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N EU R O A N E S T H E S I A
NEUROANESTHESIA
A P R O B L E M- B A S E D L E A R N I N G A P P R O A C H
EDITED BY
David E. Traul, MD
SECTION HEAD OF NEUROANESTHESIA
DE PA RTM E N T OF A N E ST HE SI OLO GY
CLEVELAND CLINIC
CLEVELAND, OHIO
and
Irene Osborn, MD
CLINICAL PROFESSOR OF ANESTHESIOLOGY
DIRECTOR OF NEUROANESTHESIA DIVISION
ALBERT EINSTEIN COLLEGE OF MEDICINE
BRONX, NEW YORK
1
1
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Printed by Sheridan Books, Inc., United States of America
For Christine, Andrew and Lauren
In loving memory of my father
DET
To my teachers, my trainees and my patients who have taught me so much
Irene Osborn
D I G I TA L M E D I A AC C O M PA N Y I N G T H E B O O K
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vi
CONTENTS
vii
CONTRIBUTOR S
ix
Marco Maurtua, MD, CHSE Wael Saasouh, MD
Department of General Anesthesia Clinical Fellow in Neuroanesthesiology
Cleveland Clinic Cleveland Clinic
Cleveland, Ohio Cleveland, Ohio
Abigail E. Meigh, DO Aleka Scoco, MD
Anesthesiologist Department of Neurosurgery
St. Joseph’s Regional Medical Center Albert Einstein College of Medicine
Paterson, NJ Montefiore Medical Center
Bronx, NY
Margaret M. Mora, MD
Fellow in Neuroanesthesia Tod B. Sloan, MD, MBA, PhD
University of Michigan Health System Professor Emeritus
Ann Arbor, MI University of Colorado School of Medicine
Aurora, Colorado
Jocelin Jones Molina, MD
Resident in Anesthesiology Joanne Spaliaras, MD
Albert Einstein College of Medicine Assistant Professor of Anesthesiology
Montefiore Medical Center Albert Einstein College of Medicine
Bronx, New York Bronx, NY
Michael R. Moore, MD Allison Spinelli, DO
Department of General Anesthesia Assistant Professor of Anesthesiology
Cleveland Clinic Albert Einstein College of Medicine
Cleveland, Ohio Montefiore Medical Center
Bronx, NY
Edward C. Nemergut, MD
Professor of Anesthesiology and Neurological Surgery David E. Traul, MD, PhD
University of Virginia School of Medicine Department of General Anesthesia
Charlottesville, VA Section Head of Neuroanesthesia
Cleveland Clinic
Irene Osborn, MD
Cleveland, Ohio
Clinical Professor of Anesthesiology
Albert Einstein College of Medicine Hui Yang, MD, PhD
Director, Division of Neuroanesthesia General Anesthesiology
Montefiore Medical Center Cleveland Clinic
Bronx, New York Cleveland, Ohio
Thomas N. Pajewski, PhD, MD Matthew Wecksell, MD
Associate Professor of Anesthesiology and Neurological Chief, General Anesthesiology
Surgery Department of Anesthesiology
Director of Neuroanesthesiology Associate Professor of Anesthesiology and Neurosurgery
University of Virginia Health System Westchester Medical Center
Charlottesville, Virginia Advanced Physician Services Member of the Westchester
Medical Center Health Network
Shobana Rajan, MD
Valhalla, New York
Staff Anesthesiologist
Cleveland Clinic Lerner College of Medicine
Cleveland, Ohio
Lauryn R. Rochlen, MD
Staff Anesthesiologist
Neuroanesthesia Fellowship Director
University of Michigan Health System
Ann Arbor, MI
x • C ontrib u tors
SECTION 1
ONCOLOGIC PROCEDURES
1.
SUPRATENTORIAL TUMOR S
David E. Traul and Rachel Diehl
WH AT MO N I TO R S A R E A P P RO P R I AT E I N T H I S WH AT I S T H E D I FFE R E N T I A L
PAT I E N T F O R H E R S U RG E RY ? S H O U L D D I AG N O S I S F O R D E L AY E D E M E RG E N C E
YO U P R E M E D I C AT E T H E PAT I E N T F O R H E R FRO M C R A N I OTO MY ?
N E RVO US N E S S ? WH AT A R E T H E G OA L S
F O R I N D U C T I O N A N D M A I N T E NA N C E The patient is now fully awake and alert and is transferred to
O F A N E S T H E S I A F O R C R A N I OTO M I E S ? the neurological intensive care unit for further monitoring.
The patient is anesthetized and positioned for surgery. Her
head is placed in Mayfield pins and the incision is made. The DISCUSSION
surgeon requests mannitol be administered.
I N C I D E N C E A N D P R E S E N TAT I O N
WH E N I S T H E B E S T T I M E TO G I V E M A N N ITO L ,
The Central Brain Tumor Registry of the United States
A N D H OW D O E S I T L OWE R I N T R AC R A N I A L
(CBTRUS) reported 379,848 cases of primary brain and other
P R E S S U R E ( I C P)? WH AT M A I N T E NA N C E FLU I D S
central nervous system (CNS) tumors from 2010 to 2014.1 The
WO U L D YO U US E A N D WH Y ?
overall incidence rate for all primary brain and CNS tumors
After the bifrontal craniotomy is performed and the or- was 22.64 per 100,000 population, with the highest incidence
bital bar removed, the surgeon states that the brain is still rate (40.82) reported in persons older than 40 years of age.
3
Normal Neuronal Function increased ICP may be temporarily alleviated by interventions
>50ml/min/100g Normal EEG such as raising the patient’s head, administration of IV hyper-
tonic fluids, or placement of an intraventricular drain.
Any comorbidity such as cardiovascular disease, respira-
Dysfunction of Neurons
tory disease, or renal disease should be adequately evaluated
<18ml/min/100g EEG slowing
with further testing completed as warranted by the spe-
cific patient requirements. Previous surgeries and anesthetic
Delayed Cell death experiences are important data prior to proceeding with sur-
<10ml/min/100g Flat EEG gery. Since the patient may develop significant bleeding during
the procedure, a complete blood count should be obtained.
Rapid Cell Death Other labwork should include a basic chemistry panel and
<6ml/min/100g Membrane Failure
coagulation studies. Patients with primary brain tumors or
metastatic disease are at a higher risk of thrombotic events,
Changes in cerebral blood flow (CBF) and corresponding
Figure 1.1.
and the use of anticoagulation therapy must be known prior
electroencephalogram (EEG) findings. Normal CBF is >50 mL/min per to surgery. Antiplatelet medications should be discontinued
100 g of tissue. EEG changes may be detected when CBF <18 mL/min 7–10 days prior to surgery. Warfarin should also be discon-
per 100 g of tissue, with cell death occurring at a CBF rate <10mL/min tinued prior to surgery, but anticoagulation may be bridged
per 100 g.
with low-molecular-weight heparin. Neuroimaging with comp
uterized tomography (CT) and MRI should be reviewed to
assist in developing a differential diagnosis and to formulate
Most of these tumors were nonmalignant (68.5%), and the
the anesthetic plan.
median age at diagnosis was 59 years. Overall, meningioma
was the most common reported histology at 36.8%, followed
by pituitary (16.2%) and glioblastoma (14.9%). The majority Vascular access and monitoring
of all tumors (>70%) were supratentorial.
Although the exact incidence of brain metastases is un- Adequate vascular access should be obtained with at least two
known, intracranial metastases from systemic malignancies large-bore peripheral IV lines. Central venous access may be
comprise the majority of brain tumors, with up to one-third justified if there is a potential for significant blood loss, in
of all cancer patients affected.2 The most common systemic patients with extensive cardiac or pulmonary comorbidities,
cancers with intracranial metastases are melanoma, lung when the risk of venous air embolism is high, or in patients
cancer, and renal cancer.3 without satisfactory peripheral access. An arterial catheter
Patients with supratentorial tumors may present with a for continuous BP monitoring should be placed in addition
wide variety of signs and symptoms depending on the location to standard monitors. Placement of the arterial catheter prior
of the tumor and its histological type. Neurological symptoms to induction may be warranted in patients with large tumors
from high-grade gliomas and brain metastases tend to man- and in situations where there is a large mass effect or increased
ifest over a shorter time course than symptoms from lower ICP. A urinary catheter should also be placed.
grade tumors. Generalized symptoms may include headache, Anxiolytics should be used with caution preopera-
nausea/vomiting, and neurocognitive dysfunction, and the tively in patients with supratentorial tumors. Sedation from
patient may have signs of increased ICP. Focal deficits may anxiolytics (such as midazolam) puts the patient at risk for
also be present, such as weakness, sensory loss, and aphasia. hypercapnia, hypoxemia, and airway obstruction that may
Seizures, either focal or generalized, are often the presenting lead to increases in PaCO2, cerebral blood flow (CBF), and
symptom and are more common in low-grade tumors.4 ICP. However, patients presenting for tumor resection may
have very high anxiety levels and associated hypertension that
increases CBF and worsens an otherwise compensated ele-
P R EO P E R AT I VE A N E S T H E S I A vated ICP. Therefore, use of preoperative anxiolytics should
C O N S I D E R AT I O N S be used on a case-by-case basis and only in a monitored set-
History and physical ting. Preoperative corticosteroids used for mass effect and an-
ticonvulsant therapies should be continued the day of surgery,
Patients with supratentorial tumors quite often present for ur-
gent, if not emergent, surgical resection. Therefore, a complete
preoperative assessment is not always feasible. When possible, P E R I O P E R AT I VE A N E S T H E S I A
the patient should be optimized as much as possible. History C O NS I D E R AT I O NS
and physical examination should include a full neurologic Induction of anesthesia
evaluation that includes mental status, cranial nerve function,
motor and sensory testing, reflexes, and coordination testing The goals of anesthesia induction for patients undergoing
that is documented prior to surgery in order to properly as- resection of supratentorial tumors are to maintain adequate
sess any postoperative deviations. Signs of increased ICP ventilatory control (avoiding hypoxemia and hypercapnia),
including altered mental status, papilledema, and hyperten- suppress sympathetic output and hypertension, and minimize
sive bradycardia should be assessed. If present, symptoms of cerebral venous outflow obstruction. This can be achieved by
4 • O ncologic P rocedures
adequately pre-oxygenating the patient followed by adminis- of cerebral ischemia.8,13 However, unlike volatile anesthetics,
tration of propofol (1–2 mg/kg) combined with fentanyl (1–2 awakening times with IV agents are often more difficult to
µg/kg) or remifentanil (1 µg/kg). Etomidate (0.2–0.4 mg/kg) predict.
may be substituted for propofol in patients with co-existing Opioid infusions (fentanyl, remifentanil, alfentanil) during
cardiac dysfunction or hemodynamic instability. intracranial surgery are particularly useful as they decrease the
Nondepolarizing muscle relaxants (NDMRs) have amount of volatile agent required to provide adequate anes-
minimal direct effect on cerebral metabolic rate, ICP, or thesia and therefore minimize the effects on CBF and ICP.
CBF. Typically, middle-to short-acting NMDRs such as Opioids also help blunt the hemodynamic response to head
rocuronium, vecuronium, or cisatracurium are used for in- pinning. Remifentanil has become a very popular opioid to
duction and maintenance of muscle relaxation during intra- use in intracranial surgery due to its short context-sensitive
cranial procedures. Pancuronium is usually avoided due to half-life and minimal effects on CBF and ICP.17 Additionally,
its long-term effect combined with its vagolytic activity that the use of remifentanil is associated with a more rapid emer-
may increase cardiac output, thereby increasing CBF and ICP. gence when compared to fentanyl.18,19
Succinylcholine may be used in the setting of rapid intubations Typically, at our institution, patients undergoing elec-
or potential difficult airways, but has several disadvantages for tive intracranial procedures are maintained with 0.5 MAC
routine use. First, succinylcholine’s depolarization of acetyl- volatile anesthetics with an opioid infusion (remifentanil or
choline receptors results in an efflux of potassium, which, in fentanyl) and muscle paralysis. Total IV anesthesia (TIVA)
the setting of profound muscle weakness or immobility, may with propofol/ remifentanil infusions is considered when
produce life-threatening hyperkalemia. Additionally, succi- difficulties with elevated ICP are anticipated.
nylcholine can cause transient increases in ICP; however if co-
administered with an IV agent (i.e., propofol) this is usually
Management of increased ICP
not clinically significant. Consideration should be given to
reports that the duration of N-Methyl-D-aspartate (NMDA) The cranial vault is a rigid, enclosed space with the volume of
muscle blockade is shortened by long-term use of anticonvul- the brain (85%), cerebrospinal fluid (10%), and blood (5%)
sant agents such as phenytoin and carbamazepine.5,6 determining the ICP. Normally, the ICP is 8–12 mm Hg.
Patient positioning should be evaluated prior to incision Since CPP depends on ICP, increased ICP puts the cerebral
to optimize jugular venous drainage and to avoid excessive tissue at risk for ischemia. Increases in volume of any one of
hyperflexion or extreme lateral extension of the head. Pinning the three components will result in increased ICP unless the
of the head in a holder device can produce a profound no- volume of another component is decreased. Therefore, normal
ciceptive stimulus and should only be performed when the ICP can be maintained in the presence of a supratentorial
patient has received adequate analgesia by local anesthetic in- tumor via decreasing CSF volume (displacement or absorp-
filtration or bolus administration of remifentanil or fentanyl. tion) and/or decreasing cerebral blood volume. However, at
If a sympathetic response does occur with head pinning, he- some point, elastance (ΔP/ΔV) in the system is maximized,
modynamic control can be regained with IV bolus of propofol and further increases in the size of the tumor (or edema) will
or an antihypertensive agent such as esmolol. cause the ICP to rise precipitously.
The anesthesiologist has several techniques at her disposal
to reduce ICP and promote adequate blood flow and surgical
Maintenance of anesthesia
conditions. When possible, avoidance of elevated ICP is best
The primary goals of anesthesia maintenance during resection done by raising the head of the bed and removing any com-
of supratentorial tumors are to control cerebral homeostasis pression on the jugular veins. Administration of IV steroids
via control of CBF and cerebral metabolic rate (CMR) and to (dexamethasone 4 mg every 6 hours) can also help prevent
provide a neuroprotective environment by decreasing cerebral increased ICP by reducing tumor-associated edema.20 Other
energy demands and minimizing areas of ischemia and edema. intraoperative interventions, such as avoiding high PEEP
The optimal anesthetic maintenance regimen required to (which may limit venous return) and ensuring adequate
achieve these goals is a subject of much debate, with the greatest muscle relaxation will also help prevent rises in ICP. When
controversy centered on the use of volatile agents versus IV increased ICP is already present, administration of osmotic
agents as maintenance anesthesia for intracranial procedures. agents can reduce brain size by decreasing interstitial water.
To date, there has been no prospective trial that definitively Mannitol is an osmotic diuretic that reduces interstitial water
favors the clinical outcomes of one technique over the other by increasing plasma oncotic pressure. Mannitol should be
in elective intracranial procedures.7–12 The advantages of vo- given as a bolus (1 g/kg body weight) around the time of in-
latile agents consist in their predictability, their titratability, cision and can lower the ICP in 1–5 minutes with peak effect
and their ability for rapid emergence. The drawback of using seen between 20 and 60 minutes.20 The effects of mannitol last
volatile agents for intracranial procedures is their ability to in- 2–3 hours, and repeat administration may actually worsen ce-
crease CBF and ICP13,14; however, this effect can be minimized rebral edema in an increase in ICP.21 Hypertonic saline and
by using lower mean alveolar concentrations (MAC) and furosemide are also effective in reducing ICP and facilitating
mild hyperventilation.14–16 IV anesthetics are an attractive op- surgical exposure.
tion for intracranial surgery since they decrease in both CBF The CMR is another important determination of CBF,
and CMR, thereby lowering ICP without increasing the risk and therefore ICP. Due to flow– metabolism coupling,
1. S upratentorial T umors • 5
Table 1.1. EFFECTS OF COMMON INHALATIONAL Blood flow and CPP
AGENT ON CEREBRAL BLOOD FLOW (CBF),
CEREBRAL METABOLIC RATE (CMR), AND Normal neuronal function in the healthy adult requires a
INTRACRANIAL PRESSURE (ICP) CBF of 50 mL/min per 100 g of tissue (Figure 1.1). CBF is
regulated at the level of the cerebral arteriole and is dependent
VOLATILE AGENT CBF CMR ICP on forward pressure gradient and PaCO2. The pressure gra-
dient is the result of CPP, which is determined by the equation
Halothane ↑↑ ↑→ ↑→
CPP = MAP –ICP. Cerebral autoregulation keeps CBF rela-
Isoflurane ↑→ ↓ ↑→ tively constant throughout a range of CPP of 50–150 mm Hg
via alterations in vasomotor tone. When CPP is inadequate,
Sevoflurane ↑→ ↓↓ → neuronal dysfunction occurs at CBF of less than 18 mL/min
Desflurane ↑→ ↓↓ ↓→ per 100 g of tissue and delayed cell death is seen when CBF is
less than 10 mL/min per 100 g of tissue.
Nitrous oxide ↑↑ ↓→ ↑↑
Changes in CBF (and therefore ICP) with isoflurane, sevoflurane, and desflurane Fluid therapy
depend on concentrations administered, with higher concentrations causing a
vasodilatory effect and therefore increasing CBF. Some of the vasodilatory effects Another area of debate in neurosurgery procedures is the
on ICP may be attenuated with hyperventilation.
choice fluid replacement therapy for intracranial surgery. As
the integrity of the blood–brain barrier is often compromised
in patients undergoing surgical resection of supratentorial
reductions in CMR will cause a parallel reduction in CBF, tumors, administration of large volumes of IV fluids is thought
and this relationship can be of benefit to the anesthesiolo- to contribute to cerebral edema. However, maintaining
gist. Hypothermia, for instance, decreases CMR by approxi- normovolemia and avoiding hypotension are important
mately 6% for every 1°C decrease in temperature. However, goals for successful surgical outcome. Dextrose-containing
due to the risks of even mild hypothermia in the surgical solutions are typically avoided in intracranial procedures as
setting (increased infection rate, coagulation disorders), hyperglycemia has been shown to worsen outcomes of cerebral
this technique is seldom used in intracranial surgery. Both ischemia.22–24 Hypotonic solutions, such as lactated Ringer’s
inhalational and IV anesthetics can decrease CMR and (273 mOsm/L), are often avoided since they are thought to
lower ICP (Table 1.1). Since all inhalational agents are exacerbate cerebral edema. Normal (0.9%) saline is slightly hy-
also vasodilators, the relationship between reduction in pertonic (308 mOsm/L), which may improve cerebral edema
CMR and MAC concentrations is not linear. Reduction in and is typically the fluid of choice for intracranial procedures.
CBF by volatile agents is more pronounced at lower MAC Colloids are also suitable alternatives for fluid replacement
(<0.5) concentrations, where flow– metabolism coupling since their ability to increase plasma oncotic pressure could
predominates. At higher MAC concentrations, the vasodil- potentially decrease brain edema.
atory property of volatile agents predominates and balances
out the reduction in CBF. IV agents, on the other hand, re-
duce CMR and are vasoconstrictors (Table 1.2). The notable E M E RG E N C E FRO M A N E S T H E S I A
exception is ketamine, which increases CMR, CBF, and ICP. The anesthetic goals at the end of intracranial surgery are a rapid
emergence and extubation in the setting of controlled hemo-
dynamic and respiratory parameters. Prior to extubation, the
Table 1.2. EFFECTS OF COMMON INTRAVENOUS PaCO2 should be allowed to gradually rise to normal levels,
AGENTS ON CEREBRAL BLOOD FLOW (CBF), adequate reversal from neuromuscular blockade should be de-
CEREBRAL METABOLIC RATE (CMR), AND termined, and the patient should be normothermic. Coughing
INTRACRANIAL PRESSURE (ICP) or “bucking” on the endotracheal tube can elevate ICP and
may be prevented with the continuation of remifentanil in-
INTRAVENOUS AGENT CBF CMR ICP
fusion or with the administration of IV lidocaine (0.5–1 mg/
Propofol ↓↓ ↓↓ ↓↓ kg). Hypertension should be promptly treated with esmolol or
other IV agents, and persistent hypertension may necessitate
Barbiturates ↓↓ ↓↓ ↓↓ calcium channel blocker infusion (nicardipine). Postoperative
Etomidate ↓↓ ↓↓ ↓ pain may be significant, especially if remifentanil was utilized
during the procedure, and should be treated with short-acting
Benzodiazepines ↓ ↓ ↓→ opioids or IV acetaminophen.
Opioids → ↓→ → In cases of delayed awakening following intracranial
procedures, the differential diagnosis includes three main
Ketamine ↑↑ ↑ ↑↑ categories: (1) neurological causes such as ongoing seizure,
hemorrhage, or stroke; (2) physiological cause, such me-
Most intravenous agents cause a reduction in CBF and CMR, with the notable
exception of ketamine. Opioids produce very little effect on CBF and CMR tabolite or electrolyte disturbances, hypothermia, or hyper-
except with high doses. glycemia; and (3) pharmacological cause such as continued
6 • O ncologic P rocedures
neuromuscular block, opioid overdose, and persistent an- Correct Answer: a. Remifentanil is frequently utilized in
esthesia. In such instance, an emergent head CT scan is neuroanesthesia to supplement volatile anesthetics, and its ef-
warranted. fect on CBF and ICP is minimal. Emergence from remifentanil
is reliable due to its short context-sensitive half-life. However,
remifentanil will not improve postoperative pain, so pain con-
R E VI EW Q U E S T I O N S trol may be necessary with a bolus of short-acting opioids in-
cluding fentanyl on emergence.
1. A patient is undergoing craniotomy for a frontal tumor
resection with general anesthesia using sevoflurane and 5. All of the following are true regarding neuromuscular
remifentanil as maintenance. The patient has the following blockade in a patient with supratentorial mass EXCEPT:
vital signs: BP 135/85, pulse 60 bpm, ETCO2 38 mm Hg, a) Succinylcholine may result in life- threatening
SpO2 99%. The surgeon asks you to facilitate more brain re- hyperkalemia.
laxation. What is the most appropriate intervention? b) Pancuronium is the preferred NDMR in cases of
a) Increase PEEP increased ICP.
b) Lower the head of the bed c) Nondepolarizing muscle relaxants have minimal effect
c) Increase sevoflurane on ICP.
d) Increase minute ventilation d) Depolarizing muscle relaxants may cause transient
increases in ICP
Correct Answer: d. Increasing the minute ventilation will
result in hypocapnia, which in turn produces cerebral vaso- Correct Answer: b. Pancuronium is not an ideal muscle re-
constriction. Assuming intact autoregulation, this will re- laxant for most neuroanesthesia procedures due to its long
sult in a reduction of brain volume and improve the surgical duration of action and its vagolytic effect, which may lead to
conditions in this case. increased CBF and ICP.
2. What is the expected effect on cerebral metabolic rate of 6. Which of the following is an appropriate goal for emergence?
oxygen consumption, CBF, and ICP when utilizing ketamine a) Normocapnia
for induction of general anesthesia in a patient with a known b) Avoiding reversal of neuromuscular blockade
supratentorial mass? c) Hypothermia
a) Decreased CBF, decreased CMR, decreased ICP d) Permissive hypertension
b) Increased CBF, increased CMR, increased ICP Correct Answer: a. The goals for emergence from intracranial
c) Increased CBF, increased CMR, decreased ICP surgery include a normal physiologic PaCO2, normothermia,
d) Decreased CBF, increased CMR, decreased ICP and complete reversal of neuromuscular blockade. In addi-
Correct Answer: b. Ketamine increases CBF, CMR, and ICP, al- tion, tight control of BP is necessary during emergence and
though the increase in CMR is minimal. This contrasts with vola- can be managed with esmolol.
tile anesthetics which decrease CBF, CMR, and ICP at 1 MAC. 7. Regarding CBF in an otherwise healthy adult, all of the fol-
3. Which of the following is the most appropriate choice for lowing are true EXCEPT:
maintenance IV fluids in an otherwise healthy adult patient a) Normal CBF is 100 mL/min per 100 g of tissue.
undergoing resection of a supratentorial mass? b) Cerebral autoregulation maintains CBF throughout a
a) D5 normal saline CPP range of 50–150 mm Hg.
b) 3% saline c) Neuronal dysfunction occurs at CBF of less than 18
c) 0.9% saline mL/min per 100 g of tissue.
d) Lactated Ringer’s d) Delayed cell death is seen when CBF is less than 10
mL/min per 100 g of tissue.
Correct Answer: c. Maintaining euvolemia is critical for suc-
cessful outcomes in neuroanesthesia. Normal saline is an ideal Correct Answer: a. CBF in a healthy adult is 50 mL/min per
choice since it is slightly hypertonic and may therefore im- 100 g of tissue.
prove cerebral edema; 3% saline may be utilized to decrease 8. Which of the following will produce the greatest decrease
ICP. However, it would not be the first choice for mainte- in ICP:
nance fluids. Fluids containing glucose should be avoided
as hyperglycemia has a negative impact on cerebral ischemia a) Hyperventilation to decrease PaCO2 from 60 to 30.
outcomes. Hypotonic solutions, including lactated Ringer’s, b) Increase volatile anesthesia agent to 2 MAC
should also be avoided as they may increase cerebral edema. c) Increase PaO2 from 80 to 100
d) Increase temperature by 1°C
4. All of the following are benefits of remifentanil except: Correct Answer: a. There is a linear relationship between
a) Improved postoperative pain control CBF and PaCO2 for PaCO2 of 20–70 mm Hg. Therefore, re-
b) Decreased requirement for volatile agents duction in PaCO2 from 60 to 30 mm Hg will result in a sig-
c) Minimal effects on CBF and ICP nificant decrease in CBF and ICP. PaO2 of less than 50 mm
d) Rapid emergence compared to fentanyl Hg can increase CBF and ICP. However, a change in PaO2
1. S upratentorial T umors • 7
within physiologic range will not cause a significant change. Propofol/ fentanyl, isoflurane/nitrous oxide, and fentanyl/ nitrous
Hypothermia, not hyperthermia, will decrease CMR by ap- oxide. Anesthesiology. 1993;78(6):1005–1020.
8. Petersen KD, Landsfeldt U, Cold GE, et al. Intracranial pressure
proximately 6% for every 1°C decrease in temperature. and cerebral hemodynamic in patients with cerebral tumors: a
9. All of the following are true regarding the actions of man- randomized prospective study of patients subjected to craniotomy in
nitol EXCEPT: propofol-fentanyl, isoflurane-fentanyl, or sevoflurane-fentanyl anes-
thesia. Anesthesiology. 2003;98(2):329–336.
a) Peak effect of mannitol is between 20–60 minutes after 9. Fraga M, Rama-Maceiras P, Rodiño S, Aymerich H, Pose P, Belda J.
administration. The effects of isoflurane and desflurane on intracranial pressure, ce-
rebral perfusion pressure, and cerebral arteriovenous oxygen content
b) Repeated doses of mannitol may cause a paradoxical in- difference in normocapnic patients with supratentorial brain tumors.
crease in ICP. Anesthesiology. 2003;98(5):1085–1090.
c) Mannitol works as an osmotic diuretic by decreasing 10. Chui J, Mariappan R, Mehta J, Manninen P, Venkatraghavan L.
plasma oncotic pressure. Comparison of propofol and volatile agents for maintenance of an-
d) Mannitol duration of action is 2–3 hours. esthesia during elective craniotomy procedures: systematic review and
meta-analysis. Can J Anaesth. 2014;61(4):347–356.
Correct Answer: c. Mannitol is an osmotic diuretic that 11. Sneyd JR, Andrews CJ, Tsubokawa T. Comparison of propofol/
decreases brain size by decreasing interstitial water via an in- remifentanil and sevoflurane/ remifentanil for maintenance
crease in plasma oncotic pressure. of anaesthesia for elective intracranial surgery. Br J Anaesth.
2005;94(6):778–783.
10. Which of the following statements about propofol 12. Citerio G, Pesenti A, Latini R, et al. A multicentre, randomised, open-
is TRUE: label, controlled trial evaluating equivalence of inhalational and in-
travenous anaesthesia during elective craniotomy. Eur J Anaesthesiol.
a) Increases CMR and decreases CBF 2012;29(8):371–379.
b) Increases CMR with induction doses only 13. Kaisti KK, Metsähonkala L, Teräs M, et al. Effects of surgical levels of
c) Maintains cerebral autoregulation propofol and sevoflurane anesthesia on cerebral blood flow in healthy
subjects studied with positron emission tomography. Anesthesiology.
d) Uncouples CBF and CMR 2002;96(6):1358–1370.
Correct Answer: c. Propofol, as well as opioids, barbiturates, 14. Kaisti KK, Långsjö JW, Aalto S, et al. Effects of sevoflurane, propofol,
and sedative- hypnotics, does not cause uncoupling of and adjunct nitrous oxide on regional cerebral blood flow, ox-
ygen consumption, and blood volume in humans. Anesthesiology.
CBF and CMR. While most IV agents maintain cerebral 2003;99(3):603–613.
autoregulation, volatile agents at high MAC levels may impair 15. Bundgaard H, von Oettingen G, Larsen KM, et al. Effects of
cerebral autoregulation. sevoflurane on intracranial pressure, cerebral blood flow and ce-
rebral metabolism. A dose- response study in patients subjected
to craniotomy for cerebral tumours. Acta Anaesthesiol Scand.
QUESTIONS AND ANSWER S 1998;42(6):621–627.
16. Holmström A, Akeson J. Desflurane increases intracranial pressure
more and sevoflurane less than isoflurane in pigs subjected to intracra-
This chapter has accompanying questions and answers nial hypertension. J Neurosurg Anesthesiol. 2004;16(2):136–143.
which are available to subscribers as part of the Oxford 17. Warner DS, Hindman BJ, Todd MM, et al. Intracranial pres-
eLearning platform. To access the questions, go to http:// sure and hemodynamic effects of remifentanil versus alfentanil
oxfordmedicine.com/neuroanesthesiaPBL in patients undergoing supratentorial craniotomy. Anesth Analg.
1996;83(2):348–353.
18. Guy J, Hindman BJ, Baker KZ, et al. Comparison of remifentanil and
fentanyl in patients undergoing craniotomy for supratentorial space-
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8 • O ncologic P rocedures
2.
ANESTHESIA FOR POSTERIOR FOSSA MASS
Valerie L. Howell, Margaret M. Collins and Lauryn R. Rochlen
9
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as determined by the eye, check measurements are taken by rule,
trams and level and final adjustments made to bring the various
parts in final proper relation to one another. For instance, the rudder
post must be perfectly vertical, as determined by a plumb line, when
the engine bearers or the top longerons are level. The various fittings
such as those for horizontal and vertical stabilizers and the engine
sections and side panels must all conform accurately to one another
so that the airplane as a whole, when it is assembled, will not contain
any inherent defects such as tail planes with slightly distorted angles
of incidence, left main panels ahead of right or over or under right
main panels, fittings so located that an initial strain must be imposed
upon them by forcing them together, etc.
After the fuselage has been lined up in the factory as described
briefly above, it is permitted to set for a week or so and then it is
checked up again and such additional slight corrections made which
would be necessitated by the sets which had occurred. The
additional fittings required are then applied and the fuselage finally
covered and sent away to have the engine and instruments applied.
When checking and truing a fuselage on the flying field after the
airplane has been assembled and flown the process is not quite so
simple as when the fuselage is checked up and trued in the factory,
largely owing to the lack of ideal factory facilities and also because
so many fittings, coverings, etc., are in the way which one must
always be cautious about removing. In general, the method of
procedure may be outlined as follows, but it must be obvious that
one can not in a series of written notes touch upon all the possible
queries and combinations of fuselage distortions which may occur
and the ways for detecting and correcting them. A certain amount of
experience in the field accompanied with some fixed habits of
inspection, and everlasting curiosity about the perfections of your
machine, and a willingness and readiness always to pitch in and help
correct the defects found, will soon develop in you the ability to
diagnose easily and quickly and remedy intelligently whatever
trouble you may run across.
For satisfactory fuselage checking and truing let us say in the field
shop, a certain minimum equipment of tools is necessary. This
equipment is:
At least two sawhorses about 3 to 4 ft. high for mounting the fuselage in flying
position.
Several wooden wedges (show taper) for easy adjustment of fuselage for cross
and lengthwise level.
About 25 yd. of strong linen line for checking center lines.
2 carpenter levels about 2 to 3 ft. long.
4 perfectly formed steel cubes about 1¼ to 1½ in. in size.
1 plumb bob.
1 small screw jack.
1 pair of wood clamps.
1 straight edge about 12 ft. long.
Several small Crescent adjustable wrenches.
Several pliers with wire-cutting attachment.
Pins for manipulating turnbuckles.
1 steel tape.
1 foot rule, 6 ft. long.
1 small brass hammer.
A small work bench equipped with a 3-in. or 4-in. vise.
1 ax.
2 crowbars.
6 lengths of iron pipe about 2 in. in diameter, 3 ft. long.
6 lengths of iron pipe about 2 in. in diameter, 4 ft. long.
100 ft. manila rope, 1 in. in diameter.
Remove propeller.
Unfasten control wires.
Unfasten main planes from fuselage and dismantle on ground.
Remove tail surfaces.
Unless machine is to be placed in box, landing gear and tail skid should remain
attached to fuselage.
Updated editions will replace the previous one—the old editions will
be renamed.