be protected from harm
still remains a problem. with either a sling, in the case of an upper extremity, or
a bulky dressing, in the case of a lower extremity. The
patient needs to be reminded that the block will dissipate
28. How is postoperative pain best controlled in
in time, and discomfort will occur. For this reason, dis-
ambulatory surgery patients? charge instructions should include recommendations to
Management of postoperative pain in the PACU and take the prescribed oral analgesic medication at the first
after discharge is of major concern to the anesthesiologist. sign of discomfort because pain is most readily treated
One important goal is to achieve adequate pain relief before it becomes excruciating.
before discharge. Prevention of postoperative pain ap- Patients who received an epidural or spinal anesthetic
pears to be much easier to accomplish than treatment of can be discharged only when full motor, sensory, and
pain that has been allowed to reach significant intensity. sympathetic function has returned. Patients should dem-
Inadequate postoperative analgesia remains a cause of onstrate the ability to void because this provides evidence
unexpected overnight hospitalization. that residual sympathetic blockade has dissipated. Before
For procedures that are expected to result in significant attempting to ambulate, it is essential to ensure that all
postoperative discomfort, addition of an opioid or a non- motor block has resolved.
steroidal antiinflammatory drug (NSAID), or both, as part Patients who have received general anesthesia may
of the anesthetic is helpful. Propofol does not provide awaken either in the operating room or shortly after
postoperative analgesia. Intraoperative administration of transfer to the PACU. Although the patient may appear
long-acting local anesthetics, such as bupivacaine or ropi- to be lucid and oriented, numerous criteria must be satis-
vacaine, at the surgical site may provide hours of postop- fied before a patient may be considered ready for dis-
erative pain relief. This technique has proven to be most charge from the facility (Box 73-3). Restoration of vital
efficacious after inguinal and umbilical hernia repairs. signs within 15%–20% of the preoperative baseline is
In the PACU, careful titration of small intravenous ordinarily required. Patients should demonstrate an in-
doses of opioids can safely provide satisfactory analgesia. tact gag reflex and the ability to cough effectively and
Blood levels of opioids that provide analgesia are less than swallow liquids without difficulty. It is not necessary for
the levels that usually result in significant respiratory de- patients to eat before discharge. Forcing patients to in-
pression or marked oversedation. Fentanyl is the narcotic gest unwanted food in the absence of hunger may serve
of choice for treating pain in the postoperative period. Its to increase the incidence of PONV. Patients ordinarily
duration of action is modest, and intravenous doses of 25– are asked to demonstrate the ability to tolerate a small
50 #g may be repeated every 5 minutes until satisfactory amount of liquid by mouth. If a patient experiences mild
pain relief has been achieved. Medicating patients with oral nausea and has been unable to ingest more than a few sips
opioid preparations before discharge provides a more com- without vomiting or increased nausea, it is foolish to
fortable trip home because the intravenous drugs adminis- persist. Discharge can still be considered if there is con-
tered in the PACU have relatively short durations of action. tinued inability to tolerate fluids, if written instructions
Home patient-controlled analgesia systems permit dis- are provided regarding steps to be taken (e.g., contact
charging patients who are expected to experience pain that facility or surgeon). It is important to ensure that a nor-
may not be sufficiently controlled with oral agents. Experi- mal state of hydration has been achieved before dis-
ments with patient-controlled analgesia in the home have charge; this is especially important after surgery in the
found this modality to be both safe and effective. Oxyco- oral cavity, where postoperative pain may preclude early
done and codeine are suitable for amelioration of mild to oral intake.
moderate pain but are not strong enough to prevent hospi- Unless the patient was previously unable to walk or
talization in a patient who experiences severe pain. the procedure performed precludes ambulation, patients
388 SECTION 13 Ambulatory Anesthesia
BOX 73-3 Guidelines for Safe Discharge after BOX 73-4 Functions of the Escort
Same-Day Surgery in Ambulatory Surgery
Stable vital signs every 15 minutes ' 4 Provide translation when patient speaks a foreign language
Oriented to time, place, and person (or returned to Receive and comprehend postoperative instructions
preoperative status) Accompany patient during transport home
Capable of walking with minimal assistance (consider Serve as companion to patient during the first 24 hours
preoperative status) after completion of surgery and assist in performing
Tolerable nausea and no active vomiting activities of daily living
Adequate pain control Remain available to summon assistance in the event of a
Good hemostasis medical, surgical, or anesthetic complication
Responsible adult present to accompany patient home
Able to tolerate oral fluids (optional)
Able to void
After gynecologic, genitourinary, groin, and perineal
procedures a responsible adult. Current definitions of “responsible
After epidural and spinal anesthetics adult” vary and may be broadened to include emanci-
pated minors or responsible older children. Ideally,
companions should remain with patients for at least 24
hours after surgery; this is especially important in the
should be able to walk with assistance and without expe- case of geriatric and debilitated patients. Problems may
riencing dizziness. If crutches are required, it should not arise when impaired patients are discharged in the com-
be assumed that the patient received preoperative in- pany of impaired escorts. Preferably, two adults should
struction and additional instruction should be offered. accompany pediatric patients home. After discharge, a
Hemostasis should be present at the surgical site, and child may suddenly experience nausea, vomiting, pain,
control of pain should be satisfactory. The preoperative fright, or disorientation. An escort who is driving a car
level of orientation should be achieved, although a mild cannot possibly pay attention to both child and traffic
degree of residual sedation is acceptable. simultaneously.
It is not essential for patients to urinate, unless genito- A clear distinction is made between “home readi-
urinary, gynecologic, or other surgery has been per- ness” and “street fitness.” “Home readiness” signals
formed in the inguinal or perineal region. Patients and that the time has arrived to discharge the patient from
escorts should be instructed to contact either the ambula- the PACU. “Street fitness” is attained after approxi-
tory facility or the surgeon if the patient has not voided mately 24 hours have elapsed, when most of the more
within 6 hours after PACU discharge. subtle and persistent CNS effects of general anesthesia
Validated postanesthesia discharge scoring systems have dissipated. Patients must be advised not to re-
have been proposed and developed for the purpose of sume normal activities immediately on returning
assessing when home readiness is achieved in the postop- home.
erative period. Criteria such as mental status, pain inten- Formal discharge criteria must be in place, and final
sity, ability to ambulate, and stability of vital signs are evaluations should be conducted immediately before a
given numeric values. A total score above a particular patient’s discharge from the PACU. All perturbations
number may indicate a high likelihood of readiness for from normal, including vital signs and unusual symp-
discharge. To be practical, a scoring system must be easily toms, can be addressed.
understood, simple to employ, and objective. Sophisti- Every attempt must be made to avoid premature dis-
cated pen-and-paper and neuropsychological tests to as- charge of the patient from the PACU. The consequences
sess recovery from anesthesia are reserved solely for of such faulty judgments may include the necessity for
research purposes. After stability in vital signs is achieved, emergency care elsewhere and possible readmission to
the ability to walk and urinate may be the best measures another health care facility. When any element of doubt
of a gross recovery from anesthesia and readiness for exists as to the stability or suitability of a patient for
discharge. These activities indicate return of motor discharge, the better part of valor is to arrange for hos-
strength, CNS functioning, and restoration of sympa- pital admission for overnight observation.
thetic tone.
Patients and escorts should receive detailed, written 30. What are the causes of unexpected
discharge instructions regarding activity, medications,
dressing care, and bathing restrictions. Instructions must
hospitalization after ambulatory surgery?
be reviewed verbally with patients and escorts. Both must Although a patient may be scheduled to return home
be advised to contact the facility in the event of untoward after surgery, admission may be required for a host
reactions or difficulties, such as bleeding, headache, of reasons. Approximately one quarter of unexpected
severe pain, or unrelenting nausea and vomiting. Most admissions after surgery are anesthesia related. The
postoperative complications occur after discharge. It is remainder result from either medical or surgical com-
important to ensure comprehension of all information by plicating factors (Box 73-5). Most ASCs experience an
the patient or designated escort (Box 73-4). unexpected hospital admission rate ranging from
Most states mandate that patients who received other !1% to approximately 4%. Unexpected hospitaliza-
than a local anesthetic be discharged in the company of tion is greater after general anesthesia than after local
73 Ambulatory Surgery 389
BOX 73-5 Reasons for Hospitalization after 32. What is the role of aftercare centers for
Ambulatory Surgery ambulatory surgery patients?
SURGICAL CAUSES Patients may experience significant postoperative pain
• Improper designation as ambulatory surgery instead of after some surgical procedures that cannot be readily con-
day-of-admission surgery trolled with oral opioids. Additionally, although they may
• Surgery extended beyond anticipated procedure require some skilled nursing observation or specialized
• Surgical complication necessitating return to surgery or care, these may be accomplished outside the setting of an
further observation acute care hospital both at lower cost and with greater
• Major intraoperative or postoperative hemorrhage comfort for the patient and family. With this in mind, the
• Additional follow-up surgical or diagnostic procedure concept of a recovery care facility was born, creating a
planned new category of inpatient postsurgical care. This health
MEDICAL REASONS care model integrates ambulatory surgery with overnight
or extended care outside of a hospital. Examples of ap-
• Poorly controlled concomitant medical condition
• Requirement for intravenous antibiotic therapy plicable procedures include hysterectomy, cholecystec-
tomy via laparotomy, shoulder repairs, and mastectomies.
ANESTHESIA-RELATED If this type of facility is unavailable, appropriate use of
• Unrelenting nausea or vomiting home care services including newer modalities of pain
• Aspiration pneumonitis control may still allow patients to avoid inpatient postop-
• Lethargy and lassitude erative care.
• Uncontrollable pain
MISCELLANEOUS FACTORS 33. Are quality assurance and continuous quality
• Patient refuses to leave for home improvement possible for ambulatory surgery?
• Surgeon requests overnight observation or additional
tests To ensure quality as well as patient satisfaction, follow-up
• No escort or suitable person to care for patient at home telephone calls by an anesthesia care team member should
be made on the first postoperative day. Some facilities
make two additional calls, one on the evening of surgery
and another call 1 week after surgery. Postage-paid post-
or regional anesthesia. As might be anticipated, the cards may be sent to patients requesting information on
addition of intravenous sedation to a local anesthetic the overall experience and specific areas of care. Space
increases the complication rate. Nausea, vomiting, may be allocated for the patient to note side effects or
dizziness, bronchospasm, and delayed emergence adverse occurrences. Depending on surgeons to provide
from anesthesia are common causes of anesthesia-re- accurate feedback regarding complications is unreliable. A
lated hospital admissions. mechanism for follow-up must be in place to uncover and
identify patterns that require remedial action.
31. When may patients operate a motor vehicle after
receiving general anesthesia? SUGGESTED READINGS
American Society of Anesthesiologists: Continuum of depth of sedation:
Current recommendations are to refrain from operating definition of general anesthesia and levels of sedation analgesia. 2004.
heavy machinery including driving a car for approxi- www.asahq.org/publicationsAndServices/standards/20.pdf
mately 24–48 hours after general anesthesia or intrave- Gan TJ, Meyer TA, Apfel CC, et al.: Society for Ambulatory Anesthesia
nous sedation. Although a patient may feel completely guidelines for the management of postoperative nausea and vomiting.
recovered and appear that way to others, subtle psycho- Anesth Analg 105:1615, 2007.
Gan TJ, Sinha AC, Kovac AL, et al.: A randomized, double-blinded,
motor disturbances and cognitive deficiencies may per- multicenter trial comparing transdermal scopolamine plus ondanse-
sist postoperatively. Important decision making and tron to ondansetron alone for the prevention of postoperative nausea
activities requiring fine motor coordination should be and vomiting in the outpatient setting. Anesth Analg 108:1498, 2009.
postponed until after the first postoperative day. Despite Matthews DM, Gaba V, Zaku B, et al.: Can remifentanil replace nitrous
oxide during anesthesia for ambulatory orthopedic surgery with
admonitions to the contrary, surveys have revealed that desflurane and fentanyl? Anesth Analg 106:101, 2008.
some patients drive their automobiles within 24 hours Sebel PS, Bowdle TA, Ghoneim MM, et al.: The incidence of awareness
after surgery, and some may even drive home from the during anesthesia: a multicenter United States study. Anesth Analg
facility. 99:833, 2004.
As a result of CNS derangements or the surgery itself, Tang J, White PF, Wender RH, et al.: Fast-track office-based anesthe-
sia: a comparison of propofol versus desflurane with antiemetic
patients may experience minor slips or even major falls prophylaxis in spontaneously breathing patients. Anesth Analg
after discharge. Some of these events could be related to 92:95, 2001.
confusion or subtle alterations in mental state. Others White PF, Rawal S, Nguyen J, et al.: PACU fast-tracking: an alternative
may be due to dizziness or pain. It is hoped that anes- to “bypassing” the PACU for facilitating the recovery process after
ambulatory surgery. J Perianesth Nurs 18:247, 2003.
thetic agents of the future will be free of the prolonged White PF, Song D: New criteria for fast-tracking after outpatient anes-
and potentially hazardous CNS dysfunction seen with thesia: a comparison with the modified Aldrete’s scoring system.
currently available drugs. Anesth Analg 88:1069, 1999.
CASE 74
Office-Based Anesthesia
Isabelle deLeon, MD • Laurence M. Hausman, MD
QUESTIONS
A 25-year-old woman presents for liposuction of the procedures to be performed safely and effectively in this
abdomen, thighs, hips, flanks, and back in the surgeon’s setting.
office. She stands 62 inches (167 cm) tall and weighs There are unique advantages for surgeons and proce-
176 lb (80 kg). She denies any medical problems but re- duralists and patients in this type of practice. Economi-
ports snoring at night. Her only medication is an oral cally, it is advantageous because the cost is significantly
contraceptive, and she has not had any previous surgery. less compared with the hospital setting. This difference
Anesthetic evaluation reveals an obese woman with a in cost is mainly due to the high overhead costs associ-
Mallampati class 3 airway. ated with hospital facility fees, which include hospital
maintenance, equipment, and staff, all of which consti-
1. What is office-based anesthesia? tutes a large component of the patient’s overall procedure
fee. In the office, this fee can be easily predicted and is
Office-based anesthesia (OBA) is defined as the “provi- often minimal compared with the hospital or an ASC.
sion of anesthesia services in an operatory or a procedure The cost savings can be passed on to the patient. In the
room that is specifically not licensed as an ambulatory interest of cost containment, insurance companies began
surgery center (ASC) by the state in which it operates offering incentives to surgeons to use their office loca-
and which is integrated into the day to day operations of tions. This venue also allows for greater surgeon and
a doctor’s office” (Koch et al. 2003). Historically, one of patient satisfaction. Scheduling is much easier in the of-
the earliest references to OBA dates back more than a fice setting. For surgeons, an office-based practice can
century ago, when Long used ether to anesthetize his eliminate much of the unproductive time associated with
patient successfully to remove a neck tumor. Since then, long operating room turnovers, patient preparation, and
the practice of OBA has changed dramatically. More driving between sites. Office-based surgery allows sur-
recent advances in surgical technology and equipment, geons to perform nonsurgical duties such as patient
along with improved anesthetic techniques and drugs consultations and follow-up examinations more easily.
have made this venue appropriate for a very wide array For patients, office-based surgery is an attractive and
of surgeries and procedures previously suitable only for convenient alternative to hospitals. It offers patients a
hospitals or ASCs. It is estimated that 10 million proce- more private and less stressful environment. There is
dures are performed in offices annually. Although many better continuity of care because staffing in the office
surgical specialties presently use this unique venue, cos- is more consistent. Exposure to nosocomial infections is
metic surgery in particular has seen a tremendous in- also diminished.
crease in volume. According to the American Society However, there are numerous potential disadvantages
of Plastic Surgeons, 37% of cosmetic procedures and to OBA. Office-based practices were once labeled as the
28% of reconstructive procedures are performed in the “wild, wild, west of health care,” with issues regarding
office-based setting. standard of care and patient safety in the office-based
practice not always being met. Most OBA practices have
2. What are the advantages and disadvantages little or no oversight by local, state, or federal govern-
of office-based anesthesia? ments regarding certification and qualification of either
surgeons or anesthesiologists, peer review, performance
OBA continues to increase in popularity for numerous improvement, documentation, general policies and pro-
reasons. Surgical and anesthesia techniques and available cedures, and reporting of adverse outcomes. At the
pharmaceuticals continue to improve. These advances present time, many states have placed regulations on
have allowed for more complex and minimally invasive office-based practices. However, these regulations vary
390
74 Office-Based Anesthesia 391
from state to state. Other states are steadily moving for- the physician must have admitting privileges and an
ward and have issued guidelines or policy statements. emergency transfer agreement with a nearby hospital.
Because of anesthesiologists’ role as patient safety advo- The facility and the physician must also have adequate
cates, it is incumbent on them to insist that the standard liability insurance.
of care achieved in hospitals or ASCs is the same in every
office in which surgery and anesthesia are performed. Office
Health care providers who wish to practice in this setting
should take advantage of the office-based surgery patient The office must be a safe location no matter where it is.
safety guidelines and recommendations published by a As previously stated, the standard of care in the office
variety of professional societies and accrediting organiza- should be no less than that of a hospital or ASC. The of-
tions. The American Society of Anesthesiologists (ASA) fice must be appropriately stocked with age-appropriate
created “Guidelines for Office-Based Anesthesia,” last and size-appropriate equipment and supplies. All equip-
affirmed on October 2009. ment must be regularly serviced and calibrated with
Another disadvantage of office-based practice is the documentation according to manufacturers’ suggestions.
limited resources available. Resources often taken for There must be a functioning waste gas scavenging sys-
granted in the hospital, such as immediate availability of tem if inhaled agents or nitrous oxide are used. An ad-
colleagues, other skilled nurses, laboratory services, and equate supply of compressed oxygen and backup supply
specialized equipment, are sparse or nonexistent. It is of for use in an emergency must be present. ASA standards
utmost importance that we ensure that the standards of for basic anesthetic monitoring must be implemented.
practice in the office, whether it is accredited or not, These include electrocardiography, noninvasive blood
meet those of the hospital or ASC to provide patients pressure, pulse oximetry, end-tidal carbon dioxide mon-
with a safe office environment. itoring, and temperature monitoring. Monitors must
be routinely serviced and should have backup battery
3. Discuss the important issues for consideration supply. All advanced cardiopulmonary life support
emergency drugs should be available, including dan-
when setting up a safe office-based practice.
trolene if malignant hyperthermia triggering agents are
There is only one way to practice medicine, and that is the used. A cardiac defibrillator with a battery backup must
safe way. In office-based practice, where surgeries and pro- be immediately available, visible, and routinely checked.
cedures are performed in an elective manner, patient safety A source of suction, including a pharyngeal catheter,
must never be compromised. Considerable consumer and must be present.
physician pressures come into play in this setting. It is of Administrative issues, such as facility and personnel
utmost importance that anesthesiologists do not succumb credentialing, development of policy and procedures
to these pressures. We must always make sure that the manual, performance improvement, emergency and in-
standard of care in an office practice is no less than that of fection control protocols, and documentation, should be
a hospital or ASC. Our level of vigilance should even be addressed as well.
heightened in this venue because we are often alone, and
resources we take for granted are limited. Patient
There are many elements that need to be carefully
considered for an office-based practice. Diligent and Appropriate patient selection is a very important aspect
careful assessment of the physician or proceduralist, the of safe OBA. Patient selection is controversial among
physical office space, the patient’s comorbidities, and office-based practitioners because there are very few
the anticipated procedure is paramount. The ASA for- data to support the inclusion or exclusion of specific
mulated “Guidelines for Non-Operating Room Anes- patient populations. The ASA “Guidelines for Office-
thetizing Locations,” “Guidelines for Office-Based An- Based Anesthesia” reads, “Patient who by reason of
esthesia,” and “Considerations for the Anesthesiologist pre-existing medical or other conditions may be at
in the Office-Based Settings,” which should be referred undue risk for complications should be referred to an
to by practitioners who are considering office-based appropriate facility for performance of the procedure
practice for guidance. and the administration of anesthesia” (American Society
of Anesthesiologists, www.asahq.org) This statement
leaves much room for interpretation. The anesthesiol-
Physician
ogist must evaluate the patient’s risk for OBA on an
The surgeon or proceduralist (e.g., gastroenterologist) individual basis.
must have the necessary and updated licensing and Determination of a patient’s suitability for OBA
credentialing information, such as medical license, reg- begins with a thorough preoperative history and phys-
istration, and Drug Enforcement Agency certificate. ical examination. Coexisting medical conditions that
The physician must be adequately trained, and board could potentially complicate the surgical procedure
certification or eligibility by the American Board of and anesthetic management must be identified. Who-
Medical Specialties is preferable. The physician should ever examines the patient preoperatively should be
have privileges to perform the proposed procedure in a familiar with the ASA physical status classifications
hospital or have training and documented competency. and implications. The American Society of Plastic
The physician should participate in peer and quality Surgeons (ASPS) and ASA have made similar recom-
review and continuing medical education. In addition, mendations that patients who are assigned an ASA
392 SECTION 13 Ambulatory Anesthesia
physical status I or II are “reasonable candidates for bleeding, which warrant hospital admission. For these
the office-based surgery setting.” The ASPS recom- reasons, it is recommended that office-based procedures
mends that ASA physical status III patients “may also should be limited to 6 hours and should be completed by
be reasonable candidates for office-based surgery fa- 3 p.m. to ensure adequate recovery time. Many surgeons
cilities when local anesthesia, with or without seda- circumvent this issue by giving their patients the option
tion,” is used. However, the ASA recommends that
patients should be evaluated by the anesthesiologist
before the day of surgery to determine their suitability BOX 74-2 Commonly Performed
for office-based surgery and anesthesia. It is impera- Office-Based Procedures
tive to consider all comorbidities when determining
patient suitability. There must be clear communication COSMETIC
between the surgeon and the anesthesia provider re- Body
garding this matter. The anesthesia provider must not Liposuction
succumb to physician and patient demands. The deci- Breast augmentation, breast reduction, mastopexy
sion regarding the patient’s clearance for anesthesia Abdominoplasty
Arm/leg lift
ultimately depends on the anesthesiologist. The ASA
Face
has also provided a list of specific patient factors that Facelift
should be taken into consideration before performing Blepharoplasty
OBA. These factors include the following: Rhinoplasty
• Known or suspected difficult airway Meloplasty
• Previous anesthetic or surgical problem Mentoplasty
• Drug allergies that are of perioperative concern Buccal fat extraction
• Substance abuse disorders including alcoholism Brow lift
• Social situation that precludes having a responsible Facial resurfacing (including laser)
adult escort GASTROINTESTINAL ENDOSCOPY
Box 74-1 lists patients that may be excluded from OBA. Upper/lower endoscopy (colonoscopy)
DENTISTRY AND ORAL AND MAXILLOFACIAL SURGERY
Procedure
Tooth (especially wisdom) extraction
A wide array of surgeries and procedures are performed in Pediatric dentistry
the office-based setting. As newer surgical techniques and ORTHOPEDICS AND PODIATRY
equipment have evolved, longer and more invasive opera-
Arthroscopy (knee, shoulder, and elbow)
tions are being performed successfully in the office. Suit-
Wrist, hand, and foot surgery
able office-based surgeries range from simple incisional
biopsies to minilaparoscopies (Box 74-2). The anesthesi- GYNECOLOGY
ologist should be medically comfortable and satisfied that Dilation and curettage
the procedure to be performed is within the scope of the Hysteroscopy
practice of the surgeon and the capabilities of the office. Mini-laparotomy
As with patient selection, there is also very little, if any, Endometrial ablation
conclusive scientific data to exclude specific procedures Ovum retrieval
from this venue. Duration of procedure has long been UROLOGY
correlated with the need for hospital admission. Longer Vasectomy
procedures and longer anesthetic times are often associ- Cystoscopy
ated with postoperative nausea and vomiting, pain, and Prostate biopsy
Laser resection
Lithotripsy/extracorporeal shock wave lithotripsy
OPHTHALMOLOGY
BOX 74-1 Patients Excluded from Cataract extraction
Office-Based Anesthesia Lacrimal duct probing
Ophthalmoplasty
ASA III and IV with poorly controlled:
Diabetes OTOLARYNGOLOGY
Hypertension Endoscopic sinus surgery
Coronary artery disease Turbinate resection
Chronic obstructive pulmonary disease Septoplasty
Obesity—BMI !35 Myringotomy
Obstructive sleep apnea
Suspicion of difficult airway VASCULAR
Malignant hyperthermia susceptible Vein stripping
History of substance abuse
History of seizure disorder PAIN
No escort Injections
Latex allergy? Radiofrequency ablation
74 Office-Based Anesthesia 393
to stay overnight in their office recovery room with a plied in the office setting. The type of anesthesia should
registered recovery room nurse. In addition, surgeries be appropriate to the patient’s overall health status and
that involve or might result in excessive blood loss, sig- surgical procedure. It should allow for rapid emergence
nificant fluid shifts, or hypothermia are not appropriate and discharge, with minimal postoperative pain and nau-
office-based surgeries. Ultimately, the patient’s overall sea. Anesthetic techniques for office-based surgery range
medical status and anticipated perioperative course is from local infiltration, with or without intravenous seda-
crucial in determining the appropriateness of a planned tion (monitored anesthesia care) to regional and general
procedure in this setting. What is considered an appro- anesthesia.
priate office-based surgery for one patient may not be Monitored anesthesia care with intravenous sedation
acceptable for another. is the most common anesthetic technique used in the
office setting. A combination of agents that provide
4. In what ways is morbid obesity a challenge to an rapid onset and fast recovery (e.g., propofol and remi-
fentanil) with local anesthetic infiltration of the surgical
office-based anesthesiologist?
site provides excellent intraoperative analgesia and re-
Morbidly obese patients present unique challenges to duces the need for postoperative opioid use. Other
anesthesiologists, and this is especially true in the office- agents commonly employed are midazolam and ket-
based setting, where resources are limited. There is only amine. However, with this technique, the anesthesia
one anesthesia provider. Anesthesia colleagues, resi- provider must be able to deepen the level of anesthesia
dents, or certified registered nurse anesthetists are not if necessary and still be able to rescue the patient from
available to assist in case of an airway emergency. Some a deep level of sedation, if indicated. It is prudent to
emergency airway equipment (e.g., fiberoptic scope, have all the necessary equipment and drugs to convert
videolaryngoscope) may be unavailable. monitored anesthesia care anesthesia to general anes-
Morbidly obese patients have associated comor- thesia at any given time.
bidities that put them at risk during the perioperative As the complexity and duration of surgical proce-
period and that are of particular concern in the office- dures performed in the office setting continue to
based setting. They are usually considered at in- evolve, the use of general anesthesia has increased.
creased risk for aspiration and require rapid-sequence With the advent of total intravenous anesthesia (TIVA)
induction for general anesthesia. Because of numer- techniques, general anesthesia can be achieved without
ous physiologic parameters, these patients may be the need of an anesthesia machine and a waste gas
difficult to intubate or ventilate. An ominous situation scavenging system. TIVA also avoids the use of agents
is created where help is sparse and backup equipment that trigger malignant hyperthermia. TIVA generally
is unavailable. consists of a mixture of propofol and an opioid, with
The option of providing monitored anesthesia care spontaneous or assisted ventilation either with or
with moderate to deep sedation for morbidly obese without a laryngeal mask airway or endotracheal tube.
patients is inadvisable because attempts at sedation Another TIVA combination includes propofol and
may quickly convert to general anesthesia and result in ketamine.
loss of airway reflexes. These patients may have ob- Regional anesthesia, such as central neuraxial blocks
structive sleep apnea and are likely to have increased (e.g., spinal, epidural) and peripheral nerve blocks (e.g.,
sensitivity to the effects of anesthesia and opioids. brachial plexus, femoral, ankle) is a useful anesthetic
This increased sensitivity predisposes them to respira- technique for orthopedic and urologic office-based pro-
tory depression or apnea during the postoperative pe- cedures. It provides excellent intraoperative and postop-
riod. For all these reasons, it would be reasonable to erative analgesia. It is not associated with significant
avoid performing OBA on morbidly obese patients, postoperative sedation, even when used in conjunction
especially patients with associated obstructive sleep with monitored anesthesia care. Nerve blocks without
apnea. intravenous opioids offer a low incidence of postopera-
Another aspect of morbid obesity that predisposes tive nausea and vomiting. Regional anesthesia is associ-
these patients to perioperative complications is the risk ated with problems ambulating, post–dural puncture
of developing deep vein thrombosis (DVT) or pulmo- headache, prolonged autonomic blockade, and inability
nary embolism. DVT with subsequent pulmonary em- to urinate.
bolism is a significant risk of abdominoplasty and lipo-
suction, two very common office-based procedures as
well as procedures morbidly obese patients are likely to SUGGESTED READINGS
undergo. Other patients who are at increased risk of American Society of Anesthesiologists: Guidelines for office-based
developing DVT are elderly patients with malignancy, anesthesia, last affirmed 2009. www.asahq.org
smokers, oral contraceptive users, patients on bed rest, ASA Committee on Ambulatory Surgical Care and the ASA Task
patients with hypercoagulation disorders, and patients Force on Office-Based Anesthesia: Office-Based Anesthesia,
Considerations for Anesthesiologists in Setting up and Maintain-
with a prior history of DVT. ing a Safe Office Anesthesia Environment. American Society of
Anesthesiologists, Park Ridge, IL, 2000.
Benumof JL: Obstructive sleep apnea in the adult obese patient: im-
5. What anesthetic techniques are appropriate plications for airway management. Anesthesiol Clin North Am
to use in an office-based practice? 20:789-811, 2002.
Grazer FM, deJong RH: Fatal outcome from liposuction: census
Most anesthetic drugs and techniques used in hospitals survey of cosmetic surgeons. Plast Reconstr Surg 105:436-446,
and ASCs can and have been safely and effectively ap- 2000.
394 SECTION 13 Ambulatory Anesthesia
Iverson R, ASPS Task Force on Patient Safety in Office-Based Surgery Koch ME, Dayan S, Barinholtz D: Office-based anesthesia: an over-
Facilities: Patient safety in office-based facilities: I. Procedure in the view. Anesthesiol Clin North Am 21:417-443, 2003.
office-based surgery setting. Plast Reconstr Surg 110:1337, 2002. Rosenquist RW: Regional anesthesia for office-based surgery. ASA
Iverson R, ASPS Task Force on Patient Safety in Office-Based Surgery Newsletter 65:12-14, 2001.
Facilities: Patient safety in office-based facilities: II. Patient selec- Twersky R: Anesthetic and management dilemmas in office-based surgery.
tion. Plast Reconstr Surg 110:1785, 2002. Ambul Surg 6:79-83, 1998.
S EC TION 1 4
TRAUMA
395
CASE 75
Thoracic Trauma
Levon M. Capan, MD • Kenneth M. Sutin, MD, FCCM • Sanford Miller, MD
QUESTIONS
1. What are the consequences of thoracic trauma? 8. How is surgery prioritized in patients with blunt
2. How are traumatic pneumothorax and hemothorax trauma and multiple injuries that include thoracic
managed in patients undergoing laparotomy for aortic damage?
splenic injury? 9. What are the current management strategies for
3. What are the mechanisms of morbidity and mortality blunt aortic injury?
from flail chest? 10. What are the perioperative clinical and anesthetic
4. What are the management options for flail chest pitfalls that can be encountered during manage-
and pulmonary contusion? ment of patients with thoracic aortic injuries, and
5. What are the perioperative management options how should they be managed?
for traumatic hemopericardium? 11. Describe the clinical management of transmedi-
6. What are the clinical implications of blunt cardiac astinal gunshot wounds.
trauma?
7. When should traumatic thoracic aortic injury be
suspected, and how is it diagnosed?
A 46-year-old man is admitted to the trauma bay of the injuries include major airway trauma with airway obstruc-
emergency department approximately 30 minutes after he tion, tension pneumothorax, open pneumothorax, cardiac
was struck by a bus. The primary survey reveals no signs tamponade, massive hemothorax, and free rupture of the
of upper airway obstruction, but there is significant respi- thoracic great vessels. Potentially life-threatening injuries
ratory distress with chest wall splinting. Systemic blood include partial tracheal disruption, contained rupture of
pressure (BP) is 130/80 mm Hg, heart rate is 120 beats the great vessels, myocardial contusion, valvular or septal
per minute, and Glasgow Coma Scale score is 15 with injuries, pulmonary contusion, esophageal disruption,
movement of all extremities. No open wounds are ob- and diaphragmatic tear. Flail chest can be immediately or
served. The secondary survey reveals a left distal humerus potentially life-threatening depending on the severity of
fracture and left (5, 6, 7, 8, and 9) and right (6, 7, and 8) associated hypoxemia. Risk factors for mortality after
rib fractures as well as abdominal guarding. Computed blunt chest trauma are patient age !65 years; three
tomography (CT) demonstrates a grade 4 splenic injury, or more rib fractures; preexisting diseases, particularly
necessitating emergency laparotomy. involving the cardiopulmonary system; and pneumonia
developing after injury.
1. What are the consequences of thoracic trauma? Although cardiothoracic trauma is a major contributor
to all trauma mortality, it coexists in 80% of cases with
Of the 112,000 annual deaths caused by unintentional inju- other injuries that commonly require major surgery.
ries, almost half result from motor vehicle–related trauma, Some serious thoracic organ injuries may be clinically
which carries a high risk of chest injury. Similarly, of the silent, and active suspicion and sophisticated diagnostic
55,000 deaths caused by intentional injuries, 20,000 are also measures may be required to detect them. Physiologic
likely to involve injuries to the chest. It is estimated that derangements from chest injuries are multi-dimensional,
12%–21% of all trauma deaths result primarily from blunt including pulmonary failure, hemorrhage, and cardiac
and penetrating chest injury. For each chest trauma–related dysfunction, and coexist in varying combinations and
death, there are approximately 100 nonfatal thoracic inju- severity. Some clinicians use the term “thoracic shock” to
ries. Not all intrathoracic organs are at equal risk of injury. describe chest injury–induced physiologic derangements
The chest wall (50%–71%) and lungs (21%–26%) are the (Figure 75-1). Individually or in combination, each of
most commonly involved structures. The heart (7%–9%), these physiologic abnormalities can interfere with oxy-
aorta and great vessels (4%), esophagus (7%), and dia- gen delivery, consumption, and extraction. They can
phragm (0.5%–7%) are less likely to be injured. potentially shift oxygen use from a flow-independent to a
The immediate threat to life also varies with different flow-dependent state, with associated anaerobic tissue
thoracic organ injuries. Immediately life-threatening metabolism and lactic acidosis.
396
75 Thoracic Trauma 397
Airway
injury Lung
laceration
Chest wall
splinting Myocardial
Lung contusion
contusion
Pericardial
tamponade
Cardiac
rupture
Diaphragmatic
injury
Cardiac Failure
Pulmonary Failure (Cardiogenic shock)
(Hypoxia, hypercarbia)
Hemorrhage
(Hypovolemic shock)
FIGURE 75-1 ■ Schematic depiction of the pathophysiology of chest injury.
2. How are traumatic pneumothorax and hemothorax The clinical signs of pneumothorax in anesthetized
managed in patients undergoing laparotomy for patients receiving positive pressure ventilation include ele-
vation of peak airway pressure, decreased lung compliance,
splenic injury?
decreasing oxygen saturation, and decreased breath sounds
Pneumothorax and hemothorax are the most frequent on the affected side. In extremis, severe hypotension and
consequences of chest injury and require timely recog- possibly cardiac arrest can ensue. Chest radiographs can
nition and treatment. They can occur after both pene- provide the diagnosis even in the supine position if the
trating and blunt chest trauma. Both can result from amount of intrapleural air is large enough; however, chest
laceration of visceral pleura by sharp objects during x-rays may be difficult or impossible to obtain during
assaults or by fractured ribs. However, pneumothorax emergency surgery.
may also occur after blunt chest trauma without rib Without a radiologically confirmed diagnosis, place-
fracture. The mechanism of this injury relates to sudden ment of a 14-gauge needle between the fourth and fifth
elevation of alveolar pressures, producing alveolar ribs (the fourth intercostal space) in the midaxillary
rupture with entry of air into the interstitial space, line, the thinnest region of the chest wall even in obese
mediastinum, and visceral pleura. patients, may be indicated for unstable patients. Never-
Concerns about exacerbating spine injuries or pro- theless, atelectasis, bronchial obstruction, or migration
ducing adverse hemodynamic changes preclude obtain- of intraabdominal contents into the chest through a
ing a chest radiograph in the sitting position, which is traumatic diaphragmatic defect can mimic the clinical
required for the diagnosis of a pneumothorax and recog- findings of pneumothorax and lead to unnecessary chest
nition of the magnitude of a hemothorax. For these tube placement. Sonographic diagnosis of pneumothorax
reasons, although supine chest radiographs are obtained has gained some recognition more recently. Normally,
routinely in all patients with major trauma, additional when the lung is imaged by a 3.5- to 7.5-MHz ultrasound
measures may be necessary to diagnose pneumothorax probe, sliding of the pleura beneath the chest wall during
and hemothorax when their presence is suspected. inspiration and expiration produces multiple echodense
CT scan of the chest obtained in the supine position spots that originate from the surface of the lungs and
is highly specific, so even a small amount of air in the project across the lung. These spots are termed comet-
pleural cavity can be recognized by this method. tail artifacts. In the presence of a pneumothorax, air be-
In some instances, an undiagnosed pneumothorax tween the chest wall and the visceral pleura prevents the
may enlarge during surgery for associated injuries. Ten- appearance of comet-tail artifacts. Ultrasonography may
sion pneumothoraces can result in severe hemodynamic be more sensitive than an anteroposterior chest x-ray for
and oxygenation abnormalities that can be lethal. Our diagnosis of pneumothorax or hemothorax.
approach is to place a chest tube for all patients with a Hemothorax may also cause hemorrhagic shock, me-
diagnosis of pneumothorax and in need of mechanical diastinal shift, and airway management difficulties.
ventilation for any reason. Not all clinicians agree with Placement of a large-bore (28F–38F) chest tube in the
this approach. It has been demonstrated that by using early phase of management, especially after penetrating
CT, the size of a traumatic pneumothorax may be injury, provides information about the rate of bleeding
classified as miniscule or limited anteriorly and antero- and often prevents development of fibrin clot over the
laterally. In most of these patients, chest tubes may lung surface, which may restrict lung expansion and
not be indicated, even during mechanical ventilation, require decortication later. Antibiotic coverage should
if close observation with appropriate monitoring is be provided for the next 24 hours.
provided. However, during emergency surgery, such The volume and rate of blood drained via the chest tube
observation and monitoring may not be easy to achieve. determine the necessity for video-assisted thoracoscopy or
398 SECTION 14 Trauma
ARDS incidence
and pulmonary contusion? 60
Diagnosis 50
The presence of a flail segment suggests underlying pul- 40
monary contusion, but if breaths are rapid and shallow,
this sign may not be evident. However, neither the extent 30
of the flail nor the number of ribs fractured accurately
20
predicts respiratory failure. Chest wall bruising, rib cage
deformities, and crepitus or pain or both during palpation 10
of the thorax suggest rib fractures or dislocation even in
the presence of a normal chest radiograph, which may not 0
0–!10% "10–!20% "20–!30% "30–!40% "40%
detect cartilaginous injuries and fractures of poorly calci- * * *
fied ribs. The initial film often does not show underlying Contusion volume
lung injury because pulmonary edema appears late. If FIGURE 75-2 ■ Correlation of pulmonary contusion volume with
present, a focal infiltrate beneath multiple rib fractures subsequent development of ARDS. (From Miller PR, Croce MA,
confirms the diagnosis of pulmonary contusion. Clinical Bee TK, et al.: ARDS after pulmonary contusion: accurate measure-
signs, such as dyspnea, tachypnea, intercostal muscle re- ment of contusion volume identifies high-risk patients. J Trauma
51:223, 2001.) ARDS, Adult respiratory distress syndrome.
traction, and use of accessory muscles, suggest underlying
lung pathology. Monitoring with pulse oximetry in the
initial stage is useful only if the patient is breathing room contusion (Figure 75-3). With any of the imaging tech-
air. Supplemental oxygen administration may mask inad- niques described, confusion may arise in differentiating
equate ventilation, delaying diagnosis and treatment to contusion from aspiration, atelectasis, hemothorax, fluid
restore functional residual capacity and lung compliance overload, transfusion-related acute lung injury, and
toward normal. Likewise, arterial blood gases measured pulmonary emboli.
with the patient breathing room air may be useful. Man-
aging these patients without supplemental oxygen neces- Management
sitates direct observation by a physician or other qualified
person. The usual pattern is a progressive decrease in As in our case, patients with pulmonary contusion fre-
arterial oxygen (PaO2) and increase in arterial carbon quently have associated injuries that may or may not re-
dioxide (PaCO2) tensions, resulting in a decrease in pH quire emergency surgery. Management may need to take
(i.e., respiratory acidosis). When patients need emergency into account treatment requirements of associated injuries
surgery, as our patient required a splenectomy, hypoxemia as well. For example, in a bleeding patient, restricting
and hypercarbia often develop intraoperatively. Frequent fluids out of a concern for exacerbating pulmonary contu-
intraoperative arterial blood gas measurements should be sion may have serious consequences. Many patients with
obtained. rib fractures and pulmonary contusion also have spinal
Although arterial hypoxemia may precede radio- fractures. Administering continuous epidural anesthesia
graphic abnormalities, it may not reflect the size of to these patients because of its salutary effect on contu-
the contusion because blood flow to the injured lung is sions would be extremely uncomfortable for the patient
restricted by hypoxic pulmonary vasoconstriction. A and may sometimes be associated with worsening of the
PaO2/FiO2 #300 after initial resuscitation is considered vertebral injury or causing spinal cord damage.
a risk factor for developing subsequent acute respiratory During the initial phase, simple measures such as
failure. Because plain chest radiography underestimates oxygen administration by mask to patients who are
contusion volume, CT scans are used for quantifying hypoxic breathing room air and maintaining the unin-
the contusion size. Patients with a contusion !28% of volved lung in a dependent position may help improve
total lung volume are very likely to require mechanical oxygenation. Patients with intratracheal bleeding may
ventilation, and patients with contusion volumes !20% need a double-lumen endotracheal tube or an endo-
of total lung volume frequently develop ARDS and bronchial blocker to prevent contamination of the
pneumonia (Figure 75-2). Although CT is the standard intact lung and possibly to tamponade the bleeding.
method of diagnosis, patients who are too unstable to be Ventilation of the intact lung alone may also be useful
transported to a CT unit may benefit from ultrasound in patients with complete unilateral contusions. In pa-
evaluation. Ultrasound may be valuable for detecting tients with bilateral contusions presenting with severe
rib fractures, pneumothorax, and contusions, although hypoxemia, differential lung ventilation via a double-
it cannot determine contusion volume. The presence of lumen tube should be considered. When hypoxemia is
multiple comet-tail artifacts at the parietal-visceral life-threatening, high-frequency jet ventilation or oscil-
pleural interface and replacement of the normal transverse latory ventilation may improve systemic oxygenation
A-line pattern by vertical B-lines suggest pulmonary effectively. These modes of ventilation may also improve
400 SECTION 14 Trauma
r
r r p
p r
* *
* *
*
*
*
A B
FIGURE 75-3 ■ Ultrasound diagnosis of pulmonary contusion. A, Ultrasound image of the normal lung showing ribs (r) and the pleural
line (p) with A-lines (asterisks), which are horizontal reverberation artifacts at equal distances. B, Ultrasound image of the contused
lung showing ribs (r) and the pleural line (p) without A-lines. Instead, there are vertical hyperechoic artifacts known as B-lines (as-
terisks), which arise from the pleural line and erase the normal A-line pattern. (From Stone MB, Secko MA: Bedside diagnosis of pulmo-
nary contusion. Pediatr Emerg Care 25:854, 2009.)
depressed cardiac function caused by concomitant myo- positive end expiratory pressure (PEEP) ventilation,
cardial contusion or ischemia. permissive hypercapnia, or high-frequency oscillatory
Early treatment is crucial. A delay of even a few hours ventilation may be considered.
may result in progression of underlying lung pathology Effective removal of tracheobronchial secretions has
with increasing morbidity and mortality. The goal is to a significant effect on outcome. Likewise, monitoring
decrease elastic recoil and the work of breathing and to with pulse oximetry, an arterial catheter, and a pulmonary
improve arterial blood gases without adverse hemodynamic artery catheter when indicated is important. A pulmo-
effects. In patients without acute respiratory failure or nary artery catheter can not only guide fluid manage-
associated injuries requiring tracheal intubation, this goal ment, which should be adjusted to the minimum consis-
can be accomplished by continuous positive airway pres- tent with adequate end-organ perfusion, but it also may
sure (CPAP) of 10–15 cm H2O applied by facemask. Non- aid ventilatory management, as it permits calculation of
invasive positive pressure ventilation using titrated bilevel oxygen delivery and intrapulmonary shunt fraction and
positive airway pressure with both inspiratory (10–12 cm thus helps to adjust the optimal level of CPAP.
H2O) and expiratory (6 cm H2O) positive pressures can Supplemental oxygen should be administered judi-
avoid tracheal intubation in more than one half of patients. ciously to permit the acquisition of maximal information
Early tracheal intubation and mechanical ventilation from the initial oxyhemoglobin saturation with pulse
with alveolar recruitment maneuvers, the usual practice oximetry or arterial blood analysis. Supplemental oxygen
before 1975, has fallen into disfavor because of a high has detrimental effects, such as absorption atelectasis, inter-
incidence of tracheobronchitis and pneumonia leading ference with hypoxic pulmonary vasoconstriction in dam-
to sepsis, multiorgan failure, and death. At the present aged lung regions, decreased mucociliary clearance, free
time, except in instances when tracheal intubation radical formation, and decreased surfactant production.
and mechanical ventilation are necessary (i.e., PaO2 Although the effect of fluids on pulmonary function
#60 mm Hg in room air, #80 mm Hg with supple- in the presence of pulmonary contusion has not been
mental oxygen, and conditions other than thoracic conclusively defined, we believe that overzealous fluid
injury), most patients do well with noninvasive positive administration may result in an increase in the size of
pressure ventilation. When impending respiratory the lung contusion and a decrease in PaO2. Although it
failure indicates tracheal intubation, airway pressure is possible to remove excess fluid with diuretics, use of
release ventilation (APRV) may be a reasonable choice. diuretics is associated with electrolyte abnormalities,
With this mode of ventilation in a spontaneously cardiac dysrhythmias, and hypovolemia. At least during
breathing patient, CPAP is intermittently decreased for initial resuscitation, the type of fluid used does not seem
short periods with the device shown in Figure 75-4. In to affect outcome. Crystalloid solutions are favored be-
other words, spontaneous breathing is superimposed cause they are less expensive. The initial enthusiasm for
on mechanical ventilation. In addition to decreased hypertonic saline in fluid management of pulmonary
work of breathing, the advantages of this technique contusion has not been substantiated. In the presence of
over controlled ventilation are improved V /Q match- concomitant blunt cardiac injury, complications of pul-
ing, increased systemic blood flow, lower sedation monary contusion can easily confuse the clinical picture.
requirements, greater oxygen delivery, shorter periods In this situation, the best guide to fluid management is
of intubation, and decreased risk of pneumonia. In pa- transesophageal echocardiography (TEE) or, if TEE is
tients with severe life-threatening pulmonary contu- unavailable, pulmonary artery and wedge pressures.
sion, ARDS, or acute lung injury unresponsive to Continuous epidural analgesia is the best pain man-
APRV or routine mechanical ventilation, lung recruit- agement technique available for patients with blunt chest
ment strategies such as high-frequency inverse ratio trauma. It improves lung function and decreases overall
ventilation, low tidal volume (6 mL/kg) and titrated morbidity. However, as mentioned earlier, concomitant
75 Thoracic Trauma 401
B
CPAP
Pressure
F
V1
H R A
Release
V2 APRV
Time
Pressure
P T
B
I E
B Time
spine or other injuries and inability of the patient to (TTE) or TEE in intubated patients without suspected
consent to the procedure preclude this technique. Con- esophageal injury can aid in diagnosing and evacuating
tinuous thoracic paravertebral block with ultrasound pericardial blood. Diastolic collapse, defined as approxi-
guidance may also be considered as a component of mation of the (usually right) ventricular walls during
multidimensional pain management. Other modalities, diastole, is a sign of tamponade and is associated with
such as parenteral opioids, are not nearly as effective, systemic BP reductions of $15%–20%. During evacua-
whereas multiple intercostal blocks are labor-intensive tion, simultaneous imaging of the needle and the peri-
and short-lasting and must be repeated at least twice a cardial sac prevents cardiac perforation.
day. Important management aspects of flail chest and The clinical signs characteristic of chronic hemopericar-
pulmonary contusion are summarized in Box 75-2. dium are virtually useless in acute traumatic tamponade.
Beck’s triad (i.e., cervical venous distention, hypotension,
5. What are the perioperative management options and muffled heart sounds) is seen in #50% of traumatic
tamponade cases. Agitation, combativeness, and cool vaso-
for traumatic hemopericardium?
constricted extremities are seen in patients with cardiac
Traumatic hemopericardium can develop after both tamponade, but they are also present in patients with hypo-
blunt and penetrating chest injuries. In contrast to volemic shock. Paradoxical inspiratory distention of the
chronic effusions, in which 600 mL of pericardial fluid neck veins (i.e., Kussmaul’s sign) is characteristic of cardiac
may not cause hemodynamic depression, even small tamponade, but it may be extremely difficult to demon-
accumulations of blood after acute injury result in car- strate in patients with acute trauma.
diac tamponade with significant hypotension and cardiac Paradoxical pulse, although not specific for cardiac tam-
arrest. Inflow occlusion of the atrioventricular valves, ponade, is probably the most reliable clinical sign in these
resulting from external compression by pericardial circumstances. Paradoxical pulse refers to a !10 mm Hg
blood, leads to decreased ventricular filling, especially in decline in systolic arterial pressure during inspiration in a
the right heart. Because a relatively small amount of spontaneously breathing patient and is simply an exaggera-
fluid accumulation can cause major hemodynamic tion of the normal 3–6 mm Hg respirophasic variation.
changes, evacuation of even a minimal quantity of blood This sign lacks specificity because it can also occur in pa-
from the pericardium usually restores BP. Hypotensive tients with uncomplicated hypovolemia. Its absence does
patients who may have cardiac tamponade could benefit not exclude cardiac tamponade. Concurrent septal defect,
from pericardiocentesis. Transthoracic echocardiography severe left ventricular failure, or aortic regurgitation may
402 SECTION 14 Trauma
BOX 75-2 Flail Chest and Pulmonary enhances the leftward septal shift. However, in hypovole-
Contusion mic trauma patients, right ventricular filling and the
septal shift are limited, rendering pulsus paradoxus less
DEFINITION perceptible.
Flail chest: rib fractures at two or more sites, with or without Equalization of elevated intrapericardial and right ven-
disarticulation tricular filling pressures is an inevitable phenomenon in
Pulmonary contusion: atelectasis, interstitial and intraalveolar compensated cardiac tamponade. With further accumula-
hemorrhage, alveolar disruption tion of blood, these pressures increase toward the left
ventricular diastolic pressure. With diastolic underfilling,
DIAGNOSIS cardiac output becomes rate dependent. A decrease in
Clinical symptoms heart rate may result in catastrophic hypotension and
Dyspnea cardiac arrest. Severe cardiac tamponade can also produce
Tachypnea a reduction in coronary blood flow, but myocardial isch-
Intercostal muscle retractions emia and decreased contractility are unlikely, probably
Use of accessory muscles of respiration because of a proportional decrease in myocardial work
Physical examination resulting from decreased systemic BP and stroke volume.
Chest wall bruising
Associated injuries often overshadow the clinical mani-
Rib cage deformities festations of cardiac tamponade even when the classic signs
Crepitus/pain on palpation of this entity are evident. It is important to be familiar with
the ancillary diagnostic findings of cardiac tamponade.
Radiologic examination Radiographic findings are not helpful. Cardiomegaly is
Chest radiograph not always diagnostic unlikely to be present in patients with traumatic cardiac
Infiltrate seen in area of trauma tamponade and is nonspecific. Findings on electrocardio-
CT scan gram (ECG) are also not specific, although ST segment
Laboratory elevation and diminished QRS voltage may be observed
if significant pericardial blood accumulates. Electrical
Progressive hypoxia
Progressive hypercarbia
alternans (i.e., phasic alteration of R wave amplitude) may
Respiratory acidosis be more specific but can also occur in patients with tension
pneumothorax. Total electrical alternans (i.e., phasic
TREATMENT alteration of P and R wave amplitudes), although rare,
CPAP 10–15 cm H2O by facemask is considered a pathognomonic sign. As mentioned, echo-
Tracheal intubation cardiography is the most reliable diagnostic tool for this
Mechanical ventilation entity. Of the four sites examined during a focused
Pressure/volume controlled ventilation abdominal sonographic study (FAST), the first involves
Airway pressure release ventilation exploration of the pericardium via a subxiphoid window.
Differential lung ventilation Transthoracic and transesophageal views can also be used.
High-frequency jet ventilation
Limit fluids
Ultrasound may demonstrate not only pericardial blood
Epidural analgesia if no contraindication exists and its volume but also right ventricular diastolic collapse.
Paravertebral block, intercostal block, or parenteral opioids Diastolic collapse may be absent in patients with a hyper-
trophic right ventricle or in patients with high intraven-
MONITORING tricular pressures from tricuspid regurgitation.
Pulse oximeter Management priorities depend on preexisting cardiac
Arterial catheter conditions, the type and extent of associated injuries, intra-
Transthoracic or transesophageal echocardiogram to dem- vascular volume, the quantity of pericardial blood, and
onstrate tricuspid regurgitation patient cooperation. If the severity of associated injuries
Pulmonary artery catheter permits, pericardiocentesis with echocardiographic guid-
Calculate oxygen delivery and intrapulmonary shunt
fraction to adjust optimal CPAP
ance or surgical drainage and intravascular volume restora-
tion should precede any anesthetic. In contrast to pleural
CPAP, Continuous positive airway pressure; CT, computed tomography. blood, pericardial blood clots easily. It may be possible
to drain only a fraction of pericardial fluid, but even
small amounts can produce significant hemodynamic
preclude a paradoxical pulse. The following two synergistic improvement.
mechanisms during inspiratory reduction of intrathoracic Any drug that decreases myocardial contractility or
pressure are responsible for development of paradoxical produces peripheral vasodilation may precipitate hemo-
pulse: dynamic depression. The classic anesthetic induction
• Increase in transmural aortic pressure and in left agent is ketamine, but even with this drug BP may dete-
ventricular afterload riorate. Positive pressure ventilation should be carefully
• Underfilling of the left ventricle because of leftward maintained with low airway pressures and without PEEP.
displacement of the interventricular septum In most instances of major trauma with pericardial tam-
Increased venous pressure during inspiration in nor- ponade, invasive monitoring other than an arterial cath-
movolemic patients makes the paradoxical pulse more eter may be difficult to place. However, a pulmonary
obvious because it increases right ventricular filling and artery catheter, if present, can be helpful to determine
75 Thoracic Trauma 403
TREATMENT
Diagnosis
Before induction of anesthesia
Pericardiocentesis with echocardiographic guidance BCI may be associated with direct precordial impact,
Surgical drainage crush injury of the chest causing compression of the heart
Volume replacement between the sternum and the spine, deceleration injuries,
and blast injuries. Suggestive signs and symptoms include
After induction of anesthesia chest pain, angina responding to nitroglycerin, dyspnea,
Avoid cardiac depressants and bradycardia chest wall ecchymosis, and fractures of ribs or sternum or
Spontaneous ventilation both. There is no “gold standard” for diagnosing blunt
If positive pressure ventilation necessary, low airway pressure, cardiac trauma. However, ECG, blood concentration of
no PEEP
troponin I, and echocardiography are important. In addi-
ECG, Electrocardiogram; PEEP, positive end expiratory pressure. tion, coronary angiography or ventriculography may
rarely be indicated to diagnose coronary lesions, cardiac
rupture, or valve injuries.
equalization of cardiac chamber pressures, cardiac out- A 12-lead ECG is the best screening test. Nonspecific
put, and response to therapeutic interventions. Bradycar- changes, such as tachycardia, bradycardia, or occasional
dia during direct laryngoscopy or surgical manipulation atrial or ventricular premature contractions, occur in 50%–
should be avoided at all costs. Important management 70% of patients and usually do not require treatment.
aspects of traumatic cardiac tamponade are summarized More serious alterations, such as ST or T wave changes,
in Box 75-3. conduction delays, and complex atrial and ventricular dys-
rhythmias, occur less frequently (4%–30%) but often need
6. What are the clinical implications of blunt cardiac to be treated. Although sensitive, ECG is not specific, and
a normal tracing cannot rule out BCI. The right ventricle,
trauma?
because of its anterior position, is injured more frequently
By definition, blunt cardiac trauma encompasses a wide than the left. Standard leads, which are primarily useful to
variety of pathologic conditions, including varying degrees detect left-sided abnormalities, miss some right heart
of myocardial damage. Examples include coronary artery events. Overall, the sensitivity, specificity, and negative
injury; cardiac free wall, interatrial, interventricular septal, predictive value of ECG for predicting cardiac complica-
or valvular rupture; and, with impalement by a fractured tions are 100%, 47%, and 90%, respectively. Although
sternum or rib, penetrating injury from blunt trauma. The delayed (!24 hours) appearance of serious ECG abnor-
term “blunt cardiac injury” (BCI) refers to myocardial malities may very rarely occur, a normal ECG on admis-
damage involving myofibrillar disintegration, edema, sion virtually eliminates the risk of complications of blunt
bleeding, or necrosis; this injury was formerly known as cardiac trauma and the need for further evaluation, as
myocardial contusion. It manifests clinically as minor long as the patient is hemodynamically stable, has no his-
ECG changes, cardiac enzyme abnormalities, complex tory of cardiac disease, is #55 years old, and does not
dysrhythmias, or cardiac failure. Some of these injuries have multiple injuries or significant chest wall trauma.
may be caused by myocardial damage from direct me- However, if these compromising conditions exist, cardiac
chanical injury or occur indirectly as a result of coronary monitoring for at least 24 hours in a telemetry ward or
occlusion or exacerbation of preexisting coronary artery intensive care unit is indicated. An abnormal ECG
disease by the stress of trauma. Cardiac lesions, seen as should be followed by continuous cardiac monitoring.
ECG abnormalities and troponin release, may also be Additionally, obtaining serum troponin I concentration 6
the result of increased catecholamine activity after severe and 12 hours after the injury in hemodynamically stable
central nervous system injury and hemorrhagic shock with patients and echocardiography in hemodynamically un-
little or no direct trauma to the heart. stable patients should be considered.
404 SECTION 14 Trauma
Serum creatine kinase (CK) and CK-MB determina- The clinical presentation of patients with BCI varies;
tions, which were frequently used to diagnose myocardial sometimes more than one compromising condition may
contusion, are no longer performed because of their low be present in the same patient. Orliguet et al. proposed an
specificity. Skeletal muscle, colon, lung, liver, and pancre- algorithm describing the management principles for each
atic tissue contain both CK and CK-MB. In patients with of these scenarios (Figure 75-5). Dysrhythmias appear to
multiple trauma, a positive value may not indicate cardiac respond readily to antiarrhythmic agents. Hypotension
injury. Troponin I is specific for cardiac muscle. However, may be caused by hypovolemia, pump failure, or both.
negative levels of CK-MB or troponin I do not rule out Fluid loading, with monitoring of cardiac function by
clinically relevant BCI because muscle disintegration is echocardiography or right heart catheterization, improves
not significant enough in many patients with cardiac hypovolemia. Pump failure is usually caused by right ven-
trauma to release detectable enzyme levels. Yet even a tricular dysfunction exacerbated by increased pulmonary
small area of myocardial damage can cause dysrhythmias, vascular resistance secondary to pulmonary contusion, as-
if it is in a critical location. piration of gastric contents, or ARDS. An initial right
Echocardiography may be helpful in many ways in BCI. ventricular free wall dilation may be followed by leftward
It provides information about myocardial function (e.g., ventricular septal shift, which alters the geometry and
wall motion abnormalities, increased end-diastolic wall compliance of the left ventricle, increasing left ventricular
thickness), cardiac structural abnormalities (e.g., echo- filling pressure and decreasing cardiac output. This condi-
dense areas on the ventricular walls, valve malfunction, tion should by no means be a signal to decrease fluid load-
hemopericardium, intracardiac thrombi), cardiac preload ing. On the contrary, volume replacement should continue
(e.g., end-diastolic area), systolic cardiac function (e.g., with concomitant use of inotropes and pulmonary vasodi-
fractional ventricular area change), and air embolism (e.g., lators. Positive pressure ventilation may also be adjusted to
air bubbles in the cardiac chambers, patent foramen ovale). minimize intrathoracic pressure and right ventricular af-
Echocardiography can help not only with the diagnosis of terload. High-frequency jet ventilation or oscillation with
BCI but also in hemodynamic management. TEE is a its relatively low mean airway pressure may be beneficial in
much more valuable monitor than TTE, whose usefulness these circumstances. As shown in the algorithm, hemo-
is limited by mechanical ventilation, pleural effusion, pericardium is treated by drainage, either surgically or by
pneumothorax, and difficulty in placing the patient in left placement of a large-bore catheter with echocardiographic
lateral decubitus position. Myocardial contusion, hemo- guidance. Anticoagulants, if used, should be stopped. Myo-
pericardium, valvular lesions, hemomediastinum, and aor- cardial infarction and valvular, septal, and coronary vascular
tic rupture are more likely to be recognized with TEE injuries are treated in the same way as they would be in the
than with TTE. Nevertheless, it is important to eliminate absence of trauma. Severe trauma may dictate surgery be-
esophageal injury before attempting TEE in patients with fore angioplasty, coronary artery bypass, repair of injured
chest trauma. Dysrhythmias, unexplained hypotension, cardiac valves, or closing a septal defect.
and heart failure are definite indications for TTE or TEE Rarely, pump failure may be unresponsive to pharma-
evaluation. cologic measures and requires cardiac assistance. The
ventricular balloon pump has been used in these rare
Perioperative Management
Depending on its type and extent, BCI can increase surgi-
cal risk. Although most patients with cardiac chamber
perforation do not reach the hospital, some, especially
patients with atrial lesions, may arrive in the operating
room. Preoperative information about the nature of injury
is important. Some retrospective reports have documented
an increased incidence of intraoperative dysrhythmias and
hypotension in patients with preoperatively diagnosed
myocardial contusion. It is unclear whether these occur-
rences were due to the myocardial injury itself or to
the complications of associated injuries. Nevertheless, the
combination of atrial fibrillation, old age, and aortic rup-
ture with myocardial contusion appears to increase periop-
erative mortality. The duration of complications is also a
relevant issue for the anesthesiologist because many
trauma patients present days to months after injury. In FIGURE 75-5 ■ Algorithm for management of various clinical sce-
most patients, dysrhythmias last no more than a few days. narios produced by severe BCI. Multiple severe trauma-induced
BCI is evaluated with ECG, troponin I, and TEE. Arrows represent
Ventricular wall motion abnormalities may persist for the frequency of occurrence of each scenario and the frequency of
1 year, but any increased risk of perioperative complications management measures. Thick arrows represent high-frequency
appears to last for no more than 1 month. An intracardiac occurrences, thin arrows represent low-frequency occurrences, and
thrombus, a well-known complication of myocardial contu- dotted arrows represent very rare occurrences. BCI, Blunt cardiac
injury; CABG, Coronary artery bypass graft; ECG, electrocardiogram;
sion, may be present !1 year after injury, further emphasiz- HFJV, high-frequency jet ventilation; TEE, transesophageal echocardiog-
ing the need for preoperative echocardiography even well raphy. (Adapted from Orliaguet G, Ferjani M, Riou G: The heart in blunt
after the accident. trauma. Anesthesiology 95:544, 2001.)
75 Thoracic Trauma 405
cases of BCI. However, in most patients, dysfunction interscapular pain, hoarseness, precordial systolic murmur,
originates from the right ventricle. If assistance is needed, or lower extremity neurologic deficit may also have an
biventricular assist devices would be preferable. aortic injury (Box 75-4).
The radiologic diagnosis of blunt aortic injury has
7. When should traumatic thoracic aortic injury be changed over the last decade. Although all patients with
major trauma receive a routine supine chest radiograph,
suspected, and how is it diagnosed?
findings with this diagnostic modality are not reliable
Traumatic thoracic cardiovascular injury is a potentially enough to confirm or eliminate blunt aortic injury. For
lethal sequela of chest trauma, associated with an almost example, in only 20%–30% of instances is mediastinal
80% mortality in the first hour after injury. It should be widening (i.e., !8 cm at the level of the aortic knob) on
suspected in every patient with blunt chest trauma. Most anteroposterior chest films associated with thoracic aortic
patients sustain thoracic vascular injury from sudden de- injury. Bleeding from the neck vessels or vertebra into the
celeration after a motor vehicle or motorcycle accident, mediastinum can produce a similar image. Absence of
free falls, or auto versus pedestrian accidents. Other mediastinal widening also is unreliable because many pa-
mechanisms, such as sudden compression of the thoracic tients who reach the hospital have a contained aortic injury
vessels between the spine and sternum or ribs, can also without much extravasation. Other chest radiographic
produce this injury. In almost 90% of cases, the aorta is findings suggestive of aortic injury are blurred aortic
injured at the isthmus, the junction of its free and fixed contour, wide paraspinal interface, opacified pulmonary
portions, which is distal to the origin of the subclavian window, broad paratracheal stripe, displaced left main
artery (Box 75-4). Most isthmus injuries occur at the stem bronchus, rightward deviation of the esophagus (or a
medial aspect of the aorta and are thought to result from nasogastric tube) and trachea, left apical pleural hematoma
sudden increases in intraluminal pressure (!1000 mm (pleural cap), and left hemothorax (Box 75-5).
Hg) and rotation of the vessel. Contrast-enhanced spiral CT and multiplanar TEE
Injuries to the ascending portion and the aortic arch are are highly accurate and are the screening methods used
much less frequent than isthmic injuries. The likelihood of currently. CT findings of traumatic aortic injury include
ascending aortic injury is enhanced by a history of violent polypoid or linear intraluminal areas of low attenuation
deceleration; impact to the side of a vehicle involved in an suggesting clot or medial flap, false aneurysm, irregular
accident; ejection of an unrestrained passenger; death of aortic wall or contour, pseudocoarctation, intramural
anyone involved in the accident; a motor vehicle and pe- hematoma, and aortic dissection.
destrian or bicycle collision; or the presence of high-
impact injuries such as diaphragmatic rupture, mesenteric
tear, or pelvic fracture. In the presence of pelvic fracture,
the overall incidence of blunt aortic injury increases from BOX 75-5 Traumatic Thoracic Aortic Injury:
#0.5% to 1.4%. Additionally, a patient with chest trauma Radiographic Findings
who develops unexplained hypotension, external signs of CHEST RADIOGRAPH
direct chest injury, a pulse deficit between the right and
left arms or between the upper and lower extremities, a Mediastinal widening
Blurred aortic contours
requirement for mechanical ventilation, retrosternal or Wide paraspinal interface
Opacified pulmonary window
Broad paratracheal stripe
BOX 75-4 Traumatic Thoracic Aortic Injury Displaced left main stem bronchus
Right deviation of esophagus and trachea
MECHANISM OF INJURY Left hemothorax
Sudden body deceleration
Compression of thoracic vessels between spine and ribs/ CONTRAST-ENHANCED CT SCAN
sternum Polypoid or linear intraluminal areas of low attenuation
False aneurysm
SITE OF INJURY Irregular aortic wall or contour
Aortic isthmus (90%) Pseudocoarctation
Ascending aorta Intraluminal hematoma
Aortic arch Aortic dissection
SUSPICIOUS OF INJURY TEE
Unexplained hypotension Dilated aortic isthmus with abnormal contour
Evidence of direct chest injury Acute false aneurysm formation
Pulse deficits Intraluminal medial flap
Between right and left upper extremities Mobile image appended to thoracic aortic wall
Between upper and lower extremities Crescentic or circumferential thickening of the aortic wall
Mechanical ventilation
Retrosternal or interscapular pain CT ANGIOGRAPHY WITH THREE-DIMENSIONAL
Hoarseness REFORMATION
Systolic precordial flow murmur Directly indicates location and type of lesion (Figure 75-7)
Lower extremity neurologic deficits
CT, Computed tomography; TEE, transesophageal echocardiography.
406 SECTION 14 Trauma
Both CT and TEE are capable of diagnosing aortic detected if there is blood between the left lung and the
injuries that require surgical intervention or conservative thoracic wall. Aortic branch injuries are difficult to detect
management. However, because of its relative invasive- by TEE. In patients with suspected esophageal injuries,
ness, conflict about its accuracy, and special skill sets that TEE is contraindicated. These patients frequently present
may be unavailable after hours, TEE has not become a with bloody nasogastric tube drainage, severe facial trauma,
routine screening method. Nevertheless, TEE is valuable unstable cervical spine injuries, and pneumoperitoneum.
in many instances. Most patients do not have major aor- Definitive diagnosis of a blunt aortic injury is currently
tic tears, and their hemodynamic abnormality generally made by CT angiography (see Box 75-5). It provides de-
originates from other injuries, such as to the spleen or tailed information about the injury, aiding treatment deci-
liver, which require immediate surgery without time for sions. Multidetector CT scans with three-dimensional
further evaluation of the chest. Intraoperative TEE in reformation have replaced invasive aortography, which
these instances eliminates uncertainty about the presence was the standard diagnostic method about a decade ago
of traumatic aortic injury and permits appropriate inter- (Figure 75-7).
vention for other problems while the diagnosis is made
by the anesthesiologist. 8. How is surgery prioritized in patients with blunt
TEE findings of traumatic thoracic aortic injury include trauma and multiple injuries that include thoracic
(Figure 75-6) the following: aortic damage?
• Grade 3
• Dilated aortic isthmus with abnormal contour or Patients with complete or nearly complete circumfer-
acute false aneurysm formation ential transection of all three layers of the aortic wall
• Grade 2 are unlikely to arrive in the operating room. These
• Intraluminal medial flap associated with subad- patients die either in the field or in the hospital within
ventitial disruption 4–6 hours. Patients who survive to surgery with this
• Grade 1 pathology generally have a small perforation, a partial
• Mobile flap attached to the thoracic aortic wall transection that is temporarily sealed with perivascular
consistent with an intimal tear or a mural thrombus clot, or a relatively large transection that bleeds at
• Crescentic or circumferential thickening of the a relatively slow rate because of hypotension and
aortic wall suggesting the presence of intramural possibly perivascular barriers such as adjacent tissues
hematoma or clot sealing the lesion. In our experience, a patient
In addition, traumatic hemomediastinum should be experiencing a 70% transection of the aortic circumfer-
considered if the distance between the esophageal probe ence survived until surgery. Most patients who arrive
and the anteromedial wall of the aortic isthmus is !3 mm, in the operating room have relatively small, sealed,
or if there is blood between the posterolateral aortic wall subadventitial, usually posterior wall, injuries, which
and the left visceral pleura. A left-sided hemothorax can be require intervention because of impending rupture. In
Ao
FIGURE 75-6 ■ TEE images of grades 1, 2, and 3 traumatic thoracic aortic injury (TAI). Ao, aorta; FA, false aneurysm. (From Goarin J-P,
Cluzel P, Gosgnach M, et al.: Evaluation of transesophageal echocardiography for diagnosis of traumatic aortic injury. Anesthesiology 93:1373, 2000.)
75 Thoracic Trauma 407
TABLE 75-1 Change in Management of Blunt cardiac free wall rupture. Likewise, as we have experi-
Thoracic Aortic Injuries from 1997 enced in the past, an aortic injury may be recognized a
to 2007 few days after injury by spiral CT or during the late
phase of a pulmonary angiogram obtained to rule out
AAST1 (N " 253) AAST2 (N " 193) pulmonary embolism.
Diagnosis
Aortogram 220 (87%) 16 (8%) Airway Management Pitfalls
CT scan 88 (35%) 180 (93%) Airway management difficulties may be encountered for
TEE 30 (12%) 2 (1%) several reasons. Bleeding from the aorta can reach the
prevertebral space. A hematoma in this area could shift the
Repair larynx and trachea anteriorly, creating difficulty during
Open 207 (100%) 68 (35%) laryngoscopy and intubation. Prevertebral hematomas are
Endovascular — 125 (65%)
easily detected by cervical CT or lateral neck film. Laryn-
goscopic visualization may be difficult in the presence
Outcomes of a cervical collar because of limited neck extension.
Mortality 53/241 (22%) 25/193 (13%) Combined with a prevertebral hematoma, limited neck
extension complicates conventional laryngoscopy. How-
Paraplegia ever, neck extension should be avoided not only because of
All patients 18 (9%) 2 (2%)
Open repair 18 (9%) 2 (3%) the possibility of cervical spine injury but also to prevent
Endovascular 0 1/125 (1%) sudden hemorrhage from an aortic arch injury. A perivas-
Renal failure 18 (9%) 17 (9%) cular hematoma that seals the injury could be distracted by
Repair site 1/207 (1%) 25/125 (20%) extension of the neck.
complication Subadventitial and perivascular hematomas or pseu-
doaneurysms may compress the left main stem bronchus
AAST1, American Association for the Surgery of Trauma 1997 study; and cause narrowing of its lumen. Double-lumen tubes
AAST2, American Association for the Surgery of Trauma 2007
study; CT, computed tomography; TEE, transesophageal
have the advantage of preventing spillage of blood into
echocardiography. the right bronchus from the left lung during dissection of
From Demetriades D, Velmahos GC, Scalea TM, et al.: Diagnosis and the aorta. However, forcing a left-sided endobronchial
treatment of blunt thoracic aortic injuries: changing perspectives. tube blindly into the left main stem bronchus may result
J Trauma 64:1415, 2008. in a burst of peribronchial bleeding. Visualization of the
left main stem bronchus with a fiberoptic bronchoscope
before advancing the endobronchial tube can diagnose
this potential problem.
specific center probably has some effect on the rate of these
complications. Although the short-term results of endovas- Central Line Placement Pitfalls
cular management are clearly superior to conventional
open repair, there is little information about its long-term Bleeding into the left or rarely into the right hemithorax
outlook. is a frequent complication of thoracic aortic rupture.
The second relatively new strategy is conservative A large quantity of blood sometimes may fill the pleural
nonoperative treatment of grades 1 and 2 injuries involv- cavity, not only causing collapse of the lung and mediasti-
ing intramural hematomas or intimal tears. Observation nal shift but also giving false information when attempting
with CT scans and BP control appears to suffice for safe to cannulate the internal jugular or subclavian vein. Free-
management of these patients. Although endovascular flowing blood may not indicate vascular puncture; it may
and conservative techniques are currently employed in be secondary to entry into the blood-filled interpleural
the management of most blunt aortic injuries, open re- space. If this situation is not recognized, rapid infusion of
pair is still used in some centers. Specific pitfalls and their fluids into the pleural space may result in catastrophic
management are discussed next. complications.
10. What are the perioperative clinical and Pitfalls Related to Use of Anesthetic Drugs
anesthetic pitfalls that can be encountered during The primary goal of anesthetic management in patients
management of patients with thoracic aortic with vascular injuries is to avoid bleeding from dislodg-
injuries, and how should they be managed? ment of perivascular clots. This goal can be accomplished
by deep anesthesia and complete muscle relaxation,
Diagnostic Pitfalls
which is easily accomplished in hemodynamically stable
More obvious coexisting injuries, failure to obtain ap- patients. However, deep anesthesia may not be possible
propriate studies, and misinterpretation of radiographic in unstable trauma victims, who tolerate only oxygen,
findings may result in diagnostic difficulties. For exam- muscle relaxation, and possibly a minimal dose of intra-
ple, an initially missed aortic injury may be recognized a venous anesthetic.
few days later during emergency sternotomy to relieve Another important objective of anesthesia is to decrease
cardiac tamponade and to control bleeding caused by viscous drag, the frictional force of flowing blood against
75 Thoracic Trauma 409
the vascular wall, which may displace a clot sealing the site last-mentioned may be achieved in several ways: partial
of injury. It is proportional to viscosity and blood flow and femoral-femoral bypass, left heart bypass (left atrioaortic
inversely proportional to the fourth power of the radius. or atriofemoral), and right atrial-to-distal aortic bypass.
It is important to decrease the force of myocardial contrac- The advantage of left or right atrial-to-distal aortic
tion. In a young, healthy patient, force of cardiac contrac- bypass techniques is that they can be used with minimal
tion may increase to maximum levels to compensate for or no anticoagulation.
hypovolemia. Interfering with compensatory mechanisms Clamping and sewing is associated with the highest
could produce a catastrophic outcome. These conflicting rate of spinal cord complications. However, the incidence
objectives may be addressed by careful titration of the an- of paraplegia is lower if clamp time is #30 minutes.
esthetic while monitoring myocardial contractility with Passive shunt placement between proximal and distal
TEE and measurement of systemic BP. Control of BP in aorta does not significantly decrease the incidence of
the preoperative period and before clamping of the aorta neurologic deficit. Partial bypass (e.g., femoral-femoral)
during surgery is crucial to prevent rupture. Preoperative decreases the rate of paraplegia, but the need for heparin-
%-adrenergic blocking or calcium channel–blocking agents ization is a significant disadvantage. Left atriofemoral
with or without sodium nitroprusside can usually maintain bypass is more frequently used than left atrioaortic or
systolic BP at 80–90 mm Hg. right atrioaortic techniques. If used with a centrifugal
As discussed previously, the surgical mortality rate pump, these approaches result in the best spinal cord
from traumatic aortic injury averages 20% (range, 5%– protection. Heparin-bound cannulas are used, which
35%). Mortality appears to correlate with patient age, obviate the need for systemic heparinization. Left heart
preoperative hypotension, delayed diagnosis and late sur- bypass also has two important additional advantages
gical treatment, and location of the lesion. Proximal aortic in that unloading of the left heart may decrease cardiac
injuries have a greater mortality than isthmic injuries. complications and possibly decreases ischemic reperfu-
Also injuries located #1 cm from the origin of the left sion injury. The particular surgical technique is dictated
subclavian artery are associated with a greater likelihood by surgeon preference and other associated injuries.
of technical difficulty, rupture, and mortality during sur-
gical manipulation than injuries in other locations. 11. Describe the clinical management
of transmediastinal gunshot wounds.
Pitfalls Related to Spinal Cord Ischemia
Injuries to internal organs caused by this type of trauma
Spinal cord ischemia resulting in paraplegia or paraparesis is are unpredictable. Any organ, even outside the thorax,
a well-known complication of thoracic aortic injury and its may be injured depending on the path of the bullet.
repair. A preoperative neurologic evaluation should be Penetrating trauma to the cardiac window, defined as a
documented to avoid confusion about neurologic deficits quadrangle bounded by the midclavicular lines laterally,
after surgery. The blood supply to the spinal cord is from the clavicles superiorly, and eleventh ribs inferiorly, is
one anterior and two posterior spinal arteries, which origi- highly likely to damage the heart. Evaluation must in-
nate from branches of the vertebral artery at the base of the clude not only the heart but also the other intrathoracic
skull and descend along the cord. The anterior spinal artery organs. Diagnostic algorithms for transmediastinal gun-
supplies the anterior two thirds and the posterior spinal shot wounds recommend transferring unstable patients
arteries the posterior one third of the cord. Anastomoses directly to the operating room. Stable patients may be
between the anterior and posterior blood supply of the cord evaluated by chest radiograph, transthoracic ultrasound,
are weak, and there are areas with marginal blood supply and spiral CT. A patient with abnormal ultrasound find-
within the spinal cord. The anterior spinal artery receives ings should be transferred directly to the operating
a few radicular branches that originate from the thoracic room. Patients with abnormal spiral CT findings may
intercostals. The largest of those is the great radicular artery need further study with esophagography, angiography,
of Adamkiewicz (arterial radicularis magna). bronchoscopy, or esophagoscopy. Positive findings in
There are two common mechanisms of spinal cord any of these examinations requires surgery.
ischemia in traumatic aortic injury. The first is occlusion Patients with penetrating injury and, to a lesser extent,
of a subclavian artery, which supplies the vertebral and the blunt injury who require intubation and ventilation may
spinal arteries. Injury or surgical clamp placement during develop systemic air embolism. This complication results
repair account for many of these cases. The second from entry of higher pressure alveolar air into injured
mechanism of spinal cord ischemia is surgical interference lower pressure pulmonary veins. Clinical signs and symp-
with intercostal vessels supplying the artery of Adamkie- toms of this frequently fatal complication include sudden
wicz. The blood supply to the artery of Adamkiewicz cyanosis, hypotension, cardiac arrest, loss of conscious-
originates from the last four thoracic segments in 75% of ness, and air bubbles in the radial, retinal, or coronary
patients, from L1 or L2 in 15%, and from the fifth to arteries. Although surgical measures, such as emergency
eighth intercostal arteries in 10%. Surgical technique is thoracotomy and clamping the hilum of the lacerated
the likeliest cause of spinal cord injury in patients without lung, have been recommended, the immediate measure
a preoperative neurologic deficit or long periods of to minimize further embolism is to ventilate with the
hypotension. lowest possible peak inspiratory pressure. Placement of a
There are three techniques for surgical repair of aortic double-lumen tube or a bronchial blocker to isolate and
injuries: clamp and sew, passive shunting between proxi- avoid ventilation to the injured lung is another measure
mal and distal aorta, and cardiopulmonary bypass. The when time and equipment become available.
410 SECTION 14 Trauma
Anesthetic management of these patients is challeng- Demetriades D: Blunt thoracic aortic injuries: crossing the Rubicon.
ing. The requirement for massive fluid and blood replace- J Am Coll Surg 214:247, 2012.
Demetriades D, Velmahos GC, Scalea TM, et al.: Diagnosis and treat-
ment necessitates insertion of large-bore intravenous lines. ment of blunt thoracic aortic injuries: changing perspectives. J Trauma
Abnormal coagulation requires factor and platelet replace- 64:1415, 2008.
ment. Airway management may be difficult because of Goarin J-P, Cluzel P, Gosgnach M, et al.: Evaluation of transesophageal
airway injury or mediastinal shift from hematoma, often echocardiography for diagnosis of traumatic aortic injury. Anesthesiology
93:1373, 2000.
necessitating fiberoptic-guided intubation to avoid entry Haynes D, Baumann MH: Management of pneumothorax. Semin
into a false passage. Acid-base and electrolyte balance Respir Crit Care Med 31:769, 2010.
should be maintained. Cardiac injuries must be repaired Hernandez G, Fernandez R, Reina-Lopez P, et al.: Noninvasive ventilation
immediately, possibly requiring cardiopulmonary bypass reduces intubation in chest trauma-related hypoxemia: a randomized
for safe repair of major coronary artery injuries. clinical trial. Chest 137:74, 2010.
Ho AM-H, Karmakar MK, Critchley LAH: Acute pain management of
patients with multiple fractured ribs: a focus on regional techniques.
Curr Opin Crit Care 17:323, 2011.
SUGGESTED READINGS Maloney JT, Fowler SJ, Chang W: Anesthetic management of thoracic
trauma. Curr Opin Anesthesiol 21:41, 2008.
Battle CE, Hutchings H, Evans PA: Risk factors that predict mortality in
Orliaguet G, Ferjani M, Riou B: The heart in blunt trauma. Anesthesiology
patients with blunt chest trauma: systematic review and meta-analysis.
95:544, 2001.
Injury 43:8, 2012.
Pretre R, Chilcott M: Blunt trauma to the heart and great vessels. N Engl
Boersma WG, Stigt JA, Smit HJM: Treatment of haemothorax. Respir
J Med 336:626, 1997.
Med 104:1583, 2010.
Round JA, Mellor AJ: Anesthetic and critical care management of thoracic
Bosman A, deJong MB, Debeij J, et al.: Systematic review and meta-
injuries. J R Army Med Corps 156:139, 2010.
analysis of antibiotic prophylaxis to prevent infections from chest drains
Singh KE, Baum VC: The anesthetic management of cardiovascular
in blunt and penetrating thoracic injuries. Br J Surg 99:506, 2012.
trauma. Curr Opin Anesthesiol 24:98, 2011.
Buckley M, Edwards H, Buckenmaier III CC, et al.: Continuous tho-
Stone MB, Secko MA: Bedside diagnosis of pulmonary contusion. Pediatr
racic paravertebral nerve block in a working anesthesia resident—
Emerg Care 25:854, 2009.
when open opioids are not an option. Milit Med 176:578, 2011.
Walkey AJ, Nair S, Papadopoulos S, et al.: Use of airway pressure
Cardarelli MG: The management of traumatic aortic rupture. Adv Surg
release ventilation is associated with a reduced incidence of venti-
37:123, 2003.
lator-associated pneumonia in patients with pulmonary contusion.
Cardarelli MG, McLaughlin JS, Downing SW, et al.: Management of
J Trauma 70:E42, 2011.
traumatic aortic rupture: a 30-year experience. Ann Surg 236:465, 2002.
Yadav K, Jalili M, Zehtbachi S: Management of traumatic occult pneumo-
Cohn SM, DuBose JJ: Pulmonary contusion: an update on recent
thorax. Resuscitation 81:1063, 2010.
advances in clinical management. World J Surg 34:1959, 2010.
CASE 76
Burns
Jaroslav Usenko, MD
QUESTIONS
1. What is the epidemiology of burns in the 7. What is the pathophysiology of carbon monoxide
United States? poisoning, and how is carbon monoxide poisoning
2. Describe how burns are classified, how the treated?
percentage of total body surface area burned is 8. What is cyanide poisoning, and how is it
estimated, and the extent of injury that occurs treated?
with different burn depths. 9. Explain the concept of direct thermal upper
3. Which patients require care in specialized burn airway injury, when it is suspected, and its
centers? consequences.
4. What is the pathophysiology of burn injury, what 10. What techniques may be used to secure the
are the local and systemic effects, and how do airway for airway management of burn patients,
burns affect different organ systems? and is succinylcholine acceptable for rapid-
5. What fluid should be used for fluid resuscitation sequence intubation?
of a burn patient, and what are the possible 11. Explain the surgical management of burns, discuss
complications of fluid resuscitation? the timing of surgery, and identify anesthetic
6. What is smoke inhalation injury, what are the considerations for burn surgery.
implications of inhalation injury, and how is
inhalation injury managed?
A 52-year-old man was brought to the emergency the United States declined 50% over a 20-year period.
department by ambulance after being injured in a This decline is attributed to prevention efforts resulting
house fire, and you were asked to assess him for inhala- in a decreased number of patients with potentially fatal
tion injury and to assist with airway management. The burns and improvements in the clinical care of patients
patient’s injuries appeared to be partial-thickness burns with severe burns.
to both upper arms, most of the anterior trunk, and
right thigh. His vital signs were heart rate 108 beats per 2. Describe how burns are classified, how the
minute, respiratory rate 25 breaths per minute, blood percentage of total body surface area burned is
pressure 158/92 mm Hg, and oxygen saturation 93% estimated, and the extent of injury that occurs
with supplemental oxygen by nasal cannula. When he with different burn depths.
complained of pain, his voice sounded hoarse, and you
noticed carbonaceous sputum. Burns are classified according to the total body surface
area (TBSA) involved, the depth of burn, and the pre-
1. What is the epidemiology of burns in the sence or absence of inhalation injury. Additionally, burns
are classified into five causal categories, as follows: injury
United States?
from flame, hot liquids (scald), hot or cold, chemicals,
Burns (thermal injuries) cause many complications and and electricity.
deaths. In the United States, !1.2 million people sustain The TBSA burned is calculated using the rule of nines
thermal injuries every year. Most cases are minor, but ap- (Figure 76-1). In adults, each upper extremity and the
proximately 50,000 burn cases are moderate to severe and head and neck are 9% each of the TBSA, the lower ex-
require hospitalizations. Of these cases, 4000–5000 patients tremities and the anterior and posterior aspects of the
die from complications of thermal injury. trunk are 18% each of the TBSA, and the perineum and
Deaths resulting from burns usually occur in a bimodal genitalia are 1% of the TBSA. Children have a larger
distribution—either immediately after injury or weeks proportion of body surface area contributed by the head
later, from multiorgan failure. About one third of burn- and neck relative to the surface area of the lower extremi-
related injuries and deaths occur in children. House fires ties. The Lund-Browder chart can be used to estimate the
account for 75% of all burn-related deaths. TBSA in children (Figure 76-2).
Morbidity and mortality rates associated with thermal Burn depth is classified according to the degree of
injury are decreasing; deaths and hospital admissions in injury in the epidermis, dermis, subcutaneous fat, and
411
412 SECTION 14 Trauma
9% A A
9% 13 13
2 2 2 2
9% 9% 1 1 1 1
9%
1 2 2
1 1 1 1
1%
B B B B
18% 18%
C C C C
1 1 1 1
FIGURE 76-1 ■ Rule of nines for determining the percentage of (Age in years)
body surface area burned in adults. (Adapted from MacLennan N, Area 0 1 5 10 15 Adult
Heimbach DM, Cullen BF. Anesthesia for major thermal injury.
A: Half of head 9- 8- 6- 5- 4- 3-
Anesthesiology 1998;89(3):749–70.)
B: Half of thigh 2- 3- 4 4- 4- 4-
C: Half of leg 2- 2- 2- 3 3- 3-
Depending on the wound environment, the zone of Burn injury affects the lungs directly and indirectly.
stasis can either survive or progress to coagulative Direct effects include upper airway obstruction and
necrosis. smoke inhalation injury (discussed in further detail sub-
• Hyperemia is characterized by vasodilation from in- sequently). Indirect injury occurs as a result of the effects
flammation surrounding the burn wound and contains of circulating inflammatory mediators, complications
viable tissue from which the healing process begins. of burn therapy, and infection. Pulmonary edema and
Mediators released from the burn wound contribute pulmonary hypertension can also occur.
to local inflammation and wound edema. Oxygen-free The kidneys are affected by diminished plasma volume
radicals, histamine, bradykinin, vasoactive amines, and and cardiac output. Increased levels of catecholamines,
interleukins have been implicated. In major burns, local angiotensin, aldosterone, and vasopressin cause systemic
injury triggers the release of inflammatory mediators into vasoconstriction and contribute to renal dysfunction. De-
the circulation, resulting in a systemic response charac- creased renal blood flow and glomerular filtration rate
terized by immune suppression, hypermetabolism, and result in oliguria, which, if left untreated, progresses to
protein catabolism. Systemic inflammation may progress acute tubular necrosis and renal failure. Early resuscita-
to sepsis and multiorgan failure. tion decreases the incidence of renal failure.
The cardiovascular system is affected by fluid shifts Mucosal atrophy, changes in digestive absorption, and
associated with major burn injury and effect of circulating increased intestinal permeability are gastrointestinal re-
mediators on contractility and systemic vascular resis- sponses to a burn. The extent of atrophy of the small
tance. Hypovolemic shock, described as burn shock, can bowel mucosa is proportional to the burn size. There is
occur immediately after a burn and primarily results from reduced uptake of glucose and amino acids and decreased
altered microvascular permeability of both burned and absorption of fatty acids. Gut permeability is increased
nonburned tissue in response to the above-described further when burn wounds become infected. Gastric
mediators. This altered microvascular permeability re- mucosal stress ulceration occurs with major burns but
sults in protein loss from the intravascular compartment may be minimized by enteral feeding.
to the interstitial compartment. There is also a marked Hypermetabolism develops after major burns and resus-
transient decrease in interstitial pressure caused by the citation. It is characterized by tachycardia, increased car-
release of osmotically active particles, causing a vacuum diac output, elevated energy expenditure, increased oxygen
effect whereby fluid is pulled in from the intravascular consumption, increased carbon dioxide production, and
space. The rapid influx of fluid into the interstitium neu- catabolism. These changes in metabolism are due partly to
tralizes the vacuum effect but does not prevent further release of catabolic hormones, which include catechol-
edema formation. Finally, an increase in interstitial space amines, glucocorticoids, and glucagon. The ambient tem-
compliance adds to changes in oncotic and hydrostatic perature when below thermoneutral (28°–32° C) further
pressures, exacerbating tissue edema formation further. increases metabolic rate in burn patients, and this should be
Initially, cardiac output is decreased independent of avoided.
intravascular volume status. Cardiac contractility is reduced Burns cause global depression in immune function,
because of circulating mediators, decreased responsiveness which places burn patients at risk for infectious compli-
to catecholamines, and decreased coronary blood flow. cations, including bacterial wound infection, pneumo-
Systemic vascular resistance is increased. After successful nia, sepsis, and multiorgan failure. Immune system
resuscitation and the first 24–48 hours after burn injury, the impairment results from depressed cellular function in
cardiovascular response evolves into systemic inflammatory all parts of the immune system, including decreased
response syndrome, manifested by increased cardiac output activation and activity of neutrophils, macrophages,
and reduced systemic vascular resistance. and T and B lymphocytes. When !20% of the TBSA
414 SECTION 14 Trauma
literature. Similarly, the use of hypertonic saline has yielded prevented by fluid restriction. However, although over-
disappointing results, with a fourfold increase in renal fail- hydration could increase pulmonary edema, inadequate
ure and a twofold increase in mortality compared with pa- fluid resuscitation increases the severity of pulmonary
tients given lactated Ringer’s solution. injury. Resuscitation is adequate if normal cardiac index
Tissue edema is a hallmark of burn pathophysiology. or urine output is maintained.
Although fluid resuscitation can correct hypovolemia, it can The management of smoke inhalation injury is directed
also exacerbate edema. The possible consequence is in- at maintaining airway patency and maximizing gas ex-
creased compartment pressure in the extremities, the abdo- change. Care is primarily supportive. In burn patients in-
men, and the orbit. The increased compartment pressures tubated for airway protection or for respiratory failure, an
may progress to compartment syndromes, and require re- important goal of mechanical ventilation is to minimize
lease by escharotomies. The abdominal compartment is barotrauma. Current Adult Respiratory Distress Syn-
clinically monitored with a Foley catheter and pressures drome (ARDS) Network protocols are widely used to
greater than 30 mm Hg require interventions, such as es- minimize positive airway pressure delivered by ventilators.
charotomy and possibly decompressive laparotomy. Permissive hypercapnia may be used to help minimize
Some burn patients do not respond to fluid resuscita- plateau pressures. Arterial oxygen tension !60 mm Hg
tion guided by the Consensus formula. Although it is is acceptable to minimize oxygen toxicity to the lungs.
sometimes impossible to predict accurately who will fail Routine pneumonia prevention strategies should be em-
fluid resuscitation, patients with electrical burns, in ployed. Prophylactic antibiotics for inhalation injury are
whom resuscitation is delayed, and patients using alcohol not indicated. As patients recover from lung injury, tra-
or illicit drugs routinely require additional fluid. Patients cheal extubation should be done as soon as clinically pos-
with smoke inhalation injury, discussed in detail next, sible to minimize the occurrence of ventilator associated
also frequently have increased fluid requirements. pneumonia and because the airway is more effectively
cleared by patient coughing than by suctioning through
6. What is smoke inhalation injury, what are the an endotracheal tube. Additionally, prolonged intubation
implications of inhalation injury, and how is risks laryngeal and tracheal injuries.
inhalation injury managed?
7. What is the pathophysiology of carbon monoxide
Smoke inhalation injury results from toxins that cause poisoning, and how is carbon monoxide poisoning
chemical damage to the airway. Products of combustion, treated?
such as ammonia, nitrogen dioxide, sulfur dioxide, and
chlorine, combine with water in the respiratory tract Carbon monoxide is a major component of most open
to produce strong acids and alkalis. These chemicals fires. It causes tissue hypoxia and metabolic acidosis by
induce bronchospasm, edema, and mucous membrane the following mechanisms:
ulceration. Another hallmark of inhalation injury is the • Carbon monoxide has 250 times more affinity for he-
separation of ciliated epithelial cells from the basement moglobin than oxygen does and, by displacing oxygen,
membrane, which contributes to exudate formation decreases oxygen-carrying capacity of hemoglobin.
within the airway. The exudate eventually coalesces to • Carbon monoxide shifts the oxyhemoglobin disso-
form fibrin casts, which can be difficult to clear. ciation curve to the left, reducing the unloading of
Patients who present with a history of a closed-space oxygen to the tissues.
fire, such as in a small apartment or a car, are at high risk • Carbon monoxide binds to cytochrome oxidase and
for smoke inhalation injury. Bronchoscopy is the “gold impairs the activity of several intracellular enzymes.
standard” for establishing the diagnosis. A clinical presen- Carbon monoxide poisoning should be considered in all
tation of facial burns, singed nasal hairs, carbonaceous patients who sustained burns in enclosed spaces. Patients
sputum, hoarseness, and respiratory distress increases the who present with smoke inhalation injury are at high risk
index of suspicion for inhalation injury. Each of these find- for carbon monoxide poisoning. Clinical presentation de-
ings has poor sensitivity and specificity, but the presence of pends on carboxyhemoglobin levels (Table 76-3). Delayed
two or more of these clinical parameters increases the neuropsychiatric sequelae have been described in patients
likelihood of positive bronchoscopic findings. exposed to toxic levels of carbon monoxide.
Smoke inhalation injury is a major factor that increases
morbidity and mortality in burn patients. It increases
the amount of time spent on mechanical ventilation. The
addition of inhalation injury to a cutaneous burn of any TABLE 76-3 Carbon Monoxide Toxicity
size doubles mortality. Acute upper airway obstruction Carboxyhemoglobin Level Signs and Symptoms
occurs in 20%–33% of hospitalized patients with inhala-
tion injury and is a major hazard because of the risk of "20% Headache, tinnitus, nausea
rapid progression from mild pharyngeal edema to com- 20%–40% Weakness, drowsiness
plete upper airway obstruction. Early tracheal intubation
!40% Severe neurologic
may be necessary. dysfunction (may be
Inhalation injury complicates fluid management of permanent), coma
burn patients. The presence of inhalation injury is associ-
55%–70% Cardiac dysrhythmias
ated with increased resuscitation fluid requirements. The (often fatal), brain injury
pulmonary edema seen in smoke inhalation injury is not
416 SECTION 14 Trauma
Carbon monoxide poisoning is diagnosed based on confirmed with fiberoptic laryngoscopy, which provides
clinical findings and by measuring carboxyhemoglobin direct information about glottic and periglottic struc-
levels. Oxyhemoglobin saturation measured by com- tures. Fiberoptic bronchoscopy can provide information
monly used pulse oximeters may be normal because the about the lower airways. Smoke inhalation injury, which
pulse oximeters read carboxyhemoglobin as saturated is primarily a chemical injury, may also be present in a
hemoglobin. A cooximeter, which measures the percent- burn patient with thermal upper airway injury.
age of hemoglobin, oxyhemoglobin, carboxyhemoglo- Glottic and periglottic edema that results from thermal
bin, and methemoglobin, is necessary to obtain accurate upper airway injury may rapidly progress to complete
oxygen saturations. airway obstruction. This is particularly concerning in
Carbon monoxide poisoning is treated with supple- pediatric patients, whose airways are of smaller diameter
mental oxygen. The patient’s inspired oxygen should be and may be occluded by minimal swelling. Prophylactic
maintained at the highest possible concentration. A frac- intubation may be required.
tional concentration of oxygen of 1.0 in inspired gas
decreases the blood half-life of carboxyhemoglobin from 10. What techniques may be used to secure
4 hours, seen when breathing room air, to 60–90 minutes. the airway for airway management of burn
Hyperbaric oxygen treatment further shortens the half-life
patients, and is succinylcholine acceptable
of carboxyhemoglobin. Hyperbaric oxygen treatment
should be considered in patients with carboxyhemoglobin for rapid-sequence intubation?
levels !30%, if this poses no delay to or interference with Airway management of burn patients requires a focused
treatment of other, more life-threatening injuries. history and physical examination to assess whether the
airway needs to be secured and to anticipate challenges in
8. What is cyanide poisoning, and how is it treated? securing the airway. Information regarding the presence
of preexisting airway abnormalities, a history of head and
Hydrogen cyanide is a product of the incomplete com- neck surgery, and a history of difficult airway manage-
bustion of certain plastics and other synthetic materials. ment should be obtained. Burn patients should be evalu-
Cyanide may be inhaled or absorbed through mucous ated for current airway injury and for signs of airway
membranes. Cyanide causes tissue asphyxia by inhibiting obstruction.
cytochrome oxidase activity, which prevents mitochon- Once the information is obtained, an important man-
drial oxygen consumption. Cyanide also interferes with agement decision is to determine if the patient requires
the tricarboxylic acid cycle, causing affected cells to rely tracheal intubation. Patients with abnormal airways,
on anaerobic metabolism to generate adenosine triphos- signs of airway obstruction, or impending respiratory
phate, which results in lactic acidosis. failure need prompt airway management. Intubation may
Similar to carbon monoxide toxicity, a history of smoke be required for associated injuries or to facilitate emer-
inhalation and fire in an enclosed space raises the suspicion gency diagnostic studies and treatment when patients are
of cyanide toxicity. In fact, carbon monoxide toxicity, agitated or uncooperative. There is also a role for pro-
smoke inhalation injury, and cyanide poisoning may be phylactic intubation in patients whose airway injuries are
present in the same patient. A definitive diagnosis can be not immediately apparent if there are concerns for edema
made only by measuring the blood cyanide level. Symp- progression and rapid airway obstruction. It is generally
toms range from dizziness, headache, and tachycardia to better to intubate a burn patient early than late.
lethargy, seizures, and cardiopulmonary failure, depending When it is decided a burn patient needs tracheal intu-
on the blood cyanide level. bation, the technique depends on whether the airway is
Initial treatment of cyanide toxicity is the administra- normal or abnormal. If there is no airway abnormality,
tion of supplemental oxygen and hemodynamic support. tracheal intubation may be achieved with rapid-sequence
The half-life of cyanide is about 1 hour. Specific antidotes induction in the emergency department trauma bay.
exist, such as sodium thiosulfate, which accelerates he- Patients should continue to receive supplemental oxygen
patic metabolism of cyanide, and nitrites, which acceler- in preparation for intubation. An induction agent (type
ate nonhepatic metabolic pathways by increasing levels of and dose based on the clinical situation) and a rapidly
methemoglobin. However, there is some controversy as acting muscle relaxant (succinylcholine or rocuronium)
to whether specific treatments are necessary or helpful, are administered, followed by rapid intubation of the
given the short half-life of cyanide. trachea with conventional direct laryngoscopy.
The use of succinylcholine warrants additional con-
9. Explain the concept of direct thermal upper sideration. After a burn, extrajunctional acetylcholine
airway injury, when it is suspected, and its receptors proliferate, which results in exaggerated release
consequences. of potassium after administration of succinylcholine.
Rapid elevations of serum potassium !9 mEq/L have
Thermal upper airway injury results from inhalation of su- been documented and are associated with cardiac arrest.
perheated air or steam. Heat is dispersed in the upper air- The process of receptor proliferation takes several days,
ways, so direct thermal injury to the lower airways and lungs and there is an initial window of safety of unknown dura-
is rare. Brief exposure of the epiglottis or larynx to either dry tion. The general agreement is that administration of
air at 300° C or steam at 100° C leads to airway edema. succinylcholine is safe in the first 24 hours after a burn
Stridor, dysphonia, hoarseness, dysphagia, facial burns, injury and should be avoided afterward.
and soot in the mouth or nose should raise the suspicion In a cooperative adult burn patient with an abnormal
of thermal upper airway injury. The diagnosis can be airway or upper airway obstruction, an awake technique
76 Burns 417
may be selected. An awake intubation is most frequently controlled with epinephrine-soaked laparotomy pads. If
achieved with a flexible fiberoptic bronchoscope. Ade- an autograft is unavailable, temporary coverage with an
quate topical anesthesia is a key requirement for a suc- allograft, xenograft, or biologic dressing is used.
cessful awake intubation. Intravenous opioids may be Early excision and grafting of burn wounds is currently
appropriate for an alert patient in pain, and small doses practiced because reports have shown benefits in terms of
of sedatives may be given to alleviate anxiety, but care survival, incidence of sepsis, and length of hospitalization.
must be taken to avoid exacerbating respiratory prob- One of the goals is to remove eschar, a potential nidus for
lems. Monitored transport to the operating room should inflammation and infection, before secondary sepsis su-
be considered for patients with markedly abnormal pervenes. The excision usually starts on days 2–5 follow-
airways. The operating room generally provides skilled ing the burn, after completion of fluid resuscitation, and
assistance, multiple airway devices, and an anesthesia is performed every 2–3 days, depending on the patient’s
machine and is the best environment for a surgical airway condition.
should that become necessary. Major burn surgery is usually performed under gen-
Pediatric patients with abnormal airways present spe- eral endotracheal anesthesia. Regional anesthesia is
cial challenges. Most young children do not cooperate often impractical given that an operation in a single
with an awake technique. Inhalation induction with oxy- patient may involve multiple excision and donor sites.
gen and a nonpungent volatile agent, such as sevoflurane, Laryngeal mask airways may be considered for minor
is likely to be the safest technique. Once the patient is cases that are not expected to result in significant blood
anesthetized, several methods of intubation are available loss and when the anesthesiologist has access to the
based on the experience of the anesthesiologist. A pediat- patient’s airway.
ric bronchoscope, a conventional laryngoscope, or one of Patients may be brought to the operating room already
the many airway devices currently available [GlideScope® tracheally intubated. The anesthesiologist should note the
(Verathon Inc. Bothell, WA), Airtraq optical laryngoscope position of the tracheal tube and ensure that it is properly
(Airtraq, Fenton, MO), LMA Fastrach™ (LMA North secured, especially if patient positioning changes are an-
America, Inc. San Diego, CA)] may be used. The key is to ticipated for the case. In patients who are not intubated,
choose a device with which one is most skillful to facilitate an airway assessment should be performed, as with any
urgent or emergent airway management. patient requiring anesthesia. Specific airway consider-
ations in burn patients have been discussed in detail ear-
11. Explain the surgical management of burns, lier; however, it bears repeating that if muscle relaxation
is used to facilitate airway management, succinylcholine
discuss the timing of surgery, and identify
must be avoided 24 hours after burn injury. Additionally,
anesthetic considerations for burn surgery. patients with large burns develop decreased sensitivity to
Deep second-degree and third-degree burns do not heal in nondepolarizing muscle relaxants and require 1.5 times
a timely fashion without surgery. The surgical manage- the usual intubating dose.
ment of burns involves excision of eschar and coverage Blood loss is a primary consideration during major
of viable tissue with an autograft or temporary cover. Tan- burn surgery. Because blood loss can be rapid and mas-
gential excision and fascial excision are the two surgical sive, blood products should be available in the operating
approaches. In tangential excision, which is a procedure room before starting the case. Blood loss may be difficult
performed more frequently, thin slices of burn eschar to estimate because it is generally not collected into the
are shaved sequentially with dermatomes until a healthy suction canister. Vigilant monitoring and close commu-
wound bed is developed. Blood loss is usually diffuse and nication with the surgical team are essential to provide
can be large. Laparotomy pads soaked with epinephrine timely resuscitation.
1:100,000 are applied to the wound to control bleeding. Hypothermia is another important consideration.
Systemic absorption of epinephrine may cause tachycardia Burn patients lose heat rapidly without intact skin and
and increases the probability of dysrhythmias. Tourniquets with large exposed surfaces. Hypothermia causes many
are usually used to minimize blood loss for tangential exci- complications and exacerbates hypermetabolism seen in
sion of extremities. major burns. The patient’s temperature should be moni-
Fascial excision involves removal of burn eschar and tored, areas out of the operative field should be covered
all the underlying fat en bloc to the level of muscle fascia and warmed, and the operating room ambient tempera-
or deeper structures. It can be performed more rapidly ture should be maintained at !28° C (thermoneutral) to
and with less blood loss than tangential excision. How- minimize heat loss.
ever, fascial excision results in marked cosmetic deformi- At the end of the case, the anesthesiologist has to
ties and functional limitations. It is generally reserved decide whether extubation is possible. Patients who are
for patients with fourth-degree burns or very extensive, brought to the operating room after tracheal intuba-
life-threatening third-degree burns. tion usually remain intubated and are transported back
After excision of tissues and attainment of hemostasis, to the burn unit. Patients who did not undergo tracheal
wounds are covered. An autograft is used for coverage intubation preoperatively may be extubated if they
when the wound bed is deemed suitable, a donor site is meet criteria. It is necessary to rule out the presence of
available, and the patient is stable. Wounds involving airway edema if a case involved large blood loss and
20%–30% of the TBSA can usually be covered with fluid resuscitation, especially if performed in the prone
an autograft of split-thickness skin, harvested from the position.
patient’s own donor site. Harvesting a split-thickness skin Additional considerations are to provide adequate post-
graft at the dermal level produces bleeding, which is operative analgesia and to ensure a smooth emergence.
418 SECTION 14 Trauma
Analgesic requirements may be difficult to estimate Gallagher JJ, Wolf SE, Herndon DN: Burns. pp. 559–585. In Townsend
because the patients are already receiving high doses of CM Jr, Beauchamp RD, Evers BM, et al. (eds.): Sabiston Textbook
of Surgery: The Biologic Basis of Modern Surgical Practice,
opioids preoperatively. If a split-thickness skin graft has 18th edition. Saunders, Philadelphia, 2008.
been applied, it is especially important to avoid uncon- Latenser BA: Critical care of the burn patient: the first 48 hours. Crit
trolled patient movement on emergence because of the Care Med 37:2819, 2009.
risk of graft dislodgment. Lee C, Luginbuehl I, Bissonnette B, et al.: Pediatric diseases. p. 581.
In Hines RL, Marschall KE (eds.): Stoelting’s Anesthesia and Co-
existing Disease, 5th edition. Churchill Livingstone, Philadelphia,
2008.
SUGGESTED READINGS MacLennan N, Heimbach DM, Cullen BF: Anesthesia for major thermal
Capan LM, Miller SM: Anesthesia for trauma and burn patients. p. 889. injury. Anesthesiology 89:749, 1998.
In Barash PG, Cullen BF, Stoelting RK, et al. (eds.): Clinical Anes- Yim KK, Berhow MT: Burn surgery. pp. 1143–1149. In Jaffe RA, Samuels
thesia, 6th edition. Lippincott Williams & Wilkins, Philadelphia, SI, Schmiesing CA, et al. (eds.): Anesthesiologist’s Manual of Surgical
2009. Procedures, 4th edition. Lippincott Williams & Wilkins, Philadelphia,
Demling RH: The burn edema process: current concepts. J Burn Care 2009.
Rehabil 26:207, 2005.
CASE 77
Abdominal Trauma
J. David Roccaforte, MD
QUESTIONS
1. What injuries and abnormalities can be anticipated 5. What are the intraoperative surgical objectives
from the history? during damage control laparotomy?
2. Explain the primary and secondary surveys 6. What is the best resuscitation fluid?
according to advanced trauma life support. 7. What are the appropriate endpoints of resuscitation
3. After the primary and secondary surveys are for this patient?
performed, what are the options for definitive 8. Explain the value of a massive transfusion protocol.
care, and what further diagnostic studies or ther-
9. What are the anesthesiologist’s intraoperative
apeutic interventions must be considered before
priorities?
transport?
10. What are the goals for subsequent postanesthesia
4. What are the airway management options?
care unit care?
A 26-year-old man shoveling snow from the roof of a surgical teams will operate concurrently. Significant in-
five-story apartment building slips and falls to the ground. traoperative blood loss is anticipated.
On arrival to the emergency department 20 minutes
later, he is awake and alert and can accurately state his 1. What injuries and abnormalities can be
name. He is not oriented to place, and he cannot recount
what happened. He is complaining of pain. On physical
anticipated from the history?
examination, he is shivering, has a grossly deformed right In general, our ability to anticipate significant injuries is
proximal femur, and has a tender abdomen to palpation. poor. The best marker of severe injuries after trauma is
His vital signs are heart rate 135 beats per minute, blood a recorded systolic blood pressure !90 mm Hg. Other
pressure 88/69 mm Hg, respirations 22 breaths per min- associations are far less valuable predictors, especially
ute, and oxygen saturation by pulse oximetry (SpO2) 99% pertaining to the mechanism of injury. Frequently,
on facemask oxygen. hearsay reports arrive before or concurrent with the
The primary survey reveals a patent, well-protected patient describing a fall of several floors, an occupant
airway; adequate oxygenation with supplemental oxy- ejected from a motor vehicle, or a through-and-through
gen; impaired ventilation secondary to pain and splint- gunshot wound. Subsequent evaluation of the patient
ing; clear breath sounds bilaterally; sinus tachycardia; reveals no injuries. Just as often, patients are brought in
hypotension responsive to rapid fluid boluses of with vague histories, such as falling from a standing
100–200 mL; intact cranial nerves; normal pupillary position, bicycling-pedestrian accident, or extremity
examination; intact sensation; and movement in all stabbing, and they are found to have significant, life-
four extremities. He has two 16-gauge intravenous threatening injuries.
(IV) catheters in his upper extremities. Because of these frequent discrepancies, all patients
After tracheal intubation, the patient is brought to the in whom significant trauma is considered possible
radiology department. He continues to have ongoing must be managed using a protocol-driven system spec-
fluid-responsive hypotension, and packed red blood cell ified by the American College of Surgeons advanced
transfusions are initiated. Computed tomography (CT) trauma life support (ATLS). The objectives of ATLS
scan of the brain is unremarkable, although diffuse axo- are quick and accurate diagnosis and initiation of
nal injury cannot be excluded. CT scan of the pelvis re- treatment for all life-threatening injuries. All patients
veals an unstable, “open-book” pelvic fracture. The ab- are managed similarly initially focusing on the primary
dominal CT scan demonstrates an avulsed, grade 5 right and secondary surveys of ATLS. The price paid to ex-
kidney injury with significant retroperitoneal bleeding. pedite diagnosis and treatment of trauma patients as
The patient proceeds directly to the operating room well as to avoid missing occult severe injury is that
for a damage control laparotomy. The planned proce- some patients receive otherwise “unnecessary” testing;
dures are exploratory and decompressive laparotomy; evaluation; and possibly even nontherapeutic interven-
right nephrectomy; and pelvic, right femoral, and right tions, such as tracheal intubation, tube thoracostomy,
ulnar external fixations. Trauma, urology, and orthopedic or exploratory laparotomy.
419
420 SECTION 14 Trauma
Specifically for this patient, it is relevant to appreciate traumatic brain injury is suspected. The GCS is a
that a fall of four stories is associated with approximately coarse screening tool that encompasses eye-opening,
50% mortality. Given that he has arrived at the hospital verbal, and motor responses (Table 77-2). GCS scores
alive and talking, it is likely that his fall was broken some- range from 3–15. A score of 3 represents a completely
how during descent. First aid initiated by bystanders and nonresponsive patient with a predicted mortality rate
emergency medical services (EMS), especially tourni- of 65%–90%. A GCS score of 13 predicts mortality
quets and pressure applied to bleeding areas, must be rates of !10%. Although the GCS score on admission
maintained during transfer to the hospital trauma team. correlates with survival outcomes, more importantly,
Injuries from the following categories can be anticipated the specific details of neurologic function should be
(Table 77-1). accurately noted. Often, loss of consciousness is re-
ported from the field, yet when patients arrive at the
hospital, they are awake with normal GCS scores.
Neurologic Injury This finding does not exclude neurologic injury; the
“lucid interval” of a potentially fatal epidural hema-
Traumatic Brain Injury
toma follows precisely this pattern. The presence of
The Glasgow Coma Scale (GCS) is the traditional seizures has a high correlation with positive findings
means of quickly assessing neurologic function when on CT scans of the brain (80%). Headache, amnesia,
Solid Organ Injuries The initial focus is on airway patency. The ability to
phonate and converse is usually sufficient proof of an
The liver and spleen are the most commonly injured in- adequate airway. Many of the criteria for immediate tra-
traperitoneal abdominal organs from blunt trauma. If the cheal intubation of trauma patients are similar to criteria
patient is hemodynamically stable, nonoperative man- typically used for other patients (i.e., hypoxemia, hy-
agement may be appropriate in select cases of hepatic and poventilation, lack of airway reflexes). The presence of
splenic trauma. The kidney is occasionally injured fol- oropharyngeal bleeding or stridor is always cause for
lowing blunt trauma, and the pancreas is injured less concern. Other times, the threshold for tracheal intuba-
frequently. Both the kidneys and the pancreas reside in tion of the trauma patient is lowered. For example, if
the retroperitoneal space. victims are intoxicated, combative, and actively bleeding,
they may need tracheal intubation expeditiously despite
the presence of adequate cough, gag and swallow re-
Systemic Abnormalities flexes. By default and until proved otherwise, trauma
Shock patients are presumed to have a full stomach and cervical
spine instability.
A reliable marker for a shock state does not exist. In Cervical spine protection begins with immobiliza-
this patient, hemorrhagic shock is presumed because tion in the field using minimally padded extrication
he has hypotension, tachycardia, altered mental sta- collars made of stiff, thin plastic. Cervical spine clear-
tus, and distended abdomen. Lactic acidosis develops ance is usually deferred until after the primary and
as a consequence of hypoperfusion. The degree of secondary surveys have been completed. If the airway
metabolic acidosis present on admission correlates needs to be secured, the risk of exacerbating a cervical
with mortality. spine injury is negligible provided that adequate pre-
cautions are maintained. These precautions include
Hypothermia manual in-line stabilization, minimizing neck exten-
sion, and management of the airway by an experienced
Although the patient was in the field for only 20 minutes, laryngoscopist.
he is shivering. The largest contributor to hypothermia is Extrication cervical spine collars and backboards
depressed metabolism that accompanies shock. Addi- can quickly lead to decubitus ulcer formation, some-
tional factors contributing to this patient’s hypothermia times in !1 hour. As soon as possible, backboards
include exposure to cold temperatures in the field and in should be removed, and the extrication collar should
the emergency department when fully disrobed and be changed to one that is padded and designed for
treatment with room temperature IV fluids. longer term use.
77 Abdominal Trauma 423
Breathing and Ventilation the secondary survey guide a further focused physical
examination as well as obtaining appropriate ancillary
In a spontaneously breathing patient, auscultation of diagnostic tests (e.g., laboratory, radiographic, ultra-
both lung fields is performed to establish the presence of sound). If the patient’s condition deteriorates, the pri-
bilateral breath sounds. In a hypotensive tracheally intu- mary survey is repeated.
bated patient, unilateral right-sided breath sounds (later
discovered to be from a right main-stem intubation) oc- 3. After the primary and secondary surveys are
casionally lead to the avoidable placement of an emer- performed, what are the options for definitive care,
gent left thoracostomy tube for suspected pneumothorax. and what further diagnostic studies or therapeutic
Trauma patients generally arrive at the emergency
interventions must be considered before transport?
department on supplemental oxygen. If the only moni-
tor of ventilatory adequacy is oxygen saturation, sig- Subsequent steps after the secondary survey involve fur-
nificant hypoventilation could be missed because oxy- ther evaluation and treatment. Possible options include
gen saturation can be maintained with a fraction of monitoring and observation, additional diagnostic evalu-
inspired oxygen (FiO2) of 100% oxygen despite very ation, interventional angiography, and surgery. Decisions
low tidal volumes. hinge on the patient’s known and suspected injuries in
addition to hemodynamic stability. Severe, refractory
Circulation with Hemorrhage Control hypotension is easy to recognize as hemodynamic insta-
bility. However, a finding of isolated tachycardia or a
Blood pressure is the initial vital sign used to establish normal blood pressure sustainable only with ongoing
adequacy of circulation. However, in severe hypovole- fluid boluses, vasoconstrictors, or both might not be as
mia, especially in young, healthy victims, compensatory obvious.
mechanisms can maintain blood pressure until precipi- For hemodynamically stable patients without obvious
tous circulatory collapse occurs. Active hemorrhage is injury, monitoring and observation are appropriate. At
controlled with applied pressure or tourniquets. If it the other extreme, a hemodynamically unstable patient
has not been done so already, large-bore peripheral IV with an acute abdomen following penetrating trauma
access is established. Fluids administered from this would likely proceed directly to the operating room for
point forward should be warmed. exploratory laparotomy. Other scenarios require a bal-
ance between the value of imaging and the risk of delay-
Disability (Neurologic Evaluation) ing treatment.
Bedside surface ultrasonography, referred to as fo-
This stage of the primary survey encompasses a quick cused abdominal sonography for trauma (FAST), has
assessment of both central and neuraxial integrity. The become the routine for evaluating intraabdominal, peri-
GCS score (Table 77-2) is correlated with survival in cardial, and intrathoracic bleeding. In experienced
traumatic brain injury and is commonly used as a short- hands, FAST is able to confirm free fluid in the perito-
hand method of communicating mental status. Patients neal cavity; however, it is an unreliable method for
with a GCS score !8 are unlikely to be able to protect excluding hollow viscera injury. Diagnostic peritoneal
their airway and may require tracheal intubation. lavage is a complementary tool for evaluating intraab-
Beyond the GCS score, it is crucial to assess and dominal bleeding and diagnosing gastrointestinal perfo-
document specific findings of an immediate baseline neu- ration (Figure 77-1).
rologic examination, including cranial nerve function, Whenever possible, as dictated by hemodynamic stabil-
pupillary size, movement of extremities, lateralizing ity, further delineation of injuries by radiologic evaluation
signs, sensation (if the patient is able to cooperate), and (e.g., CT scan) can be accomplished before an interven-
higher functions. Any deterioration from baseline re- tion or procedure. Bleeding from certain injuries may be
quires immediate investigation. addressed by angiography with arterial embolization. Inju-
ries amenable to embolization include pelvic fractures,
Exposure and Environmental Control splenic and hepatic lacerations, and occasionally renal in-
juries (Figure 77-2).
The patient should be fully undressed (exposure) while This patient’s secondary survey reveals obvious
maintaining cervical spine immobilization and kept warm bony distortions of the right forearm and femur; mul-
with blankets (environmental control); this facilitates the tiple scrapes and soft tissue contusions; and a dis-
head-to-toe examination, which is part of the secondary tended, tender abdomen. Initial x-rays demonstrate an
survey. unstable pelvic fracture; essentially normal chest; and
confirmed comminuted, displaced right ulnar and fe-
Secondary Survey mur fractures.
FAST was negative for free fluid, and diagnostic
When the primary survey objectives are met and stable peritoneal lavage was normal. Throughout this period
(or supported) and adequate vital signs are achieved, the (20 minutes), the patient’s systolic blood pressure de-
secondary survey can begin. The secondary survey com- creased into the low 80s with maintained mental status.
prises a head-to-toe physical examination and a review Intermittent crystalloid solution boluses of 100–200 mL
of the patient’s history, if available. The findings during increased the systolic blood pressure "90 mm Hg. He
424 SECTION 14 Trauma
US DPL
Hemodynamically Unstable?
- Aspiration of
gross blood
No Free Yes - RBC !100K/mm3 No
fluid identified? - WBC !500/mm3
- Particulate matter
- Bile
?
Hemodynamically
Stable
Yes No
Reliable PE?
- Abdominal tenderness
- Multiple rib fractures
Yes CT Scan CT Scan
- Abdominal wall contusion
or US?
- Equivocal findings
?
No US
No
- Repeat US Yes No
Exploratory Free
CT Scan - Observation
laparotomy fluid identified?
- CT scan*
had received 2 L of normal saline (NS) in the field, and while transporting the patient to radiology for a CT
another 2 L were infusing. There were 4 units of packed scan to evaluate his brain, abdomen, and pelvis. Until
red blood cells (PRBCs) and fresh frozen plasma (FFP) serious injuries have been objectively excluded, appro-
in the process of crossmatching. priate monitoring and personnel must accompany
Anticipating the source of bleeding to be a retro- trauma patients when they are transported. Personnel
peritoneal hematoma secondary to pelvic fracture, the must be able to recognize physiologic deterioration and
plan was to continue monitoring and resuscitation, respond. Before transport, this patient was tracheally
77 Abdominal Trauma 425
intubated and sedated to alleviate pain, optimize imag- survival benefits with either succinylcholine (1.5 mg/kg),
ing, and facilitate transition to a definitive care or rocuronium (1.2 mg/kg) for rapid-sequence induction.
procedure, such as angiography with embolization or The choice may be guided by the anticipation of difficult
surgery. intubation (favoring succinylcholine) or by concerns for
hyperkalemia (favoring rocuronium). Regardless, a neuro-
muscular blocking agent should not be excluded or underdosed.
4. What are the airway management options?
Laryngoscopy without neuromuscular blockade can
The decision to secure this patient’s airway is a judgment stimulate gagging and a vigorous Valsalva response,
call. Anticipating that the patient will soon require tra- which can increase intraabdominal (risking regurgitation
cheal intubation for a definitive procedure, the author and pulmonary aspiration), venous (disrupting formed
prefers to secure the airway in a controlled manner, clots), and intracranial (compromising cerebral blood
rather than emergently during transport or while in the flow) pressures.
CT scanner. The disadvantage of sedation and tracheal Successful denitrogenation is accomplished with high-
intubation is the inability to assess the patient’s neuro- flow oxygen and an airtight facemask seal. SpO2 values
logic status. Neurologic assessment of the awake patient of 100% are insufficient proof that oxygen has replaced
is the best monitor of brain function. Consequently, CT nitrogen in the lungs. For adequate preoxygenation,
evaluation of the brain for bleeding, contusion, or mass 3 minutes of spontaneous ventilation or eight maximum
effect becomes the priority. breaths in 60 seconds is generally recommended. Al-
As long as full stomach and cervical spine precau- though prolonged hyperventilation is no longer recom-
tions are maintained, there is no evidence-based strat- mended to treat closed head trauma, slight hyperventila-
egy for managing induction and tracheal intubation tion with 100% oxygen before induction helps prevent
that yields superior outcomes. Generally, there is no hypoxia during laryngoscopy and avoids elevated arterial
benefit to awake, nasal, blind, or fiberoptic intubation carbon dioxide tension (PaCO2) exacerbating increased
compared with asleep oral direct laryngoscopy. On the intracranial pressure (ICP).
contrary, awake techniques are likely to result in exces- There is no need to wait for hypnosis before dosing the
sive patient movement, Valsalva, coughing, bleeding, neuromuscular blocker. The induction agent and neuro-
and delay of treatment and should be employed only muscular blocker should be dosed in rapid sequence
for specific indications. (except for thiopental, which must be flushed before ro-
Airway management begins with ensuring appropriate curonium administration to avoid precipitation). Likewise,
personnel and equipment, such as oxygen, vascular ac- there is no need to wait for defasciculations or twitches on
cess, medications, endotracheal tubes, laryngoscope the neuromuscular monitor to disappear before removing
blades, and suction. Next, the plan is articulated to in- the facemask and attempting to open the mouth. Care
volved personnel, and contingencies are outlined in the must be taken not to induce a gag or cough reflex, but
event that primary intubation attempts fail. Optimally, advances should be made to secure the airway as long as
there should be one person assigned to administer medi- the patient tolerates gentle laryngoscopy. The greatest
cations, a second to hold cricoid pressure, a third to risk of aspiration occurs between the time when patients
maintain in-line cervical stabilization, and a fourth to cannot protect their airway and inflation of the tracheal
manage the airway. tube’s cuff in the trachea.
A theoretical concern about cricoid pressure is the
potential for an unstable C5 vertebral body to be dis- 5. What are the intraoperative surgical objectives
placed posteriorly into the spinal cord. In many cases, the
force applied during Sellick maneuver is insufficient to during damage control laparotomy?
occlude the esophagus. Consequently, cricoid pressure Traditionally, surgery follows the standard sequence: ac-
must be firm but not excessive. cess, exposure, hemostasis, resection, and reconstruction.
The choice of medications administered is controver- Damage control surgery endeavors to complete the min-
sial. Of induction agents available, etomidate is often imum life-threatening repairs that are necessary and then
chosen for induction because of its ability to maintain seek safe harbor in the postanesthesia care unit (PACU)
hemodynamic stability in euvolemic patients. Although or intensive care unit. Further repair of additional inju-
etomidate has been associated with adrenal suppression, ries and reconstruction are done in a staged manner.
this is of questionable clinical significance. Propofol ad- Objectives for damage control laparotomy are as follows:
ministered to hypovolemic patients with high sympa- • Control bleeding. Bleeding from arteries and large
thetic drive often results in severe hypotension, especially veins is addressed with clamps and staples. Bleeding
after institution of positive pressure ventilation, which from smaller veins is controlled with packing. Time-
impairs venous return and cardiac preload. Reduced consuming microvascular repair is not attempted.
doses of propofol, especially following small doses of a • Control enteric spillage. Control is accomplished
benzodiazepine, provide sufficient hypnosis (and often quickly with stapling devices or creating blind loops,
amnesia), while preserving blood pressure better. Ket- if necessary. Time-consuming complex anastomoses
amine offers several advantages, such as analgesia, better and ostomies are not performed.
preservation of respiratory drive and airway reflexes, and • Immobilize long bone and unstable pelvic fractures. Im-
increased sympathetic tone. mobilization is accomplished with external fixation
Choice of neuromuscular blocking agents is equally devices or splinting. It is important to minimize
controversial. No prospective trial has demonstrated bony fragments from moving past each other, which
426 SECTION 14 Trauma
alone is used to assess the need for further resuscitation, a frequently arrive without medical histories. The best
vicious cycle is initiated that can lead to excessive fluid strategy for treating a trauma patient in shock is to collect
administration. and trend as many endpoints of resuscitation as reason-
LRS does not cause a hyperchloremic acidosis because ably possible and determine which parameters improve
lactate is metabolized by the liver into bicarbonate, which or deteriorate as bleeding and resuscitation continue.
helps to maintain a normal pH balance. LRS is the most Endpoints of resuscitation can be categorized as mark-
commonly used trauma resuscitation crystalloid solution ers of global (Table 77-3) or regional (Table 77-4) organ-
in hospitals. However, LRS has some shortcomings. specific perfusion. The goal is to narrow the focus to at
• LRS contains potassium. Trauma patients typically are least one marker from each group that together would
exposed to multiple renal insults, including episodes optimize the ability to assess the degree to which the
of hypotension, hypoxia, anemia, IV contrast, and patient is resuscitated and provide an early warning of
rhabdomyolysis. When LRS is used, judicious at- deterioration.
tention must be paid to serum potassium levels to Vital sign targets are not clear-cut. It may be unneces-
avoid hyperkalemia. sary to return blood pressure and heart rate to normal,
• LRS contains calcium. This may be beneficial be- especially before surgical hemostasis. Resuscitation objec-
cause transfusion of multiple PRBC units can lead tives vary depending on the status of surgical bleeding and
to severe hypocalcemia from the sodium citrate the ability of the patient to tolerate compensated hypovo-
used as an anticoagulant. However, combining lemia and hypotension. Aiming for supranormal end-
LRS and PRBCs in the same infusion set results in points of resuscitation, although associated with better
clotting. As a precaution, infusion sets should be survival retrospectively, has not been shown to improve
flushed with NS between PRBC transfusions and outcomes in prospective randomized trials and probably
LRS. simply reflects the patient’s baseline physiologic reserve.
• LRS is slightly hypotonic. Theoretically, this may Permissive hypotension, similar to the strategy em-
exacerbate cerebral edema, increasing ICP in pa- ployed for leaking abdominal aortic aneurysms, may de-
tients with traumatic brain injury. crease blood loss before obtaining hemostasis. Low mean
The functional improvement to coagulation with arterial pressures (MAPs) must be tolerated with caution
colloid infusions (e.g., FFP, cryoprecipitate, platelets) in the setting of traumatic brain injury and elevated ICP
provides utility above and beyond their volume expan- because even brief episodes of low cerebral perfusion
sion properties. There is no survival benefit associated pressure (CPP) are associated with significantly worse
with nonfunctional colloid solutions (e.g., albumin, het- neurologic outcomes. The default approach is to target
astarch). The only potential advantage of nonfunctional normotension and allow hypotension only with MAP
colloid solutions may be to “catch up” quickly with $55 mm Hg when ICP is normal and no evidence of
severe hypovolemia. However, albumin-based resuscita- cardiac ischemia exists. With ongoing blood loss such as
tion is associated with worse outcomes in patients with the case described, even targeting hypotensive endpoints
traumatic brain injury. Hetastarch infused in larger vol- of resuscitation may still require tremendous volumes of
umes is associated with platelet dysfunction and bleeding. resuscitation fluids. When surgical and medical hemosta-
In adults, hetastarch is typically limited to 1000 mL in sis is achieved, resuscitation goals should target restora-
24 hours. tion of normal vital signs.
The idea that crystalloid-based resuscitation causes
edema is not supported by physiology. In the setting of 8. Explain the value of a massive transfusion
an inflammatory response, capillary pores leak (especially
in the gut), even large molecules such as albumin, and the protocol.
lymphatic system shuts down. Excess interstitial fluid is Traditionally, massive transfusion was defined as the infu-
not cleared, resulting in edema formation. Although total sion of one blood volume in 24 hours. Trauma patients
body water increases in this setting, intravascular volume often receive this amount in 10–15 minutes, and multiple
decreases. The result is organ hypoperfusion and dys- blood volumes are replaced over the first 24 hours. In
function and hypovolemic shock. In the absence of an reality, survival of patients with massive hemorrhage is
inflammatory response, excess crystalloid administration determined in the first few hours, during which hemosta-
is eliminated by the kidneys and does not result in edema sis must be obtained surgically. The objective of resusci-
formation. tation in this context is to keep up with blood loss, and
speed is essential. For ongoing, uncontrolled bleeding,
blood products are transfused without regard to vital
7. What are the appropriate endpoints of
signs or laboratory values. When bleeding is controlled,
resuscitation for this patient? further resuscitation and blood products are adminis-
A universal marker of adequate resuscitation does not tered based on objective triggers, such as vital signs and
exist. Single endpoints of resuscitation have the poten- laboratory values.
tial to provide a false sense of security or generate un- A massive transfusion protocol serves to expedite blood
necessary cause for alarm. Patient comorbidities often product availability, especially FFP and platelets. These
render commonly used parameters unreliable. For in- protocols decrease the amount of time required for the
stance, %-adrenergic blockers could prevent tachycardia blood bank to provide adequate blood products; this is
in response to hypovolemia, and hepatic insufficiency beneficial in the initial stage of management, when a
may interfere with lactate clearance. Trauma patients bleeding patient is at risk for exsanguination. Controversy
428 SECTION 14 Trauma
ETCO2, End-tidal carbon dioxide; FiO2, fraction of inspired oxygen; PaCO2, arterial carbon dioxide tension; PaO2, arterial oxygen tension;
SvO2, mixed venous oxygen saturation; V Q , ventilation/perfusion.
TABLE 77-4 Endpoints of Resuscitation— exists regarding the optimal ratio of blood products to
Markers of Regional Perfusion administer. The approximate ratios present in whole
blood are effectively reconstituted with 1 unit of PRBCs
Markers of Re- & 1 unit of FFP & 1 unit of platelets. Although no pro-
gional Perfusion Notes/Pitfalls spective randomized data have demonstrated a survival
Mental status Unavailable during general anesthesia benefit of transfusing a 1:1:1 ratio, it would seem as good
Unreliable with intoxication as any strategy in the initial severe blood loss stage. When
Urine output Unreliable with acute or chronic renal
bleeding has been controlled, the massive transfusion
failure, SIADH, or neurogenic DI protocol ends, and the 1:1:1 ratio may not be necessary.
Because transfusions can be harmful, subsequent blood
Electrocardiogram Unknown baseline for comparison
products are administered to correct documented abnor-
Echocardiography Requires special operator skills malities, not to meet a predetermined ratio.
Absent esophageal or gastric pathology
Capillary refill Unknown baseline for comparison 9. What are the anesthesiologist’s intraoperative
Sublingual Not routinely available priorities?
tonometry
Besides volume resuscitation, anesthesiologists have other
Jugular bulb Not routinely available responsibilities that must be prioritized. For complex cases
saturation
such as the one described here, it is impossible for a single
NIR spectrometry Not routinely available anesthesiologist to keep up with all the necessary tasks.
CPK levels Too slow for acute changes Help of additional anesthesiologists is required to do the
following:
Troponin levels Too slow for acute changes
• Provide immobility and amnesia. Although awareness
CPK, Creatinine phosphokinase; DI, diabetes insipidus; NIR, near in- under anesthesia can be devastating, when blood
frared; SIADH, syndrome of inappropriate antidiuretic hormone. pressure is already marginal, depth of anesthesia is
77 Abdominal Trauma 429
generally reduced. The initial priority should be to transition to correction of abnormal physiology. Imme-
provide neuromuscular blockade and amnesia. Agents diately on arrival in the PACU, this patient would re-
to consider are benzodiazepines at low doses, scopol- quire active warming, correction of coagulopathies and
amine, nitrous oxide (if oxygenation is adequate), and anemia, invasive monitoring, sedation, and antibiotics.
ketamine (provided that ICP is normal). If blood Complete blood count, coagulation profile, electrolyte
pressure is inadequate, short-term vasopressor ther- panel, arterial blood gas, and creatinine phosphokinase
apy may be used until intravascular volume is im- (to screen for rhabdomyolysis) should be obtained.
proved. If hypotension persists, alternative explana- If possible, sedation should be decreased, and a basic
tions of shock (i.e., cardiogenic, distributive, neurologic examination should be performed. If a neuro-
mechanical) should be investigated. When blood logic examination is not possible or if any gross neuro-
pressure is stable, other agents can be added to pro- logic abnormalities are noted, repeat CT scan of the
vide balanced anesthesia addressing hypnosis (volatile brain should be considered. A chest x-ray is performed to
anesthetics) and analgesia (opioids). confirm line placement, to confirm tracheal tube location
• Establish reliable IV access. In the field, two short length above the carina, and to rule out pneumothorax. A head-
catheters are routinely placed in the antecubital fossae. to-toe physical examination is repeated, and additional
As resuscitation proceeds, edema formation in subcu- imaging is obtained as indicated to evaluate for missed
taneous tissue expands the distance between vein and injuries (commonly hand, foot, or digital fractures). IV
skin where the IV catheter is fixed. Consequently, the catheters placed in the field or under less than sterile
tip of the IV catheter begins to retract out of the vessel. conditions are removed. Tetanus booster injection should
For massive transfusions, large-bore (introducer) ve- be administered. Extrication cervical spine collar is
nous access should be established. Femoral or saphe- changed to one designed for long-term use (Miami-J or
nous venous lines should be used with caution if inju- Philadelphia type).
ries involve the pelvic or abdominal central veins. Worsening shock should prompt rapid evaluation for
• Monitor arterial blood pressure. An arterial catheter new surgical bleeding, which is treated with either angio-
should be inserted to monitor blood pressure con- graphic embolization or surgery. Sequential compression
tinuously, to calculate CPP accurately, and to enable devices are placed on uninjured limbs for deep vein throm-
frequent arterial blood gas sampling. Femoral, dor- bosis prophylaxis, and subcutaneous heparin is started as
salis pedis, or axillary arteries may be used if the soon as acute bleeding concerns have ceased. A plan for
radial arteries are unavailable. nutrition should be established. Family members should be
• Manage CPP. For patients with concomitant head contacted and updated regarding the patient’s condition
injuries, ICP monitoring should be initiated in the and prognosis. When the patient’s abnormalities are cor-
operating room as soon as possible, and CPP should rected, one should anticipate returning to the operating
be maintained "55 mm Hg (CPP ' MAP # ICP). room in 24–48 hours for staged procedures including inter-
This may require augmentation of blood pressure nal fixation of orthopedic fractures, removal of abdominal
using (-agonist agents or efforts to decrease ICP packing, and reconstruction and closure of the abdomen.
(e.g., mannitol, hypertonic saline), or both.
• Maintain normothermia. Shock induces hypothermia as
metabolism slows. It can be challenging to maintain SUGGESTED READINGS
normothermia in an exsanguinating trauma patient. Abdul Rahman YS, Al Den AS, Maull KI: Prospective study of validity
All fluids should be infused through warmers, and of neurologic signs in predicting positive cranial computed tomogra-
warming blankets should be placed on all exposed, phy following minor head trauma. Prehosp Disaster Med 25:59,
2010.
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perature continues to decrease, ambient temperature vanced Trauma Life Support for Doctors. American College of
in the operating room may need to be increased. Surgeons, Chicago, 2008.
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trauma patient. Curr Opin Crit Care 15:542, 2009.
ties. Occasionally, vehicular trauma and falls may oc- Healey MA, Samphire J, Hoyt DB, et al.: Irreversible shock is not ir-
cur after a person loses consciousness from a medical reversible: a new model of massive hemorrhage and resuscitation.
condition (e.g., stroke, sepsis, myocardial infarction, J Trauma 50:826, 2001.
arrhythmia, hypoglycemia, seizures). Those medical Herman NL, Carter B, Van Decar TK: Cricoid pressure: teaching the
conditions warrant investigation and treatment con- recommended level. Anesth Analg 83:859, 1996.
Ho AM, Dion PW, Yeung JH, et al.: Prevalence of survivor bias in
currently with the management of traumatic injuries. observational studies on fresh frozen plasma: erythrocyte ratios in
Prophylactic antibiotics may need to be redosed if trauma requiring massive transfusion. Anesthesiology 116:716, 2012.
blood levels are diluted by large-volume resuscitation. Hoff WS, Holevar M, Nagy KK, et al.; Eastern Association for the
• Maintain accurate documentation. Accurate recording Surgery of Trauma: practice management guidelines for the evalua-
tion of blunt abdominal trauma: the East Practice Management
of medications, fluids, and blood products should be Guidelines Work Group. J Trauma 53:602, 2002.
ongoing. Kohn MA, Hammel JM, Bretz SW, et al.: Trauma team activation
criteria as predictors of patient disposition from the emergency de-
partment. Acad Emerg Med 11:1, 2004.
10. What are the goals for subsequent Kouraklis G, Spirakos S, Glinavou A: Damage control surgery: an
postanesthesia care unit care? alternative approach for the management of critically injured pa-
tients. Surg Today 32:195, 2002.
After surgical bleeding has been addressed and opera- Lapostolle F, Gere C, Borron SW, et al.: Prognostic factors in victims
tive damage control objectives have been met, priorities of falls from height. Crit Care Med 33:1239, 2005.
430 SECTION 14 Trauma
Lieurance R, Benjamin JB, Rappaport WD: Blood loss and transfusion in recommendations of the National Expert Panel on Field Triage,
patients with isolated femur fractures. J Orthop Trauma 6:175, 1992. 2011. MMWR Recomm Rep 61(RR-1):1, 2012.
Mitra B, Mori A, Cameron PA, et al.: Fresh frozen plasma (FFP) use Snyder CW, Weinberg JA, McGwin G Jr, et al.: The relationship
during massive blood transfusion in trauma resuscitation. Injury of blood product ratio to mortality: survival benefit or survival bias?
41:35, 2010. J Trauma 66:358; discussion 362, 2009.
Riskin DJ, Tsai TC, Riskin L, et al.: Massive transfusion protocols: the Stahel PF, Smith WR, Moore EE: Current trends in resuscitation strat-
role of aggressive resuscitation versus product ratio in mortality egy for the multiply injured patient. Injury 40(Suppl 4):S27, 2009.
reduction. J Am Coll Surg 209:198, 2009. Tanoubi I, Drolet P, Donati F: Optimizing preoxygenation in adults.
Sasser SM, Hunt RC, Faul M, et al.; Centers for Disease Control and Can J Anaesth 56:449, 2009.
Prevention (CDC): guidelines for field triage of injured patients:
SEC TION 1 5
POSTANESTHESIA
CARE UNIT
431
CASE 78
Asthma
Andrew B. Leibowitz, MD • Elvis Umanzor Velasquez, MD
QUESTIONS
1. What is asthma, and how is it diagnosed? if the patient said that she was just recovering from
2. What are the characteristic pulmonary function test a “bad cold” and had a few scattered wheezes on
findings seen in obstructive and restrictive lung auscultation?
disease, asthma, and chronic obstructive pulmonary 6. Would you choose general anesthesia (endotra-
disease? cheal intubation versus laryngeal mask airway)
3. What is the pharmacology of medications available or a neuraxial block for this patient?
to treat asthma; which medications are used for 7. What are the signs and potential causes of perioper-
long-term control, and which medications are used ative bronchospasm?
for acute attacks; and what would be a treatment 8. After uneventful induction of general anesthesia
plan based on the degree of severity? and intubation, the patient’s peak airway pressures
4. What are the indications for mechanical ventila- suddenly increased during the procedure, and
tion in severe asthma (status asthmaticus), and wheezing was heard on auscultation; what would
what are the specific concerns? you do?
5. What preoperative evaluation and preparation would
you order for this patient; would you cancel the case
A 30-year-old woman presented for elective uterine myo- normal ratio of forced expired volume in the first second
mectomy. She had a long history of asthma, treated with (FEV1) to forced vital capacity (FVC), but the more sen-
an unknown inhaler, as needed. Preoperatively, her chest sitive forced expiratory flow between 25% and 75% of
was clear to auscultation. FVC (FEF25%-75%) would be decreased. Also, the FEV1/
FVC ratio is effort dependent and requires patient coop-
eration for accurate measurement, whereas FEF25%-75%
1. What is asthma, and how is it diagnosed?
does not depend on patient effort. FEF25%-75% is obtained
Asthma is a common disease characterized by reversible by dividing the volume expired between 25% and 75%
airway obstruction with components of hyperresponsive- of the FVC by the time elapsed between these two
ness and inflammation. Asthma “attacks” are character- points. Occasionally, bronchospasm may be intentionally
ized by episodes of shortness of breath, wheezing, and triggered during PFT evaluation with methacholine
often cough. These episodes usually follow exposure to or histamine to assess airway reactivity in patients with
known triggers (e.g., pollen, dust, animal dander, smoke, normal baseline PFTs who are suspected to have asthma.
change in weather, viral illness). The diagnosis is most For patients with chronic obstructive pulmonary dis-
commonly made by history and examination alone. Mea- ease (COPD), measurements are repeated after inhaled
surements of peak expiratory flow (PEF) rate and forced bronchodilators to evaluate the degree of reversibility.
expiratory volumes and their response to bronchodilator The fixed component of COPD is due to inflammation
administration may sometimes be necessary. and airway destruction.
Flow-volume curves may also be helpful. A normal
2. What are the characteristic pulmonary function curve and typical curves from patients with obstructive
test findings seen in obstructive and restrictive and restrictive disease are shown in Figure 78-1. By con-
lung disease, asthma, and chronic obstructive vention, inspiration is below the x axis, and expiration is
above the x axis. In restrictive disease, airway resistance is
pulmonary disease?
normal with no flow limitation, whereas lung volumes are
Pulmonary function tests (PFTs) comprise spirometry reduced. In obstructive disease, the expiratory flow curve
and flow-volume loops. An arterial blood gas and diffu- shows a characteristic flattening secondary to increased
sion of carbon monoxide can also be included. Typical airway resistance.
values in obstructive and restrictive lung disease are Curves from patients with fixed airway obstruction and
shown in Table 78-1. variable extrathoracic and intrathoracic obstructions are
Asthmatics usually have normal PFTs between exacer- shown in Figure 78-2. Fixed obstruction, exemplified by
bations. Narrowing limited to small airways may yield a tracheal stricture or compression by a tumor or goiter,
432
78 Asthma 433
COPD, Chronic obstructive pulmonary disease; DLCO, diffusion capacity of the lung for carbon
monoxide; FEF25%-75%, forced expiratory flow between 25% and 75% of forced vital capacity;
FEV1, forced expired volume in the first second; FVC, forced vital capacity; MBC, maximum
breathing capacity; MMEFR, maximal midexpiratory flow rate; RV, residual volume; TLC, total
lung capacity.
Acute attacks not responding to a self-administered modern ventilators allow auto-PEEP to be measured
metered-dose inhaler !2 agonist are usually treated with by triggering an expiratory pause (provided that the
!2-agonist nebulizers and systemic steroids (e.g., methyl- patient is sedated enough to prevent spontaneous
prednisolone, 40-60 mg intravenously), which are tapered breathing). Occasionally, in patients with extreme
over a few days. bronchospasm, neuromuscular blockade might be used
to increase chest wall compliance and make ventilation
4. What are the indications for mechanical easier.
ventilation in severe asthma (status asthmaticus),
and what are the specific concerns? 5. What preoperative evaluation and preparation
would you order for this patient; would you cancel
The indications for tracheal intubation and mechanical the case if the patient said that she was just
ventilation in severe asthma are hypercapnia and impend- recovering from a “bad cold” and had a few
ing physical exhaustion, despite treatment. Hypoxemia scattered wheezes on auscultation?
and somnolence likely indicate that tracheal intubation
was delayed too long. Tracheal intubation can acutely History and physical examination usually suffice for the
worsen airway obstruction because of bronchial hyperre- preoperative evaluation. The key historical points to
sponsiveness, and a treatment plan for this possibility ascertain are the frequency and severity of attacks, re-
needs to be established ahead of time. sponse to treatment, need for emergency department
The main concerns of mechanically ventilating asth- visits, hospital admissions and mechanical ventilation, use
matic patients are increased airway resistance, high of systemic steroids (dose, duration, last use), and long-
peak insufflation pressures, prolonged expiration times, term medications. If the patient uses a PEF device, the
auto-PEEP (positive end expiratory pressure), and best PEF and the current value should be compared.
breath “stacking.” Reasonable initial settings are frac- There is no benefit in obtaining preoperative PFTs for a
tion of inspired oxygen (FiO2) of 1.0, respiratory rate of patient with asthma.
8–12 breaths per minute, and tidal volume of 6–8 mL/kg The key physical examination finding is the pres-
of lean body weight. Increasing expiratory time, high ence or absence of wheezing. If there is any wheezing,
inspiratory peak flows (80–100 L per minute if using an prolongation of the expiratory phase of respiration and
intensive care unit–style ventilator), and low inspira- use of accessory muscles should be noted. Severe bron-
tory/expiratory ratio (e.g., 1:4–1:6) are helpful. Most chospasm may manifest with absence of breath sounds
78 Asthma 435
and no wheezing, but many asthmatics when examined increase in inflation pressures is usually noted first in
carefully always wheeze, even when asymptomatic. anesthetized mechanically ventilated patients. In addition
Patients who are asymptomatic with a history of mild to asthma, other causes of bronchospasm include tracheal
asthma do not need any special testing or preparation. tube obstruction (e.g., kink, secretions), congestive heart
Their usual medications should be continued per usual failure, allergic reactions (e.g., drugs, blood transfusion
routine, and an inhaled !2 agonist should be adminis- reaction), increased histamine release (e.g., secondary to
tered before entering the operating room. Perioperative morphine), and rarely pneumothorax and pulmonary
steroids should be reserved for asthmatics with moderate embolus.
or severe asthma. Treatment should be initiated the day
before surgery with prednisone, 40 mg daily, or its 8. After uneventful induction of general anesthesia
equivalent. A postoperative nausea and vomiting pro- and intubation, the patient’s peak airway
phylactic dose of dexamethasone (e.g., 8 mg) is equiva- pressures suddenly increased during the
lent to approximately 50 mg of prednisone. In the procedure, and wheezing was heard on
absence of problematic asthma complicating the imme- auscultation; what would you do?
diate perioperative course, this dose of steroid either can
be discontinued after 2–3 days or rapidly tapered over An orderly approach to wheezing, even in the absence of
4–7 days without risk. a history of asthma, is a basic skill every anesthesiologist
A history of recent respiratory viral infection increases must be able to perform reflexively. A reasonable checklist
airway reactivity in normal patients and is one of the that can be modified to suit the specific patient, operation,
main triggers for exacerbations in asthmatics. In an adult and incident severity follows:
patient with a clear chest examination, it is probably safe 1. Immediately increase FiO2 to treat or in anticipa-
to proceed, but postponement may be the safer course of tion of decreased oxygen saturation. Short-term
action in the presence of fever, erythematous throat, and FiO2 of 1.0 is completely safe.
productive cough. In this patient, with known asthma 2. Rule out mechanical causes of wheezing, including
and an abnormal chest examination, postponement is main stem intubation, tracheal tube tip abutting
indicated. the carina, tracheal tube kink, and obstruction by
secretions (pass a “whistle tip” suction catheter
6. Would you choose general anesthesia through the tracheal tube). Always consider pneu-
(endotracheal intubation versus laryngeal mask mothorax in the differential diagnosis.
3. Deepen the anesthetic by increasing the volatile
airway) or a neuraxial block for this patient?
agent concentration, and optimize neuromuscular
Regional anesthesia is generally preferable because blockade if diaphragmatic or chest wall compliance
airway instrumentation would be avoided, but patients is possibly contributory.
undergoing regional anesthesia are not completely 4. Administer an inhaled short-acting !2 agonist (e.g.,
immune from intraoperative bronchospasm. Two of- albuterol) by metered-dose inhaler or nebulizer.
ten cited concerns that are rarely an issue are (1) a High doses may be given with minimal side effects.
high block may adversely affect pulmonary function, 5. Administer steroids (e.g., hydrocortisone 100–
and (2) sympathetic blockade would cause unopposed 200 mg or methylprednisolone 40–60 mg intrave-
vagal tone leading to bronchospasm. As with any re- nously). Onset might take 6 hours, but if bron-
gional anesthetic, there is a risk of failure and need for chospasm persists, early administration would be
general anesthesia. advantageous.
General anesthesia can almost always be safely admin- 6. If life-threatening bronchospasm occurs, consider
istered. Basic principles include the need to obtain a deep magnesium sulfate (e.g., 2 g intravenously) and as a
plane of anesthesia before laryngoscopy and tracheal in- last resort intravenous epinephrine (e.g., 5–10 "g).
tubation and consideration of ketamine as the induction 7. Consider inhaled ipratropium in patients with a
agent. Laryngeal mask airway insertion has been shown chronic obstructive component or if the patient
to be associated with less increased airway resistance also takes a ! blocker.
compared with endotracheal intubation and might be 8. Remember basic mechanical ventilation principles.
preferable. However, a laryngeal mask airway does not A normal or low tidal volume with prolonged expi-
always protect against aspiration of gastric contents, and ratory time would be advantageous. Respiratory
in the case of abdominal surgery in which there is perito- acidosis is generally very well tolerated.
neal irritation and need for neuromuscular blockade, a
tracheal tube is preferable.
SUGGESTED READINGS
7. What are the signs and potential causes Brenner B, Corbridge T, Kazzi A: Intubation and mechanical ventilation
of the asthmatic patient in respiratory failure. Proc Am Thorac Soc
of perioperative bronchospasm? 6:371, 2009.
Bronchospasm is recognized by auscultation of expira- Brown RH, Wagner EM: Mechanism of bronchoprotection by anes-
thetic induction agents: propofol vs. ketamine. Anesthesiology 90:
tory wheezing accompanied by a prolonged expiratory 822, 1999.
time. Tachypnea and dyspnea are usually present in an Busse WW, Camargo CA, Boushey HA, et al.: Expert Panel Report 3:
awake patient, but increased airway resistance with an Guidelines for the diagnosis and management of asthma. National
436 SECTION 15 Postanesthesia Care Unit
Heart, Blood, and Lung Institute. NIH Publication No. 08-4051, Manthous CA, Chatila W, Schmidt GA, et al.: Treatment of broncho-
2007. spasm by metered-dose inhaler albuterol in mechanically ventilated
Groeben H, Schwalen A, Irsfeld S, et al.: High thoracic epidural anesthe- patients. Chest 107:210, 1995.
sia does not alter airway resistance and attenuates the response to an Tait AR, Malviya S, Voepel-Lewis T, et al.: Risk factors for perioperative
inhalational provocation test in patients with bronchial hyperreactivity. adverse respiratory events in children with upper respiratory tract
Anesthesiology 81:868, 1994. infections. Anesthesiology 95:299, 2001.
Kabalin CS, Yarnold PR, Grammer LC: Low complication rate of Warner DO, Warner MA, Barnes RD, et al.: Perioperative respiratory
corticosteroid-treated asthmatics undergoing surgical procedures. complications in patients with asthma. Anesthesiology 85:460, 1996.
Arch Intern Med 155:1379, 1995. Woods BD, Sladen RN: Perioperative considerations for the patient with
Kil HK, Rooke GA, Ryan-Dykes MA, et al.: Effect of prophylactic asthma and bronchospasm. Br J Anaesth 103(Suppl 1):i57, 2009.
bronchodilator treatment on lung resistance after tracheal intubation.
Anesthesiology 81:43, 1994.
CASE 79
Hypothermia
Andrew B. Leibowitz, MD • Gene Tulman, MD
QUESTIONS
1. How is hypothermia defined and graded? 5. Are there any benefits to mild intraoperative
2. What mechanisms lead to hypothermia in surgical hypothermia?
patients under general anesthesia? 6. Where are the commonly used temperature
3. Explain the physiologic responses to monitoring sites?
hypothermia. 7. How is hypothermia prevented?
4. Describe the physiologic consequences of 8. Is hypothermia prevention warranted for patients
hypothermia. receiving central neuraxial blockade?
A 71-year-old man underwent subtotal colectomy com- In other settings, hypothermia can result from loss of
plicated by hypothermia. He was brought to the postan- central thermoregulation (e.g., stroke, head trauma, spinal
esthesia care unit (PACU) with a temperature of 31.9° C. cord injury), drugs (e.g., alcohol or barbiturate overdose),
or metabolic derangement (e.g., hypoglycemia, hypothy-
roidism, sepsis, burns, hepatic failure).
1. How is hypothermia defined and graded?
Hypothermia is defined as a core body temperature 3. Explain the physiologic responses to hypothermia.
!35° C. It is often further characterized as mild (32°–35° C),
moderate (28°–32° C), and severe (!28° C). There are three physiologic responses to hypothermia.
Shivering in the postoperative period can increase activity. This mechanism may double the metabolic heat
oxygen consumption by 300%–500% contributing to a production in infants, but it does not play a significant
potentially significant oxygen/demand mismatch that can role in adults. (See Chapter 64 for a detailed explanation
lead to myocardial ischemia in susceptible patients. It can of nonshivering thermogenesis.)
also increase the serum potassium level.
4. Describe the physiologic consequences
Nonshivering Thermogenesis of hypothermia.
Nonshivering thermogenesis is the mechanism of heat The physiologic consequences of hypothermia are sum-
production in infants that is not associated with muscle marized in Table 79-1. Electrocardiogram (ECG) changes
CO2, Carbon dioxide; HLA-DR, human leukocyte antigen, DR subregion; IL-10, interleukin-10; MAC, minimum alveolar concentration;
PaCO2, arterial carbon dioxide tension; TNF-#, tumor necrosis factor-#.
79 Hypothermia 439
include sinus bradycardia, widened P–R interval, widened but are comatose has become widely accepted in recent
QRS, and prolonged Q–T interval. The Osborn wave is years. Recommendations at the present time are for cool-
characteristic for hypothermia (Figure 79-1). This wave is ing to 32°–34° C for 12–24 hours.
a deflection at the J point (the junction between the QRS
complex and the ST segment) in the same direction as 6. Where are the commonly used temperature
that of the QRS complex, with a height proportional to monitoring sites?
the degree of hypothermia. It is frequently mistaken for
genuine ST segment elevation. Temperature may be monitored via oral, rectal, esophageal,
Several deleterious clinical consequences have been nasopharyngeal, and tympanic membrane sites. It can also
well documented, including the following: be monitored via pulmonary artery catheter or urinary
• Impaired coagulation has been shown to lead to bladder catheter. With the exception of the oral route, all
higher transfusion requirements in patients under- other methods provide a generally accurate and reproduc-
going total hip replacement. ible measurement of core temperature in general surgical
• The incidence of wound infection is increased because patients.
of direct impairment of the immune function and a Skin temperature monitoring is usually accomplished
decrease in oxygen delivery to the tissue edges. using liquid crystal–containing strips or probes with
• The incidence of postoperative myocardial infarction thermistor tips, but the potential large difference between
and ventricular dysrhythmias is increased. core and peripheral temperature makes skin monitoring
• Hospital length of stay is increased. suboptimal intraoperatively and may be inaccurate on
The current recommendation is to maintain tempera- admission to the PACU.
ture at $36° C to avoid hypothermia-related adverse During hypothermic cardiopulmonary bypass, signifi-
outcomes. This temperature goal is emerging as a standard cant gradients can exist between core, blood, and periph-
for reporting to various regulatory authorities. Failure eral temperatures. Pulmonary artery catheters measure
to maintain normothermia could subject institutions temperature of blood from the cardiopulmonary bypass
to financial penalties. Hypothermic patients, especially pump. Core temperature (esophageal, nasopharyngeal,
patients with coronary artery disease, might benefit from and tympanic) lags behind. Envelope (rectal) temperature
remaining under anesthesia into the postoperative period takes even more time to equilibrate during both cooling
until adequate rewarming is achieved to avoid the poten- and rewarming.
tial shivering-related increased oxygen consumption and
resultant myocardial ischemia. 7. How is hypothermia prevented?
5. Are there any benefits to mild intraoperative The four mechanisms of heat loss should be kept
in mind. Redistribution and loss that is primarily due
hypothermia?
to radiation are the largest largely preventable mecha-
For years, hypothermia had been postulated to confer pro- nisms by early application of skin warming. Even in the
tection against cerebral hypoxia. However, the Intraopera- absence of active warming, simply increasing the ambi-
tive Hypothermia for Aneurysm Surgery Trial (IHAST) ent (room) temperature is very helpful because radiation
failed to demonstrate any neuroprotective benefits of mild heat loss is proportional to the fourth power of the dif-
hypothermia in patients undergoing temporary clipping ference between the absolute temperatures of surfaces.
during cerebral aneurysm surgery. In contrast, hypother- Radiation heat loss can be limited simply by increasing
mia acutely applied to patients who survive cardiac arrest ambient (room) temperature. Radiant warmers are used
only for infants and are effective only while the patient is
exposed. Use of radiant warmers can preclude the need
to increase room temperature. However, intervening
drapes render radiant warmers ineffective, and increasing
distance between the patient and the warmer diminishes
its effectiveness.
Warming of inspired gas and intravenous fluid has
limited efficacy. Less than 10% of heat loss occurs in the
respiratory tract. Fluid warming becomes more important
Osborn as larger volumes are administered over shorter times.
wave
Body temperature is decreased by about 0.25° C with 1 L
of crystalloid at room temperature or 1 unit (250 mL) of
refrigerated blood.
T wave Insulation with one layer of fabric (sheet or blanket)
decreases heat loss by only 30%. There is little additional
benefit from additional layers. Forced-air warming
Q–T (e.g., Bair Hugger Blanket; Arizant Healthcare Inc.,
Q–T interval Eden Prairie, MN) is the most effective warming and
Prolonged: 0.60 sec rewarming method. It works best when patients are vaso-
dilated. It is better to maintain normothermia from the
FIGURE 79-1 ■ Osborn wave and prolonged Q–T interval seen on time of entry into the operating room rather than to have
ECG in hypothermic patients. to rewarm postoperatively. Rewarming a vasoconstricted
440 SECTION 15 Postanesthesia Care Unit
patient can lead to hypotension secondary to vasodilation, vasodilation. Additionally, shivering is precluded by motor
especially if volume status is not maintained, which is a blockade. Central control is impaired secondary to elevated
frequently seen complication in the PACU. Circulating- skin temperature from cutaneous vasodilation. Significant
water mattresses placed on the operating room table have hypothermia can occur, leading to discomfort and possible
little efficacy. A minimal amount of the patient’s body shivering, although the shivering threshold is reduced in
surface area actually contacts the mattress, substantially this setting. Measures to prevent hypothermia should be
limiting its effectiveness. used during central neuraxial blockade.
Forced-air warmers are effective but must be used with
caution. They can produce burns if applied directly to the
skin. Hot-water bottles and forced hot air warming with- SUGGESTED READINGS
out the appropriate blanket should absolutely be avoided. Bremmelgaard A, Raahave D, Beier-Holgersen R, et al.: Computer-aided
They are frequent causes of perioperative thermal injury surveillance of surgical infections and identification of risk factors.
according to the American Society of Anesthesiologists J Hosp Infect 13:1, 1989.
Clifton GL, Valadka A, Zygun D, et al.: Very early hypothermia induction
Closed Claims Project database. in patients with severe brain injury (the National Acute Brain Injury
Shivering can be treated by skin-surface warming and Study: hypothermia II): a randomised trial. Lancet Neurol 10:131, 2011.
pharmacologically, most commonly with meperidine, Hindman BJ, Bayman EO, Pfisterer WK, et al.: No association between
12.5–50 mg intravenously. The exact mechanism of intraoperative hypothermia or supplemental protective drug and neu-
action of meperidine is unknown, but it is likely rologic outcomes in patients undergoing temporary clipping during
cerebral aneurysm surgery: findings from the intraoperative hypother-
associated with its multireceptor activity including mia for aneurysm surgery trial. Anesthesiology 112:86, 2010.
the #2b-adrenergic receptor and the kappa receptor. Michelson AD, MacGregor H, Barnard MR, et al.: Reversible inhibition
Dexmedetomidine, an #2 agonist, has also been reported of human platelet activation by hypothermia in vivo and in vitro.
to be effective but is a very expensive option with a pro- Thromb Haemost 71:633, 1994.
Morrison LJ, Deakin CD, Morley PT, et al.: Part 8: Advanced Life Sup-
pensity to reduce blood pressure and promote bradycar- port: 2010 International Consensus on Cardiopulmonary Resuscita-
dia. The mechanism of action of dexmedetomidine tion and Emergency Cardiovascular Care Science with Treatment
involves a decrease of vasoconstriction and shivering Recommendations. Circulation 122(16 Suppl 2):S345, 2010.
thresholds. Another rarely employed adjunct in the Pitoni S, Sinclair HL, Andrews PJD: Aspects of thermoregulation
PACU is buspirone, a serotonin 5-HT1A partial agonist, physiology. Curr Opin Crit Care 17:115, 2011.
Qadan M, Gardner SA, Vitale DS, et al.: Hypothermia and surgery:
which is now frequently used in post–cardiac arrest immunologic mechanisms for current practice. Ann Surg 250:134,
hypothermia–related shivering algorithms. 2009.
Schmied H, Kurz A, Sessler DI, et al.: Mild hypothermia increases blood
loss and transfusion requirements during total hip arthroplasty. Lancet
8. Is hypothermia prevention warranted for patients 347:289, 1996.
receiving central neuraxial blockade? Sessler DI: Perioperative heat balance. Anesthesiology 92:578–596,
2000.
Neuraxial blockade results in a functional sympathectomy Sessler DI: Thermoregulatory defense mechanisms. Crit Care Med
in the anesthetized area causing loss of autoregulation and 37(Suppl):S203, 2009.
CASE 80
QUESTIONS
1. What is the cause of nausea and vomiting? 6. What complications occur in the postanesthesia
2. What are the risk factors for postoperative nausea care unit?
and vomiting? 7. What are the commonly applied postanesthesia
3. What are the incidence and implications of care unit discharge criteria?
postoperative nausea and vomiting? 8. Describe a postanesthesia care unit scoring system
4. What are the strategies to reduce the incidence used to assess readiness for discharge.
and severity of postoperative nausea and vomiting?
5. What are the treatment considerations for
postoperative nausea and vomiting?
A 36-year-old woman underwent uneventful laparoscopic maintenance infusion. Etomidate is associated with an
salpingo-oophorectomy under general anesthesia. In the increased risk of PONV and should be used only when
postanesthesia care unit (PACU), she complained of hemodynamic stability is of paramount importance.
severe nausea and vomited. She wanted to be discharged The incidence of PONV is similar regardless of type
home. of opioid administered; opioid-sparing techniques
should contribute to a risk reduction of PONV. A
meta-analysis showed that a single perioperative intra-
1. What is the cause of nausea and vomiting?
venous dose of 60 mg of ketorolac was associated with
The vomiting center is located in the medulla. It receives a potentially clinically significant opioid-sparing effect
input from the chemoreceptor zone and gastrointestinal and a statistically significant reduction in PONV. Intra-
tract. The vomiting center may be activated by various venous acetaminophen, which became available in the
stimuli, including medications, body motion, stimulation United States more recently, can be expected to result
of the posterior pharynx, odors, and visual images. in similar improved outcomes. Regional anesthetic
techniques (e.g., peripheral nerve blocks) without in-
2. What are the risk factors for postoperative nausea travenous opioid supplementation are also effective in
reducing the risk of PONV.
and vomiting?
Risk factors for postoperative nausea and vomiting 3. What are the incidence and implications of
(PONV) are related to patient characteristics, type postoperative nausea and vomiting?
of surgery, and anesthetic. The main patient character-
istics that increase the risk of PONV are female gender PONV is the most common postoperative complica-
(especially if pregnant or menstruating), prior history tion and the leading cause of delayed discharge from
of PONV, history of motion sickness, and being a the PACU. It has been estimated that 25%–30% of
nonsmoker. surgical patients experience PONV within 24 hours of
Operative procedures particularly associated with an surgery. In high-risk surgical patients, the incidence
increased incidence of PONV are laparoscopy, breast, stra- of PONV may be 70%–80%. The incidence of periop-
bismus, and ear-nose-throat procedures. Surgical duration erative vomiting in children has been estimated to be
!30 minutes also increases the risk of PONV. twice that of adults. In one review of 8995 pediatric
General anesthesia entailing potent volatile agents, outpatient cases, 26 patients required admission for
nitrous oxide, and intravenous opioids increases the risk persistent nausea and vomiting, accounting for 36% of
of PONV, whereas use of a propofol-based general an- all unanticipated hospital admissions. PONV may con-
esthetic reduces the incidence and severity of PONV. tribute to high levels of patient discomfort, delayed
There is little benefit if propofol is used only as an PACU discharge, increased need for nursing care, and
induction agent and a significant benefit if it is used as a potential hospital admission. All of these factors may
441
442 SECTION 15 Postanesthesia Care Unit
increase avoidable periprocedural cost and are a main hydrocortisone). It is usually administered prophy-
cause of patient dissatisfaction. lactically in a dose of 4–10 mg intravenously after
induction of general anesthesia. Administration may
4. What are the strategies to reduce the incidence be associated with acute vaginal burning in awake
female patients and with scrotal burning in male
and severity of postoperative nausea and vomiting?
patients, which can be quite disturbing. Routine
The 2007 Society of Ambulatory Anesthesia Guide- administration should be standard after induction of
lines for the Management of Postoperative Nausea general anesthesia. Some studies have suggested
and Vomiting recommend the following strategies to that smaller doses (4 mg) are as effective as larger
reduce PONV: doses. The antiemetic mechanism of action is not
• Use of regional anesthesia with no or minimal intra- well understood. No clinically significant adverse
venous opioid supplementation events have been noted after a single bolus dose of
• Use of propofol for induction and maintenance of dexamethasone but caution is warranted in diabetic
general anesthesia patients who are prone to hyperglycemia. The
• Avoidance of nitrous oxide effectiveness of dexamethasone in treating estab-
• Avoidance of volatile anesthetics lished PONV is not nearly as well documented as
• Avoidance or minimization of intraoperative and the prophylactic effect.
postoperative opioids • Droperidol is a pharmacologic relative of the more
• Avoidance or minimization of neostigmine given for widely used antipsychotic drug haloperidol. It is a
muscle relaxant reversal potent "-adrenergic antagonist. In small doses
• Administration of adequate hydration (0.625–1.25 mg intravenously), it significantly de-
• Prophylactic administration of 5-HT3 antagonists creases the incidence of PONV. When given in
• Prophylactic administration of additional antiemetic higher doses, it may be associated with excessive
medications to high-risk patients sedation and delayed discharge from the PACU. In
2001, the U.S. Food and Drug Administration
5. What are the treatment considerations for (FDA) issued a “black box” warning noting that
droperidol can cause Q–T interval prolongation,
postoperative nausea and vomiting?
has been associated with lethal arrhythmias (e.g.,
Although there may be no consensus to administer an- torsade de pointes), and should not be administered
tiemetic prophylaxis to all surgical patients, routine in the presence of known Q–T interval prolonga-
administration of some generically available agents is tion. In the absence of a prolonged Q–T interval, it
commonplace because of their minimal cost and risk. was recommended that patients receiving droperi-
Considerations to administer pharmacologic antiemetic dol should have electrocardiogram (ECG) monitor-
prophylaxis and treatment of established PONV should ing for 2–3 hours after administration. The FDA
be individualized based on the previously discussed risk was widely criticized for these warnings and recom-
factors. Patients with several risk factors frequently mendations because this decision was mostly based
require more than one agent. The following drugs are on reported cases involving much higher doses of
commonly administered either prophylactically or as the drug than were clinically used in the United
treatment. They are listed in order of clinical useful- States and that low doses had not been associated
ness and ease of use-to-risk ratio: 5-HT3 receptor an- with arrhythmia or cardiac arrest. Nonetheless, the
tagonists, dexamethasone, droperidol, scopolamine, “black box” warning has contributed to a significant
and metoclopramide. reduction in the use of droperidol for prevention
• Ondansetron, dolasetron, granisetron, and palonosetron and treatment of PONV. However, in high-risk
are currently available 5-HT3 receptor antagonists patients, early administration of droperidol allows
approved for the prevention of PONV; ondansetron for the requisite ECG monitoring period while con-
is the most widely studied. There is no significant ferring significant reduction in the risk of PONV.
difference in efficacy among these drugs when com- • Scopolamine is an anticholinergic drug that is usually
paring equipotent doses. The recommended adult applied as a transdermal patch and is better known
dose of ondansetron is 4 mg intravenously. Ondan- for the prevention of motion sickness. It reduces
setron is effective when administered after general PONV with minimal side effects but should be ap-
anesthesia induction or approximately 30 minutes plied well before the induction of general anesthesia.
before the end of surgery. 5-HT3 receptor antago- Intramuscular or intravenous administration is much
nists are the first choice for prophylaxis in children. more likely to cause a central cholinergic syndrome
Although frequently administered to treat estab- consisting of sedation, amnesia, and euphoria. Con-
lished PONV, they are not effective if already sequently, intramuscular and intravenous routes of
administered prophylactically within the previous delivery are less desirable. The transdermal patch
4 hours. They all have minimal, if any, clinically may be associated with complaints of dry mouth and
significant side effects; however, there have been visual disturbances.
reports of Q–T interval prolongation similar to that • Metoclopramide is a methoxychlorinated derivative
seen with droperidol. of procainamide and is a dopamine antagonist. It
• Dexamethasone is a potent synthetic glucocorticoid is the weakest of all of the medications discussed
(0.75 mg of dexamethasone is equivalent to 20 mg of here, and its ability to prevent PONV or treat
80 Postanesthesia Care Unit Discharge Criteria 443
established PONV has been questioned. Its anti- rigorously applied to all patients. Although criteria may
emetic effect results primarily from increasing vary from center to center, the following summarizes
gastric emptying and lowering esophageal sphinc- what typically occurs on discharge.
ter pressure. Although it may be administered
orally and intramuscularly, 10 mg administered Examination
intravenously is the standard clinical dose. Extra-
pyramidal effects are common and frequently 1. The patient should have stable vital signs for at
very disturbing to patients. Its poor efficacy and least 30 minutes and consistent with his or her age
substantial side effects have led many clinicians to and preanesthetic examination.
abandon the use of metoclopramide. It is not even 2. The patient should be able to swallow and cough.
mentioned in the 2007 SAMBA guidelines for the 3. The patient should be able to walk or return to
management of PONV. preoperative status.
• Aprepitant is a newer NK1 receptor antagonist 4. The patient should have minimal nausea and
that is very expensive and not widely used by vomiting allowing for the ability to swallow and
anesthesiologists. retain liquids.
Administration of intraoperative fraction of inspired 5. The patient should have little or no dizziness al-
oxygen (Fio2) of 0.8 and postoperative supplemental lowing for ambulation.
oxygen (Fio2 !0.3) has been associated with decreased 6. The patient should have no respiratory distress.
PONV in patients receiving general anesthesia; this may 7. The patient should be appropriately alert and
be the result of eliminating nitrous oxide administration oriented.
rather than increasing oxygen concentration. Other 8. The patient should have no surgical contraindication
nonpharmacologic therapies that are effective include to discharge (e.g., excessive pain, bleeding).
the following:
• Acupuncture Instructions to Patient
• Acupoint stimulation via wristband
• Acupressure 1. “You may experience sleepiness or fatigue and
Combining available therapies in management of should not drive, operate machinery, or make any
PONV has been shown to be highly effective, with vom- complex decisions until tomorrow.”
iting rates approaching 0% versus 7% with ondansetron 2. “You may have a sore throat and should gargle with
alone and 22% with placebo. Although gastric suctioning dilute salt water or take acetaminophen.”
before the completion of surgery empties the stomach 3. “You may experience muscular soreness that may
and theoretically would reduce the incidence of PONV, also be treated with acetaminophen.” (This is more
this has not been shown to be efficacious. likely if succinylcholine has been administered.)
4. “In case of any unforeseen emergent problem, call
6. What complications occur in the postanesthesia ….” (The patient should be provided with an
emergency phone number to contact.)
care unit?
5. “An adult escort must accompany you home.”
The incidence of complications in the PACU is high. A (The availability of an escort should be ascer-
review of !18,000 PACU admissions in a university tained before starting surgery because local law
hospital showed an overall complication rate of 26%; the likely mandates this and forbids the discharge
most common complication was PONV (9.8%). Other of even fully recovered patients on their own
complications are airway compromise (6.9%), hypoten- recognizance.)
sion (2.7%), dysrhythmias (1.4%), hypertension (1.1%),
altered mental status (0.6%), suspected myocardial Follow-Up
infarction (0.3%), and other major cardiac events (0.3%).
Another review of 120 incidents occurring in the PACU A member of the anesthesia care team should call the
found that two thirds were related to respiratory compli- patient on the day after surgery and confirm that there
cations. The incidence of complications and specific are no complaints and that the recovery is as expected.
frequency of each of these complications are signifi-
cantly influenced by the patient population and types of 8. Describe a postanesthesia care unit scoring
surgery performed. Healthy young patients undergoing system used to assess readiness for discharge.
ambulatory procedures most frequently experience
PONV, whereas elderly patients with American Society The Aldrete scoring system (Table 80-1) and Postanes-
of Anesthesiologists Physical Status 4 undergoing major thesia Discharge Scoring System (PADSS) (Table 80-2)
abdominal, thoracic, and vascular procedures experience are two commonly used systems. Many variations,
respiratory and cardiac complications. combinations, and permutations of these systems are
employed. The Aldrete scoring system is primarily
7. What are the commonly applied postanesthesia used to determine suitability for discharge from the
PACU to an inpatient bed, and most PACUs would
care unit discharge criteria?
require a summative score of at least 9. The PADSS is
Discharge of patients to home after surgery and anesthe- more appropriate for determination of discharge to
sia is safest when predetermined discharge criteria are home; many PACUs look for a score of 9.
444 SECTION 15 Postanesthesia Care Unit
TABLE 80-1 Aldrete Scoring System TABLE 80-2 Postanesthesia Discharge Scoring
System
Criteria Points
Criteria Points
Respiration
Able to take deep breath and cough 2 Vital Signs
Dyspnea or shallow breathing 1 BP and pulse within 20% of preoperative values 2
BP and pulse within 20%–40% of preoperative 1
Apnea 0
values
SUGGESTED READINGS Hines R, Barash PG, Watrous G, et al.: Complications occurring in the
Broemling N, Campbell F: Anesthetic management of congenital tra- postanesthesia care unit: a survey. Anesth Analg 74:503, 1992.
cheoesophageal fistula. Pediatr Anesth 21:1092, 2011. Scuderi PE, James RL, Harris L, et al.: Antiemetic prophylaxis does
De Oliveira GS, Agarwal D, Benzon HT: Perioperative single dose not improve outcome after outpatient surgery when compared to
ketorolac to prevent postoperative pain: a meta-analysis of randomized symptomatic treatment. Anesthesiology 90:360, 1999.
trials. Anesth Analg 114:424, 2012. Scuderi PE, James RL, Harris L, et al.: Multimodal antiemetic management
Gan TJ: Postoperative nausea and vomiting: can it be eliminated? prevents early postoperative vomiting after outpatient laparoscopy.
JAMA 287:1233, 2002. Anesth Analg 91:1408, 2000.
Gan TJ, Meyer T, Apfel CC, et al.: Consensus guidelines for managing Van der Walt JH, Webb RK, Osborne GA, et al.: The Australian incident
postoperative nausea and vomiting. Anesth Analg 97:62, 2003. monitoring study: recovery room incidents in the first 2000 incident
Gan TJ, Meyer TA, Apfel CC, et al.: Society for ambulatory anesthesia reports. Anaesth Intensive Care 21:653, 1993.
guidelines for the management of postoperative nausea and vomiting. Yogendran S, Asokumar B, Cheng DC, et al.: A prospective randomized
Anesth Analg 105:1615, 2007. double-blinded study of the effect of intravenous fluid therapy on
Goll V, Akca O, Greif R, et al.: Ondansetron is no more effective than adverse outcomes on outpatient surgery. Anesth Analg 80:682, 1995.
supplemental intraoperative oxygen for prevention of postoperative
nausea and vomiting. Anesth Analg 92:112, 2001.
Greif R, Laciny S, Rapf B, et al.: Supplemental oxygen reduces the in-
cidence of postoperative nausea and vomiting. Anesthesiology 91:
1246, 1999.
CASE 81
QUESTIONS
1. What are the possible causes, work-up, and 3. On the following day, the patient responded to
treatment for delayed emergence after general noxious stimuli with extensor posturing, and his
anesthesia? pupils were 4 mm, fixed, and nonreactive to light;
2. Computed tomography scan showed a large left is this patient brain dead, and what are the criteria
thalamic hemorrhage with intraventricular blood for brain death?
and a midline shift, and the patient remained 4. What is an apnea test, and how is it performed?
comatose; how would you manage this patient
in the intensive care unit?
A 66-year-old man underwent craniotomy for clipping of a continuous infusion of naloxone is required to prevent
a saccular aneurysm of the right middle cerebral artery. “renarcotization.”
The aneurysm was discovered during the work-up of per- Residual neuromuscular blockade must always be
sistent headache and did not bleed preoperatively. At the suspected. The response to train-of-four stimulation
conclusion of the procedure, the patient did not wake up. (train-of-four ratio !0.9) can easily assess residual neu-
romuscular blockade. Care must be taken not to stimu-
late nerves in an area where upper motor neuron disease
1. What are the possible causes, work-up, and is present (e.g., hemiplegia) because the response can be
treatment for delayed emergence after general normal-appearing, while neuromuscular blockade exists
anesthesia? in normally innervated muscle. The typical behavior of
a patient with residual neuromuscular blockade is rapid,
Anesthetic Medication Effect
shallow breathing and “flapping” of the limbs, described
The effects of intravenous and inhalation anesthetics can as “a fish out of water.” When in doubt, additional cho-
be prolonged especially in advanced age and in the pres- linesterase inhibitors (usual maximum adult dose of
ence of hepatic and renal dysfunction. The total amount neostigmine regardless of weight is 5 mg) can be given
of medications administered should be reviewed, and spe- for reversal, or one can allow for more time to elapse.
cial attention should be given to when the last doses were If the latter option is chosen, the patient should be ade-
administered. The effects of propofol, midazolam, and quately sedated to avoid an awake but paralyzed patient.
volatile agents should rarely last "30–60 minutes if there Inadequate reversal of neuromuscular blockade (despite
was no “overdose.” Analysis of expired gases can rule out administration of an adequate reversal dose of neostig-
the persistence of volatile agents. Benzodiazepines can be mine or edrophonium) may result from several circum-
reversed by administration of flumazenil intravenously in stances, including (1) the original block was too dense to
0.2-mg increments up to 1.0 mg, and physostigmine can overcome, (2) severe acidosis, (3) hypothermia, (4) marked
reverse the effect of some sedatives, especially the central hypocalcemia, and, more rarely, (5) administration of anti-
effects of anticholinergic agents such as scopolamine. biotics (e.g., aminoglycosides) or other medications (e.g.,
A prolonged opioid effect is more common. The patient magnesium) that potentiate neuromuscular blockade.
typically presents with pinpoint pupils, a slow respiratory
rate, and normal to high tidal volumes. Both diagnosis and Metabolic Disorders
treatment are accomplished by carefully titrating naloxone
intravenously in 40-#g increments, up to 400 #g, or in rare The blood glucose should be measured to rule out hypo-
cases higher doses if the suspicion is high. Complete opioid glycemia or marked hyperglycemia and hyperosmolar
reversal is undesirable because it might lead to severe pain coma. Hypoglycemia should be treated with intravenous
or withdrawal symptoms, with tachycardia, dysrhythmias, dextrose, at least 50 mL of 50% dextrose (25 g). If the
hypertension, increase in intracranial pressure (ICP), suspicion is high, treatment should be initiated without
myocardial ischemia, and pulmonary edema. Occasionally, waiting for the laboratory results. Blood analysis for
445
446 SECTION 15 Postanesthesia Care Unit
electrolytes and an arterial blood gas (ABG) should be • Cerebral perfusion pressure (CPP) should be main-
performed, and any significant abnormality (especially tained "70 mm Hg and is calculated as follows:
hypoxemia, hypercapnia, and hyponatremia or hyperna-
CPP $ MAP % CVP or ICP (whichever is the higher value)
tremia) should be corrected. In patients whose immediate (MAP $ mean arterial pressure, CVP $ central venous pressure.)
preoperative neurologic status is unknown or question-
able, other etiologies such as hypothyroidism or adrenal • Mechanical ventilation
insufficiency should be considered. • Airway protection
• Maintain normal oxygenation
• Mild hyperventilation (see subsequently)
Neurosurgical Disorders
• Decrease ICP
A neurologic examination for focal deficits should be per- • Elevate head of the bed 30 degrees (easiest and
formed. If the cause of delayed awakening remains unclear, most effective measure).
especially after a craniotomy, a computed tomography • Avoid excessive (e.g., "5 cm H2O) positive end
(CT) scan of the brain must be performed to search for expiratory pressure.
intracranial pathology, such as intracranial hemorrhage. • Avoid agitation and “bucking.”
Ischemic cerebrovascular accidents are often not immedi- • Consider administration of mannitol (0.5–1 g/kg
ately seen on CT scan. Less commonly, CT scan may intravenously) or hypertonic saline (3% or 25%)
demonstrate tension pneumocephalus, caused by nitrous to increase serum osmotic pressure.
oxide, or global cerebral hypoxic damage. Cerebral hypoxia • Hyperventilate to arterial carbon dioxide tension
of any cause results in a reduced level of consciousness that (PaCO2) of 30–35 mm Hg.
may first appear as delayed emergence. • Consider insertion of ICP monitor (e.g., ventricu-
lostomy), which also permits cerebrospinal fluid
removal to manage cases of acute intracranial
Other Causes
hypertension.
Alcohol and other recreational drugs ingested preopera- • In extreme cases, craniectomy can be performed
tively should be considered, especially in trauma patients. to remove part of the skull vault to control ICP.
Blood and urine could be quickly sent for a toxicology • Avoid rebleeding
screen. • Control blood pressure.
Table 81-1 summarizes the differential diagnosis and • Correct any coagulopathy.
work-up for delayed awakening. • Avoid anticoagulants (e.g., prophylactic doses of
heparin subcutaneously for deep vein thrombosis
2. Computed tomography scan showed a large left are controversial but usually avoided).
thalamic hemorrhage with intraventricular blood • Prevent seizures
and a midline shift, and the patient remained • Administer fosphenytoin, 1500 mg (or 15 to
comatose; how would you manage this patient in 20 mg/kg) intravenously (equivalent to 1000 mg of
phenytoin but less likely to cause hypotension in
the intensive care unit?
high doses) over 30 minutes, then phenytoin, 100 mg
The following parameters should be monitored and man- intravenously every 8 hours, adjusted based on
aged accordingly: plasma levels. Free phenytoin level rather than
• Maintain close to normal hemodynamics total phenytoin level may need to be checked.
• Fluid administration as necessary • Prevent hyperthermia
• Vasopressors or inotropes as indicated • Although the cerebral protective effect of hypo-
thermia is still controversial, the deleterious ef-
fect of hyperthermia to the injured brain is well
established.
• Administer antipyretics and active cooling as needed.
TABLE 81-1 Differential Diagnosis and Work-up • Glucose control
for Delayed Awakening • Hyperglycemia predicts increased risk of mortality
and poor outcome in patients with intracerebral
Metabolic Hypoxia ABG hemorrhage. However, more recent studies reveal
Hypercapnia an increased risk of hypoglycemic events and as-
Hypoglycemia Laboratory testing sociated increased risk of mortality in patients
Electrolyte disturbance
Hypothyroidism
treated with tight glucose control regimens. At the
Adrenal insufficiency present time, the optimal target glucose is unclear
but &180 g/dL is a reasonable goal. Hypoglycemia
Neurologic Cerebrovascular accident CT scan
Pneumocephalus
should be avoided and treated expeditiously.
Global cerebral hypoxia • Prevent gastrointestinal bleeding
• Administer anti–histamine H2 agents (e.g., famoti-
Other Alcohol intoxication Blood and urine
Recreational drug use toxicology
dine) or proton pump inhibitors (e.g., omeprazole).
• Prevent deep vein thrombosis
ABG, Arterial blood gas; CT, computed tomography. • Apply sequential compression stockings.
81 Delayed Emergence, Coma, and Brain Death 447
3. On the following day, the patient responded to • Clinical observations compatible with the diagnosis
noxious stimuli with extensor posturing, and his of brain death
pupils were 4 mm, fixed, and nonreactive to light; The following manifestations are occasionally seen
is this patient brain dead, and what are the and are not evidence of brainstem function:
criteria for brain death? • Spontaneous movements of limbs other than patho-
logic flexion or extension response
The patient is not brain dead, but if he survives, the like- • Respiratory-like movements (shoulder elevation and
lihood of a persistent vegetative state is very high. If the adduction, back arching, intercostal expansion with-
patient does not have a living will stating his wishes, the out significant tidal volumes)
discussion with the family should first provide informa- • Sweating, flushing, tachycardia
tion regarding the current status and prognosis in a way • Normal blood pressure without pharmacologic sup-
that nonmedical people could comprehend. The discus- port or sudden increases in blood pressure
sion should center on trying to determine what the • Absence of diabetes insipidus
wishes of the patient are. If no wishes were clearly stated, • Deep tendon reflexes, superficial abdominal reflexes,
the patient’s values should be explored to reach a decision triple flexion response
regarding pursuit or withdrawal of treatment. • Babinski reflex
The criteria for brain death are the irreversible ab- Confirmatory tests, such as a cerebral angiogram or a
sence of brain function including cortex and brainstem in radionuclide scan, demonstrating the absence of blood
the absence of hypothermia, toxins (e.g., drugs, especially flow to the brain are sufficient to affirm brain death. An-
sedative-hypnotics and muscle relaxants), and metabolic cillary tests can be used when uncertainty exists about the
disturbances (e.g., marked abnormalities in sodium, hy- reliability of parts of the neurologic examination or when
pothyroidism). Precise protocols for determining brain the apnea test cannot be performed. Transcranial Dop-
death vary among institutions. pler showing small systolic peaks with no diastolic flow
Determination of brain death requires two clinical as- has similar value. The absence of signal on both electro-
sessments of brain function, separated by a period of at encephalogram and brainstem evoked potentials is also
least 6 hours. The apnea test is typically performed after sufficient. Some of these tests are required by policy in
the second evaluation of brainstem reflexes. The three some institutions; however, brain death is commonly
essential findings in brain death are coma or unrespon- determined on clinical criteria alone.
siveness, absence of brainstem reflexes, and apnea. The All evidence should be adequately documented in the
determination of brain death verifies these findings by chart, and two concurring physicians should affirm the
the following clinical indicators: diagnosis of brain death. Legally, all physicians are al-
• Coma or unresponsiveness lowed to determine brain death in most states. Neurolo-
• No cerebral motor response to verbal command gists, neurosurgeons, and intensive care specialists may
or painful stimulation in all extremities (nail-bed have specialized expertise. It seems reasonable to require
pressure) and supraorbital pressure that all physicians making a determination of brain death
• Absence of brainstem reflexes be intimately familiar with brain death criteria and have
• Pupils demonstrated competence in this complex examination.
• No response to bright light The family can be approached for solid organ and tissue
• Size: midposition (4 mm) to dilated (9 mm) donation. In children, the criteria are slightly different
• Ocular movement and beyond the scope of this chapter.
• No oculocephalic reflex (testing is appropriate
only when no fracture or instability of the cervi-
4. What is an apnea test, and how is it performed?
cal spine or skull base is apparent); this entails
turning the head rapidly from side to side and An apnea test reveals the patient’s response to hypercap-
observing the abnormal lack of eye movement nia and helps to confirm the diagnosis of brain death (i.e.,
in the direction opposite to the head movement no response in the case of brain death). It is performed as
• No deviation of the eyes to irrigation in each follows:
ear with 50 mL of cold water (tympanic mem- • Baseline ABG is obtained
branes intact; allow 1 minute after injection • Establish reliable pulse oximeter signal and disconnect
and at least 5 minutes between testing on each ventilator
side) • Deliver oxygen into the trachea by placement of
• Facial sensation and motor response nasal cannula deep into the tracheal tube taking
• No corneal reflex care not to occlude the lumen and prevent efflux
• No jaw reflex (optional) of gas
• No grimacing to deep pressure on nail bed, • Look closely for any respiratory movements
supraorbital ridge, or temporomandibular joint • Measure arterial oxygen tension, PaCO2, and pH
• Pharyngeal and tracheal reflexes after approximately 8 minutes and reconnect ventilator
• No response after stimulation of the posterior If respiratory movements are absent and PaCO2 is
pharynx !60 mm Hg, or there is a 20 mm Hg increase in PaCO2
• No cough response to tracheobronchial suc- over a baseline normal PaCO2, the apnea test result
tioning is positive (i.e., supports the diagnosis of brain death).
448 SECTION 15 Postanesthesia Care Unit
CRITICAL CARE
449
CASE 82
Neonatal Resuscitation
Francine S. Yudkowitz, MD, FAAP
QUESTIONS
A 42-year-old woman was in labor. The fetal heart rate changes lead to a dramatic decrease in PVR, although not
monitor showed intermittent variable decelerations with to the normal adult values. At the same time, the umbili-
good recovery. The obstetrician ruptured membranes and cal cord is clamped, and the low-resistance placenta is
noted that the amniotic fluid was meconium stained. Because removed from the circulation; this results in an abrupt
the fetal heart rate monitor showed good beat-to-beat vari- increase in SVR. These changes lead to the following:
ability, it was decided to allow the mother to continue in labor • Functional closure of the patent foramen ovale
and deliver vaginally. The infant was delivered vaginally because the pressure on the left side of the heart
2 hours later and was noted to be meconium stained. (SVR) is greater than the pressure on the right
side (PVR)
• Functional closure of the ductus arteriosus because
1. Describe the fetal circulation.
of an increase in arterial pO2; the ductus arteriosus
The fetal circulation (Figure 82-1) is a parallel circuit, becomes the ligamentum arteriosum
in contrast to a series circuit in the adult. In the fetus, gas • Functional closure of the ductus venosus because of
exchange occurs at the placenta and not the lungs. Blood removal of the placenta
leaving the placenta enters the fetus via the umbilical vein. This pattern of circulation closely resembles the adult
This relatively well-oxygenated blood (pO2 30–35 mm Hg) circulation. However, it is referred to as the transitional
enters the fetus and predominantly bypasses the liver via the circulation because of the reversibility of the above-
ductus venosus. Most of this blood on entering the right mentioned changes during adverse events, such as hypoxia
atrium is preferentially shunted across the patent foramen or acidosis. Any insult that increases pulmonary vascular
ovale to the left side of the heart and out the ascending aorta resistance results in reopening of the functionally closed
to the cerebral and coronary circulation. The brain and fetal shunts. Factors that adversely affect PVR are hypoxia,
heart receive most of the relatively well-oxygenated blood. hypercarbia, acidosis, hypothermia, and sympathetic stim-
Blood returning from the cerebral circulation via the supe- ulation. It is imperative in the initial management of the
rior vena cava, which is considerably less oxygenated (pO2 neonate in the delivery room to pay meticulous attention
12–14 mm Hg), enters the right side of the heart. This to ensuring adequate oxygenation, ventilation, and main-
blood is preferentially directed to the right ventricle and tenance of normothermia. Reversion to fetal circulation is
exits through the pulmonary artery. Because of the high referred to as persistent pulmonary hypertension of the
pulmonary vascular resistance (PVR) that exists in utero, newborn.
only 10% of this blood enters the pulmonary circulation to
provide nutrients for lung growth. The remaining blood is 3. How is neonatal resuscitation managed
shunted across the ductus arteriosus because of the low in the delivery room?
systemic vascular resistance (SVR). SVR is low in the fetus
because of the relatively large ductus arteriosus and the As soon as the newborn is delivered, a rapid assessment
placenta. Blood enters the descending aorta and supplies the should be performed to determine the need for resuscita-
lower fetal body, returning to the placenta via the iliac veins tion (Figure 82-2). This rapid assessment answers the
to the umbilical arteries. following three questions:
• Is the newborn full term?
• Is the newborn crying or breathing?
2. What physiologic changes occur at birth?
• Is the muscle tone good?
When the neonate is delivered, the first breaths expand If the answer to all three questions is yes, resuscitation is
the lungs with air, and alveolar pO2 increases. These not necessary, and the newborn can remain with the
450
82 Neonatal Resuscitation 451
To head
To arm To arm
Pulmonary artery
Left atrium
Foramen ovale
Right atrium
Right lung Left
Right ventricle
Hepatic vein
Left ventricle
Ductus venosus
Liver
Inferior vena cava
Umbilical vein
Aorta
Umbilical
Umbilicus arteries
Hypogastric arteries
To left leg
Umbilical cord
Arterial blood
Placenta Bladder
Venous blood
Mixed
arterial-venous
blood
FIGURE 82-1 ■ Fetal circulation. (From Miller RD, Cucchiare RF, Miller ED, editors.: Anesthesia, 5th ed. Philadelphia: Churchill Livingstone;
2000. p. 1807.)
mother. If the answer to any of these questions is no, and, if needed, administration of supplemental oxygen or
resuscitation should be initiated in the following order: positive pressure ventilation. Positive pressure ventilation
• Initial steps should be at a rate of 40–60 breaths per minute, and the
• Warm by radiant heat source minimal inflation pressure to achieve a heart rate !100 beats
• Clear the airway if needed per minute should be applied. Heart rate is assessed by
• Dry the newborn auscultation of the precordium or palpation of the
• Stimulate breathing umbilical artery. When supplemental oxygen or positive
• Ventilation pressure ventilation or both are begun, the assessment now
• Chest compressions consists of evaluation of respirations, heart rate, and oxy-
• Administration of epinephrine or volume expansion genation (see Box 82-1). Oxygenation is ideally monitored
or both by pulse oximetry. However, it may take 1–2 minutes
In the first 60 seconds, known as the “golden minute,” before pulse oximetry is functional, and in low-flow states
the following should be completed: the initial steps; reas- it may not work at all. During every intervention, success is
sessment of the respiratory status and heart rate (Box 82-1); measured by an increase in heart rate.
452 SECTION 16 Critical Care
Newborn Resuscitation
No Labored breathing
HR below 100,
30 sec or persistent
gasping, or apnea?
cyanosis?
Yes
Yes
Clear airway
PPV, SpO2 monitoring
SpO2 monitoring Consider CPAP
60 sec
No
HR below 100?
Yes
Take ventilation
corrective steps Postresuscitation
care
No
HR below 60?
Yes
Consider intubation
Chest compressions
Coordinate with PPV
Take ventilation
corrective steps
HR below 60?
Intubate if
no chest rise!
Yes
IV epinephrine
Consider:
• Hypovolemia
• Pneumothorax
FIGURE 82-2 ■ Neonatal resuscitation in the delivery room. (Adapted from Kattwinkel J, Perlman JM, Aziz K, et al.: Part 15. Neonatal
resuscitation: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation
122(Suppl 3):S909, 2010.)
BOX 82-1 Assessment Parameters for Endotracheal intubation should be considered in the
Respirations and Heart Rate following circumstances:
• Nonvigorous newborn with meconium staining
• Respirations • Prolonged or ineffective bag and mask ventilation
• Apnea • Chest compressions are performed
• Gasping • Special circumstances, such as congenital diaphrag-
• Labored or unlabored breathing
matic hernia, “micropreemie”
• Heart rate
• ! or " 100 beats per minute Correct placement of the endotracheal tube should result
• Oxygenation in an increase in heart rate. An exhaled carbon dioxide
• Appropriate preductal oxygen saturation by age detector is the recommended method to confirm correct
endotracheal tube placement. However, if there is little
82 Neonatal Resuscitation 453
60 seconds of adequate ventilation, the oxygen concentra- for medical intervention. The Apgar score (Table 82-2)
tion should be increased to 100%. consists of five parameters that are assessed at 1 minute
and 5 minutes after birth: heart rate, respiratory effort,
5. How is a newborn managed when meconium muscle tone, reflex irritability, and color. A score of 0,
1, or 2 is assigned to each parameter. A score of 8–10 is
is present?
normal and requires no additional treatment. A score
Meconium aspiration syndrome (MAS) occurs when of 5–7 indicates moderate impairment; supplemental
meconium is aspirated in utero, at delivery, or during oxygen and tactile stimulation may be needed. A score
resuscitation. Previously, the recommendation consisted of 0–4 indicates the need for immediate resuscitation.
of suctioning the oropharynx after delivery of the shoul- The 1-minute score is said to be inversely proportional
ders, but subsequent studies have shown this to be of no to the risk of infant mortality, whereas the 5-minute
value. Elective intubation and suctioning of the trachea score may relate to the degree of future neurologic
in meconium-stained vigorous newborns were found to impairment.
be of no value; in addition, complications associated with The Apgar score, although still widely performed, is
tracheal suctioning, such as laryngeal trauma, may occur. not used to guide resuscitation efforts in the delivery
Although MAS is more likely to occur in nonvigorous room. One should not wait until 1 minute after birth to
meconium-stained newborns, elective intubation and tra- begin resuscitative efforts.
cheal suctioning have not been associated with a decreased
incidence of MAS. However, there are not enough ran-
domized controlled trials to change current practice rec-
ommendations of tracheal suctioning of meconium-stained SUGGESTED READINGS
nonvigorous newborns. During this maneuver, an assistant Kattwinkel J, Perlman JM, Aziz K, et al.: Part 15: neonatal resuscitation:
2010 American Heart Association Guidelines for Cardiopulmonary
should monitor the heart rate continuously. If there is Resuscitation and Emergency Cardiovascular Care. Circulation
persistent bradycardia, this maneuver should be aban- 122(Suppl 3):S909, 2010.
doned, and resuscitation should be initiated. Rabi Y, Rabi D, Yee W: Room air resuscitation of the depressed new-
born: a systematic review and meta-analysis. Resuscitation 72:353,
2007.
6. What is the Apgar score? Shukla AC, Steven JM, McGowan F: Cardiac physiology and pharmacol-
ogy. p. 361. In Cote CJ, Lerman J, Todres ID, (eds.): A practice of an-
Apgar, an anesthesiologist, devised a scoring system to esthesia for infants and children, 4th edition. Saunders, Philadelphia,
assess newborns for their clinical condition and need 2009.
CASE 83
Pediatric Cardiopulmonary
Resuscitation
Cheryl K. Gooden, MD, FAAP
QUESTIONS
1. What is the etiology of cardiac arrest in children? 7. Are calcium and vasopressin recommended for
2. How do survival rates from cardiac arrest differ routine use during pediatric cardiopulmonary
when comparing in-hospital with out-of-hospital arrest?
settings? 8. What are the cardiopulmonary resuscitation
3. What changes occurred to pediatric chest com- recommendations for infants and children with
pression depth and compression/ventilation ratios congenital heart disease?
with the 2010 American Heart Association guide- 9. How is symptomatic bradycardia treated?
lines? 10. How is pulseless electrical activity treated?
4. What are the recommendations for the delivery of 11. How is ventricular fibrillation or pulseless
breaths with and without an advanced airway? ventricular tachycardia treated?
5. What are the latest recommendations for 12. How is supraventricular tachycardia treated?
automated external defibrillators or manual 13. What are the recommendations for supplemental
defibrillators in infants? oxygen use after return of spontaneous
6. Is intraosseous access an acceptable form of circulation?
vascular access during pediatric advanced life
support?
A 6-year-old, obese boy with genu valgum underwent 2. How do survival rates from cardiac arrest differ
an uneventful anesthetic for removal of bilateral lower when comparing in-hospital with out-of-hospital
extremity hardware. While in the postanesthesia care settings?
unit, he received intravenous fentanyl and shortly thereaf-
ter became unresponsive with ensuing respiratory arrest. Infants and children who experience in-hospital cardiac
He developed pulseless ventricular tachycardia (VT) that arrest are more likely to survive the event than infants
deteriorated quickly to ventricular fibrillation (VF). and children in the out-of-hospital setting. However,
overall there remains room for improvement in this area.
For the most part, the numbers are low for infants and
1. What is the etiology of cardiac arrest in children?
children who survive to discharge from the hospital after
Most cardiac arrest events in infants and children are in-hospital (33%) or out-of-hospital (4%–13%) cardiac
precipitated by respiratory failure or shock. Sudden arrest. The American Heart Association (AHA) main-
cardiac arrest may be observed less frequently. Typi- tains an ongoing focus on early recognition and rapid
cally, sudden cardiac arrest is the result of an arrhyth- intervention of respiratory failure or shock to prevents
mia, such as pulseless VT or VF. Genetic mutations progression to cardiac arrest. When cardiac arrest occurs,
resulting in channelopathies have been linked to sudden early recognition and high-quality cardiopulmonary
cardiac arrest, such as in sudden infant death syndrome resuscitation (CPR) are important to improve survival.
and sudden death in children. Channelopathies are a
group of diseases that are characterized by abnormal 3. What changes occurred to pediatric chest
myocyte ion channels or the proteins that regulate them compression depth and compression/ventilation
resulting in fatal arrhythmias. ratios with the 2010 American Heart Association
Primary factors that may lead to cardiac arrest in guidelines?
pediatric patients are respiratory failure, shock, and
sudden arrhythmias (pulseless VT or VF). Secondary A major change in the 2010 AHA Guidelines is to begin
factors that may contribute to cardiac arrest and should CPR with chest compressions as opposed to providing
be considered when managing arrest victims are listed breaths. With this in mind, the initial “look, listen, and
in Box 83-1. feel for breathing,” was eliminated. For many of us who
455
456 SECTION 16 Critical Care
BOX 83-1 Factors Contributing to Cardiac • A bystander who is not a skilled health care provider
Arrest may be more inclined to initiate CPR with chest
compressions than rescue breaths. Because of this,
PRIMARY FACTORS the AHA has advocated for a number of years
Respiratory failure “hands-only” (chest compression–only) CPR for the
Shock bystander who is reluctant to perform rescue breath-
Sudden arrhythmias (pulseless VT or VF) ing. A bystander providing only chest compressions
is better than not performing CPR at all.
SECONDARY FACTORS (“H’S AND T’S”) • For the ease of learning CPR, especially for unskilled
Hypoxia providers, the C-A-B sequence, although better
Hypovolemia suited for adult victims, is taught for both adult and
Hydrogen ions (acidosis) pediatric resuscitation.
Hypoglycemia The 2010 recommendation for chest compression
Hypokalemia/hyperkalemia
depth (“push hard”) is approximately one third of the
Hypothermia
Thrombosis—coronary or pulmonary anterior-posterior diameter of the chest wall. This cor-
Tamponade—cardiac relates with approximately 1.5 inches (4 cm) for an infant
Tension pneumothorax and 2 inches (5 cm) for a child (Table 83-1). Full chest
Toxins recoil should occur between chest compressions.
Trauma During cardiac arrest, it is crucial that chest compres-
sions are performed early and effectively without fre-
VT, ventricular tachycardia; VF, ventricular fibrillation. quent or prolonged interruptions to generate a better
cardiac output. To some extent, the cardiac output pro-
vides essential organs with much needed blood flow to
restore baseline circulation as close as possible. Cycles of
learned the phrase “airway, breathing, and circulation CPR should continue uninterrupted for 2 minutes before
(A-B-C),” it now has become “circulation, airway, and checking for a rhythm and pulse and should resume
breathing (C-A-B).” The reason for this change was to within 10 seconds. The number of compressions per
prevent delayed chest compressions even though the minute changed from 100 to at least 100 compressions
most common origin of cardiac arrest in pediatrics is of a per minute (“push fast”). During resuscitation by more
respiratory nature. The impetus for this change is multi- than one health care provider, the person doing chest
factorial, as follows: compressions should change after each 2-minute cycle
• Because high-quality chest compressions are the because fatigue is associated with lower quality chest
basis for effective CPR, time to initiation of chest compressions.
compressions is important to survival. The time to
deliver two breaths, particularly by nonskilled pro- 4. What are the recommendations for the delivery of
viders, delays chest compressions for a greater pe-
breaths with and without an advanced airway?
riod of time (!18 seconds) than would the delay to
first breath ("18 seconds) if chest compressions are Without an advanced airway (e.g., endotracheal tube,
performed initially. Even though respiratory causes laryngeal mask airway), breaths should be synchronized
of cardiac arrest are more likely in pediatric popula- with chest compressions. Two breaths are given after
tions, the time to first breath would not be signifi- 30 compressions (30:2) with one rescuer and after 15
cantly delayed. chest compressions (15:2) with two rescuers. Each breath
should not last !1 second and should be terminated better option than no defibrillation at all (Table 83-2).
when chest rise is detected (see Table 83-1). Excessive The recommended initial dose is 2–4 J/kg. If a second
ventilation interferes with cardiac output and coronary shock is necessary, following a cycle (approximately
artery perfusion. Excessive ventilation also could cause 2 minutes) of CPR, a dose of 4 J/kg is recommended.
gastric distention, which would increase the risk of If additional shocks are necessary, the minimum dose is
aspiration. 4 J/kg and may increase to 10 J/kg.
With an advanced airway, breaths and chest com-
pressions are asynchronous. One breath is given every 6. Is intraosseous access an acceptable form of
6–8 seconds (i.e., 8–10 breaths per minute). Care must vascular access during pediatric advanced life
be taken to avoid excessive ventilation by terminating support?
inflation when chest rise is achieved.
When an endotracheal tube is placed during resuscita- Intraosseous (IO) cannulation is considered an excellent
tion, capnography should be used to confirm placement. If alternative option for vascular access. It can be obtained
possible, continuous monitoring of end-tidal carbon diox- quickly, particularly in the setting of resuscitation, and is
ide (ETCO2) should be used during CPR as an indirect acceptable in patients of any age. Similar to intravenous
measure of the quality of chest compressions. An ETCO2 (IV) access, medications, crystalloids, colloids, and blood
of at least 10–15 mm Hg is associated with effective car- products can be administered through an IO access.
diac compressions. Return of spontaneous circulation Additionally, the IO route is better for administering
(ROSC) is associated with increased ETCO2, usually to medications than through an endotracheal tube because
!40 mm Hg. uptake of medications through the endotracheal tube
route tends to be unpredictable.
5. What are the latest recommendations for Several locations exist for placement of IO access in
automated external defibrillators or manual children. The most commonly used site is the proximal
tibia. Additional locations include the anterior-superior
defibrillators in infants?
iliac spine, distal femur, and distal tibia. Contraindica-
Defibrillation with an automated external defibrillator tions to IO placement are listed in Box 83-2.
(AED) or manual defibrillator is reserved for shockable There are various techniques for IO placement. IO or
rhythms (i.e., VF, pulseless VT). Ideally, defibrillation bone marrow needles are most commonly used for IO
should be provided early during resuscitation. However, access. IO drills have appeared on the market more re-
CPR should not be delayed while awaiting an AED or cently, and their use is becoming quite popular. If these
manual defibrillator. are unavailable, spinal needles, hypodermic needles, and
AEDs have become ubiquitous in most public settings. even butterfly needles may be used.
The 2010 AHA Guidelines include recommendations for
its use in infants. Before these guidelines, AEDs were not 7. Are calcium and vasopressin recommended for
recommended for infants. routine use during pediatric cardiopulmonary
As the name implies, an AED with pads applied to the arrest?
patient’s chest determines whether a shockable rhythm ex-
ists, charges to the manufacturer’s set dose, and advises the Compared with the 2005 AHA Guidelines, the 2010
user when to administer a shock. Many AEDs are capable guidelines deemphasize calcium administration during
of providing an energy dose that is appropriate for infants resuscitation because it does not offer any known advan-
or children #8 years old. If the AED is not equipped with tages. The indications for calcium administration are
this capability, it can still be used in infants and children. documented hypocalcemia or hyperkalemia. It can be
Many manual defibrillators are equipped with infant considered for the treatment of hypermagnesemia or
paddles. If not, adult paddles may be used. When avail- calcium-channel blocker overdose.
able, a manual defibrillator is preferable to an AED for Either calcium chloride (20 mg/kg) or calcium gluconate
use in infants. However, defibrillation with an AED is a (60 mg/kg) may be administered. In an arrest situation,
During the resuscitation, underlying causative factors complex and whether hemodynamic instability is pres-
for cardiac arrest should be sought and treated (see ent. The first step is to differentiate narrow complex
Box 83-1). tachycardia (QRS width #0.09 second) from wide com-
plex tachycardia (QRS width !0.09 second). Treatment
11. How is ventricular fibrillation or pulseless options for narrow complex tachycardia pivots on dis-
tinguishing sinus tachycardia from SVT (Table 83-4).
ventricular tachycardia treated?
Treatment of sinus tachycardia requires identification
There should be no hesitation to begin CPR for of an underlying cause (e.g., dehydration, fever). Con-
the treatment of VF or pulseless VT. VF and pulseless trolling SVT begins with vagal maneuvers (Box 83-3)
VT are shockable rhythms. The most important while obtaining IV/IO access. When IV/IO access is
measure in managing these rhythms is defibrillation, secured, adenosine should be administered as a rapid
with either a manual defibrillator or AED (see bolus and immediately followed by a saline flush. SVT
Question 5). that is unresponsive to vagal maneuvers and adenosine
IV/IO epinephrine is the mainstay of drug therapy is treated with synchronized cardioversion (Table 83-5).
for VF or pulseless VT. The first dose of epinephrine When it is clinically acceptable, sedation may be pro-
(0.1 mg/kg of 1:10,000) is indicated after the second vided before synchronized cardioversion.
delivered shock, while the next cycle of CPR is in prog- The treatment of wide complex SVT depends on
ress. Epinephrine is delayed until this time because whether cardiopulmonary compromise (i.e., hypoten-
defibrillation alone may result in a life sustainable sion, acutely altered mental status, shock) is present. If
rhythm. cardiopulmonary compromise is present, synchronized
During resuscitation, the endotracheal route has been cardioversion should be performed immediately. In the
used for delivering certain medications (e.g., epineph- absence of cardiopulmonary compromise, a cardiology
rine, atropine, lidocaine, naloxone) when the IV/IO consultation should be obtained. Adenosine may be
route was unavailable. However, this route has been administered if the rate is regular and the QRS com-
strongly discouraged for the following reasons: plex is monomorphic. Further management includes
• Blood levels attained with the endotracheal route are administration of either amiodarone (5 mg/kg) or pro-
less than the blood levels attained by the IV/IO cainamide (15 mg/kg). Verapamil may be considered as
routes a treatment option in SVT in an older child. Verapamil
• Evidence indicates that epinephrine administered is not the drug of choice for the treatment of SVT
through the endotracheal route can result in over- in infants and young children. Consultation with a
riding &-adrenergic effects
• Chest compressions must be stopped
Amiodarone (5 mg/kg) for VF or pulseless VT is
a second-line drug therapy. Lidocaine (1 mg/kg)
also may be considered for use in VF or pulseless
VT when amiodarone is unavailable. Secondary BOX 83-3 Vagal Maneuvers
factors should be investigated for treatable causes (see INFANT/YOUNGER CHILD
Box 83-1).
Place a small ice pack on the face
Electrical
Synchronized Initial shock: 0.5–1 J/kg
cardioversion
Next shock: 2 J/kg If initial shock ineffective
Cardiopulmonary Resuscitation
Amanda J. Rhee, MD • David L. Reich, MD • Yaakov Beilin, MD
QUESTIONS
1. What is the initial response to a witnessed cardiac 9. How are ventricular fibrillation and pulseless
arrest? ventricular tachycardia managed?
2. How do chest compressions produce a cardiac 10. What is the management of asystole and pulse-
output? less electrical activity?
3. What is the optimal airway management during 11. How is symptomatic bradycardia managed?
cardiopulmonary resuscitation? 12. How are supraventricular tachyarrhythmias
4. What are the complications of cardiopulmonary managed?
resuscitation? 13. What are the indications for magnesium therapy?
5. What is the optimal dose of epinephrine? 14. What are the indications for a pacemaker?
6. What is the indication for vasopressin in cardio- 15. Why is it important to monitor serum glucose?
pulmonary resuscitation? 16. What are the indications for open cardiac massage?
7. What are the indications for sodium bicarbonate 17. What is the role for therapeutic hypothermia?
administration?
18. What are the special considerations for cardio-
8. What are the indications for calcium administration pulmonary resuscitation in a pregnant patient?
during cardiopulmonary resuscitation?
An 86-year-old woman with congestive heart failure, coro- Basic life support (BLS) protocol (Figure 84-1) is
nary artery disease, and syncopal episodes presented for followed during the initial phase of cardiac arrest.
elective permanent pacemaker insertion. A recent 24-hour Although these steps are described in sequence, they
ambulatory electrocardiogram (ECG) demonstrated mul- may occur simultaneously in the hospital setting. The
tiple episodes of severe sinus bradycardia associated with initial response to a witnessed cardiac arrest is to con-
presyncopal symptoms. Monitored anesthesia care was firm that the patient is unresponsive and apneic or has
requested because of the patient’s advanced age and associ- abnormal breathing (i.e., gasping). The health care
ated medical conditions. Infiltration of local anesthesia and provider immediately calls for assistance and a defibril-
isolation of the cephalic vein in the left deltopectoral lator. The recommendation to call for assistance before
groove proceeded uneventfully. During placement of the initiating chest compressions was established to de-
ventricular pacing lead, ventricular ectopy occurred. As the crease the time from cardiac arrest to first defibrilla-
lead was repositioned, ventricular tachycardia was induced tion, if appropriate. This recommendation is important
and rapidly deteriorated into ventricular fibrillation. because the highest survival rates are in patients who
experience a witnessed cardiac arrest and have ventric-
1. What is the initial response to a witnessed ular fibrillation (VF) or pulseless ventricular tachycar-
dia (VT) and who receive early chest compressions and
cardiac arrest?
defibrillation.
In 2010, the American Heart Association (AHA) pub- The next step is to check for a pulse (carotid artery)
lished updated Guidelines for Cardiopulmonary Arrest for no longer than 10 seconds before initiating cardio-
and Emergency Cardiovascular Care. The guidelines dif- pulmonary resuscitation (CPR). One starts with high
fer for lay rescuers and health care providers. This review quality chest compressions. The essential element in
focuses only on the recommendations for health care treating cardiac arrest is beginning high-quality chest
providers. The following major changes were made: compressions without delay, to provide oxygenated
• Elimination of “look, listen, and feel” blood to the heart and brain while advanced cardiopul-
• Deemphasis on pulse check monary life support (ACLS) protocols are initiated.
• Sequence of resuscitation is circulation, airway, Components of high-quality chest compressions are as
breathing (C-A-B) follows:
• Changed from airway, breathing, circulation • “Push hard and push fast”
(A-B-C) • Adequate rate (at least 100 compressions per minute)
• Continued focus of ensuring high-quality chest • Adequate depth (2 inches)
compressions • Full chest recoil between chest compressions
461
462 SECTION 16 Critical Care
Optimal airway management during CPR depends on 4. What are the complications of
the experience of the rescuer. When unskilled providers
cardiopulmonary resuscitation?
attempted to place endotracheal tubes (ETT), the fol-
lowing complications occurred: Complications of CPR include skeletal (especially rib
• Trauma to the oropharynx fractures), visceral, airway, and skin and integument
• Unacceptably long periods of interrupted chest (skin, teeth, lips) injuries. Some of these complications
compressions and ventilation may require therapy and prolong hospitalization. Exam-
• Hypoxemia ples include rib and sternal fractures, myocardial and
• Failure to recognize misplacement or dislodgment pulmonary contusions, pneumothorax, pericardial hema-
Tracheal intubation, particularly by unskilled providers, toma, tracheal and laryngeal injuries, liver and spleen
is no longer considered the optimal way to manage the ruptures, and gastric perforation and dilation. Of these
airway. In these circumstances, bag and mask ventilation complications, !0.5% are considered life-threatening.
or the use of alternative airways is preferable. Serious harm occurring to patients while performing
Bag and mask ventilation is performed initially in the CPR is uncommon and should not dissuade bystanders
nonintubated patient but risks gastric inflation, regurgi- from performing CPR.
tation, and aspiration. Despite these risks, the routine
application of cricoid pressure during CPR is not recom-
5. What is the optimal dose of epinephrine?
mended. In certain circumstances where regurgitation is
of particular concern, cricoid pressure may be used. Epinephrine is the therapy of choice for VF, pulseless
However, if effective ventilation is impeded, the pressure VT, asystole, and pulseless electrical activity (PEA).
should be relaxed, adjusted, or ultimately released. Vasoconstriction caused by the #-adrenergic effects of
There is no specific recommendation regarding the epinephrine during CPR increases arterial pressure and
timing of tracheal intubation. Whenever the decision is improves myocardial and cerebral perfusion pressure.
made to perform tracheal intubation, the following con- This is most likely a dose-dependent phenomenon.
cepts apply: The presence of coronary artery disease in many
• CPR should not be interrupted for "10 seconds. patients limits coronary artery blood flow even in the pres-
• The compressor should be prepared to resume chest ence of higher aortic diastolic pressures. The $-adrenergic
compressions as soon as the ETT is passed through effects of epinephrine may actually worsen the outcome by
the vocal cords. increasing myocardial oxygen requirements.
• Confirmation of ETT placement should consist of: Animal models have shown better outcomes from
• Visualization of bilateral chest rise experimental cardiac arrest using 0.1–0.2 mg/kg of epi-
• Auscultation over the epigastrium and bilateral nephrine, compared with the present recommended
lung fields dose of 0.01 mg/kg. However, two more recent large
• Detection of ETCO2 multicenter investigations did not demonstrate survival
• Continuous waveform capnography differences in patients treated with larger doses of epi-
• Colorimetric or nonwaveform nephrine. This lack of clinical efficacy may be related to
Absence of ETCO2 does not always indicate misplace- the increased time that elapsed before the initial dose of
ment of the ETT (Box 84-1). In situations in which epinephrine in clinical situations versus the animal stud-
ETCO2 is absent, a second method of confirmation should ies. Until further studies clarify this issue, the current
include either direct visualization of the ETT passing recommendation is 1 mg administered intravenously or
through the vocal cords or an esophageal detector device. intraosseously of a 1:10,000 epinephrine solution every
Supraglottic devices, such as laryngeal mask airways, 3–5 minutes. Higher doses (up to 0.2 mg/kg) are not
are acceptable alternatives to bag and mask ventilation recommended and may be harmful.
464 SECTION 16 Critical Care
6. What is the indication for vasopressin 8. What are the indications for calcium administration
in cardiopulmoanry resuscitation? during cardiopulmonary resuscitation?
Vasopressin, also known as antidiuretic hormone, is a potent Routine administration of calcium during CPR is not
vasoconstrictor. The vasoconstrictive effect of vasopressin recommended. Specific indications for calcium therapy
increases blood flow to the brain and heart during CPR. during CPR include hyperkalemia, documented hypocal-
The vasoconstrictive effect is mediated via V1 receptors cemia, and calcium-channel blocker overdose.
and is independent of the adrenergic receptor–mediated
effect of epinephrine. Vasopressin appears to lack the 9. How are ventricular fibrillation and pulseless
$-adrenergic–mediated adverse effects of epinephrine, such
as increased myocardial oxygen demand and tachycardia. ventricular tachycardia managed?
Studies comparing outcomes after cardiac arrest After CPR has been initiated and the underlying rhythm
showed no difference whether vasopressin or epineph- recognized as VF and pulseless VT, immediate defibrilla-
rine was administered. Repeated doses of vasopressin tion is indicated. Depending on whether the defibrillator
during resuscitation did not result in improved survival is monophasic or biphasic, the shock current is set to
rates compared with repeated doses of epinephrine. 360 J or 120–200 J. The 2010 guidelines recommend one
Based on these studies, the current recommendation is shock followed immediately by five cycles (2 minutes) of
that 40 units of vasopressin administered intravenously CPR without checking the rhythm or feeling for a pulse.
or intraosseously may be substituted for the first or sec- After 2 minutes of CPR, the rhythm is checked, and if it
ond dose of epinephrine in all the algorithms. Because is a shockable rhythm, defibrillation is repeated. Either
of the longer half-life of vasopressin (10–20 minutes) epinephrine or vasopressin should be administered at this
compared with epinephrine (3–5 minutes) and lack of time. If during the next rhythm check (after 2 minutes of
supportive evidence in human trials, repeated doses are CPR) pulseless VT and VF still exist, another shock
not recommended at this time. should be delivered. A dose of epinephrine or vasopressin
(depending on what the first drug administered was)
7. What are the indications for sodium should be administered if 3 minutes has elapsed since the
previous dose. If repeated defibrillation, epinephrine and
bicarbonate administration?
vasopressin administration, and appropriately adminis-
Sodium bicarbonate (NaHCO3) previously was used rou- tered CPR are ineffective (i.e., refractory VF or VT),
tinely during CPR, even without knowledge of the acid-base amiodarone should be administered as a 300-mg intrave-
status. Although acidosis inhibits myocardial contractility nous bolus, after the third shock (Table 84-1). This
and catecholamine efficacy, this does not appear clinically can be followed by a second dose of 150 mg intrave-
significant in the range of pH commonly encountered and nously. If hypomagnesemia is suspected or polymorphic
the catecholamine doses administered during resuscitation. VT with long QT syndrome (e.g., torsades de pointes) is
The detrimental effects of NaHCO3 are as follows: present, magnesium sulfate, 1–2 mg intravenously, should
• Hypernatremia leads to hyperosmolarity. Hyperos- be given.
molarity may cause decreased aortic pressures leading
to a reduction in coronary perfusion pressure. 10. What is the management of asystole and pulseless
• Intracellular acidosis develops. As is apparent from the
equilibrium equation, every 50 mEq of bicarbonate electrical activity?
administered produces large amounts of carbon dioxide Asystole, the absence of cardiac electrical activity, and
(CO2) gas that freely diffuses across cellular membranes PEA, cardiac electrical activity without a detectable pulse,
and causes a paradoxical exacerbation of intracellular
acidosis. Intracellular CO2 tensions "300 mm Hg and
pH values !6.1 have been recorded.
[HCO3%] & [H&] I[H2CO3] I [CO2] & [H2O] TABLE 84-1 Therapy for Ventricular Fibrillation
and Pulseless Ventricular
• Extracellular alkalosis shifts the oxyhemoglobin disso- Tachycardia
ciation curve to the left impairing oxygen delivery.
The routine use of NaHCO3 is not recommended. Defibrillation
Special circumstances when NaHCO3 administration is Monophasic 360 J
desirable include preexisting metabolic acidosis, hyper- Biphasic 120–200 J (as recommended by
manufacturer, if known use highest
kalemia, or tricyclic antidepressant overdose. Otherwise, energy level)
NaHCO3 should be administered only based on laboratory
findings of a low bicarbonate concentration or calculated Epinephrine 1 mg 1:10,000 IV every 3–5 minutes
base deficit. Calculation of the base deficit is as follows: Vasopressin 40 units IV (instead of first or second
dose of epinephrine)
Patient’s weight (kg) ' base deficit ' 0.3
Amiodarone 300 mg IV, may be repeated as 150 mg
To minimize the risk of iatrogenic alkalosis, the full calcu-
Magnesium 1–2 g IV (polymorphic VT with long
lated correction dose should not be administered. Most cli- sulfate QT interval, torsades de pointes)
nicians administer half the calculated dose and recheck the
base deficit before any further administration of NaHCO3. IV, Intravenously; VT, ventricular tachycardia.
84 Cardiopulmonary Resuscitation 465
are managed in the same way. Once cardiac arrest is Atropine may be ineffective in the heart transplant patient.
identified, help should be called for, and CPR should If the bradycardia is due to type II second-degree or
immediately be performed until monitoring or a defibril- third-degree heart block, atropine is unlikely to be effec-
lator is attached to the patient. The rhythm should be tive. Transcutaneous pacing or $-adrenergic therapy is
checked, and if asystole or PEA is identified, CPR warranted until transvenous pacing can be established.
should continue for 2 minutes while intravenous access is If atropine is ineffective, transcutaneous pacing, dopa-
established (if not already present), epinephrine 1 mg mine infusion (2–10 (g/kg per minute), or epinephrine
intravenously is administered (repeated every 3–5 minutes infusion (2–10 (g per minute) is indicated (Table 84-2).
during resuscitation), and placement of an advanced airway
with capnography monitoring is considered. Vasopressin, 12. How are supraventricular tachyarrhythmias
40 U intravenously, can be administered once instead of
the first or second dose of epinephrine. If the rhythm
managed?
remains the same after 2 minutes of CPR, reversible Tachycardia is defined as a heart rate "100 beats per min-
causes should be investigated (Box 84-2). Further treat- ute. However, clinically significant tachycardia does not
ment should be customized to the suspected underlying usually occur until the heart rate is "150 beats per minute.
cause. After every 2 minutes of CPR, the rhythm should The most important initial step in the management of
be checked, and further management is determined by the tachyarrhythmias is to evaluate whether the patient is stable
current rhythm identified. For example, if VF is identified or unstable. If the patient is unstable (i.e., presence of hypo-
during a rhythm check, the algorithm for VF manage- tension, signs of shock, acutely altered mental status, acute
ment should be followed (i.e., defibrillation). heart failure, or ischemic chest discomfort), immediate syn-
chronized electrical cardioversion should be performed
(Table 84-3). Wide irregular complexes should be managed
11. How is symptomatic bradycardia managed? the same as pulseless VT and VF with unsynchronized
Bradycardia is defined as a heart rate !60 beats per minute. shocks (i.e., 360 J monophasic, 120–200 J biphasic).
Clinically significant bradycardia is defined as bradycardia If the patient is stable, the next treatment (Table 84-4)
inappropriate for the clinical condition. Most patients do decision is based on the width of the QRS complex. If the
not become symptomatic until the heart rate is !50 beats width of the QRS complex is !0.12 second (narrow com-
per minute. Because the most common cause of bradycar- plex), preferred management consists of vagal maneuvers
dia is hypoxia, the initial management of symptomatic and adenosine (if regular rhythm). Adenosine is given as
bradycardia is directed at evaluation of the respiratory sys- a rapid bolus of 6 mg intravenously that is repeated in
tem. Patency of the airway, signs of increased work of
breathing, and oxygen saturation should be determined.
Supplemental oxygen should be administered if the patient TABLE 84-2 Therapy for Symptomatic
is hypoxic, and electrocardiogram (ECG) monitoring and Bradycardia
intravenous access should be established. Immediate treat-
ment is indicated if further assessment determines the pres- Atropine 0.5 mg IV, every 3–5 minutes,
maximum 3 mg
ence of any of the following: Caution in presence of ACS or MI
• Hypotension May be ineffective in presence
• Altered mental status of heart transplant or type II
• Heart failure second-degree and third-
degree heart block
• Shock
• Angina Transcutaneous pacing
The first-line treatment is atropine, 0.5 mg intrave- Dopamine 2–10 (g/kg/min
nously, repeated every 3–5 minutes to a maximum of
Epinephrine 2–10 (g/min
3 mg. If poor perfusion is present, external pacing should
not be delayed by administration of atropine. Atropine ACS, Acute coronary syndrome; IV, intravenously; MI, myocardial
should be given with caution in the presence of acute infarction.
coronary syndrome or myocardial infarction because
it may exacerbate ischemia or increase infarct size.
TABLE 84-3 Therapy for Unstable
Supraventricular Tachycardia
Synchronized Electrical Cardioversion
BOX 84-2 Treatable Causes (5 H’s and 5 T’s) Narrow complex 50–100 J
of Asystole and Pulseless Electrical
Activity Narrow irregular 200 J monophasic
100–200 J biphasic
Hypovolemia Tension pneumothorax Wide regular 100 J
Hypoxia Tamponade (cardiac)
Hydrogen ion (acidosis) Toxins Unsynchronized Shocks
Hypokalemia or hyperkalemia Thrombosis (coronary) Wide irregular 360 J monophasic
Hypothermia Thrombosis (pulmonary) 120–200 J biphasic
466 SECTION 16 Critical Care
2 minutes as 12 mg intravenously if the rhythm does not When the diagnosis of atrial fibrillation/flutter is con-
convert. Sometimes vagal maneuvers or adenosine may firmed, treatment usually consists of electrical cardiover-
be diagnostic in that the true underlying arrhythmia is sion, $-adrenergic blockers, calcium-channel blockers (e.g.,
revealed when the rate is slowed (e.g., atrial fibrillation, diltiazem), or digoxin. Amiodarone is preferred in unstable
atrial flutter). If these treatments do not convert the patients or patients with impaired ventricular function.
rhythm, the rhythm recurs, or they disclose a different
type of tachyarrhythmia, $-adrenergic blocker or calcium-
channel blocker therapy should be instituted. 13. What are the indications for magnesium therapy?
If the width of the QRS is "0.12 second (wide complex), Magnesium deficiency is associated with ventricular
adenosine should be administered only if the rhythm is ectopy, sudden cardiac death, and congestive heart fail-
regular and the complexes are monomorphic. If adminis- ure. It can also precipitate refractory VF and impede
tered when the rhythm is irregular or the complexes poly- correction of hypokalemia. Hypomagnesemia should be
morphic, adenosine may precipitate VF. Other treatment corrected in cases of refractory VT or VF. Magnesium
options include antiarrhythmic infusions of procainamide, sulfate is the treatment of choice for polymorphic
amiodarone, or sotalol. wide-complex tachycardia associated with congenital
If atrial fibrillation/flutter is suspected as the underlying or acquired long QT syndrome (e.g., torsades de
rhythm, it is imperative to evaluate the patient before fur- pointes). Magnesium supplementation may also reduce
ther management is initiated. If possible, the patient’s car- the incidence of ventricular arrhythmias after myocar-
diac function should be assessed, Wolff-Parkinson-White dial infarction.
syndrome should be ruled out, and the time of onset of
atrial fibrillation should be determined (i.e., !48 hours
or "48 hours). The goals are to treat unstable patients 14. What are the indications for a pacemaker?
urgently to control the rate, convert the rhythm, and pro- Electrical pacing is generally ineffective, and no studies
vide anticoagulation. Patients with an onset of symptoms have observed a survival benefit when pacemakers are
"48 hours should be evaluated for thrombi in the atria used during cardiac arrest. The use of transcutaneous or
using transesophageal echocardiography before electrical transvenous pacemakers in ACLS is indicated in pa-
cardioversion is attempted. tients with symptomatic bradyarrhythmias (i.e., myo-
Wolff-Parkinson-White syndrome is preferably treated cardial ischemia, hypotension, mental status changes,
with electrical cardioversion or amiodarone. Adenosine, pulmonary edema), in patients with high-degree AV
$-adrenergic blockers, calcium-channel blockers, and di- block when intravenous access is unavailable, and for
goxin are contraindicated because they can lead to an overdrive pacing in patients with refractory tachyar-
increased ventricular response or may precipitate VF by rhythmias. It is reasonable to initiate transcutaneous or
selectively blocking the AV node in the presence of coexist- transvenous pacing in unstable patients who are unre-
ing accessory conduction pathways. sponsive to atropine.
84 Cardiopulmonary Resuscitation 467
Do Not Resuscitate
Leila Hosseinian, MD
QUESTIONS
1. Does the American Society of Anesthesiologists 3. What course of action can be taken if the anesthe-
have guidelines for do not resuscitate orders or siologist and the patient or surgeon cannot come
other directives that limit treatment in the operating to an agreement?
room? 4. How long should the agreed on adjustments to do
2. What options regarding resuscitation efforts in not resuscitate status be continued?
the operating room should be discussed with the 5. How would you counsel this patient on her do not
patient or patient’s surrogate before administration resuscitate or intubate status before proceeding
of anesthesia? with surgery?
A 64-year-old woman presented for right hip replace- 2. What options regarding resuscitation efforts
ment. She had a history of myasthenia gravis, unrespon- in the operating room should be discussed
sive to therapy. When healthy, her exercise tolerance was with the patient or the patient’s surrogate
equal to 4 METS; however, exacerbations precipitated by
before administration of anesthesia?
minor illness confined her to bed. She has refused cardio-
pulmonary resuscitation (“do not resuscitate” [DNR]) or Because administration of anesthesia and surgery involve
intubation (“do not intubate” [DNI]) in the event of an procedures and practices that overlap with resuscitation,
emergency. You informed the patient you would like to the anesthesiologist can provide the following alternatives
discuss her DNR/DNI orders, and the patient did not to full dismissal of DNR status:
understand why because the procedure was going to be • Full attempt at resuscitation: Because the period of
done under spinal anesthesia. time under anesthesia and in the immediate postop-
erative period is an alternate state, the patient or
1. Does the American Society of surrogate may request full suspension of existing
Anesthesiologists have guidelines directives during this time. All resuscitative efforts
for do not resuscitate orders or other can then be brought to bear.
directives that limit treatment? • Limited attempt at resuscitation defined with regard to
specific procedures: The patient or surrogate may
The American Society of Anesthesiologists (ASA) last choose to refuse specific resuscitation procedures.
affirmed ethical guidelines for the anesthesia care of The anesthesiologist discusses with the patient or
patients with DNR orders or other directives that limit surrogate the procedures that may need to be per-
treatment in 2008. The ASA guidelines apply to compe- formed, highlighting which procedures are essential
tent patients and incompetent patients who previously for the success of anesthesia and surgery versus the
expressed their preferences. Before the early 1990s, when procedures that are not essential and can be refused.
the guidelines were first written, it was assumed that Procedures that are frequently discussed include
DNR orders were automatically revoked while a patient chest compressions, defibrillation, tracheal intuba-
was in the operating room because anesthesia and sur- tion, administration of resuscitative medications,
gery were deemed to be a temporary altered state. Also, use of supplemental oxygen, placement of central
many procedures and drugs used routinely in the operat- lines, invasive monitoring, and use of bag and mask
ing room can be considered as resuscitative. Guidelines ventilation. The procedure-related DNR approach
recommending automatic suspension violate patients’ requires anticipation of the most likely problems
rights of self-determination in a responsible and ethical that may occur and limits the physician when an
manner. Instead, communication between the physician unexpected situation arises. However, this ap-
and the patient is an essential element of the preoperative proach does make it easier to implement DNR
preparation to determine goals of care. orders successfully when multiple caregivers are
468
85 Do Not Resuscitate 469
involved. There is a concern that when faced with anesthesiologist must proceed with reasonable adherence
limited treatment options, the anesthesiologist may to the patient’s directives.
provide a “light” anesthetic to decrease the likeli-
hood of needing any form of resuscitation, ulti- 4. How long should the agreed on adjustments
mately resulting in inadequate anesthesia. to do not resuscitate status be continued?
• Limited attempt at resuscitation defined with regard to
the patient’s goals and values: The patient or surrogate Reinstitution of the prior DNR/DNI status needs to be
may allow the anesthesiologist to make decisions discussed with patients during the preoperative evalua-
regarding acceptable treatments based on the pa- tion. Some patients prefer to reinstitute full DNR/DNI
tient’s goals and values rather than on individual status on arrival to the postanesthesia care unit; others
procedures. Some patients may find certain treat- agree on extending the limited DNR/DNI status to
ments acceptable if the clinical event is temporary cover the perioperative period.
and quickly reversible but would want treatment
withheld if the condition is or becomes irreversible 5. How would you counsel this patient on her
or would result in permanent damage. Patients are do not resuscitate or intubate status before
often less concerned with the technical details of proceeding with surgery?
resuscitation and more concerned with issues such
as the potential for pain and long-term outcomes of Although the patient is having hip replacement surgery
resuscitation. This approach allows for treatment of under regional anesthesia, it is important to explain to
unexpected cardiac or respiratory events as long as the patient the risk of a high spinal anesthetic. The ability
that treatment complies with the patient’s care goals. to intubate or mask ventilate for a defined period is nec-
However, some anesthesiologists may be uncom- essary for resuscitation, even though this is a rare event.
fortable with the goal-directed DNR approach. Also, hypotension may occur requiring the use of vaso-
They may have legal and ethical concerns regarding pressor medications. The approach to this discussion can
their decisions based on their best judgment during be as follows:
the time of the critical event. This method works • Full resuscitation: The DNR/DNI order is fully
only if the team caring for the patient throughout rescinded during the operative and postanesthesia
the case maintains consistency. There is too great care unit period.
a risk of misinterpretation of patient’s goals if they • Procedure-related: Anesthesia-related procedures that
are passed on from one anesthesiologist to another. overlap with resuscitative efforts should be dis-
Ideally, the individuals taking care of the patient cussed. An explanation of these procedures and their
should have first-hand knowledge of the patient and expected time course is helpful for patients to un-
were involved in the discussion of the patient’s goals. derstand them. A definitive end time needs to be
Most physicians prefer the adaptability and flexibil- established as well. For example, the patient may
ity of this approach, but it does require a high de- agree to intubation in the event of a high spinal but
gree of trust between the patient and physicians, only for the duration of the spinal.
which is not always possible. Documentation of the • Goal-related: The patient’s goals of care need to be
goal-directed DNR approach should include a nar- understood. If the patient rejects machines or drugs
rative that summarizes the discussions that occurred to maintain cardiac function, an agreement may
between the patient and physicians. allow treatment if the condition is considered to be
temporary and due to the surgery. It is important
3. What course of action can be taken if the that all parties involved agree on what is considered
anesthesiologist and the patient or surgeon temporary.
If the patient refuses any alteration in status, the anes-
cannot come to an agreement?
thesiologist either can agree to proceed after explaining
When the anesthesiologist finds the patient’s or surgeon’s the risks to limiting care or can refuse to care for the
limitation of interventions to conflict with his or her patient if another anesthesiologist is available.
moral views, withdrawal from the case is appropriate after
obtaining a replacement to provide care. If the limitation
of interventions is in conflict with generally accepted
SUGGESTED READINGS
standards of care, the anesthesiologist should voice these
concerns to the appropriate hospital committee (e.g., eth- American Society of Anesthesiologists: Ethical guidelines for the anes-
thesia care of patients with do-not-resuscitate orders or other direc-
ics committee). For example, an anesthesiologist can re- tives that limit treatment. 2008. Available from: http://www.asahq.
fuse to comply with a patient declining intubation for an org/for-members/standards-guidelines-and-statements.aspx.
exploratory laparoscopy. (In the United States, it is not Bastron RD: Ethical concerns in anesthetic care for patients with do-not-
common practice to substitute supraglottic devices for resuscitate orders. Anesthesiology 85:1190, 1996.
Truog RD, Waisel DB, Burns JP: NR in the OR: a goal-directed ap-
tracheal intubation during laparoscopy). If surgery is ur- proach. Anesthesiology 90:289, 1999.
gent or emergent and an alternative anesthesiologist is Waisel DB, Truog RD: The end-of-life sequence. Anesthesiology
unavailable in an appropriate time frame, the original 87:676, 1997.
CASE 86
QUESTIONS
A 52-year-old man presented for exploratory laparotomy. American-European Consensus Conference Committee
He complained of fever, severe abdominal pain, and vom- (AECC) as follows:
iting for 3 days. Past medical history was significant for • Acute onset
Crohn’s disease, hypertension, and multiple bowel resec- • Bilateral infiltrates on chest radiograph
tions, the last of which was done 1 week ago. He weighed • Pulmonary capillary wedge pressure (PCWP)
176 pounds (80 kg) and stood 5 feet 9 inches (175 cm) !18 mm Hg or absence of clinical evidence of left
tall. Clinically significant vital signs included heart rate, atrial hypertension
123 beats per minute, blood pressure, 90/65 mm Hg, • Acute lung injury considered to be present if PaO2/
and respiratory rate, 29 breaths per minute. Laboratory FiO2 ratio !300
findings included hematocrit of 46% and white blood cell • Acute respiratory distress considered to be present if
count of 23,000/mm3. Sodium and creatinine were mildly PaO2/FiO2 ratio !200
elevated. Intraoperatively, the patient was hemodynami- There has been some criticism regarding the AECC
cally unstable. Postoperatively, he remained intubated and oxygenation criteria because they do not account for
ventilated in the intensive care unit. Overnight he became variations in the PaO2/FiO2 ratio in response to varying
more difficult to ventilate with elevated peak airway pres- levels of positive end expiratory pressure (PEEP). With
sures and increasing fraction of inspired oxygen (FiO2) the current definition, a patient with a PaO2/FiO2 ratio
requirements. "200 on a PEEP of 12 cm H2O is considered equivalent
to a patient with a similar PaO2/FiO2 ratio on a PEEP of
5 cm H2O. Investigators have advocated that a standard-
1. Define acute respiratory distress syndrome.
ized PEEP/FiO2 assessment is necessary to classify ARDS
Acute respiratory distress syndrome (ARDS) is character- severity accurately. The PaO2/FiO2 ratio has failed to
ized by inflammation of the lung parenchyma leading to predict ARDS outcomes consistently in epidemiologic
impaired gas exchange, hypoxemia, and nonhydrostatic studies. This failing is likely due to ignoring PEEP in
pulmonary edema. The incidence of ARDS in the inten- their evaluation.
sive care unit (ICU) ranges from 4%–9%, with a mortal- In a study from Spain by Cortes et al. (2012), one third
ity rate of approximating 40%–45%. ARDS was first of patients who died with a clinical diagnosis of ARDS
described in 1967 by Ashbaugh et al. in 12 patients, who did not have histologic evidence of diffuse alveolar dam-
had cyanosis refractory to oxygen therapy, decreased age on autopsy. This finding questions the current clini-
lung compliance, and diffuse infiltrates on chest radio- cal criteria used for diagnosis of ARDS. With regard to
graph. By 1994, a new definition was established by the the AECC chest radiograph definition of ARDS, there is
470
86 Acute Respiratory Distress Syndrome 471
some controversy regarding the lack of acknowledgment reduced lung compliance with increased alveolar dead
of the severity or distribution of infiltrates. Furthermore, space and interstitial fibrosis. For most patients who
the distribution of infiltrates seen on chest radiographs survive, pulmonary function returns to normal within
and computed tomography (CT) scans often disagree, 6–12 months. Most deaths are due to sepsis or multior-
questioning the use of chest radiograph rather than CT gan failure and not hypoxia.
scan findings to diagnose ARDS. Finally, the criteria re-
quiring PCWP "18 mm Hg is not easy to assess nonin- 4. Describe the ventilatory strategies for acute
vasively and is flawed by interobserver measurement respiratory distress syndrome.
variability. Some authors have argued for the use of echo-
cardiography; however, it is also dependent on interpre- ARDS is treated with mechanical ventilation to correct
tation and availability. hypoxemia and hypercapnia (Box 86-1). The goals are to
maintain acceptable gas exchange, minimize ventilator-
2. What are the common causes of acute respiratory induced lung injury, and treat underlying causes of illness.
Although mechanical ventilation is the modality keep-
distress syndrome?
ing these patients alive, it can also extend inflammation
ARDS is most often part of a systemic inflammatory in response to cyclic tidal alveolar hyperinflation. Cyclic
process. Sepsis is associated with the highest risk of overdistention produced by excessive transpulmonary
progression to ARDS. Various precipitating events can pressure is a determinant of ventilator-induced lung
either directly or indirectly result in lung injury and
eventually ARDS (Table 86-1).
The inciting cause can be used to predict progression
and prognosis of ARDS. For example, ARDS associated BOX 86-1 National Heart, Lung, and Blood
with trauma has a better prognosis compared with non– Institute Acute Respiratory
trauma-related injury. In terms of disease progression, Distress Syndrome Clinical
pulmonary infections are associated with a higher risk Network Mechanical Ventilation
of ARDS progression compared with nonpulmonary Protocol Summary
infections.
1. Calculate PBW
A. Males # 50 $ 2.3 (height inches % 60)
3. Explain the pathophysiology of acute respiratory B. Females # 45.5 $ 2.3 (height inches % 60)
distress syndrome. 2. Set any ventilatory mode
3. Set ventilator to achieve initial VT # 8 mL/kg PBW
ARDS develops when inflammatory cytokines injure 4. Reduce VT by 1 mL/kg until VT # 6 mL/kg PBW
the epithelium and endothelium of the lungs. In early 5. Adjust VT and RR to achieve
phases, alveolar macrophages release proinflammatory A. pH goal of 7.3–7.45
cytokines such as tumor necrosis factors (TNF) and in- B. Pplat goal !30 cm H2O
terleukin (IL)-1, IL-6, and IL-8. These cytokines attract 6. Maintain PaO2 55–80 mm Hg or oxygen saturation
neutrophils to the lungs, where they release a wide vari- 88%–95% using
ety of substances (e.g., reactive oxygen species, prote- A. Minimum PEEP of 5 cm H2O
B. Minimum FiO2
ases). These substrates injure alveolar epithelium and C. Use incremental increases in PEEP and FiO2 to
endothelium, leading to increased capillary permeability, achieve goals
which is the hallmark of ARDS. This results in leakage of 7. Pplat goal !30 cm H2O
protein-rich edema into the interstitium and air spaces. A. If Pplat &30 cm H2O
Protein-rich edema fluid in the alveolus inactivates sur- i. Decrease VT by 1 mL/kg PBW at a time
factant and creates diffuse alveolar damage. ARDS may (minimum 4 mL/kg PBW)
resolve completely in some patients, after the acute B. If Pplat "25 cm H2O and VT "6 mL/kg PBW
phase. In others, the disease progresses to persistent i. Increase VT by 1 mL/kg PBW until
a. Pplat &25 cm H2O or
b. VT # 6 mL/kg PBW
8. pH goal 7.3–7.45
9. Acidosis management (pH "7.3)
A. pH 7.15–7.3
TABLE 86-1 Causes of Acute Respiratory i. Increase RR until pH &7.3 or PaCO2 "25
Distress Syndrome (maximum RR # 35)
B. pH "7.15
Direct Lung Injury Indirect Lung Injury i. VT may be increased by 1 mL/kg PBW
Common Pneumonia Sepsis increments until pH &7.15
Aspiration Severe trauma a. Pplat may exceed 30 cm H2O
Multiple blood C. May give sodium bicarbonate
transfusions 10. Alkalosis management (pH &7.45)
Less common Inhalational injury Acute pancreatitis A. Decrease RR if possible
Air embolism Drug overdose
Fat embolism Post–cardiopulmonary FiO2, Fraction of inspired oxygen; PBW, predicted body weight; PEEP,
Near drowning bypass positive end expiratory pressure; Pplat, plateau pressure;
RR, respiratory rate; VT, tidal volume.
472 SECTION 16 Critical Care
injury (VILI). Dreyfuss et al. (1988) studied rat lungs improve oxygenation by relieving atelectasis, enhance ven-
to determine whether VILI resulted from a pressure- tilation/perfusion matching, increase end expiratory lung
mediated or lung volume (stretch)–mediated injury. volume, and more uniformly distribute lung stress and
These investigators subjected rats to incremental peak strain with tidal cycling. Although oxygenation in patients
inspiratory pressure, and the tidal volume was with ARDS can be improved with prone positioning, there
restricted in one group using a thoracoabdominal binder is no evidence of decreased mortality. A meta-analysis pool-
to limit chest wall excursion. High tidal volume ventila- ing patient populations with the most severe ARDS sug-
tion, independent of airway pressure, produced severe gested that prone positioning should be considered as a
lung injury, otherwise known as volutrauma. The inves- rescue regimen for patients with intractable hypoxemia.
tigators also found PEEP to be protective, preventing The potential risks of prone positioning are primarily
pulmonary epithelial damage and alveolar edema. related to physical injury and tube dislodgment during
The ARDS Clinical Network (ARDSnet) completed a turning maneuvers.
landmark trial in 2000 with 861 patients with ARDS
(Acute Respiratory Distress Syndrome Network, 2000). 7. Can recruitment maneuvers improve oxygenation
Improved mortality was seen when a tidal volume of in patients with acute respiratory distress
6 mL/kg based on predicted body weight (PBW) was syndrome?
used compared with the traditional value of 12 mL/kg
based on PBW. The group with tidal volume 6 mL/kg Recruitment maneuvers are transient increases in trans-
was restricted to a plateau pressure !30 cm H2O, and pulmonary pressure intended to promote reopening of
the group with tidal volume 12 mL/kg was restricted collapsed alveoli. The maneuver is accomplished by in-
to a much higher plateau pressure of !50 cm H2O creasing continuous positive airway pressure to 35–50 cm
(Table 86-2). The low tidal volume group was found to H2O for 30 seconds. Several studies have shown improved
have reduced levels of inflammatory mediators, which gas exchange and decreased hypoxia after recruitment
reflect less severe lung injury. maneuvers; however, there are no randomized controlled
No particular ventilator mode has improved ARDS trials to show benefit on ARDS mortality. In addition,
mortality. The ARDSnet trial used volume control mode, patients can become hypotensive with recruitment maneu-
and PEEP was used to improve oxygenation. There are vers because they decrease cardiac preload.
three types of alveoli in ARDS:
• Normal—always inflated and participating in gas 8. Is extracorporeal membrane oxygenation an
exchange evidence-based treatment for acute respiratory
• Flooded—unable to participate in gas exchange distress syndrome?
• Atelectatic or partially flooded—with the right
amount of PEEP can be recruited to participate in Extracorporeal membrane oxygenation (ECMO) was first
gas exchange applied to patients with ARDS in 1972. ECMO is the
The goal of “lung protective” ventilation (i.e., reduced optimal method for oxygenating blood while maintaining
tidal volumes) is to avoid excessive pulmonary stress and total lung protection. However, the risks of ECMO (bleed-
strain; higher PEEP prevents regional excessive stress ing from anticoagulation and infection from intravascular
and strain by avoiding alveolar collapse and reopening catheters) mitigate its potential benefit. At this point,
during mechanical ventilation. However, the optimal ECMO should be applied only in experienced institutions
level of PEEP remains unclear. Several randomized and should be reserved for patients for whom safe
controlled trials comparing higher versus lower levels mechanical ventilation is impossible.
of PEEP in patients with ARDS showed improved
oxygenation with higher levels of PEEP without signifi- 9. Is high-frequency jet ventilation an effective
cant differences in mortality rates. ventilation mode for patients with acute
respiratory distress syndrome?
5. What role does permissive hypercapnia have in
High-frequency jet ventilation (HFJV) is a mode of
current lung protective strategies?
mechanical ventilation that uses rapid respiratory rates
Reduced tidal volume avoids stretch-induced lung injury (100–200 breaths per minute) and small tidal volumes
and provides lung protective ventilation; however, it gener- (2–5 mL/kg). Although tidal volumes are often smaller
ally leads to elevations in PaCO2. This increase has been an than traditional estimates of both anatomic and physi-
accepted approach termed “permissive hypercapnia.” ologic dead space, adequate oxygenation and ventilation
There is some evidence that hypercapnic acidosis may con- can be achieved. HFJV administers oxygen under high
tribute to the benefits seen with protective lung ventilation. pressure through a small-bore aperture into an endotra-
However, it can be detrimental in patients with elevations cheal tube. Valves control the intermittent delivery of
in intracranial pressure or pulmonary vascular resistance. gas jets. Smaller tidal volumes help avoid injury from
excessive end inspiratory lung volumes. The disadvan-
6. Can prone positioning help improve oxygenation in tages include hypercapnia with respiratory acidosis and
associated circulatory depression, auto-PEEP, increased
patients with acute respiratory distress syndrome?
cerebral blood flow, elevated intracranial pressures, and
The distribution of pulmonary infiltrates is not uniform in enhanced requirements for sedation and neuromuscular
ARDS. Consequently, positioning a patient prone could blockade. A mortality benefit from HFJV has not been
86 Acute Respiratory Distress Syndrome 473
shown; however, oxygenation can be improved within and lower plateau pressures and PEEP versus the liberal
the first 24 hours of therapy. fluid management group (average net gain of almost 7 L
over the first 7 days). There was no difference in the de-
velopment of shock or the need for renal replacement
10. Do inhaled nitric oxide and other vasodilators
therapy between the two groups. However, mortality
improve ventilation/perfusion mismatch? rates were not significantly different between the two
Nitric oxide is a potent vasodilator that is delivered to the groups.
pulmonary vasculature by inhalation, without causing sys-
temic vasodilation. It has been shown to protect type II
pneumocytes from stretch injury and may be protective of SUGGESTED READINGS
endothelial tissue by decreasing platelet and leukocyte Acute Respiratory Distress Syndrome Network: Ventilation with lower
adhesion to endothelium. Inhaled nitric oxide (iNO) also tidal volumes as compared with traditional tidal volumes for acute
vasodilates the microcirculation, which allows for increased lung injury and the acute respiratory distress syndrome. N Engl J
Med 342:1301, 2000.
perfusion of tissue beds and improved ventilation/perfusion Artigas A, Bernard GR, Carlet J, et al.: The American- European con-
matching, resulting in better oxygenation. More recent tri- sensus conference on ARDS, Part 2. Am J Respir Crit Care Med
als have shown no effect on either mortality or the duration 157:1332, 1998.
of mechanical ventilation when using iNO for patients with Bernard GR, Artigas A, Brigham KL, et al.: The American- European
consensus conference on ARDS. Definitions, mechanisms, relevant
ARDS. It may be useful as a rescue therapy in patients with outcomes, and clinical trial coordination. Am J Respir Crit Care Med
refractory hypoxia, but the benefit of improved oxygen- 149:818, 1994.
ation is temporary. Treatment with less selective vasodila- Brower RG, Lanken PN, MacIntyre N, et al.: Higher vs lower positive
tors (sodium nitroprusside, epoprostenol, and alprostadil) end-expiratory pressures in patients with the acute respiratory distress
has also not been proven to be beneficial. syndrome. N Engl J Med 351:327, 2004.
Cortes I, Penuelas O, Esteban A: Acute respiratory distress syndrome:
evaluation and management. Minerva Anestesiol 78:343, 2012.
11. Can the antiinflammatory property of steroids Donahoe M: Acute respiratory distress syndrome: a clinical review.
Pulm Circ 1:192, 2011.
inhibit progression of inflammation contributing Dreyfuss D, Soler P, Basset G, et al.: High inflation pressure pulmonary
to acute respiratory distress syndrome? edema: respective effects of high airway pressure, high tidal volume,
and positive end-expiratory pressure. Am Rev Respir Dis 137:1159,
Patients with ARDS have persistent elevations in plasma 1988.
levels of inflammatory cytokines (TNF-', IL-1(, and Gurka DP, Balk RA: Acute respiratory failure. p. 773. In Parrillo JE,
IL-6). Theoretically, suppression of these substances Dellinger RP (eds.): Critical care medicine: Principles of diagnosis
could reverse the inflammatory component of ARDS. and management in the adult, 3rd edition. Mosby, Philadelphia,
2008.
In a more recent study, although treatment with meth- Krishnan JA, Brower RG: High-frequency ventilation for acute lung
ylprednisolone increased the number of ventilator-free injury and ARDS. Chest 118:795, 2000.
days, shock-free days, and ICU-free days, it did not Laffey JG, O’Croinin D, McLoughlin P, et al.: Permissive hypercapnia—
change the mortality rate from ARDS. role in protective lung ventilatory strategies. Intensive Care Med
30:347, 2004.
National Heart, Lung, and Blood Institute Acute Respiratory Distress
12. Does fluid restriction help lung function? Syndrome (ARDS) Clinical Trials Network: Pulmonary-artery
versus central venous catheter to guide treatment of acute lung
One consequence of ARDS is increased pulmonary capil- injury. N Engl J Med 354:2213, 2006.
lary permeability resulting in pulmonary edema. The Pierrakos C, Karanikolas M, Scolletta S, et al.: Acute respiratory distress
syndrome: pathophysiology and therapeutic options. J Clin Med Res
Fluid and Catheter Therapy Trial (FACTT), published 4:7, 2012.
in the New England Journal of Medicine in 2006, evaluated Tsushima K, King L, Aggarwal NR, et al.: Acute lung injury review.
whether fluid restriction would improve outcomes in Intern Med 48:621, 2009.
patients with acute lung injury. The conservative fluid Ware LB, Matthay M: The acute respiratory distress syndrome. N Engl
J Med 342:1334, 2000.
strategy group (average loss of 136 mL over 7 days) Wiedermann HP, Wheeler AP, Bernard GR, et al.: Comparison of two
showed better lung injury scores, oxygenation indices, fluid-management strategies in acute lung injury. N Engl J Med
increased number of ventilator-free and ICU-free days, 354:2564, 2006.
CASE 87
Respiratory Failure
Andrew B. Leibowitz, MD
QUESTIONS
1. What is postoperative respiratory failure? 6. How would you treat this patient?
2. Describe the two main types of acute respiratory 7. What are the most common ventilatory modes?
failure. 8. How does pulmonary embolism manifest, and how
3. What are the indications for tracheal intubation in is it diagnosed and treated?
a patient with dyspnea? 9. What criteria are used to determine if extubation
4. When should noninvasive ventilation be considered, should be performed?
and how is it prescribed?
5. What are the four primary causes of hypoxemia,
how are they distinguished, and which is most
likely in this patient?
A 59-year-old woman with carcinoma underwent a left excessive carbon dioxide (CO2) production (e.g., malignant
hemicolectomy. She had a history of chronic obstructive hyperthermia, thyroid storm). Ineffective minute ventila-
pulmonary disease (COPD) secondary to long-standing tion has three main clinical causes, as follows:
tobacco use and type 2 diabetes mellitus. Surgery was com- • Decreased respiratory rate (e.g., secondary to opioids,
plicated by aspiration after extubation and reintubation. brainstem lesions)
Arterial blood gas (ABG) values are pH 7.35, carbon diox- • Decreased tidal volume (e.g., residual neuromuscu-
ide tension (PaCO2) 37 mm Hg, and oxygen tension lar blockade, myasthenia gravis, splinting)
(PaO2) 54 mm Hg on controlled mechanical ventilation • Increased physiologic dead space (e.g., COPD, later
(CMV) with a rate of 12 breaths per minute, tidal volume stages of acute respiratory distress syndrome [ARDS],
of 650 mL, fraction of inspired oxygen (FiO2) of 0.5, and shock)
positive end expiratory pressure (PEEP) of 5 cm H2O. Hypercapnia can also result in hypoxemia, as is discussed
Peak inspiratory pressures are 26 cm H2O. After several in Question 5.
days in the intensive care unit (ICU), the patient’s respira-
tory status improved. 3. What are the indications for tracheal intubation
in a patient with dyspnea?
1. What is postoperative respiratory failure?
Clinical indications include patient fatigue, accessory
Postoperative respiratory failure is the postoperative muscle use, paradoxical breathing pattern, and inability
need for continued mechanical ventilation or the need to protect the airway. PaO2 !60 mm Hg (i.e., oxygen
for reintubation and mechanical ventilation after extuba- saturation "90%), FiO2 #0.5, and increasing PaCO2
tion in the early postoperative period (i.e., 24–48 hours). (e.g., 10 mm Hg above baseline or #50 mm Hg) are
ABG abnormalities that alone, and especially in combina-
2. Describe the two main types of acute respiratory tion with any of the clinical indications, support the need
to intubate and initiate mechanical ventilation.
failure.
The two main types of acute respiratory failure are as 4. When should noninvasive ventilation be
follows: considered, and how is it prescribed?
• Type I—hypoxemic
• Type II—hypercapnic Noninvasive ventilation may be effective in place of tra-
Occasionally both types may coexist. cheal intubation when respiratory distress is expected to
Hypoxemic acute respiratory failure is discussed in de- be short-lived (e.g., ideally "24 hours), and the patient
tail in Question 5. Hypercapnic acute respiratory failure can cooperate with the requisite mask fitting and protect
occurs when a patient develops acute respiratory acidosis, the airway. Mild to moderate pulmonary edema respond-
usually with a PaCO2 $50 mmHg. It is caused by either ing to medical therapy, COPD exacerbation, and perhaps
ineffective minute ventilation or, much less commonly, splinting are reasonable postoperative conditions for
474
87 Respiratory Failure 475
consideration of noninvasive ventilatory support. Generally, feature of significant shunting is the failure of PaO2 to
noninvasive ventilation is set with inspiratory pressure increase in response to increasing FiO2. The degree of
support (PS) and continuous positive airway pressure shunting is calculated by the shunt equation, as follows:
(CPAP), which together are termed BPAP (bilevel
positive airway pressure). A common initial setting is QS (CcO2 " CaO2 )
10 cm H2O/5 cm H2O (PS/CPAP) adjusted by appear- !
QT CcO2 " CvO2 )
ance, respiratory rate, oxygen saturation by pulse oxime-
try (SpO2), and measured PaCO2. The success rate for
avoidance of eventual tracheal intubation is highly depen- where Q̇S and Q̇T refer to the shunt and total pulmonary
dent on respiratory care team effort and patient selection. blood flows, and CcO2, CaO2, and Cv–O2 refer to the
Extreme care must be taken to avoid the unobserved need oxygen content of pulmonary end-capillary, arterial, and
to progress to tracheal intubation. mixed venous blood.
Arterial oxygen content is calculated as follows:
5. What are the four primary causes of hypoxemia,
how are they distinguished, and which is most CaO2 ! ( Hgb "1.34 " SaO2 ) # 0.003 " PaO2
likely in this patient?
where Hgb is the hemoglobin concentration in g/dL,
The four primary causes of hypoxemia are hypoventilation SaO2 is the arterial oxygen saturation of Hgb, and PaO2
˙ /Q)
(i.e., hypercapnia), shunt, ventilation/perfusion ( V ˙ is the arterial oxygen tension. Hemoglobin concentration
mismatch, and diffusion impairment. Low FiO2 and low and SaO2 are the main determinants of blood oxygen
barometric pressure can cause hypoxemia but do not content, with PaO2 playing a comparatively small role
warrant consideration in this context. except in special situations such as severe anemia or
Hypoventilation is a reduction in gas flow to the hyperbaric oxygen therapy.
alveoli. This reduction occurs whenever there is ineffec- Ventilation/perfusion (V ˙ /Q)
˙ mismatch is the most
tive minute ventilation (see Question 2). The hallmark common cause of hypoxemia and the hardest to under-
feature is an increased PaCO2. Two basic equations relate stand. In this condition, there is inefficient and incom-
to this condition. plete transfer of gas from the alveoli to the capillary
The first equation demonstrates the relationship be- because of mismatching of blood flow and ventilation.
tween PaCO2 and alveolar ventilation: Mismatching varies in different areas of the lungs at any
point in time. Elements of shunt and hypoventilation
VCO2 may exist. Hypercapnia is not prominent unless mis-
PaCO2 ! "K
VA matching is severe. Essentially, when hypoventilation,
shunt, and diffusion impairment (see later) are excluded
where V̇CO2 is the CO2 produced, VA is the alveolar as primary causes of an increased alveolar to arterial (A-a)
ventilation, and K is a constant equal to 0.863. This gradient, V ˙ /Q
˙ mismatch is the cause.
equation demonstrates that if the alveolar ventilation is Diffusion impairment is the result of incomplete equi-
halved, PaCO2 doubles, and vice versa. librium between alveolar gas and capillary blood because
The second equation is the alveolar gas equation: of an abnormality in the thin-walled and easily crossed
alveolar-capillary barrier. This condition may occur in a
(
PA O2 ! FiO2 Patm " PH2O " ) PaCO2
RQ
variety of chronic lung diseases such as interstitial fibro-
sis, asbestosis, and sarcoidosis but is not commonly seen
in acute respiratory failure. Although diffusion capacity
where PAO2 is the alveolar partial pressure of oxygen, Patm may be measured in a pulmonary function laboratory us-
is the atmospheric pressure (760 mm Hg at sea level), PH2O ing carbon monoxide, bedside quantification of diffusion-
is the saturated pressure of water at 37° C (47), and RQ is limited hypoxemia using standard laboratory tests is
the respiratory quotient (approximately 0.8). This equation impossible.
predicts that although hypoventilation causes a decrease In this patient, the A-a gradient is 256, whereas the
in PAO2, this may be overcome by administration of PaO2/FiO2 ratio is 108 (diagnostic for ARDS). V ˙ /Q
˙ mis-
an increased FiO2. Postoperative patients with respiratory match and shunt are the most likely pathophysiologic
depression receiving supplemental oxygen may have a explanations and are commonly seen in ARDS. PaCO2 is
delayed diagnosis of hypoventilation (e.g., SpO2 $90% normal, which excludes hypoventilation, and diffusion
and PaCO2 $60 mm Hg). For this patient, the PAO2 abnormality is uncommon in acute situations. Significant
calculates to 310 mm Hg. shunt can be excluded if an increase in FiO2 is associated
Shunt occurs when blood passes from the venous cir- with a commensurate increase in PaO2.
culation to the arterial circulation without exposure to
ventilated alveoli. Ventricular septal defects and extrapul-
6. How would you treat this patient?
monary shunts sometimes allow significant amounts of
venous blood to pass to the arterial side without oxygenat- The first measure should focus on improving the A-a gra-
ing. Such physiology creates large right-to-left shunts. dient. Manual recruitment maneuvers help to minimize
This is the most glaring example of a shunt, but less obvi- atelectasis and open up new lung units. These maneuvers
ous intrapulmonary shunting, involving the vasculature of require the administration of several supraphysiologic tidal
the lung, is common in respiratory diseases. The primary volumes (e.g., $20 mL/kg). Increasing PEEP increases
476 SECTION 16 Critical Care
the functional residual capacity and allows a greater por- be detected by the generation of either negative
tion of ventilation to occur in opened alveoli during each pressure (AC mode) or inspiratory flow (PS mode).
breath. Incrementally increasing PEEP to 15 cm H2O “Breath goal” refers to the set desired breath; gener-
may be required. ally, this is either a volume or a pressure delivered by the
Maintenance of PaO2 $60 mm Hg with FiO2 !0.6 is a ventilator. In the case of SIMV, the patient-generated
short-term goal because hypoxemia can be injurious, and breaths are entirely determined by patient effort. Type of
FiO2 $0.6 may cause oxygen toxicity and result in ARDS. breath delivered is ventilator setting derived (CMV, AC,
FiO2 of 1.0 is almost always toxic within 24–48 hours, so PC modes), entirely patient derived (intermittent breaths
reduction of FiO2 toward 0.6 is a good short-term (i.e., in taken in SIMV mode), or patient assisted (PS mode).
"12–24 hours) goal. When shunt is a significant issue, CMV is used only in the operating room setting. The
reduction in high FiO2 levels frequently results in little respiratory rate and tidal volume are set, and the patient
change in PaO2, so frequent ventilatory changes with cannot take any spontaneous breaths. It is an appropriate
vigilant SpO2 and ABG monitoring are necessary. mode only under general anesthesia.
Shortly after achieving adequate oxygenation, a low tidal AC ventilation allows a patient to receive a preset
volume strategy as outlined in the ARDS Network investi- number of ventilator breaths per minute and detects
gation (i.e., 6 mL/kg of lean body weight with peak inflation additional inspiratory efforts by the patient and delivers
pressure "30 cm H2O) should be instituted. Another a ventilator breath with the same set tidal volume. PC
ARDS-specific treatment is maintenance of a relatively ventilation delivers breaths determined by pressure, not
“dry” state versus liberal fluid administration. Other general volume. It is a mode used almost exclusively by intensiv-
intensive care unit (ICU) measures include gastrointestinal ists in the management of ARDS but can be helpful
bleeding prophylaxis, deep vein thrombosis prevention, whenever lung compliance is grossly abnormal (e.g.,
early enteral feeding, and daily sedation breaks. obese patients undergoing laparoscopic surgery). Im-
proved oxygenation and ventilation occur in this mode
because the pressure-time curve characteristics of each
7. What are the most common ventilatory modes?
breath are associated with better alveolar ventilation.
A complete overview of mechanical ventilation is beyond Tidal volume is completely determined by the pressure
the scope of this chapter. The most commonly used ven- set and lung compliance, so extra vigilance needs to be
tilatory modes are outlined in Table 87-1. maintained by observing the delivered tidal volume,
Generally, mechanical ventilation is required to assist SpO2, and either end-tidal CO2 or PaCO2.
a patient who is: SIMV combines ventilator breaths at a set rate syn-
• Unable to contribute any respiratory effort (e.g., chronized not to interfere with spontaneous breaths that
CMV, assist controlled [AC], and pressure controlled the patient takes.
[PC] mode) PS ventilation is used to assist spontaneous breaths.
• Able to contribute only some effort (e.g., synchro- The ventilator detects an inspiratory effort by the patient
nized intermittent mechanical ventilation [SIMV] and maintains a preset pressure until the inspiratory
and SIMV/PS mode) flow decreases, usually to 25% of the peak flow. A PS of
• Able to contribute significant effort (e.g., PS mode) 5–10 cm H2O should be equivalent to breathing sponta-
“Trigger” refers to the event that initiates a breath. neously without a tracheal tube and associated ventilator
The trigger can be either of the following: hoses and valves because it compensates for the resistance
• Time—the set respiratory rate determines when a contributed by these items. A higher PS provides addi-
breath will be delivered This is the most common tional support.
intraoperative method. If the rate is set at 12 breaths Combinations of these modes are also frequently used,
per minute, a breath is delivered every 5 seconds. especially SIMV with PS in which the patient-generated
• Patient—the ventilator detects an inspiratory effort breaths given between the ventilator-generated breaths
generated by the patient. The inspiratory effort can are supported with a PS mode. This combination may be
AC, Assist controlled; CMV, controlled mechanical ventilation; PC, pressure controlled; PS, pressure support; SIMV, synchronized intermittent
mandatory ventilation.
87 Respiratory Failure 477
more comfortable for a patient transitioning from a fully or surgical interventions, especially if transportation
supported mode (AC or PC) to a minimally supported out of the ICU will be required shortly after the
mode (PS alone) than SIMV alone. Newer ventilators planned extubation.
provide AC modes with the ability to regulate pressure Respiratory-specific criteria are as follows:
over the course of the respiratory cycle (i.e., pressure regu- 1. Patients should maintain SpO2 $90% on FiO2
lated volume control), which provides some of the same !0.4 and a minute ventilation requirement "10 L
benefits of PC ventilation but without the need for deep per minute while on mechanical ventilation.
sedation or paralysis. 2. Patients should undergo a spontaneous breathing
trial for at least 30–60 minutes during which they are
8. How does pulmonary embolism manifest, and how placed on a PS of 5–10 cm H2O or on a T-piece.
A grossly successful trial is judged by absence of
is it diagnosed and treated?
tachycardia, bradycardia, hypertension, hypotension,
Pulmonary embolism usually manifest as an acute decrease distress (e.g., respiratory, agitation), diaphoresis, ac-
in PaO2 without infiltrate on radiograph. Common alter- cessory muscle use, paradoxical breathing, and SpO2
native causes for an acute decrease in PaO2 are asthma !90%. More specifically, a rapid shallow breathing
(even in the absence of wheezing) that is also associated index (RSBI) should be calculated, as follows:
with no infiltrate on radiograph, and pneumonia, usually
associated with a new infiltrate on radiograph. In pulmo- respiratory rate per minute
RSBI %
nary embolus, the patient usually is tachycardic. The tidal volume in liters
patient usually is tachycardic and dyspneic and might
develop a new supraventricular arrhythmia. Presentation A value "100 is predictive of success.
in critically ill ventilated patients is variable, and the diag- An ABG is not required at the end of the spontaneous
nosis is usually made by computed tomography angiogram, breathing trial, but it may be helpful, especially in
although lower extremity duplex, ventilation/perfusion borderline patients whose appearance and RSBI are not
scanning, and occasionally pulmonary angiogram may completely reassuring. Also, despite best efforts and
be performed. Treatment consists of anticoagulation. In adherence to these guidelines, approximately 10% of
this setting, intravenous heparinization, guided by partial patients in ICUs require reintubation !24 hours after
thromboplastin time monitoring, or subcutaneous low- extubation.
molecular-weight heparin may be administered. In patients
whose risk of bleeding from anticoagulation is high, infe-
rior vena cava filter placement should be considered.
SUGGESTED READINGS
9. What criteria are used to determine if extubation Acute Respiratory Distress Syndrome Network: Ventilation with lower
tidal volumes as compared with traditional tidal volumes for acute
should be performed? lung injury and the acute respiratory distress syndrome. N Engl J
Med 342:1301, 2000.
Several extubation criteria need to be met. They are best Chao DC, Scheinhorn DJ: Determining the best threshold of rapid
grouped into two categories, general and respiratory- shallow breathing index in a therapist-implemented patient-specific
specific. weaning protocol. Respir Care 52:159, 2007.
General criteria are as follows: National Heart, Lung, and Blood Institute Acute Respiratory Distress
Syndrome (ARDS) Clinical Trials Network, Wiedemann HP, Wheeler
1. Patients should be awake, alert, and cooperative AP, Bernard GR, et al.: Comparison of two fluid-management strate-
with the ability to protect the airway. gies in acute lung injury. N Engl J Med 354:2564, 2006.
2. Patients should be hemodynamically stable with Organized Jointly by the American Thoracic Society, the European Re-
minimal or no vasopressor requirement. spiratory Society, the European Society of Intensive Care Medicine,
3. Patients should not have a high fever or gross and the Société de Réanimation de Langue Française, and approved by
the ATS Board of Directors. December 2000 ATS Board of Directors
manifestations of sepsis (e.g., rigors). International Consensus Conferences in Intensive Care Medicine:
4. Patients should not require tests (e.g., computed noninvasive positive pressure ventilation in acute respiratory failure.
tomography scan or magnetic resonance imaging) Am J Respir Crit Care Med 163:283, 2001.
CASE 88
Cardiovascular System
Paula Trigo, MD • Gregory W. Fischer, MD
QUESTIONS
1. What are the etiology and pathophysiology of right 4. Explain the treatment strategies for right ventricular
ventricular failure? failure.
2. What is the impact of chronic pulmonary 5. What intraoperative monitoring is recommended
arterial hypertension on right ventricular for patients with right ventricular failure?
function? 6. What is the prognosis of patients with right
3. How is right ventricular failure diagnosed? ventricular failure?
A 74-year-old woman was admitted for elective mitral values progressively increased reaching a maximum of
valve repair. Her past medical history was significant 8 mmol/L. TEE performed on the morning of postopera-
for hypertension, diabetes, and hyperlipidemia. After an tive day 1 showed a severely depressed right ventricle and
uneventful induction of general anesthesia, a pulmonary severe tricuspid regurgitation. Left ventricular ejection
artery catheter (PAC) was placed via the right internal fraction was 50%.
jugular vein. Her baseline pulmonary artery pressures The decision was made to return to the operating
were elevated (45/20 mm Hg). All other clinical and room for emergent implantation of a right ventricular
laboratory parameters were within normal limits. A assist device (RVAD) (Thoratec Centrimag; Thoratec,
transesophageal echocardiogram (TEE) obtained before Pleasanton, CA). The procedure was uneventful, and the
cardiopulmonary bypass showed prolapse of the poste- patient returned to the CTICU for further management.
rior mitral valve leaflet (P2 segment) with severe mitral Over the course of the next 12 hours, the patient showed
regurgitation and a dilated left ventricle with normal a dramatic improvement in hemodynamic status. The
ejection fraction. The right ventricle was mildly dilated signs of early multiorgan failure (i.e., low urine output,
and showed mild impairment of function. There was elevated transaminases) were reversed. Over the course
mild tricuspid regurgitation. of the next few days, the RVAD could be progressively
After successful surgical repair of the mitral valve, the weaned, and the patient was taken back to the operating
patient was weaned off cardiopulmonary bypass on moder- room on postoperative day 7 for RVAD explantation,
ate inotropic support (epinephrine 0.1 !g/kg per minute). which proceeded without difficulty. Her trachea was
The left ventricular ejection fraction was 40%. There was extubated 3 days after RVAD explantation, and she was
now moderate right ventricular (RV) dysfunction accom- subsequently weaned off all vasoactive support. The
panied by moderate tricuspid regurgitation (Figure 88-1). patient was discharged home on postoperative day 37.
The pulmonary artery pressures remained elevated
(50/22 mm Hg), and central venous pressure was within 1. What are the etiology and pathophysiology of right
normal limits (10–12 mm Hg). Cardiac index was
2.0 L/min/m2, and mixed venous saturation was 72%. The ventricular failure?
patient was transferred to the cardiothoracic intensive RV failure results from any structural or functional
care unit (CTICU) for further postoperative management. disorder that makes the right ventricle unable to eject
The patient was initially stable in the CTICU with blood into the pulmonary circulation. The most com-
good hemodynamic function. The epinephrine infusion mon etiologies of RV failure are listed in Table 88-1.
was progressively weaned. However, during the first post- RV failure is also a prominent feature of various forms
operative night, she received large amounts of intravenous of congenital heart disease, such as tetralogy of Fallot,
fluids in an attempt to improve borderline systemic blood transposition of the great arteries, Ebstein anomaly,
pressure. As a result, the patient’s central venous pressure and Eisenmenger syndrome. Acute RV failure can also
increased from 10 mm Hg to 20 mm Hg, without be seen in patients with sickle cell disease during acute
improvement in systemic blood pressure (85/45 mm Hg). chest syndrome.
Despite increasing vasoactive support, the clinical status The pathophysiology of RV failure is complex. It de-
continued to deteriorate, showing signs of progressive velops from functional impairment of the underlying
low cardiac output and beginning multiorgan failure. The free wall and interventricular septum. Myocyte fiber
patient’s cardiac index and mixed venous oxygen saturation orientation is the key to RV performance. The septum is
declined to 1.5 L/min/m2 and 45%, respectively. Lactate composed of oblique and transverse fibers. This specific
478
88 Cardiovascular System 479
FIGURE 88-1 ■ Moderate tricuspid regurgitation. 2. What is the impact of chronic pulmonary arterial
hypertension on right ventricular function?
In chronic PAH, the right ventricle adapts to increased
afterload with concentric hypertrophy and flattening of the
interventricular septum; this decreases compliance of the
TABLE 88-1 Etiologies of Right Ventricular left ventricle leading to diastolic dysfunction. Consequently,
Failure diastolic dysfunction is commonly seen in patients with
chronic PAH. Plasma levels of brain natriuretic peptide
Left ventricular failure
and troponin T correlate well with pulmonary vascular
Right ventricular ischemia resistance (PVR), and increases in these parameters are
Intrinsic myocardial disease associated with increased mortality in patients who have
idiopathic PAH.
Pressure overload
Pulmonary valve stenosis
If PAH remains untreated, and the right ventricle
Chronic pulmonary hypertension from any cause continues to eject blood into a high pulmonary pressure
system, the hypertrophied right ventricle deteriorates to
Acute pulmonary hypertension
Severe left ventricular dysfunction
dilation and ultimately failure, with a decrease in cardiac
Protamine reaction output and end-organ perfusion. This reduced perfusion,
Hypoxemia along with increased myocardial oxygen demand, can
Acidosis result in RV ischemia even in the absence of significant
Tension pneumothorax coronary atherosclerotic disease.
Acute pulmonary embolism
Transfusion-related acute lung injury
Sepsis 3. How is right ventricular failure diagnosed?
Cardiac tamponade The clinical presentation of RV failure is fluid reten-
Post–cardiothoracic surgery states tion (i.e., peripheral edema, ascites, and anasarca), low
Inadequate myocardial protection cardiac output that may lead to exercise intolerance or
Myocardial stunning fatigue, and arrhythmias. Cardiac magnetic resonance
Coronary air embolism imaging (MRI) is a useful tool to assess RV structure
and function. Some studies show that MRI is the most
accurate method of measuring right ventricular ejec-
tion fraction (RVEF). Radionuclide-based techniques
provide independent assessments of RV function. Car-
orientation of fibers is essential for ventricular function diac catheterization can measure hemodynamic data
and determines the ejection fraction. The concept of the and accurately assess PVR. Another test to provide
septum as the “biventricular motor” is useful to under- anatomic and functional characteristics is pulmonary
stand the interdependence of both ventricles. The cen- angiography.
tral role of the septum in RV function provides the basis The most reliable, versatile, and available method to
of treatment for RV infarction and RV dysfunction after assess RV structure and performance is echocardiog-
cardiac surgery. raphy. In two-dimensional echocardiography, RVEF can
In the case presented, the etiology of RV failure is be measured with Simpson’s rule and the area-length
multifactorial. On the one hand, the patient had pulmo- method. RV fractional area change is measured in the
nary arterial hypertension (PAH) preoperatively. This four-chamber view. In end-stage pulmonary disease,
chronic increase in afterload leads to increased wall RVEF and RV fractional area change are well correlated.
tension, which produces increased metabolic demand. Tricuspid annular plane systolic excursion is another
Consequently, the ischemic state of the heart during quantitative assessment of RV function, and it is usually
480 SECTION 16 Critical Care
BSA, Body surface area; CI, cardiac index; CO, cardiac output; CVP, central venous pressure;
LVSWI, left ventricular stroke work index; MAP, mean arterial pressure; MPAP, mean pulmonary
arterial pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance;
PVRI, pulmonary vascular resistance index; RVSWI, right ventricular stroke work index; SI, stroke
index; SV, stroke volume; SVR, systemic vascular resistance; SVRI, systemic vascular resistance
index.
6. What is the prognosis of patients with right Haddad F, Doyle R, Murphy DJ, et al.: Right ventricular function in
ventricular failure? cardiovascular disease, part II: pathophysiology, clinical importance,
and management of right ventricular failure. Circulation 117:
RV failure is associated with increased morbidity and 1717, 2008.
mortality. There are select markers of RV failure associ- Haddad F, Hunt SA, Rosenthal DN, et al.: Right ventricular function in
cardiovascular disease, part I: anatomy, physiology, aging, and functional
ated with prognosis, such as hemodynamics (e.g., right assessment of the right ventricle. Circulation 117:1436, 2008.
atrial pressure, cardiac index), systolic performance indices Harvey S, Harrison DA, Singer M, et al.: PAC-Man study collabora-
(e.g., RVEF, RV fractional area change, tricuspid annular tion: Assessment of the clinical effectiveness of pulmonary artery
plane systolic excursion), and diastolic filling profiles. catheters in management of patients in intensive care (PAC-Man): a
However, most patients who have an initial hemodynamic randomised controlled trial. Lancet 366:472, 2005.
Kaplan JA, Reich DL, Savino JS: Kaplan’s cardiac anesthesia: The
insult and subsequently survive have spontaneous early echo era, 6th edition. Elsevier, St Louis, 2011.
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function. More recent strategies aimed at using long-term ment of acute right ventricular failure. J Am Coll Cardiol 56:1435, 2010.
ventricular assist devices either as primary therapy or as Markel TA, Wairiuko GM, Lahm T, et al.: The right heart and its
distinct mechanisms of development, function, and failure. J Surg
bridge to recovery have significantly improved survival Res 146:304, 2008.
rates. Sandham JD, Hull RD, Brant RF, et al.: Canadian Critical Care Clinical
Trials Group: A randomized, controlled trial of the use of pulmonary-
artery catheters in high-risk surgical patients. N Engl J Med 348:
5, 2003.
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Bojar R: Manual of perioperative care in adult cardiac surgery, tricular function. Eur J Cardiothorac Surg 29(Suppl 1):S126, 2006.
4th edition. Blackwell Publishing, Malden, MA, 2005. Schwann NM, Hillel Z, Hoeft A, et al.: Lack of effectiveness of the
Buckberg G, Athanasuleas C, Saleh S: Septal myocardial protection pulmonary artery catheter in cardiac surgery. Anesth Analg 113:994,
during cardiac surgery for prevention of right ventricular dysfunc- 2011.
tion. Anadolu Kardiyol Derg 8(Suppl 2):108, 2008. [Erratum in: Voelkel NF, Quaife RA, Leinwand LA, et al.: Right ventricular function
Anadolu Kardiyol Derg 8(6):471, 2008.] and failure: report of a National Heart, Lung, and Blood Institute
Chin KM, Kim NH, Rubin LJ: The right ventricle in pulmonary working group on cellular and molecular mechanisms of right heart
hypertension. Coron Artery Dis 16:13, 2005. failure. Circulation 114:1883, 2006.
CASE 89
QUESTIONS
1. Distinguish among systemic inflammatory 3. How are sepsis and multisystem organ dysfunction
response syndrome, sepsis, severe sepsis, syndrome treated?
septic shock, and multisystem organ dysfunction 4. How is catheter-related sepsis evaluated, managed,
syndrome. and prevented?
2. What are the pathophysiology and manifestations 5. What patient subgroups may require different
of sepsis-related organ dysfunction? therapeutic approaches?
A 57-year-old man with a history of diabetes mellitus and SIRS or cardiogenic shock. Although these conditions
Helicobacter pylori infection is admitted to the intensive share many features, recent years have seen an effort to
care unit after exploratory laparotomy for perforated standardize and clarify their nomenclature.
duodenal ulcer. Vital signs are heart rate of 113 beats per
minute, blood pressure of 83/40 mm Hg, respiratory rate
2. What are the pathophysiology and manifestations
of 18 breaths per minute, temperature of 38.9° C, and
oxygen saturation by pulse oximetry (SpO2) of 98%. He of sepsis-related organ dysfunction?
subsequently remains hypotensive despite fluid resuscita- Numerous theories have been proposed to explain the
tion and develops oliguria and coagulopathy. cascade of events that results in sepsis. Most of these
theories share the general concept that sepsis is the result
1. Distinguish among systemic inflammatory response of an initial infectious insult. The infection results in im-
syndrome, sepsis, severe sepsis, septic shock, and mune activation, with subsequent detrimental hyperac-
multisystem organ dysfunction syndrome. tivity of the immune system. The initial insult is most
commonly a localized or blood-borne bacterial infection.
Sepsis has been recognized as a clinical syndrome for The cell membranes of gram-negative bacteria contain
many years. Systemic inflammatory response syndrome various elements that may initiate strong immune re-
(SIRS) is a more recent development, defined by the sponses, such as lipopolysaccharide, thought to be the
American College of Chest Physicians in 1992. Both main factor in gram-negative sepsis. Gram-positive bac-
conditions are recognized as part of a continuum of dis- teria do not contain lipopolysaccharides, and much of
ease processes that involve similar pathophysiologic their pathogenicity is thought to be due to exotoxins,
mechanisms. SIRS is defined by four cardinal criteria that which are immunogenic toxins secreted by bacteria.
are indicators of inflammation (Table 89-1). Numerous proinflammatory cytokines are released in
Although SIRS is frequently associated with infection, response to these stimuli, such as interleukin (IL)-1, IL-2,
it can be caused by many noninfectious etiologies, such as IL-6, and IL-10; interferon-!, and tumor necrosis factor
pancreatitis, trauma, surgery, cardiopulmonary bypass, (TNF)-". TNF-" creates a positive feedback loop, in
burns, anaphylaxis, drugs, or aortic dissection. If SIRS is which it acts to increase its own production and the pro-
associated with positive blood cultures or other conclu- duction of other inflammatory mediators. This process is
sive indicators of infection, it is referred to as sepsis. Se- initially beneficial as a response to bacterial invasion but
vere sepsis indicates that the patient has developed organ can become deleterious. Cytokine production results in
dysfunction secondary to sepsis. In septic shock, a closely activation of immune cells as well as complement, which
related entity, sepsis results in hypoperfusion or arterial can cause apoptosis and endothelial cell dysfunction. Ac-
hypotension or both. Multisystem organ dysfunction tivated endothelial cells express molecules, such as tissue
syndrome (MODS) indicates the dysfunction of two or factor, that are prothrombotic. The result is microvascu-
more systems such that intervention is needed to main- lar thrombosis and ischemia that is thought to underlie
tain homeostasis. MODS can result from sepsis but can the development of organ dysfunction. In addition, en-
also be due to other conditions, such as noninfectious dothelial cells produce increased levels of nitric oxide
482
89 Sepsis and Multisystem Organ Dysfunction Syndrome 483
If the patient remains malperfused but is no longer vol- the aforementioned techniques to maintain organ perfu-
ume-responsive, inotropes are indicated. Traditionally, sion and reduce complications, support or replacement
dopamine and dobutamine have been used, although of organ function is sometimes necessary. Most com-
epinephrine and milrinone may be desirable in certain monly, this support takes the form of mechanical ventila-
circumstances. tion or renal replacement therapy (RRT). If mechanical
Patients with septic shock may remain hypotensive ventilation is necessary, the aforementioned prophylactic
even after circulating volume and cardiac output are measures should be taken to reduce VAP and decrease
restored. Certain tissue beds, such as the brain and time spent on the ventilator. In patients developing ALI/
kidney, tend to be more pressure-dependent and may ARDS, a ventilation strategy using lower tidal volumes
experience ischemia in this circumstance. It may be (6 mL/kg of ideal body weight) has been shown to reduce
necessary to administer vasopressor agents to maintain mortality. Use of higher levels of positive end expiratory
arterial pressure. Phenylephrine may be used, especially pressure and recruitment maneuvers to prevent atelecta-
if the patient has no central access, because it is less sis may also be beneficial. Early use of neuromuscular
likely to cause tissue ischemia if it extravasates. If cen- blocking agents has been shown more recently to reduce
tral access is available, norepinephrine is considered mortality in ARDS, but because these drugs can have
first-line therapy because it is a more potent vasocon- significant undesirable effects (i.e., myopathies, neurop-
strictor and has some '-adrenergic activity, making it a athies, alterations of the neuromuscular junction), it may
more “physiologic” choice. More recently, vasopressin be too early to adopt this treatment broadly.
has become popular because many septic patients RRT can be lifesaving in cases of refractory hyperka-
quickly become AVP-depleted and are expected to ben- lemia or other electrolyte abnormalities. It is also useful
efit from “hormone replacement.” AVP may also have to treat severe acidosis, volume overload, uremia, or drug
some benefits over norepinephrine because it seems to intoxication. Despite some enthusiasm for its use to
increase urine output and may lead to improved out- modulate cytokine response and alter the course of sep-
comes in patients with less severe sepsis. Although do- sis, trials for this purpose have been disappointing. RRT
pamine traditionally has been a first-line pressor and may be performed continuously or intermittently. Both
inotrope in sepsis and other shock states, it can cause approaches provide comparable outcomes, although con-
tachyarrhythmias. Although dopamine is believed by tinuous therapies seem to be associated with slightly
many to preserve renal function in shock, a large body better hemodynamic stability in critically ill patients.
of literature refutes this idea. However, intermittent therapy has benefits in terms of
catheter maintenance and resource use. With continuous
therapy, hemofiltration or hemodialysis may be selected;
Prophylaxis to Prevent Complications
this decision frequently depends on local standards.
Many patients with sepsis die of complications that can be Replacement of other vital organ functions is not easily
avoided with appropriate prophylactic measures. Because accomplished. Blood products and growth factors are
of hypotension and gut hypoperfusion, endogenous de- available to replace inadequate erythropoiesis, thrombo-
fenses against gastric acidity may fail resulting in peptic poiesis, and leukocyte production. However, there are
ulcers and upper gastrointestinal bleeding. Histamine-2 negative effects of blood transfusions, such as immunosup-
blockers and proton pump inhibitors are preventive mea- pression, transfusion reactions, and transfusion-associated
sures. Sepsis is a hypercoagulable state, and even patients lung injury. Although there have been some successes with
with mild thrombocytopenia and coagulopathy may be liver replacement therapies for acute liver failure, there is
prone to thrombosis, primarily venous thrombosis. little experience with sepsis-related liver failure. Critically
Thromboprophylaxis with subcutaneous unfractionated ill patients may exhibit relative adrenal insufficiency. Al-
or low-molecular-weight heparin and sequential com- though many experts endorse corticosteroid therapy in
pression devices may prevent morbidity and mortality. these circumstances, it is still uncertain whether such
Despite the lifesaving nature of mechanical ventilation, it therapy improves morbidity and mortality.
can leave patients vulnerable to ventilator-associated
pneumonia (VAP), worsen hemodynamics, and may 4. How is catheter-related sepsis evaluated,
necessitate additional sedation. Placing patients in a semi-
recumbent position, which reduces microaspiration and managed, and prevented?
incidence of VAP, and routine use of spontaneous breath- One particular infectious process that bears special
ing trials and sedation interruption, which can lessen the mention is central line–associated bloodstream infec-
duration of mechanical ventilation, may reduce these tion (CLABSI). CLABSI is an important cause of mor-
risks. Much evidence suggests that prevention of severe bidity and mortality in the intensive care unit and may
hyperglycemia using insulin infusions prevents infectious be responsible for $2.3 billion per year in excess health-
and neuromuscular complications. However, it is unclear care costs.
how tight glycemic control must be to benefit patients; When an indwelling catheter is placed, bacteria can
this is an area of much ongoing research. colonize the catheter tip via intraluminal or extralu-
minal routes. The extraluminal route seems to be
more important in the initial period after placement,
Support and Replacement of Organ Function
before the catheter tract can heal and reepithelialize.
Despite all efforts to prevent it, many patients go on to Conversely, the intraluminal route becomes more
develop organ dysfunction as a result of sepsis. Besides important the longer the catheter remains in place.
486 SECTION 16 Critical Care
Catheter-related infection should be suspected in any cases of combined septic shock and heart failure, the
patient with bacteremia or sepsis and an indwelling addition of short-term cardiac support, such as an
catheter. This is especially true if the catheter site intraaortic balloon pump, may be extremely helpful.
appears indurated or purulent, although these are Patients with renal failure may warrant more careful
unreliable predictors of infection. volume management and may require early dialysis.
When a catheter-related bloodstream infection is sus- However, this does not mean that fluid resuscitation
pected, blood cultures should be drawn from another should be withheld.
(preferable peripheral) site to prove bacteremia defini- Likewise, patients with impaired immune systems
tively. If cultures are positive, the culprit line should be often warrant more careful consideration. They may
removed and, if necessary, replaced at another site. Bac- not show the usual clinical indicators of infection, espe-
teremia, despite appropriate antimicrobial therapy, is cially if they are receiving corticosteroids, and generally
particularly suspicious for catheter-related infection. If require broader antimicrobial coverage. The range of
suspicion is very high, a potentially infected line should pathogens that may cause a severe systemic response in
be removed even in the absence of definitive culture these individuals is much greater than in immunocom-
evidence. Antimicrobial medications are indicated and petent patients. Fungi, mycobacteria, and viruses must
should broadly cover common pathogens, such as staphy- be considered as targets for therapy. Also, it may be
lococci, enterococci, and gram-negative bacilli. desirable to minimize the use of indwelling catheters
CLABSI is increasingly being documented as a senti- and other devices, even more than is the standard of
nel event. Much research has focused on the best ways to care, because of the decreased ability of immunosup-
prevent catheter colonization and infection. Several ap- pressed patients to resist invasion by environmental
proaches have met with success (Box 89-1). Conse- microorganisms.
quently, these practices are implemented widely through- Lastly, in patients who have a poor prognosis, such as
out the health care system. Although catheter removal patients with advanced age or metastatic cancer, it may be
is a useful technique to prevent infection, the strategy of inappropriate to proceed with aggressive care. In these
routine catheter exchange has repeatedly failed to de- cases, careful attention should be paid to the patient’s
crease infection rates. This approach may lead to in- wishes before falling ill. Depending on the patient’s de-
creased rates of mechanical complications, such as sires and the likelihood of recovery, it may be better to
thrombosis and pneumothorax. make a transition to palliative care rather than engage in
interventions that are unlikely to improve length or qual-
ity of life. Such decisions should always be made with the
5. What patient subgroups may require different
participation of the patient’s family members and, in se-
therapeutic approaches? lect cases, a hospital ethics committee.
Any patient population that is not expected to respond to
therapeutic measures in a predictable fashion may re-
quire special consideration. For example, the usual early SUGGESTED READINGS
goal-directed resuscitation for patients with sepsis gives Ventilation with lower tidal volumes as compared with traditional tidal
specific targets for CVP to guide initial fluid loading. volumes for acute lung injury and the acute respiratory distress syn-
However, in patients with heart failure, particularly right drome. The Acute Respiratory Distress Syndrome Network (ARD-
heart failure with or without pulmonary hypertension, SNet). N Engl J Med 342:1301, 2000.
this may be a deleterious strategy. In a patient with right Bone RC, Balk RA, Cerra FB: Definitions for sepsis and organ failure
and guidelines for the use of innovative therapies in sepsis. Chest
heart failure, this approach may lead to overdistention of 101:1644, 1992.
the right ventricle, shifting the interventricular septum to Briel M, Meade M, Mercat A, et al.: Higher vs. lower positive end-
the left, decreasing left ventricular preload and compli- expiratory pressure in patients with acute lung injury and acute
ance, and resulting in impaired myocardial performance. respiratory distress syndrome: systematic review and meta-analysis.
JAMA 303:865, 2010.
Such patients may warrant a more balanced approach De Backer D, Biston P, Devriendt J, et al.: Comparison of dopamine and
that includes earlier use of inotropes and the addition of norepinephrine in the treatment of shock. N Engl J Med 362:779, 2010.
pulmonary vasodilators such as inhaled NO. In extreme Dellinger RP, Carlet JM, Masur H, et al.: Surviving Sepsis Campaign
guidelines for management of severe sepsis and septic shock. Crit
Care Med 32:858, 2004.
Ely EW, Goyette RE: Sepsis with acute organ dysfunction. In Hall JB,
Schmidt GA, Wood LD (eds): Principles of Critical Care, 3rd edi-
BOX 89-1 Evidence-Based Practices to tion. McGraw-Hill, New York, 2005.
Reduce Catheter-Related Infection Frasca D, Dahyot-Fizelier C, Mimoz O: Prevention of central venous
catheter-related infection in the intensive care unit. Crit Care
Adherence to checklists and use of standard protocols 14:212, 2010.
Staff education and training Hack CE, Zeerleder S: The endothelium in sepsis: source of and a
Use of catheter materials and coatings that reduce bacterial target for inflammation. Crit Care Med 29(Suppl):S21, 2001.
Hooper MH, Girard TD: Sedation and weaning from mechanical ven-
adhesion and growth tilation: linking spontaneous awakening trials and spontaneous
Preference for subclavian vein over other sites breathing trials to improve patient outcomes. Crit Care Clin 25:515,
Good hand hygiene 2009.
Use of chlorhexidine-alcohol preparation solution Khan RZ, Badr KF: Endotoxin and renal function: perspectives to the
Removal of catheters when no longer needed understanding of septic acute renal failure and toxic shock. Nephrol
Dial Transplant 14:814, 1999.
89 Sepsis and Multisystem Organ Dysfunction Syndrome 487
Kollef MH, Sherman G, Ward S, Fraser VJ: Inadequate antimicrobial Papazian L, Forel J-M, Gacouin A, et al.: Neuromuscular blockers in early
treatment of infections: a risk factor for hospital mortality among acute respiratory distress syndrome. N Engl J Med 363:1107, 2010.
critically ill patients. Chest 115:462, 1999. Rabindranath KS, Adams J, MacLeod AM, Muirhead N: Intermittent
Landry DW, Oliver JA: The pathogenesis of vasodilatory shock. versus continuous renal replacement therapy for acute renal failure
N Engl J Med 345:588, 2001. in adults. Cochrane Database Syst Rev (3):1, 2007.
MacFie J: Current status of bacterial translocation as a cause of surgical Rivers E, Nguyen B, Havstad S, et al.: Early goal-directed therapy in
sepsis. Br Med Bull 71:1, 2004. the treatment of severe sepsis and septic shock. N Engl J Med
Marik PE, Baram M, Vahid B: Does central venous pressure predict 345:1368, 2001.
fluid responsiveness? A systematic review of the literature and the Ruiz BM: Reversible myocardial dysfunction in critically ill, noncardiac
tale of seven mares. Chest 134:172, 2008. patients: a review. Crit Care Med 30:1280, 2002.
Marinelli WA, Leatherman JW: Neuromuscular disorders in the Russell JA, Walley KR, Singer J, et al.: Vasopressin versus norepinephrine
intensive care unit. Crit Care Clin 18:915, 2002. infusion in patients with septic shock. N Engl J Med 358:877, 2008.
Papadopoulos MC, Davies DC, Moss RF, et al.: Pathophysiology of Santoro A, Mancini E, Ferramosca E, Faenza S: Liver support systems.
septic encephalopathy: a review. Crit Care Med 28:3019, 2000. Contrib Nephrol 156: 396, 2007.
CASE 90
Renal System
Leila Hosseinian, MD • Insung Chung, MD • Adam Evans, MD
QUESTIONS
1. How is acute kidney injury defined? 8. Identify the risk factors for and probability of
2. What are the incidence and outcome of developing contrast-induced nephropathy.
acute kidney injury in the intensive care unit? 9. What are the options for preventing contrast-
3. Explain the pathophysiology of acute kidney induced nephropathy?
injury. 10. What are the indications for dialysis in the
4. How is the etiology of acute kidney injury intensive care unit?
determined in the intensive care unit? 11. What are the options for renal replacement
5. Discuss acid-base balance regulation, and identify therapy?
acid-base disturbances resulting from acute 12. Discuss problems encountered with renal
kidney injury. replacement therapy.
6. What is contrast-induced nephropathy? 13. How is the most appropriate renal replacement
7. Describe the pathogenesis of contrast-induced therapy selected?
nephropathy.
A 62-year-old man presented for emergency repair of a than if creatinine doubles in 3 days, but this is not re-
type A dissecting ascending aortic aneurysm. He had a flected within the RIFLE criteria. Change in urine
history of hypertension, diabetes, and hyperlipidemia. In output is generally the most important criterion used in
the emergency department, he complained of acute onset the intensive care unit (ICU) to determine renal dys-
of chest pain. The work-up included a computed tomog- function because it can more rapidly help identify risk.
raphy scan with intravenous contrast agent administra- The Acute Kidney Injury Network (AKIN), recogniz-
tion. On postoperative day 1 in the cardiothoracic inten- ing the importance of time course to kidney injury, modi-
sive care unit, his creatinine level increased twofold, with fied the RIFLE criteria (Table 90-2). Their diagnostic
a decrease in urine output and a metabolic acidosis. criteria for AKI include an abrupt (!48 hours) reduction
in kidney function defined as one of the following:
• Absolute increase in serum creatinine of "0.3 mg/dL
1. How is acute renal injury defined?
• Increase in serum creatinine of "50% (1.5-fold
Acute renal failure (ARF) is the sudden development of from baseline)
renal insufficiency that results in the retention of urea and • Reduction in urine output (documented urine
other nitrogenous waste products as well as dysregulation output of #0.5 mL/kg/hour for "6 hours)
of extracellular volume and electrolytes. It is also known as Risk from the RIFLE criteria is equivalent to stage 1 of
acute kidney injury (AKI). AKI encompasses the entire the AKIN classification system, injury is equivalent to
range of renal dysfunction, from minor to requiring renal stage 2, and failure is equivalent to stage 3. Loss of renal
replacement therapy. The measurement of serum creati- function and end-stage renal disease were removed from
nine, which measures glomerular filtration rate (GFR), has the AKIN classification. Both criteria are based on creati-
been used to evaluate kidney function loss. The Acute nine as a marker for renal injury, which is a routine blood
Dialysis Quality Initiative developed criteria for different test. However, there are limitations to the usefulness
stages of renal injury. The RIFLE criteria consist of three of creatinine as a marker because many factors affect
graded levels of risk, injury, and failure, which are based on creatinine levels, including body size, catabolic state,
the magnitude of elevation of serum creatinine and urine rhabdomyolysis, dilutional effects, and drugs. Blood urea
output (Table 90-1). There are also two outcome mea- nitrogen (BUN) has also been used as a marker of renal
sures, loss of renal function and end-stage renal disease. function, but it too is affected by various factors, including
The RIFLE scoring system has some disadvantages. excessive protein intake, protein catabolism, total paren-
The RIFLE criteria do not have a time component for teral nutrition, acute myocardial infarction, gastrointesti-
creatinine levels; this does not allow for analysis of nal bleeding, steroid administration, and dehydration.
renal function as a dynamic process. For example, a New markers of AKI are under investigation. Cystatin C
doubling of creatinine in 24 hours is more significant is an endogenous cysteine-proteinase inhibitor that is
488
90 Renal System 489
TABLE 90-1 RIFLE Classification System TABLE 90-3 Conditions Associated with
Acquired Renal Failure in the
Class GFR UO Intensive Care Unit
Risk Decreased by "25% #0.5 mL/kg/ Condition Incidence (%)
or hour "6
Baseline SCr increased $ 1.5 hours Multiorgan failure 30–75
Injury Decreased by "50% #0.5mL/kg/ Sepsis 30–50
or hour "12
Baseline SCr increased $ 2 hours Drugs 20–40
acid, and trimetazidine have not been shown to add any Uremia typically results when GFR is decreased to
additional benefit; these agents have not been thoroughly #10 mL/min and BUN levels are %100 mg/dL. Common
studied to recommend routine use in the prophylactic causes include excessive protein ingestion (parenteral or
treatment of CIN. enteral), gastrointestinal bleeding, and corticosteroid use.
Reducing the risk of acquiring CIN requires a multifac- Prompt initiation of dialysis is advised when patients de-
torial approach. Issues for consideration include using velop encephalopathy, pericarditis, or hemorrhage.
nonionized, low-osmolar to isoosmolar contrast media and Critically ill patients tend to be severely hypervolemic
limiting the volume. All common nephrotoxic drugs, such as a result of aggressive fluid resuscitation and reduction in
as NSAIDs and metformin, should be discontinued before filtered sodium load. Dialysis is indicated when aggressive
receiving radiocontrast. Isotonic sodium bicarbonate (add diuretic therapy fails to achieve optimal volume status.
three 50-mL ampules of 1 mEq/mL sodium bicarbonate to
850 mL of sterile water) should be administered at 3 mL/kg Nonrenal Indications
1 hour before the procedure, followed by 1 mL/kg for
6 hours after completion of the procedure. Acetylcysteine Hemodialysis is indicated for the treatment of life-
can also be administered (1200 mg twice daily orally) the threatening toxic ingestions and any severe metabolic
day before and the day of radiocontrast injection. acidosis that occurs from ingestion. Volume overload
from congestive heart failure is another common indica-
10. What are the indications for dialysis in the tion for renal replacement therapy. These patients often
have low cardiac outputs and resultant renal hypoperfu-
intensive care unit?
sion. They tend to retain sodium and fluid as a result of
ARF is marked by a swift decline in kidney function increased circulating levels of catecholamines and neuro-
leading to azotemia and oliguria. There is no consensus hormonal factors. When patients become refractory to
regarding the optimal timing for dialysis therapy in a treatment with diuretics and inotropic agents, dialysis
critically ill patient. Box 90-1 lists the most common ultrafiltration is often effective. Finally, patients with
reasons for dialysis in the ICU. liver failure are predisposed to developing azotemia and
hepatorenal syndrome. Renal replacement therapy is
commonly used to assist with solute and fluid clearance.
Renal Indications
Hyperkalemia as a result of decreased renal excretion can 11. What are the options for renal replacement therapy?
be life-threatening in patients with ARF. Exogenous
sources such as intravenous fluids, potassium replace- Options for renal replacement therapy include hemodi-
ment, and medications (e.g., ACE inhibitors) all need to alysis and continuous renal replacement therapies. Inter-
be carefully regulated. Nonrenal causes of hyperkalemia, mittent hemodialysis is the most common therapy for
such as tumor lysis syndrome, rhabdomyolysis, or hema- ARF in the ICU. A session typically lasts 4 hours and
toma reabsorption, can also lead to life-threatening hy- requires a dialysis machine and trained personnel. The
perkalemia by causing a rapid shift in potassium from the dialysis machine is primarily diffusion dependent with a
intracellular to the extracellular space. higher dialysate rate (%500 mL/min) compared with
When renal function is severely impaired, accumula- blood flow (300 mL/min). Blood flow runs countercur-
tion of acids can lead to a high anion gap acidosis. When rent to the dialysate and produces a rapid decrease in
severe acidosis (pH #7.20) occurs, treatment with exog- plasma solute concentration.
enous sodium bicarbonate is often initiated. This treat- Continuous renal replacement therapy (CRRT) in-
ment may be detrimental in patients at risk for volume cludes multiple different modalities, and therapies are
overload and hypernatremia or in cases of concomitant generally run continuously. They are better tolerated in
respiratory acidosis. In these patients or in patients re- patients who are hemodynamically unstable because they
fractory to medical treatment, dialysis affords another use a lower blood flow rate. The most commonly used
option for clearance of acidic waste. are continuous arteriovenous hemofiltration (CAVH),
continuous arteriovenous hemodialysis (CAVHD), con-
tinuous venovenous hemofiltration (CVVH), continuous
venovenous hemodialysis (CVVHD), and slow continu-
BOX 90-1 Common Indications for Dialysis ous ultrafiltration (SCUF). CAVH and CAVHD use the
in the Intensive Care Unit patient’s mean arterial pressure as the impetus for blood
flow across the membrane. An arteriovenous circuit is
RENAL used, which avoids the need for a blood pump, and solute
• Hyperkalemia removal occurs by convection. CAVHD includes dialysis
• Uremia allowing for the diffuse clearance of solute. Blood flow
• Acidosis ranges from 50–100 mL/min. CVVH and CVVHD are
• Hypervolemia secondary to renal failure similar to CAVH and CAVHD except that they require
NONRENAL central venous access and connection to an extracorpo-
• Toxins
real blood pump to maintain the transmembrane pres-
• Congestive heart failure sure gradient. SCUF is similar to CAVH and CVVH but
• Liver failure functions to remove fluid and not solute. SCUF is pri-
marily used in patients with heart failure.
90 Renal System 493
QUESTIONS
1. What is subarachnoid hemorrhage? 6. What are the risks of acute ischemic stroke, and
2. How is subarachnoid hemorrhage diagnosed? how is stroke diagnosed and treated?
3. How are patients with subarachnoid hemorrhage 7. How common are seizures after head injury, and
managed? how are they treated?
4. How is elevated intracranial pressure diagnosed 8. What is encephalopathy, and how is it treated?
and treated? 9. What is brain death, and how is it diagnosed?
5. What is traumatic brain injury?
A 35-year-old man sustained injuries in a motor vehicle factors for SAH. Genetic diseases such as polycystic kid-
accident and was taken to the nearest emergency depart- ney disease and connective tissue diseases (e.g., Marfan
ment. His vital signs, x-rays, and laboratory values were syndrome, Ehlers-Danlos syndrome) increase the risk of
normal. As his wounds were sutured, he complained of the developing aneurysms. In certain populations, such as the
worst headache of his life. His mental status acutely dete- Japanese and Finnish, a familial syndrome is associated
riorated. He was diagnosed with subarachnoid hemorrhage with intracranial aneurysms. The strongest risk factor for
(SAH) and increased intracranial pressure (ICP), which SAH is a history of previous SAH. There appears to be a
were treated. After an uneventful course in the intensive higher incidence of SAH in winter and spring months
care unit (ICU), he was transferred to the floor, where he as well as an association between atmospheric pressure
experienced a seizure. After the seizure, he remained con- changes and number of SAHs per day; the reasons are
fused and combative. Later, he sustained an unwitnessed unknown.
cardiac arrest from which he had return of spontaneous
circulation after 30 minutes. However, he never regained 2. How is subarachnoid hemorrhage diagnosed?
consciousness.
The symptom classically associated with aneurysmal SAH
is described as “the worst headache of my life” and is re-
1. What is subarachnoid hemorrhage?
ported in nearly 80% of awake patients. Many patients
SAH is the extravasation of blood into the subarachnoid also report a sentinel headache, which generally occurs
space, which is located between the pia and the arachnoid 2–8 weeks before a major SAH. Other symptoms include
membrane. The most common cause of SAH is trau- nausea, vomiting, pain radiating to the legs (blood pool-
matic head injury. Traumatic SAH in elderly adults often ing in lumbar cistern), nuchal rigidity, meningeal signs,
occurs after falls and head injury, whereas the most com- cranial nerve palsies, focal neurologic symptoms, loss
mon cause in young people is motor vehicle accidents. of consciousness, and seizures. Death occurs in 12% of
Nontraumatic SAH is most commonly associated with people before receiving treatment.
intracranial aneurysm rupture (approximately 80%–90%). Timely diagnosis is essential for SAH because prompt
Approximately 5% of the population harbor an aneurysm, treatment has a significant impact on outcome. SAH is
and 20%–30% of people with an aneurysm have multiple misdiagnosed in 12% of patients, leading to delayed treat-
aneurysms; however, very few aneurysms rupture sponta- ment and is associated with a fourfold higher risk of death
neously. Although SAH is responsible for about 5% of all or disability at 1 year. Although SAH accounts for only
strokes, the incidence of spontaneous SAH is only 25 per 1% of all patients with headaches presenting to the emer-
100,000 in the United States. The peak incidence of gency department, approximately 20% of all patients with
aneurysmal SAH is between 50 and 60 years of age, with SAHs present with sentinel headaches before major SAH.
a higher prevalence in women and African Americans. When a patient presents to the emergency department
Other nontraumatic causes include vascular malforma- with a headache, a high index of suspicion for possible
tions, tumors, and infections. leak (sentinel headache) could prevent rerupture and be
Risk factors for aneurysmal SAH are multifold, consist- lifesaving.
ing of both modifiable and genetic factors. In the United Noncontrast computed tomography (CT) scan of
States, smoking, hypertension, alcohol abuse, and cocaine the head is the diagnostic test of choice for acute SAH.
abuse (especially in young people) are independent risk The probability of detecting SAH by CT scan is related
494
91 Central Nervous System 495
coiling excludes aneurysms from the circulation by filling depletion, low cardiac output, smoking, fever, and vaso-
the aneurysm with platinum coils, which results in clot spasm on initial angiography (higher risk of subsequent
formation, decreasing the potential for rebleeding. vasospasm).
There is still controversy at the present time regarding The “gold standard” for diagnosis of cerebral vaso-
whether open surgical clipping or endovascular coiling is spasm is cerebral angiography. Transcranial Doppler
superior. The decision whether to coil or clip is determined (TCD) ultrasound can be used at the bedside to diagnose
on a patient-by-patient basis taking into account the size, vasospasm. Although changes in mean flow velocities of
shape, and location of each aneurysm, patient condition, the middle cerebral artery of "200 cm/second are highly
and the experience of available physicians. The Interna- suggestive of cerebral vasospasm, other vascular territories
tional Subarachnoid Aneurysm Trial (ISAT) showed a sta- are unreliable. TCD scans can be performed daily, and
tistically significant improvement in disability and death at elevated velocities on TCD scans can precede symptoms
1 year in patients who had endovascular coiling compared by 2 days. If TCD suggests vasospasm, further investiga-
with surgical clipping (24% vs. 31%). At 7-year follow-up, tion (e.g., CTA, MRA, cerebral angiography) should be
the surgical cohort had significantly higher mortality and performed to confirm the diagnosis.
seizure rates. However, early rebleeding was higher in the Most patients with SAH are treated prophylactically
endovascular group. Although endovascular coiling has to prevent vasospasm. At the present time, nimodipine is
become more common and widely available, preference the only medication shown in clinical trials to improve
among centers is largely related to the culture, familiarity, outcomes. Nimodipine is usually given for 2–3 weeks,
and comfort of the facility with either clipping or coiling. and the dose is based on blood pressure. A suggested
Some recommendations suggest that surgical clipping is protocol is 60 mg every 4 hours for systolic blood pres-
preferable for aneurysms "10 mm or aneurysms with wide sure (SBP) "140 mm Hg, 30 mg for SBP 120–140 mm
necks. Hg, and no drug for SBP !120 mm Hg. Normovolemia
Whether clipping or coiling is preferred at a particular should be the goal in patients with SAH.
institution, early treatment is recommended. In a follow- The treatment for patients who develop symptomatic
up article looking at the ISAT data, early intervention with vasospasm includes “triple H” therapy and direct arterial
either clipping or coiling resulted in improved outcomes. calcium channel blocker injection by cerebral angiography.
Past recommendations dictated that treatment should “Triple H” therapy includes hypertension, hydration, and
either occur early (0–3 days) or, if a patient’s condition hemodilution. The goal is to increase the SBP 20–30 mm
warranted, be delayed (after 10 days). Intervention was not Hg above baseline but not "220 mm Hg. This goal can be
recommended between days 4 and 10 because of the in- accomplished with pressors, fluids, or both. Hemodilution
creased risk for vasospasm. However, more recent studies is generally achieved by administering crystalloids to dilute
have shown that intervention during days 5–10 yielded the hematocrit, which also accomplishes hydration. If pos-
better outcomes than late interventions. The practice of sible, repeat angiography should be performed to facilitate
delaying treatment is now questionable. Early intervention intraarterial injection of calcium channel blockers to relax
resulted in the best outcomes. the cerebral artery.
Medical management of SAH focuses on treating the Hydrocephalus and elevated ICP can occur. Hydro-
complications of SAH. Rebleeding is the most treatable cephalus is treated with an external ventricular device to
cause of poor outcomes. In unrepaired patients, the risk divert CSF flow, which also treats increased ICP. Other
of rebleeding is 3%–4% within the first 24 hours, 2% on management strategies for elevated ICP are hypertonic
day 2, up to 20% within the first 2 weeks, and up to 50% saline and mannitol to decrease brain swelling.
by 6 months. Seizures are associated with increased risk Seizures are a possible complication of SAH, and
of rebleeding in patients with untreated aneurysms. The most patients are placed on prophylactic anticonvulsant
only certain way to prevent rebleeding is aneurysmal therapy for the first 7 days. If the patient has a seizure or
clipping or coiling. Antifibrinolytics, such as aminoca- the aneurysm is not treated, anticonvulsant therapy is
proic acid (2–4 g loading dose, followed by 1 g/hour infu- warranted for a longer period.
sion) or tranexamic acid (1 g loading dose, followed by Hyponatremia usually occurs secondary to cerebral salt
1 g every 6–8 hours), have been used to prevent early wasting syndrome and is not due to syndrome of inappro-
rebleeding. However, because antifibrinolytics are associ- priate antidiuretic hormone (SIADH). Cerebral salt wast-
ated with vasospasm, the current recommendation is to ing is characterized by hyponatremia and dehydration with
limit their use to the first 3 days. Both antifibrinolytics are excessive urine output. Treatment entails correcting the
to be employed cautiously in patients with histories of myo- hyponatremia with salt tablets or hypertonic saline and
cardial infarction, hypercoagulopathy, deep vein thrombo- maintaining balanced fluid and urine outputs. It is impor-
sis, or pulmonary embolus. Lowering blood pressure with tant to rule out SIADH because treatment for SIADH
labetalol, nicardipine, or clevidipine has been shown to (which is fluid restriction) should be avoided as it can
decrease risk of rebleeding. worsen the patient’s volume status and increase risk of
Cerebral artery vasospasm can lead to worse mortality vasospasm from dehydration.
and disability in patients with SAH. It usually occurs be-
tween days 3 and 14 after SAH. Symptomatic vasospasm, 4. How is increased intracranial pressure diagnosed
defined as clinical deterioration secondary to vasospasm, and treated?
is seen in 20%–40% of patients. Risk factors for the de-
velopment of vasospasm include poor clinical status, thick The cranial vault comprises brain (80%), blood (10%),
blood on CT scan ("1 mm thick), hypertension, volume and CSF (10%). Because the volume in the cranial vault
91 Central Nervous System 497
mild confusion to coma. Papilledema may indicate ele- neurologic emergencies related to cerebral edema and
vated ICP; however, it can be observed in patients with elevated ICP. There are no data showing superiority of
normal ICP. Uncal herniation produces an ipsilateral either mannitol or hypertonic saline. However, mannitol
fixed and dilated pupil (cranial nerve [CN] III palsy). CN should be administered with caution to patients with a
VI palsy, inability to turn the eye outward, may be pres- low ejection fraction or renal failure.
ent. Posturing, either decorticate (flexor) or decerebrate More recently, small volumes of high-osmolarity solu-
(extensor), is a nonspecific sign of elevated ICP. Decorti- tions (23.4% saline) have been used to treat intracranial
cate posturing occurs when the injury is between the hypertension crises. The theory behind the use of high-
cortex and the red nucleus. Decerebrate posturing occurs osmolarity solutions is that they create a driving force to
when the injury is below the red nucleus. Posturing pro- mobilize water from the interstitial and intracellular
vides only general localizations and not absolute ana- compartments of the brain into the intravascular com-
tomic diagnoses. Abnormal respiratory patterns, such as partment. Reduction in brain water can lead to a "50%
Cheyne-Stokes respiration, central neurogenic hyper- reduction in ICP in the acute setting allowing additional
ventilation, sustained inspiratory effort, clustered breath- time to arrange for other diagnostic or therapeutic inter-
ing, and ataxic breathing, can also be observed in patients ventions. Advantages of high-osmolarity saline include
with elevated ICP. The only definitive way to diagnose low cost; amenable to repeat administrations; low total
elevated ICP is to measure it directly. volume; and freedom from allergenicity, which mannitol
The concept of CPP-directed treatment of increased is not. Treatment with high-osmolarity saline does have
ICP was introduced "30 years ago. There has been a some risks, although complications are uncommon. Rec-
small improvement in outcome statistics, but mortality ognized complications include hyperosmolarity, central
still ranges from 20%–30%. When increased ICP is di- pontine myelinolysis, subdural hematomas, congestive
agnosed, emergent treatment must be initiated. Surgical heart failure, acid-base derangements, and coagulop-
consultation should be sought immediately for possible athies. This treatment still requires further investigation
evacuation of blood or excess fluid or ventricular drain- to determine the optimal dose as well as the safest and
age of CSF. The goals of therapy are to reduce ICP and most effective mode of administration.
attain a CPP of 60–100 mm Hg. CPP is optimized by ICP monitoring is considered the standard of care in
increasing MAP and reducing ICP (Box 91-3). If ICP most clinical centers, although some studies have shown
remains elevated, osmotherapy with either mannitol or no change in mortality with ICP monitoring versus
hypertonic saline should be considered. Mannitol and monitoring with imaging and clinical examinations only.
hypertonic saline are the mainstays of treatment of Several techniques are available for ICP monitoring
(Table 91-3). The goal of all these monitoring devices is
to provide early warning of impending brain hypoxia or
ischemia as well as improving cerebral hemodynamics
BOX 91-3 Treatment of Elevated Intracranial and oxygenation. Some noninvasive methods allow the
Pressure medical team to look for additional signs of elevated ICP.
Surgical intervention varies depending on the under-
Immediate surgical consultation lying cause of elevated ICP, the patient’s clinical status,
Increase MAP
Vasopressors
imaging studies, and overall prognosis. The two most
Isotonic fluids common causes requiring surgical intervention are epi-
Decrease intracranial pressure dural hematoma and acute subdural hematoma. The
Elevate head of bed 30–45 degrees most recent recommendations for treatment are based on
Avoid administration of free water the Brain Trauma Foundation guidelines published in
Maintain mildly elevated plasma sodium levels 2007. Epidural hematomas "30 mL should be surgically
(150–155 mEq/L) evacuated regardless of the patient’s Glasgow Coma Scale
Avoid increases in cerebral metabolic rate score. There is no ideal surgical intervention, but crani-
Avoid hyperthermia otomy allows for a more significant evacuation of the
Avoid shivering hematoma. An epidural hematoma !30 mL with !5 mm
Prevent seizures
Control pain
midline shift can be managed nonoperatively by serial CT
Continue normocarbia (pCO2 37–40 mm Hg) scans and close neurologic monitoring. Acute subdural
May institute short-term hyperventilation hematomas that are !10 mm thick or are causing a mid-
(pCO2 30-32 mm Hg) line shift "5 mm on CT scan should undergo surgical
If intracranial pressure remains elevated intervention. Emergent surgery should also be performed
Osmotherapy if the subdural hematoma is !10 mm thick and there is
Mannitol 20% !5 mm midline shift and one of the following conditions
0.5–1 g/kg bolus followed by 0.5 g/kg every 4–6 hours are present:
Goal: 300–320 mOsm/L in serum • Glasgow Coma Scale score decreased by "2 points
Caution in patients with low ejection fractions or since the time of the injury
renal failure
Hypertonic saline (3% NS)
• Signs of brainstem involvement (e.g., asymmetric or
1 mg/kg/hour fixed and dilated pupils)
Goal: Sodium 150–155 mEq/L • ICP "20 mm Hg
Other treatment options that may be implemented are
NS, Normal saline; pCO2, carbon dioxide tension. sedation, external ventricular CSF drainage, hypothermia,
91 Central Nervous System 499
opioids, benzodiazepines, or both are abruptly stopped. such injury. CT scan or MRI is useful to demonstrate
Withdrawal is a common cause of delayed encephalopathy damage to the brain. All reversible factors that could ac-
in patients treated with benzodiazepines for suspected alco- count for altered brain function, including hypothermia
hol withdrawal syndrome. Tacrolimus, an important drug (temperature !32.2 °C), drug intoxication or poisoning,
in transplant patients, is associated with encephalopathy. sedative drugs, neuromuscular blocking agents, severe
electrolyte abnormalities, severe acid-base abnormalities,
shock, and endocrine disorders, need to be corrected. In
9. What is brain death, and how is it diagnosed?
addition, the neurologic examination must not show im-
The concept of brain death became applicable after the provement over time. There is no minimal amount of
introduction of positive pressure mechanical ventilators time a patient needs to be observed before declaring
in the 1950s. Before the advent of ventilators, death was brain death.
determined by loss of respiration or circulation. How-
ever, with ventilators, physicians were able to keep pa- Absence of Neurologic Function
tients “alive” despite irreversible destruction of the brain
that would have previously led to termination of cardio- Total absence of functioning of the entire brain is a fun-
respiratory function. The first widely accepted criteria damental feature of brain death. All brainstem functions
for diagnosing brain death, the Harvard Criteria, were are absent. The pupils are fixed and unreactive to light.
published in 1968 in the Journal of the American Medical Ocular movements are absent to oculocephalic and ocu-
Association. lovestibular reflex testing. Corneal, pharyngeal (gag), and
Only 1%–2% of all deaths per year in the United tracheal reflexes are absent. The patient does not grimace
States are brain deaths. Brain death requires an irrevers- or move in response to painful stimuli (unresponsive
ibly nonfunctional brain; however, the determination of coma). The presence of spontaneous motor responses in
brain death varies according to state law and hospital the limbs secondary to spinal reflexes do not negate the
policies. In 1981, the Uniform Determination of Death diagnosis of brain death. However, decorticate or decer-
Act was published by a presidential commission providing ebrate posturing does negate the diagnosis of whole brain
guidelines on the determination of brain death in the death.
United States. The Act states that patients are dead if they
have irreversible cessation of circulatory or respiratory Apnea
functions or if they have irreversible cessation of all func-
tions of the entire brain, including the brainstem. Al- Before performing the apnea test, the patient should be
though state laws and hospital policies may vary slightly, normotensive, normothermic, euvolemic, eucapnic, and
they all must follow the guidelines determined by the not hypoxic. PaCO2 must increase sufficiently (generally to
Uniform Determination of Death Act. at least 60 mm Hg) to stimulate spontaneous respirations.
In 1995, the American Academy of Neurology (AAN) Patients with lung disease may not tolerate this period of
published practice parameters for establishing brain apnea because of oxygen desaturation before achieving a
death in adult patients. The guidelines stress the need for high enough PaCO2 to stimulate respirations. In patients
determination of whole brain death and irreversible loss with chronic obstructive pulmonary disease, a higher target
of function. According to an evidence-based guideline PaCO2 may be necessary to stimulate respirations. Gener-
update by the AAN in 2010, there were no published ally, a good rule is to target a PaCO2 20 mm Hg higher
reports of recovery of neurologic function after the clini- than the patient’s baseline. Hypoxia should be avoided dur-
cal diagnosis of brain death had been established accord- ing apnea testing because it may result in exacerbation of
ing to the 1995 AAN practice parameters. neurologic injury in patients who are not brain dead.
The diagnosis of brain death needs to be made by a
physician. Some hospitals require brain death testing to Additional Confirmatory Tests
be done by a neurologist or neurosurgeon. Some states
require that two physicians make the determination. Confirmatory tests are not required for the diagnosis of
Brain death usually follows some form of neurologic in- brain death, which is a clinical diagnosis. However, in
jury, of which trauma is the most frequent cause. Other some European countries, confirmatory tests are manda-
etiologies include hypertensive hemorrhage, aneurysmal tory. Their use is recommended when the clinical exami-
hemorrhage, brain tumors, and anoxic brain injury. nation, including the apnea test, cannot be performed
There is no evidence regarding how many examina- completely or reliably; if the cause of brain death has not
tions are required or what time period of observation is been established; or if there is a questionable confounder
required before a declaration of brain death. There are mimicking brain death. These tests evaluate either cere-
four elements that are fundamental to all published brain bral function or intracranial blood flow. They each have
death criteria based on the Uniform Determination of limitations and should be used only in conjunction with
Death Act: (1) irreversibility, (2) absence of neurologic other established criteria for brain death.
function, (3) apnea, and (4) additional confirmatory tests. The most sensitive confirmatory test for brain death is
cerebral angiography. A lack of intracerebral filling at the
level of the carotid bifurcation or the circle of Willis sup-
Irreversibility
ports the diagnosis of brain death. This test is rarely used
Irreversibility requires determination of the mechanism because it is difficult to perform, requires administration
of injury to the brain and the anatomic findings to prove of contrast medium, and is expensive.
506 SECTION 16 Critical Care
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Index
A Abruptio placentae (Continued) Acute respiratory distress syndrome
Abdominal trauma risk factors, 291 (ARDS)
airway management options, 425 signs and symptoms, 291–292 case background, 470
case, 419 Accelerography, 107 causes, 471, 471t
resuscitation endpoints, 427, 428t Acetylcholinesterase defined, 470–471
damage control laparotomy, surgical anticholinergic drug and, 104–105 ECMO and, 472
objectives, 425–426 doses and durations, 104, 104t fluid restriction and, 473
definitive care options, 423–425, 424f inhibition techniques, 103–104 HFJV and, 472–473
evaluation, 424f inhibitors, 104 nitric oxide and, 473
injuries and abnormalities anticipated Acidemia, hyperkalemia and, 192 pathophysiology, 471
after, 419–422, 420t ACL. See Anterior cruciate ligament permissive hypercapnia and, 472
abdominal injuries, 422 Acquired factor inhibitors, 239 prone positioning and, 472
aortic injury, 421–422 Acquired pseudocholinesterase deficiency, recruitment maneuvers and, 472
blunt cardiac injury, 421 85, 85b sepsis and, 483, 483t
bowel injury, 422 disease related, 85 steroids and, 473
coagulopathy, 422 medication related, 85 ventilation/perfusion mismatch
diaphragmatic rupture, 421 Acromegaly and, 473
GCS and, 420–421, 421t airway management concerns, 92 ventilatory strategies, 471–472
hemothorax, 421 anesthetic considerations, 92 Acute vasoocclusive crisis, 257–258
hypothermia, 422 case background, 91 Addiction, pain and, 353–354
long bone fractures, 421 described, 91 Addison disease, 137–138, 138t
neurologic injury, 420–421 DI and, 93, 93b Adenotonsillectomy (AT)
orthopedic injuries, 421 postoperative concerns, 93 case background, 341
pelvic fractures, 421 symptoms, 91 indications, 341
penetrating wounds, 421 airway changes, 92b intraoperative management, 343
pneumothorax, 421 peripheral effects, 92b OSA and, 341, 342b, 342f
pulmonary contusion, 421 transsphenoidal surgical field and, 92–93 postadenotonsillectomy bleeding
rib fractures, 421 treatment, 91 management, 344, 344b
shock, 422 Acute chest syndrome (ACS), 258 postoperative admittance, 344
solid organ injuries, 422 Acute extravascular hemolytic transfusion postoperative problems, 343
spinal injury, 421 reaction, 231 premedication and, 342
systemic abnormalities, 422 Acute intravascular hemolytic transfusion preoperative evaluation, 342, 342b
TBI, 420–421 reaction (AIHTR), 230–231 Adrenal reverse, 139
thoracic injuries, 421–422 Acute isovolemic hemodilution (AIHD) Adrenal suppression, 138
intraoperative priorities, 428–429 accomplishment of, 246 !-Adrenergic blockers
massive transfusion protocol and, advantages of, 246b CAD and, 4, 53
427–428 described, 245 myocardial ischemia and, 3
postanesthesia goals, 429 patients suitable for, 246–247, 247b recommendations, 4
primary and secondary surveys and, performance of, 246b AHA. See American Heart Association
422–423 monitoring, 246 AIHD. See Acute isovolemic hemodilution
resuscitation fluid objectives, 426–427 removal, 246 AIHTR. See Acute intravascular hemolytic
anemia avoidance, 426 retransfusion, 246 transfusion reaction
coagulopathy treatment, 426 physiologic response to, 245–246, 246b Air embolism, 324-325. See also Venous air
hypovolemia avoidance, 426–427 Acute kidney injury (AKI) embolism
Abdominal wall defects acid-base balance and, 490–491 Airway
case, 313 AKIN and, 488, 489t burns and, 416–417
intraoperative management, 314 case background, 488 CPAP and, 68
gastroschisis CIN and CPR, pediatric and, 456–457, 456t
compared with omphalocele, 313, 314t described, 491 laryngoscopy and, 215–216, 219–220
preoperative concerns for, 313 pathogenesis, 491 management
surgical treatment for, 315 preventing, 491–492 abdominal trauma, 425
omphalocele risk factors, 491, 491t acromegaly, 92
compared with gastroschisis, 313, 314t CRRT and, 492 burns and, 416–417
preoperative concerns for, 313 problems, 493 during CPR, 463
surgical treatment for, 315 selection, 493 Difficult Airway Algorithm and, 211f
Abruptio placentae. See also Fetal distress defined, 488–489, 489t FESS and, 225
case background, 291 dialysis indications, 492, 492b thoracic trauma, 408
cesarian delivery for, 295–296, 296b nonrenal, 492 trauma standardized approach to, 422
coagulation changes in pregnancy and, renal, 492 preterm infant, 336, 338
292, 292b etiology, 490, 490t retinal detachment and, 201
described, 291 incidence and outcome, 489, 489t thermal upper airway injury, 416
diagnosis, 291–292 pathophysiology, 489–490 trauma and, 422
labor analgesia consultation, 295 RIFLE and, 488, 489t AKI. See Acute kidney injury
massive obstetric hemorrhage and, Acute Kidney Injury Network (AKIN), 488, AKIN. See Acute Kidney Injury Network
297–298 489t Alcohol neurolysis, 373, 373t
obstetric management, 292 Acute lung injury (ALI), 483, 483t Alcoholic cardiomyopathy, 13, 13t
placenta previa versus, 297t Acute renal failure. See Acute kidney injury Aldrete scoring system, 443, 444t
509
510 Index
ALI. See Acute lung injury Aorta (Continued) Asystole, 464–465, 465b
Allergic transfusion reactions, 231 TAVI and, 19–20 AT. See Adenotonsillectomy
Ambulatory surgery traumatic thoracic aortic injury, 405–406, Atlantoaxial instability, 350, 350b
aftercare centers and, 389 405b Atracurium, 100t
anesthetic choices, 379, 380t airway management pitfalls, 408 Atrial septal defects (ASDs), 326, 329,
appropriate surgery types for, 376–377 anesthetic drugs pitfalls, 408–409 329b
benzodiazepine and, 385 central line placement pitfalls, 408 Atrioventricular sepal defects (AV), 330,
cancellation or postponement, 379 chest radiograph, 405 332b
candidates, 376 clinical and anesthetic pitfalls, Atropine, 152
case background, 375 408–409 Autologous blood sources, 245, 250–251,
diabetic patients and, 376 contrast-enhanced CT scan, 405 250t. See also Preoperative autologous
discharge criteria, 387–388 CT angiography with three- blood donation
escort functions, 388b dimensional reformation, 405, 407f AV. See Atrioventricular sepal defects
guidelines, 388b diagnosis, 405–406, 405b Awake fiberoptic intubation, 86
empty stomach and, 377–378 diagnostic pitfalls, 408
evaluation, 378 mechanism of injury, 405
by internist before, 378–379 radiographic findings, 405b B
ex-preterm infants and, 376 site of injury, 405 Bacteria-contaminated transfusion, 232
fasting time and, 377 spinal cord ischemia pitfalls, 409 Balloon angioplasty, 162, 162b
general anesthesia contraindications, 379 suspicious of injury, 405 Balloon pump, intraaortic, 53
hospitalization after, 388–389 TEE, 405, 406, 406f Bare metal stent (BMS), 162, 162b
reasons for, 389b Aortic aneurysm Benzodiazepine, 385
ideal anesthetic, 379 case background, 161 Biliopancreatic diversion/duodenal switch
moderate sedation and, 384–385 cross-clamping and, 163–164 (BPD/DS), 179, 179f
motor vehicle operation and, 389 natural history of, 161 Birth physiologic changes, 450
nausea and vomiting, 385–387 postoperative analgesia and, 164 Bladder perforation, 171
factors associated with postoperative, preoperative evaluation and, 161–162, Blood loss compensation, 244–245
386b 162b Blood replacement
prophylaxis and treatment of preoperative medications and, 162–163 AIHD and, 245, 246b
postoperative, 386t surgery autologous blood sources and, 245
nerve block techniques anesthetic agents, 163 case background, 244
advantages and disadvantages, 381 monitoring, 163 cell salvage and, 247
complications, 382 TEE and, 163 hemoglobin concentration and, 245
postoperative pain control, 387 Aortic stenosis (AS) oxygen transport and, 244
premedication, 379 anesthetic management, 18–19 PABD and, 248
preoperative laboratory studies and, 378 aortic valve area and, 18, 18t Blood salvage, postoperative, 250
propofol and, 383 bradyarrhythmias and, 18 Blood transfusion
quality and, 389 case background, 17 avoiding homologous, 255, 255b
regional anesthesia etiology of, 17–18 JWs and, 252–253
advantages and disadvantages, 379–381 hemodynamic goals in, 19, 19t acceptable blood components, 254f
intravenous, 381–382 hypotension treatment and, 18 minor children and, 253
sedatives to supplement, 382 prognosis for, 17 Blunt cardiac injury
succinylcholine myalgias and, 385 sinus rhythm and, 18 abdominal trauma and, 421
TIVA and, 383–384, 384b supraventricular tachyarrhythmias thoracic trauma and, 403–405
tracheal intubation and, 382–383 and, 18 diagnosis, 403–404
volatile agents and, 385 symptoms, 17 perioperative management, 404–405,
American Heart Association (AHA), 455 TAVI anesthetic considerations, 19–20 404f
Guidelines for Cardiopulmonary Arrest, Aortic valve area, 18, 18t BMI. See Body mass index
461–462, 462f Apgar score, 454, 454t BMS. See Bare metal stent
American Society of Anesthesiologists (ASA) Apnea. See also Obstructive sleep apnea Body mass index (BMI)
Difficult Airway Algorithm, 210, 211f brain death and, 447–448, 505 defined, 175
DNR and, 468 Apneic oxygenation, 218 example, 176f
Anemia avoidance, 426 Aqueous humor dynamics, 196 obesity classification and, 176t
Aneurysm. See also Aortic aneurysm; ARDS. See Acute respiratory distress pediatric population and, 177t
Intracranial aneurysm syndrome Bowel injury, 422
clipping Arrhythmia. See also Bradyarrhythmias; BPD/DS. See Biliopancreatic diversion/
monitors indicated for, 77–78 Supraventricular tachyarrhythmias duodenal switch
rupture management during, 78 CHD and, 329, 329b Brachial plexus
SAH and, 77–78, 495b CHF, 16 anatomic structure, 266, 267f
Ankle block, 276, 276t AS. See Aortic stenosis block effects, 266–268
Anterior cruciate ligament (ACL), surgery ASA. See American Society of axillary, 268
anesthetic options, 271–273 Anesthesiologists infraclavicular nerve, 268
femoral nerve catheter and, 273 ASDs. See Atrial septal defects interscalene nerve, 266–268
nerves affected during, 271, 273t Asthma supraclavicular nerve, 268
Anticholinergics case, 432 case background, 266
acetylcholinesterase and, 104–105 anesthesia choices, 435 LAST
heart transplantation and, 51 challenges following anesthesia diagnosis, 269–270
Antiemetic therapy, 203 induction, 435 treatment, 270, 270b
Antiplatelet agents, 53 patient evaluation, 434–435 supraclavicular nerve block performance,
Anxiolytic premedication, 379 described, 432 269
Aorta. See also Endovascular aortic repair diagnosis, 432 surgical site and, 266–268
abdominal trauma and, 421–422 medications and, 433–434, 434t terminal branches, 266, 267t
blunt aortic injury management, 407–408 perioperative bronchospasm and, 435 ultrasound and, 269
CAD and, 53 PFTs and, 432–433, 433f, 433t Bradyarrhythmias, 18
coarctation of, 330 ventilation and, 434 Bradycardia, 458, 458t
Index 511
CHF. See Congestive heart failure Congenital heart disease (Continued) Coronary artery disease (Continued)
Child-Pugh score, 154–155, 156t pediatric CPR and, 458 reductase inhibitors, 53
Cholinergic crisis, 114–115 right-to-left shunting with reduced risk factors, 53b
Choroidal blood volume, 196 pulmonary blood flow treatment, 53
Chronic obstructive pulmonary disease anesthetic considerations, 328, 328b !-Adrenergic blockers, 53
(COPD), 432–433, 433f, 433t common intracardiac lesions, 327–328 antiplatelet agents, 53
CIEDs. See Cardiac implantable electronic complex lesions and TGA, 328 Coronary Artery Revascularization
devices hypercyanotic spells and, 327, 327t Prophylaxis (CARP) study, 10
Cimetidine, 152 tetralogy of Fallot, 327–328 Coronary perfusion pressure (CPP), 52
CIN. See Contrast-induced nephropathy surgical options, 328 Cortisol, 137–138
Cisatracurium, 100t systolic murmur differential diagnosis and, CPAP. See Continuous positive airway
Citrate toxicity, 233 324 pressure
Coagulation, 307 Congenital or acquired factor deficiency, CPP. See Cerebral perfusion pressure;
Coagulopathy. See also Perioperative 239 Coronary perfusion pressure
coagulopathies Congestive heart failure (CHF) CPR. See Cardiopulmonary resuscitation
abdominal trauma and, 422, 426 anesthetic management, 15–16, 16b Craniotomy
DIC, 292–293, 293b arrhythmia management, 16 anesthesia induced and maintained, 76
TURP and, 171–172 induction, 16 awake, 76
Coarctation of aorta, 330, 332b inotropic support, 16 case background, 70
Cobb method, 252, 253f maintenance, 16 cerebral autoregulation and, 70–71, 71b,
Complex regional pain syndrome (CRPS) monitoring, 16 71f
case background, 367 vasodilators, 16 intracranial pressure
diagnosis, 368–369 case background, 13 anesthetic agents and vasoactive drugs
etiology theories, 367 DCM etiologies and, 13–14 and, 71–73, 72t
nerve blocks and, 369 alcoholic cardiomyopathy, 13, 13t contributing factors, 71
signs and symptoms, 368 genetic form, 13 monitoring, 74
stages, 368, 368t inflammatory variety, 13 signs and symptoms, 73–74, 74b
acute or hyperemic, 368 noninflammatory variety, 13 treatment, 74, 74b
atrophic, 368 DCM pathophysiology and, 14–15, 14f sitting position and, 75–76
dystrophic, 368 backward failure, 14–15 VAE and
treatment, 369 forward failure, 14–15 detection, 75, 75b
type 1 and type 2, 367 ventricular failure manifestations, 15b treatment, 75, 75b
Computed tomography (CT) scan hemodynamic goals regarding, 15–16, Cricoid pressure, 152
aorta and, 405, 407f 15t Cricothyroid puncture ventilation, 212–213,
traumatic thoracic aortic injury and, 405, perioperative monitoring, 15 212f, 213f
407f Continuous positive airway pressure (CPAP), Cross-clamping, aortic, 163–164
Congenital diaphragmatic hernia (CDH) 68 CRPS. See Complex regional pain syndrome
anesthetic considerations, 318, 318b Continuous renal replacement therapy CRRT. See Continuous renal replacement
case background, 316 (CRRT), 492 therapy
clinical features, 317, 317b problems, 493 CSII. See Continuous subcutaneous insulin
embryology and pathophysiology, selection, 493 infusion
316–317 Continuous subcutaneous insulin infusion CT. See Computed tomography scan
fetal surgery techniques, 318 (CSII), 191 Cushing syndrome, 138, 138t
intraoperative and postoperative Contrast-induced nephropathy (CIN) CVP. See Central venous pressure
problems, 318 described, 491 Cyanide poisoning, 416
permissive hypercapnia and, 317–318 pathogenesis, 491
preoperative management of neonate preventing, 491–492
with, 317, 317b risk factors, 491, 491t D
PVR and, 317, 317b Controlled or deliberate hypotensive Dabigatran, 264
types of, 317t anesthetic technique Dantrolene, 118
Congenital heart disease (CHD) FESS and, 224 DBS. See Double-burst stimulation
anesthetic considerations, 324–325 medications, 255, 255t DCM. See Dilated cardiomyopathy
air embolism prevention, 324–325 risks and benefits of, 224–225 Defibrillators, 457, 457t. See also Implantable
endocarditis prophylaxis, 325, 325t COPD. See Chronic obstructive pulmonary cardioverter-defibrillator
extracardiac defects, 324 disease Delayed acquired transfusion-transmitted
arrhythmia following surgery, 329, 329b Coronary artery bypass grafting (CABG). See infections, 233
case background, 324 also Off-pump coronary artery bypass Delayed emergence
incidence, 324, 325t grafting apnea test and, 447–448
left-to-right shunting anesthetic technique, 54 case, 445
ASDs and, 326 case background, 52 brain death and, 447
common intracardiac lesions, 326 on-pump versus off-pump, 54–55 patient management, 446
lesion anesthetic considerations, Coronary artery disease (CAD) causes, work-up, and treatment, 445–446,
326–327, 327b !-Adrenergic blockade and, 4, 53 446t
PDAs and, 326 aorta and, 53 metabolic disorders, 445–446
VSDs and, 326 case background, 2 neurosurgical disorders, 446
lesion surgical repair and sequelae, 329–332 DES considerations, 4 other causes, 446
ASD, 329, 332b intraaortic balloon pump, 53 Delayed hemolytic transfusion reaction
AV, 330, 332b intraoperative monitoring, 4 (DHTR), 233
coarctation of aorta, 330, 332b myocardial ischemia, pharmacologic Deliberate hypotensive anesthetic technique
single ventricle and Fontan operation, alternatives, 3–4 FESS and, 224
331–332, 332b myocardial oxygen medications, 255, 255t
tetralogy of Fallot, 330, 332b demand determinants and, 2–3 risks and benefits of, 224–225
transposition of great arteries, 330–331, supply determinants and, 2 Depolarizing neuromuscular blockade
332b PCI and, 162, 162b case background, 95
VSD, 329–330, 332b preanesthetic concerns, 53–54 healthy patient, not waking up and, 95
Index 513
FESS. See Functional endoscopic sinus Gastroschisis Hip replacement, total, case (Continued)
surgery compared with omphalocele, 313, 314t risks and benefits, 262
Fetal circulation, 450, 451f preoperative concerns for, 313 stent thrombosis and, 261–262
Fetal distress diagnosis, 293–295 surgical treatment for, 315 HOCM. See Hypertrophic obstructive
Fetal heart rate (FHR) monitoring, 293, Glasgow Coma Scale (GCS), 420–421, 421t, cardiomyopathy
293b 500t Hunt-Hess clinical grade classification, 77,
early decelerations, 294 Glidescopes, 86 78t
good variability, 293–294, 293f Glucocorticosteroids, 137 Hypercalcemia
late decelerations, 294–295, 295f Glycine, 172 anesthetic care complication by,
poor variability, 293–294, 294f Glycopyrrolate, 152 134–135
variable decelerations, 295, 296f Graft-versus-host disease (GVHD), 233 clinical features of, 134, 135t
FFL. See Flexible fiberoptic laryngoscope Guidelines for Cardiopulmonary Arrest, treatment of, 134
FHR. See Fetal heart rate monitoring 461–462, 462f Hypercarbia, daytime, 178
Flail chest, 402b Gunshot wounds, 409–410 Hypercyanotic spells, 327, 327t
clinical symptoms, 402 GVHD. See Graft-versus-host disease Hyperfibrinolysis, 239
defined, 402 Hyperglycemic hyperosmolar states (HHS),
diagnosis, 399, 399f, 400f, 402 126–127, 127t
laboratory, 402 H management of, 127–128, 127b
management, 399–401, 401f Heart transplantation Hyperkalemia
monitoring, 402 immunosuppressive medications used acidemia and, 192
morbidity and mortality mechanisms, after, 48–49, 49t management of, 192t
398–399 noncardiac surgery after transfusion reactions and, 233
physical examination, 402 anesthetic techniques, 50 Hypertension, preeclampsia and, 288, 289t
radiologic examination, 402 anticholinergics, 51 Hypertensive disorders of pregnancy, 285,
treatment, 402 case background, 47 285b
Flexible fiberoptic laryngoscope (FFL), 210 emergency drugs, 50 Hypertrophic obstructive cardiomyopathy
FNHTR. See Febrile nonhemolytic intraoperative monitors, 50 (HOCM)
transfusion reaction preanesthetic concerns, 49–50 afterload and, 26, 26t
Food and Drug Administration (FDA), physiology of transplanted heart, 47–48, anatomic abnormalities in, 25
category ratings 48f anesthetic management, 27–28, 27t
of anesthetic agents, 302t reinnervation and, 48 in labor and delivery, 28
of drugs during pregnancy, 302t HeartMate II, LVAD and, 41, 41f case background, 25
Foreign body aspiration alarm conditions, 45–46, 45f contractility and, 26, 26t
case background, 345 battery life, 45 heart rate and, 26, 26t
described, 345 console parameters, 44–45, 44f hemodynamic goals in, 26, 26t
intraoperative management, 346–347, Hemoglobin concentration, 245 monitoring of, 26–27
347b Hemolytic crisis, 258 preload and, 26, 26t
foreign body ingestion, 347 Hemothorax treatment options, 26
postoperative concerns, 347 abdominal trauma and, 421 Hypocalcemia, 136
preoperative concerns, 345–346 thoracic trauma and, 398, 398b Hypotension, 18
presentation of, 345, 346f indications for thoracotomy, 398 Hypotensive anesthetic technique
Fractures splenic injury laparotomy and, 397 FESS and, 224
long bone, 421 symptoms, 398 medications, 255, 255t
pelvic, 421 Heparin risks and benefits of, 224–225
rib, 421 excess, 239 Hypotensive transfusion reaction, 232
Full stomach. See Pulmonary aspiration low-molecular-weight, 309 Hypothermia
Functional endoscopic sinus surgery (FESS) anesthetic experience with, 310 abdominal trauma and, 422
anatomic structures related to, 221, 222f pregnancy and, 309, 310, 310b case background, 437
case background, 221 recommendations for parturient taking, defined, 437
comorbidities and, 223–224, 223t 310, 310b grading of, 437
complications, 221–222, 222t Hepatic resection, major mechanisms leading to, 437
considerations, 222–223 case background, 154 mild intraoperative, benefits of, 439
described, 221 fluid management and, 159 physiologic consequences of, 438–439,
goals, 222–223, 223t incisions for, 158f 438t, 439f
hypotensive anesthetic technique and, 224 intraoperative considerations, in noncir- physiologic responses to, 437–438
postoperative pain reduction, 227–228 rhotic patient, 157–158 nonshivering thermogenesis, 438
regional anesthesia, 227–228, 227f, postoperative pain management, 160 shivering thermogenesis, 437–438
228f Pringle maneuver and, 159 vasoconstriction, 437
preoperative assessment, 223 right and left liver lobectomies and, 158, prevention, 439–440
Samter’s triad and, 223–224 159f central neuraxial blockade and, 440
surgical field improvement techniques, total caval isolation and, 159, 160 temperature monitoring sites, 439
225–226 transfusion avoidance and, 159f therapeutic, CPR and, 467
airway management, 225 Herniated nucleus pulposus, 361 TURP and, 172
emergence, 226 spinal stenosis versus, 361, 361t Hypovolemia avoidance, 426–427
maintenance of anesthesia, 225–226, HFJV. See High-frequency jet ventilation Hypoxemia, 475
226t HHS. See Hyperglycemic hyperosmolar OLV and, 63–64, 68, 63b, 64b
positioning, 225 states
preoperative medications, 225 High-frequency jet ventilation (HFJV),
ventilation choice, 226 472–473 I
Hip replacement, total, case, 261 ICD. See Implantable cardioverter-
anesthetic technique, 264–265 defibrillator
G lumbar plexus and femoral blockade, 265 ICP. See Increased intracranial pressure
Gabapentin, oral, 87 neuraxial anesthesia and, 262–264, 263t IDD. See Internal disk disruption
Gas bubble injection, 201 postoperative pain management, 265 Immunosuppressive medications,
Gastroparesis, 124 preoperative anesthetic considerations, 261 48–49, 49t
Index 515
Left ventricular assist device (Continued) Magnet, 35 MRI. See Magnetic resonance imaging
pacemaker perioperative management Magnetic resonance imaging (MRI) Multisystem organ dysfunction syndrome
and, 43 case background, 348 (MODS)
postoperative considerations, 46 described, 348 case background, 482
preanesthetic considerations, 42 Down syndrome and patient subgroups and, 486
Left ventricular end-diastolic pressure anesthetic alternatives, 350–351 sepsis compared with, 482
(LVEDP), 2 postanesthetic concerns, 351 treatment, 484–485
Left ventricular wall tension (T), 2, 52–53 magnetic field problems associated with, complications prevention, 485
Left-to-right shunting 348, 349b initiating infection control, 484
ASDs and, 326 patient-related problems associated with, organ function support and
common intracardiac lesions, 326 349, 349b replacement, 485
lesion anesthetic considerations, 326–327, physiologic monitors and equipment organ perfusion resuscitation
327b problems associated with, 348–349 and maintenance, 484–485
PDAs and, 326 Malignant hyperthermia (MH) Myalgias, succinylcholine, 385
VSDs and, 326 cart, 120b Myasthenia gravis (MG)
LES. See Lower esophageal sphincter case background, 116 case background, 111
LGS. See Laparoscopic gastric sleeve clinical characteristics of, 117, 117b, cholinergic crisis and, 114–115
Liver. See also Hepatic resection, major 117t classification, 111–112, 112t
cirrhosis dantrolene and, 118 described, 111
anesthetic agent choice and, 154–156, described, 116 diagnosis, 111–112
157t diagnosing, 120 extubation criteria and, 114, 114t
Child-Pugh score and, 154–155, 156t genetic testing for, 120 nondepolarizing muscle relaxants
complications of end-stage, 155t medicolegal issues in, 120 and, 113
described, 154 MMR and, 117 postoperative ventilation and, 115
patient evaluation, 154 NMS and, 120 rapid-sequence intubation and, 113–114
preoperative assessment of, 156f nontriggering agents and, 118b succinylcholine and, 113
lobectomies, 158, 159f pathophysiology of, 116 surgery patient optimization, 113
preterm infant and, 336 preparation for known case of, 118–120, transcervical thymectomy, anesthetic
Local anesthesia systemic toxicity (LAST) 120b technique, 113
diagnosis, 269–270 treating suspected case of, 118, 119t treatment alternatives, 112–113
treatment, 270, 270b triggering agents for, 117 Myocardial infarction (MI)
Long bone fractures, 421 Marshall Classification of Head Injury, 501t case background, 6
Low back pain Mask ventilation noncardiac surgery considerations, 6–9
case background, 360 case background, 204 additional drugs, 12
differential diagnosis, 360 predictors of difficult, 204, 205b anesthetic technique, 12
ESIs and, 362 Masseter muscle rigidity (MMR), 117 cardiac status, 9–10, 9b
evaluation, 360–361 Massive obstetric hemorrhage, 297–298 for case presented, 10
facet joints and, 362 Mechanomyography (MMG), 107 clinical risk assignment, 6–8, 7t
FBS and, 363–364 Meconium, 454 initial approach, 6
herniated nucleus pulposus and, 361 MEPs. See Motor evoked potentials intraoperative monitoring, 11, 12f
spinal stenosis versus, 361, 361t Metabolic equivalents (METs), 6, 7f management algorithm, 9f
IDD and, 362 Methadone, 87 METs, 6, 7f
incidence of, 360 Metoclopramide, 152 PCI and, 10–11, 11t
myofascial syndrome and, 361–362 METs. See Metabolic equivalents risk factors, 7b
oral medications, 363, 363t MG. See Myasthenia gravis surgical risk assignment, 8–9
SI disease and, 362 MH. See Malignant hyperthermia Myocardial ischemia
Lower esophageal sphincter (LES), 150 MI. See Myocardial infarction hemodynamic goals, to optimize coronary
anesthetic agents effects on, 152–153 Mineralocorticoid, 138 perfusion pressure, 3t
Lower extremity anesthesia Mitral stenosis intraoperative monitoring techniques, 54
ACL and afterload and, 22, 22t pharmacologic alternatives for treating,
anesthetic options, 271–273 anesthesia and, 23, 23t 3–4
femoral nerve catheter, 273 case background, 21 !-Adrenergic blockers, 3
nerves affected during surgery, 271, 273t contractility and, 22, 22t calcium-channel entry blockers, 4
ankle block, 276, 276t etiology of, 21–22 nitroglycerin, 3
block types and, 274–275, 275t heart rate and, 22, 22t phenylephrine, 4
case background, 271 hemodynamic goals in, 22, 22t Myocardial oxygen
postoperative posterior knee pain hypotension treatment and, 23 demand determinants, 2–3, 52–53
and, 275 intraoperative monitoring, 22–23 balance and, 2, 3f
regional anesthetic options, 275–276 pathophysiology of, 21–22, 21f basal oxygen requirements, 52
sensory innervation and, 271, 272f percutaneous mitral valve commissurot- contractility, 2, 53
LRS. See Lactated Ringer solution omy and, 24 heart rate, 2, 53
Lumbar plexus preload and, 22, 22t T, 2, 52–53
blocks, 274–275, 275t preoperative management, 22 supply determinants, 2, 52–53
hip replacement and, 265 RV failure therapies and, 23–24, 24b arterial oxygen content, 52
sensory distribution, 273t surgical mitral valve replacement balance and, 2, 3f
Lund-Browder chart, 412f and, 24 coronary anatomy, 52
LVAD. See Left ventricular assist device Mivacurium, 100t coronary perfusion pressure, 52
LVEDP. See Left ventricular end-diastolic MMG. See Mechanomyography heart rate, 52
pressure MMR. See Masseter muscle rigidity Myofascial syndrome, 361–362
Mode switching, 31
Moderate sedation, 384–385
M MODS. See Multisystem organ dysfunction N
Macintosh blade, 209–210 syndrome Nasogastric tubes (NGTs), 151–152
Magnesium Morbid obesity. See Obesity; NASPE/BPEG. See North American Society
sulfate, 287–288, 287b, 288t Superobesity of Pacing and Electrophysiology/British
therapy, 466 Motor evoked potentials (MEPs), 87 Pacing and Electrophysiology Group
Index 517
Nausea and vomiting. See also Postoperative Nitrous oxide Office-based anesthesia (Continued)
nausea and vomiting retinal detachment and, 201 physician, 391
ambulatory surgery, 385–387 tympanomastoidectomy and, 202–203 procedure, 392–393, 392b
factors associated with postoperative, NMBDs. See Neuromuscular blocking drugs obesity and, 393
386b NMS. See Neuroleptic malignant syndrome Off-pump coronary artery bypass grafting
prophylaxis and treatment of postoper- Nondepolarizing muscle relaxants, 113 (OPCAB)
ative, 386t Nondepolarizing neuromuscular blockade anesthetic considerations, 55
retinal detachment and, 201 case background, 99 on-pump versus, 54–55
Neonatal resuscitation disease states affect on, 101 OHS. See Obesity hypoventilation syndrome
apgar score and, 454, 454t factors augmenting, 115b Oliguria, 490t
birth physiologic changes and, 450 NMBDs and OLV. See One-lung ventilation
case background, 450 burns and, 101 Omphalocele
emergency equipment, 453b drug interactions and, 99–101, 101t compared with gastroschisis, 313, 314t
fetal circulation and, 450, 451f metabolic derangements effects on, 101 preoperative concerns for, 313
management, 450–453, 452f properties of, 99, 100t surgical treatment for, 315
meconium and, 454 skeletal muscle relaxation and, 99 One-lung ventilation (OLV)
oxygen administration, 453, 453t other drugs affect on, 101 anesthetic evaluation before, 57–58
respiration and heart rate, assessment Nondepolarizing neuromuscular blockade, bronchial blockers, 59
parameters, 451, 452b antagonism of case background, 57
Neostigmine, 104, 104t acetylcholinesterase and complications following, 64–65, 65b
Nerve block anticholinergic drug and, 104–105 DLT
ambulatory surgery and doses and durations, 104, 104t left or right side, 59
advantages and disadvantages, 381 inhibition techniques, 103–104 placement, 59–60
complications, 382 inhibitors, 104 placement problems, 62
brachial plexus and, 269 case background, 103 positioning assessment, 60–62, 60f, 62f
CRPS and, 369 principles underlying, 103 hypoxemia and, 63–64, 68, 63b, 64b
Neuraxial analgesia sugammadex and, 105 indications, 58
advantages of, 356b Nonshivering thermogenesis, 438 lateral decubitus position complications
local anesthetics and, 357–358, 358t Normal neuromuscular transmission, 95–96, and, 62–63, 62b
opioids and, 357 96f noninvasive monitoring of oxygenation, 58
parenteral opioid analgesia versus, 356, North American Society of Pacing and perfusion and ventilation effects during,
356b, 356t Electrophysiology/British Pacing and 63, 63b
Neuraxial anesthesia Electrophysiology Group (NASPE/ pleural drainage and, 64
anesthetic experience with, 310 BPEG), 30–31, 30t single-lumen endotracheal tubes, 59
anticoagulation therapy and, 262–264, 263t thoracostomy tube and, 64
dabigatran, 264 OPCAB. See Off-pump coronary artery
factor Xa inhibitors, 264 O bypass grafting
INR, 264 OBA. See Office-based anesthesia Open cardiac massage, 467
Neuroleptic malignant syndrome (NMS), 120 Obesity. See also Superobesity Open eye injury. See also Intraocular pressure
Neurology BMI and, 175, 176f, 176t, 177t anesthetic considerations, 196–197, 197b
abdominal trauma and, 420–421 case background, 175 case background, 196
alcohol and phenol neurolysis, 373 classification emergent or urgent repair, 198
brain death and, 505 body fat percentage, 175, 177t succinylcholine and, 197–198, 198t
CEA and, 80–81 pediatric population and, 175, 176f, 177t Opioid
trauma and, 424f surgical literature, 176t extended-duration, 371t
Neuromuscular blocking drugs (NMBDs) WHO, 175, 176t neuraxial analgesia and, 357
neuromuscular blockade monitoring OBA and, 393 parenteral opioid analgesia, 356, 356b,
and, 106 OHS and, 178 356t
nondepolarizing OSA and rapid-onset, 372, 372t
burns and, 101 diagnosis, 178 set-dose extended-release, 371
drug interactions and, 99–101, 101t pathophysiology, 177–178 use prevention, 355–356
metabolic derangements effects on, 101 STOP-Bang and, 178, 178t Orthopedic injuries, 421
properties, 99, 100t surgical procedures, 178–180 OSA. See Obstructive sleep apnea
skeletal muscle relaxation and, 99 BPD/DS, 179, 179f Oxygen transport, 244
Neuromuscular junction monitoring laparoscopic adjustable gastric banding,
case background, 106 179f, 180
devices, 107–108 LGS, 179f, 180 P
accelerography, 107 Roux-en Y gastric bypass, 179–180, 179f PABD. See Preoperative autologous blood
EMG, 107 Obesity hypoventilation syndrome donation
KMG, 108 (OHS), 178 PAC. See Pulmonary artery catheter
MMG, 107 Obstructive sleep apnea (OSA) Pacemakers
peripheral nerve stimulators, 107 AT and, 341, 342b, 342f best practices, 32–33
NMBDs and, 106 associated conditions, 342b case background, 29
no response to train-of-four stimulation diagnosis, 178 codes, 30–31, 30t
and, 109–110 pathophysiology, 177–178, 341, 342b, 342f CPR and, 466
principles, 106 STOP-Bang and, 178, 178t determination of dependence on, 34
stimulation patterns, 108–109 Oculocardiac reflex, 201 determining type of, 33, 33f
DBS, 109, 109f Office-based anesthesia (OBA) ECT and, 83–84
PTF and PTC, 109, 109f advantages and disadvantages, 390–391 EMI and, 33–34
single twitch, 108 anesthetic techniques and, 393 how they work, 29–30
tetanic stimulation, 108, 108f case background, 390 ICDs and, 32
train-of-four, 108–109, 108f commonly performed procedures, 392b indications for implantation, 29, 29b
supramaximal stimulus and, 107 defined, 390 interrogation of, 35, 36b
NGTs. See Nasogastric tubes issues for safe practice, 391–393 LVAD perioperative management
Nitric oxide, ARDS and, 473 office, 391 regarding, 43
Nitroglycerin, 3 patient, 391–392, 392b magnet use on, 35
518 Index
TEE. See Transesophageal echocardiography Thromboelastogram, 307, 308f Transfusion reaction (Continued)
TEF. See Tracheoesophageal fistula Thromboelastography (TEG), 240, 240f, AIHTR, 230–231
TEG. See Thromboelastography 241f allergic transfusion reactions, 231–232
Teratogens, 301–303 Thrombotic events, 239 bacteria-contaminated transfusion, 232
Tetanic stimulation, 108, 108f Thyroid disease citrate toxicity, 233
Tetralogy of Fallot (TOF), 330, 332b case background, 129 delayed acquired transfusion-
CHD hormone production and, 129 transmitted infections, 233
lesion surgical repair and sequelae, 330, problems associated with, 130b delayed reactions, 233
332b surgery DHTR, 233
right-to-left shunting and, 327–328 complications of, 130–131, 131b FNHTR, 231
TGA. See Transposition of great arteries intraoperative anesthetic considerations GVHD, 233
Thermal upper airway injury, 416 for, 131–132 hyperkalemia, 233
Third-trimester bleeding, 291, 292b preoperative evaluation for, 130 hypotensive transfusion reaction, 232
Thoracic trauma regional anesthesia and, 132, 132f of immediate, 230–233
blunt aortic injury management, 407–408, thyrotoxicosis and, 129 other acute reactions, 233
408t Thyroid storm, 129–130, 130t septic transfusions, 232
blunt cardiac trauma, 403–405 Thyrotoxicosis, 129 TACO, 233
diagnosis, 403–404 Tight glucose control, 126 TRALI, 232
perioperative management, 404–405, TIVA. See Total intravenous anesthesia immediate, 230
404f TOF. See Tetralogy of Fallot; Train-of-four incidence of, 230
cardiac tamponade and, 403b Tolerance, pain, 353–354 management, 233–234
case background, 396 Total body surface area (TBSA), 411–412, prevention, 234
consequences, 396 412f Transfusion-associated circulatory overload
flail chest, 402b Total caval isolation, 159, 160 (TACO), 233
clinical symptoms, 402 Total intravenous anesthesia (TIVA), Transfusion-related lung injury (TRALI),
defined, 402 383–384, 384b 232
diagnosis, 399, 399f, 400f, 402 Tourniquets, 259 Transmediastinal gunshot wounds, 409–410
laboratory, 402 Tracheal intubation Transposition of great arteries (TGA), 328,
management, 399–401, 401f methods to verify successful, 213, 213b 330–331, 332b
monitoring, 402 most reliable, 213 Transsphenoidal hypophysectomy. See also
morbidity and mortality mechanisms, reliable, 213 Acromegaly
398–399 very reliable, 213 case background, 91
physical examination, 402 respiratory failure and, 474 DI and, 93, 93b
radiologic examination, 402 Tracheoesophageal fistula (TEF) postoperative concerns, 93
treatment, 402 associated anomalies and, 319, 320t transsphenoidal surgical field and, 92–93
hemothorax, 398, 398b case background, 319 Transtracheal ventilation, 212–213, 212f,
indications for thoracotomy, 398 described, 319, 320f 213f
splenic injury laparotomy and, 397 intraoperative management, 320–321, Transurethral resection of prostate (TURP)
symptoms, 398 321b anesthetic options, 172–173, 172b
pathophysiology, 397f postoperative concerns, 321 complications, 171–172, 171b
pneumothorax, 398, 398b preoperative concerns, 319–320 bladder perforation, 171
diagnosis, 398 types, 320t bleeding, 171
differential diagnosis, 398 typical presentation, 319 coagulopathy, 171–172
signs and symptoms under anesthesia, VACTERL association and, 320t hypothermia, 172
398 Train-of-four (TOF) toxicity of irrigation fluids, 172
splenic injury laparotomy and, 397 neuromuscular junction monitoring and, transient bacteremia and septicemia,
surgery prioritization, 406–407 108–109, 108f 172
transmediastinal gunshot wounds and, no response to, 109–110 glycine and, 172
409–410 TRALI. See Transfusion-related lung irrigating fluids used for, 172
traumatic hemopericardium, 401–403 injury regional anesthesia, 172–173
traumatic thoracic aortic injury, 405–406, Transcatheter aortic valve implantation benefits, 172b
405b (TAVI), 19–20 sensory innervation and, 173, 173b
airway management pitfalls, 408 Transcervical thymectomy, 113 sodium level and, 173
anesthetic drugs pitfalls, 408–409 Transesophageal echocardiography (TEE) syndrome
central line placement pitfalls, 408 aortic aneurysm surgery and, 163 cardiovascular effects, 170, 171b
chest radiograph, 405 EAR and, 168 case background, 170
clinical and anesthetic pitfalls, myocardial ischemia and, 54 central nervous system effects, 170, 171b
408–409 traumatic thoracic aortic injury and, 405, described, 170–171
contrast-enhanced CT scan, 405 406, 406f minimally invasive modalities for, 174
CT angiography with three- Transfusion surgery for minimizing incidence
dimensional reformation, 405, 407f AIHD and, 246 of, 173
diagnosis, 405–406, 405b avoiding homologous, 255, 255b treatment, 170–171
diagnostic pitfalls, 408 hepatic resection and, 159f Transversus abdominis plane (TAP) block,
mechanism of injury, 405 JWs and, 252–253 193, 193f
radiographic findings, 405b acceptable blood components, 254f Trauma. See also Abdominal trauma;
site of injury, 405 minor children and, 253 Thoracic trauma
spinal cord ischemia pitfalls, 409 massive transfusion protocol, 427–428 definitive care options, 423–425, 424f
suspicious of injury, 405 PABD and, 250 standardized approach to, 422–423
TEE, 405, 406, 406f SCD and, 258–259 airway maintenance, 422
Thoracoscopy. See Video-assisted Transfusion reaction breathing and ventilation, 423
thoracoscopy blood products causing, 230 cervical spine protection, 422
Thoracostomy tube, 64 case background, 230 circulation with hemorrhage control,
Thoracotomy, 64–65, 65b delayed, 230, 233 423
Three-in-one blocks, 274–275, 275t etiologies and presentations, 230–233 disability, 423, 424f
Thrombocytopenia. See Pregnancy, acute extravascular hemolytic environmental control, 423
thrombocytopenia in transfusion reaction, 231 exposure, 423
522 Index