CHAPTER 1

V O L U M E T H I R T Y - T H R E E

SUPRATENTORIAL TUMORS:
ANESTHETIZED, AWAKE,
AND COMPUTER-ASSISTED
MANAGEMENT

AUDRÉE A. BENDO, M.D.

PROFESSOR AND VICE CHAIR FOR EDUCATION
DEPARTMENT OF ANESTHESIOLOGY
SUNY/DOWNSTATE MEDICAL CENTER
BROOKLYN, NEW YORK

EDITOR: ALAN JAY SCHWARTZ, M.D., [Link].

ASSOCIATE EDITORS: M. JANE MATJASKO, M.D.
JEFFREY B. GROSS, M.D.

The American Society of Anesthesiologists, Inc.

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 Supratentorial Tumors: Anesthetized,
Awake, and Computer-assisted Management
Audrée A. Bendo, M.D.
Professor and Vice Chair for Education
Department of Anesthesiology
SUNY/Downstate Medical Center
Brooklyn, New York

Each year, more than 200,000 people in the United States are diagnosed with brain
tumors.1 Primary brain tumors comprise approximately 40,000 of these diagnoses.
Most brain tumors are metastatic, usually from breast and lung cancer. Brain tumors
are the leading cause of cancer death in children less than 20, now surpassing acute
lymphocytic leukemia, and the second leading cause of cancer death in males ages 20
to 29.1 The distribution of all primary brain and central nervous system (CNS) tumors
by site reveals that the majority are supratentorial.1

Pathophysiology
Supratentorial tumors (meningiomas, gliomas, and metastatic lesions) change intra-
cranial dynamics predictably. Initially, when the lesion is small and slowly expanding,
volume–spatial compensation occurs by compression of the cerebrospinal fluid (CSF)
compartment and nearby cerebral veins, which prevents increases in intracranial pres-
sure (ICP). As the lesion grows, compensatory mechanisms become exhausted, and any
further increase in tumor mass will cause progressively greater increases in ICP. Primary
or metastatic tumors or chronic subdural hematomas can present as chronic mass
lesions. Because of the ability of the intracranial compartment to compensate up to a
point, patients may exhibit minimal neurologic dysfunction despite the presence of a
large mass, elevated ICP, and shifts in the position of brain structures.
Significant changes in ICP can occur with supratentorial tumors if they develop
a central area of hemorrhagic necrotic tissue or a wide border of brain edema. As the
tumor enlarges, it can outstrip its blood supply, developing a central hemorrhagic area
that may expand rapidly, increasing ICP. Brain edema surrounding the tumor increases
the effective bulk of the tumor and represents an additional portion of the brain that
is not autoregulating. In such situations of compromised intracranial compliance, small
increases in arterial pressure may produce large increases in cerebral blood flow (CBF),
which can markedly increase intracranial volume and ICP with its attendant compli-
cations, that is, cerebral ischemia and herniation. In addition to hypertension, other
causes of increased cerebral blood volume such as hypercarbia, hypoxia, vasodilating
agents, and jugular venous obstruction can adversely affect cerebral hemodynamics
and must be avoided perioperatively.

Anesthetic Techniques and Drugs

The goal of neuroanesthetic care for patients with supratentorial tumors is to maxi-
mize therapeutic modalities that reduce intracranial volume. ICP must be controlled

1
2 BENDO

before the cranium is opened and optimal operating conditions obtained by produc-
ing a slack brain that facilitates surgical dissection. Various maneuvers and pharmaco-
logic agents have been used to reduce brain bulk (Table 1). For example, administra-
tion of diuretics or steroids, hyperventilation, and systemic blood pressure control may
be implemented preoperatively to reduce cerebral edema and brain bulk, thereby
reducing ICP. The application of these methods selectively or together, when neces-
sary, is often accompanied by marked clinical improvement.

Clinical Control of Intracranial Hypertension

Rapid brain dehydration and ICP reduction can be produced by administering the
osmotic diuretic, mannitol, or the loop diuretic, furosemide. Mannitol is given as an intra-
venous infusion in a dose of 0.25 to 1.0 g/kg−1. Its action begins within 10 to 15 minutes
and is effective for approximately 2 hours. Larger doses produce a longer duration of
action but do not necessarily reduce ICP more effectively. Furthermore, larger doses
and repeated administration can result in metabolic derangement. Mannitol is effec-
tive when the blood–brain barrier is intact. By increasing the osmolality of blood rela-
tive to the brain, mannitol pulls water across an intact blood–brain barrier from brain
to blood to restore the osmolar balance. When the blood–brain barrier is disrupted,
mannitol may enter the brain and increase its osmolality. Mannitol could pull water into
the brain as the plasma concentration of the agent declines and cause a rebound increase
in ICP. This rebound increase in ICP may be prevented by maintaining a mild fluid deficit.
Mannitol has been shown to cause vasodilation of vascular smooth muscle, which is
dependent on dose and rate of administration. Mannitol-induced vasodilation affects
intracranial and extracranial vessels and can transiently increase cerebral blood volume

TABLE 1. Clinical Control of Intracranial Hypertension

Diuretics: Osmotic: Mannitol (0.25 to 1 g/kg IV), hypertonic saline (under

investigation).
Furosemide: (0.5 to 1 mg/kg IV alone or 0.15 to 0.3 mg/kg IV in
combination with mannitol).
Corticosteroids: Dexamethasone (effective for localized cerebral edema surrounding
tumors; requires 12 to 36 hours).
Adequate ventilation: PaO2 ≥ 100 mm Hg, PaCO2 33 to 35 mm Hg; hyperventilation on
demand.
Optimize hemodynamics (MAP, CVP, PCWP, HR):
Target normotension and maintain cerebral perfusion pressure
(CPP = MAP − ICP) to avoid cerebral ischemia.
Fluid therapy: Target normovolemia before anesthetic induction to prevent
hypotension.
Use glucose-free isoosmolar crystalloid solutions to prevent
increases in brain water content (from hypoosmolality) and
ischemic damage (from hyperglycemia).
Position to improve cerebral venous return (neutral, head-up position).
Drug-induced cerebral vasoconstriction (e.g., thiopental, propofol).
Temperature control: Avoid hyperthermia perioperatively. Consider using mild intra-
operative hypothermia.
Cerebral spinal fluid drainage to acutely reduce brain tension.

IV = intravenous; MAP = mean arterial pressure; CVP = central venous pressure; PCWP = pulmonary
capillary wedge pressure; HR = heart rate; CPP = cerebral perfusion pressure; ICP = intracranial pressure.
 SUPRATENTORIAL TUMORS 3

and ICP while simultaneously decreasing systemic blood pressure. Because mannitol
may initially increase ICP, it should be given slowly (≥10-minute infusion) and in con-
junction with maneuvers that decrease intracranial volume (for example, steroids or
hyperventilation). Prolonged use of mannitol may produce dehydration, electrolyte
disturbances, hyperosmolality, and impaired renal function.
Hypertonic saline, another osmotic diuretic, is currently under investigation as an
agent to control ICP.2 Hypertonic saline solutions have been shown to reduce ICP in
animal models and in human studies and may be more effective than other diuretics
in certain clinical conditions, for example, patients with refractory intracranial hyper-
tension or in those who require brain debulking and maintenance of intravascular vol-
ume.2,3 Hypertonic saline also can be used as an alternative or adjunct to intraopera-
tive use of mannitol. There are several potential adverse effects of hypertonic saline
therapy (Table 2). Significant complications such as central pontine myelinolysis and
intracranial hemorrhage have not been reported in human studies. Different types of
hypertonic saline solutions with different methods of infusion (bolus and continuous)
have been reported in the literature. Published data are encouraging, but more studies
are required to determine dose–response curves and the safety and efficacy of these
solutions.
Hypertonic agents, either mannitol or hypertonic saline, should be administered
cautiously in patients with preexisting cardiovascular disease. In these patients, the
transient increase in intravascular volume may precipitate left ventricular failure.
Furosemide may be a better agent to reduce ICP in patients with impaired cardiac reserve.
The loop diuretic furosemide reduces ICP by inducing a systemic diuresis, decreas-
ing CSF production, and resolving cerebral edema by improving cellular water transport.
Furosemide lowers ICP without increasing cerebral blood volume or blood osmolality;
however, it is not as effective as mannitol in reducing ICP. Furosemide can be given
alone as a large initial dose (0.5 to 1 mg/kg−1) or as a lower dose with mannitol (0.15 to
0.30 mg/kg−1). A combination of mannitol and furosemide diuresis has been shown to
be more effective in reducing ICP and brain bulk than mannitol alone, but causes more
severe dehydration and electrolyte imbalances. With combined therapy, it is necessary
to monitor electrolytes intraoperatively and replace potassium as indicated.
Corticosteroids reduce edema around some brain tumors; however, steroids require
many hours or days before a reduction in ICP becomes apparent. The administration
of steroids preoperatively frequently causes neurologic improvement that can precede
the ICP reduction. One explanation for this is that the neurologic improvement is
accompanied by partial restoration of the previously abnormal blood–brain barrier.

TABLE 2. Hypertonic Saline: Potential Adverse Effects of Intravenous Administration

Central Nervous System Systemic

Decreased level of consciousness Hyperosmolality

Seizures Hypernatremia
*Central pontine myelinolysis Congestive heart failure
*Subdural and intraparenchymal hemorrhage Hypokalemia
Rebound cerebral edema Hyperchloremic acidosis
Coagulopathy
Phlebitis
Renal failure

*Not reported in human studies.

4 BENDO

Postulated mechanisms of action for steroidal reduction in brain edema are brain dehy-
dration, blood–brain barrier repair, prevention of lysosomal activity, enhanced cerebral
electrolyte transport, improved brain metabolism, promotion of water and electrolyte
excretion, and inhibition of phospholipase A2 activity. The potential complications of
continuous perioperative steroid administration are hyperglycemia, glucosuria, gastro-
intestinal bleeding, electrolyte disturbances, and increased incidence of infection. There-
fore, the potential risks and benefits of continuous steroid administration need to be
evaluated in these patients.
Hyperventilation reduces brain volume by decreasing CBF through cerebral vasocon-
striction. For every 1-mm Hg change in PaCO2, CBF changes by 1 to 2 mL/100 g−1/min−1.
The duration of effectiveness of hyperventilation for lowering ICP may be as short as
4 to 6 hours, depending on the pH of the CSF. Hyperventilation is only effective when
the CO2 reactivity of the cerebrovasculature is intact. Impaired responsiveness to
changes in CO2 tension occurs in areas of vasoparalysis, which are associated with
extensive intracranial disease such as ischemia, trauma, tumor, and infection.
The typical target PaCO2 is 30 to 35 mm Hg. A PaCO2 less than 25 to 30 mm Hg in
some pathologic conditions may be associated with ischemia caused by extreme cere-
bral vasoconstriction.4,5 By monitoring global cerebral oxygenation with jugular
venous oxygen saturation (SjvO2), for example, the therapeutic effectiveness of hyper-
ventilation can be determined and more safely applied.
The autoregulation of CBF has been discussed, as has the relationship between
blood pressure and ICP when autoregulation is disturbed. The therapeutic goals are to
maintain CPP and to control intracranial dynamics so that cerebral ischemia, edema,
hemorrhage, and herniation are avoided. Severe hypotension results in cerebral
ischemia and should be treated with volume replacement, inotropes, or vasopressors
as dictated by clinical need. Severe hypertension, conversely, can worsen cerebral
edema and cause intracranial hemorrhage and herniation. The β-adrenergic blockers,
propranolol and esmolol, and the combination α- and β-adrenergic blocker, labetalol,
are effective in reducing systemic blood pressure in patients with raised ICP resulting
in minimal or no effect on CBF or ICP.
Restricted fluid intake was a traditional approach to intracranial decompression
therapy but is now rarely used to lower ICP. Severe fluid restriction over several days
is only modestly effective in reducing brain water content and can cause hypovolemia,
resulting in hypotension, inadequate renal perfusion, electrolyte and acid-base distur-
bances, hypoxemia, and reductions in CBF. In patients who are dehydrated preoper-
atively, intravascular volume must be restored to normal before induction of anesthe-
sia to prevent hypotension in response to anesthetic agents and positive-pressure
ventilation. Fluid resuscitation and maintenance fluids in the routine neurosurgical
patient are provided with glucose-free isoosmolar crystalloid solutions to prevent
increases in brain water content from hypoosmolality. For routine craniotomy, the
patient receives hourly maintenance fluids and replacement of urine output. Blood loss
is replaced at approximately a 3:1 ratio (crystalloid:blood) down to a hematocrit of
approximately 25% to 30% depending on the patient’s physiological status.
Solutions containing glucose are avoided in all neurosurgical patients with normal
glucose metabolism, because these solutions exacerbate ischemic damage and cere-
bral edema. Hyperglycemia augments ischemic damage by promoting neuronal lactate
production, which worsens cellular injury. Intravenous fluids containing glucose and
water (D5W0.45%, NaCl or D5W) are particularly problematic because the glucose is
metabolized and the free water remains in the intracranial fluid compartment, result-
ing in brain edema. Brain water can interfere with surgical exposure and, after closure
 SUPRATENTORIAL TUMORS 5

of the skull, can compromise cerebral perfusion. In normal patients, both preopera-
tive dexamethasone treatment and general anesthesia-induced gluconeogenesis may
increase resting glucose levels. Therefore, blood glucose levels should be monitored
during craniotomy and maintained at near low-normal range. This should be accom-
plished mainly by withholding glucose.
For most neurosurgical patients, a neutral head position, mildly elevated to 15° to
30°, is recommended to decrease ICP by improving venous drainage. Flexing or turn-
ing of the head may obstruct cerebral venous outflow, causing a dramatic ICP elevation
that has been shown to resolve with resumption of a neutral head position. Lowering
the head impairs cerebral venous drainage, which can quickly result in an increase in
brain bulk and ICP.
The application of positive end-expiratory pressure (PEEP) to mechanically venti-
lated patients can potentially increase ICP. This effect occurs when PEEP increases
mean intrathoracic pressure, impairing cerebral venous outflow and cardiac output.
When PEEP is required to maintain oxygenation, it should be applied cautiously and
with appropriate monitoring to minimize decreases in cardiac output and increases in
ICP. PEEP levels of 10 cm H2O or less have been used without significant increases in
ICP or decreases in CPP. When higher levels of PEEP are required to optimize the
PaO2–PEEP–CPP relationship, both central venous pressure (CVP) and ICP monitoring
are indicated.
The administration of pharmacologic agents that increase cerebral vascular resis-
tance can acutely reduce ICP. Thiopental and propofol are potent cerebral vasocon-
strictors that can be used for this purpose. These agents are usually administered dur-
ing induction of anesthesia but may also be administered in anticipation of noxious
stimuli or to treat persistently elevated ICP in the intensive care unit.
Although rarely used to reduce ICP, hypothermia does this by decreasing brain
metabolism, CBF, cerebral blood volume, and CSF production.6 Drugs that centrally
suppress shivering, muscle relaxants, and mechanical ventilation are required when
hypothermic techniques are used. Intraoperatively, a modest degree of hypothermia,
approximately 34°C, has been recommended as a way to confer neuronal protection
during focal ischemia. Hypothermic techniques are also used to cool febrile neuro-
surgical patients. Hyperthermia is particularly dangerous in neurosurgical patients
because it increases brain metabolism, CBF, and the propensity for cerebral edema.
To acutely reduce brain tension, CSF drainage either by direct surgical puncture of
the lateral ventricle or by lumbar spinal catheter can be used. Lumbar CSF drainage
should be used cautiously and only when the dura is open and the patient is at least
mildly hyperventilated to prevent acute brain herniation. Brain tension can be effec-
tively reduced by draining 10 to 20 mL of CSF.

Premedication
Lethargic patients do not receive premedication. Patients who are alert and anxious
may receive an anxiolytic (for example, 5 mg midazolam orally) before coming to the
operating room. If there is any doubt about the patient’s level of consciousness, the
patient may be given sedation or analgesics in the operating room after an intravenous
route is established. For the preinduction insertion of invasive monitoring devices in
an awake, conversant patient, premedicants (for example, small doses of opioids)
should be considered to alleviate the discomfort from needle punctures.
6 BENDO

Monitoring
In addition to the routine monitors, measurement of intraarterial blood pressure,
arterial blood gases, CVP, and urine output is recommended for all major neurosurgi-
cal procedures. An arterial cannula is inserted before induction of anesthesia to con-
tinuously monitor blood pressure and to estimate CPP. When the arterial pressure
transducer is at midhead level (usually the level of the external auditory meatus), mean
arterial pressure (MAP) approximates the pressure at the level of the circle of Willis.
Cerebral perfusion pressure is calculated as the difference between MAP and CVP in
patients without intracranial hypertension or the ICP in those with intracranial hyper-
tension. When the cranium is open, ICP equals atmospheric pressure and CPP equals
MAP. With direct arterial pressure monitoring, the hemodynamic consequences of the
pharmacologic agents administered during anesthesia are recognized instantly. In addi-
tion, the arterial catheter provides ready access for intraoperative measurement of arte-
rial blood gases, hematocrit, serum electrolytes, glucose, and osmolality. Arterial blood
gas measurement is necessary to verify the adequacy of hyperventilation. In the elderly
and those with ventilation/perfusion mismatch, end-tidal CO2 may correlate poorly
with the PaCO2. Therefore, the difference between PaCO2 and end-tidal CO2 must be
determined for a given patient in a given position. Radial, femoral, or brachial arteries
are suitable for short-term cannulation; however, after ulnar artery collateral blood
flow is tested, cannulation of the radial artery is preferred.
Because most neurosurgical patients are dehydrated preoperatively and then sub-
jected to intraoperative diuresis, the measurement of cardiac preload and urine out-
put is important. A right atrial catheter reflects cardiac preload and is used to deter-
mine the preoperative fluid deficit and rate of intraoperative fluid infusion. When
possible, the CVP catheter should be inserted through an antecubital vein instead of
the jugular or subclavian veins. This avoids increased ICP from both the head-down
position and decreased cerebral venous outflow. The position of the antecubital placed
CVP catheter can be verified by chest x-ray, transducer pressure waveform, or p-wave
configuration on the electrocardiogram.
Urine output is also measured as an indicator of perioperative fluid balance. Dur-
ing craniotomy, a diuresis occurs initially after the administration of osmotic or loop
diuretics. Reduced urine output may reflect either hypovolemia or release of anti-
diuretic hormone.
Preoperative ICP monitoring is rarely used in patients for elective supratentorial
tumor operations. ICP monitoring is an invasive procedure that can cause bleeding or
infection. When performed with local anesthesia before induction, the procedure can
be uncomfortable to the patient.

Induction, Maintenance, and Emergence

When the patient is brought into the operating room, a gross neurologic exami-
nation should be repeated and documented because changes in the patient’s neuro-
logic status can occur overnight. In patients with elevated ICP by clinical examina-
tion, computed tomography scan, and/or ICP measurement, osmotherapy may be
indicated before induction of anesthesia. After appropriate monitoring devices are
applied, the cooperative patient is asked to hyperventilate while preoxygenation is
provided. Before laryngoscopy and intubation of the trachea, the patient is smoothly
and deeply anesthetized with agents that reduce ICP. In the presence of elevated ICP,
 SUPRATENTORIAL TUMORS 7

thiopental is commonly used to induce anesthesia; however, alternative agents such

as propofol or midazolam can be used depending on the patient’s medical condi-
tion. The following induction sequence is suggested: The intravenous administra-
tion of thiopental (3 to 5 mg/kg−1) or propofol (1.25 to 2.5 mg/kg−1) is followed by
an opioid (3 to 5 µg/kg−1 fentanyl) and muscle relaxant. If no airway difficulties are
anticipated, a nondepolarizing muscle relaxant is administered while controlled hyper-
ventilation with 100% oxygen is instituted. In patients who have been vomiting because
of elevated ICP, cricoid pressure is applied during mask ventilation. To deepen the
anesthetic, fentanyl is administered in 50 µg increments to a total dose of 10 µg/kg−1,
depending on the blood pressure response. Lidocaine (1.5 mg/kg−1) is also adminis-
tered intravenously 90 seconds before intubation to suppress laryngeal reflexes. When
the peripheral muscle twitch response disappears, an additional 2 to 3-mg/kg−1 bolus of
thiopental is administered, and tracheal intubation is performed as rapidly and smoothly
as possible. An esmolol infusion or bolus may also be used to reduce the heart rate and
blood pressure response to laryngoscopy and intubation. After induction of anesthesia,
ventilation of the lung is controlled mechanically. Arterial blood gases are measured
after intubation to establish the arterial–end-tidal CO2 gradient.
Routine institution of hyperventilation is no longer recommended in neurosurgical
patients because of the risk of cerebral ischemia in some pathologic conditions. Surgi-
cal conditions should define the PaCO2 level for each patient. For example, in patients
with significant intracranial hypertension or when using volatile agents, PaCO2 is usu-
ally adjusted between 30 and 35 mm Hg to reduce brain bulk.7 After direct visualiza-
tion of the brain and/or discussion with the neurosurgeon, the PaCO2 level should be
adjusted as necessary.
Because anesthetics affect the intracranial environment, there continues to be
controversy over the best choice of anesthetic technique for neurosurgical patients,
that is, intravenous- or volatile-based techniques. In practice, the anesthetics most
frequently administered to neurosurgical patients are either propofol–opioid or
isoflurane–opioid.8 The opioids selected are usually fentanyl or remifentanil. There
have been no large clinical outcome studies conducted comparing anesthetic tech-
niques. Our choice of anesthetics has been based primarily on information derived
from experimental and clinical studies of cerebral hemodynamics (CBF, CMRO2), ICP,
and recovery characteristics of different agents.
A popular maintenance technique for neurosurgical patients is the continuous
infusion of propofol with remifentanil or fentanyl. In patients with brain tumors, this
technique has been shown to reduce ICP more effectively than either isoflurane or
sevoflurane,8 and in nonneurosurgical patients, propofol with remifentanil produced
a quicker emergence than either desflurane or sevoflurane.9 This technique would
seem ideal for neurosurgical patients; however, questions have been raised regarding
the risk of cerebral hypoperfusion with propofol anesthesia.10,11 Studies suggest that
propofol anesthesia produces a reduction of CBF larger than a reduction of cerebral
metabolic rate (CMR), resulting in a decrease of the CBF/CMR ratio.11,12 In susceptible
patients, the risk of cerebral hypoperfusion may be even greater when patients are
hyperventilated under propofol anesthesia.11,12
Nitrous oxide, 50% to 70% in oxygen, is administered by some to decrease the total
dose of intravenous agent or the required concentration of volatile agent. The cere-
brovascular effects of nitrous oxide are not benign,6,13 and studies report that at equi-
potent doses, isoflurane has less adverse effects on ICP and CBF than nitrous oxide.6 In
patients with elevated ICP or low compliance, some clinicians avoid the administration
of either nitrous oxide or high concentrations of isoflurane (that is, greater than 1.0%).
8 BENDO

Alternatively, an opioid—thiopental or propofol anesthetic technique may be used

with midazolam or low-dose isoflurane added for amnesia. When severe intracranial
hypertension exists and the brain is tight despite adequate hyperventilation and the
administration of steroids and diuretics, a totally intravenous technique using a thiopen-
tal infusion (2 to 3 mg/kg−1/hr−1) and fentanyl boluses or infusion (1 to 4 µg/kg−1/hr −1)
is recommended.
In the usual craniotomy for excision of a supratentorial tumor, the conduct of the
anesthetic is aimed at awakening and extubating the patient at the end of the proce-
dure to permit early assessment of surgical results and postoperative neurologic fol-
low up. The risks and benefits of an early versus delayed recovery in neurosurgical
patients have been reviewed.14 The authors recommend extubation of the neuro-
surgical patient only when there is complete systemic and brain homeostasis. There
are several conditions listed in Table 3 that can delay awakening in neurosurgical
patients and should be considered before developing an extubation plan.
Intracranial hematoma and major cerebral edema are the most feared complications
after intracranial surgery. In a retrospective study of 11,214 craniotomy patients, a rela-
tionship was demonstrated between perioperative hypertension and the development
of postoperative hematomas.15 Therefore, emergence from anesthesia should be as
smooth as possible, avoiding straining or bucking on the endotracheal tube. Bucking
can cause arterial hypertension and elevated ICP, which can lead to postoperative
hemorrhage and cerebral edema. To avoid bucking, muscle relaxants are not reversed
until the head dressing is applied. Intravenous lidocaine (1.5 mg/kg−1) can be admin-
istered 90 seconds before suctioning and extubation to minimize cough, straining, and
hypertension. Antihypertensive agents such as labetalol and esmolol also are also
administered during emergence to control systemic hypertension.
The patient is extubated only when fully reversed from paralysis, and when he or
she is awake and following commands. If the patient is not responsive, the endotra-
cheal tube remains in place until the patient is awake and following commands. A brief
neurologic examination is performed before and after extubation of the trachea. The
patient is positioned with the head elevated 15° to 30° and transferred to the recovery
room or intensive care unit (ICU) with oxygen by mask, oxygen saturation monitor-
ing, and continued hemodynamic monitoring. Close monitoring and care, including
frequent neurologic examinations, are continued in the recovery room (ICU).

Awake Craniotomy
Awake craniotomy with functional mapping is recommended for removal of tumors
involving the eloquent cortex. Functional mapping is performed by stimulating the

TABLE 3. Causes of Delayed Awakening

Preoperative decreased level of consciousness

Large intracranial tumor
Residual anesthetics
Metabolic or electrolyte disturbances
Residual hypothermia
Surgical complications
Seizures
Cerebral edema
Hematoma
Pneumocephalus
 SUPRATENTORIAL TUMORS 9

brain with a small electrical charge. A neuropsychologist then performs neurocognitive

testing and/or monitors motor responses during mapping and later tumor resection.
This technique allows maximal tumor resection with minimal postoperative neurologic
deficits from retraction, edema, and/or resection of eloquent tissue. Other advantages
include avoidance of general anesthesia and need for more intensive monitoring intra-
operatively and postoperatively, a low complication rate, and reduction in resource
utilization (for example, shorter intensive care time and total hospital stay).16,17
Preoperative selection, evaluation, and preparation of the patients for awake craniot-
omy are slightly different than for general anesthesia. The patient must be cooperative
and able to participate in neurocognitive testing. In addition, the patient must have an
uncomplicated airway and be a candidate for general anesthesia. Most centers provide
the patient with detailed information about the procedure and what to expect in verbal,
written, and visual form.
In the operating room, there are several challenges for the anesthesiologist. Like
with any craniotomy, optimal operating conditions providing adequate surgical
exposure and brain relaxation are required. For the awake craniotomy, the patient
must be positioned very comfortably with bolsters and additional padding. Adequate
analgesia and sedation are needed for head frame application, skin incision, crani-
otomy, and opening of the dura. During cortical mapping and tumor resection, the
patient must be fully alert, cooperative, and able to participate in complex neuro-
cognitive testing.
Several different anesthetic protocols have been reported for awake craniotomy.16
These include neurolept anesthesia, propofol with or without opioid infusions, and
asleep, awake, asleep techniques using laryngeal mask airways. Dexmedetomidine, a
highly specific α-2 adrenoreceptor agonist, has been recommended for use during
awake craniotomy.18 It has the advantage of providing sedation and analgesia without
respiratory depression.
All awake procedures with sedation run the risk of respiratory depression and poor
patient cooperation. Complications such as seizures, increased ICP, hypertension, nau-
sea, and vomiting, which are more likely to occur during craniotomy, also require
prompt treatment.16,19 Most anesthetic protocols include prophylaxis with antihyper-
tensives, anticonvulsants, and antiemetics.

Neuronavigation/Computer-assisted Surgery
Neuronavigation allows precise anatomic mapping and orientation of tumors
before the operation and throughout the procedure.20–23 Image-guided surgery can be
performed with a magnetic resonance image (MRI) in the operating room or in a “twin
operating theater,” the MRI suite is in close proximity to the conventional operating
room. A study comparing the impact of neuronavigation on patients undergoing
glioblastoma surgery found that absolute and relative residual tumor volumes were
significantly lower with neuronavigation.24 Furthermore, radical tumor resection was
associated with a highly significant prolongation in survival. In another study, image-
guided resection of meningiomas was associated with less complications and shorter
hospital stays when compared with conventional surgery.25 Anesthetic management
concerns regarding intraoperative MRI have been discussed in recent articles.26–28
Along with concerns of administering an anesthetic in a remote location and using
MRI-compatible anesthesia equipment, neuroanesthetic principles must also be
applied when caring for these patients.
10 BENDO

Summary
There are several challenges to anesthetizing patients with an intracranial mass
lesion. The anesthesiologist must balance the needs of the patient (for example, opti-
mizing cerebral homeostasis and cardiorespiratory status) with those of the surgeon
(for example, unusual position, brain exposure without retraction, early emergence
for neurologic examination). Appropriate selection of anesthetics and monitoring with
meticulous general management of the patient’s respiration, circulation, fluid replace-
ment, and positioning are all essential to improving outcome.

References
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intracranial hypertension. Crit Care Med 2000; 28:3301–13.
3. Vialet R, Albanese J, Thomachot L, et al.: Isovolume hypertonic solutes (sodium chloride or
mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mg/kg
7% saline is more effective than 2 ml/kg 2% mannitol. Crit Care Med 2003; 31:1683–7.
4. Obrist WD, Langfitt TW, Jaggi JL, et al.: Cerebral blood flow and metabolism in comatose
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