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Neurocritical Care Management of The Neurosurgical Patient 1St Edition Edition Monisha Kumar Full Chapter
Neurocritical Care Management of The Neurosurgical Patient 1St Edition Edition Monisha Kumar Full Chapter
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In medicine there are a few nodes of care where over a short knowledge of the events that occur in the operating room
period of time a person’s life lies in the balance. The neuro- is equally essential. However, the emergency department
critical care unit (NICU) is one such node. Though postop- is a much more familiar environment for the neurointensi-
erative care units for neurosurgical patients have existed vist than the operating room. This textbook, written by
for many decades the multidisciplinary neurocritical care neurosurgeons, neuroanesthesiologists, and neurointensi-
field is still very young, dating back only to the 1980s. vists, defines the key issues needed to meld these two
As a result, the evidence-base that underlies much of the approaches.
decision-making in the NICU is still being assembled. The Dr. Kumar and her co-authors bring a unique viewpoint
lessons-learned from experienced neurointensivists remains that mimics the reality of the NICU where the patient care is
the bedrock of the art of neurocritical care. a complicated dance with multiple caregivers, the patient
This textbook incorporates the wisdom of an impressive and family. From my position at NIH it’s also important
cadre of dedicated physicians who clearly communicated to note that many of the chapters identify the evidence gaps
their art, as well as describing the evidence-base for their that need to be addressed to inform decision-making in the
craft. The focus on the neurosurgical patient places the NICU. Outlining these should enable neurointensivists to
book in a special position in medical literature. Close work- engage in research to understand those interventions asso-
ing relationships between the patient’s neurosurgeon, neu- ciated with clinically important outcomes in specific
roanesthesiologist, and the neurointensivist is crucial for patients. Though professional agendas differ among care-
good patient care in the NICU, but is not by itself a replace- givers, a good final clinical outcome is shared by all, and
ment for a working knowledge of each others concerns, the body of knowledge displayed in the text is a wonderful
abilities, and processes. Understanding the neurosurgery guide to the care of the neurosurgical patient in the NICU.
is as essential for the neurointensivist, as neurointensive
care is to the neurosurgeon. It would be impossible to pro- Walter Koroshetz, MD
vide quality care for the person transferred to the NICU Director, National Institute of
from the emergency department without knowledge of Neurological Disorders and Stroke
what occurred in the emergency department. A similar
ix
Preface
Neurocritical Care is a burgeoning field dedicated to the Furthermore, the options and methods for intraoperative
management of patients with life-threatening neurological monitoring have grown over the past decade and will con-
and neurosurgical illness as well as those at risk for neuro- tinue to do so. Physiological data gleaned from novel mon-
logical complications of systemic disease. Much of neuro- itors provide critical information about the individual
intensive care unit (Neuro ICU) management focuses on patient’s response to surgery and anesthesia. Understand-
the postoperative neurosurgical patient. Treating neuro- ing the advantages and disadvantages of these monitoring
surgical patients without a comprehensive understanding techniques is imperative to the provision of exemplary care
of what occurs in the operating room (OR) may severely of the neurocritically-ill patient. Similarly, mounting evi-
hinder the intensivist in the provision of optimal care. It is dence suggests that critical information is progressively
imperative that neuro-intensivists be aware of the relevant omitted during points of transitions of care. Anticipatory
neuroanatomical structures, surgical approach, and anes- inquiry may enhance communication between OR and
thetic considerations as well as the range of known compli- ICU staff if providers receiving the patients are knowledge-
cations of elective and non-elective neurosurgery. This is able enough to ask probing questions and to elicit details
fundamental to the practice of neurocritical care. However, that may be lost in translation.
the preoperative evaluation, perioperative assessment and The aim of this text, Neurocritical Care Management of the
intraoperative management are not comprehensively Neurosurgical Patient, is to serve as the premier reference for
taught in the neurocritical care curriculum. This book is the intensive care management of neurosurgical patients.
intended to grant deeper insight into perioperative neuro- Many available neurocritical care textbooks have focused
surgical evaluations and anesthetic considerations that on particular disease states, pathophysiological conditions,
may affect the intensive care management of these patients. or medical complications. However, none has described the
It is critical that this knowledge gap be sealed as the field specific neurosurgical procedures or anesthetic consider-
of neurocritical care matures. The knowledge gap is further ations that impact the critical care management of these
compounded by the fact that practitioners of neurocritical patients.
care hail from a wide variety of primary specialties includ- This textbook is divided into 6 sections. Section 1 offers a
ing Internal Medicine, Emergency Medicine, General Sur- review of core neuroanesthesiology principles applied to the
gery, Anesthesiology and Neurology. The diversity of operative care of neurosurgical patients. Chapters in this
specialties allows practitioners a varied skill set; however, section focus on neurophysiological effects of anesthetic
a standard and comprehensive set of skills may be elusive. agents, procedural patient positioning, specific anesthetic
Although a fundamental understanding of neurosurgery, considerations for brain, spinal cord and endovascular neu-
including proper patient positioning, operative techniques rosurgery, intraoperative neuromonitoring, and intrao-
and relevant neuroanatomy, remain a prerequisite for perative catastrophes.
those caring for postoperative neurosurgical patients, it is The lion’s share of the volume is contained within
an oft-overlooked segment of clinical training. Sections 2-5. For the most part, a neurosurgeon or
Transitions in care and patient handoffs have evolved neuro-interventionalist collaborated with a neurointensivist
dramatically over the last decade. Hand-offs in surgical spe- to write each chapter. Section 2 focuses on types of craniot-
cialties often focus on the operative intervention, whereas omy procedures, including vascular neurosurgery, neuro-
hand-offs in medical specialties focus on the history of pre- oncologic surgery, epilepsy surgery, functional neurosurgery
sent illness. These distinct approaches intersect in the and trauma neurosurgery. Section 3 is devoted to spinal
Neuro ICU, which is frequently a mixed medical-surgical surgery and Section 4 focuses on endovascular neurosur-
ICU. Surgical ICU sign-out rounds involves a review of gery. Section 5 is dedicated to specialty procedures
the anatomy, anesthesia and complications of the surgery including ventricular shunts and neuro-monitor placement,
performed for each postoperative patient, in contradistinc- combined neurosurgical procedures (e.g. with Otorhinolar-
tion to the individual patient’s initial presentation and yngology or Plastic Surgery) and peripheral neurosurgery.
symptom chronology as is often done in the Neuro ICU. Chapters in Sections 2-5 adhere to a prescribed struc-
Although reviewing the patient’s initial symptomatology ture and format. Each chapter is divided into 3 parts: Neu-
may be important, it is likely that the early ICU course roanatomy and Procedure, Perioperative Considerations,
might be as much related to the operative procedure, as and ICU Complications. The first part, Neuroanatomy and
to the presenting signs and symptoms. We are unaware Procedure, reviews the relevant neuroanatomy and opera-
of a reference for the intensivist that provides this type of tive steps of the procedure. The second part, Perioperative
perioperative information regarding neurosurgical patients Considerations, describes the related neuro-monitoring,
in a clear and concise manner. This was the impetus for this operative position and anesthetic choices for the procedure.
textbook. The remainder of the chapter, ICU Complications, comprises
xi
xii Preface
an evidence-based review of the potential procedural com- internationally recognized. These academic and clinical
plications and the relevant critical care management strat- endeavors have resulted in partnerships with experts in
egies. Section 6 is exclusively devoted to potential ICU neuroanesthesia, neurocritical care and neurosurgery,
complications of neurosurgery including delayed emer- many of whom have graciously contributed to this volume.
gence, intracranial hypertension, hemodynamic complica- We believe that this textbook will have broad applicability
tions, intracranial hypertension, or status epilepticus. and will serve neurosurgeons, anesthesiologists, medical
The editors are grateful that the Neuro ICUs at the Uni- intensivists, surgical intensivists as well as neurointensi-
versity of Pennsylvania foster collaborative endeavors vists. We hope that it will also serve as a reference for
between Neurology, Neurosurgery and Anesthesiology. It trainees of varied backgrounds.
is likely due to the fact that from its inception, the Penn
Neuro ICU represented a shared vision of the chairpersons M. A. Kumar, MD
of the Departments of Neurology, Neurosurgery and Anes- W. A. Kofke, MD, MBA
thesiology & Critical Care. The inherent nature of this J. M. Levine, MD
Neuro-ICU program has borne fruitful clinical, academic J. M. Schuster, MD, PhD
and research programs that are nationally and
List of Contributors
xiii
xiv List of Contributors
We would like to express our sincere gratitude and appre- the seed that would grow into this textbook. Also we would
ciation to all the contributors to this volume. We also thank like to thank the nurses in the clinic, operating room and
the editorial, design and production staff at Elsevier, in par- intensive care unit who care for our patients as we could
ticular: Charlotta Kryhl, Sharon Nash, Trinity Hutton, and not do our job without them. Finally, we would like to
Julie Taylor who have been particularly helpful in produc- thank our patients and their families; we are grateful for
ing this volume. We would like to thank Dr. Rae Allain, for- the opportunity to be a part of their treatment, cure and
merly of the Massachusetts General Hospital, for planting recovery.
xxi
Dedications
xxiii
1 Effects of Anesthetics,
Operative Pharmacotherapy,
and Recovery from Anesthesia
ZIRKA H. ANASTASIAN and JOHN G. GAUDET
3
4 SECTION 1 • Neuroanesthesia and Perioperative Care
Propofol in low doses is an antiemetic of an unclear mech- brain.78,79 Also numerous retrospective studies have
anism. The residual antiemetic properties postoperatively reported an association between hyperglycemia and
make propofol a popular choice or adjunct for an anesthetic adverse outcomes in humans with various types of neuro-
in a patient who is at high risk for nausea and vomiting logical problems.80 Sieber et al. reported that routine elec-
postoperatively.68 tive neurosurgery was associated with levels of
Phenothiazines (promethazine and prochlorperazine) hyperglycemia thought to be high enough to exacerbate
are D2 antagonists with moderate antihistamine and anti- ischemic brain damage.81 Thus the stage was set for needed
cholinergic properties.70 They can produce extrapyramidal prospective randomized studies. In 2001 Van den Berghe
reactions.68 et al. reported on the use of intensive insulin therapy
Phenylethylamine (ephedrine) is a sympathomimetic targeted to tight blood glucose control (target range 80–
agent that has been used as an antiemetic in the obstetrical 110 mg/dL) in critically ill surgical patients. This and
and abdominal surgery populations.73 It does increase subsequent studies from her group resulted in
heart rate and blood pressure. recommendations calling for the widespread use of inten-
Butyrophenones (droperidol, haloperidol) are D2 recep- sive insulin therapy (IIT) in critically ill patients.82 To
tor antagonists.70 They have minimal effect on cerebral address the safety of IIT administered to postoperative neu-
hemodynamics or intracranial pressure and tend to rosurgical patients, tight blood glucose control with IIT
decrease blood pressure. Side effects include mild sedation, resulted in a three-fold increase in the risk of iatrogenic
dysphoria, and extrapyramidal side effects. It is therefore hypoglycemia.83 The Normoglycemia in Intensive Care
contraindicated in patients with Parkinson’s disease and Evaluation-Survival Using Glucose Algorithm Regulation
prolonged QT interval. trial, a large (6104 patients), multicenter, international,
Antihistamines (dimenhydrinate, hydroxyzine) block randomized trial, reported that in adult intensive care unit
histamine receptors in the nucleus of the solitary tract. (ICU) patients, IIT targeted to tight blood glucose control
They can produce some sedation.68 (target range 81–108 mg/dL), compared with conven-
Anticholinergic (transdermal scopolamine) medica- tional glucose control (target <144–180 mg/dL), resulted
tions act centrally and block impulses from vestibular in higher mortality.84
nuclei to higher areas in the central nervous system Optimal glucose management, particularly in patients
and reticular activating system.68,74 The central cholin- with acute brain injury and those undergoing neurosur-
ergic antagonism can lead to delirium, which can be gery, remains a controversial issue. Both hypoglycemia
reversed with physostigmine, a centrally acting cholines- and hyperglycemia appear to result in critical adverse
terase inhibitor. It also can result in mild sedation and effects. Although there may be benefit in controlling hyper-
dizziness. glycemia in neurocritical care and neurosurgical ICU
Neurokinin antagonists (aprepitant) act by blocking the patients,85–87 the actual incidence and impact of hypogly-
binding of substance P (a regulatory neuropeptide) to NK1 cemia remain unknown. This may be due to the fact that
receptors in vagal afferents in the gastrointestinal tract and the temporal relationship to ictus, optimal level of control,
in regions of the central nervous system. Common side and the impact of confounding factors such as stress or ste-
effects include fatigue, headache, and constipation.75 roid administration remains unknown. More information is
In general, combination therapy has superior efficacy needed about the correlation of peripheral glucose levels
compared with monotherapy for PONV prophylaxis, and with intracellular levels in the brain, particularly in the
drugs with different mechanisms of action should be used ischemic or potentially ischemic brain. Current guidelines
in combination to optimize efficacy.76 suggest that hyperglycemic levels above 180 to 200 mg%
Postoperatively, when a prophylactic dose of an antie- warrant insulin therapy.88
metic has failed, a rescue dose should be chosen from The widespread use of glucocorticoids in the neurosur-
another mechanistic class. To repeat a prophylactic dose gical ICU affects optimal glucose management. Glucocor-
in the first 6 hours after administration has not been shown ticoids stabilize the blood–brain barrier and increase
to be effective.77 absorption of cerebrospinal fluid. They are beneficial
when administered in low doses (e.g., 10 mg of dexa-
methasone) in preventing PONV and are commonly used
Effects of Anesthetics and Surgery on in neurosurgery to reduce vasogenic edema in primary
and metastatic tumors. The administration of a single
Postoperative Glycemic Control dose of dexamethasone will, however, increase blood
glucose concentration significantly in both diabetic and
Key Concept nondiabetic patients.89,90
Effects of Anesthetics and Surgery The effects of general and/or neuraxial anesthesia may
either balance or exacerbate temperature changes com-
on Temperature Regulation monly observed in brain or spinal cord injury. After brain
injury, hypothalamic dysfunction or stress-induced
Key Concepts immune modulation may result in hypothermia or hyper-
thermia.104 In patients with altered mental status, fever is
• Hypothermia has both deleterious and potentially also commonly due to environmental exposure and
neuroprotective effects when performed intraoperatively and bronchoaspiration. After spinal cord injury, although pro-
postoperatively. longed immobility may present with hyperthermia due to
• Rewarming should be done gradually and with caution to infectious or thrombotic complications, neurogenic vaso-
avoid complications. plegia can be responsible for significant heat loss.105
Fever is clearly associated with worse clinical outcomes
Abnormal body temperature results from an imbalance in patients with neurological injury.106 Although hypo-
between heat loss and heat production. Radiation, conduc- thermia has multiple systemic deleterious side effects, it
tion, convection, and evaporation mechanisms contribute may also have neuroprotective effects in patients with trau-
to heat loss.91 The hypothalamus is responsible, in large matic brain injury (TBI) or massive stroke.107,108 Mild
part, for maintaining core temperature within a normal hypothermia attenuates secondary cerebral insults due to
range (35.0–37.5°C, 95.0–99.5°F).92 It receives afferent intracranial hypertension after TBI.109 In stroke patients,
peripheral input from C (warm) and Aδ (cold) fibers and reg- therapeutic effects of hypothermia are equivocal despite
ulates both heat production (basal metabolic rate, shivering) robust benefits in animal models. In absence of strong evi-
and heat distribution (peripheral vasomotor tone, sweat) via dence from clinical trials, therapeutic hypothermia should
efferent autonomic and endocrine signals.93 Disruption of be considered for treatment of massive stroke with intracra-
afferent or efferent signaling, as well as hypothalamic dys- nial hypertension.110 Unclear benefits of therapeutic hypo-
function, may lead to hypothermia (any core temperature thermia in a clinical setting are due in part to the
below 35°C) or hyperthermia (any core temperature above deleterious effects of rewarming.111 Patients with brain
37.5°C) as measured centrally (pulmonary artery, bladder, or spinal cord injury should be rewarmed carefully before
nasopharynx, lower esophagus, tympanic membrane) or initiation of emergence. As a general rule, the more severe
peripherally (axilla, mouth, rectum). Core temperature is the injury and/or degree of hypothermia, the more progres-
usually higher than peripheral temperature. Core hypother- sive and closely monitored rewarming should be. In all
mia is graded as mild (32–35.0°C, 90–95.0°F), moderate cases of brain or spinal cord injury, hyperthermia should
(28–32°C, 82–90°F), severe (20–28°C, 68–82°F), or pro- be avoided, as it is clearly deleterious.112
found (less than 20°C, 68°F). Severe hyperthermia (any core
temperature above 40.0°C, 104.0°F) is sometimes referred
to as hyperpyrexia.94 Clinical Pearl
Whereas hypothermia is frequently observed following
administration of general anesthesia, the onset of hyper- Hypothermia is common during and after surgery and may
be neuroprotective in some cases, but hyperthermia is clearly
thermia is rare but should prompt immediate investigation
deleterious and should be avoided.
because it may be the expression of anaphylaxis or abnor-
mal drug reaction.95 Malignant hyperthermia is most con-
cerning and potentially lethal, but quite rare. Most general
anesthetic drugs affect both peripheral vasomotor tone and Effects of Anesthetics and Surgery
hypothalamic function but preserve sweat mechanisms on Pain and Pain Control
and afferent hypothalamic input.96 Initially after induction
of general anesthesia, heat loss is accelerated due to redis-
tribution of blood flow to peripheral tissues. Skin warming Key Concepts
before induction attenuates this phenomenon by reducing
the thermic gradient between the central and peripheral • Multimodal analgesia, including acetaminophen, nonsteroidal
compartments.97 Drugs such as ketamine98 and midazo- antiinflammatory drugs (NSAIDs), local anesthetics,
lam,99 as well as nitrous oxide100 may help preserve vaso- gabapentinoids, ketamine, and opioids, should be considered
in chronic pain patients or patients at risk of developing
motor tone and decrease heat loss. During maintenance of
chronic pain.
general anesthesia, the hypothalamic temperature set • Whenever necessary, collaboration with a pain specialist
point gets readjusted to a lower temperature due to drug- should be considered.
related effects. Inhibition of shivering by muscle relaxants
further decreases heat production.101 During neuraxial
anesthesia, the combination of sympatholytic vasoplegia Up to two-thirds of patients suffer from postoperative pain
and altered afferent signaling leads to hypothermia from after craniotomy.113 Compared with supratentorial proce-
accelerated heat loss and abnormal elevation in apparent dures, patients undergoing infratentorial craniotomy report
temperature, respectively.102 Under such circumstances, more severe pain scores. Such poor outcomes are at least in
skin warming may fail to prevent hypothermia.103 Heat part due to avoidance or underutilization of opioids to reduce
loss is also exacerbated by the frequent administration of the sedation associated with their use. They also result from
hypnotic drugs to produce sedation in combination with a presumed lack of need for analgesics, as well as difficulties
neuraxial anesthesia. in assessing pain during recovery from brain surgery.
1 • Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia 9
Pain after spine surgery represents a particularly difficult decreasing opioid consumption without increasing the risk
challenge. These patients often have chronic pain, signifi- of aberrant excitatory cortical, hippocampal, and limbic
cant disability, and psychological distress, and many have hallucinogenic activity observed at higher dosages.
had prior neurosurgery.114 The challenge in managing Although the use of ketamine during craniotomy remains
pain after spine surgery resides in treating patients with very controversial, there is preliminary clinical evidence
multiple predictors of severe postoperative pain and analge- indicating ketamine may be beneficial in sedated, ventilated
sic consumption.115 Factors clearly associated with difficult patients with severe traumatic brain injury.130 It should be
postoperative pain management include chronic pain inde- considered for patients with chronic pain and opioid depen-
pendent of opioid tolerance, significant disability with psy- dence undergoing spine surgery.131
chological distress, major surgery, or reoperation after Gabapentinoids, such as gabapentin and pregabalin, are
failed surgery.114 In the presence of such risk factors, the oral anticonvulsant drugs. They block calcium channels,
perioperative analgesic plan should be made and adjusted which are upregulated in dorsal root ganglia and contrib-
in collaboration with a pain specialist. ute to neuropathic pain symptoms (hyperalgesia, allody-
Opioids remain the mainstay of analgesia after neurosur- nia) after nerve injury. A heterogeneous body of clinical
gical procedures. Although most share common pharma- studies shows they may also have antinociceptive, opioid-
codynamical properties (μ receptor agonism), their sparing, and anxiolytic properties.128 Their use as analge-
pharmacokinetic profiles tend to differ significantly.116 sic premedication before craniotomy is very controversial
Whenever rapid neurological recovery from anesthetic due to a high incidence of dizziness and sedation, most com-
effect is required, drugs with shorter half-lives are usually monly in the elderly and/or in patients with renal dysfunc-
favored. Unless complemented with other nonopioid anal- tion.132 Gabapentinoids appear to be most beneficial in
gesics, use of such short-acting drugs may result in subop- patients undergoing major spine surgery; however, timing
timal postoperative analgesia. Alternatively, drugs with and optimal dosage remain unclear.133
longer half-lives may be preferred to optimize analgesia dur- Finally, postoperative pain may also be attenuated using
ing emergence and recovery whenever pain management is local anesthetics to reduce transmission of the nociceptive
anticipated to be problematic. Opioid-induced side effects signal from the peripheral to the central nervous system.
include respiratory depression, sedation, and prolonged During craniotomy, regional scalp block using lidocaine,
immobilization. Perioperative analgesia should be managed bupivacaine, or ropivacaine before incision has been shown
in collaboration with a pain specialist in presence of respira- to reduce postoperative pain and opioid consumption.
tory risk factors such as obesity, sleep apnea, or obstructive Addition of low-dose epinephrine to the local anesthetic
or restrictive lung disease. Nausea, vomiting, constipation, solution may help prolong duration of the block without
and slow gastric emptying with delayed enteral nutrition systemic hemodynamic effects.134 Local anesthetics may
may also complicate their use.117 Prolonged duration of also be administered in the epidural space or intravenously
high opioid plasma levels has been associated with increas- in patients undergoing major spine surgery. Combined epi-
ing sensitivity to noxious stimuli (opioid-induced hyperalge- dural/general anesthesia with postoperative epidural anal-
sia)118 and immunosuppression.119 In order to reduce the gesia may produce better pain control and a lower surgical
incidence and severity of opioid-induced side effects, modern stress response than general anesthesia with postoperative
analgesic management relies on a multimodal approach that systemic opioid analgesia. However, patients with epidural
combines opioids with coanalgesics.120 catheters should be carefully monitored and referred to a
Acetaminophen may be used as an adjunctive to treat pain specialist postoperatively due to the potential signifi-
mild to moderate postoperative pain. In patients with fever, cant side effects of sympathetic blockade.135 Alternatively,
it may also induce a significant decrease in temperature perioperative IV administration of lidocaine may improve
within 15 minutes. Compared with the oral or rectal routes, postoperative pain management after complex spine proce-
IV acetaminophen may be beneficial. However, due to the dures. The evidence supporting this strategy remains lim-
relatively high cost of the IV formulation, physicians ited; further research is needed to confirm preliminary
remain hesitant to use it.121 results, demonstrate safety, and clarify dosage.136
The use of NSAIDs such as ketorolac after neurosurgical
procedures remains controversial. On one hand, ketorolac
is a nonsedating drug with potent analgesic activity that Effects of Anesthetics and Surgery
has been demonstrated to reduce postoperative opioid
requirements.122 On the other hand, ketorolac has an inhib- on Consciousness and Cognition
itory effect on both platelet function123 and bone
formation,124 a key determinant for the success of spinal Key Concepts
fusion procedures. In the absence of strong clinical evidence,
ketorolac should be used cautiously, if at all, after intracra- • Postoperative delirium (POD) and postoperative cognitive
nial surgery125 or spinal fusion procedures.126 In addition, decline (POCD) are frequently encountered in the elderly after
NSAIDs should be avoided in patients with, or at risk for, surgery.
renal dysfunction and gastrointestinal bleeding.127 • Management should rely on early identification of patients at
Ketamine has potent antinociceptive effects in the spinal risk and avoidance of any disruption of cerebral physiology
cord at subanesthetic concentrations.128 It may also have until the mechanisms leading to POD and POCD are
beneficial antiinflammatory effects.129 The combination of elucidated.
a low-dose bolus (0.1–0.5 mg/kg preferably administered • Treatment can include reduction of psychological and
physiological perioperative stress and use of
before incision) and a continuous infusion (2–5 mcg/kg/ dexmedetomidine and antipsychotics.
min) may improve postoperative pain management while
10 SECTION 1 • Neuroanesthesia and Perioperative Care
POD and POCD are two distinct forms of brain dysfunc- Table 1.2 Predisposing and Precipitating Factors
tion that are frequently encountered mostly in the elderly for Postoperative Delirium
after major surgery.137 Although it is unclear whether both
disorders share common pathophysiological mechanisms, Predisposing factors Precipitating factors
they have clearly been associated with an increased Reduced cognitive reserve Polymedication
risk of complications leading to longer hospital stays, (advanced age, cognitive Drugs affecting the central nervous
significantly higher costs, and higher mortality rates.138 impairment) system
Rapid, often fluctuant alterations of consciousness are Sensory impairment Pain
the hallmark of POD. Psychomotor changes (agitation or, (visual, auditory) Urinary obstruction/catheterization
more commonly, hypoactivity) and acute cognitive distur- Frailty Hypoxemia
bances are other important signs frequently observed (malnutrition, dehydration) Hypotension
alongside an abnormal sleep/wake cycle or disturbed
visual/auditory perception. POD typically presents 1 to Substance dependence Infection
(alcohol, drugs) Electrolyte abnormalities
3 days after surgery; it may persist for several days to
weeks. Several diagnostic scales using Diagnostic and Statis- Severe illness with organ Environmental changes
tical Manual of Mental Disorders criteria are available for use dysfunction
in multiple settings, including the ICU.139 In some situa- Apolipoprotein E4 genotype Sleep/wake disturbances
tions of an apparent hypoactive cognitive state, consider-
ation should be given to nonconvulsive seizures, which
have been reported in up to 19% of ICU patients.140
POCD has a subtler, subacute presentation dominated by
memory loss and executive dysfunction leading to inability been shown to increase the risk of POD irrespective of
to perform simple activities of daily living. POCD usually dose or duration of administration, dexmedetomidine
presents weeks to months after surgery; it may be only may be advantageous and should be considered for seda-
partially reversible over a period of several months. The tion or as a complement for general anesthesia in patients
diagnosis of POCD must be confirmed by the results of a at risk.147 Interestingly, recent evidence indicates excessive
time-consuming battery of neurocognitive tests, adminis- depth of anesthesia, as measured with electroencephalog-
tered by trained personnel, showing significant decline raphy, may correlate with a higher risk of both POD and
from baseline evaluation.141 Education and awareness of POCD.148
POCD are of considerable importance because many Anticholinergic drugs used for reversal of muscle paral-
patients and their families may not be aware of the poten- ysis have been suspected to contribute to the development
tial scope of this disease. of POD and POCD; however, recent reports have failed to
Because the stress response to surgery appears to play a confirm this hypothesis.149 Antipsychotic medications
central role in development of postoperative brain dysfunc- have been successfully used for prevention and treatment
tion, strategies aimed at reducing tissue injury and/or lim- of hyperactive POD. The precise underlying mechanism
iting its impact on the brain may be beneficial. Minimally remains unclear; some authors suggest it may convert
invasive surgical techniques are associated with lower rates hyperactive episodes of POD into hypoactive ones without
of POD.142 Their role in decreasing the risk of POCD resolving the issue.150 In absence of a reversible cause for
remains unclear. Similarly, effective attenuation of the brain dysfunction, they may be administered cautiously.
pain-induced stress response using a multimodal, opioid- Atypical antipsychotics such as risperidone or olanzapine
sparing analgesic strategy may be beneficial during have a better side effect profile but are available for oral
and after surgery.143 Other neuroprotective strategies tar- administration only. Alternatively, haloperidol may be
geting the perioperative inflammatory activation or the administered intravenously or intramuscularly.151
neuroendocrine response are being investigated.144
Finally, reduction of psychological perioperative stress
using reassurance, orientation, and maintenance of sen- Clinical Pearl
sory input from visual or auditory aids has been shown
to be as efficient as, if not more than, other strategies.145 Management of POD and POCD should focus on early
identification of patients at risk and minimizing disruption of
Clearly, management should rely on early identification
cerebral physiology.
of patients at risk (Table 1.2) and avoidance of any disrup-
tion of cerebral physiology until the mechanisms leading to
POD and POCD are elucidated. Patient management rely-
ing on a multimodal, multidisciplinary strategy is most suc- Summary
cessful when initiated before surgery and continued
postoperatively.146 Overall, conditions associated with The effects of anesthetics, agents given during surgery, and
insufficient cerebral oxygen or energy delivery (hypoxemia, surgery itself can have an effect on the recovering patient.
anemia, hypotension, hypoglycemia, stroke), excessive Patients who are at an increased risk for postoperative
cerebral metabolism (hyperthermia, seizure activity, sub- respiratory dysfunction, PONV, hyperglycemia, hypother-
stance withdrawal), and any acute homeostatic imbalance mia, pain, and cognitive dysfunction should be identified
(renal or hepatic dysfunction, drug toxicity, systemic by preoperative risk factors, and the postoperative manage-
inflammation) should be identified as early as possible ment should take into consideration the intraoperative
and treated promptly. Whereas most hypnotic drugs have course and management.
1 • Effects of Anesthetics, Operative Pharmacotherapy, and Recovery from Anesthesia 11
hypercapnia in anesthetized rats. Anesthesiology. 2007;107 intragastric nutrition in critically ill patients. JPEN. 2008;32
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2 Patient Positioning for
Neurosurgical Procedures
SHAUN E. GRUENBAUM, BENJAMIN F. GRUENBAUM, YORAM SHAPIRA, and
ALEXANDER ZLOTNIK
15
16 SECTION 1 • Neuroanesthesia and Perioperative Care
Table 2.1 Positioning Strategies of the Upper and Lower HEAD FIXATION
Extremities to Reduce the Risk of Perioperative Peripheral Fixing the head in a stereotaxic Mayfield frame is com-
Neuropathies
monly done prior to neurosurgical procedures. Placing
A. UPPER EXTREMITY the stereotaxic frame requires the placement of 3–4 exter-
nal pins on the patient’s scalp at a pressure of 60–80
Positioning Strategy
pounds per square inch (psi). Head pinning has a pro-
BRACHIAL PLEXUS Arm abduction should not exceed 90 foundly stimulating effect, similar to that of a surgical inci-
NEUROPATHY degrees sion. If not properly anticipated and treated, pinning can
ULNAR NEUROPATHY Avoid pronation of the hands or result in a large catecholamine release and associated
(ELBOW) forearms hypertension and tachycardia. Furthermore, if the patient’s
RADIAL NEUROPATHY Avoid pressure in the spiral groove of
head moves after being fixed in the stereotaxic frame, this
(ARM) the humerus from prolonged contact can result in significant lacerations to the patient’s scalp or
with a hard surface cervical spine injury.
The severe hypertension that results from head pinning
MEDIAN NEUROPATHY Avoid extending the elbow beyond
(ELBOW) what is comfortable for the patient may result in exacerbation of cerebral edema or hemor-
during the preoperative examination rhage at the surgical site or, rarely, at another intracranial
site remote from the surgical area.4,5 If the hemorrhage is
B. LOWER EXTREMITY
large enough, it may require surgical evacuation. Worsen-
Positioning Strategy ing edema due to fixation-related hypertension may com-
promise exposure during an intracranial procedure. It is
SCIATIC NEUROPATHY Avoid stretching the hamstring muscle
beyond what is comfortable for the therefore very important to anticipate the sequelae of head
patient during the preoperative pinning, ensure adequate pain control, and maintain the
examination blood pressure within the normal range. This is especially
Avoid extreme hip flexion important for patients with vascular lesions in the brain
(such as arteriovenous malformations or cerebral aneu-
PERONEAL Avoid pressure near the fibular head rysm), known coagulation disorders or on anticoagulants,
NEUROPATHY from contact with a hard surface or rigid
support
and disrupted blood–brain barrier function. Blood pressure
should be frequently monitored, preferably with an arterial
Adapted from the American Society of Anesthesiologists Practice Advisory for line, during head pinning.
the Prevention of Perioperative Peripheral Neuropathies. Anesthesiology. Patients with chronically uncontrolled hypertension are
2011 Apr;114(4):741–54.
at particularly high risk of severe hypertension during pin-
ning. Head fixation requires constant communication
between the surgery and anesthesia team to ensure patient between the surgical and anesthesia teams, and the hemo-
safety, and the patient should be reconnected to the venti- dynamic responses associated with head pinning should be
lator and monitors in a timely manner. anticipated and preemptively treated. Prior to head pinning
in both the awake and anesthetized patient, the patient’s
scalp should be infiltrated with local anesthetic.6 The anes-
Clinical Pearl thesia should be deepened, and when appropriate, muscle
relaxation should be administered to anesthetized patients.
Rotating the bed 90 to 180 degrees often necessitates that When one plans to administer an opioid infusion during the
monitors, vascular lines, and ventilation circuit be neurosurgical procedure, it should ideally be started prior
disconnected from the patient; this is a moment of risk and to head pinning to further blunt the response to pinning.
should be accomplished efficiently and with the cooperation It is important to note that the hemodynamic response
of the surgical and anesthesia teams.
from pinning is typically short lived, and after the patient’s
head is fixed, the stereotaxic frame is no longer stimulating.
For this reason, a bolus of a short-acting opioid (such as
Head Fixation and Positioning remifentanil 1 mcg/kg), with or without propofol, may be
advantageous over large doses of propofol or volatile anes-
thetics that may result in profound hypotension after the
Key Concepts head is fixed.
Fixing the head in the Mayfield frame is associated with
• Fixing the head with pins in a Mayfield frame is profoundly
stimulating, and severe hypertension and tachycardia can
several additional complications.7 In children or adults
ensue if not anticipated and pharmacologically prevented. with thin skulls, the use of excessive force may cause a
• Positioning the head and neck is one of the most important depressed skull fracture. Occasionally, the fracture may
considerations when positioning patients for neurosurgical be so severe that it results in a poor outcome. Similarly,
procedures, and proper positioning ensures optimal surgical in trauma patients with a known or suspected skull frac-
approach and exposure. ture, fixing the head should be done with extreme caution.
• To facilitate venous and lymphatic drainage and minimize the In the immediate postoperative period, the clinician
chance of endotracheal tube kink when the neck is flexed, a should be cognizant of potential complications related to
distance of at least 2–3 fingerbreadths must be maintained head pinning (Table 2.2). When the pins are removed at
between the mandibular protuberance and the manubrium of
the end of the procedure, bleeding is common at the pin
the sternum at all times.
sites. Typically, a pressure dressing with gauze is sufficient
2 • Patient Positioning for Neurosurgical Procedures 17
Table 2.2 Postoperative Complications That May Result from compression of the vertebral arteries, resulting in cerebral
Neurosurgery in the Various Positions ischemia, and difficulties in oxygenation and ventilation.
It is therefore recommended that a distance of at least
Risk Factor Postoperative Complications 2–3 fingerbreadths be maintained between the mandibular
Head Pinning ■ Bleeding at the pin sites protuberance and the manubrium of the sternum at all
■ VAE times. Furthermore, the surgical and anesthesia team
Head and Neck ■ Neck discomfort or pain
should be cognizant to avoid a position that maintains pres-
Positioning ■ Brachial plexus injury sure on the patient’s chin, which can result in skin break-
■ Postoperative airway obstruction from down or pressure necrosis.
inadequate cerebral venous or lymphatic Complications related to head and neck positioning
drainage might present in the immediate postoperative period6
■ Cervical spine ischemia and quadriplegia
from vertebral or carotid artery obstruction (Table 2.2). Excess strain of the neck may cause brachial
plexus injury or postoperative discomfort or pain. Skin
Supine Position ■ Lower back pain and peripheral breakdown or pressure necrosis may result from prolonged
neuropathies (especially ulnar) from
inadequate padding of pressure points pressure on the patient’s chin. Swelling of the neck and air-
■ Complications related to neck rotation or way from inadequate cerebral venous or lymphatic drain-
flexion (see earlier) age may result in postoperative airway obstruction.
Lateral Position ■ Brachial plexus injury from axillary artery
Furthermore, if the vertebral or carotid arteries were
compression obstructed during surgery for a prolonged period, cervical
■ Pressure and stretch palsies (especially spine ischemia and quadriplegia may ensue.
peroneal nerve and lateral femoral
cutaneous nerve injury due to improper
positioning of the lower extremities)
Prone position ■ Postoperative blindness (most commonly
Body Positioning
due to OIN)
■ Pressure sores
■ Brachial plexus injuries Key Concepts
■ Vascular compression with subsequent
quadriplegia • The supine position is the easiest, most common position
used for neurosurgical procedures and does not require any
Sitting position ■ Pneumocephalus special equipment.
■ Quadriplegia (due to cervical spine ischemia
• Risks of neurosurgical procedures in the lateral position
from extreme head and neck flexion)
■ Pressor support and mechanical ventilation include kinking of the jugular vein and brachial plexus injury,
for severe VAE peripheral nerve injury, and ventilation-perfusion mismatch.
• Turning a patient prone may necessitate being disconnected
OIN, optic ischemic neuropathy; VAE, venous air embolism. from monitors, vascular lines, and the ventilator and should be
done carefully but efficiently.
• VAE is a potentially catastrophic complication that can occur
to stop the bleeding. Occasionally, the holes may require in the sitting position, and the risk-to-benefit ratio of
closure with sutures or staples. Furthermore, the removal performing procedures in this position has been heavily
of the pins may increase the risk of venous air embolism debated.
(VAE). For procedures in the sitting position, where the risk
of VAE is highest, the placement of antibiotic ointment on
Neurosurgical procedures are generally performed with
the pins is advocated to prevent VAE.6
the patient in the supine, lateral, prone, or sitting position
or in a variation of one of these positions. Each of these
HEAD AND NECK POSITIONING positions has unique associated benefits and risks that
should be considered in the preoperative assessment
The positioning of the head and neck is one of the most
(Table 2.3). A comprehensive understanding of the risks
important aspects of patient positioning for neurosurgical
associated with each of these positions is essential for
procedures8 because the orientation of the head provides
ensuring patient safety during the neurosurgical proce-
the neurosurgeon with the appropriate surgical approach
dure. Especially after long procedures, an incorrectly posi-
and exposure. There are a few basic principles of positioning
tioned patient may be at increased risk of postoperative
the head and neck that are important to consider, and vig-
complications.
ilance on the part of the surgeon and anesthesiologist are
vital in preventing complications. First, the patient’s neck
mobility and stability should be assessed prior to surgery SUPINE POSITION
and should dictate the extent of intraoperative head and
neck positioning. If a patient reports neurological symptoms The supine position is the most common position employed
associated with neck mobility, one should avoid or minimize for neurosurgical procedures.8 The supine position is easily
hyperflexion, hyperextension, lateral flexion, or rotation.6 achieved and is arguably associated with the lowest risk of
Extreme hyperflexion of the neck may result in obstruc- complications. Moreover, the supine position does not
tion of venous and lymphatic drainage from the head, require any special equipment.
resulting in tongue and face swelling, and increased intra- For patients in the supine position, special attention
cranial pressure. Extreme hyperflexion can also cause should be paid to the extremities. The arms are typically
18 SECTION 1 • Neuroanesthesia and Perioperative Care
Table 2.3 Advantages and Risks Associated with the Four Primary Patient Positions Employed in Neurosurgical Procedures
Advantages Risks
LATERAL ■ Best surgical access for temporal lobe ■ Kinking of the jugular vein and brachial plexus injury
■ Three-quarter prone position allows for access to the posterior ■ Peripheral nerve injury
cranial fossa with less risk of venous air embolism and increased ■ Ventilation/perfusion mismatch
surgeon comfort (compared with the sitting position) ■ Fluid accumulation in the dependent lung
PRONE ■ Best surgical access to the suboccipital region or posterior spine ■ Typically necessitates disconnection from monitors, vascular
■ Low risk of venous air embolism compared with the sitting position lines, and ventilator
■ Potential injury when turning prone
■ Decreased pulmonary compliance with increased peak
airway pressure
■ Increased intracranial pressure
■ Poor airway access
■ If arms are tucked at the patient’s sides, vascular access may
be lost
■ Postoperative blindness
SITTING ■ Best surgical access for posterior cranial fossa ■ Significant hypotension and reduced cerebral perfusion
■ Reduced tissue retraction results in improved exposure and pressure
reduced risk of cranial nerve damage ■ Highest risk of venous air embolism (compared with other
■ Improved cerebrospinal fluid drainage, resulting in reduced positions)
intracranial pressure ■ Many clinicians advocate for screening for a patent foramen
■ Improved cerebral venous drainage, resulting in potentially ovale
reduced surgical blood loss
■ Good airway access
Clinical Pearl
When placing patients in the lateral position, one should be
especially careful to place an axillary roll under the upper
part of the chest to prevent brachial plexus injury.
PRONE POSITION
Fig. 2.2 Three-quarters (lateral oblique) positioning. The principles
of three-quarter positioning resemble those for the lateral position, but The prone position is often preferred for surgical access to
the head may be placed on the table or in pins, and the dependent the suboccipital region or posterior spine.12 A variety of
(lower) arm may be placed behind the body or in a sling below the face prone configurations and support frames are used
for a so-called park bench modification. If a suboccipital approach is
required, the nondependent (upper) shoulder may need to be taped (Fig. 2.3). Prior to turning the patient prone, the patient
down toward the foot. However, this can cause additional stretching is typically induced under general anesthesia on the hospi-
of the brachial plexus with associated risk of postoperative neuropa- tal bed in the supine position. Venous and arterial access is
thy. (Adapted from Goodkin R, Mesiwala A. General principles of oper- established, and the bladder is catheterized. The head is
ative positioning. In: Winn RH, ed. Youmans Neurological Surgery, 5th ed.
Philadelphia: Saunders; 2004; with permission.)
then fixed in the Mayfield frame (for intracranial and cervi-
cal spine procedures), and the patient is subsequently
A B
C D
Fig. 2.3 Examples of positioning frames for spinal surgery designed to minimize vertebral venous distension: (A) Tuck position; (B) Canadian frame;
(C) Relton Hall type frame; (D) Andrews frame; (E) Wilson frame. (Adapted from Schonauer C, Bocchetti A, Barbagallo G, Albanese V, Moraci A. Posi-
tioning on surgical table. European Spine Journal. 2004;13(Suppl. 1):S50–S5.)
2 • Patient Positioning for Neurosurgical Procedures 21
turned onto the operating room table. Alternatively, special cerebral perfusion pressure. Compared with the sitting posi-
operating tables (such as the RotoProne) have the ability to tion, surgery in the prone position may provide excellent
rotate the patient prone without having to transfer the posterior access with a significantly lower risk of VAE.
patient to a different bed.
Turning the patient prone should be done with extreme
caution and with the coordination of several staff members. Clinical Pearl
The surgeon, not the anesthesiologist, should be responsi-
ble for controlling the head and spine during the turn as the The most common risk factors associated with postoperative
anesthesiologist ensures security of the endotracheal tube. visual loss include the prone position, length of surgery over
The surgeon must be especially careful to maintain the 6 hours, intraoperative hypotension, and significant
blood loss.
head in a stable and neutral position during the turn to pre-
vent any spinal injury. Turning the patient prone may
require that the patient be disconnected from the ventilator
circuit and monitors, causing a brief temporary period of no Postoperative visual loss is a rare but devastating com-
monitoring or ventilation. During the turn, special care plication after surgery in the prone position (Table 2.2).
must be made to monitor all lines, urinary catheter, and The incidence and mechanism of visual loss are poorly
endotracheal tube. There must be cooperation between understood.17 The four causes of postoperative visual loss
the surgical and anesthesia team to ensure that the patient include ischemic optic neuropathy (most common cause,
is efficiently turned and reconnected to the ventilator and accounting for approximately 89% of cases of postopera-
monitors in a timely fashion. tive visual loss), central retinal artery occlusion, cortical
Once the patient is turned and reconnected to the ven- infarction, and external ocular injury. The most common
tilator circuit and monitors, the patient’s body, extremities, risk factors associated with postoperative visual loss
and eyes should be examined. When positioning the body, include the prone position, length of surgery over 6 hours,
special care should be taken to avoid excessive intraab- intraoperative hypotension, and significant blood loss. It
dominal pressure. Pressure on the abdomen may occlude should be noted, however, that the risk factors are specu-
the inferior vena cava, thereby decreasing venous return lative based on associations made in retrospective
and increasing bleeding for lumbar surgery (Chapter 7), reports.18 There is no effective treatment for ischemic optic
and may prevent or impair optimal diaphragmatic excur- neuropathy (see also Chapter 4). Other potential postoper-
sion during ventilation. Providing adequate chest support ative complications include pressure sores, brachial plexus
may reduce pressure on the abdomen. The arms and knees injuries, and vascular compression with subsequent
should be padded over the bony prominences to prevent quadriplegia.6
skin breakdown due to mechanical pressure. The shoul-
ders should not be abducted more than 90 degrees, and SITTING POSITION
the arms should be flexed. The knees should be flexed,
and one should avoid excessive plantar flexion of the feet. The sitting position (Fig. 2.4) has traditionally been the pre-
Male genitalia should hang freely, the eyes should be taped ferred position to surgically access the posterior cranial
shut and free from orbital compression, and the breasts fossa or posterior cervical spine.12 Although the prone
should be adequately padded. The head should be fixed and lateral positions may also be used when operating on
in the neutral or flexed position as indicated by the the posterior cranial fossa, the sitting position offers several
surgery. physiological advantages. The effects of gravity facilitate an
If the patient’s head is not fixed in a Mayfield frame, a improvement in cerebrospinal fluid drainage, consequently
prone foam pillow with cutouts for the eyes, nose, and air- lowering intracranial pressure more than any other posi-
way should be used. It should be noted that a prone pillow is tion.19 Compared with other positions, there is improved
only available in one height, and neck hyperextension may exposure of the posterior cranial fossa due to less tissue
occur in smaller patients.7 During the procedure, the eyes retraction, and there is a reduced risk of cranial nerve dam-
should be checked at least every 15 minutes to ensure that age. Cerebral venous drainage is also improved, thereby
there is no orbital compression.15 During long procedures draining blood away from the surgical field. This results
in the prone position, there may be significant facial edema in optimal surgical conditions and potentially less surgical
that occurs. After letting the endotracheal tube cuff down, blood loss than other positions.
the absence of a leak around the cuff may necessitate post- Compared with the prone position, the patient’s airway is
operative ventilation. easily accessible to the anesthesiologist when in the sitting
Compared with the supine position, the prone position position. Furthermore, intrathoracic pressure is lower in
may lower the patient’s pulmonary compliance, resulting the sitting position, allowing for easier ventilation. In the
in higher peak airway pressure. Furthermore, the prone event of cardiac arrest, cardiopulmonary resuscitation
position results in decreased venous return to the heart, (CPR) in the sitting position is easier than in the prone posi-
with increased systemic and pulmonary vascular resis- tion, and the bed can be positioned to facilitate CPR.
tance.6 The prone position also increases intracranial pres- Neurosurgery in the sitting position is associated with
sure and should be used with caution in patients with significant and potentially life-threatening risks. The effects
reduced intracranial compliance.16 The prone position is of gravity on venous drainage make patients prone to
advantageous in that it improves matching of ventilation potentially significant hypotension, thereby reducing cere-
and perfusion, resulting in improved arterial oxygenation bral perfusion pressure. The drop in blood pressure may be
and cerebral tissue oxygenation, as well as increased partially ameliorated by a fluid bolus prior to positioning,
22 SECTION 1 • Neuroanesthesia and Perioperative Care
Fig. 2.4 “Sitting” position with Mayfield head pins. This is actually a modified recumbent position because the legs are kept as high as possible to pro-
mote venous return. Arms must be supported to prevent shoulder traction. Note that the head holder support is preferably attached to the back section
of the table so that the patient’s back may be adjusted or lowered emergently without first detaching the head holder. If the head holder is connected to
the thigh section of the table, this cannot be done. (Reprinted from Cassorla L, Lee J-W. Patient positioning and anesthesia. In: Miller RD, ed. Miller’s
Anesthesia. Maryland Heights: Churchill-Livingstone; 2009: pp. 1151–70.).
administration of vasopressors, application of elastic bands VAE is typically detected with end-tidal CO2, precordial
to the lower extremities, and positioning the patient to the Doppler, or transesophageal echocardiogram, although
sitting position in increments. Furthermore, the sitting no single monitoring modality will accurately predict all
position is associated with an increase in pulmonary and cases of VAE.22 In the event of a VAE, hypoxemia can
systemic vascular resistance.20 quickly ensue due to an increase in dead space in the lungs.
VAE is a potentially catastrophic complication that can Right heart strain can further result in cardiac ischemia
occur when neurosurgery is performed in the sitting posi- and significant hypotension and cardiac arrest. A paradox-
tion. VAE can occur when there is an open vein and a pres- ical air embolism can lead to significant neurological
sure gradient between the surgical site and the heart. The sequelae, including stroke and quadriplegia. Patients with
risk of VAE in the sitting position greatly varies depending VAE can also develop thrombocytopenia, increasing the
on the type of procedure. The noncollapsible venous sinuses patient’s risk of bleeding.23
are exposed during posterior cranial fossa surgery, making Due to the increased risk of VAE in patients with a PFO,
these procedures particularly high risk. The presence of a many clinicians advocate for routine preoperative screen-
patent foramen ovale (PFO) further increases the risk of ing with contrast-enhanced transesophageal, transtho-
introducing a paradoxical embolism into the systemic cir- racic echocardiography. In recent years, transcranial
culation. Stendel and colleagues21 demonstrated a preva- Doppler has emerged as an inexpensive, noninvasive, and
lence of PFO in 27% of patients with a posterior cranial easy method of assessing for PFO.21 In short, a contrast
fossa lesion. They further demonstrated the presence of agent with a small amount of air is injected into the ante-
VAE in 75% of patients during posterior cranial fossa sur- cubital vein. If a right to left shunt is present, the contrast
gery in the sitting position. It should be noted that the risk will bypass the pulmonary circulation and result in micro-
of VAE is not unique to the sitting position and can occur embolic signals in the basal cerebral arteries. The quantity
during surgery in the prone or lateral position as well, pro- of microbubbles indicates the severity of PFO. When a neu-
viding the venous pressure in the surgical bed is subatmo- rosurgical procedure is preferred in the sitting position and
spheric, which typically can arise when the level of the a PFO is found on screening, some authors recommend that
surgery is above the heart. the PFO be surgically closed prior to surgery.24
2 • Patient Positioning for Neurosurgical Procedures 23
Postoperative tension pneumocephalus can occur in up position may occur with or without the use of nitrous oxide.
to 3% of posterior cranial fossa surgeries in the sitting posi- With extreme head and neck flexion, quadriplegia may
tion.25 Tension pneumocephalus may result when air result from cervical spine ischemia. In the event of a signif-
enters the epidural space in large enough volumes to cause icant VAE, continued pressor support and mechanical ven-
a mass effect, which can result in life-threatening brain her- tilation may be needed in the postoperative period.
niation. Some authors recommend that minute ventilation
be decreased to allow for brain expansion as the dura is
closed,26 and nitrous oxide should be avoided in the first Summary
14 days after posterior cranial fossa surgery. The risk is fur-
ther decreased by the placement of a ventriculostomy The long duration of neurosurgical procedures and the fact
drain, which is commonly placed after major posterior fossa that patients are completely covered by drapes makes
surgeries in the sitting position. proper patient positioning especially critical. When decid-
Extreme neck flexion, in which the chin rests on the ing the patient’s position during surgery, the benefits
chest, combined with the use of an oropharyngeal airway of optimal surgical access and surgeon comfort should
or transesophageal probe that obstructs venous and lym- be weighed against the risks of a particular position. A com-
phatic drainage, can result in significant postoperative ton- prehensive preoperative assessment is vital, and the
gue edema.26 This can result in postoperative airway position decided on should be communicated to the anes-
obstruction and hypoxemia. Careful positioning of the neck thesiologist and nursing staff as early as possible. Proper
and proper placement of a bite block rather than an oropha- patient positioning requires the cooperation and communi-
ryngeal airway may reduce this risk. cation between all operating room personnel.
Rarely, peripheral neuropathies can result from neuro- Fixing the patient’s head in a Mayfield stereotaxic frame,
surgical procedures in the sitting position. The most com- positioning the head and neck, and positioning the body
monly injured nerve in the sitting position is the all deserve special attention and consideration. Pinning
common peroneal nerve, resulting in foot drop. Injury to the head may result in significant hypertension and tachy-
the common peroneal nerve may be due to ischemic com- cardia and should be anticipated by the anesthesiologist.
pression or from stretching the sciatic nerve. Prior to pinning, patients should be preemptively treated
The risk-to-benefit ratio of neurosurgical procedures in with an opioid or anesthetic agent, and blood pressure
the sitting position has been considerably debated.24,27 In should be carefully monitored during this time. During
recent years, the sitting position has largely fallen out of positioning of the head and neck, a patient’s preoperative
favor in the United States due to fear of its associated com- mobility should be considered. Extreme hyperflexion is
plications. Today, the most common procedure done in the discouraged, and at least 2–3 fingerbreadths should be
sitting position in the United States is an insertion of a deep- maintained between the mandibular protuberance and
brain stimulator8 or occasionally for difficult-to-access manubrium at all times.
lesions such as pineal tumors. In Europe, the sitting posi- Each patient position is associated with unique benefits
tion is still very popular and is the preferred position for sur- and risks and should be considered for all neurosurgical
gery of the posterior cranial fossa.28 patients. Peripheral nerve injury is possible in all positions,
It has never been firmly established that neurosurgical pro- and care should be taken when positioning the extremities.
cedures in the lateral or prone position are safer than the sit- Similarly, there is a risk of VAE in all procedures in which
ting position. Many authors have argued that the fear of the operative site is above the heart, with the highest risk in
catastrophic complications related to the sitting position the sitting position.
seems unwarranted.29 With an experienced surgical and
anesthesia team, neurosurgery in the sitting position may
be done safely and may be advantageous to the prone References
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analyzed 85 pediatric patients undergoing craniotomy for associated with anesthesia. Anesthesiology. 1990;73(2):202–207.
2. McCaig C. Review: positioning for neurosurgery. AORN J. 1978;28
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experienced fewer intraoperative and postoperative compli- Perioperative Peripheral N. Practice advisory for the prevention of
cations, with a shorter intensive care and hospital stay. perioperative peripheral neuropathies: an updated report by the
When the sitting position is preferred for a neurosurgical American Society of Anesthesiologists Task Force on prevention of
perioperative peripheral neuropathies. Anesthesiology. 2011;114
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in the early detection of VAE. The presence of a right to left 4. Brisman MH, Bederson JB, Sen CN, Germano IM, Moore F, Post KD.
intracardiac shunt has generally been considered an absolute Intracerebral hemorrhage occurring remote from the craniotomy site.
contraindication to surgery in the sitting position, although Neurosurgery. 1996;39(6):1114–1121. discussion 21–2.
5. Koller M, Ortler M, Langmayr J, Twerdy K. Posterior-fossa haemor-
this premise has been challenged in recent years. Limited data rhage after supratentorial surgery—report of three cases and review
suggest that even patients with a PFO may be safely operated of the literature. Acta Neurochir. 1999;141(6):587–592.
on in the sitting position, with minimal risk of VAE.33–35 Rel- 6. Rozet I, Vavilala MS. Risks and benefits of patient positioning during
ative contraindications include severe atherosclerotic coro- neurosurgical care. Anesthesiol Clin. 2007;25(3):631–653.
7. Silverman RB. Ruskin KJ, Rosenbaum SH, Rampil IJ, eds. Positioning
nary artery disease and severe hypotension or hypertension. for Neurosurgery. New York: Oxford University Press; 2014.
In the immediate postoperative period, pneumocephalus 8. Lapointe G, Kemp J, Rajan G, Walter GE, Abdulrauf SI. Ellenbogen RG,
is common and may persist for weeks after surgery6 Abdulrauf SI, Sekhar LN, eds. Principles of Surgical Positioning.
(Table 2.2). Pneumocephalus after surgery in the sitting Philadelphia: Saunders; 2012.
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9. Fan JY. Effect of backrest position on intracranial pressure and cere- 22. Lindroos AC, Niiya T, Randell T, Romani R, Hernesniemi J, Niemi T.
bral perfusion pressure in individuals with brain injury: a systematic Sitting position for removal of pineal region lesions: the Helsinki expe-
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perfusion pressures in traumatically brain-injured adults. Am J Crit cytopenia. Anaesthesia. 2011;66(1):25–30.
Care: An Official Publication, American Association of Critical-Care 24. Fathi AR, Eshtehardi P, Meier B. Patent foramen ovale and neurosur-
Nurses. 2000;9(6):373–380. quiz 81–2. gery in sitting position: a systematic review. Br J Anaesth. 2009;102
11. Rosner MJ, Coley IB. Cerebral perfusion pressure, intracranial pres- (5):588–596.
sure, and head elevation. J Neurosurg. 1986;65(5):636–641. 25. Standefer M, Bay JW, Trusso R. The sitting position in neurosurgery: a
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13. Shimizu S, Sato K, Mabuchi I, Utsuki S, Oka H, Kan S, et al. Brachial 26. Porter JM, Pidgeon C, Cunningham AJ. The sitting position in neuro-
plexopathy due to massive swelling of the neck associated with crani- surgery: a critical appraisal. Br J Anaesth. 1999;82(1):117–128.
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3 Anesthetic Considerations
for Craniotomy
DEEPAK SHARMA and K.H. KEVIN LUK
25
26 SECTION 1 • Neuroanesthesia and Perioperative Care
Table 3.1 ASA Classification of Physical Status Cushing’s reflex (hypertension, bradycardia, and irregular
breathing) in a patient with intracranial mass lesions trig-
ASA Physical gers rapid intervention to acutely decrease the intracranial
Status Disease State
pressure (ICP). Finally, preexisting motor deficits are iden-
1 A normal healthy patient tified to avoid life-threatening hyperkalemia secondary to
succinylcholine.13
2 A patient with mild systemic disease
Review of neuroimaging is pertinent to anesthetic
3 A patient with severe systemic disease management. Computed tomography (CT) and magnetic
4 A patient with severe systemic disease that is a resonance imaging scans are reviewed to predict intra-
constant threat to life operative brain swelling and risk of bleeding. The degree
of midline shift, peritumoral edema, and a diagnosis of
5 A moribund patient who is not expected to survive
without the operation
glioblastoma multiforme or metastasis are independent
predictors of brain swelling.14 The presence of subdural
6 A patient declared brain-dead whose organs are hematoma on imaging is associated with intraoperative
being removed for donor purposes hyperglycemia, as well as intraoperative hypotension, dur-
ASA, American Society of Anesthesiologists. ing emergent craniotomy.15,16 Cerebral angiograms provide
Excerpted from the Relative Value Guide 2008 of the American Society of information regarding collateral vessels, which is helpful in
Anesthesiologists. A copy of the full text can be obtained from ASA, 520 N. anticipating the risk of cerebral ischemia (and hence the
Northwest Highway, Park Ridge, IL 60068-2573.
need for neuroprotective interventions) during temporary
clipping for aneurysm surgery. Tumors adjacent to the
superior sagittal sinus or other dural sinuses suggest a risk
perioperative seizure. Discussion of relevant social/religious of hemorrhage and venous air embolism.
background (e.g., Jehovah’s Witnesses, who may not want
to receive blood transfusion), as well as personal prefer-
ences (such as “do not resuscitate” orders), is imperative Clinical Pearl
to anesthetic planning. Establishing a rapport with the
patient preoperatively is invaluable if an awake craniotomy Proper preanesthesia evaluation is critical—a consultation
is being planned. with an internist and routine screening tests do not replace
A comprehensive physical examination is critical for preanesthesia evaluation.
anesthetic planning. Preoperative correction of dehydra-
tion in patients with reduced intake of fluids, vomiting,
or the use of diuretics and contrast agents can prevent
hypotension after induction of anesthesia. Recording of
preoperative vital parameters provides baseline values to Goals of Anesthetic Management
direct hemodynamic management. Assessment of the
airway is mandatory to ensure the ability to adequately The general goal of intraoperative anesthetic management
oxygenate and ventilate under anesthesia. Modified Mal- is to render the patient unconscious and immobile to facil-
lampati scoring, thyromental distance, presence of overbite itate surgery, to provide adequate analgesia, and to main-
or underbite, and the range of neck flexion-extension tain homeostasis and vital functions. The anesthetic goals
collectively provide an estimate of the risk for difficult intu- specific to craniotomy are listed in Box 3.1. These goals are
bation. Difficult airway should be anticipated in patients accomplished by selection of appropriate pharmacological
who have recently undergone a frontotemporal craniot- agents, careful titration of hemodynamic and ventilation
omy and may have developed a pseudoankylosis of the tem- parameters, and vigilant neuromonitoring and will be
poromandibular joint,10 acromegalic patients undergoing described in detail later.
pituitary surgery,11 and patients with cervical spine lesions
or with cervical immobilization devices (internal or exter-
nal). Recognition of potential airway difficulty allows
proper planning with the availability of equipment and
resources and formulation of a backup plan. Patients with Box 3.1 Anesthetic Goals for Craniotomy
depressed level of consciousness are likely to have a reduced
need for anesthetic agents and are more likely to emerge 1. Provide adequate amnesia, analgesia, and immobility
from anesthesia slowly postoperatively. The presence of 2. Optimize cerebral blood flow and oxygenation
brainstem lesions or lower cranial nerve dysfunction pre- 3. Control intracranial pressure
disposes patients to an increased risk of aspiration, and 4. Avoid secondary physiological insults (hypotension, hypoxia,
extubation of the trachea may electively be delayed. hyper-/hypoglycemia, hyper-/hypocarbia, hyperthermia,
Patients with ruptured intracranial aneurysms with higher seizures)
Hunt and Hess grades are more likely to have impaired 5. Provide optimal operating conditions (brain relaxation)
6. Facilitate intraoperative neurophysiological monitoring
cerebral autoregulation (and, hence, susceptibility to 7. Provide intraoperative neuroprotection
hemodynamic fluctuations) in addition to the higher 8. Avoid positioning-related complications
chance of associated diminished airway reflexes and cardio- 9. Accomplish early emergence after surgery to facilitate
pulmonary, metabolic, and electrolyte imbalances com- neurological assessment
pared with patients with lower Hunt and Hess grades.12
3 • Anesthetic Considerations for Craniotomy 27
patients under propofol anesthesia may lead to excessive Hemodynamic Management under
cerebral vasoconstriction and can cause cerebral
ischemia.23 Anesthesia
Positron emission tomography studies demonstrate that
although both sevoflurane and propofol similarly reduce Key Concepts
CMR in all brain areas, sevoflurane decreases CBF in some
and propofol in all brain structures, and only propofol • According to the Brain Trauma Foundation guidelines, the
reduces cerebral blood volume in the cortex and cerebel- recommended CPP for TBI is 50 to 70 mm Hg.
lum.19 In an open-label study of patients with supratentor- • Hypertension should be avoided in patients with unsecured
ial cerebral tumors randomized to propofol-fentanyl, aneurysms.
isoflurane-fentanyl, or sevoflurane-fentanyl anesthesia, • Blood pressure is actively decreased after resection of large
the ICP was significantly lower and cerebral perfusion arteriovenous malformations to prevent normal perfusion
pressure (CPP) higher in patients who received propofol pressure breakthrough and hyperemia.
• Emerging data suggest that the lower and upper limits of
anesthesia.21 The cerebral swelling after opening of the
cerebral autoregulation may be more variable and the range
dura was also lower in patients who received propofol, of autoregulation narrower than previously believed.
but the arteriovenous oxygen difference was higher and • Warm, nonglucose-containing isotonic fluids are preferred
jugular venous saturation and carbon dioxide reactivity during craniotomy.
lower in patients anesthetized with propofol.21 Moreover,
cerebral autoregulation is impaired at 1.5 MAC by isoflur-
ane and desflurane, whereas propofol preserves it.24 These Optimization of hemodynamic parameters is important
and similar other findings indicate the potential benefit of to ensure adequate cerebral perfusion during craniotomy.
propofol anesthesia in patients with intracranial tumors. Patients with neurosurgical disorders are likely to have
Importantly, propofol-induced burst suppression after trau- impaired cerebral autoregulation31 and, hence, increased
matic brain injury (TBI) may not reduce the level of susceptibility to hemodynamic fluctuations. The hemody-
regional ischemic burden measured by arterial-jugular namic goals differ depending on the intracranial pathology
venous oxygen differences.25 However, low-dose inhaled as well as comorbid conditions. The current guidelines rec-
agents as part of balanced anesthesia are often effectively ommend maintaining CPP between 50 and 70 mm Hg and
used by neuroanesthesiologists to provide optimal opera- mean arterial pressure above 90 mm Hg in patients with
tive conditions during craniotomy.26 severe TBI. Intraoperative hypotension is anticipated
Numerous other factors, such as the effect on evoked in patients with multiple lesions on the CT, subdural
potential signal quality, are considered in selecting an hematoma, and thickness of lesion15 and is frequently
anesthetic agent. Although the inhalational agents cause encountered after decompression of the brain. Hypoten-
dose-dependent increases in latency and decreases in sion is also undesirable in patients with occlusive cerebro-
amplitude of somatosensory-evoked potentials (SSEPs), vascular disease such as Moyamoya and intracranial
less than 1.0 MAC concentration is generally compatible arterial stenosis. Conversely, in patients undergoing crani-
with monitoring of cortical SSEPs, although propofol otomy for aneurysm clipping, the goal is to avoid acute
anesthesia does not affect SSEPs.27 However, if motor- increases in blood pressure that may risk rebleeding due
evoked potential monitoring is contemplated, many neu- to increase in the transmural pressure. Calcium channel
roanesthesiologists prefer propofol anesthesia, especially blockers such as nicardipine and short-acting beta-
in patients who may have preexisting neurological defi- blockers like esmolol are sometimes used to actively
cits. It should be noted that despite the apparent pre- decrease the blood pressure. However, during the periods
ference for propofol, <0.5 MAC of desflurane is also of temporary clipping, the blood pressure may be actively
compatible with motor-evoked potentials.28,29 Ketamine raised to ensure blood flow through the collateral channels
is also often added to support motor-evoked potentials, to avoid cerebral ischemia. Once the aneurysm is secured,
but its use requires consideration of potential for increased the blood pressure goals are normalized. Occasionally, in
CMR and CBF. Motor-evoked potentials also preclude order to facilitate clipping of giant basilar tip aneurysms,
the use of neuromuscular blocking agents, whereas intraoperative temporary cardiac standstill is provided
brainstem-evoked potentials are, in general, most resis- using high-dose adenosine (0.2–0.3 mg/kg).32 Blood pres-
tant to the effect of anesthetic agents. The choice of sure is actively reduced after the resection of arteriovenous
anesthetic agents is also determined by the need for malformation to prevent hyperemia and normal perfusion
intraoperative electrocorticography or motor mapping. pressure breakthrough.
There is growing evidence regarding potential epilepto- Invasive arterial blood pressure monitoring is used to
genicity of sevoflurane.30 titrate hemodynamic goals during craniotomy. Myocardial
stunning is not uncommon after aneurysmal subarachnoid
hemorrhage, which can result in a Takotsubo-like cardio-
Clinical Pearl
myopathy. Myocardial dysfunction has also been described
in the setting of TBI. Although the effects of vasopressor
Volatile anesthetic agents cause cerebral vasodilatation
only in concentrations above 1.0 MAC. agents on cerebral vasculature have not been fully deci-
Low-concentration volatile anesthetics may be safely used phered, the inotropic and vasopressor medication choices
in combination with mild hyperventilation without can contribute to such comorbidities. The arterial pressure
causing brain swelling. transducer is zeroed and positioned at the level of the exter-
nal auditory meatus to ensure adequate CPP and CBF, and
3 • Anesthetic Considerations for Craniotomy 29
is especially prudent in patients undergoing craniotomy in feasible.35 Jugular venous oximetry can be used intraopera-
the sitting position. tively to optimize oxygen delivery to the brain.36 Jugular
Patients undergoing craniotomy typically receive venous saturation maintained between 50% and 70%
nonglucose-containing warm, isotonic intravenous fluids. serves as a surrogate for the balance between the global
Hypotonic fluids like lactated Ringer’s solution are avoided cerebral oxygen delivery and metabolic requirement and
because they can worsen cerebral edema and brain swell- is useful in individualizing blood pressure and ventilation
ing. Despite the use of diuretics to facilitate brain relaxation, parameters intraoperatively.36
the goal is to maintain normovolemia during the proce-
dure. Albumin may be associated with poor outcomes in
patients with TBI and hence is often avoided.33 Because Intracranial Pressure Management
cerebral salt wasting, diabetes insipidus, hypokalemia,
and hypocalcemia are often associated with intracranial
and Brain Relaxation
disease, electrolytes are periodically monitored under anes-
thesia and corrected accordingly. Surgical blood loss can Key Concepts
sometimes be substantial, requiring blood transfusion.
Some typical examples include resection of a large arterio- • Hyperventilation should be used selectively—prolonged and
venous malformation or meningioma, intraoperative excessive hyperventilation must be avoided.
rupture of an aneurysm, and inadvertent vascular injury. • Steroids should not be administered to patients with TBI.
The transfusion triggers for neurosurgical patients are
somewhat elusive, although historically, a hemoglobin Patients presenting for craniotomy often have elevated
level of 10 g/dL was often considered to be a balance ICP. In addition, brain relaxation is desirable to facilitate
between optimal oxygen-carrying capacity and rheology surgical exposure and brain retraction. The various inter-
of blood to facilitate perfusion of cerebral microvasculature. ventions used intraoperatively for brain relaxation and
However, more recently, lower hemoglobin values have ICP reduction are listed in Box 3.2. Briefly, maintenance
been advocated in neurosurgical patients. Anemia in neu- of adequate anesthesia and analgesia is essential to avoid
rosurgical patients is associated with poor outcomes, but so cerebral metabolic demand associated with increase in
is the use of transfusion of blood. Intraoperative decision to CBF, which may cause swelling of a poorly compliant brain.
transfuse blood is often made based on overall fluid and Volatile anesthetic agents are used in low concentrations to
hemodynamic status, hemoglobin value, and rapidity of avoid direct cerebral vasodilation, and in patients where
blood loss, taking into account the patient’s cardiac comor- brain swelling is anticipated, intravenous anesthesia with
bidity and neurological dysfunction, including estimates of propofol (but avoiding hypotension) is often preferred.21
cerebrovascular reserve (i.e., capability to vasodilate in Optimal patient positioning is critical because excessive
compensation for anemia). Although the safety of acute flexion or rotation of the neck can lead to obstruction of
normovolemic hemodilution during craniotomy has been cerebral venous drainage, resulting in brain swelling.
demonstrated,34 the practice has not gained substantial Slight head elevation is desirable to facilitate cerebral
popularity. venous drainage. Avoidance of hypercarbia with controlled
ventilation is critical, and moderate hypocarbia (PaCO2
Clinical Pearl
Nonglucose-containing warm, isotonic intravenous fluids Box 3.2 Strategies for Intraoperative Brain
are preferable during craniotomy. Strict hemodynamic Relaxation and Control of Intracranial Pressure
control is critical.
1. Maintenance of adequate depth of anesthesia and analgesia
2. Selection of appropriate anesthetic agents (intravenous
anesthetics for patients with anticipated brain swelling)
3. Optimal positioning with slight head elevation and avoiding
excessive neck flexion or rotation
Intraoperative Monitoring 4. Optimization of hemodynamic parameters
5. Controlled ventilation with normocarbia to moderate
The details of intraoperative neuromonitoring are dis- hypocarbia (PaCO2 30–35 mm Hg)*
cussed in Chapter 6. Briefly, the ASA recommends monitor- 6. Mannitol (osmotic diuretic)
ing electrocardiography, blood pressure, pulse oximetry, 7. Furosemide
capnography, temperature, and anesthetic concentration 8. Hypertonic saline
monitoring for inhaled anesthetics. Arterial lines are also 9. Cerebrospinal fluid drainage (external ventricular drainage)
useful for hemodynamic monitoring and to sample PaO2, 10. Steroids in patients with tumors/vasogenic edema#
PaCO2, glucose levels, and electrolytes. Evoked potential 11. Treatment of fever/seizures
monitoring and electroencephalography are increasingly 12. Burst suppression with propofol/thiopental bolus
being used. In addition, monitoring for venous air embo- *Brief periods of hypocarbia with PaCO2 < 30 mm Hg should be used only
lism may include transesophageal echocardiography or in emergent conditions or when other ICP reduction maneuvers have
precordial Doppler. Monitoring cerebral blood flow velocity failed.
using transcranial Doppler ultrasonography may provide #
Steroids should not be administered in patients with traumatic brain
useful information in surgeries where probe placement is injury.
30 SECTION 1 • Neuroanesthesia and Perioperative Care
over the conventional balanced volatile technique in terms are closely monitored for adequacy of oxygenation and
of recovery and cognitive functions after craniotomy.43,44 ventilation, hemodynamic stability, pain control, neurolog-
However, patients who receive desflurane are likely to have ical recovery, and any complications. Data on the effect of
a shorter extubation and recovery time compared with craniotomy site on the severity of pain are somewhat con-
those who receive sevoflurane.44 Desflurane also provides flicting. Despite the associated risk of overdosing-related
earlier postoperative cognitive recovery and reversal to adverse effects such as respiratory depression with hypox-
normocapnia and normal pH in overweight and obese emia and/or carbon dioxide retention and increased
patients after craniotomy. Incorporation of dexmedetomi- CBF and ICP, judicious use of potent opioids such as fenta-
dine in the anesthetic regimen is another strategy to facil- nyl, morphine, and hydromorphone, including patient-
itate shorter emergence and recovery time in neurosurgical controlled analgesia (PCA), remains the cornerstone of
patients45 with attenuation of delirium, and scalp blocks postoperative pain management.47 The use of scheduled
have been shown to improve recovery profiles. tramadol in addition to narcotics may provide better
The adrenergic surge associated with emergence may be pain control in some patients, decrease the side effects asso-
treated with a short-acting opioid or an antihypertensive ciated with narcotic pain medications, encourage earlier
such as esmolol or nicardipine. Coughing and straining postoperative ambulation, and reduce total hospitalization
on the tracheal tube during emergence can be prevented costs.48 Importantly, tramadol does present a small
with lidocaine or judicious use of remifentanil. Dexmedeto- increased risk of seizure in addition to the high incidence
midine has both sedative and analgesic properties, but does of vomiting. The cyclooxygenase-2 inhibitor parecoxib
not cause respiratory depression and is also useful in facil- has been found to offer no benefit in addition to local anes-
itating timely and smooth emergence. Perioperative hyper- thetic scalp infiltration, intravenous paracetamol, and mor-
tension has been associated with increased incidence in phine PCA after supratentorial craniotomy.49 Preoperative
postoperative intracranial hemorrhage in patients under- oral gabapentin used for antiepileptic prophylaxis in
going craniotomy and should be avoided.46 Unexpected patients undergoing craniotomy for supratentorial tumor
delay in emergence mandates ruling out potential con- resection can decrease the postoperative pain scores and
founding factors such as nonconvulsive status epilepticus, the total morphine consumption, albeit with increased
drug overdose, hypothermia, and hypoglycemia before an sedation postoperatively. Regional scalp blocks attenuate
imaging study will be performed to rule out an intracranial the postcraniotomy pain and stress responses but appear
cause. to remain underutilized. Although the published random-
ized controlled trials of regional scalp block are small and
of limited methodological quality, metaanalysis shows
Clinical Pearl reduced postoperative pain.50
PONV after elective craniotomy may affect up to two
Patients should almost never be extubated under deep thirds of patients. Selective serotonin (5-HT3) receptor
anesthesia after craniotomy. Extubation should be smooth antagonists are considered first-choice drugs for prophy-
and without hemodynamic response with a patient who can laxis of PONV due to their favorable safety profile. Ondan-
yield a valid neurological examination.
setron 4 mg given at the time of dural closure is safe and
effective in preventing emetic episodes after elective crani-
otomy. However, the effectiveness may be substantially
variable. Granisetron 1 mg provides comparable preven-
tion of emesis after supratentorial craniotomy. Metaanaly-
Immediate Postoperative sis of published data indicates that the cumulative
incidence of emesis but not nausea is significantly reduced
Management with 5-HT3 receptor antagonists at 24 and 48 hours.51
A single 600-mg dose of gabapentin also reduces the 24-
Key Concepts hour incidence of PONV. Other options, based on disparate
antiemetic mechanisms, for rescue of PONV include meto-
• Opioids are the mainstay of postcraniotomy pain control but clopramide, droperidol, and scopolamine.
should be used judiciously to avoid respiratory and Maintenance of adequate ventilation and oxygenation
neurological depression. postoperatively is critical. Some common indications for
• Regional scalp block prevents and attenuates the reintubation are neurological deterioration, respiratory
postcraniotomy pain and stress responses. distress, copious oropharyngeal secretions, and seizures.
• Selective serotonin (5-HT3) receptor antagonists are first- The neurological deterioration may be related to residual
choice drugs for prophylaxis of postoperative nausea and tumor with surrounding edema, intracerebral hemor-
vomiting (PONV).
rhage, or cerebral infarction. Patients who are not extu-
• Patients with neurological deterioration, respiratory distress,
copious oropharyngeal secretions, or seizures may need
bated at the end of surgery or require reintubation
reintubation. usually undergo imaging followed by transfer to the ICU.
• Effective hand-off with adequate communication is critical for A systematic and detailed hand-off communication is crit-
patient safety. ical to facilitate a smooth transition of care from the anes-
thesia providers to the ICU. Table 3.2 summarizes some
possible perioperative complications related to craniotomy
Immediate postoperative recovery arises in the posta- that may require special attention while transitioning to
nesthesia care unit or neurology ICU, where the patients intensive care.
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— Millainen hän sitten on? — kysyi Aljoša. — Onko hän kantelija?
Poika odotti ääneti ja uhmailevana vain sitä, että Aljoša nyt toki
välttämättömästi hyökkäisi hänen kimppuunsa. Kun hän näki että
tämä nytkään ei aio sitä tehdä, niin hän vimmastui kuin peto: hän
syöksyi paikaltaan ja hyökkäsi Aljošan kimppuun, eikä tämä
ennättänyt liikahtaakaan, kun ilkeä poika taivuttaen päänsä alas ja
tarttuen molemmin käsin hänen vasempaan käteensä puraisi
kipeästi hänen keskisormeaan. Poika pureutui siihen hampaineen
eikä noin kymmeneen sekuntiin päästänyt sitä irti. Aljoša huudahti
kivusta ja nyki kaikin voimin sormeaan. Poika päästi sen viimein irti
ja juoksi pois entisen välimatkan päähän. Sormea hän oli purrut
kipeästi aivan kynnen kohdalta syvälle luuhun asti, ja siitä virtasi
verta. Aljoša otti taskustaan liinan ja kääri sen tiukasti haavoitetun
käden ympäri. Käärimiseen meni melkein kokonainen minuutti. Poika
seisoi kaiken aikaa ja odotti. Viimein Aljoša kohotti häneen
rauhallisen katseensa.
— No, hyvä, — sanoi hän, — näette, kuinka kipeästi olette minua
purrut, kai se jo riittää? Sanokaa nyt, mitä minä olen teille tehnyt?
4.
Hohlakovien luona
— Sain kyllä.
Mutta heti kun Lise näki raosta Aljošan sormen, hän avasi oven
selko selälleen.
— Minä tuon heti kaikki, Lise, älä vain huuda äläkä ole levoton.
Näetkö, kuinka lujana Aleksei Fjodorovitš kantaa onnettomuutensa.
Missä te olettekaan voinut niin kamalasti haavoittua, Aleksei
Fjodorovitš?
— Se jäi sinne.
— Minkä tähden?
— Te loukkaatte minua!
— Enhän minä voinut tietää, että hän tulee tänne sormi purtuna,
muutenhan tosiaankin olisin voinut tehdä sen tahallani. Enkelini,
äitikulta, te alatte puhua tavattoman teräväjärkisesti.
— No, riittää jo, Lise, kenties minä tosiaankin olin liian kärkäs
puhumaan hullusta pojasta ja sinä teit jo omat johtopäätöksesi. Heti
kun Katerina Ivanovna sai kuulla teidän tulleen, Aleksei Fjodorovitš,
hän syöksyi luokseni, hänellä on hirveä, hirveä halu nähdä teitä.
— Ah, äiti! Menkää sinne yksin, hän ei voi nyt heti lähteä, hän
kärsii kovin.
— Ah, Lise, tuo on vain leikkiä sinun puoleltasi, vaan mitäpä, jos
tosiaankin nukkuisit! — huudahti rouva Hohlakov.
— Minä en tiedä, millä olen… Minä jään vielä noin kolmeksi tai, jos
niin tahdotte, viideksi minuutiksi, — mutisi Aljoša.
Mullerrus vierashuoneessa