Chapter 63 – Neurosurgical Anesthesia.pdf

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63 Neurosurgical Anesthesia

John C. Drummond and Piyush M. Patel

Key Points

1. For the purposes of planning a control strategy for intracranial pressure (ICP), the clinician should consider the four subcompartments of the intracranial space: cells, interstitial and intracellular fluid, cerebrospinal fluid, and blood.

2. The venous side of the cerebral circulation is a largely passive compartment that is often the cause of increased ICP or “tightness” of the surgical field, but that is commonly overlooked by clinicians.

3. Cerebral perfusion pressure (CPP) should be supported at or near waking normal levels in patients with recent cerebral injuries (e.g., traumatic brain injury [TBI], subarachnoid hemorrhage [SAH]) because of low resting cerebral blood flow and impaired autoregulation.

4. When patients are managed in the sitting position, blood pressure should be corrected to the level of the external auditory meatus, and mean arterial pressure (MAP) should be maintained at 60 mm Hg in normotensive adults.

5. The minimal standard of care for monitoring to detect venous air embolism in at-risk situations includes the precordial Doppler and end-tidal carbon dioxide analysis.

6. Despite encouraging preclinical data, therapeutic mild hypothermia cannot currently be advocated in the care of head-injured patients in the intensive care unit or during the operative management of patients with

intracranial aneurysms because of negative human trials in those patient groups.

7. The most important consideration in the anesthetic management of patients undergoing clipping or coiling after acute SAH is the prevention of paroxysmal hypertension with its attendant risk of aneurysm rerupture. Nonetheless, adequate perfusion pressure is needed if temporary clips are used or during management of cerebral vasospasm.

8. Although induced hypotension is very rarely employed electively in aneurysm surgery, the clinician must be ready to reduce blood pressure immediately and accurately in the event of aneurysm rupture.

9. Tracheal intubation of a head-injured patient with an undefined cervical spine injury can be accomplished using a rapid-sequence induction with manual in-line stabilization (occiput held rigidly to the backboard) with only a very small risk of injury to the spinal cord.

10. CPP (CPP = MAP − ICP) should be supported at 60 mm Hg in the first 48 hours after TBI in adults.

11. Hypocapnia has the potential to cause cerebral ischemia, particularly in recently injured brain and in brain beneath retractors; it should be used only when absolutely necessary for the control of critically increased or uncertain ICP.

This chapter provides guidelines for the management of common situations in neurosurgical anesthesia. First, issues that arise in connection with a variety of neurosurgical procedures are reviewed. These issues constitute a checklist that the practitioner should review before undertaking anesthesia for any neurosurgi-cal procedure. Procedure-specific discussions follow. This chapter assumes familiarity with the cerebral physiology and effects of anesthetics as described in Chapter 13. Neurologic monitoring is described in Chapter 46, and carotid endarterectomy is discussed in Chapter 62.

Recurrent Issues in Neuroanesthesia

Several basic elements of neurosurgical/neuroanesthetic manage-ment are recurrent and, in the absence of an established under-standing between the surgeon and anesthesiologist, should be discussed and agreed on at the outset of every neurosurgical procedure. The list varies with the procedure and may include the

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intended surgical position and requisite positioning aids; inten-tions with respect to the use of steroids, diuretics, anticonvulsants, and antibiotics; the surgeon’s perception of the “tightness” of the intracranial space and the remaining intracranial compliance reserve; appropriate objectives for the management of blood pres-sure, Paco2, and body temperature; anticipated blood loss; the intended use of neurophysiologic monitoring (which may impose constraints on the use of anesthetics or muscle relaxants, or both); and, occasionally, the perceived risk of air embolization. The con-siderations driving the decisions made about these issues are pre-sented in this section. One additional recurrent issue, brain protection, is discussed briefly in the section on aneurysms and arteriovenous malformations and in detail in Chapter 13.

Control of Intracranial Pressure and Brain Relaxation

The necessity of preventing increases in intracranial pressure (ICP) or reducing an ICP that is already elevated is recurrent in neuroanesthesia. When the cranium is closed, the objective is to maintain adequate cerebral perfusion pressure (CPP) (CPP = mean arterial pressure [MAP] − ICP), and prevent the herniation of brain tissue between intracranial compartments or through the foramen magnum (Fig. 63-1). When the cranium is open, the issue may be one of providing relaxation of the intracranial con-tents to facilitate surgical access or, in extreme circumstances, reverse the process of brain herniation through a craniotomy. The principles that apply are similar whether the cranium is open or closed.

The various clinical indicators of increased ICP include headache (particularly headache that awakens the patient at night), nausea and vomiting, blurred vision, somnolence, and papilledema. Suggestive findings on computed tomography (CT)

include midline shift, obliteration of the basal cisterns, loss of sulci, ventricular effacement (or enlarged ventricles in the event of hydrocephalus), and edema. Edema appears on a CT scan as a region of hypodensity. The basal cisterns appear on CT as a black (fluid) halo around the upper end of the brainstem (Fig. 63-2). They include the interpeduncular cistern, which lies between the two cerebral peduncles; the quadrigeminal cistern, which overlies the four colliculi; and the ambient cisterns, which lie lateral to the cerebral peduncles.

Figure 63-3 shows the pressure-volume relationship of the intracranial space. The plateau phase occurring at low volumes reveals that the intracranial space is not a completely closed one, and that there is some compensatory latitude. Compensation is accomplished principally by the translocation of cerebrospinal

Figure 63-1 Schematic representation of various herniation pathways: (1) subfalcine, (2) uncal (transtentorial), (3) cerebellar, and (4) transcalvarial. (From Fishman RA: Brain edema. N Engl J Med 293:706-711, 1975.)

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2

3

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Figure 63-2 CT scan depicting normal (left) and compressed (right) basal cisterns. The basal, or perimesencephalic, cerebrospinal fluid space consists of the interpeduncular cistern (anterior), the ambient cisterns (lateral), and the quadrigeminal cisterns (posterior). In the right panel, in a patient with diffuse cerebral swelling (owing to sagittal sinus thrombosis), the cisterns have been obliterated. (Image provided by Ivan Petrovitch, MD.)

Figure 63-3 The intracranial pressure-volume relationship. The horizontal portion of the curve indicates that there is initially some latitude for compensation in the face of an expanding intracranial lesion. That compensation is accomplished largely by displacement of cerebrospinal fluid (CSF) and venous blood from intracranial to extracranial spaces. When the compensatory latitudes are exhausted, small volume increments result in large increases in intracranial pressure with the associated hazards of herniation or of decreased cerebral perfusion pressure (CPP) resulting in ischemia.

Intracranial volume

Volume compensation(CSF, blood)

Volume compensationmechanisms reaching

exhaustion

CP

P r

educ

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fluid (CSF) to the spinal CSF space and venous blood to the extracranial veins. Ultimately, when the compensatory potential is exhausted, even tiny increments in volume of the intracranial contents can result in substantial increases in ICP. These increases have the potential to result in either herniation of brain tissue from one compartment to another (or into the surgical field) (see Fig. 63-1), with resultant mechanical injury to brain tissue, or reduction in perfusion pressure, leading to ischemic injury.

Several variables can interact to cause or aggravate intra-cranial hypertension (Fig. 63-4). For clinicians faced with the problem of managing increased ICP, the objective is, broadly speaking, to reduce the volume of the intracranial contents. For mnemonic purposes, the clinician can divide the intracranial space into four subcompartments (Table 63-1): cells (including neurons, glia, tumors, and extravasated collections of blood), fluid (intracellular and extracellular), CSF, and blood.

1. The cellular compartment: This compartment is largely the province of the surgeon. It may be the anesthesiologist’s responsibility, however, to pose a well-placed diagnostic question. When the brain is bulging into the surgical field at the conclusion of evacuation of an extradural hematoma, the clinician should ask whether a subdural or extradural hematoma is present on the contralateral side that warrants either immediate bur holes or immediate postprocedure radiologic evaluation.

2. The CSF compartment: There is no pharmacologic manipu-lation of the CSF space, the time course and magnitude of which are relevant to the neurosurgical operating room. The only relevant means for manipulating the size of this compartment is by drainage. A tight surgical field some-times can be improved by passage of a brain needle by the surgeon into a lateral ventricle to drain CSF. Lumbar CSF drainage can be used to improve surgical exposure in situ-ations with no substantial hazard of uncal or transforamen magnum herniation.

3. The fluid compartment: This compartment can be addressed with steroids and diuretics. The use of these agents is dis-cussed subsequently.

4. The blood compartment: This is the compartment that receives the anesthesiologist’s greatest attention because it is the most amenable to rapid alteration. The blood com-partment should be considered as two separate compo-nents: venous and arterial.

We suggest giving first consideration to the venous side of the circulation. It is largely a passive compartment that is fre-quently overlooked. Passive though it is, engorgement of this compartment is a common cause of increased ICP or poor condi-tions in the surgical field (Fig. 63-5). A head-up posture to ensure

Figure 63-4 The pathophysiology of intracranial hypertension. The figure depicts the manner in which increases in the volumes of any or all of the four intracranial compartments—blood, cerebrospinal fluid (CSF), fluid (interstitial or intracellular) and cells—result in intracranial pressure (ICP) increases and eventual neurologic damage. The elements that are potentially under the control of the anesthesiologist are indicated by asterisks (*). (Control of CSF volume requires the presence of a ventriculostomy catheter.) BP, blood pressure.

Neurologicinjury

Airway orintrathoracic

pressure Herniation or

perfusionpressure

Intracranial volume

Bloodvolume

CSFvolume*

CellularCompartment

Mass Lesions

Fluid*Compartment

Edema

Jugularvenous

pressure*

TumorHematoma

subduralextraduralintracerebral

Some anesthetics*

Vasodilators*

Seizures

PaCO2

PaO2

Mechanical injuryor

ischemia

ICP

(If autoregulation defective)

BP

BP

Arterial pressure*

Table 63-1 Intracranial Compartments and Techniques for Manipulation of Their Volume

Compartment Volume Control Methods

Cells (including neurons, glia, tumors, and extravasated blood)

Surgical removal

Fluid (intracellular and extracellular) Diuretics

Steroids (principally tumors)

CSF Drainage

Arterial blood Decrease CBF

Venous blood Improve cerebral venous drainage

CBF, cerebral blood flow; CSF, cerebrospinal fluid.

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good venous drainage is the norm in neurosurgical anesthesia and critical care. Obstruction of cerebral venous drainage by extremes of head position or circumferential pressure (e.g., Phila-delphia collars, endotracheal tube ties) should be avoided. Phe-nomena occurring downstream from the venous structures of the neck also may be relevant, including any condition that can increase central venous pressure, such as positive end-expiratory pressure (PEEP) or cardiac failure. Anything that causes increased intrathoracic pressure can result in obstruction of cerebral venous drainage. Various commonplace events can lead to obstruction, including kinked or partially obstructed endotracheal tubes, tension pneumothorax, coughing or straining against the endotra-cheal tube, or gas trapping as a result of bronchospasm. These events also should be sought and remedied. Most practitioners carefully maintain paralysis during craniotomies, unless a contraindication is present, because a sudden cough can result in dramatic herniation of cerebral structures through the craniotomy.

Thereafter, the anesthesiologist should consider the arterial side of the circulation. Attention to the effect of anesthetic drugs and techniques on cerebral blood flow (CBF) (see Chapter 13) is an established part of neuroanesthesia. Such attention is relevant because increases in CBF generally are associated with increases in cerebral blood volume (CBV).1-3 The notable exception to this rule occurs in the context of cerebral ischemia caused by hypo-tension or vessel occlusion, at which times CBV may increase as the cerebral vasculature dilates in response to a sudden reduction in CBF. The relationship generally applies, however, and attention to the control of CBF is relevant in situations in which volume compensation mechanisms are exhausted, or ICP is already increased. The general approach is to select anesthetics and control the physiologic parameters in a manner that avoids unnecessary increases in CBF. The parameters that influence CBF are listed in Table 63-2 and are discussed in Chapter 13.

Selection of Anesthetics

The question of which anesthetics are appropriate, especially in the context of unstable ICP, arises often. Chapter 13 provides rel-evant information in detail, and only broad generalizations are offered here. Generally, intravenous anesthetic, analgesic, and

sedative drugs are associated with parallel reductions in CBF and cerebral metabolic rate (CMR) and do not have adverse effects on ICP. Ketamine, given in large doses to patients with a generally normal level of consciousness before anesthesia, may be the exception. Autoregulation and carbon dioxide (CO2) responsive-ness are generally preserved during the administration of intra-venous drugs (see Chapter 13).

By contrast, all of the volatile anesthetics can be, depending on physiologic and pharmacologic circumstances, dose-depend-ent cerebral vasodilators. The order of vasodilating potency is approximately halothane >> enflurane > desflurane > isoflurane > sevoflurane. As noted in Chapter 13, the CBF differences among isoflurane, desflurane, and sevoflurane are probably not signifi-cant to the clinician. The net CBF effect of introducing a volatile anesthetic depends on the interaction of several factors, including the concentration of the anesthetic, the extent of previous CMR depression, simultaneous blood pressure changes acting in con-junction with previous or anesthetic-induced autoregulation abnormalities, and simultaneous changes in Paco2 in conjunction with any disease-related impairment in CO2 responsiveness.

Nitrous oxide (N2O) is also a cerebral vasodilator, the CBF effect of which is the most profound when it is administered as a sole anesthetic, and least when it is administered against a back-

Figure 63-5 The effect of cerebral venous outflow obstruction on intracranial pressure (ICP) in a patient with an intracerebral hematoma. Bilateral jugular compression was applied briefly to verify the function of a newly placed ventriculostomy. The ICP response illustrates the importance of maintaining unobstructed cerebral venous drainage. BP, blood pressure.

BP

(m

m H

g)IC

P (

mm

Hg)

Table 63-2 Factors That Influence Cerebral Blood Flow*

Pao2

Paco2

Cerebral metabolic rateArousal/painSeizuresTemperatureAnesthetics

Blood pressure/status of autoregulationVasoactive agents

AnestheticsPressorsInotropesVasodilators

Blood viscosityNeurogenic pathways (intra-axial and extra-axial)

*See Chapter 13 for detailed discussion.

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ground of narcotics, propofol, or benzodiazepines, and to a lesser extent when administered with volatile anesthetics (see Chapter 13). Nonetheless, experience dictates that N2O and volatile anes-thetics, the latter usually in concentrations less than the minimum alveolar concentration (MAC), when administered as compo-nents of a balanced anesthetic technique in combination with narcotics, can be used in most elective and many emergency neurosurgical procedures. Exceptions are rare, but when they occur (e.g., a somnolent, vomiting patient with papilledema, a large mass, and compressed basal cisterns, or a head injury victim with an expanding mass lesion or obliterated cisterns and sulci on CT scan), the clinician may be well advised to use a predomi-nantly intravenous technique until the cranium and dura are open, and the effect of the anesthetic technique can be assessed by direct observation of the surgical field. Inhaled anesthetics are entirely acceptable components of most anesthetics for neurosur-gery. In circumstances in which ICP is persistently elevated (in a closed-cranium procedure), or the surgical field is persistently “tight,” N2O and volatile anesthetics should be viewed as potential contributing factors,4 however, and should be eliminated from the anesthetic in favor of intravenous anesthetics.

Muscle relaxants (see Chapter 29) that have the potential to release histamine (mivacurium, atracurium) should be given in small, divided doses. Although succinylcholine increases in ICP, these increases are small and transient. The increases can be blocked by a preceding dose of metocurine, 0.03 mg/kg5 (and probably other nondepolarizers), and, in at least some instances, are not evident in patients with common emergency neurosurgi-cal conditions (i.e., head injury, subarachnoid hemorrhage [SAH]).6 In a clinical situation that calls for rapid relaxation for the purpose of controlling or protecting the airway, succinylcho-line in conjunction with proper management of the airway and MAP is reasonable.

From the material just presented and the discussion of cerebral physiology in Chapter 13, a systematic clinical approach should follow readily. A schema for approaching the problem of an acute increase in ICP or acute deterioration in conditions in the surgical field is presented in Table 63-3. If the problem has not resolved satisfactorily after following the approach in Table 63-3, Table 63-4 presents other options.

Table 63-3 High Intracranial Pressure/“Tight Brain” Checklist

1. Are the relevant pressures controlled?Jugular venous pressure

Extreme head rotation or neck flexion?Direct jugular compression?Head-up posture?

Airway pressureAirway obstruction?Bronchospasm?Straining, coughing, adequately relaxed?Pneumothorax?

Paco2 and Pao2

Arterial pressure2. Is metabolic rate controlled?

Pain/arousal?Seizures?

3. Are any potential vasodilators in use?N2O, volatile agents, nitroprusside, calcium channel blockers

4. Are there any unrecognized mass lesions?Blood, air with or without N2O

Table 63-4 Methods for Rapid Reduction of Intracranial Pressure and Brain Volume*

Further titration of Paco2 (≥25 mm Hg)CSF drainage (ventriculostomy, brain needle)Diuresis (usually mannitol)CMR suppression (barbiturates, propofol)MAP reduction (if dysautoregulation)Surgical control (i.e., removal of bone flap or lobectomy)

*After review of the checklist in Table 63-3.CMR, cerebral metabolic rate; CSF, cerebrospinal fluid; MAP, mean arterial pressure.

CSF drainage was discussed earlier. The use of additional osmotic diuretics is theoretically limited by an upper acceptable osmolarity limit of approximately 320 mOsm/L. In extremis, the use is frequently empirical, however, and repeated doses (e.g., 12.5 g) are administered until a clinical response is no longer observed. Barbiturates have long been the most widely used drugs for inducing a reduction in CMR, with the objective of causing a coupled reduction in CBF and CBV. Propofol is gaining popular-ity for this application. Although the use of barbiturates is sup-ported by intensive care unit (ICU) experience showing efficacy in ICP control7 (if not outcome), no such experience has been accumulated for propofol. A frequently fatal syndrome of meta-bolic acidosis and rhabdomyolysis has been recognized in patients who have received prolonged propofol infusions in the ICU.8,9 MAP reduction occasionally reduces vascular engorgement and reduces total brain bulk, but should be applied with extreme caution if patients have compromised intracranial collateral cir-culation. This approach is most likely to be relevant in the event of dysautoregulation occurring in the context of resection of arte-riovenous malformations (AVMs) (see the later section on aneu-rysms and arteriovenous malformations).

Management of Paco2

At the outset, the anesthesiologist and the surgeon should agree on the objectives with respect to Paco2. Induction of hypocapnia is a time-honored part of the management of intracranial neuro-surgical procedures. The rationale is principally that the concomi-tant reduction in CBF (see Fig. 13-4) and CBV results in a reduction in ICP, or “brain relaxation.” The rationale is valid.10 Two considerations should influence the clinician’s use of hyper-ventilation, however. First, the vasoconstrictive effect of hypocap-nia has the potential to cause ischemia in certain situations. Second, the CBF-lowering and ICP-lowering effect is not sustained.11

Hypocapnia-Induced Cerebral IschemiaAt first, clinicians were skeptical that hyperventilation could result in ischemia, and normal brain seems unlikely to be damaged by the typical clinical use of hyperventilation. This may not be the case, however, in certain pathologic conditions.

Normal Brain. Available data12-16 indicate that in normal sub-jects, ischemia does not occur at a Paco2 greater than 20 mm Hg. This generalization seems also to apply during induced hypoten-sion.17-19 Physiologic alterations, as evidenced by metabolic and electroencephalogram (EEG) abnormalities, have been observed,

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however, in human volunteers13,15,20 with severe hypocapnia. In one of these studies,15 EEG abnormalities and paresthesias occurred in volunteers hyperventilating to Paco2 values less than 20 mm Hg, and these effects were reversed by hyperbaric oxy-genation, suggesting that they may truly have been caused by ischemia. Given that a Paco2 of less than 20 to 25 mm Hg offers very little additional benefit in terms of improvement in intra-cranial compliance, it seems prudent to limit acute Paco2 reduc-tion to 25 mm Hg in previously normocapnic individuals. Normal brain should not be injured by this degree of hypocapnia.

Injured Brain. Although preventing herniation, maintaining ICP less than 20 mm Hg, minimizing retractor pressure, and facilitating surgical access remain priorities that may justify hypocapnia, evidence also is accumulating that hyperventilation is potentially deleterious and should not be overused. Available evidence indicates that hyperventilation can result in ischemia,21-31 especially when baseline CBF is low,32 as is com-monly the case in the first 24 hours after injury.33-39 An increased frequency of brain regions with very low CBF has been shown in head-injured patients who were acutely hyperventilated.21,30,31 In addition, from centers that monitor jugular venous oxygen satu-ration (Sjvo2), there have been numerous observations that low Sjvo2 values can be increased, and that lactate levels in the jugular venous effluent can be decreased by reducing the degree of hyper-ventilation,23,32,40 although the inability of Sjvo2 monitoring to detect ischemia consistently also has been reported.29-31

At present, there is little information to confirm a deleteri-ous effect of hyperventilation. The closest thing to “proof ” resides in a subset analysis from a study of patients with moderate head injuries by Muizelaar and colleagues.24 The study included a near-normocapnic group, in which Paco2 was maintained at approximately 35 mm Hg, and a hypocapnic group, in which Paco2 was maintained at approximately 25 mm Hg. Outcomes 3 and 6 months after injury revealed a poorer status in a subpopula-tion of the hyperventilation group. That subpopulation included patients with the best initial motor scores, a subgroup in which the severity of injury was such that they merited intubation by conventional criteria, but whose clinical condition may have been such that hyperventilation was not required for control of ICP and who had little to gain from hyperventilation.

Hyperventilation should not be an automatic component of every “neuroanesthetic.” It should be treated in a manner any other therapeutic intervention. There should be an indication for instituting it (usually elevated or uncertain ICP or the need to improve conditions in the surgical field, or both). Hyperventila-tion should be used with the knowledge that it has the potential for causing an adverse effect, and as is the case with any other therapeutic intervention, it should be withdrawn as the indication for it subsides. The concern regarding the hazards of hypocapnia, which evolved in the context of head injury, has influenced all of neurosurgery. In particular, hyperventilation is now widely avoided in the management of SAH because of the low-CBF state that is known to occur.41 In addition, brain tissue beneath retrac-tors can have a similarly reduced CBF.26,42

Duration of Hypocapnia-Induced Reduction in Cerebral Blood FlowThe effect of hypocapnia on CBF is not sustained. Figure 63-6 is a nonquantitative representation of changes in CBF and CSF pH occurring in association with a sustained period of hyperventila-

tion. With the onset of hyperventilation, the pH of CSF and the brain’s extracellular fluid space increases, and CBF decreases abruptly. The cerebral alkalosis is not sustained, however. By alterations in the function of the enzyme carbonic anhydrase, the concentration of bicarbonate in CSF and the brain’s extracellular fluid space is reduced, and in a time course of 6 to 18 hours, the pH of these compartments returns to normal.43 Simultaneously, CBF returns toward normal levels.43,44

The implications are twofold. First, the clinician ideally should hyperventilate patients for only as long as a reduction in brain volume is required. Prolonged, but unnecessary, hyperven-tilation may lead to a circumstance wherein subsequent clinical events call for additional maneuvers to reduce the volume of the intracranial contents. However, if carbon dioxide tension is already in the 23 to 25 mm Hg range, it would be difficult to impose sufficient additional hyperventilation to once again accomplish the original reduction in CBF without the hazard of pulmonary barotrauma. Second, in a patient who has been hyper-ventilated for a sustained period (e.g., 2 days in the ICU), rapid restoration of Paco2 from values in the vicinity of 25 mm Hg to typical normal values (e.g., 40 mm Hg) ideally should be accom-plished slowly. A sudden increase in Paco2 from 25 to 40 mm Hg in an individual who has been chronically hyperventilated would have the same physiologic effect that a rapid change from 40 to 55 mm Hg would have in a previously normocapnic subject. If hypocapnia has been required as an adjunct to brain relaxation during craniotomy, Paco2 also should be allowed to increase when the retractors are removed (if dural closure requirements permit) to minimize the residual intracranial pneumatocele (see later section on pneumocephalus).

Management of Arterial Blood Pressure

Acceptable blood pressure limits should be agreed on at the beginning of a neurosurgical procedure. A prominent theme of contemporary neurosurgery is that CPP should be maintained at normal or even high-normal levels after acute central nervous

Figure 63-6 Paco2, cerebral blood flow (CBF), and cerebrospinal fluid (CSF) pH changes with prolonged hyperventilation. Although the decreased arterial Paco2 (and the systemic alkalosis) persist for the duration of hyperventilation, the pH of the brain and CBF return toward normal over 8 to 12 hours.

Time (hours)

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FC

SF

pH

PaC

O2

2 6 10 14 18

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system insults and during most intracranial neurosurgical proce-dures. This concept has evolved from the growing understanding that CBF is frequently very low in some brain regions after acute neurologic insults, in particular, head injury (see discussion in the later section on head injury) and SAH. Two additional factors should be considered. The first is that the autoregulatory response to decreasing blood pressure may not be intact throughout the brain. Figure 63-7 depicts the ischemic hazard that attends the circumstance of a low resting CBF and absent autoregulation even at blood pressure levels considered safe when autoregulation is intact. Second, there is the understanding that maintenance of arterial pressure also is relevant to brain compressed under retrac-tors26 because the effective perfusion pressure there is reduced by increased local tissue pressure.

Although little other than anecdotal data support the notion, we believe that an aggressive attitude toward blood pres-sure support should be extrapolated to patients who have sus-tained a recent spinal cord injury, to patients whose spinal cord is under compression or at risk for compression or vascular com-promise because of a disease process (most commonly cervical spinal stenosis with or without ossification of the posterior lon-gitudinal ligament) or an intended surgical procedure, and to patients undergoing surgery involving retraction of the spinal cord. Were we empowered to “legislate” the standard of care, we would mandate that blood pressure during anesthesia in these patients be maintained as close as possible to, and certainly within 10% of, average awake values.

Steroids

The administration of steroids for the purpose of reducing or limiting the formation of edema is another time-honored practice in neurosurgery. The efficacy of steroids in reducing the edema and increasing blood-brain barrier permeability associated with tumors is well confirmed.45-47 The time course of this effect is rapid, although not so rapid that it is relevant to the management of acute intraoperative events. Administration beginning 48 hours before an elective surgical procedure has the potential, however,

to reduce edema formation and improve the clinical condition by the time of craniotomy.45,48,49

Although clinical improvement—specifically, a decreased frequency of ICP plateau waves and an improvement in the pres-sure-volume response (the increment in ICP in response to a standardized intracranial volume challenge)—occurs within 24 hours,48 a reduction in ICP may not occur for 48 to 72 hours after the initiation of therapy.48 This finding has been interpreted to indicate that steroids in some way improve the “viscoelastic prop-erties” of the intracranial space before a reduction in edema occurs, although the mechanism is undefined.49 Steroids are often given intraoperatively and postoperatively to maintain the effects achieved by preoperative treatment. The practice of administering steroids to adult head injury patients has been abandoned as a result of controlled trials that showed either no benefit or deleteri-ous effects.50

Diuretics

Diuretics are used widely in neurosurgery to reduce the volume of the brain’s intracellular and extracellular fluid compartment. It is probably largely the extracellular compartment that is influ-enced because neurons and glia have quick and efficient cell volume regulation mechanisms. Osmotic and loop diuretics have been employed. Although data suggest that loop diuretics can be effective,51 osmotic diuretics, principally mannitol, are preferred clinically because of their speed and efficacy. The only U.S. Food and Drug Administration approved osmotic diuretic available on most formularies is mannitol. Hypertonic saline is an understud-ied alternative for which there is a small favorable experience and some enthusiasm in the neurosurgical community.52,53 There is no confirmation of superiority to mannitol, however.

Data indicate that mannitol enters brain and, over a short time course, appears in the CSF space.54 The possibility that the mannitol that gains access to the parenchyma aggravates swelling has resulted in varying degrees of reluctance among clinicians to administer mannitol.55 Nonetheless, most clinicians find it a mainstay of ICP management. There is the concern that mannitol is effective only when some degree of blood-brain barrier integ-rity is preserved in a significant portion of the brain. Most clini-cians respond to this concern by making empirical use of this agent (i.e., if it is effective in reducing ICP or improving condi-tions in the surgical field, repeated doses can be administered). If it is ineffective (or if serum osmolarity reaches the traditional limit of 320 mOsm/L), its administration is withheld.

The doses of mannitol employed vary from 0.25 g/kg to 100 g “for all comers”; 1.0 g/kg seems to be the most common dose. A systematic study in head-injured patients showed, however, that an equivalent initial ICP-reducing effect can be achieved with 0.25 g/kg, although that effect may not be as well sustained as with greater doses.56 Mannitol should be adminis-tered by infusion (e.g., over 10 to 15 minutes). Sudden exposure of the cerebral circulation to extreme hyperosmolarity can have a vasodilatory effect, which can produce brain engorgement and increased ICP that does not occur with slower infusions.

Some clinicians advocate the combined administration of a loop diuretic (usually furosemide) and an osmotic diuretic. The superficial rationale is that mannitol establishes an osmotic gradi-ent that draws fluid out of brain parenchyma, and that the furo-semide, by hastening excretion of water from the intravascular

Figure 63-7 Normal and absent autoregulation curves. The “absent” curve indicates a pressure-passive condition in which cerebral blood flow (CBF) varies in proportion to cerebral perfusion pressure. This curve is drawn to indicate subnormal CBF values during normotension, as have been shown to occur immediately after head injury23 and subarachnoid hemorrhage.41 The potential for modest hypotension to cause ischemia is apparent. MAP, mean arterial pressure.

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75

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space, facilitates the maintenance of that gradient. A second mechanism may add additional justification for the practice of combining the two agents. Neurons and glia, as mentioned earlier, seem to have powerful homeostatic mechanisms to ensure regula-tion of cell volume. Neurons and glia that shrink in response to an increased osmolarity in the external environment recover their volume rapidly as a consequence of the accumulation of so-called idiogenic osmoles that serve to minimize the gradient between the internal and external environment. One of those idiogenic osmoles is chloride. The loop diuretics inhibit the chloride channel through which this ion must pass and retard the normal volume-restoring mechanism.57,58

The normal volume regulatory mechanisms of neurons and glia also may be relevant to the phenomenon of rebound swelling. Rebound is commonly attributed to the prior use of mannitol and assumed to be a function of the accumulation of mannitol in cerebral tissue. Although this may be part of the story, the rebound may be “hypertonic rebound,” rather than “mannitol rebound.” After a sustained period of hyperosmolarity of any etiology, rebound swelling of neurons and glia (which have accumulated idiogenic osmoles) may occur in the event that systemic osmolar-ity decreases rapidly toward normal levels. It is well known that rebound cerebral swelling can occur after an episode of extreme increases in blood glucose concentration. Hypertonic saline rather than mannitol may not obviate this phenomenon.

Anticonvulsants

The general principle is that any acute irritation of the cortical surface has the potential to result in seizures; this includes acute neurologic events such as head injury and SAH.59,60 Cortical inci-sions and brain surface irritation by retractors may similarly be potential foci. Given the benign nature of diphenylhydantoin, routine administration in patients undergoing most supratento-rial craniotomies and in patients who have sustained a significant recent head injury59 or SAH seems appropriate in the absence of a contraindication. Diphenylhydantoin should be administered at rates not more rapid than 50 mg/min. There is no need for rapid administration to prevent postoperative seizures, and it should be administered at a significantly slower rate.

Positioning

The intended surgical position and the necessary position aids should be agreed on at the outset. Table 63-5 lists the commonly used positions and positioning aids and supports (see also Chapter 36).

General ConsiderationsThe prolonged duration of many neurosurgical procedures should be taken into account in all positions. Pressure points should be identified and padded carefully. Pressure and traction on nerves must be avoided. Given the high risk of thromboembolic compli-cations in neurosurgical patients, precautions including support hose and sequential compression devices are indicated. For cranial procedures, almost invariably some component of head-up pos-turing (e.g., 15 to 20 degrees) is appropriate to ensure optimal venous drainage. The conspicuous exception occurs with evacu-ation of a chronic subdural hemorrhage, after which patients are

Table 63-5 Common Neurosurgical Positions and Positioning Aids

PositionsSupineLateral (park bench)Semilateral (Janetta)ProneSitting

Positioning Aids and SupportsPin (Mayfield) head holderRadiolucent pin head holderHorseshoe head restFoam head support (e.g., Voss, O.S.I., Prone-View)Vacuum mattress (“bean bag”)Wilson-type frameAndrews (“hinder binder”)-type frameRelton-Hall (four-poster) frame

usually nursed flat to discourage reaccumulation. Patients also are often maintained flat after CSF shunting to avoid too-rapid col-lapse of the ventricles.

SupineThe supine position is used with the head neutral or rotated for frontal, temporal, or parietal access. Extremes of head rotation can obstruct the jugular venous drainage, and a shoulder roll can attenuate this problem. The head is usually in a neutral position for bifrontal craniotomies and transsphenoidal approaches to the pituitary. The head-up posture is best accomplished by adjusting the operating table to a chaise lounge (lawn chair) position (flexion, pillows under the knees, slight reverse Trendelenburg). This orientation, in addition to promoting cerebral venous drain-age, decreases back strain.

SemilateralThe semilateral position, also known as the Janetta position after the neurosurgeon who popularized its use for microvascular decompression of the fifth cranial nerve, is used for retromastoid access. It is achieved by lateral tilting of the table 10 to 20 degrees combined with a generous shoulder roll. Extreme head rotation, sufficient to cause compression of the contralateral jugular by the chin, should be avoided.

LateralThe lateral position can be used for access to the posterior parietal and occipital lobes and the lateral posterior fossa, including tumors at the cerebellopontine angle and aneurysms of the ver-tebral and basilar arteries. An axillary roll is important for pre-venting brachial plexus injury.

ProneThe prone position is used for spinal cord, occipital lobe, cranio-synostosis, and posterior fossa procedures. The prone position also has been referred to, aptly, as the Concorde position because, for cervical spine and posterior fossa procedures, the final posi-tion commonly entails neck flexion, reverse Trendelenburg, and elevation of the legs. This orientation brings the surgical field to a horizontal position.

The anesthesiologist should have a plan for detaching and reattaching monitors in an orderly manner to prevent an exces-sive monitoring “window.” Awake tracheal intubation and prone positioning can be employed in patients with an unstable cervical

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spine, in whom an unchanged neurologic status should be con-firmed before induction of anesthesia in the final surgical posi-tion. It also is occasionally done in very obese patients.

The head can be positioned in a pin head holder (applied before the turn), a horseshoe head rest, or a disposable foam head rest. A complication of the prone position is retinal ischemia and blindness owing to orbital compression causing central retinal vessel occlusion; constant attention must be directed toward avoiding this complication. It must be intermittently confirmed (e.g., every 15 minutes), and confirmed after any surgery-related head or neck movement that pressure has not come to bear on the eye.

Not all postoperative visual loss is a result of direct orbital compression, however. Ischemic optic neuropathy (ION) seems to be a more frequent cause of postoperative visual loss than pressure causing occlusion of central retinal vessels. The cause-and-effect relationships associated with ION are uncertain, but low arterial pressure, low hematocrit, and lengthy surgical pro-cedures are statistically associated with the phenomenon.61 Ophthalmologists have long recognized the phenomenon of ante-rior ION in nonanesthetized patients, and have identified as risk factors many causes of vascular disease (e.g., hypertension, dia-betes, smoking, hyperlipidemia) and hypotension, especially when it occurs in hypertensives.62,63 It also is suspected that certain normal anatomic and physiologic variations, including poor collateralization or absence of autoregulation of the vascu-lature of the optic nerve head,62 a small and anatomically “crowded” optic nerve head (the “disk at risk”64), an increase in intraocular pressure that has been observed to occur during pro-longed prone spine surgery,65 and impaired cerebral venous drainage,66 may contribute to the intraoperative occurrence of ION. The notion that ION is merely a function of arterial hypo-tension is probably an inaccurate oversimplification of a phenom-enon that almost certainly involves the interplay of numerous preoperative and intraoperative factors.67,68

Direct pressure also can result in various degrees of pres-sure necrosis of the forehead, maxillae, and chin, especially with prolonged spinal procedures. The clinician should ensure that pressure is as evenly distributed as possible over facial structures. Other pressure points to be checked include the axillae, breasts, iliac crests, femoral canals, genitalia, knees, and heels. When the arms are placed in the “stick-em up” position, traction on the brachial plexus must be avoided. That can usually be accom-plished by not exceeding a “90-90” position (arms abducted not greater than 90 degrees; elbows extended not greater than 90 degrees) with care taken to ensure that the elbow is anterior to the shoulder to prevent wrapping of the brachial plexus around the head of the humerus. An antisialogogue (e.g., glycopyrrolate) and adhesive (e.g., benzoin) may help reduce loosening of tape used to secure the endotracheal tube.

An objective during prone positioning, especially for lumbar spine surgery, is the avoidance of compression of the inferior vena cava. Impairment of vena caval return diverts blood to the epidural plexus and increases the potential for bleeding during spinal surgery. Optimizing venous return is an objective of all of the spinal surgery frames and is accomplished very effec-tively by the Relton-Hall, Wilson, and Andrews variants. Use of these frames introduces a risk of air embolism,69,70 although clini-cal occurrences have been very rare.71

Attention should be directed toward preventing injury to the tongue in the prone position. With cervical and posterior

fossa procedures, it is frequently necessary to flex the neck sub-stantially to facilitate surgical access. This flexion reduces the anterior-posterior dimension of the hypopharynx, and compres-sion ischemia of the base of the tongue (and the soft palate and posterior wall of the pharynx) can occur in the presence of foreign bodies (i.e., endotracheal tube, esophageal stethoscope, oral airway). The consequence can be macroglossia, caused by accu-mulation of edema after reperfusion of the ischemic tissue causing postextubation airway obstruction of rapid onset (see later). Unnecessary paraphernalia in the oral cavity and pharynx should be avoided. Omitting the oral airway entirely is unwise because the tongue may then protrude between and be trapped by the teeth as progressive swelling of facial structures occurs during a prolonged prone procedure. A rolled gauze bite block prevents this problem without adding bulk to the hypopharynx.

SittingThere have been several reviews of large experiences with the sitting position.72-76 All concluded that the sitting position can be employed with acceptable rates of morbidity and mortality. These reports were prepared by groups that perform 50 to 100 or more of these procedures per year, however, and the hazards of the sitting position may be greater for teams who have less frequent occasion to use it. With increasing frequency, the sitting position is being avoided through the use of one of its alternatives (i.e., prone, semilateral, lateral). We are likely to continue encountering it, however, because even surgeons who are inclined to use alter-native positions may opt for the sitting position when access to midline structures (i.e., the floor of the fourth ventricle, the pon-tomedullary junction, and the vermis) is required. Nonetheless, alternative positions for posterior fossa surgery exist and should be considered when there are contraindications to the sitting position.

Achieving the Sitting Position. A properly positioned patient is more commonly in a modified recumbent position as shown in Figure 63-8, rather than truly sitting. The legs should be kept as high as possible (usually with pillows under the knees) to promote venous return. Ideally, the head holder should be attached to the back portion of the table (see Fig. 63-8A), rather than to the portions under thighs or legs (see Fig. 63-8B). This permits lowering of the head, and closed chest massage if necessary, without the necessity of first taking the patient out of the head holder.

When procedures are performed in the sitting position, the clinician should think in terms of measuring and maintaining perfusion pressure at the level of the surgical field. This is best accomplished by referencing transducers to the interaural plane. If a manual blood pressure cuff on the arm is employed, a cor-rection* to allow for the hydrostatic difference between the arm and the operative field should be applied.

A series of hazards are associated with the sitting position. Circulatory instability, macroglossia, and quadriplegia are dis-cussed in this section. Pneumocephalus is discussed in the section on pneumocephalus. Venous air embolism (VAE) and paradoxi-cal air embolism (PAE) are discussed in the section on venous air embolism. Several of these hazards also are relevant when cervical spine and posterior fossa procedures are done in nonsitting posi-tions, but occur with greater frequency in the sitting position.

*A column of water 32 cm high exerts a pressure of 25 mm Hg.

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Cardiovascular Effects of the Sitting Position. Placing the anesthetized patient in the sitting position conveys some risk of impaired cardiovascular function, in particular, hypoten-sion. Pressor administration is required in some patients. Meas-ures to avoid hypotension include prepositioning hydration, wrapping of the legs with elastic bandages to counteract gravita-tional shifts of blood, and slow, incremental adjustment of table position. Aggressive volume loading and the G suit (also known as pneumatic antishock trousers or military antishock trousers) attenuate the effects of assuming the sitting position.77-79 Neither of these measures has been widely applied, however.

In most healthy subjects, the hemodynamic changes are of a nonthreatening magnitude. In a study of healthy anesthetized adult subjects, 22 to 64 years old, Marshall and colleagues80 observed modest changes. MAP was relatively unaffected, whereas wedge pressure, stroke volume, and cardiac index decreased—the last-mentioned by approximately 15%—although there was some variation with the anesthetic drugs employed. The combination of an unchanged MAP (which generally requires the use of a “light,” high sympathetic tone anesthetic) and a reduced cardiac index implies that systematic vascular resistance increased. Their calculations and the observations of other investigators81 reveal significant elevation of systematic vascular resistance. For patients in whom an abrupt increase in systematic vascular resistance may be poorly tolerated, the sitting position may represent a physio-logic threat, and alternative positions should be considered. A pulmonary arterial catheter may be warranted when there is clini-cal or historical evidence of antecedent coronary artery or valvu-lar heart disease and arbitrarily in patients older than 60 to 65 years.

During procedures performed in the sitting position, MAP should be corrected to head level to obtain a meaningful index of

CPP. Specifically, CPP (MAP − estimated ICP) should be main-tained at a minimum value of 60 mm Hg in healthy patients in whom it is reasonable to assume a normal cerebral vasculature. The safe lower limit should be increased for elderly patients, for patients with hypertension or known cerebrovascular disease, and for patients with degenerative disease of the cervical spine or cervical spinal stenosis who may be at risk for decreased spinal cord perfusion, and in the event that substantial or sustained retractor pressure must be applied to brain or spinal cord tissue.

Macroglossia. There have been sporadic reports of upper airway obstruction after posterior fossa procedures in which swelling of pharyngeal structures, including the soft palate, pos-terior wall, pharynx, and base of the tongue, has been observed.82 These episodes have been attributed to edema formation at the time of reperfusion after trauma or prolonged ischemia occurring as the result of foreign bodies (usually oral airways) causing pres-sure on these structures in the circumstances of lengthy proce-dures with sustained neck flexion (which is usually required to improve access to posterior structures). It is customary (and we think ideal, although there is no science to support the practice) to maintain at least two fingerbreadth’s distance between the chin/mandible and the sternum/clavicle to prevent excessive reduction of the anterior-posterior diameter of the oropharynx. In addition, we position patients with the oral airway in place and then, after the final head position is achieved, withdraw it until its tip func-tions as a bite block between the teeth. The macroglossia phe-nomenon also may be relevant as clinicians contemplate the use of transesophageal echocardiography (TEE) in the neurosurgery suite. The centers that routinely employ TEE in neurosurgery, for the most part, use either pediatric or custom-made small-diameter probes to avoid trauma to pharyngeal and perilaryngeal structures.

Quadriplegia. The sitting position per se has been implicated as a cause of rare instances of unexplained postoperative paraple-gia. It has been hypothesized83 that the neck flexion that is a common concomitant of the seated position may result in stretch-ing or compression of the cervical spinal cord. This possibility may represent a relative contraindication to the use of this posi-tion in patients with significant degenerative disease of the cervi-cal spine, especially when there is evidence of associated cerebrovascular disease. The implications for blood pressure management are mentioned in the preceding section on cardio-vascular effects. It also may represent a justification for somato-sensory evoked response monitoring during the positioning phase of a sitting procedure for patients perceived to be at high risk.

Pneumocephalus

The issue of pneumocephalus arises most often in connection with posterior fossa craniotomies performed with a head-up posture.84,85 During these procedures, air may enter the supraten-torial space, much as air enters an inverted bottle. Depending on the relationship of the brainstem and temporal lobes to the incisura, the pressure in the air collection may or may not be able to equilibrate with atmospheric pressure. This phenomenon has relevance to the use of N2O because any N2O that enters a trapped gas space would augment the volume of that space. In (probably

Figure 63-8 A and B, The sitting position. The patient is typically semirecumbent rather than sitting. In A, the head holder support is correctly positioned such that the head can be lowered without the need to detach the head holder first. The configuration in B, with the support attached to the thigh portion of the table, should be avoided. (From Martin JT: Positioning in Anesthesia and Surgery. Philadelphia, WB Saunders, 1988.)

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uncommon) intraoperative circumstances in which there is a completely closed intracranial gas space, the use of N2O may result in an effect comparable to that of an expanding mass lesion. We do not view N2O as absolutely contraindicated because, before dural closure, intracranial gas is probably only rarely trapped. Nonetheless, attention to this possibility is important when one is presented with the problem of an increasingly “tight” brain during a posterior fossa craniotomy.86,87

During a posterior fossa procedure done in a head-up posture, when surgical closure has reached a stage such that the intracranial space has been completely sealed from the atmos-phere, N2O should not be given because of the possibility of contributing to a tension pneumocephalus. The use of N2O up to the point of dural closure may represent a clinical advantage88 because the gas pocket can be expected to shrink more rapidly owing to the presence of N2O (because N2O diffuses out much more quickly than nitrogen does). Tension pneumocephalus is often naively viewed as exclusively a function of the use of N2O. Tension pneumocephalus can occur, however, as a complication of intracranial neurosurgery entirely unrelated to the use of N2O.89

Tension pneumocephalus is one of the causes of delayed awakening or nonawakening after posterior fossa and supratento-rial procedures (Fig. 63-9).89,90 It occurs because air enters the cranium while the patient is in a head-up position at a time when the volume of the intracranial contents has been reduced as a result of some combination of hypocapnia, good venous drainage, osmotic diuresis, and CSF loss from the operative field. When the cranium is closed, and the patient is returned to the near-supine position, CSF, venous blood volume, and extracellular fluid return or reaccumulate, and the air pocket becomes an unyielding mass

lesion (because of the very slow diffusion of nitrogen). This mass may cause delayed recovery of consciousness or severe headache. Among supratentorial craniotomies, the largest residual airspaces occur after frontal skull base procedures in which energetic brain relaxation measures are used to facilitate subfrontal access (see Fig. 63-9). At the end of these procedures, typically done in a supine/brow-up position, it is not feasible to fill the intracranial dead space with normal saline as is commonly done with smaller craniotomy defects, and there may be a large residual pneu-matocele. We doubt that the possible occurrence of this phenom-enon represents a contraindication to N2O. Withdrawal of N2O may be appropriate at the time of cranial closure, however. The diagnosis of pneumocephalus is confirmed by a brow-up lateral x-ray or CT scan. The treatment is a twist-drill hole followed by needle puncture of the dura.

Residual intracranial air should be considered at the time of repeat anesthesia, neurosurgical or non-neurosurgical. Air fre-quently remains evident on CT scan for more than 7 days after a craniotomy.91 Pneumocephalus also can develop de novo in the postoperative period in patients who have a residual dural defect and a communication between the nasal sinuses and the intra-cranial space.92

Venous Air Embolism

The rate of occurrence of VAE varies according to the procedure, the intraoperative position, and the detection method used. During posterior fossa procedures done in the sitting position, VAE is detectable by precordial Doppler in approximately 40% of patients and by TEE in 76%.93-96 The incidence of VAE during posterior fossa procedures performed in nonsitting positions is much less (12% using precordial Doppler in the report of Black and colleagues74), and it is probable, but unproven, that the average volume of air entrained per event also is smaller. The rate of VAE is apparently lower with cervical laminectomy (25% using TEE in the sitting position versus 76% for posterior fossa procedures95). Although VAE is principally a hazard of posterior fossa and upper cervical spine procedures, especially when they are performed in the sitting position, it can occur with supratentorial procedures. The most common situations involve tumors, most often para-sagittal or falcine meningiomas, that encroach on the posterior half of the sagittal sinus (Fig. 63-10) and craniosynostosis proce-dures, typically performed in children.97,98 Pin sites and trapped gas under pressure also can lead to VAE, although clinically rele-vant events have been very rare.

The common sources of critical VAE are the major cerebral venous sinuses, in particular, the transverse, the sigmoid, and the posterior half of the sagittal sinus, all of which may be non-collapsible because of their dural attachments. Air entry also may occur via emissary veins, particularly from suboccipital muscu-lature, the diploic space of the skull (which can be violated by the craniotomy and pin fixation), and the cervical epidural veins. We believe, although this has not been confirmed by systematic study, that the VAE risk associated with cervical laminectomy is greatest when the exposure requires dissection of suboccipital muscle with the potential to open emissary veins to the atmosphere at their point of entry into occipital bone. There also is anecdotal evidence99 that air under pressure in the ventricles or subdural space occasionally can enter the venous system, perhaps following the normal egress route of the CSF.

Figure 63-9 Postoperative CT scan shows a large pneumocephalus after a subfrontal approach to a suprasellar glioma. Immediately postoperatively, the patient was confused and agitated and complained of severe headache.

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Detection of Venous Air EmbolismThe monitors employed for the detection of VAE should provide (1) a high level of sensitivity, (2) a high level of specificity, (3) a rapid response, (4) a quantitative measure of the VAE event, and (5) an indication of the course of recovery from the VAE event. The combination of a precordial Doppler and expired CO2 moni-toring meet these criteria and are the current standard of care. Doppler placement in a left or right parasternal location between the second and third or third and fourth ribs has a very high detection rate for gas embolization,100 and when good heart tones are obtained, maneuvers to confirm adequate placement seem to be unnecessary. TEE is more sensitive than precordial Doppler to VAE (Fig. 63-11),101 and offers the advantage of identifying right-to-left shunting of air.95,102-104 Its safety during prolonged use (especially with pronounced neck flexion) is not well established, however. Expired nitrogen analysis is theoretically attractive. The expired nitrogen concentrations involved in anything less than catastrophic VAE are very small, however, and push the available instrumentation to the limits of its sensitivity (see Fig. 63-11).105

Figure 63-12 shows the physiologic and monitor response to an air embolic event. Table 63-6 presents an appropriate man-agement response to such an event.

Right Heart CatheterEssentially all patients who undergo sitting posterior fossa pro-cedures should have a right heart catheter. Although catastrophic, life-threatening VAE is relatively uncommon, a catheter that permits immediate evacuation of an air-filled heart occasionally is the sine qua non for resuscitation. The latitudes are much wider

with the nonsitting positions, and it is frequently appropriate, after a documented discussion with the surgeon, to omit the right heart catheter. The variables that contribute to this decision are the perceived risks of VAE associated with the intended proce-dure and the patient’s physiologic reserve.

An example of a procedure for which the right heart cath-eter is usually omitted is microvascular decompression of the fifth cranial nerve for tic douloureux or the seventh cranial nerve for hemifacial spasm. The essentially horizontal semilateral position and the very limited retromastoid craniectomy these procedures require have resulted (at our institution) in a very low incidence of Doppler-detectable VAE. One should come to know the local surgical practices, however, particularly with respect to the degree of head-up posture, before becoming casual about omitting the right atrial catheter. With regard to the Janetta procedure, the necessary retromastoid craniectomy is performed in the angle between the transverse and sigmoid sinuses, and venous sinusoids and emissary veins in the suboccipital bone are common. If this procedure is performed with any degree of head-up posturing, the risk of VAE may still be substantial.

Which Vein Should Be Used for Right Heart Access. Although some surgeons may ask that neck veins not be used, a skillfully placed jugular catheter is usually acceptable. In a very few patients, high ICP may make the head-down posture undesir-able. In others, unfavorable anatomy with an increased likelihood of a difficult cannulation and hematoma formation also may encourage the use of alternative access sites. Access to the brachial

Figure 63-10 Horizontal (top) and coronal (bottom) MR images of a parasagittal meningioma. Resection of meningiomas arising from the dural reflection overlying the sagittal sinus or from the dura of the adjacent convexity or falx entails a risk of venous air embolism because of the proximity of the sagittal sinus (the triangular structure at the superior end of the interhemispheric fissure in the bottom panel).

Figure 63-11 The relative sensitivity of various monitoring techniques to the occurrence of venous air embolism (VAE). BP, blood pressure; CO, cardiac output; CVP, central venous pressure; ECG, electrocardiogram, ET-CO2, end-tidal carbon dioxide; PAP, pulmonary arterial pressure; physiol, physiological; T-echo, transesophageal echo.

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Table 63-6 Management of an Acute Air Embolic Event

Prevent further air entryNotify surgeon (flood or pack surgical field)Jugular compressionLower the head

Treat intravascular AirAspirate right heart catheterDiscontinue N2OFio2: 1.0Pressors/inotropesChest compression

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veins has been greatly facilitated by the commercial availability of multiorificed catheters that use a Seldinger cannulation tech-nique and a lengthy J-tipped guidewire to negotiate the axilla or deltopectoral groove.

Positioning the Right Heart Catheter. Bunegin and col-leagues106 suggested that a multi-orificed catheter should be located with the tip 2 cm below the superior vena caval–atrial junction, and a single-orificed catheter should be located with the tip 3 cm above the superior vena caval–atrial junction. Although these small distinctions in location may be relevant for optimal recovery of small volumes of air when cardiac output is well maintained, for the recovery of massive volumes of air in the face of cardiovascular collapse, anywhere in the right atrium should suffice. Right heart placement can be confirmed by (1) x-ray, (2) pull back from the right ventricle while monitoring intravascular pressure, or (3) intravascular electrocardiogram (ECG).107 Although there is no literature to support the practice, with cath-eter access via the right internal jugular vein, a measured place-ment to the level of the second or third right intercostal space should suffice when the catheter passes readily.

The intravascular ECG technique makes use of the fact that an ECG “electrode” placed in the middle of the right atrium ini-tially “sees” an increasing positivity as the developing P-wave vector approaches it (Fig. 63-13), and then an increasing negativ-ity as the wave of atrial depolarization passes and moves away from it. The resultant biphasic P wave is characteristic of an intra-atrial “electrode” position. The technique requires that the CVP

catheter becomes an exploring ECG electrode. This is accom-plished by filling the catheter with an electrolyte solution (bicar-bonate is best) and attaching an ECG lead (the leg lead if lead II is selected) to the hub of the CVP catheter. Commercial CVP kits with an ECG adapter are available. The ECG configurations that are observed at various intravascular locations are shown in Figure 63-13. To minimize the microshock hazard, a battery-operated ECG unit is preferable, and unnecessary electric appa-ratus should be detached from the patient during catheter placement (see Table 63-6).

Paradoxical Air EmbolismThere has been much concern about the possibility of the passage of air across the interatrial septum via a patent foramen ovale (known to be present in approximately 25% of adults).108 The concern is that this phenomenon carries the risk of major cerebral or coronary morbidity, although there has been no precise defini-tion of the morbidity that can realistically be attributed to PAE. Although the minimal pressure required to open a probe patent foramen ovale is not known with certainty, it is thought that the necessary gradient may be 5 mm Hg. In a clinical investigation, Mammoto and colleagues104 observed that PAE occurred only in the context of major air embolic events, suggesting that signifi-cant increases in right heart pressures are an important predis-posing factor of the occurrence of PAE.

Several clinical investigations have examined factors that influence the right atrial pressure (RAP) to left atrial pressure (LAP) gradient. The use of PEEP was shown to increase the inci-

Figure 63-12 The responses of electrocardiogram (ECG), arterial pressure (blood pressure [BP]), pulmonary arterial pressure (PAP), pan-tidal carbon dioxide (CO2) concentration, precordial Doppler, and central venous pressure (CVP) to the intravenous administration of 10 mL of air over 30 seconds to an 11-kg dog.

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Figure 63-13 Electrocardiogram (ECG) configurations observed at various locations when a central venous catheter is used as an intravascular ECG electrode. The configurations in the figure are observed when “lead II” is monitored and the positive electrode (the leg electrode) is connected to the catheter. P indicates the sinoatrial node. The heavy black arrow indicates the P wave vector. Note the equi-biphasic P wave when the catheter tip is in the mid right atrial position.107

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dence of a positive RAP to pulmonary wedge pressure gradient,109 and generous fluid administration (e.g., 2800 mL/patient versus 1220 mL/control patient110) was shown to reduce it. As a result, the use of PEEP, which was previously advocated as a means of preventing air entrainment, diminished, and the practice of more generous fluid administration for patients undergoing posterior fossa procedures evolved. Subsequent data indicated, however, that even when mean LAP exceeds mean RAP, PAE can still occur because transient reversal of the interatrial pressure gradient can occur during each cardiac cycle.111

Some centers have advocated performing bubble studies preoperatively with either precordial echocardiography96 or tran-scranial Doppler (TCD)112 or prepositioning TEE113 to identify patients with a patent foramen ovale with a view to using alterna-tives to the sitting position in this subpopulation.95,114 Some centers thereafter advocate the use of TEE to identify PAE intra-operatively.95,103 This practice is not universal,76 however, and at the time of writing (2009) it is not a community-wide standard of care. Because the morbid events attributable to PAE have been infrequent, surgeons who are convinced that the sitting position is optimal for a given procedure76 are loath to be dis-

suaded from using it on the basis of what may seem like the very minor possibility of an injury to the patient occurring by this mechanism.

Transpulmonary Passage of AirAir apparently can occasionally traverse the pulmonary vascular bed to reach the systemic circulation.115,116 Transpulmonary passage is more likely to occur when large volumes of air are presented to the pulmonary vascular “filter.”117,118 There is also evidence suggesting that pulmonary vasodilators, including vola-tile anesthetics, may decrease the threshold for transpulmonary passage.117-119 Differences among anesthetics are negligible. N2O should be discontinued promptly after even apparently minor VAE events, however, because of the possibility that air may reach the left-sided circulation via a patent foramen ovale or the pul-monary vascular bed.

Techniques for Reducing the Incidence of Venous Air EmbolismAs noted previously, PEEP has been advocated in the past as a means of reducing the incidence of VAE or of responding to an acute VAE event to prevent further air entry. Perkins and Bedford109 suggest that PEEP increases the risk of PAE, however, and argue against the use of PEEP in seated neurosurgical proce-dures. As these authors point out, even 10 cm of PEEP would be unlikely to result in positive venous pressures in cerebral venous structures, which may be 25 cm above the heart. The ineffective-ness of PEEP120 and the relative superiority of jugular venous compression121,122 in increasing cerebral venous pressures have been confirmed by several investigations. An inflatable neck tour-niquet available for rapid inflation in the event of VAE has been studied in animals and used in humans by Pfitzner and McLean.123 There are additional arguments against the acute use of increased positive airway pressure in the event of VAE. The release of a Valsalva maneuver promotes paradoxical embolism. In addition, the impairment of systemic venous return caused by the sudden application of substantial PEEP may be undesirable in the face of the cardiovascular dysfunction already caused by the VAE event.

It has been associated that a patient who has sustained a hemodynamically significant VAE should be placed in a lateral position with the right side up. The rationale is that air would remain in the right atrium, where it would not contribute to an air lock in the right ventricle, and where it would remain amena-ble to recovery via a right atrial catheter. The first difficulty is that this repositioning is all but impossible with a patient in a pin head holder. In addition, the only systematic attempt to examine the efficacy of this maneuver, albeit performed in dogs, failed to identify any hemodynamic benefit.124

Nitrous Oxide. N2O diffuses into air bubbles trapped in the vascular tree; N2O should be eliminated after a clinical VAE event to avoid aggravating the cardiovascular impact. As noted earlier, the PAE phenomenon adds an additional reason for eliminating N2O after the occurrence VAE. When major VAE occurs, no matter how the RAP-LAP gradient was manipulated before the event, RAP increases abruptly with respect to LAP,125 and major VAE results in an acutely increased risk of PAE in patients with a patent foramen ovale.104 Should N2O be used at all in patients at risk for VAE? Some clinicians may decide that it is the “path of least resistance” simply to avoid it, and to avoid having to worry

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about the considerations it creates. N2O can be used, however, with the knowledge that it neither increases the incidence of VAE126 nor aggravates the hemodynamic response to VAE, pro-vided that it is eliminated when VAE occurs.127

Monitoring

Neurologic monitoring techniques are discussed in Chapter 46. Invasive monitoring is frequently appropriate in neurosurgery Table 63-7 lists indications for an arterial catheter.

Patients with increased ICP may be intolerant of the vas-cular engorgement associated with sudden hypertension occur-ring as a consequence of light anesthesia. Surgical relief of increased ICP may be associated with sudden hypotension as brainstem compression is relieved. Beat-by-beat arterial pressure monitoring also serves as an important monitor of depth of anesthesia and as an early warning system for neurologic injury. Much of the brain is insensate. Consequently, the intracranial portion of many neurosurgical procedures is not very stimulat-ing, and to achieve circulatory stability, light anesthesia is often necessary. The anesthesiologist should be constantly aware of the possibility of sudden arousal (most often associated with cranial nerve traction or irritation). This is especially important when paralysis is precluded by the use of electromyographic recording from facial muscles to monitor cranial nerve integrity. Blood pressure responses may reveal imminent arousal. Blood pressure responses also may serve to warn a surgeon of excessive or unrec-ognized irritation, traction, or compression of neurologic tissue.

Table 63-7 Relative Indications for Intra-arterial Pressure Monitoring

Elevated ICPIschemia or incipient ischemia of neurologic tissue

Recent SAHRecent head injuryRecent spinal cord injuryIntended or potential temporary vessel occlusion

Circulatory instabilityTraumaSpinal cord injury (spinal shock)Sitting positionPossible barbiturate coma

Possibility of induced hypotensionPossibility of induced hypertensionAnticipated/potential major blood loss

Aneurysm clippingArteriovenous malformationsVascular tumorsTumors involving major venous sinusesCraniofacial reconstructionExtensive craniosynostosis procedures

Anticipated light anesthesia without paralysisBrainstem manipulation/compression/dissectionAnticipated cranial nerve manipulation (especially CN V)Advantageous for postoperative intensive care

Hypervolemic therapyHead injuryDiabetes insipidus

Incidental cardiac disease

CN, cranial nerve; ICP, intracranial pressure; SAH, subarachnoid hemorrhage.

These occur most often with posterior fossa procedures involving brainstem or cranial nerves, and abrupt changes should be reported to the surgeon immediately.

The use of right heart catheters for air retrieval is discussed in the section on venous air embolism. Thereafter, anticipated blood loss and fluid flux (including aggressive mannitol use) and an evaluation of the patient’s physiologic reserve should deter-mine the necessity for CVP or pulmonary arterial catheters. The use of the precordial Doppler also is described in the section on venous air embolism.

Intravenous Fluid Management

The general principles of fluid management (see Chapter 54) for neurosurgical anesthesia are (1) maintain normovolemia, and (2) avoid reduction of serum osmolarity. The first principle is a deriv-ative of the concept presented in the section on management of blood pressure that it is generally ideal to maintain a normal MAP in patients undergoing most neurosurgical procedures and neu-rosurgical critical care. Maintaining normovolemia is simply one element of maintaining a normal MAP. The second principle is a derivative of the often repeated observation that reducing serum osmolarity results in edema of normal and abnormal brain.128 Administering fluids that provide free water (i.e., fluids that do not have sufficient nonglucose solutes to render them iso-osmolar with respect to blood) reduces serum osmolarity if the amount of free water administered is greater than that required to main-tain ongoing free water loss.

Normal saline and lactated Ringer’s solution are the fluids most often used intraoperatively. At 308 mOsm/L, normal saline is slightly hyperosmolar with respect to plasma (295 mOsm/L). It has the disadvantage that in large volumes it can cause a hyper-chloremic metabolic acidosis.129 The physiologic significance of this acidosis, which involves the extracellular, but not the intracel-lular, fluid space, is unclear. At a minimum, it has the potential to confuse the diagnostic picture when acidosis is present. As a result, many clinicians use predominately lactated Ringer’s solu-tion. Although lactated Ringer’s solution (273 mOsm/L) theoreti-cally is not ideal for individual replacement of blood and third space loss or insensible losses, it serves as a reasonable compro-mise for meeting both needs simultaneously and is very suitable in most instances. It is a hypo-osmolar fluid, however, and in a healthy experimental animal, it is possible to reduce serum osmo-larity and produce cerebral edema with a large volume of lactated Ringer’s solution.128 In the setting of large-volume fluid adminis-tration (e.g., significant blood loss, multiple trauma), we alternate, liter by liter, lactated Ringer’s solution and normal saline.

The crystalloid versus colloid discussion is a recurrent one. This discussion usually arises in the context of a head injury victim. Although there are numerous fervent beliefs regarding this issue, there has been only a single demonstration that the reduction of colloid oncotic pressure in the absence of a change of osmolarity can contribute to an augmentation of cerebral edema in the setting of experimental head injury.130 The transcap-illary membrane pressure gradients that can be produced by reduction of colloid oncotic pressure are very small compared with those created by changes in serum osmolarity. Nonetheless, it seems that those small gradients have the potential—probably in the setting of a blood-brain barrier injury of intermediate severity—to augment edema. It seems reasonable then to select a

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fluid administration pattern that, in addition to maintaining normal serum osmolarity, would prevent substantial reductions in colloid oncotic pressure. For most elective craniotomies, this would not require the administration of colloid solutions. In situ-ations requiring substantial volume administration (e.g., multiple trauma, aneurysm rupture, cerebral venous sinus laceration, fluid administration to support filling pressure during barbiturate coma), a combination of isotonic crystalloid and colloid may be appropriate.

Which Colloid Solutions Should Be EmployedOn the basis of empirical local experience, we view albumin to be a reasonable choice as a colloid solution. There are conflicting opinions and cross-currents in the literature, however. A more recent analysis of the subset of patients in the Saline versus Albumin Fluid Evaluation (SAFE) trial with severe head injury (Glasgow Coma Scale [GCS] score 3 to 8) revealed increased mortality in patients who received saline.131 There is no accepted explanation. The formation of cerebral edema, which is more dif-ficult to clear, is an inevitable suspicion. By contrast, a nonconcur-rent, retrospective (i.e., less than scientifically ideal) comparison of outcome after volume support in patients with vasospasm after SAH revealed deterioration in outcomes when albumin was abandoned in favor of saline.132 Finally, an evolving literature, containing preclinical and clinical data, suggests an improvement in neurologic outcome when albumin is administered after stroke.133 These data have been sufficient to justify a phase III trial in human stroke, which began in 2006.134 At most, the exist-ing literature might justify consideration of limiting albumin volumes in patients with severe head injury, although the driving observations should be replicated before any firm principle is established.

The dextran-containing solutions are generally avoided because of their effects on platelet function. The various starch-containing solutions should be used cautiously in neurosurgery because, in addition to a dilutional reduction of coagulation factors, they interfere directly with platelets and the factor VIII complex.135 The literature addressing the coagulation effects of starches should be read with the understanding that the effects on coagulation are proportional to the average molecular weight of the starch preparation. In North America, preparations with the greatest molecular weights are used. When hetastarch solu-tions are used in neuroanesthesia, the clinician should respect the manufacturers’ recommended dose restrictions, and should use additional restraint in situations where there are other reasons for impairment of the coagulation mechanism. Several reported instances of bleeding in neurosurgical patients have been attrib-uted to hetastarch administration. All of those instances have involved circumstances in which the manufacturer’s recom-mended limit of 20 mL/kg/day was exceeded,136 or in which het-astarch was administered up to the recommended limit on successive days, probably resulting in an accumulation effect.137 The decision to use or not use these products frequently is a matter of local bias. If the products are used, the manufacturers’ recommended limit (20 mL/kg/24 hr) should be observed.

There is substantial current interest in the use of hypertonic fluids for the resuscitation of multiple trauma victims in general138 and of patients with neurologic injuries in particular.52,139 Improve-ment in outcome has yet to be shown in the latter group in asso-ciation with hypertonic solutions, however.139 It seems unlikely that the initial ICP effect of these fluids on the brain is substan-

tially different from an equiosmolar exposure to mannitol140,141 (although that notion should be qualified that there are reports of patients who had become refractory to mannitol who then responded to hypertonic saline).53,142 For the time being, when decisions about the appropriateness and relevance of these fluids in the resuscitation process are eventually made, it seems unlikely that those decisions should be made on the basis of specific cer-ebral effects. It seems more likely that the final judgment regard-ing this class of fluids would be made on the basis of their effects on the systemic circulation. Generally, an intervention that has the advantage of more effectively restoring systemic hemodynam-ics is likely to be advantageous to the injured brain. That assertion is made with the proviso that sustained hyperosmolarity (e.g., >320 mOsm/L) caused by any fluid has the potential to result in rebound swelling of the brain.

Hypothermia

The effects of hypothermia on cerebral physiology and its poten-tial cerebral protective mechanisms are presented in Chapter 13. The efficacy of mild hypothermia (32°C to 34°C) in reducing the neurologic injury occurring after standardized cerebral and spinal cord ischemic insults has been shown in numerous laboratories. On that basis, the use of induced hypothermia in the management of cerebrovascular procedures, in particular, aneurysms and occa-sionally AVMs, became widespread. An international, multicenter trial of mild hypothermia in 1001 relatively good-grade patients undergoing aneurysm surgery revealed no improvement, however, in neurologic outcome.143 The routine use of intraoperative hypo-thermia is likely to diminish.

Although mild hypothermia is perceived to increase the risk of coagulation dysfunction and dysrhythmias, neither of those problems has been evident in the temperature ranges typi-cally used (32°C to 34°C). The issue of where body temperature should be recorded to reflect best brain temperature during crani-otomy has been addressed.144 Esophageal, tympanic membrane, pulmonary artery, and jugular bulb temperature all are similar and provide a reasonable reflection of deep brain temperature, whereas bladder temperature does not. Superficial layers of cortex may be substantially cooler than deep brain and central temperatures.

Because ischemia is recognized to make a post insult con-tribution to neuronal injury after head injury,23,145 hypothermia was also studied in the laboratory in the context of traumatic brain injury.146 It was effective and this resulted in at least four single institution trials of 24 to 48 hours of mild hypothermia after head injury.147-150 These investigations revealed some physi-ologic dysfunction associated with more prolonged mild hypo-thermia, all of which was reversible with restoration of normal temperature. This included decreased creatinine clearance, eleva-tion of pancreatic enzymes, and a suggestion of an increased infection rate. A decreased incidence of seizures was an apparent adjunctive benefit in one study. As a result, a multicenter, pro-spective trial of hypothermia was performed but did not show a benefit of hypothermia (33°C) induced within 8 hours of injury and maintained for 48 hours.151 Post hoc subgroup analysis indi-cated that patients younger than age 45 years who arrived at the tertiary care facility with a temperature less than 35°C who were randomly assigned to the cooling limb of the trial did have an improved outcome. A follow-up trial in which the protocol seeks to achieve cooling more rapidly is under way.

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On the basis of lack of demonstrated efficacy in humans, routine use of hypothermia in neurosurgery cannot be advocated in a standard text. The decision to employ it, usually in the context of aneurysm surgery, will be a local one. We continue to use mild hypothermia selectively, most commonly in patients perceived to be at especially high risk of intraoperative ischemia. If hypother-mia is employed, it should be done so with attention to the pos-sibility of cardiac dysrhythmias and coagulation dysfunction if temperatures become too low and with attention to the necessity to rewarm adequately before emergence to avoid shivering and hypertension.

Yet another application of mild hypothermia is evolving. Two multicenter trials have shown improved neurologic outcome among survivors of witnessed cardiac arrest cooled to 32°C to 34°C within 4 hours and maintained at that temperature for 12 to 24 hours.152,153 Widespread clinical application has been advo-cated by an international task force.154 Systematic clinical applica-tion is evolving slowly, however, probably because of the time necessary for technical and ICU protocol developments.

Emergence from Anesthesia

Most practitioners of neuroanesthesia believe that there is a premium on a “smooth” emergence—one free of coughing and straining and arterial hypertension. The avoidance of arterial hypertension is considered desirable because of the belief that arterial hypertension can contribute to intracranial bleeding and increased edema formation.155-158 In the face of a poorly autoregu-lating cerebral vasculature, hypertension also has the potential, through vascular engorgement, to contribute to elevation of ICP. Much of the concern with coughing and straining has a similar basis. The sudden increases in intrathoracic pressure are transmit-ted to arteries and veins, producing transient increases in cerebral arterial and venous pressure with the same potential conse-quences: edema formation, bleeding, and elevation of intracranial pressure.

Coughing is a specific concern with certain individual pro-cedures. In transsphenoidal pituitary surgery in which a surgeon has opened, and subsequently taken pains to close, the arachnoid membrane to prevent CSF leakage, coughing has the potential to disrupt this closure because of the sudden and substantial increases in CSF pressure. Opening a pathway from the intracra-nial space to the nasal cavity conveys a substantial risk of post-operative meningitis. In other procedures, notably operations that have violated the floor of the anterior fossa, there is also the theo-retical potential for air to be driven into the cranium and, in the event of a flap-valve mechanism, to cause a tension pneumo-cephalus. This latter event can occur only when coughing occurs after the endotracheal tube has been removed.

There is a paucity of systematically obtained clinical data to give a perspective to the actual magnitude of the risks associ-ated with emergences that are not “smooth.” A retrospective study revealed that elevated postoperative arterial blood pressure was a correlate of intracerebral bleeding after craniotomy.159 Hyperten-sion occurring at emergence is not correlated with postoperative intracerebral bleeding, however. Although one clinical investiga-tion reported an association of increased CBF velocity with hypertension occurring during emergence,160 a second study observed that 60% increases in CBF velocity occurred even in the absence of hypertension, and concluded that hyperemia may be

a normal concomitant of arousal at the end of an anesthetic.161 A relationship between hypertensive transients at emergence and edema formation also is unconfirmed. Sudden, substantial increases in arterial pressure in anesthetized animals can result in a breach of the blood-brain barrier with extravasation of tracers such as Evans blue.156 There are no data, however, to confirm that the pressure transients associated with the typical coughing episode or typical emergence hypertensive transient are associated with increased edema formation. Nonetheless, it seems reasonable to take measures, to the extent that these measures do not themselves add potential patient morbidity, to prevent these occurrences.

A common method for managing systemic hypertension during the last stages of a craniotomy is the expectant or reactive (or both) administration of vasoactive agents, most commonly labetalol and esmolol.162 Other agents, including enalapril, nicar-dipine, and diltiazem, have been used to good effect. Administra-tion of dexmedetomidine during the procedure also has been reported to reduce the hypertensive response to emergence.163

There are also many approaches to the prevention of cough-ing and straining. We have several biases. We encourage trainees to include in their anesthetic technique “as much narcotic as is consistent with spontaneous ventilation at the conclusion of the procedure.” This practice is based on the same physiologic effect that justifies the administration of codeine and related com-pounds as antitussive medication (i.e., the depression of airway reflexes by narcotics). We also have the bias that patients emerge more rapidly and smoothly when the last inhaled agent to be withdrawn is N2O, and that clinicians should seek to avoid the “neither here nor there” phase of anesthesia that occurs in patients who are stimulated in the face of residual exhaled concentrations of volatile agent on the order of 0.2 to 0.3 MAC. A common practice among neuroanesthesiologists near the conclusion of a craniotomy is the relatively early discontinuation of the volatile agent with supplementation of residual N2O with propofol by either bolus increments or infusion at rates of 25 to 100 µg/kg/min.

An additional principle relevant to the emergence from neurosurgical procedures that practitioners may learn from a book or by bad experience is that emergence should be timed to coincide not with the final suture, but rather with the conclusion of the application of the head dressing. Good anesthetics for neurosurgery have been spoiled by severe coughing and straining occurring in association with endotracheal tube motion during the application of the head dressing. Another nuance of our prac-tice has been to withhold administration of neuromuscular antagonists as long as possible as a “hedge” against misjudgment while lightening a patient in the later stages of the procedure. The administration of lidocaine is another apparently effective tech-nique for reducing airway responsiveness and the likelihood of coughing and straining as depth of anesthesia is reduced in antici-pation of emergence. Bolus doses of approximately 1.5 mg/kg, usually given as the application of the head dressing begins, are appropriate for this purpose.

The premium placed on minimizing coughing and straining and hypertension results, in most instances, in patients being extubated expediently when extubation is appropriate. In some instances, anesthesiologists may be tempted to extubate patients before complete recovery of consciousness. This early extubation may be acceptable in some circumstances. It should be undertaken with caution, however, when the circumstances of the surgical

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procedure make it possible that neurologic events have occurred that would delay recovery of consciousness, or when there may be lower cranial nerve dysfunction. In these circumstances, it generally is best to wait until the likelihood of the patient’s recovery of consciousness is confirmed or wait until patient cooperation and airway reflexes are likely to have recovered.

Specific Procedures

Many of the considerations relevant to individual neurosurgical procedures are generic ones that have been presented in the pre-ceding section on recurrent issues. The descriptions that follow highlight only procedure-specific issues.

Supratentorial Tumors

Craniotomies for excision or biopsy, or both, of supratentorial tumors are common neurosurgical procedures. Gliomas and meningiomas are among the most frequent tumors. Relevant preoperative considerations include the patient’s ICP status and the location and size of the tumor. Location and size give the anesthesiologist an indication of the surgical position and the potential for blood loss, and occasionally reveal a risk of air embolism. Risk of VAE is quite low for most supratentorial tumors. However, lesions (usually convexity meningiomas) that encroach on the sagittal sinus may convey a substantial risk of VAE. Full VAE precautions, including a right atrial catheter, are usually reserved for only supratentorial tumors that lie near the posterior half of the superior sagittal sinus.

Excision of craniopharyngiomas and pituitary tumors with suprasellar extension may entail dissection in and around the hypothalamus. Irritation of the hypothalamus can elicit sympathetic responses, including hypertension. Damage to the hypothalamus can result in a spectrum of physiologic distur-bances, notably in water balance. Diabetes insipidus is the most likely disturbance, although cerebral salt-wasting syndrome can potentially occur. The latter has been very rare. The various dis-turbances of water balance typically have a delayed onset, begin-ning 12 to 24 hours postoperatively, rather than in the operating room. Postoperative temperature homeostasis also may be disturbed.

Patients who undergo a craniotomy involving a subfrontal approach occasionally may manifest a disturbance of conscious-ness in the immediate postoperative period. Retraction and irrita-tion of the inferior surfaces of the frontal lobes can result in a patient who is lethargic and does not awaken “cleanly,” and who may exhibit delayed emergence or some degree of disinhibition, or both. Patients exhibiting this phenomenon are sometimes referred to as “frontal lobey.” The phenomenon is more likely to be evident when there has been bilateral subfrontal retraction than when it occurs only unilaterally. The anesthetic implication is that the clinician should be more inclined to confirm return of consciousness before extubating the patient than to extubate expectantly. We also believe (although this has not been con-firmed by any systematic study) that a less liberal use of intrave-nous anesthetics (e.g., narcotics, benzodiazepines) may be appropriate when there is to be bilateral, subfrontal retraction. This is based on the rationale that low residual concentrations of

these agents that would be compatible with reasonable recovery of consciousness in the majority of patients, may be less well tol-erated in this population. Subfrontal approaches are most com-monly employed in patients with olfactory groove meningiomas and patients with suprasellar tumors (craniopharyngiomas and pituitary tumors with suprasellar extension).

Preoperative PreparationPatients with a significant tumor-related mass effect, especially if there is tumor-related edema, should receive preoperative ster-oids. A 48-hour course is ideal (see previous discussion of ster-oids), although 24 hours is sufficient for a clinical effect to be evident. Dexamethasone is the most commonly used agent; a regimen such as 10 mg intravenously or orally followed by 10 mg every 6 hours is typical. Because of the concern about producing CO2 retention in a patient whose intracranial compliance is already abnormal, patients with any substantial mass effect are usually not premedicated outside of the operating room.

MonitoringFrequently, the nature of the procedure does not require anything more than routine monitoring (see Chapter 46). Some situations may warrant invasive monitors (see Table 63-7). Preinduction placement of an arterial catheter may be appropriate in patients with severe mass effect and little residual compensatory latitude. It is the period of induction during which hypertension, with its attendant risks in a patient with impaired compliance and autoregulation, is most likely to occur. Procedures with a substan-tial blood loss potential (e.g., tumors encroaching on the sagittal sinus, large vascular tumors) also may justify arterial or CVP catheters. If not already present for other indications, is ICP monitoring ever warranted for intraoperative management? In our opinion, the answer is generally “no.” Anesthesiologists have a sufficient understanding of the potential impact of anes-thetic agents and techniques that they should be able to manage induction of anesthesia “blind.” When the cranium is open, obser-vation of conditions in the surgical field provides equivalent information.

Management of AnesthesiaThe principles governing the choice of anesthetic agents were presented earlier in the section on control of intracranial pressure and brain relaxation.

Aneurysms and Arteriovenous Malformations

Contemporary management of intracranial aneurysms calls for early intervention after SAH, ideally within 24 hours and defi-nitely within 48 hours. Intervention may entail either operative clipping or an endovascular approach. The latter is discussed in the subsequent section on interventional neuroradiology.

Early intervention was originally undertaken only in patients in the better neurologic grades—grades I through III and perhaps IV of the World Federation of Neurosurgeons classifica-tion (Table 63-8) or grades I through III of the Hunt-Hess classi-fication (Table 63-9)—but more recently has been extended to patients of higher grades.164 If early intervention is not feasible, and a surgical approach is intended, surgery is usually delayed for

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Table 63-8 World Federation of Neurosurgeons (WFNS) Subarachnoid Hemorrhage Scale

WFNS Grade GCS Score Motor Deficit

I 15 Absent

II 14-13 Absent

III 14-13 Present

IV 12-7 Present or absent

V 6-3 Present or absent

GCS, Glasgow Coma Scale.

Table 63-9 Hunt-Hess Classification of Neurologic Status after Subarachnoid Hemorrhage

Grade Criteria*

I Asymptomatic, or minimal headache and slight nuchal rigidity

II Moderate to severe headache, nuchal rigidity, no deficit other than cranial nerve palsy

III Drowsiness, confusion, or mild focal deficit

IV Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances

V Deep coma, decerebrate rigidity, moribund appearance

*Serious systemic diseases, such as hypertension, diabetes, severe arteriosclero-sis, chronic pulmonary disease, and severe vasospasm seen on arteriography, result in placement of the patient in the next less favorable category.

10 to 14 days to be safely beyond the period of maximal vaso-spasm risk (i.e., days 4 to 10 post-SAH).

The rationale for early intervention is severalfold. First, the sooner the aneurysm is clipped or obliterated, the less likelihood of rebleeding (and rebleeding is the principal cause of death for patients hospitalized after SAH165). Second, the management of the ischemia caused by vasospasm involves volume loading and induced hypertension. Early occlusion of the aneurysm elimi-nates the risk of rebleeding associated with this therapy. Vaso-spasm seems to be related to the presence of blood in the basal cisterns in the vicinity of the circle of Willis. Some of this blood can be removed at the time of the aneurysm clipping, and intra-cisternal fibrinolytics (for which there is limited proof of effi-cacy166) can be administered. Early operative clipping not only makes the therapy of vasospasm safer, but also may reduce the incidence and severity of the problem. Prior surgical practices entailed maintaining the patient at bed rest until approximately day 14, when the period of spasm risk had passed. Early aneu-rysm clipping reduces the period of hospitalization and reduces the incidence of the medical complications (e.g., deep vein throm-bosis, atelectasis, pneumonia) associated with a lengthy period of enforced bed rest.

Early intervention can make the surgeon’s task more diffi-cult. The brain in the early post-SAH period is likely to be more edematous than after a 2-week delay. A mild degree of hydro-cephalus is common after blood contaminates the subarachnoid space. Ten percent to 20% of SAH patients may require CSF diversion at some point in their course.167 Early intervention also may enhance the risk of intraoperative aneurysmal rupture because of the shorter period of time for clot to organize over the site of the initial bleed. All of this places a substantial premium on techniques designed to reduce the volume of the intracranial contents (see the section on control of intracranial pressure and brain relaxation) to facilitate exposure and minimize retraction pressures.

Preoperative EvaluationMany patients scheduled for intracranial aneurysm clipping come directly from the ICU, and elements of their management in the ICU may influence their immediate preoperative status.

Fluid Management. Some patients develop the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after SAH and are appropriately managed with fluid restriction. However, hyponatremia after SAH is more likely to be the result of the cerebral salt-wasting syndrome, which probably occurs as a result of the release of a natriuretic peptide by the brain (similar

to that which occurs in the heart).168 Cerebral salt-wasting syn-drome is characterized by the triad of hyponatremia, volume contraction, and high urine sodium concentrations (>50 mmol/L). The distinction between this syndrome and SIADH is impor-tant. SIADH, which is characterized by normovolemia or mild hypervolemia, is treated by volume restriction. Cerebral salt wasting is associated with a contracted intravascular volume. Fluid restriction and further volume contraction may be espe-cially deleterious in a patient after SAH169,170 and should be avoided. Although the clinical distinction between these two causes of hyponatremia (SIADH and cerebral salt-wasting syn-drome) may be difficult, management of both is simple: admin-istration of isotonic fluids using intravascular normovolemia as the end point.

Vasospasm. The anesthesiologist should determine whether vasospasm has occurred, and what, if any, therapies for it have been undertaken. Vasospasm is thought to be caused by the breakdown products of hemoglobin from the blood that has accumulated around the vessels of the circle of Willis after SAH. A specific mechanism/mediator has not been identified, but the current focus is on endothelin.171,172 A phase II trial of the endothe-lin A receptor antagonist clazosentan indicated effective reversal of established vasospasm and a substantial reduction in the inci-dence of new infarctions.173 A phase III trial is under way, and a preliminary report of drug-related reductions in vasospasm-related hypoperfusion in those patients has appeared.174

When there is a clinical suspicion of vasospasm (typically because of a change in sensorium or new neurologic deficit), surgery is deferred, and TCD, angiography, or other imaging is performed.175-177 Confirmed vasospasm is commonly treated with the “triple H” therapy described in the next paragraph and some-times by balloon angioplasty or intra-arterial vasodilators.

For patients proceeding to surgery, CPP should be main-tained intraoperatively in a high-normal range. Despite the former popularity of induced hypotension, the potential for induced hypotension to cause or aggravate cerebral ischemia in a patient with some degree of vasospasm is now recognized.178,179 This concern extends even to a patient classified as World Federation of Neurosurgeons grade I who may have regions of cerebral ischemia41 that are subclinical when the patient is normotensive.

In the ICU, the regimens employed to treat vasospasm usually involve some combination of hypervolemia, hemodilu-tion, and hypertension. The science behind hypervolemic-

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hypertensive therapy is “soft,” and the efficacy of neither “triple H” therapy nor volume expansion in isolation has been proved by prospective study.180,181 The importance of the rheologic and the pressure effects is undefined, although there is evidence for the relevance of blood pressure elevation in isolation.182,183 Phen-ylephrine and dopamine are the most commonly employed pres-sors; the specific pressor choice should be governed primarily by systemic cardiovascular considerations. The end point for pressor administration varies. Most commonly, the objective is an increase in MAP of approximately 20 to 30 mm Hg above “baseline” sys-tolic pressure. It has been reported, however, that augmentation of cardiac output with dobutamine, without simultaneous MAP increase, augments CBF in vasospastic territories.184 Some authors believe that the hematocrit should be reduced to the low 30s. Commonly, hematocrit reduction occurs secondarily as a result of attempts to produce hypervolemia (usually with colloid solu-tions) as a part of the effort to increase blood pressure.

Calcium Channel Blockers. Calcium channel blockers are now an established part of the management of SAH. Administra-tion of nimodipine has been shown to decrease the incidence of morbidity from cerebral ischemia occurring after SAH.185-187 These studies failed to show any reduction in the incidence of vasospasm, however, as detected by angiography.186 The beneficial effect of these agents may be the result of effects on neurons, rather than vascular smooth muscle. Patients coming to the oper-ating room after SAH should be receiving nimodipine. Nimodi-pine must be administered orally; nicardipine has been evaluated as an intravenous alternative. The multicenter nicardipine trial188,189 revealed a reduced incidence of symptomatic vasos-pasm, but no improvement in outcome. Consequently, nimodipine is more commonly employed. Because papaverine may be neuro-toxic, intra-arterial calcium entry blockers, including verapamil and nicardipine, are being increasingly used as a primary treat-ment for medically refractory vasospasm.

Magnesium, Statins, and Endothelin Antagonists. More recent clinical trials have identified several agents that may soon become part of the routine management of patients with SAH. The endothelin antagonist clazosentan was mentioned earlier in this section. A randomized, blinded, placebo-controlled trial reported fewer new ischemic deficits and improved outcome among patients who received magnesium sulfate starting within 4 days of SAH. Two phase II trials have examined the post-SAH administration of statins. Together, these trials showed reductions in vasospasm, delayed ischemic deficits, and improvement in outcome.190,191 Although some centers have already implemented some of these therapies as part of the local routine, widespread adoption is not likely until the completion of larger trials that confirm these initial results.

Antifibrinolytics. Antifibrinolytics have been administered in an attempt to reduce the incidence of rebleeding. Meta-analysis suggests, however, that although they accomplish the latter, they do so at the cost of an increased incidence of ischemic symptoms and hydrocephalus with the result being no net improvement in outcome.192

Subarachnoid Hemorrhage–Associated Myocardial Dys-function. SAH can result in a reversible, “stunning”-like myo-cardial injury. The severity of the dysfunction correlates best with

the severity of the neurologic injury,193 and occasionally is suffi-cient to require pressor support.194 The mechanism is uncertain, but it is thought to be catecholamine mediated.195 This suspicion is supported by the observation that more severe dysfunction occurs in SAH patients with genetic polymorphisms associated with greater catecholamine receptor sensitivity. Troponin eleva-tion occurs commonly, although typically reaching levels less than the diagnostic threshold for myocardial infarction.196 Peak troponin levels correlate with the severity of neurologic injury and echocardiographic myocardial dysfunction.194

ECG abnormalities are common after SAH.193 In addition to the classic “canyon T waves” (Fig. 63-14), nonspecific T-wave changes, Q-T prolongation, ST-segment depression, and U waves have been described. There is typically no relationship between the ECG changes and echocardiographic myocardial dysfunc-tion.196 ECG abnormalities do not herald evolving or impending cardiac disease.197 When ECG patterns other than those that are typical of myocardial ischemia are observed, no specific interven-tions or modifications of patient management are warranted, other than attention to the possibility of dysrhythmias. In particu-lar, an increased Q-T interval (>550 msec) occurs frequently after SAH, especially in patients with more severe SAH,198 and has been associated with an increased incidence of malignant ventricular rhythms, including torsades de pointes.199,200

Anesthetic TechniqueThe important considerations in anesthetic technique include the following:

1. Absolute avoidance of acute hypertension with its attend-ant risk of rerupture

2. Provision of intraoperative brain relaxation to facilitate surgical access to the aneurysm

3. Maintenance of a high-normal mean arterial (perfusion) pressure to prevent critical reduction of CBF in recently insulted and now marginally perfused areas of brain, or regions critically dependent on collateral pathways

4. Preparedness to perform precise manipulations of MAP as the surgeon attempts to clip the aneurysm or to control bleeding from a ruptured aneurysm, including manage-ment of temporary vascular occlusion

Monitoring. An arterial line is invariably appropriate. CVP may be relevant if the institutional practices involve large doses of mannitol to promote brain relaxation and may be used in older patients to guide volume replacement in the event of bleeding.

Anesthetic Selection. Any technique that permits proper control of MAP is acceptable. In the face of increased ICP or a tight surgical field, an inhaled agent technique may be less suita-ble. The prevention of paroxysmal hypertension is the only abso-lute requirement in patients undergoing aneurysm clipping. Rebleeding kills,165 and a poorly organized clot over the aneu-rysms of patients undergoing early post-SAH clipping makes them particularly prone to rebleeding. A rebleed at induction is frequently fatal. The escaping arterial blood is more likely to pen-etrate brain substance because it cannot dissect through the CSF space (filled with clot), and the ICP increase is extreme because of the poor compliance of the intracranial space (swollen brain, hydrocephalus).

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Induced Hypotension. The routine use of induced hypoten-sion is diminishing (see previous section on management of arte-rial blood pressure). Nonetheless, the anesthesiologist should be prepared to reduce blood pressure immediately and precisely if called on to do so. Preparation must occur before the episode of bleeding. We prepare a sodium nitroprusside infusion before induction. It is placed in line at a Y-injection port at the hub of the CVP or intravenous catheter. A carrier drip flows steadily such that any change in nitroprusside infusion rate is reflected as rapidly as possible in the central compartment. There are theoreti-cal pros and cons for various hypotensive agents. The data indi-cate that regimens that entail the use of an agent that is also a cerebral vasodilator (e.g., isoflurane, nitroprusside) are preferable in terms of brain oxygen delivery to approaches that do not involve cerebral vasodilation (e.g., trimethaphan, controlled hypovolemia).201 The choice should ultimately be made on the basis of which regimen, in the hands of the individual practi-tioner, results in the most precise control of MAP. Occasionally, the anesthesiologist may be asked to control MAP in the range of 40 to 50 mm Hg, in the face of the active arterial bleeding. This can be extremely difficult in a patient who is hypovolemic at the beginning of the bleeding episode. It is our practice to maintain normovolemia.

Induced Hypertension. Hypertension may be requested during periods of temporary arterial occlusion (see the later section on trapping) to augment collateral CBF. In addition, after clipping of the aneurysm, some surgeons puncture the dome of the aneurysm to confirm adequate clip placement, and may request transient elevation of the systolic pressure to 150 mm Hg. Phenylephrine is suitable in either instance.

Hypocapnia. Hypocapnia traditionally has been employed as an adjunct to brain relaxation. The practice has been questioned, however, because of the concern that it would aggravate ischemia (see the earlier section on management of Paco2). The circum-stances regarding ICP and brain relaxation should probably dictate its use or avoidance.

Lumbar Cerebrospinal Fluid Drainage. Some surgeons employ elective CSF drainage to facilitate exposure. Its use seems to be diminishing, however, because surgeons have appreciated that the same brain-relaxing effect can be achieved by release of CSF from the basal cisterns. It is appropriate, when placing a lumbar CSF drain, to avoid excessive loss of CSF. Sudden reduc-tion of the transmural pressure gradient across the dome of the aneurysm (by sudden reduction of ICP consequent on substantial

Figure 63-14 Electrocardiogram abnormalities associated with subarachnoid hemorrhage (SAH). The “canyon” T waves that may be seen after SAH are evident.

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CSF drainage) should be avoided because of the theoretical concern that this decompression might encourage rebleeding. The common practice is, having verified the patency of the lumbar drainage system, to leave it closed until such time as the surgeon is opening the dura. The drain may be opened at that time and allowed to drain freely with the bag at floor level. Drainage should be discontinued promptly after final withdrawal of the retractors to allow CSF to reaccumulate and to reduce the size of the poten-tial pneumocephalus. The drain is usually removed immediately postoperatively.

Mannitol. Some surgeons make relatively aggressive use of mannitol (e.g., 2 g/kg). It is used, in part, to shrink the brain and to facilitate exposure and reduce retractor pressures. There is evidence that mannitol may have additional benefits. Specifically, data derived in animals and humans indicate that mannitol may have a CBF-enhancing effect in regions of moderate CBF reduc-tion.202-205 The mechanism is not defined. Reduction of interstitial tissue pressure around capillaries or an alteration of blood rheol-ogy, or both, have been proposed to contribute. Typically, man-nitol is administered in a dose of 1 mg/kg just before dural opening. Surgeons who believe in the flow-enhancing effect may request a second 1 mg/kg dose approximately 15 minutes before an anticipated temporary occlusion.

TrappingIt is occasionally necessary for the surgeon to “trap” the aneurysm (i.e., to occlude the vessel on either side of the aneurysm tempo-rarily) to complete dissection of the neck and apply the clip. The need for trapping is more common with larger aneurysms. With giant aneurysms in the vicinity of the carotid siphon, the inferior occlusion may be performed at the level of the internal carotid artery via a separate incision in the neck. A clinical survey by Samson and coworkers206 of the neurologic outcome after tempo-rary occlusion in normothermic, normotensive adults revealed that occlusion times of less than 14 minutes were invariably toler-ated. The likelihood of an ischemic injury increased with longer occlusions and reached 100% with occlusions longer than 31 minutes.206 In another institution, the threshold for ischemic injury was 20 minutes of occlusion.207 Typically, it is appropriate to support MAP at high normal levels during periods of occlusion to facilitate collateral CBF.

Brain ProtectionImportant brain protection techniques include maintenance of MAP to ensure collateral flow and perfusion under retractors, efficient brain relaxation to facilitate surgical access and reduce retractor pressures, limitation of the duration of episodes of tem-porary occlusion, and perhaps mild hypothermia. Specific anes-thetic agents also have been used to protect the brain (see the discussion in Chapter 13). Propofol and etomidate are currently used. However, no convincing laboratory studies have shown that propofol provides any greater tolerance to a standardized ischemic insult than anesthesia with a volatile agent. Attempts to show protection by etomidate in an animal model of focal ischemia showed an adverse effect of etomidate.208 A clinical investigation during aneurysm clipping revealed decreases in brain tissue Po2 in association with administration of etomidate, which contrasted with the brain Po2 increases that occurred with the introduction of desflurane. During subsequent temporary

vessel occlusion, tissue pH decreased alarmingly in patients receiving etomidate and was unchanged with desflurane.209

Although the available data collectively do not support an assertion that etomidate is harmful in the setting of aneurysm surgery, we think that they should dissuade any anesthesiologist from advocating the administration of etomidate as a uniquely protective substance in the context of aneurysm surgery. With respect to the volatile agents, attempts in the laboratory to confirm the once proclaimed protective efficacy of isoflurane have shown that there are no differences among the various volatile agents in terms of their influence on outcome after focal or global ischemia.208,210-212 In addition, there has been no demonstration of greater protective efficacy with concentrations of volatile agents sufficient to cause EEG suppression as opposed to more modest (e.g., 1.0 MAC) levels.212,213 Nonetheless, these animal investiga-tions suggest that a standardized experimental ischemic insult is better tolerated, relative to the awake state, by animals receiving a volatile anesthetic.211,212,214 Data derived in animals also suggest that there may be a relative protective advantage to an anesthetic that includes a volatile agent compared with a strict N2O-narcotic technique.212,214

The magnitude of the differences among anesthetics and the absence of proof of relevance in patients precludes advocacy of a particular anesthetic regimen in a standard text. The impor-tant anesthetic objectives are precise hemodynamic control and timely wake-up, and these two constraints should dictate the choice of the anesthetic regimen for most aneurysm procedures. Among anesthetic agents, only for the barbiturates has additional protective efficacy been shown convincingly (see Chapter 13). Because of their potentially adverse effects on hemodynamics and wake-up, barbiturates are not ideal for routine administration. They probably should be reserved for situations in which a pro-longed vessel occlusion is unavoidable, and in that circumstance it would be ideal that the ischemic hazard be first confirmed by observation of the EEG response to a temporary occlusion.215

HypothermiaAs noted in the earlier section on hypothermia, a prospective trial of mild hypothermia in patients undergoing aneurysm surgery revealed no improvement in neurologic outcome. Nonetheless, many neurosurgical teams that were already employing mild hypothermia (32°C to 34°C) are continuing its use for procedures in which temporary vessel occlusion may occur. Institutions that use the lower temperatures are those in which the team is willing to accept a delay in emergence from anesthesia to achieve suffi-cient rewarming to avoid the extreme hypertension that can occur when a patient is awakened during hypothermia.

Neurophysiologic MonitoringEvoked responses and EEG (see Chapter 46) have been employed for monitoring,215,216 although neither technique has been used widely. EEG monitoring can be used as a guide to management during the period of flow interruption or to guide the administra-tion of CMR-reducing anesthetic agents given before occlusion.215 An electrode strip can be placed over the region of cortex at risk during the intended occlusion. However, the more commonly used skin surface frontal-mastoid derivation is probably sufficient to reveal a major ischemic event. The EEG can be either the con-ventional “raw” polygraph or a processed derivative. In most cir-cumstances, if occlusion is deemed necessary, a temporary

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occlusion is done, and the EEG is observed. If the EEG shows significant slowing, the clip can be repositioned, or MAP can be increased by some combination of phenylephrine and lightening of anesthesia to find a way of temporary clipping without a major EEG disturbance. If this cannot be accomplished, and a sustained period of occlusion seems likely, barbiturates (see earlier) should be given to produce burst suppression.

Intraoperative AngiographyIntraoperative angiography is an increasingly common compo-nent of the management of intracranial aneurysms. It does not have substantial implications for the anesthesiologist. Apparatus around the patient’s head must be organized, however, so as to allow C-arm access without snagging of airway and monitoring equipment. In addition, the radiologist must have access to groin vessels. The vascular access sheath, for a patient who will ulti-mately be in the lateral position, is easiest to use when the non-dependent femoral artery is chosen. The rate of administration of heparin “flush” via the vascular access sheath should be monitored.

Special Considerations for Specific AneurysmsThe most common procedures are done for aneurysms arising in or close to the circle of Willis. The vessel of origin may be the anterior communicating artery, the middle cerebral artery, the anterior cerebral artery, the ophthalmic artery, the tip of the basilar artery, the posterior communicating artery, or, less frequently, the posterior cerebral artery. These procedures all are similar for the anesthesiologist and typically require a supine position with the head turned slightly away from the operative side.

Ophthalmic Artery Aneurysms. Access to the origin of the ophthalmic artery, which is the first intradural branch of the carotid artery, is made difficult by the anterior clinoid process and the optic nerve. As a result, these aneurysms frequently require temporary vascular occlusion. The surgeon commonly first exposes the carotid artery in the neck. When the surgeon reaches the stage of seeking definitive access to the neck of the aneurysm, he or she will occlude first the carotid artery in the neck and then the intracranial portion of the carotid artery immediately proxi-mal to the origin of the posterior communicating artery.

Vertebrobasilar Aneurysms. These procedures are typi-cally performed in the lateral position. The exposure may involve a combined middle and posterior fossa approach, with some attendant, although minor, risk of venous air embolism. Cortical or skin surface EEG monitoring is of less relevance with verte-brobasilar aneurysms. Auditory or somatosensory evoked responses, or both, have been employed.217 As in any other pro-cedure involving the potential for mechanical or vascular injury to the brainstem, cardiovascular responses should be monitored, and sudden changes in response to surgical manipulation should prompt immediate notification to the surgeon. Spontaneous ven-tilation may be appropriate for procedures involving surgical manipulation of the vertebral arteries, the vertebrobasilar junc-tion, and the middle portion of the basilar artery. Apnea, gasping, or other sudden changes in ventilatory pattern during manipula-tion of the vasculature provide important, although nonspecific, warning of compromise of the vascular supply of the brainstem.218

Now largely supplanted by endovascular approaches, manage-ment of these aneurysms occasionally requires cardiopulmonary bypass and deep hypothermic circulatory arrest.219

Vein of Galen Aneurysms. Vein of Galen “aneurysms” are congenital dural arteriovenous fistulas, usually treated in neonates using endovascular methods, and share considerations relevant to AVMs. These include anticipation of the possibility of the cerebral dysautoregulation phenomenon and are considered subsequently.

Arteriovenous Malformations

For most intracranial AVMs, the general considerations are similar to the considerations appropriate to aneurysm surgery: avoidance of acute hypertension and the capability to manipulate blood pressure accurately in the event of bleeding. A problem that is specific to AVMs is the phenomenon known as “perfusion pres-sure breakthrough,” or cerebral dysautoregulation.220,221 It is char-acterized by an often sudden engorgement and swelling of the brain, sometimes with a relentless cauliflower-like protrusion from the cranium. This phenomenon tends to occur in the advanced stages of lengthy procedures on large AVMs, or accounts for otherwise unexplained postoperative swelling and hemor-rhage. The phenomenon is not entirely understood and is almost certainly related to the “hyperemic” complications seen after carotid endarterectomy or angioplasty.

In textbooks, this syndrome has been described as relating to the acute obliteration of a high-volume, low-resistance pathway (the AVM) that has chronically diverted blood from adjacent, marginally perfused vascular territories. It has been theorized that these tissues have long been maximally vasodilated without the need ever to vasoconstrict and have become incapable of doing so. Experimental data are not generally consistent with this mechanism, however.221-223 The observed “hyperemic” complica-tions are probably not passive. One might speculate that the vasodilation is neurogenic in origin, or involves some kind of paracrine signaling. Such events might lead to vascular wall pro-tease activation and vasogenic edema or vascular rupture. Supranormal flow rates also can activate protease activity. The area is in need of further study.

Anesthetic TechniqueThe management constraints are essentially the same as those relevant to aneurysm surgery, although the risk of intraoperative rupture is much less. Institutional practices vary. We do not employ induced hypotension unless required to by bleeding. We reason that the effects on the surrounding brain of devasculariz-ing the AVM would be best appreciated if the devascularization occurs at normal pressures. If refractory brain swelling occurs, tight blood control is essential; decreasing MAP may be useful to control swelling. The hyperemic complications with carotid surgery seem to be related, but not uniquely determined, by poor post-treatment blood pressure control. The speculation is that blood flow through the involved area is pressure-passive and decreases as MAP is reduced.

With severe episodes of swelling, we have employed (in addition to hypotension, which we use cautiously because of the associated ischemia risk) hypocapnia, hypothermia, and barbitu-

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rates. These three techniques probably reduce the bulk of only normal brain tissue—hypocapnia via a direct effect on CBF, and barbiturates and hypothermia via the coupled effects of reduction of CMR on CBF. Induced hypothermia also is an adjunct to minimizing the barbiturate doses. In all of neurosurgery, we seek to prevent postoperative hypertension; however, in AVM surgery, this should be accomplished with greatest care because of the concern that the “dysautoregulating” brain adjacent to the resected AVM will develop edema or hemorrhage if hypertension occurs.

Head Injury

Intubating a Head-Injured PatientThe anesthesiologist’s first encounter with a patient who has sus-tained a traumatic brain injury (TBI) may come as a result of a request for assistance with airway management. Patients with GCS scores of 7 or 8 or less (Table 63-10) require intubation and controlled ventilation for ICP or airway control or both. Patients with less severe head injuries also may require intubation because of trauma-related cardiopulmonary dysfunction or, when unco-operative, to facilitate diagnostic procedures.

In choosing the intubation technique, the anesthesiologist may encounter numerous conflicting constraints (Table 63-11), including (1) elevated ICP, (2) a full stomach, (3) uncertain cervi-cal spine status, (4) uncertain airway status (e.g., presence of blood, possible laryngotracheal injury, possible skull base frac-ture), (5) uncertain volume status, (6) an uncooperative or com-bative patient, and (7) hypoxemia. There is no “correct” way, and the “best” approach is determined by the relative weight of these various factors along with the degree of urgency. The anesthesi-ologist must not become distracted by placing an excessive initial emphasis on ICP. The anesthesiologist needs to keep sight of the ABCs of resuscitation: Securing the airway, guaranteeing gas exchange, and stabilizing the circulation are higher initial priori-ties than ICP. One must not risk losing the airway or causing severe hypotension for the sake of preventing coughing on the tube or brief hypertension with intubation.

Cervical SpineThe possibility of causing or aggravating an injury to the cervical spine is a relevant concern. Approximately 2% of blunt trauma victims who survive to reach a hospital and 8% to 10% of TBI victims with GCS less than 8 have a fracture of the cervical spine.224,225 This incidence suggests that a “hypnotic-relaxant-direct laryngoscopy” approach for all patients with a closed-head injury might convey a measurable risk of injuring the cervical cord. Nonetheless, although the literature contains con-tradictions, several published series have concluded that a rapid-sequence induction does not convey significant risk of neurologic injury.226-230 It is possible, however, that the incidence of intuba-tion-related neurologic injury is underreported. An informal survey reported by Criswell and colleagues226 indicated that there have been more such events than one can infer from the pub-lished literature.231,232

Nonetheless, the literature argues that we will “get away with it” most of the time, and most TBI patients requiring airway control are intubated using a hypnotic-relaxant-direct laryngos-copy sequence. It is our (probably minority) opinion, however, that the possibility of devastating spinal cord injury exists, prob-ably most so with injuries in the atlanto-occipital region, which are also difficult to identify radiologically,233 and that the anesthe-siologist should identify circumstances in which time latitudes allow more detailed examination or radiologic evaluation. When there is any uncertainty regarding the airway or the cervical spine, direct laryngoscopy (with vigorous atlanto-occipital extension) should probably be avoided, unless the exigencies of airway control demand it (which often is the case). The nasal route can be considered if the clinical context warrants, bearing in mind that risk of infection may be increased with skull base fracture and CSF leak. The anesthesiologist needs to use discretion (e.g., in the pres-ence of an obvious facial smash, the nasal route should be avoided because of the possibility of entering the cranium) and be sensitive to unusual resistance in passing the endotracheal tube.

When a hypnotic muscle-relaxant sequence is used, the standard approach includes the use of cricoid pressure and in-line axial stabilization. In-line traction previously was favored, but has been supplanted by stabilization because of the perceived risk of overdistraction and cord injury in the event of gross instability. The largest of the clinical series that concluded that oral intuba-tion with anesthesia and relaxation is reasonable227 used in-line stabilization with the patient’s occiput held firmly on the back-board, limiting the amount of “sniff ” that was feasible (Fig. 63-15). There is no question that in-line stabilization, properly performed, makes laryngoscopy more difficult, but it decreases the amount

Table 63-10 Glasgow Coma Scale

Eyes open Never 1

To pain 2

To speech 3

Spontaneously 4

Best verbal responses None 1

Garbled/incomprehensible sounds 2

Inappropriate words 3

Confused but converses 4

Oriented 5

Best motor responses None 1

Extension (decerebrate rigidity) 2

Abnormal flexion (decorticate rigidity) 3

Withdrawal 4

Localizes pain 5

Obeys commands 6

Total 3-15

Table 63-11 Factors That May Be Relevant during Intubation of a Head-Injured Patient

Full stomachUncertain cervical spineUncertain airway

BloodAirway injury (larynx, cricoarytenoid cartilage)Skull base fracture

Uncertain volume statusUncooperative/combativeHypoxemiaIncreased ICP

ICP, intracranial pressure.

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Figure 63-15 Intubating an acute trauma patient with an uncertain cervical spine injury . A hypnotic and a relaxant have been administered. One assistant maintains in-line axial stabilization with the occiput held firmly to the back-board; a second applies cricoid pressure. The posterior portion of the cervical collar remains in place to “discourage” atlantoaxial extension. (From Stene JD: Anesthesia for the critically ill trauma patient. In Siegel JH [ed]: Trauma: Emergency Surgery and Critical Care. Melbourne, Churchill Livingstone, 1987, pp 843-862.)

of atlanto-occipital extension necessary to achieve visualization of the glottis.234 This is probably because performing the laryn-goscopy against the assistant’s counter pressure results in greater compression of the soft tissue structures of the tongue and floor of the mouth. Some recommend leaving the back half of the Philadelphia collar in place during laryngoscopy (see Fig. 63-15) because it functions as a strut between the shoulder and the occiput limits atlanto-occipital extension.

In the resuscitation situation, before initiating a hypnotic-relaxant sequence, the anesthesiologist should confirm the avail-ability of cricothyrotomy equipment and of someone to make immediate, skilled use of it if necessary. The recently injured brain is very intolerant of hypoxia and hypotension.235 The occasional failed intubation is inevitable. In the extensive experience of the Cowley Shock-Trauma Center in Baltimore, the cricothyrotomy/tracheostomy rate is 0.3%.236 As is the case in many other situa-tions, the laryngeal mask may be a useful device for temporizing in the face of a failed intubation, and may provide access for intubation as an alternative to cricothyrotomy.

As noted Chapter 13, although succinylcholine can cause ICP increases, these increments are small; they probably do not occur at all in patients with serious cerebral injuries.6 Succinyl-choline should not be contraindicated in a patient with TBI. If there is an urgent need to secure the airway (to guarantee oxy-genation and control Paco2), and if succinylcholine is in other respects the appropriate drug to achieve that end, it should be used.

The situation of a patient whose cervical spine has not been “cleared” should arise with decreasing frequency in unconscious patients because of the proliferation of multidetector CT scan-ners, which allow rapid, thin-slice evaluation, with sagittal recon-struction, of the cervical spine. The combination of a three-view plain film series and CT scanning (and most of these patients require CT evaluation for other reasons) is reported by one reviewer to have a false-negative rate for serious injury of less than 0.1%.237 Another survey reported, however, that CT may

miss a significant number of ligamentous injuries.238 With respect to a conscious patient who has not yet undergone complete radio-logic evaluation, several clinical surveys have confirmed that patients who are alert, nonintoxicated, and free of significant dis-tracting injuries invariably have pain, midline tenderness, limita-tion of voluntary movement, or neurologic signs239-241 if they have a cervical spine fracture.

Despite the frequency with which an anesthesiologist may encounter a patient still wearing a Philadelphia collar because his or her neck has not yet been “cleared,” no special precautions seem warranted in an asymptomatic, alert patient. If the clinical situa-tion or examination is suspicious for a cervical spine injury, a normal lateral x-ray (the anteroposterior and through-the-mouth odontoid views are frequently not taken during initial evaluation) cannot provide complete reassurance. The lateral view has been reported to miss 15%242 to 26%239 of fractures.

Anesthetic Technique

Choice of Anesthetic Drugs. Craniotomies most commonly are performed for the evacuation of subdural, epidural, or intra-cerebral hematomas. The anesthetic approach is similar for all three. The guiding principles have been discussed in the section on control of intracranial pressure and brain relaxation. Gener-ally, anesthetics that are cerebral vasoconstrictors are preferable to anesthetics that have the potential to dilate the cerebral circula-tion. All of the intravenous anesthetics except perhaps ketamine cause some cerebral vasoconstriction and are reasonable choices, provided that they are consistent with hemodynamic stability. All of the inhaled anesthetics (N2O and all of the vapors) have some cerebral vasodilatory effect. Although their administration fre-quently is consistent with acceptable ICP levels and appropriate conditions in the surgical field, when the ICP is out of control (or unknown), or the surgical field is “tight,” eliminating the inhaled agents in favor of fixed agents is appropriate.

For patients who are likely to remain intubated postopera-tively, an anesthetic based primarily on a narcotic (e.g., fentanyl) and a muscle relaxant usually serves well. Any muscle relaxant is acceptable with the proviso that agents that can release histamine should be titrated in careful increments. When immediate tra-cheal extubation is a possibility (e.g., a patient with an acute epi-dural hematoma who had a lucid interval before witnessed deterioration), the technique should be modified after the opening of the cranium. Introduction of inhaled anesthetics or the use of shorter acting intravenous anesthetics, or both, can be under-taken as guided by observation of the surgical field. If N2O is contemplated at any time, the anesthesiologist must remember the possibility, in the setting of missile injury or compound skull fracture, of intracranial air.

Monitoring. The anesthesiologist should appreciate that the priority is to open the cranium as rapidly as possible. After achiev-ing intravenous access, the risks and benefits of delaying craniot-omy for line placement should be carefully considered. An arterial line, often placed after induction in urgent situations, is appropri-ate for essentially all acute trauma craniotomies. The decision to achieve central venous access can be made on the basis of the patient’s hemodynamic status. Cardiovascular collapse after dural opening with high ICP may occur243; adequate volume resuscita-tion may mitigate this complication. Infrequently, the manage-ment of a depressed skull fracture over the sagittal sinus justifies

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a precordial Doppler and, subject to the surgeon’s assessment of VAE risk, a right heart catheter.

Blood Pressure Management. The concept that the injured brain is extremely vulnerable to what would otherwise be a minor insult (e.g., modest hypotension, moderate hypoxia) has been well confirmed in the laboratory.244,245 Although there are as yet no completely conclusive data derived in humans, several clinical surveys confirm the association of otherwise minor degrees of hypotension and hypoxia and poor outcome in TBI patients.235,246-250 The explanation for this vulnerability to hypoten-sion probably relates partly to the observation that some patients in the postinjury period have regions of brain with precariously low CBF,23,33,38,251 in which autoregulation also may be defec-tive.37,252 Although it has been argued that reduced CBF is partly a normal concomitant of the reduced CMR that commonly occurs after TBI, there is nonetheless ample reason to worry about the occurrence of ischemia. First, a large percentage of patients who die after TBI have pathologic changes consistent with ischemia.145 Second, there is considerable evidence that the low postinsult CBF values correlate with a poor eventual outcome.23,36,247,253,254 These observations have resulted in a much greater emphasis among neurosurgeons, neurointensivists, and anesthesiologists on aggressive support of blood pressure in the TBI patient.

What constitutes an appropriate blood pressure? System-atic studies, in particular the studies conducted at the University of Edinburgh, revealed that indices of the adequacy of cerebral perfusion derived from Sjvo2 and TCD data begin to deteriorate below a mean CPP (CPP = MAP − ICP) of 70 mm Hg,247,255,256 and many centers adopted 70 mm Hg as the target CPP. A clinical investigation by Robertson and colleagues257 comparing the ICU management of TBI patients at CPPs of 70 mm Hg and 50 mm Hg showed that although indices of cerebral well-being were improved by the former, there was no outcome advantage, apparently because of the cardiopulmonary morbidity associated with achieving a sustained CPP of 70 mm Hg. As a result, many groups and authorities have adopted 60 mm Hg as the minimum CPP management objective.258-261 The most recent recommenda-tions of the Brain Trauma Foundation give clinicians wide lati-tude in recommending CPP target values “within the range of 50-70 mm Hg.”59

There are at least two alternative opinions regarding blood pressure management (Fig. 63-16). The first, promoted by the neurosurgery group at the University of Alabama, Birmingham, is that induced hypertension can be employed as an adjunct to ICP control.23,262 This idea is based on the belief that autoregula-tion is at least partially preserved after head injury, and that an increased CPP results in autoregulation-mediated vasoconstric-tion with a concomitant reduction in CBV and ICP. These inves-tigators reported a very satisfactory local experience262 with this approach, but it has not been applied widely, and others have reported that induced hypertension was either ineffective or del-eterious as a means of reducing increased ICP.10,263 The second alternative is the so-called Lund concept, which is based on the premise that high blood volume and hydrostatically driven edema accumulation make a substantial contribution to increased ICP.264-266

As originally described, the Lund approach entailed dehy-dration; hyperosmolarity; and the administration of metoprolol, clonidine, and dihydroergotamine to reduce blood pressure to a

CPP target of 50 to 55 mm Hg. At its inception, the approach was controversial because it ran counter to the perceptions of many clinicians of the importance of maintaining a CPP of 70 mm Hg, and because of the later demonstration that a negative fluid balance in patients with TBI is deleterious.249 Over time (and in parallel with a relaxation the CPP targets by others59,258-260), the Lund proponents have modified their approach, and now “a CPP of 60-70 is considered optimal,” and normovolemia is the clinical objective.266

The essence of the previously controversial Lund approach is no longer the aggressive CPP reduction that was the originally proclaimed cornerstone, although sedatives, clonidine, and meto-prolol are administered to prevent hypertension. The Lund con-cept’s distinguishing features are now (1) the routine infusion of low-dose thiopental (to reduce the “stress response” and to decrease CMR and CBV); (2) the maintenance of colloid osmotic pressure at unspecified levels by the generous administration of albumin; and (3) the cautious administration of dihydroergot-amine, also to reduce CBV (by a putative selective cerebral veno-constrictive effect).266 Although there is a theoretical basis for each of the components, the existing literature provides no com-pelling support. Although the proponents of the Lund approach assert improvements in outcome, those reports invariably entail either no control group or comparisons with nonconcurrent controls.267-269 The approach has not been adopted in North America.

What should an anesthesiologist managing a TBI patient do in the face of these various approaches? The approaches have in common perfusion pressure support of varying degrees. The characteristic behavior of CBF after head injury is an initially low CBF followed by a gradual increase over 48 to 72 hours to normal or sometimes even slightly hyperemic levels.23,33,37,38,251,258,270 Aggressive support of CPP in the 60 to 70 mm Hg range during

Figure 63-16 The relationship of cerebral blood flow (CBF) to blood pressure after head injury. There are three cerebral perfusion pressure (CPP) management strategies (see text) driven by differing beliefs about common pathophysiologic derangements. The most commonly used strategy, “Edinburgh” (named for the institution of the original proponents), emphasizes low postinjury CBF, impaired autoregulation, and the necessity to support CPP (mean arterial pressure [MAP] − intracranial pressure [ICP]) to 70 mm Hg. The “Lund” concept emphasizes the contribution of hyperemia to the occurrence of elevated ICP. This approach uses antihypertensive agents to reduce blood pressure, while maintaining CPP greater than 50 mm Hg.264 That CPP target has increased, in the most recent iteration, to 60 to 70 mm Hg with allowance for occasional reduction to 50 mm Hg.266 An approach from the University of Alabama, identified as “Birmingham,” entails pharmacologically induced hypertension. This approach is based on the belief that autoregulation is largely intact, and that hypertension would result in cerebral vasoconstriction with concomitantly reduced cerebral blood volume and ICP.262,331

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that period would be the most reasonable general approach. In patients with subarachnoid blood, a second period of low CBF may occur from days 2 to 13 postinjury, apparently on a vaso-spasm-related basis.35,271 Phenylephrine, norepinephrine, and dopamine all have been employed to increase blood pressure. Norepinephrine has been reported to accomplish CBF augmenta-tion more consistently than dopamine.272

There are exceptions to the foregoing generalizations about CBF after TBI. Although an initially low postinjury CBF is prob-ably the most common clinical occurrence, hyperemia does occur.35,39,270,271,273 It tends to occur in patients with mass lesions rather than contusions, although patients with contusions have an immediate postinjury period of low CBF, with delayed hyper-emia peaking at 24 hours or later.34,35,253,270,273 Hyperemia also may be common in children.274 In the ideal situation, CPP man-agement should be “targeted” to the pathophysiology that prevails in the individual patient.275 There is substantial evidence that not all TBI patients benefit from increases in perfusion pressure. Patients with impaired autoregulation, low baseline flows, and increased ICP are most likely to benefit.276-278 Techniques to discriminate the various flow states (CBF measurement, TCD, Sjvo2, brain tissue Po2—see later) are not universally available or applied, however, and in their absence, the common practice is to maintain CPP 60 to 70 mm Hg in the first 72 hours after TBI.256,258,261,279-281 A CPP target of 45 mm Hg has been recom-mended for children.282 With these firm recommendations offered, it must be acknowledged that convictions vary, and anesthesiolo-gists should come to an understanding with the local traumatolo-gists and neurosurgeons regarding blood pressure targets.

Hyperventilation. The use of hypocapnia has been reviewed in detail in the section on management of Paco2. Hyperventila-tion has long been a component of the management of TBI patients, and the effectiveness of acute hypocapnia in reducing ICP is well confirmed.10 There is substantial evidence, however, that hyperventilation is potentially deleterious23,24,29-31,283 and should not be overused. The evidence suggests that hyperventila-tion and the concomitant vasoconstriction can result in ischemia,21,29-32 especially when baseline CBF is low,32 as is likely to be the case in the first 48 to 72 hours after head injury.23,33,38,39 The expert panel convened by the Brain Trauma Foundation specified that prophylactic hyperventilation is “not recom-mended,” and that “hyperventilation should be avoided during the first 24 hours after injury when CBF is often critically reduced.”59 The available information argues that hyperventilation should be used selectively rather than routinely in the management of TBI patients. Maintaining ICP less than 20 mm Hg, preventing or reversing herniation, minimizing retractor pressure, and facilitat-ing surgical access are still important objectives in the manage-ment of TBI patients and to the extent that hyperventilation contributes to these objectives, it is still appropriate. The anesthe-siologist should agree on management parameters with the surgi-cal team at the outset of a procedure.

Fluid Management. Fluid management of head-injured patients was addressed in the earlier section on intravenous fluid management. The important principles are that fluids should be chosen invariably to prevent reduction of serum osmolarity and should probably be chosen to prevent profound reduction of colloid oncotic pressure; in the circumstances of a large-volume resuscitation (arbitrarily, greater than half a circulating volume),

a mix of colloids and crystalloids is probably appropriate. The clinical objective should be to maintain intravascular normovo-lemia, in part as an adjunct to MAP and CPP support. A chronic negative fluid balance, as can occur with the combination of modest fluid restriction and liberal use of osmotic diuretics, has been shown to be deleterious and should be avoided.249 The severely injured brain can liberate sufficient thromboplastin into the circulation to result in a consumptive coagulopathy.284 Appro-priate laboratory tests and replacement should be performed. The clinician also may find a serum osmolarity determination early in the course of anesthetic management useful in appreciating the cumulative effects of prior mannitol administration. The use of hypertonic solutions and the relevant attributes of colloid solutions were discussed in the section on intravenous fluid management.

Jugular Venous Oxygen SaturationNumerous centers have studied or made use of Sjvo2 monitoring as a guide to the clinical management of head-injured patients.29-32,40,247,256,257,281,285 The underlying concept is that a mar-ginal or inadequate CBF results in an increasing oxygen extrac-tion, a widening arteriovenous content difference, and reduction of Sjvo2. Normal subjects at rest may have Sjvo2 values between 55% and 75%. Sjvo2 less than 50% for 5 minutes is commonly accepted as constituting “jugular desaturation.” There have been numerous reports of low Sjvo2 values improving with interven-tions including reducing hyperventilation, increasing MAP, or inducing hypervolemia. Sjvo2 measurement makes an assessment of global oxygen extraction. It might be expected to have limited sensitivity to highly focal events, and instances in which focal inadequacy of perfusion was not reflected by low Sjvo2 have been reported.29-31,39 One of those investigations offers a possible expla-nation for normal Sjvo2 in the face of significant focal ischemia. Coles and colleagues39 showed the coexistence of areas of hyper-emia and hypoperfusion in individual TBI patients. The former would tend to mask the Sjvo2 reduction that would occur if the latter (hypoperfusion) were to occur in isolation. An additional limitation inherent to the unilateral placement of the catheter was found by Stocchetti and associates,286 who observed that there was an average side-to-side difference between simultaneous jugular bulb saturations of 5.3 ± 5%, and that side-to-side differences in hemoglobin saturation of 15% were common.

Despite the reported successes with Sjvo2 monitoring,40,287,288 we do not believe that the method is sufficiently well defined to justify advocating widespread intraoperative application. In the ICU, it seems potentially useful as a trend monitor that may serve to identify the level of CPP or hyperventilation below which cer-ebral perfusion begins to be compromised, with the proviso that there is a significant potential for false-negative results.29-31,39 The technique also has a potential use beyond using Sjvo2 values to warn of inadequate perfusion. High Sjvo2 values may serve to identify a patient with elevated ICP in whom hyperemia is an important contributing factor, and in whom aggressive attempts to decrease CBF (e.g., hyperventilation, barbiturates) may be beneficial.

Brain Tissue Po2 MonitoringThere are small-diameter intraparenchymal electrodes that allow measurement of brain tissue Pbo2 (and sometimes pH and Pbco2). They have been used to monitor cerebral well-being during the ICU management of TBI and SAH patients, and to

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assess the effect of operative interventions.289 A Pbo2 of 20 mm Hg or greater is viewed as normal, and values of 10 mm Hg or less are assumed to convey a substantial risk of hypoxic injury. Pbo2 monitors have the inverse of the problem that prevails with Sjvo2 monitoring—they provide very focal information about the oxy-genation status of only small regions of brain surrounding the tip. If they are placed remote from focal injuries to provide a “global” measure of oxygenation, they may not “see” adverse events in at-risk but salvageable perilesional tissue. They may similarly fail to be a useful therapeutic guide if they are within irredeemably injured brain.

So far, the use of Pbo2 monitoring is neither standardized nor widespread. One center has reported, however, on the basis of a comparison with a historic control group, a reduction in mortality when established management guided by CPP and ICP was supplemented with Pbo2-directed care, with the probe placed in white matter adjacent to, but not within, areas of severe injury.290 The same group has reported that 29% of TBI patients with a GCS score of 8 or less have brain regions with Pbo2 of 10 mm Hg or less despite meeting CPP and ICP targets of 60 mm Hg and greater (CPP) or less than 25 mm Hg (ICP).261

HypothermiaThere is clearly an ischemic component to the pathophysiology of TBI, and mild induced hypothermia was shown to be highly protective in experimental cerebral ischemia (see also the preced-ing section on hypothermia). On that basis, study of hypothermia after experimental head injury was undertaken, and improve-ments in outcome were shown.146 Hypothermia in the manage-ment of TBI patients was the subject of at least four small, prospective controlled trials.147-150 Because those trials seemed to indicate good patient tolerance of sustained mild hypothermia (32°C to 34°C) and improvement in ICP, cerebral oxygen supply and demand, and outcome, a multicenter trial was performed. This trial revealed no overall benefit of hypothermia.151 As a result, there is no established role for hypothermia in head injury management as of this writing.

Post hoc analysis showed that patients younger than age 45 who were already hypothermic (≤35°C) at the time of admission to the hospital did have an improved outcome. This finding led to the concern that the protocol, which required induction of hypothermia within 8 hours of injury, was not achieving hypo-thermia rapidly enough to achieve the potential benefits. A follow-up trial is under way. Patients 16 to 45 years old, with a GCS score less than 8, who arrive at the hospital with a bladder temperature of 35°C or less are to be randomly assigned to cooling to 32.5°C to 33.5°C (within 4 hours of injury) for 48 hours or passive rewarming to normothermia. Outcome is to be assessed at 6 months.

Intracranial Pressure Monitoring for Non-neurologic Surgery in a Head-Injured PatientIn the ideal situation, neurosurgical consultation will be readily available, and, appropriately, the anesthesiologist will rarely have to make the decision regarding ICP monitoring. It may be neces-sary, however, for the anesthesiologist to participate in this deci-sion. The relevant variables are as follows:

1. The level of consciousness. If there has been a loss of con-sciousness at any time, or if the GCS score is less than 15, a CT scan should be obtained. If the CT scan reveals com-

pressed basal cisterns (indicative of an exhaustion of supratentorial compensatory latitudes), midline shift, or effaced ventricles, and probably any intracranial lesion (e.g., contusion, small subdural), an ICP monitor should be placed. Excessive comfort should not be taken from a good GCS score. Patients with good GCS scores can “talk and deteriorate” or “talk and die” after a head injury associated with loss of consciousness. Delayed deterioration has been observed 48 hours after the initial injury (average 17 hours).291 Patients with lesions, usually contusions, in the frontotemporal region and especially patients with medial temporal lesions are most at risk for this phenomenon. Modest expansion of lesions in this location (i.e., close to the uncus and the incisura where herniation occurs) can result in herniation even at relatively low ICPs (e.g., approx-imately 20 mm Hg). At our institution, neurosurgeons would recommend avoiding an anesthetic in these patients and would advise ICP monitoring if general anesthesia were unavoidable.

2. Time since injury. The longer the patient has had to declare his or her clinical course, the less pressing is the need for ICP monitoring. Delayed deterioration, as noted previ-ously, has been observed for up to 48 hours,291 however, and a patient with a demonstrable CT lesion is a candidate for a monitor for at least this period of time.

3. Intended aortic occlusion (i.e., repair of ruptured aorta). Dramatic increases in ICP have been associated with aortic occlusion. This may in large part be the result of the abrupt increase in blood pressure or the agents used to control it, or both. In addition, the increased airway and venous pres-sures associated with the lateral position and one-lung ventilation plus occasional difficulties in maintaining hypocapnia during one-lung ventilation should result in a low threshold for ICP monitoring in this situation. The intent to heparinize systemically essentially precludes the placement of a monitor, although lumbar drains have been used with cardiopulmonary bypass.219

4. Nature and duration of the intended procedure. The risks of an untoward ICP event are inevitably greater in a 6-hour spine instrumentation in the prone position than for a 20-minute débridement and suturing of an arm laceration.

Posterior Fossa Procedures

Most of the topics relevant to posterior fossa procedures (Table 63-12) have been discussed in the section on recurrent issues. These include the sitting position and its cardiovascular effects and complications (e.g., quadriplegia, macroglossia), pneumo-cephalus, and VAE and PAE. The use of the sitting position to facilitate surgery in the posterior fossa increases the likelihood of all of these phenomena, although they are relevant to nonsitting positions as well. This section reviews the cardiovascular events associated with direct stimulation of the brainstem and their pos-sible implications for postoperative management.

Brainstem StimulationIrritation of the lower portion of the pons and of the upper medulla and of the extra-axial portion of the fifth cranial nerve can result in numerous cardiovascular responses. The former two areas are most often stimulated during procedures on the floor of

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Table 63-12 Considerations Relevant to Posterior Fossa Procedures and the Location (Section, Subsection) of the Related Discussion in Chapter

Consideration Section, Subsection

Hemodynamic effects of sitting position Positioning, Sitting

Venous air embolism Venous Air Embolism

Paradoxical air embolism Venous Air Embolism

Hemodynamic effects of brainstem and cranial nerve manipulation

Posterior Fossa Procedures

Macroglossia Positioning, Sitting

Pneumocephalus Pneumocephalus

Quadriplegia Positioning, Sitting

the fourth ventricle and the last during surgery at or near the cerebellopontine angle (e.g., acoustic neuromas, microvascular decompression of fifth [tic douloureux], seventh [hemifacial spasm], or ninth [glossopharyngeal neuralgia] cranial nerves). The cardiovascular responses may include bradycardia and hypo-tension, tachycardia and hypertension, bradycardia and hyper-tension, and ventricular dysrhythmias.292 Meticulous attention to the ECG and a directly transduced arterial pressure during manipulation in this region are necessary to provide the surgeon with immediate warning of the risk of damage to the adjacent cranial nerve nuclei and respiratory centers. Pharmacologic treat-ment of the dysrhythmias that occur may attenuate the very warning signs that should be sought.

Balloon compression of the trigeminal ganglion is another situation in which a dysrhythmia may occur. The procedure attempts to produce a neurapraxia of the fifth cranial nerve by the rapid inflation of a Fogarty-type balloon within Meckel’s cave.293,294 The balloon is introduced percutaneously through the cheek and beneath the maxilla. The procedure is best accom-plished with a general anesthetic because the entry of the needle into Meckel’s cave and the balloon compression (lasting several minutes) are intensely stimulating. A relatively profound, although transient, bradycardia occurs and is sought as confirmation of adequate compression. External pacemaker pads have been advo-cated, but in our experience are unnecessary.

Irritation and injury of posterior fossa structures that may have occurred during surgery should be taken into account in planning extubation and postoperative care. In particular, proce-dures involving dissection on the floor of the fourth ventricle entail the possibility of injury to cranial nerve nuclei or postop-erative swelling in that region, or both. Cranial nerve dysfunc-tion, particularly of cranial nerves IX, X, and XII, can result in loss of control and patency of the upper airway, and swelling of the brainstem can result in impairment of cranial nerve function and respiratory drive. The posterior fossa is a small space, and its compensatory latitudes are even more limited than those of the supratentorial space. Relatively little swelling can result in disor-ders of consciousness, respiratory drive, and cardiomotor func-tion. A meeting should occur between the anesthesiologist and the surgeon to make decisions as to whether extubation is appro-priate, and where postoperative observation should occur (i.e., ICU or non-ICU).

Spontaneous ventilation was previously advocated for pro-cedures that entailed a risk of damage to the respiratory centers.

Spontaneous ventilation is now rarely used because the proximity of the cardiomotor areas to the respiratory centers should permit cardiovascular signs to serve as an indicator of impending injury to the latter. In our opinion, respiratory pattern is more likely to be a relevant monitor when the “threat” to the brainstem is the result of vessel occlusion (as might occur with accidental inter-ruption of perforating vessels during vertebrobasilar aneurysm surgery295) than when it is because of direct mechanical damage caused by retraction of or dissection in the brainstem.

Various electrophysiologic monitoring techniques may be used during posterior fossa surgery, including somatosensory evoked responses, brainstem auditory evoked responses, and elec-tromyographic monitoring of the facial nerve. Electromyography requires that the patient not be paralyzed or have a constant state of incomplete paralysis. Somatosensory evoked response moni-toring imposes some constraints with respect to the selection of anesthetic agents. These are discussed in Chapter 46.

Transsphenoidal Surgery

The transsphenoidal approach to the sella turcica is used for the excision of tumors that lie within the sella or that have extended to or originated in the immediate suprasellar area. The most common lesions are prolactin-secreting microadenomas and nonsecreting macroadenomas. Patients with the former are usually women who present with secondary amenorrhea. Nonse-creting adenomas tend to manifest with mass effects (i.e., head-ache, visual disturbance, hypopituitarism) and are typically larger at the time of diagnosis. There are three other, less common pitui-tary tumors: Growth hormone–secreting lesions result in acro-megaly, adrenocorticotropic hormone (ACTH)–secreting tumors cause Cushing’s disease, and a very rare thyroid-stimulating hormone–secreting lesion results in hyperthyroidism. A detailed review of the perioperative management of this group of patients is available.296

Preoperative EvaluationThe important preoperative considerations relate to the patient’s endocrine status. Generally, as a pituitary lesion expands and compresses the pituitary tissue, the sequence in which hormonal function is lost is first gonadotropins; second, growth hormone; third, ACTH; and fourth and last, thyroid-stimulating hormone. The precise definition of the adrenal status of these patients is often not critical because the patients commonly receive adrenal hormone supplementation at least temporarily. Profound hypocortisolism, with associated hyponatremia, should be cor-rected preoperatively. It is uncommon for thyroid deficiency to occur. Hypothyroidism should be sought and corrected preopera-tively, however, because hypothyroid patients have a diminished tolerance to the cardiovascular depressant effects of anesthetic agents. Hypertension, diabetes, and central obesity are common concomitants of ACTH-secreting adenomas (Cushing’s disease). Patients with advanced acromegaly can develop an enlarged tongue and a narrowed glottis, and the airway should be evaluated accordingly (Table 63-13).

MonitoringMany practitioners place an arterial catheter, but it is not abso-lutely necessary. Access for blood sampling is a valuable adjunct to postoperative care if diabetes insipidus develops. Blood loss is

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Table 63-13 Tumors of the Pituitary Region

Location Hormone Secreted Clinical Presentation Comment

Anterior pituitary Prolactin Galactorrhea, amenorrhea, hypogonadism, infertility

Bromocriptine sensitive

Adrenocorticotropin Cushing’s disease (hypercortisolism) Basophilic adenoma; centripetal obesity; diabetes mellitus; friable tissues

Growth hormone Acromegaly/gigantism, glucose intolerance Eosinophilic adenoma; difficult airway; thick skin (difficult cannulation); hypertension/cardiomyopathy

Nonsecretory Mass effect, panhypopituitarism Chromophobic adenoma; consider preoperative hormone replacement

Suprasellar Nonsecretory Panhypopituitarism, SIADH, visual symptoms, hydrocephalus

Craniopharyngioma, Rathke cleft cyst, or suprasellar extension of pituitary lesion

SIADH, syndrome of inappropriate secretion of antidiuretic hormone.

usually modest. The cavernous sinus is in immediate lateral rela-tion of the pituitary, however, and may be entered during the resection of large tumors. The carotid arteries pass through the cavernous sinuses and are similarly at risk. In addition, in some patients, there is a venous sinusoid that lies in front of the pitui-tary gland and connects the two cavernous sinuses. This can be the origin of substantial blood loss. It has occasionally precluded this approach to the pituitary gland.

Anesthetic TechniqueThe latitudes are broad with respect to choice of agent, although tumors with suprasellar extension can cause hydrocephalus and add increased ICP constraints to the anesthetic technique. The procedure is performed in a supine position usually with some degree of head-up posture to avoid venous engorgement. A pha-ryngeal pack prevents an accumulation of blood in the stomach (which causes vomiting) or in the glottis (which contributes to coughing at extubation). A RAE-type tube secured to the lower jaw at the corner of the mouth opposite the surgeon’s dominant hand (e.g., left corner of mouth for a right-handed surgeon) is suitable. A small esophageal stethoscope and temperature probe can lie with the endotracheal tube. Covering the entire bundle with a towel drape (a plastic sheet with an adhesive edge) placed just below the lower lip so that it hangs from the lower jaw like a veil protects it from the preparation solutions.

The procedure is commonly performed with a C-arm image intensifier (lateral views), and the head and arms are rela-tively inaccessible when the patient is draped. It is appropriate to establish the nerve stimulator at a lower extremity site. The surgi-cal approach is via the nasal cavity, usually through an incision made under the upper lip. During the approach, the mucosal surfaces within the nose are infiltrated with a local anesthetic and epinephrine solution, and the patient should be observed for the occurrence of dysrhythmias.

Surgical preferences for CO2 management vary. In some instances, hypocapnia is requested to reduce brain volume and minimize the degree to which the arachnoid bulges into the sella. An important surgical consideration is the avoidance, where pos-sible, of opening the arachnoid membrane. Postoperative CSF leaks can be persistent and are associated with a considerable risk of meningitis. By contrast, when there is suprasellar extension of a tumor, normal or increased CO2 helps to deliver the lesion into the sella for excision.297 As an alternative way to accomplish this,

some surgeons have resorted to “pumping” of saline or air into the lumbar CSF space.298,299

Diabetes insipidus is a potential complication of this pro-cedure. Antidiuretic hormone is synthesized in the supraoptic nuclei of the hypothalamus and is transported down the supraop-tic-hypophyseal tract to the posterior lobe of the pituitary. This portion of the pituitary gland is frequently spared. Even when it is excised, water homeostasis commonly normalizes, presumably because antidiuretic hormone is released from the cut-end of the tract. When the pituitary stalk is transected, and occasionally even when the posterior lobe of the pituitary is left intact, tran-sient diabetes insipidus may occur. Diabetes insipidus very rarely arises intraoperatively. It usually occurs 4 to 12 hours postopera-tively and is typically transient. The clinical picture is one of polyuria in association with an increasing serum osmolality. The diagnosis is made by comparison of the osmolalities of urine and serum. Hypo-osmolar urine in the face of an increased and increasing serum osmolality strongly supports the diagnosis. Urine specific gravity is a useful bedside test. In the presence of bona fide diabetes insipidus, specific gravity is low (i.e., ≤1.002).

When the diagnosis of diabetes insipidus is established, an appropriate fluid management regimen is hourly maintenance fluids plus two thirds of the previous hour’s urine output. (An acceptable alternative is previous hour’s urine output minus 50 mL plus maintenance.) The choice of fluid is dictated by the patient’s electrolyte picture. Generally, the patient is losing fluid that is hypo-osmolar and relatively low in sodium. Half-normal saline and 5% dextrose in water are commonly used as replace-ment fluids. Hyperglycemia is a risk when large volumes of 5% dextrose in water are employed. An unacceptable fluid regimen that has been employed calls for maintenance fluids plus previous hour’s urine output. This has the potential to put the anesthesiolo-gist and the patient in a “chase your tail” situation. Should the patient become iatrogenically fluid overloaded, this regimen pre-cludes his or her returning to isovolemia, and when the mainte-nance fluid allowance is generous, it guarantees that the patient will become increasingly hypervolemic. If the hourly requirement exceeds 350 to 400 mL, desmopressin (DDAVP) is usually administered.

A smooth emergence (see the section on emergence from anesthesia) is desirable especially if the CSF space has been opened (and resealed with fibrin glue or by packing the sphenoid sinus with fat or muscle). Repeated, intense Valsalva maneuvers,

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as with coughing or vomiting, may contribute to the reopening of a CSF leak and worsen the risk of a subsequent meningitis. The airway should be cleared of debris, including formed clot. In situ-ations in which there is concern that a persistent CSF leak may occur, the surgeon may place a lumbar CSF drain to maintain CSF decompression in the early postoperative period.

Awake Craniotomy and Seizure Surgery

Awake craniotomies are performed when tumors or epileptic foci lie close to cortical areas required for either speech or motor function or to mesiotemporal structures critical to short-term memory. Many patients have so-called temporal lobe epilepsy. There is commonly a structural lesion visible on magnetic reso-nance imaging (MRI). Sometimes there is a history of trauma. More commonly, the etiology is presumed to be an asphyxial birth injury.

Presurgical EvaluationBefore the resection, most patients have undergone a Wada test or video-telemetry or both. More recently, functional testing employing MRI or positron emission tomography, or both, has been introduced to the presurgical evaluation. The Wada test involves selectively anesthetizing the cerebral hemispheres, usually by injection of sodium amytal into the carotid artery to localize the hemisphere that controls speech or to confirm that there is bilateral representation for short-term memory, or both. Speech is an issue when the posterolateral portions of the tempo-ral lobe are involved, and memory is the concern when the involvement is medial.

Anesthesia for Electroencephalogram Electrode PlacementVideo-telemetry is performed to permit localization of the seizure focus that is responsible for the clinically problematic events. This evaluation usually requires prior placement of either subdural strip electrodes (via bur holes) or a subdural electrode grid (requiring a craniotomy). Occasionally, electrodes are placed deep into parenchyma, usually within the temporal lobe (placed stere-otactically via bur holes), or are positioned so as to “look at” the inferior surfaces of the temporal lobe. The latter is commonly accomplished with so-called foramen ovale electrodes. These are placed using a needle similar to an epidural needle. The point of entry is about 2 cm lateral to the angle of the mouth. The needle is passed through soft tissue, under the temporal process of the zygomatic bone and medial to the ramus of the mandible, up to the base of the skull in the vicinity of the foramen ovale. Typically, this procedure is performed as a “MAC,” although small doses of anesthetics, most often propofol, are usually required at the time of stimulation by the needle of the periosteum at the base of the skull. After placement of the relevant electrodes, the patient’s seizure medication is discontinued, and the patient remains in an observation unit with EEG and patient behavior recorded con-tinuously. In this manner, the EEG events associated with the clinically significant seizure events and their anatomic origin can be identified.

Preanesthetic Evaluation and PreparationAt the preoperative interview, the patient should be educated about the nature and duration of the procedure and the limita-

tions on patient movement. One should obtain a description of the aura and the seizures to facilitate recognition of them. One should ascertain whether the patient is subject to grand mal con-vulsions. If intraoperative electrocorticography to identify seizure foci is intended, it is common to discontinue or reduce by half the anticonvulsants according to the perceived risk of uncon-trolled seizures. Premedicants with an anticonvulsant effect (e.g., benzodiazepines) should not be used because they may interfere with intraoperative EEG localization.

Anesthetic TechniqueThe objectives of the anesthetic technique are as follows:

1. To minimize patient discomfort associated with the poten-tially painful portions of the procedure and with the pro-longed restriction of movement

2. To ensure patient responsiveness and compliance during the phases of the procedure that require assessment of either speech or motor/sensory responses to cortical stimulation

3. To select anesthetic techniques that produce minimal inhi-bition of spontaneous seizure activity.

There are probably many ways of providing sedation that are consistent with the above-listed objectives. The techniques employed range from minimal sedation approaches, to deep sedation during which intermittent unresponsiveness is achieved with spontaneous ventilation and an unprotected airway, to asleep-awake-asleep techniques with intermittent airway man-agement with a laryngeal mask airway (LMA), sometimes with positive-pressure ventilation.

At the outset, the anesthesiologist should appreciate that the essential element of an “anesthetic” for an awake craniotomy is the surgeon’s local anesthetic technique. “Sedation” cannot compensate for inadequate anesthesia of the scalp, as accom-plished by nerve blocks (Fig. 63-17), and pin site infiltration. Although the anesthesiologist can contribute enormously to the patient’s comfort and tolerance of the painful components of the procedure and the prolonged immobilization, the anesthesi-ologist must not get trapped into thinking that it is his or her responsibility to provide a general anesthetic-equivalent in a spontaneously breathing patient with an unprotected and all but inaccessible airway.

For sedation, some clinicians use principally propofol by either physician-controlled or patient-controlled infusion.300,301 The combination of propofol with either fentanyl or remifentanil in low dose (e.g., remifentanil, 0.02 to 0.05 µg/kg/min) also is reasonable.302,303 Great care should be taken in administering additional sedative agents, especially narcotics, whose respiratory depressant effects would be synergistic with propofol. This is especially relevant with the use of pin fixation, which severely restricts the anesthesiologist’s capacity to intervene quickly in the event of excessive respiratory depression or loss of patency of the airway.

Propofol should be discontinued at least 15 minutes before EEG recording. Despite prompt awakening, propofol leaves a residual EEG “footprint” characterized by high-frequency, high-amplitude beta activity, which can obscure the abnormal activity that is being sought in the cortical surface EEG.300 The use of dexmedetomidine, which in addition to sedation and anxiolysis provides some analgesia with minimal respiratory depression, is

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Figure 63-17 Cutaneous nerves to the scalp.

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Zygmaticotemporal

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increasing.304-306 The authors of those series report satisfactory conditions for functional testing, including brain stimulation for speech mapping and electrocorticography with the dexmed-etomidine infusion ongoing at 0.1 to 0.5 µg/kg/hr during the testing.305,307,308 The occurrence of delays in achieving satisfactory patient responsiveness has been reported,306,309 however, and employing modest infusion rates (i.e., 0.1 to 0.3 µg/kg/hr) during neurocognitive testing seems advisable.307 Administration of antiemetics (i.e., ondansetron, dexamethasone, or both) probably should be routine, especially if narcotics are administered.

Various groups have reported the use of the LMA, com-monly with narcotic-propofol sedation and spontaneous ventila-tion during the craniotomy, with cessation of sedative administration and LMA removal after the brain surface is exposed.304-307,310 Many approaches can be effective, but, to our knowledge, the LMA techniques have not been reported in patients in pin fixation.

Routine, noninvasive monitors are almost always suffi-cient. Reliable capnography, to provide breath-by-breath confir-mation of airway patency and respiratory drive, is an essential component of the technique if deep sedation is intended for any portion of the procedure. These procedures are often lengthy, and attention to the details of patient comfort (e.g., warming blankets, a sheepskin, room temperature) improves patient tolerance.

The uncomfortable phases of the procedure are pin head holder placement (not all groups use a pin head holder) and the craniotomy. Many patients also find manipulation of the dura, in particular traction on subtemporal dura, painful. The actual manipulation of supratentorial brain parenchyma is painless. The volume of local anesthetic used to infiltrate pin sites and perform the scalp nerve blocks can be substantial. It is appropriate for the

anesthesiologist to keep track of the doses of local anesthetic agents used.

The anesthesiologist should participate actively at the time of head positioning. The more “sniff ” that can be achieved before the final lock-down of the head holder, the wider the latitudes will be for sedating the patient, while maintaining spontaneous ventilation and a patent airway. During positioning of the patient, the clinician also should pay attention to the need to maintain visual access to the face. A clear line of sight to the face is neces-sary to present the patient with images to name as part of speech testing and to identify the occurrence of facial motor responses during mapping of the motor strip.

Generally, after the dural opening is complete, cortical surface EEG recording is performed to locate the seizure focus. If no seizure activity is observed, provocative maneuvers may be requested.311 Methohexital in a dose of approximately 0.3 mg/kg is generally safe and effective. Etomidate, approximately 0.05 to 0.1 mg/kg, also has been used. Localization of seizure focus also can be accomplished during light general anesthesia (e.g., N2O/fentanyl/low-dose isoflurane). During general anesthesia, alfen-tanil in a bolus dose of 30 to 50 µg/kg,312,313 etomidate in doses of 0.2 to 0.3 mg/kg,314,315 and remifentanil in a bolus dose of 2.5 µg/kg316 have been reported to be effective in activating seizure foci.

After localization by EEG, functional testing may be per-formed by stimulating the cortical surface electrically and observ-ing for motor, sensory, or speech interruption effects. During stimulation, the anesthesiologist should be prepared to treat grand mal convulsions when they are not self-limited (e.g., with propofol in 0.5 to 1 mg/kg increments). Propofol should be with-held, however, until it is clear that the seizure is not going to ter-minate spontaneously because propofol may interfere with subsequent EEG localization of the seizure focus for some time.300

Stereotactic Procedures

Stereotactically guided procedures are done for numerous indica-tions, including biopsy of small, deep-seated lesions; placement of deep brain stimulation electrodes, the latter; occasionally for seizure control and, more commonly, for the treatment of move-ment disorders (e.g., Parkinson’s disease, essential tremor, dysto-nias).317 Procedures related to movement disorders most often target the subthalamic nucleus, the internal segment of the globus pallidus, or the ventral intermediate nucleus of the thalamus (Fig. 63-18).317 The mechanism of the beneficial effect is not well understood. A prominent theory is that the abnormal motor pat-terns are caused by abnormally synchronized oscillations in neural circuits involving several basal ganglia nuclei and the cortex, and that high-frequency stimulation of any of several points along the pathway can interfere with the oscillation.318

The issues with which the anesthesiologist must contend include restriction of airway access by the frame, restriction regarding choice of sedative when electrophysiologic recordings are to be performed as a guide to device placement, and the detec-tion and management of complications (principally, seizures and intracerebral hematomas). Preoperative evaluation should include attention to ensuring that the coagulation process is intact, and that the patient has not been taking platelet-inhibiting agents (including herbal medications). There should be careful explana-

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tion of the procedure, its likely duration, and the necessary restraints on patient movement.

Commonly, the stereotactic frame, of which there are many variations, is placed using local anesthetic, and the patient undergoes an imaging study before being brought to the operat-ing room. In some instances, the frame prevents mask applica-tion and ventilation, laryngoscopy, and neck extension. If a general anesthetic is to be employed, an awake intubation occa-sionally may be required. If sedation is to be employed, the anesthesiologist should have certain knowledge as to how to remove the device rapidly in an urgent situation (including knowledge of the whereabouts of the requisite “key” or spanner device).

When electrophysiologic recordings are not intended, sed-ative regimens similar to those used for awake craniotomy (see earlier) may be appropriate. For thalamic and subthalamic nucleus stimulator placements, part of the localization process entails identifying the typical electrophysiologic “footprint” of specific nuclei. Because the nature and duration of the effects of anesthetic agents on these signals have not been systematically defined, some surgeons and electrophysiologists may request that no seda-tive agent whatsoever be given. The patient’s tremor is an impor-tant end point for determining the adequacy of stimulator position and current and must not be suppressed by the sedative agents. Such suppression may occur with propofol. However, Rozet and colleagues319 reported satisfactory electrophysiologic recordings and preservation of tremor when dexmedetomidine was used for deep brain stimulator placement in patients with Parkinson’s disease. They administered dexmedetomidine in a dose sufficient to maintain a lethargic response to normal speech.

An additional issue that arises in some patients with move-ment disorders is the problem of obtaining high-quality radio-logic images in the presence of a persistent tremor. Sedation immediately preceding the stereotactic placement may be inevi-table. Propofol has been employed, but the window between pro-pofol administration and subsequent recording should be as long as possible. If sedatives are administered, they must be given in a manner that ensures the ability to perform precise intermittent neurologic examinations of the patient.

During the subsequent procedure, among the anesthesiolo-gist’s objectives is the prevention or treatment of hypertension. The concern is that, in the face of multiple needle passes through the brain, hypertension would precipitate development of an intracerebral hematoma. Dexmedetomidine has the added advan-tage that it may reduce hypertension. In the event of a substantial hematoma, an urgent craniotomy may be required, and the anesthesiologist should be prepared from the outset for this eventuality.

Neuroradiologic Procedures

Magnetic Resonance ImagingThe major constraints of MRI are created by the powerful mag-netic field employed. It creates at least two conditions that have an impact on anesthetic technique. First, any ferromagnetic object that approaches the magnet has the potential to become a dangerous projectile. Second, many of the monitoring devices used in the operating room do not function properly in the vicin-ity of the magnet. The equipment limitations have largely been

circumvented, however. MRI-compatible ECG machines, oxime-ters, capnographs, noninvasive blood pressure monitors, and gas machines are now widely available. Only temperature monitoring cannot be readily accomplished, and with that exception, there is no longer any justification for incomplete monitoring of patients undergoing MRI.

Most frequently, it is children, claustrophobic adults, and patients with painful conditions who require anesthesia to undergo MRI. Sedation with propofol and an unprotected airway, and general anesthesia with either an LMA or an endotracheal tube have been employed successfully.

Interventional NeuroradiologyA wide variety of procedures are available to evaluate and treat intracranial and extracranial disease. These include, principally, attempts to obliterate aneurysms or devascularize tumors and AVMs. An extensive review is available.320

Tumors and Arteriovenous Malformations. Hyperventi-lation may be appropriate in an attempt to divert flow away from normal brain and toward a lesion that is intended to receive the occlusive device or material. The anesthesiologist may be asked

Figure 63-18 Deep brain stimulation electrode target sites. The most commonly targeted nuclei for the treatment of movement disorders are the subthalamic nucleus, the ventral intermediate nucleus of thalamus (Vim), and the internal segment of globus pallidus (GPi).

Caudate

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to reduce systemic blood pressure, which reduces flow through fistulous lesions. Hypotension is usually requested to obtain greater precision for delivery of cyanoacrylate glues and to prevent glue passage into the draining veins or systemic venous system. The choice of hypotensive agent depends on the anesthesiologist’s experience and systemic cardiovascular considerations. Adenos-ine is occasionally effective.321

Intracranial Aneurysms. A discussion of the relative merits of open clipping and endovascular management (usually coiling) for intracranial aneurysms is beyond the scope of this chapter. The International Subarachnoid Aneurysm Trial (ISAT) has con-firmed the broad applicability of endovascular treatment,322 and most aneurysms are currently managed by endovascular approaches. Nonetheless, numerous patients continue to undergo operative clipping323—primarily patients with wide-necked aneu-rysms or otherwise complex anatomies. At present, the durability of coil therapy is inferior to direct clipping324; a small but signifi-cant number of patients treated with coils need additional treat-ment, usually determined during routine follow-up angiography. Attempts to define the characteristics of patients best managed by operative clipping are ongoing.

Many of these procedures—in particular, procedures involving the treatment of vasospasm by selective intra-arterial installation of papaverine or more commonly by balloon dila-tion—can be accomplished without the involvement of an anesthesiologist. The duration of a procedure, individual patient factors, and, occasionally, the necessity for precise physiologic control may result in requests for monitored anesthesia care or general anesthesia. A chin-tucked position (to remove the bones of the face from the line of the anteroposterior x-ray source) and absolute immobility are commonly needed by the radiologist, and, consequently, when the anesthesiologist’s assistance is requested, a general anesthetic often is necessary. In addition, anesthesiologists may become involved during the resuscitation stage in the event of vascular rupture or of the migration of an intravascular device to an incorrect location. In the event of rupture, the interventionist may request blood pressure reduction while the coil packing of the aneurysm is completed hastily. Immediate reversal of heparinization also would be required. When detachable devices (i.e., coils, balloons) are misplaced, and ischemia ensues, fluid loading and pressor administration may be requested to improve collateral CBF while the device is retrieved.

Carotid Angioplasty and Stenting. The role of carotid angioplasty is undefined. Carotid angioplasty and stenting (CAS) was originally proposed as an alternative for patients deemed to be of the highest medical risk. An early prospective comparison of CAS and carotid endarterectomy (CEA) among moderately high-risk patients revealed similar outcomes for the two proce-dures.325 Reports have subsequently appeared of two additional trials, one of which was halted when an interim data analysis revealed a greater “any stroke or death” rate among CAS patients.326 The second trial reported similar rates of any stroke or death for CAS and CEA.327 There was a nonsignificant trend, however, toward an increase in the rate of occurrence of “disabling stroke or death” in the CAS group.

Finally, an interim report on patients enrolled in the ongoing Carotid Revascularization versus Stent Trial (CREST) revealed an unexpectedly high rate of stroke and death among patients older than 75 years of age, which was not explained by adjustment for comorbidities.328 The suspicion is that the increased stroke incidence may be related to embolism from the arch of the aorta or the carotid, and it has been reported unofficially that some centers have discontinued enrollment of patients older than 75 years. It may evolve that some of the patients who were origi-nally viewed as part of the target population (the very elderly) for this procedure may be among the patients for whom the proce-dure is relatively contraindicated.

It seems probable that the future holds a place for CAS and CEA, in part, because there are numerous relative contraindica-tions to both procedures. The relative contraindications to CAS include antiplatelet agent intolerance, other pending surgery that precludes antiplatelet agents, aortic arch disease (age), and various elements of carotid morphology, including carotid tortuosity, concentric calcification (which entails a risk of vessel rupture), heavy thrombus burden, and unstable plaque (the latter two entail increased embolization risk). The relative contraindications to CEA include prior irradiation, prior radical neck surgery, trache-ostomy, restenosis after CEA, high carotid bifurcation, contralat-eral recurrent laryngeal nerve palsy, and (perhaps) severe coronary or pulmonary disease (or both).

The procedure is almost always accomplished using mon-itored anesthesia care. Vascular access is most often achieved via the femoral artery. The anesthesiologist is usually asked to titrate heparin by bolus and infusion to achieve an activated clotting time of 250 to 300 seconds. Thereafter, the principal concern is the occurrence of what may be a profound brady-cardia first with balloon dilation of the stenotic region and sub-sequently with expansion of the stent across the same region. Our practice is to titrate glycopyrrolate from the beginning of the procedure to achieve a heart rate of about 70 beats/min before the dilation and to have atropine at the ready and an external pacemaker in the room. We have never had to use the latter. In our institution, the presence of an anesthesia provider for this procedure is typically requested for only the most phys-iologically compromised patients. In this population, we have found it advantageous to have an independent (i.e., radial) arte-rial line.

Cerebrospinal Fluid Shunting Procedures

CSF shunts are inserted for the relief of various hydrocephalic states and pseudotumor cerebri. Hydrocephalus can be commu-nicating or noncommunicating. In a noncommunicating hydro-cephalus, CSF egress from the ventricular system is obstructed. This can occur as a result of blood or infection in the ventricular system or tumors in or adjacent to the ventricular system. In communicating hydrocephalus, the CSF escapes from the ven-tricular system, but is not absorbed by the arachnoid villi; this occurs most commonly secondary to infection or blood in the CSF space. Some degree of communicating hydrocephalus is par-ticularly common after SAH.

The ventriculoperitoneal shunt is the most commonly employed device. Usually, a catheter is inserted via a bur hole into

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the frontal horn of the lateral ventricle on the nondominant (usually the right) side. A reservoir is placed subcutaneously adja-cent to the bur hole, and the drainage limb passes via a subcutane-ous tunnel to a point near the epigastrium, where it is inserted into the peritoneal space via a very small laparotomy. A moderate degree of muscle relaxation may be helpful. A distended stomach can result in an inadvertent “gastrostomy.” Occasionally, most commonly in pediatric patients, there may be an obstruction at more than one level in the ventricular system, and a so-called double-barreled shunt becomes appropriate. In this instance, there are two proximal ends—usually one in the lateral ventricle and one in the fourth ventricle. This latter procedure is usually performed in the prone position, whereas most ventriculoperito-neal shunts are done supine.

Occasionally, when there is a communicating hydrocepha-lus, a lumboperitoneal shunt is inserted. The patient is placed in a lateral position, and a catheter is put in the lumbar CSF space via a Tuohy-type needle. The catheter is tunneled subcutaneously around to the anterior abdominal wall and inserted into the peri-toneal space via a small laparotomy.

Anesthetic ManagementInvasive monitoring is generally not required. The anesthetic technique should be chosen to avoid further increases in ICP. Moderate hyperventilation (Paco2 25 to 30 mm Hg) is customary. The procedure is usually performed in the supine position, with the table turned 90 degrees and the head turned toward the anesthesiologist. Blood pressure may decrease abruptly (as brain-stem pressure is relieved) when the ventricle is first cannulated. Infrequently, brief pressor support is required. Burrowing the subcutaneous tunnel can produce a sudden painful stimulus. There is only minor postoperative discomfort.

In contrast to most neurosurgical patients, shunt patients are often nursed flat after their procedures in an attempt to prevent an excessively rapid collapse of the ventricular system. Empirically, there is a small incidence of subdural hematoma after shunting, and the tearing of bridging veins at the time of rapid brain shrinkage is a suspected cause.

Pediatric Ventriculoperitoneal ShuntsShunts are probably more commonly performed in children than in adults. Common indications are hydrocephalus occur-ring in association with meningomyelocele, neonatal intraven-tricular hemorrhage, and posterior fossa tumors. Although one can never be casual about the management of these patients, open fontanelles seem to provide some margin for error in younger patients, and palpation of the fontanelles provides on-line trend monitoring of “ICP.” Despite the theoretical considera-tions, inhaled inductions using volatile agents are empirically well tolerated, even in children with closed fontanelles. We would avoid inhaled induction in a child who was already stu-porous, however. When an intravenous line is available, we usually employ a propofol-relaxant induction sequence. For chil-dren in whom cannulation of a peripheral vein cannot be accom-plished readily, an inhalation induction with sevoflurane is a

common approach, with initiation of controlled ventilation, by bag and mask, as rapidly as possible. After establishing control-led ventilation, an ideal course at this point is to establish an intravenous line and administer a muscle relaxant and perhaps an intravenous anesthetic, and to intubate the trachea in these optimal circumstances.

Anesthesia is most commonly maintained thereafter with 60% to 70% N2O, mechanical hyperventilation, and isoflurane or sevoflurane as required. For children older than 6 months who were not stuporous at the outset, we commonly administer 2 to 3 µg/kg of fentanyl in the belief that this procedure is not entirely pain-free postoperatively, and that a smoother emergence can be accomplished with a narcotic background.

Pediatric Neurosurgery

Table 63-14 lists common pediatric procedures and their anes-thetic considerations (see Chapter 82). The most frequent proce-dures are probably the placement and revision of CSF shunts. These are discussed in the preceding section. Most pediatric tumors occur in the posterior fossa. Most are near the midline, and many are associated with hydrocephalus. For pediatric pos-terior fossa procedures, VAE risk, monitoring, and treatment are similar for adults and children and have been discussed previ-ously. A Doppler is invariably indicated, and right heart catheters are generally placed when procedures are done in the sitting posi-tion. Craniosynostosis procedures have the potential for substan-tial blood loss that is roughly proportional to the number of sutures involved. There is a significant VAE risk that justifies the use of a precordial Doppler.97

Spinal Surgery

Table 63-15 summarizes the many issues that may arise in the context of spinal cord or spinal column procedures undertaken by neurosurgeons. The physiology of the spinal cord is generally similar to that of the brain: CO2 responsiveness, blood-brain barrier, autoregulation, high metabolic rate and blood flow (although less than the brain), and substantial ischemic vulnera-bility of gray matter. Measures to reduce spinal cord swelling, analogous to ICP reduction maneuvers, are, however, rarely used. The relevant electrophysiologic monitoring techniques are described in Chapter 46. Prone positioning considerations and the phenomenon of postoperative visual loss are addressed in the discussion of the prone position.

Acknowledgment

The authors gratefully acknowledge the contribution of Harvey M. Shapiro to the origins of this chapter.

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Table 63-14 Common Pediatric Neurosurgical Disorders and Anesthetic Considerations

Age Group Lesion Pathogenesis Anesthetic Considerations

Neonates Intraventricular hemorrhage Subependymal vascular rupture Associated problems of prematurity

Depressed skull fracture Forceps injury Associated cerebral edema

Infants Hydrocephalus Varied Increased ICP, especially dangerous in shunt-dependent revisions

Meningocele Outpouching of meninges through skull defect Large size creates airway management problems

Prone or lateral position

Substantial blood loss

Repair may increase ICP

Encephalocele Outpouching of meninges through skull defect with brain tissue enclosed

Myelomeningocele Protrusion of spinal meninges and roots through spina bifida

Prone or lateral position


Respiratory restriction after covering large defects

Arnold-Chiari malformation Impaction of posterior fossa contents into foramen magnum

Brainstem compression with head flexion

With or without hydrocephalus Increased ICP

Latex allergy

With or without myelomeningocele Postoperative respiratory depression

Craniosynostosis Premature cranial suture fusion Substantial blood loss

Air embolism

Supine or prone position

Craniofacial dysostosis Developmental abnormality Lengthy procedures


Brain retraction

Air embolism

Endotracheal tube damage

Vascular malformations Varied Congestive heart failure

Large blood loss

Elective hypotension

Subdural hematoma/effusion Trauma Associated injuries

Older children Posterior fossa tumors Ependymoma Malnutrition/dehydration

Astrocytoma Hydrocephalus

Increased ICP

Prone or sitting position

Air embolism

Brainstem compression

Postoperative cranial nerve dysfunction or brainstem swelling or compression

ICP, intracranial pressure.

Table 63-15 Anesthetic Considerations and Position Requirements Associated with Various Spinal Surgical Procedures

Spinal Segment and Surgical Condition Problems/Considerations Positions Used and Comments

Thoracolumbar region: degenerative disease, spinal stenosis, trauma

Major position change Prone, lateral, or knee-chest position

Awake intubation and position If unstable after trauma and major position change required

Blood loss Especially with redos, instrumentation, and spinal stenosis; risk of occult aortoiliac or major venous injury

Air embolism Infrequent; perhaps increased with knee-chest position and Relton-Hall frame

Postoperative visual loss Etiology unclear; associated with long prone procedures, low hematocrit, large estimated blood loss, and hypotension. Patient variables may contribute

See Section on Positioning, Prone

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Spinal Segment and Surgical Condition Problems/Considerations Positions Used and Comments

Cervical region: degenerative disk disease, stenosis, trauma, rheumatoid arthritis

Maintain neutral neck position to avoid cord compression

Supine/anterior approach for most diskectomies. Posterior approach (prone or sitting) for laminectomy and occasional diskectomy

Maintain perfusion pressure at waking normal levels

If existing cord compression or recent cord injury or if cord retraction required

Hypotension (spinal shock) Occurs with complete cervical cord injury

Postoperative respiratory insufficiency Occurs with cervical cord injury

Methylprednisolone329,330 30 mg/kg over 1 hr period, then 5.4 mg/kg for 23 hr

Air embolism With sitting laminectomies

Anterior cervical diskectomy Traction required for anterior graft insertion

Retractor compression of airway

Postoperative swelling/airway compression

Postoperative cranial nerve dysfunction

Cervical instability Awake intubation

Awake positioning Prone or supine

Axial stabilization for intubation If awake intubation not feasible

Vertebral metastasis Large blood loss Prone or anterolateral/retroperitoneal

Double-lumen tube for lesions above L1

Spinal cord tumors Maintain perfusion pressure during retraction

Prone

Methylprednisolone

Procedures with major neurologic risk Wake-up test Prone. Rehearse with patient

Somatosensory evoked responses Anesthetic restrictions

Motor evoked responses Anesthetic/relaxant restrictions

Pedicle screw electromyogram Relaxant restriction

EMG, electromyogram.

References

1. Grubb RL, Raichle ME, Eichling JO, et al: The effects of changes in Paco2 on cerebral blood volume, blood flow, and vascular mean transit time. Stroke 5:630-639, 1974.

2. Archer DP, Labreque P, Tyler JL, et al: Cerebral blood volume is increased in dogs during adminis-tration of nitrous oxide or isoflurane. Anesthesiol-ogy 67:642-648, 1987.

3. Greenberg JH, Alavi A, Reivich M, et al: Local cer-ebral blood volume response to carbon dioxide in man. Circ Res 43:324-331, 1978.

4. Petersen KD, Landsfeldt L, Cold GE, et al: Intracra-nial pressure and cerebral hemodynamics in patients with cerebral tumors: A randomized prospective study of patients subjected to craniotomy in pro-pofol-fentanyl, isoflurane-fentanyl, or sevoflurane- fentanyl anesthesia. Anesthesiology 98:329-336, 2003.

5. Stirt JA, Grosslight KR, Bedford RF, et al: “Defas-ciculation” with metocurine prevents succinylcho-line-induced increases in intracranial pressure. Anesthesiology 67:50-53, 1987.

6. Kovarik DW, Mayberg TS, Lam AM, et al: Succinyl-choline does not change intracranial pressure, cerebral blood flow velocity, or the electroencepha-logram in patients with neurologic injury. Anesth Analg 78:469-473, 1994.

7. Eisenberg HA, Frankowski RF, Constant CJ, et al: High-dose barbiturate control of elevated intracra-nial pressure in patients with severe head injury. J Neurosurg 69:15-23, 1988.

8. Cremer OL, Moons KG, Bouman EA, et al: Long-term propofol infusion and cardiac failure in adult-injured patients. Lancet 357:117-118, 2001.

9. Cannon ML, Glazier SS, Bauman LA: Metabolic acidosis, rhabdomyolsis, and cardiovascular col-lapse after prolonged propofol infusion. J Neuro-surg 95:1053-1056, 2001.

10. Oertel M, Kelly DF, Lee JH, et al: Efficacy of hyper-ventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury. J Neurosurg 97:1045-1053, 2002.

11. Steiner LA, Balestreri M, Johnston AJ, et al: Sus-tained moderate reductions in arterial CO2 after brain trauma time-course of cerebral blood flow velocity and intracranial pressure. Intensive Care Med 30:2180-2187, 2004.

12. Grote J, Zimmer K, Schubert R: Effects of severe arterial hypocapnia on regional blood flow regula-tion, tissue PO2 and metabolism in the brain cortex of cats. Pflugers Arch 391:195-199, 1981.

13. Alexander SC, Smith TC, Stroebel G, et al: Cerebral carbohydrate metabolism of man during respira-tory and metabolic alkalosis. J Appl Physiol 24:66, 1968.

14. Hansen NB, Nowicki PT, Miller RR, et al: Altera-tions in cerebral blood flow and oxygen consump-tion during prolonged hypocarbia. Pediatr Res 20:147-150, 1986.

15. Reivich M, Cohen PJ, Greenbaum L: Alterations in the electroencephalogram of awake man produced

by hyperventilation: Effects of 100% oxygen at 3 atmospheres (absolute) pressure. Neurology 16:304, 1966.

16. Bruce DA: Effects of hyperventilation on cerebral blood flow and metabolism. Clin Perinatol 11:673-680, 1984.

17. Artru AA: Cerebral vascular responses to hypocap-nia during nitroglycerin-induced hypotension. Neurosurgery 16:468-472, 1985.

18. Artru AA, Katz RA, Colley PS: Autoregulation of cerebral blood flow during normocapnia and hypocapnia in dogs. Anesthesiology 70:288-292, 1989.

19. Boarini DJ, Kassell NF, Sprowll JA, et al: Cerebro-vascular effects of hypocapnia during adenosine-induced arterial hypotension. J Neurosurg 63:937-943, 1985.

20. VanderWorp HB, Kraaier V, Wieneke GH, et al: Quantitative EEG during progressive hypocarbia and hypoxia: Hyperventilation-induced EEG changes reconsidered. Electroencephalogr Clin Neurophysiol 79:335-341, 1991.

21. Cold GE: Does acute hyperventilation provoke cerebral oligaemia in comatose patients after acute head injury? Acta Neurochir 96:100-106, 1989.

22. Sutton LN, McLaughlin AC, Dante S, et al: Cerebral venous oxygen content as a measure of brain energy metabolism with increased intracranial pressure and hyperventilation. J Neurosurg 73:927-932, 1990.

Table 63-15 Anesthetic Considerations and Position Requirements Associated with Various Spinal Surgical Procedures—cont’d

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23. Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia. J Neuro-surg 75:685-693, 1991.

24. Muizelaar JP, Marmarou A, Ward JD, et al: Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trial. J Neurosurg 75:731-739, 1991.

25. Sheinberg M, Kanter MJ, Robertson CS, et al: Con-tinuous monitoring of jugular venous oxygen satu-ration in head-injured patients. J Neurosurg 76:212-217, 1992.

26. Andrews RJ, Muto RP: Retraction brain ischaemia: Cerebral blood flow, evoked potentials, hypotension and hyperventilation in a new animal model. Neurol Res 14:19-25, 1992.

27. Ruta TS, Drummond JC, Cole DJ: The effect of acute hypocapnia on local cerebral blood flow during middle cerebral artery occlusion in isoflu-rane anesthetized rats. Anesthesiology 78:134-140, 1993.

28. McLaughlin MR, Marion DW: Cerebral blood flow and vasoresponsivity within and around cerebral contusions. J Neurosurg 85:871-876, 1996.

29. Imberti R, Bellinzona G, Langer M: Cerebral tissue PO2 and SjvO2 changes during moderate hyperven-tilation in patients with severe traumatic brain injury. J Neurosurg 96:97-102, 2002.

30. Coles JP, Minhas PS, Fryer TD, et al: Effect of hyperventilation on cerebral blood flow in trau-matic head injury: Clinical relevance and monitor-ing correlates. Crit Care Med 30:1950-1959, 2002.

31. Coles JP, Fryer TD, Coleman MR, et al: Hyperven-tilation following head injury: Effect on ischemic burden and cerebral oxidative metabolism. Crit Care Med 35:568-578, 2007.

32. Gopinath SP, Robertson CS, Contant CF, et al: Jugular venous desaturation and outcome after head injury. J Neurol Neurosurg Psychiatry 57:717-723, 1994.

33. Bouma GJ, Muizelaar JP, Stringer WA, et al: Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neurosurg 77:360-368, 1992.

34. Kelly DF, Martin NA, Kordestani R, et al: Cerebral blood flow as a predictor of outcome following traumatic brain injury. J Neurosurg 86:633-641, 1997.

35. Martin NA, Patwardhan RV, Alexander MJ, et al: Characterization of cerebral hemodynamic phases following severe head trauma: Hypoperfusion, hyperemia, and vasospasm. J Neurosurg 87:9-19, 1997.

36. Schroder ML, Muizelaar JP, Kuta AJ, et al: Thresh-olds for cerebral ischemia after severe head injury: Relationship with late CT findings and outcome. J Neurotrauma 13:17-23, 1996.

37. Hlatky R, Furuya Y, Valadka AB, et al: Dynamic autoregulatory response after severe head injury. J Neurosurg 97:1054-1061, 2002.

38. van Santbrink H, Schouten JW, Steyerberg EW, et al: Serial transcranial Doppler measurements in traumatic brain injury with special focus on the early posttraumatic period. Acta Neurochir (Wien) 144:1141-1149, 2002.

39. Coles JP, Fryer TD, Smielewski P, et al: Incidence and mechanisms of cerebral ischemia in early clini-cal head injury. J Cereb Blood Flow Metab 24:202-211, 2004.

40. Matta BF, Lam AM, Mayberg TS, et al: A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures. Anesth Analg 79:745-750, 1994.

60. Lin CL, Dumont AS, Lieu AS, et al: Characteriza-tion of perioperative seizures and epilepsy follow-ing aneurysmal subarachnoid hemorrhage. J Neurosurg 99:978-985, 2003.

61. Lee LA, Roth S, Posner KL, et al: The American Society of Anesthesiologists Postoperative Visual Loss Registry: Analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 105:652-659, 2006.

62. Hayreh SS: Anterior ischemic optic neuropathy. Clin Neurosci 4:251-263, 1997.

63. Stammen J, Unsold R, Arendt G, et al: Etiology and pathogenetic mechanisms of optic disc swelling with visual loss. Ophthalmologica 213:40-47, 1999.

64. Wakakura M, Ishikawa S: Neuro-ophthalmic aspects of vascular disease. Curr Opin Ophthalmol 5:18-22, 1994.

65. Cheng MA, Todorov A, Tempelhoff R, et al: The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 95:1351-1355, 2001.

66. Williams EL, Hart WM, Tempelhoff R: Postopera-tive ischemic optic neuropathy. Anesth Analg 80:1018-1029, 1995.

67. Cheng MA, Sigurdson W, Tempelhoff R, et al: Visual loss after spine surgery: A survey. Neurosur-gery 46:625-631, 2000.

68. Roth S, Barach P: Postoperative visual loss: Still no answers—yet. Anesthesiology 95:575-577, 2001.

69. Albin MS, Ritter RR, Pruett CE, et al: Venous air embolism during lumbar laminectomy in the prone position: Report of three cases. Anesth Analg 73:346-349, 1991.

70. Sutherland RW, Winter RJ: Two cases of fatal air embolism in children undergoing scoliosis surgery. Acta Anaesthesiol Scand 41:1073-1076, 1997.

71. Brown J, Rogers J, Soar J: Cardiac arrest during surgery and ventilation in the prone position: A case report and systematic review. Resuscitation 50:233-238, 2001.

72. Standefer M, Bay JW, Trusso R: The sitting position in neurosurgery: A retrospective analysis of 488 cases. Neurosurgery 14:649-658, 1984.

73. Matjasko J, Petrozza P, Cohen M, et al: Anesthesia and surgery in the seated position: Analysis of 554 cases. Neurosurgery 17:695-702, 1985.

74. Black S, Ockert DB, Oliver WC, et al: Outcome following posterior fossa craniectomy in patients in the sitting or horizontal positions. Anesthesiology 69:49-56, 1988.

75. Duke DA, Lynch JJ, Harner SG, et al: Venous air embolism in sitting and supine patients undergoing vestibular schwannoma resection. Neurosurgery 42:1286-1287, 1998.

76. Harrison EA, Mackersie A, McEwan A, et al: The sitting position for neurosurgery in children: A review of 16 years’ experience. Br J Anaesth 88:12-17, 2002.

77. Murr R, Biller H, Enzenbach R: Influence of volume loading on the cardiovascular pattern in the sitting position. Br J Anaesth 56:1305P, 1984.

78. Brodrick PM, Ingram GS: The antigravity suit in neurosurgery. Anaesthesia 43:762-765, 1988.

79. Meyer PG, Cuttaree H, Charron B, et al: Prevention of venous air embolism in paediatric neurosurgical procedures performed in the sitting position by combined use of MAST suit and PEEP. Br J Anaesth 73:795-800, 1994.

80. Marshall WK, Bedford RF, Miller ED: Cardiovascu-lar responses in the seated position: Impact of four anesthetic techniques. Anesth Analg 62:648-653, 1983.

81. Dalrymple DG, MacGowan SW, MacLeod GF: Cardiorespiratory effects of the sitting position

41. Ishii R: Regional cerebral blood flow in patients with ruptured intracranial aneurysms. J Neurosurg 50:587-594, 1979.

42. Xu W, Mellergard P, Ungerstedt U, et al: Local changes in cerebral energy metabolism due to brain retraction during routine neurosurgical procedures. Acta Neurochir 144:679-683, 2002.

43. Raichle ME, Posner JB, Plum F: Cerebral blood flow during and after hyperventilation. Arch Neurol 23:394-403, 1970.

44. Muizelaar JP, Poel HG, Li ZC, et al: Pial arteriolar vessel diameter and CO2 reactivity during pro-longed hyperventilation in the rabbit. J Neurosurg 69:923-927, 1988.

45. Miller JD, Sakalas R, Ward JD, et al: Methylpred-nisolone treatment in patients with brain tumors. Neurosurgery 1:114-117, 1977.

46. Yeung WTI, Lee TY, Maestro RFD, et al: Effect of steroids on iopamidol blood-brain transfer constant and plasma volume in brain tumors measured with x-ray computed tomography. J Neuro-Oncol 18:53-60, 1994.

47. Wilkinson ID, Jellineck DA, Levy D, et al: Dexam-ethasone and enhancing solitary cerebral mass lesions: Alterations in perfusion and blood-tumor barrier kinetics shown by magnetic resonance imaging. Neurosurgery 58:640-646, 2006.

48. Miller JD, Leech P: Effects of mannitol and steroid therapy on intracranial volume-pressure relation-ships in patients. J Neurosurg 42:274-281, 1975.

49. Bell BA, Kean KM, Macdonald HL, et al: Brain water measured by magnetic resonance imaging: Correlation with direct estimation and changes after mannitol and dexamethasone. Lancet 1:66-69, 1987.

50. Edwards P, Arango M, Balica L, et al: Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury—outcomes at 6 months. Lancet 365:1957-1959, 2005.

51. Cottrell JE, Robustelli A, Post K, et al: Furosemide- and mannitol-induced changes in intracranial pres-sure and serum osmolality and electrolytes. Anesthesiology 47:28-30, 1977.

52. Ogden AT, Mayer SA, Connolly ES Jr: Hyperosmolar agents in neurosurgical practice: The evolving role of hypertonic saline. Neurosurgery 57:207-215, 2005.

53. Khanna S, Davis D, Peterson B, et al: Use of hyper-tonic saline in the treatment of severe refractory posttraumatic intracranial hypertension in pediat-ric traumatic brain injury. Crit Care Med 28:1144-1151, 2000.

54. Rudehill A, Gordon E, Ohman G, et al: Pharma-cokinetics and effects of mannitol on hemodynam-ics, blood and cerebrospinal fluid electrolytes, and osmolality during intracranial surgery. J Neurosurg Anesthesiol 5:4-12, 1993.

55. Kaufmann AM, Cardoso ER: Aggravation of vasogenic cerebral edema by multiple-dose manni-tol. J Neurosurg 77:584-589, 1992.

56. Marshall LF, Smith RW, Rauscher LA, et al: Man-nitol dose requirements in brain-injured patients. J Neurosurg 48:169-172, 1978.

57. Staub F, Stoffel M, Berger S, et al: Treatment of vasogenic brain edema with the novel chloride ion transport inhibitor torasemide. J Neurotrauma 11:679-690, 1994.

58. Ringel F, Chang RC, Staub F, et al: Contribution of anion transporters to the acidosis-induced swelling and intracellular acidification of glial cells. J Neuro-chem 75:125-132, 2000.

59. Guidelines for the management of severe traumatic brain injury. J Neurotrauma 24(Suppl 1):S1-S106, 2007.

A


ection

V A

dult Sub

specialty M

anagement

in neurosurgery. Br J Anaesth 51:1079-1082, 1979.

82. Pivalizza EG, Katz J, Singh S, et al: Massive macroglossia after posterior fossa surgery in the prone position. J Neurosurg Anesthesiol 10:34-36, 1998.

83. Wilder BL: Hypothesis: The etiology of midcervical quadriplegia after operation with the patient in the sitting position. Neurosurgery 11:530-531, 1982.

84. Toung TJK, McPherson RW, Ahn H, et al: Pneumo-cephalus: Effects of patient position on the inci-dence and location of aerocele after posterior fossa and upper cervical cord surgery. Anesth Analg 65:65-70, 1986.

85. Hernandez-Palazon J, Martinez-Lage JF, Rosa- Carrillo VN, et al: Anesthetic technique and devel-opment of pneumocephalus after posterior fossa surgery in the sitting position. Neurochirurgia 14:216-221, 2003.

86. Drummond JC: Tension pneumocephalus and intermittent drainage of ventricular CSF [letter]. Anesthesiology 60:609-610, 1984.

87. Goodie D, Traill R: Intraoperative subdural tension pneumocephalus arising after opening of the dura. Anesthesiology 74:193-195, 1991.

88. Skahen S, Shapiro HM, Drummond JC, et al: Nitrous oxide withdrawal reduces intracranial pres-sure in the presence of pneumocephalus. Anesthe-siology 65:192-195, 1986.

89. Prabhakar H, Bithal PK, Garg A: Tension pneumo-cephalus after craniotomy in supine position. J Neu-rosurg Anesthesiol 15:278-281, 2003.

90. Toung TT, Donham RT, Lehner A, et al: Tension pneumocephalus after posterior fossa craniotomy: Report of four additional cases and review of post-operative pneumocephalus. Neurosurgery 12:164-168, 1983.

91. Reasoner DK, Todd MM, Scamman FL, et al: The incidence of pneumocephalus after supratentorial craniotomy. Anesthesiology 80:1008-1012, 1994.

92. Satyarthee GD, Mahapatra AK: Tension pneumo-cephalus following transsphenoid surgery for pitui-tary adenoma—report of two cases. J Clin Neurosci 10:495-497, 2003.

93. Michenfelder JD, Miller RH, Gronert GA: Evalua-tion of an ultrasonic device (Doppler) for the diag-nosis of venous air embolism. Anesthesiology 36:164-167, 1972.

94. Marshall WK, Bedford RF: Use of a pulmonary-artery catheter for detection and treatment of venous air embolism. Anesthesiology 52:131-134, 1980.

95. Papadopoulos G, Kuhly P, Brock M, et al: Venous and paradoxical air embolism in the sitting posi-tion: A prospective study with transesophageal echocardiography. Acta Neurochir 126:140-143, 1994.

96. Schwarz G, Fuchs G, Weihs W, et al: Sitting position for neurosurgery: Experience with preoperative contrast echocardiography in 301 patients. J Neuro-surg Anesth 6:83-88, 1994.

97. Faberowski LW, Black S, Mickle P: Incidence of venous air embolism during craniectomy for craniosynostosis repair. Anesthesiology 92:20-23, 2000.

98. Tobias JD, Johnson JO, Jimenez DF, et al: Venous air embolism during endoscopic strip craniectomy for repair of craniosynostosis in infants. Anesthesiol-ogy 95:340-342, 2001.

99. Matjasko J: Lessons learned [editorial]. J Neurosurg Anesthesiol 8:1-2, 1996.

100. Schubert A, Deogaonkar A, Drummond JC: Pre-cordial Doppler probe placement for optimal detec-

119. Yahagi N, Furuya H, Sai Y, et al: Effect of halothane, fentanyl, and ketamine on the threshold for transpulmonary passage of venous air emboli in dogs. Anesth Analg 75:720-723, 1992.

120. Zentner J, Albrecht T, Hassler W: Prevention of an air embolism by moderate hypoventilation during surgery in the sitting position. Neurosurgery 28:705-708, 1991.

121. Grady MS, Bedford RF, Park TS: Changes in supe-rior sagittal sinus pressure in children with head elevation, jugular venous compression and PEEP. J Neurosurg 65:199-202, 1986.

122. Toung TJK, Miyabe M, McShane AJ, et al: Effect of PEEP and jugular venous compression on canine cerebral blood flow and oxygen consumption in the head elevated position. Anesthesiology 68:53-58, 1988.

123. Pfitzner J, McLean AG: Controlled neck compres-sion in neurosurgery. Anaesthesia 40:624-629, 1985.

124. Geissler HJ, Allen SJ, Mehlhorn U, et al: Effect of body repositioning after venous air embolism. Anesthesiology 86:710-717, 1997.

125. Sokoll MM, Gergis SD: Effects of venous air embo-lism on the cardiovascular system and acid base balance in the presence and absence of nitrous oxide. Acta Anaesthesiol Scand 28:226-231, 1984.

126. Losasso TJ, Muzzi DA, Dietz NM, et al: Fifty percent nitrous oxide does not increase the risk of venous air embolism in neurosurgical patients operated upon in the sitting position. Anesthesiol-ogy 77:21-30, 1992.

127. Losasso TJ, Black S, Muzzi DA, et al: Detection and hemodynamic consequences of venous air embo-lism: Does nitrous oxide make a difference? Anesthesiology 77:148-152, 1992.

128. Tommasino C, Moore S, Todd MM: Cerebral effects of isovolemic hemodilution with crystalloid or colloid solutions. Crit Care Med 16:862-868, 1988.

129. Kellum JA: Saline-induced hyperchloremic meta-bolic acidosis. Crit Care Med 30:259-261, 2002.

130. Drummond JC, Patel PM, Cole DJ, et al: The effect of reduction of colloid oncotic pressure, with and without reduction of osmolality, on post trau-matic cerebral edema. Anesthesiology 88:993-1002, 1998.

131. Myburgh J, Cooper J, Finfer S, et al: Saline or albumin for fluid resuscitation in patients with trau-matic brain injury. N Engl J Med 357:874-884, 2007.

132. Suarez JI, Shannon L, Zaidat OO, et al: Effect of human albumin administration on clinical outcome and hospital cost in patients with subarachnoid hemorrhage. J Neurosurg 100:585-590, 2004.

133. Palesch YY, Hill MD, Ryckborst KJ, et al: The ALIAS Pilot Trial: A dose-escalation and safety study of albumin therapy for acute ischemic stroke, II: Neu-rologic outcome and efficacy analysis. Stroke 37:2107-2114, 2006.

134. Ginsberg MD, Palesch YY, Hill MD: The ALIAS (ALbumin In Acute Stroke) phase III randomized multicentre clinical trial: Design and progress report. Biochem Soc Trans 34:1323-1326, 2006.

135. Kozek-Langenecker SA: Effects of hydroxyethyl starch solutions on hemostasis. Anesthesiology 103:654-660, 2005.

136. Cully MD, Larson CP, Silverberg GD: Hetastarch coagulopathy in a neurosurgical patient [letter]. Anesthesiology 66:706-707, 1987.

137. Trumble ER, Muizelaar JP, Myseros JS, et al: Coagu-lopathy with the use of hetastarch in the treatment of vasospasm. J Neurosurg 82:44-47, 1995.

138. Kreimeier U, Messmer K: Small-volume resuscita-tion: From experimental evidence to clinical

tion of venous air embolism during craniotomy. Anesth Analg 102:1543-1547, 2006.

101. Mirski MA, Lele AV, Fitzsimmons L, et al: Diagno-sis and treatment of vascular air embolism. Anesthesiology 106:164-177, 2007.

102. Cucchiara RF, Seward JB, Nishimura RA, et al: Identification of patent foramen ovale during sitting position craniotomy by transesophageal echocardi-ography with positive airway pressure. Anesthesiol-ogy 63:107-109, 1985.

103. Black S, Muzzi DA, Nishimura RA, et al: Preopera-tive and intraoperative echocardiography to detect right-to-left shunt in patients undergoing neurosur-gical procedures in the sitting position. Anesthesiol-ogy 72:436-438, 1990.

104. Mammoto T, Hayashi Y, Ohnishi Y, et al: Incidence of venous and paradoxical air embolism in neuro-surgical patients in the sitting position: Detection by transesophageal echocardiography. Acta Anaes-thesiol Scand 42:643-647, 1998.

105. Drummond JC, Prutow RJ, Scheller MS: A com-parison of the sensitivity of pulmonary artery pres-sure, end-tidal carbon dioxide, and end-tidal nitrogen in the detection of venous air embolism in the dog. Anesth Analg 64:688-692, 1985.

106. Bunegin L, Albin MS, Helsel PE, et al: Positioning the right atrial catheter: A model for reappraisal. Anesthesiology 55:343-348, 1981.

107. Martin JT: Anesthetic adjuncts to patients in the sitting position, III: Intravascular electrocardiogra-phy. Anesth Analg 49:793-808, 1970.

108. Hagen PT, Scholz DG, Edwards WD: Incidence and size of patent foramen ovale during the first 10 decades of life: An autopsy study of 965 normal hearts. Mayo Clin Proc 59:17-20, 1984.

109. Perkins NAK, Bedford RF: Hemodynamic conse-quences of PEEP in seated neurological patients—implications for paradoxical air embolism. Anesth Analg 63:429-432, 1984.

110. Colohan ART, Perkins AK, Bedford RF, et al: Intravenous fluid loading as prophylaxis for para-doxical air embolism. J Neurosurg 62:839-842, 1985.

111. Black S, Cucchiara RF, Nishimura RA, et al: Param-eters affecting occurrence of paradoxical air embo-lism. Anesthesiology 71:235-241, 1989.

112. Engelhardt M, Folkers W, Brenke C, et al: Neuro-surgical operations with the patient in sitting position: Analysis of risk factors using transcranial Doppler sonography. Br J Anaesth 96:467-472, 2006.

113. Kwapisz MM, Deinsberger W, Muller M, et al: Transesophageal echocardiography as a guide for patient positioning before neurosurgical proce-dures in semi-sitting position. J Neurosurg Anesthe-siol 16:277-281, 2004.

114. Leonard IE, Cunningham AJ: The sitting position in neurosurgery—not yet obsolete! Br J Anaesth 88:1-3, 2002.

115. Bedell EA, Berge KH, Losasso TJ: Paradoxic air embolism during venous air embolism: Trans-esophageal echocardiographic evidence of transpul-monary air passage. Anesthesiology 80:947-950, 1994.

116. Tommasino C, Rizzardi R, Beretta L, et al: Cerebral ischemia after venous air embolism in the absence of intracardiac defects. J Neurosurg Anesth 8:30-34, 1996.

117. Butler BD, Hills BA: The lung as a filter for micro-bubbles. J Appl Physiol 47:537-543, 1979.

118. Katz J, Leiman BC, Butler BD: Effects of inhalation anaesthetics on filtration of venous gas emboli by the pulmonary vasculature. Br J Anaesth 61:200-205, 1988.

A


routine: Advantages and disadvantages of hyper-tonic solutions. Acta Anaesthesiol Scand 46:625-638, 2002.

139. Cooper DJ, Myles PS, McDermott FT, et al: Prehos-pital hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: A randomized controlled trial. JAMA 291:1350-1357, 2004.

140. Qureshi AI, Suarez JI: Use of hypertonic saline solu-tions in treatment of cerebral edema and intracra-nial hypertension [review]. Crit Care Med 28:3301-3313, 2000.

141. Doyle JA, Davis DP, Hoyt DB: The use of hypertonic saline in the treatment of traumatic brain injury. J Trauma 50:367-383, 2001.

142. Horn P, Munch E, Vajkoczy P, et al: Hypertonic saline solution for control of elevated intracranial pressure in patients with exhausted response to mannitol and barbiturates. Neurol Res 21:758-764, 1999.

143. Todd MM, Hindman BJ, Clarke WR, et al: Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med 352:135-145, 2005.

144. Crowder CM, Tempelhoff R, Theard A, et al: Jugular bulb temperature: Comparison with brain surface and core temperatures in neurosurgical patients during mild hypothermia. J Neurosurg 85:98-103, 1996.

145. Graham DI, Ford I, Adams JH, et al: Ischaemic brain damage is still common in fatal non-missile head injury. J Neurol Neurosurg Psychiatry 52:346-350, 1989.

146. Clifton GL, Jiang JY, Lyeth BG, et al: Marked protec-tion by moderate hypothermia after experimental traumatic brain injury. J Cereb Blood Flow Metab 11:114-121, 1991.

147. Marion DW, Obrist WD, Carlier PM, et al: The use of moderate therapeutic hypothermia for patients with severe head injuries: A preliminary report. J Neurosurg 79:354-362, 1993.

148. Shiozaki T, Sugimoto H, Taneda M, et al: Effect of mild hypothermia on uncontrollable intracranial hypertension after severe head injury. J Neurosurg 79:363-368, 1993.

149. Clifton GL, Allen S, Barrodale P, et al: A phase II study of moderate hypothermia in severe brain injury. J Neurotrauma 10:263-273, 1993.

150. Metz C, Holzschuh M, Bein T, et al: Moderate hypo-thermia in patients with severe head injury: Cere-bral and extracerebral effects. J Neurosurg 85:533-541, 1996.

151. Clifton GL, Miller ER, Choi SC, et al: Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 344:556-563, 2001.

152. Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 346:557-563, 2002.

153. Hypothermia After Cardiac Arrest Study Group: Mild therapeutic hypothermia to improve the neu-rologic outcome after cardiac arrest. N Engl J Med 346:549-556, 2002.

154. Nolan JP, Morley PT, Vanden Hoek TL, et al: Thera-peutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscita-tion. Circulation 108:118-121, 2003.

155. Johansson B, Li CL, Olsson Y, et al: The effect of acute arterial hypertension on the blood-brain barrier to protein tracers. Acta Neuropathol (Berl) 16:117-124, 1970.

156. Forster A, Horn KV, Marshall LF, et al: Anesthetic effects on blood-brain barrier function during acute

175. Hertel F, Walter C, Bettag M, et al: Perfusion-weighted magnetic resonance imaging in patients with vasospasm: A useful new tool in the manage-ment of patients with subarachnoid hemorrhage. Neurosurgery 56:28-35, 2005.

176. Munch E, Vajkoczy P: Current advances in the diag-nosis of vasospasm. Neurol Res 28:703-712, 2006.

177. Weidauer S, Lanfermann H, Raabe A, et al: Impair-ment of cerebral perfusion and infarct patterns attributable to vasospasm after aneurysmal sub-arachnoid hemorrhage: A prospective MRI and DSA study. Stroke 38:1831-1836, 2007.

178. Chang HS, Hongo K, Nakagawa H: Adverse effects of limited hypotensive anesthesia on the outcome of patients with subarachnoid hemorrhage. J Neu-rosurg 92:971-975, 2000.

179. Foroohar M, Macdonald RL, Roth S, et al: Intraop-erative variables and early outcome after aneurysm surgery. Surg Neurol 54:304-315, 2000.

180. Treggiari MM, Walder B, Suter PM, et al: Systematic review of the prevention of delayed ischemic neu-rological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg 98:978-984, 2003.

181. Rinkel GJ, Feigin VL, Algra A, et al: Circulatory volume expansion therapy for aneurysmal sub-arachnoid haemorrhage. Cochrane Database Syst Rev CD000483, 2004.

182. Muizelaar JP, Becker DP: Induced hypertension for the treatment of cerebral ischemia after subarach-noid hemorrhage. Surg Neurol 25:317-325, 1986.

183. Raabe A, Beck J, Keller M, et al: Relative importance of hypertension compared with hypervolemia for increasing cerebral oxygenation in patients with cerebral vasospasm after subarachnoid hemorrhage. J Neurosurg 103:974-981, 2005.

184. Kim DH, Joseph M, Ziadi S, et al: Increases in cardiac output can reverse flow deficits from vaso-spasm independent of blood pressure: A study using xenon computed tomographic measurement of cerebral blood flow. Neurosurgery 53:1044-1052, 2003.

185. Pickard JD, Murray GD, Illingworth R, et al: Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 298:636-642, 1989.

186. Petruk KC, West M, Mohr G, et al: Nimodipine treatment in poor-grade aneurysm patients. J Neu-rosurg 68:505-517, 1988.

187. Barker FG, Ogilivy CS: Efficacy of prophylactic nimodipine for delayed ischemic deficit after sub-arachnoid hemorrhage: A meta-analysis. J Neuro-surg 84:405-414, 1996.

188. Haley EC, Kassell NF, Torner JC, et al: A rand-omized controlled trial of high-dose intravenous nicardipine in aneurysmal subarachnoid hemor-rhage: A report of the Cooperative Aneurysm Study. J Neurosurg 78:537-547, 1993.

189. Haley EC, Kassell NF, Torner JC, et al: A rand-omized trial of nicardipine in subarachnoid hemor-rhage: Angiographic and transcranial Doppler ultrasound results: A report of the Cooperative Aneurysm Study. J Neurosurg 78:548-553, 1993.

190. Tseng MY, Czosnyka M, Richards H, et al: Effects of acute treatment with pravastatin on cerebral vaso-spasm, autoregulation, and delayed ischemic defi-cits after aneurysmal subarachnoid hemorrhage: a phase II randomized placebo-controlled trial. Stroke 36:1627-1632, 2005.

191. Lynch JR, Wang H, McGirt MJ, et al: Simvastatin reduces vasospasm after aneurysmal subarachnoid hemorrhage: results of a pilot randomized clinical trial. Stroke 36:2024-2026, 2005.

arterial hypertension. Anesthesiology 49:26-30, 1978.

157. Hatashita S, Hoff JT, Ishii S: Focal brain edema asso-ciated with acute arterial hypertension. J Neurosurg 64:643-649, 1986.

158. Mayhan WG: Disruption of blood-brain barrier during acute hypertension in adult and aged rats. Am J Physiol 258:H1735-H1738, 1990.

159. Kalfas IH, Little JR: Postoperative hemorrhage: A survey of 4992 intracranial procedures. Neurosur-gery 23:343-347, 1988.

160. Lewelt W, Hummel R, Littlewood K, et al: Recovery from anesthesia and cerebral blood flow velocity [abstract]. Anesth Analg 74:S186, 1992.

161. Bruder N, Pellissier D, Grillot P, et al: Cerebral hyperemia during recovery from general anesthesia in neurosurgical patients. Anesth Analg 94:650-654, 2002.

162. Grillo P, Bruder N, Auquier P, et al: Esmolol blunts the cerebral blood flow velocity increase during emergence from anesthesia in neurosurgical patients. Anesth Analg 96:1145-1149, 2003.

163. Tanskanen PE, Kytta JV, Randell TT, et al: Dex-medetomidine as an anaesthetic adjuvant in patients undergoing intracranial tumour surgery: A double-blind, randomized and placebo-controlled study. Br J Anaesth 97:658-665, 2006.

164. Laidlaw JD, Siu KH: Poor-grade aneurysmal sub-arachnoid hemorrhage: Outcome after treatment with urgent surgery. Neurosurgery 53:1275-1282, 2003.

165. Broderick JP, Brott TG, Duldner JE, et al: Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage. Stroke 25:1342-1347, 1994.

166. Amin-Hanjani S, Ogilvy CS, Barker FG II: Does intracisternal thrombolysis prevent vasospasm after aneurysmal subarachnoid hemorrhage? A meta-analysis. Neurosurgery 54:326-334, 2004.

167. Dorai Z, Hynan LS, Kopitnik TA, et al: Factors related to hydrocephalus after aneurysmal subarach-noid hemorrhage. Neurosurgery 52:763-771, 2003.

168. Tisdall M, Crocker M, Watkiss J, et al: Disturbances of sodium in critically ill adult neurologic patients: A clinical review. J Neurosurg Anesthesiol 18:57-63, 2006.

169. Wijdicks EFM, Vermeulen M, tenHaaf JA, et al: Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol 18:211-216, 1985.

170. Okuchi K, Fujioka M, Fujiikawa A, et al: Rapid natriuresis and preventive hypervolaemia for symp-tomatic vasospasm after subarachnoid haemor-rhage. Acta Neurochir 138:951-957, 1996.

171. Dumont AS, Kassell NF: Vasospasm. J Neurosurg 103:1-3, 2005.

172. Lin CL, Winardi W, Jeng AY, et al: Endothelin-converting enzyme inhibitors for the treatment of subarachnoid hemorrhage-induced vasospasm. Neurol Res 28:721-729, 2006.

173. Vajkoczy P, Meyer B, Weidauer S, et al: Clazosentan (AXV-034343), a selective endothelin A receptor antagonist, in the prevention of cerebral vasospasm following severe aneurysmal subarachnoid hemor-rhage: Results of a randomized, double-blind, placebo-controlled, multicenter phase IIa study. J Neurosurg 103:9-17, 2005.

174. Barth M, Capelle HH, Munch E, et al: Effects of the selective endothelin A (ET(A)) receptor antagonist Clazosentan on cerebral perfusion and cerebral oxygenation following severe subarachnoid hemor-rhage—preliminary results from a randomized clinical series. Acta Neurochir (Wien) 149:911-918, 2007.

A


ection

V A

dult Sub

specialty M

anagement

192. Roos Y, Rinkel G, Vermeulen M, et al: Antifibrino-lytic therapy for aneurysmal subarachnoid hemor-rhage. Stroke 34:2308-2309, 2003.

193. Macrea LM, Tramer MR, Walder B: Spontaneous subarachnoid hemorrhage and serious cardiopul-monary dysfunction—a systematic review. Resusci-tation 65:139-148, 2005.

194. Naidech AM, Kreiter KT, Janjua N, et al: Cardiac troponin elevation, cardiovascular morbidity, and outcome after subarachnoid hemorrhage. Circula-tion 112:2851-2856, 2005.

195. Banki NM, Kopelnik A, Dae MW, et al: Acute neu-rocardiogenic injury after subarachnoid hemor-rhage. Circulation 112:3314-3319, 2005.

196. Bulsara KR, McGirt MJ, Liao L, et al: Use of the peak troponin value to differentiate myocardial inf-arction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarach-noid hemorrhage. J Neurosurg 98:524-528, 2003.

197. Brouwers PJAM, Wijdicks EFM, Hasan D, et al: Serial electrocardiographic recording in aneurys-mal subarachnoid hemorrhage. Stroke 20:1162-1167, 1989.

198. Lorsheyd A, Simmers TA, Robles De Medina EO: The relationship between electroencephalographic abnormalities and location of the intracranial aneu-rysm in subarachnoid hemorrhage. Pacing Clin Electrophysiol 26:1722-1728, 2003.

199. Lanzino G, Kongable GL, Kassell NF: Electrocar-diographic abnormalities after nontraumatic sub-arachnoid hemorrhage. J Neurosurg Anesth 6:156-162, 1994.

200. Randell T, Tanskanen P, Scheinin M, et al: QT dis-persion after subarachnoid hemorrhage. J Neuro-surg Anesth 11:163-166, 1999.

201. Maekawa T, McDowall DG, Okuda Y: Brain-surface oxygen tension and cerebral cortical blood flow during hemorrhagic and drug-induced hypoten-sion in the cat. Anesthesiology 51:313-320, 1979.

202. Meyer FB, Anderson RE, Sundt TM, et al: Treat-ment of experimental focal cerebral ischemia with mannitol. J Neurosurg 66:109-115, 1987.

203. Jafar JJ, Johns LM, Mullan SF: The effect of mannitol on cerebral blood flow. J Neurosurg 64:754-759, 1986.

204. Bouma GJ, Muizelaar JP: Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation. J Neurosurg 73:368-374, 1990.

205. Ogilvy CS, Chu D, Kaplan S: Mild hypothermia, hypertension, and mannitol are protective against infarction during experimental intracranial tempo-rary vessel occlusion. Neurosurgery 38:1202-1210, 1996.

206. Samson D, Batjer HH, Bowman G, et al: A clinical study of the parameters and effects of temporary arterial occlusion in the management of intracra-nial aneurysms. Neurosurgery 34:22, 1994.

207. Ogilvy CS, Carter BS, Kaplan S, et al: Temporary vessel occlusion for aneurysm surgery: Risk factors for stroke in patients protected by induced hypo-thermia and hypertension and intravenous manni-tol administration. J Neurosurg 84:785-791, 1996.

208. Drummond JC, Cole DJ, Patel PM, et al: Focal cer-ebral ischemia during anesthesia with etomidate, isoflurane or thiopental: A comparison of the extent of cerebral injury. Neurosurgery 37:742-749, 1995.

209. Hoffman WE, Charbel FT, Edelman G, et al: Com-parison of the effect of etomidate and desflurane on brain tissue games and pH during prolonged middle cerebral artery occlusion. Anesthesiology 88:1188-1194, 1998.

210. Ridenour TR, Warner DS, Todd MM, et al: Com-parative effects of propofol and halothane on

230. Shatney CH, Brunner RD, Nguyen TQ: The safety of orotracheal intubation in patients with unstable cervical spine fracture or high spinal cord injury. Am J Surg 170:676-680, 1995.

231. Hastings RH, Kelley SD: Neurologic deterioration associated with airway management in a cervical spine-injured patient. Anesthesiology 78:580-583, 1993.

232. Muckart DJJ, Bhagwanjee S, vanderMerwe R: Spinal cord injury as a result of endotracheal intubation in patients with undiagnosed cervical spine fractures. Anesthesiology 87:418-420, 1997.

233. Kirschenbaum KJ, Nadimpalli SR, Fantus R, et al: Unsuspected upper cervical spine fractures associ-ated with significant head trauma: Role of CT. J Emerg Med 8:183-198, 1990.

234. Hastings RH, Wood PR: Head extension and laryn-geal view during laryngoscopy with cervical spine stabilization maneuvers. Anesthesiology 80:825-831, 1994.

235. Chesnut RM, Marshall LF, Klauber MR, et al: The role of secondary brain injury in determining outcome from severe head injury. J Trauma 34:216-222, 1993.

236. Stephens C, Kahntroff S, Dutton R: Success of emer-gency endotracheal intubation in trauma patients at a major trauma referral center [abstract]. Anesthe-siology A:1298, 2007.

237. Morris CG, McCoy EP, Lavery GG: Spinal immobi-lisation for unconscious patients with multiple inju-ries. BMJ 329:495-499, 2004.

238. Stassen NA, Williams VA, Gestring ML, et al: Mag-netic resonance imaging in combination with helical computed tomography provides a safe and efficient method of cervical spine clearance in the obtunded trauma patient. J Trauma 60:171-177, 2006.

239. Bachulis BL, Long WB, Hynes GD, et al: Clinical indications for cervical spine radiographs in the traumatized patient. Am J Surg 153:473-477, 1987.

240. Fischer RP: Cervical radiographic evaluation of alert patients following blunt trauma. Ann Emerg Med 13:905-907, 1984.

241. Stiell IG, Clement CM, McKnight RD, et al: The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med 349:2510-2518, 2003.

242. Ross SE, Schwab CW, David ET, et al: Clearing the cervical spine: Initial radiologic evaluation. J Trauma 27:1055-1060, 1987.

243. Miller P, Mack CD, Sammer M, et al: The incidence and risk factors for hypotension during emergent decompressive craniotomy in children with trau-matic brain injury. Anesth Analg 103:869-875, 2006.

244. Marmarou A, Anderson RL, Ward JD, et al: Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 75:S59-S66, 1991.

245. Laurer HL, Bareyre FM, Lee VM, et al: Mild head injury increasing the brain’s vulnerability to a second concussive impact. J Neurosurg 95:859-870, 2001.

246. Pietropaoli JA, Rogers FB, Shackford SR, et al: The deleterious effects of intraoperative hypotension an outcome in patients with severe head injuries. J Trauma 33:403-407, 1992.

247. Jones PA, Andrews PJ, Midgley S, et al: Measuring the burden of secondary insults in head-injured patients during intensive care. J Neurosurg Anesthe-siol 6:4-14, 1994.

248. Stocchetti N, Furlan A, Volta F: Hypoxemia and arterial hypotension at the accident scene in head injury. J Trauma 40:764-767, 1996.

outcome from temporary middle cerebral artery occlusion in the rat. Anesthesiology 76:807-812, 1992.

211. Warner DS, Todd MM, McFarlane C, et al: Sevoflu-rane and halothane reduce focal ischemic brain damage in the rat: Possible influence on thermoreg-ulation. Anesthesiology 79:985-992, 1993.

212. Engelhard K, Werner C, Reeker W, et al: Desflurane and isoflurane improve neurological outcome after incomplete cerebral ischaemia in rats. Br J Anaesth 83:415-421, 1999.

213. Baughman VL, Hoffman WE, Miletich DJ, et al: Neurologic outcome in rats following incomplete cerebral ischemia during halothane, isoflurane, or N2O. Anesthesiology 69:192-198, 1988.

214. Soonthon-Brant V, Patel PM, Drummond JC, et al: Fentanyl does not increase brain injury after focal cerebral ischemia in rats. Anesth Analg 88:49-55, 1999.

215. Young WL, Solomon RA, Pedley TA, et al: Direct cortical EEG monitoring during temporary vascu-lar occlusion for cerebral aneurysm surgery. Anesthesiology 71:794-799, 1989.

216. Symon L, Wang AD, Silva IEC, et al: Perioperative use of somatosensory evoked responses in aneu-rysm surgery. J Neurosurg 60:269-275, 1984.

217. Little JR, Lesser RP, Luders H: Electrophysiological monitoring during basilar aneurysm operation. Neurosurgery 20:421-427, 1987.

218. Manninen PH: Spontaneous ventilation is a useful monitor of brain stem function during posterior fossa surgery. J Neurosurg Anesthesiol 7:63-65, 1995.

219. Mack WJ, Ducruet AF, Angevine PD, et al: Deep hypothermic circulatory arrest for complex cerebral aneurysms: Lessons learned. Neurosurgery 60:815-827, 2007.

220. Batjer HH, Devous MD, Meyer YJ, et al: Cerebro-vascular hemodynamics in arteriovenous malfor-mation complicated by normal perfusion pressure breakthrough. Neurosurgery 22:503-509, 1988.

221. Young WL, Kader A, Ornstein E, et al: Cerebral hyperemia after arteriovenous malformation resec-tion is related to “breakthrough” complications but not to feeding artery pressure. Neurosurgery 38:1085-1095, 1996.

222. Young WL, Prohovnik I, Ornstein E, et al: Pressure autoregulation is intact after arteriovenous malfor-mation resection. Neurosurgery 32:491-497, 1993.

223. Meyer B, Schaller C, Frenkel C, et al: Distributions of local oxygen saturation and its response to changes of mean arterial blood pressure in the cer-ebral cortex adjacent to arteriovenous malforma-tions. Stroke 30:2623-2630, 1999.

224. Morris CG, McCoy E: Clearing the cervical spine in unconscious polytrauma victims, balancing risks and effective screening. Anaesthesia 59:464-482, 2004.

225. Crosby ET: Airway management in adults after cer-vical spine trauma. Anesthesiology 104:1293-1318, 2006.

226. Criswell JC, Parr MJ, Nolan JP: Emergency airway management in patients with cervical spine injuries. Anaesthesia 49:900-903, 1994.

227. Stene JD: Anesthesia for the critically ill trauma patient. In Siegel JH (ed): Trauma: Emergency Surgery and Critical Care. Melbourne, Churchill Livingstone, 1987, pp 843-862.

228. Talucci RC, Shaikh KA, Schwab CW: Rapid sequence induction with oral endotracheal intuba-tion in the multiply injured patient. Am Surg 54:185-187, 1988.

229. Suderman VS, Crosby ET, Lui A: Elective oral tra-cheal intubation in cervical spine-injured adults. Can J Anaesth 38:785-789, 1991.

A


249. Clifton GL, Miller ER, Choi SC, et al: Fluid thresh-olds and outcome from severe brain injury. Crit Care Med 30:739-745, 2002.

250. McHugh GS, Engel DC, Butcher I, et al: Prognostic value of secondary insults in traumatic brain injury: Results from the IMPACT study. J Neurotrauma 24:287-293, 2007.

251. Diringer MN, Videen TO, Yundt K, et al: Regional cerebrovascular and metabolic effects of hyperven-tilation after severe traumatic brain injury. J Neuro-surg 96:103-108, 2002.

252. Schmidt EA, Czosnyka M, Steiner LA, et al: Asym-metry of pressure autoregulation after traumatic brain injury. J Neurosurg 99:991-998, 2003.

253. Marion DW, Darby J, Yonas H: Acute regional cer-ebral blood flow changes caused by severe head injuries. J Neurosurg 74:407-414, 1991.

254. Soustiel JF, Glenn TC, Shik V, et al: Monitoring of cerebral blood flow and metabolism in traumatic brain injury. J Neurotrauma 22:955-965, 2005.

255. Chan K-H, Miller JD, Dearden NM, et al: The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg 77:55-61, 1992.

256. Chan KH, Dearden NM, Miller JD, et al: Multimo-dality monitoring as a guide to treatment of intrac-ranial hypertension after severe brain injury. Neurosurgery 32:547-553, 1993.

257. Robertson CS, Valadka AB, Hannay HJ, et al: Pre-vention of secondary ischemic insults after severe head injury. Crit Care Med 27:2086-2095, 1999.

258. Bruzzone P, Dionigi R, Bellinzona G, et al: Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury. Acta Neurochir 71:111-113, 1998.

259. Marshall LF: Head injury: Recent past, present and future [editorial]. Neurosurgery 47:546-561, 2000.

260. Robertson CS: Management of cerebral perfusion pressure after traumatic brain injury. Anesthesiol-ogy 95:1513-1517, 2001.

261. Stiefel MF, Udoetuk JD, Spiotta AM, et al: Conven-tional neurocritical care and cerebral oxygenation after traumatic brain injury. J Neurosurg 105:568-575, 2006.

262. Rosner MJ, Rosner SD, Johnson AH: Cerebral per-fusion pressure: Management protocol and clinical results. J Neurosurg 83:949-962, 1995.

263. Czosnyka M, Smielewski P, Piechnik S, et al: Cere-bral autoregulation following head injury. J Neuro-surg 95:756-763, 2001.

264. Asgeirsson B, Grande PO, Nordstrom CH: A new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regula-tion. Intensive Care Med 20:260-267, 1994.

265. Asgeirsson B, Grande PO, Nordstrom CH: The Lund concept of post-traumatic brain oedema therapy. Acta Anaesthesiol Scand 39:103-106, 1995.

266. Grande PO, Asgeirsson B, Nordstrom CH: Volume-targeted therapy of increased intracranial pressure: The Lund concept unifies surgical and non-surgical treatments. Acta Anaesthesiol Scand 46:929-941, 2002.

267. Naredi S, Eden E, Zall S, et al: A standardized neu-rosurgical/neurointensive therapy directed toward vasogenic edema after severe traumatic brain injury: Clinical results. Intensive Care Med 24:446-451, 1998.

268. Eker C, Asgeirsson B, Grande P-O, et al: Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation. Crit Care Med 26:1881-1886, 1998.

samples in the internal jugular veins. Neurosurgery 34:38, 1994.

287. Schneider GH, Helden AV, Lanksch WR, et al: Con-tinuous monitoring of jugular bulb oxygen satura-tion in comatose patients—therapeutic implications. Acta Neurochir 134:71-75, 1995.

288. Gopinath SP, Cormio M, Ziegler J, et al: Intraopera-tive jugular desaturation during surgery for trau-matic intracranial hematomas. Anesth Analg 83:1014-1021, 1996.

289. Nortje J, Gupta AK: The role of tissue oxygen moni-toring in patients with acute brain injury. Br J Anaesth 97:95-106, 2006.

290. Stiefel MF, Spiotta A, Gracias VH, et al: Reduced mortality rate in patients with severe traumatic brain injury treated with brain tissue oxygen moni-toring. J Neurosurg 103:805-811, 2005.

291. Marshall LF, Toole BM, Bowers SA: The National Traumatic Coma Data Bank, part 2: Patients who talk and deteriorate: Implications for treatment. J Neurosurg 59:285-288, 1983.

292. Drummond JC, Todd MM: Acute sinus arrhythmia during surgery in the fourth ventricle: An indicator of brain-stem irritation. Anesthesiology 60:232-236, 1984.

293. Lobato RD, Rivas JJ, Sarabia R, et al: Percutaneous microcompression of the gasserian ganglion for tri geminal neuralgia. J Neurosurg 72:546-553, 1990.

294. Skirving DJ, Dan NG: A 20-year review of percuta-neous balloon compression of the trigeminal gan-glion. J Neurosurg 94:913, 2001.

295. Manninen PH, Cuillerier DJ, Nantau WE, et al: Monitoring of brainstem function during vertebral basilar aneurysm surgery: The use of spontaneous ventilation. Anesthesiology 77:681-685, 1992.

296. Nemergut EC, Dumont AS, Barry UT, et al: Periop-erative management of patients undergoing trans-sphenoidal pituitary surgery. Anesth Analg 101:1170-1181, 2005.

297. Korula G, George SP, Rajshekhar V, et al: Effect of controlled hypercapnia on cerebrospinal fluid pres-sure and operating conditions during transsphenoi-dal operations for pituitary macroadenoma. J Neurosurg Anesthesiol 13:255-259, 2001.

298. Nath G, Korula G, Chandy MJ: Effect of intrathecal saline injection and Valsalva maneuver on cerebral perfusion pressure during transsphenoidal surgery for pituitary macroadenoma. J Neurosurg Anesthe-siol 7:1-6, 1995.

299. Spaziante R, DeDivitiis E: Forced subarachnoid air in transsphenoidal excision of pituitary tumors (pumping technique). J Neurosurg 71:864-867, 1989.

300. Drummond JC, Iragui-Madoz VJ, Alksne JF, et al: Masking of epileptiform activity by propofol during seizure surgery. Anesthesiology 76:652-654, 1992.

301. Herrick IA, Craen RA, Gelb AW, et al: Propofol sedation during awake craniotomy for seizures: Patient-controlled administration versus neurolept analgesia. Anesth Analg 84:1280-1284, 1997.

302. Manninen PH, Balki M, Lukitto K, et al: Patient satisfaction with awake craniotomy for tumor surgery: A comparison of remifentanil and fentanyl in conjunction with propofol. Anesth Analg 102:237-242, 2006.

303. Keifer JC, Dentchev D, Little K, et al: A retrospec-tive analysis of a remifentanil/propofol general anesthetic for craniotomy before awake functional brain mapping. Anesth Analg 101:502-508, 2005.

304. Mack PF, Perrine K, Kobylarz E, et al: Dexmed-etomidine and neurocognitive testing in awake craniotomy. J Neurosurg Anesthesiol 16:20-25, 2004.

269. Naredi S, Olivecrona M, Lindgren C, et al: An outcome study of severe traumatic head injury using the “Lund therapy” with low-dose prostacyc-lin. Acta Anaesthesiol Scand 45:402-406, 2001.

270. Steiger HJ, Ciessinna E, Seiler RW: Identification of posttraumatic ischemia and hyperfusion by deter-mination of effect of induced arterial hypertension on carbon dioxide reactivity. Stroke 27:2048-2051, 1996.

271. Romner B, Bellner J, Kongstad P, et al: Elevated trans cranial Doppler flow velocities after severe head injury: Cerebral vasospasm or hyperemia? J Neurosurg 85:90-97, 1996.

272. Steiner LA, Johnston AJ, Czosnyka M, et al: Direct comparison of cerebrovascular effects of norepin-ephrine and dopamine in head-injured patients. Crit Care Med 32:1049-1054, 2004.

273. Kelly DF, Kordestani RK, Martin NA, et al: Hyper-emia following traumatic brain injury: Relationship to intracranial hypertension and outcome. J Neuro-surg 85:762-771, 1996.

274. Muizelaar JP, Marmarou A, DeSalles AAF, et al: Cerebral blood flow and metabolism in severely head-injured children, part 1: Relationship with GCS score, outcome, ICP, and PVI. J Neurosurg 71:63-71, 1989.

275. Warner DS, Borel CO: Treatment of traumatic brain injury: One size does not fit all. Anesth Analg 99:1208-1210, 2004.

276. Coles JP, Steiner LA, Johnston AJ, et al: Does induced hypertension reduce cerebral ischaemia within the traumatized human brain? Brain 127:2479-2490, 2004.

277. Cremer OL, van Dijk GW, Amelink GJ, et al: Cer-ebral hemodynamic responses to blood pressure manipulation in severely head-injured patients in the presence or absence of intracranial hyperten-sion. Anesth Analg 99:1211-1217, 2004.

278. Hlatky R, Valadka AB, Robertson CS: Intracranial pressure response to induced hypertension: Role of dynamic pressure autoregulation. Neurosurgery 57:917-923, 2005.

279. Bouma GJ, Muizelaar JP, Bandoh K, et al: Blood pressure and intracranial pressure-volume dynam-ics in severe head injury: Relationship with cerebral blood flow. J Neurosurg 77:15-19, 1992.

280. Juul N, Morris GF, Marshall SB, et al: Intracranial hypertension and cerebral perfusion pressure: Their influence on neurological deterioration and outcome in severe head injury. J Neurosurg 92:1-6, 2000.

281. Clayton TJ, Nelson RJ, Manara AR: Reduction in mortality from severe head injury following intro-duction of a protocol for intensive care manage-ment. Br J Anaesth 93:761-767, 2004.

282. Chambers IR, Treadwell L, Mendelow AD: Deter-mination of threshold levels of cerebral perfusion pressure and intracranial pressure in severe head injury by using receiver-operating characteristic curves: An observational study in 291 patients. J Neurosurg 94:412, 2001.

283. Stocchetti N, Maas AI, Chieregato A, et al: Hyper-ventilation in head injury: A review. Chest 127:1812-1827, 2005.

284. Nekludov M, Antovic J, Bredbacka S, et al: Coagula-tion abnormalities associated with severe isolated traumatic brain injury: Cerebral arterio-venous dif-ferences in coagulation and inflammatory markers. J Neurotrauma 24:174-180, 2007.

285. White H, Baker A: Continuous jugular venous oxi-metry in the neurointensive care unit—a brief review. Can J Anesth 49:623-629, 2002.

286. Stocchetti N, Paparella A, Bridelli F, et al: Cerebral venous oxygen saturation studied with bilateral

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305. Ard J, Doyle W, Bekker A: Awake craniotomy with dexmedetomidine in pediatric patients. J Neuro-surg Anesthesiol 15:263-266, 2003.

306. Bekker AY, Kaufman B, Samir H, et al: The use of dexmedetomidine infusion for awake craniotomy. Anesth Analg 92:1251-1253, 2001.

307. Souter MJ, Rozet I, Ojemann JG, et al: Dexmedeto-midine sedation during awake craniotomy for seizure resection: Effects on electrocorticography. J Neurosurg Anesthesiol 19:38-44, 2007.

308. Talke P, Stapelfeldt C, Garcia P: Dexmedetomidine does not reduce epileptiform discharges in adults with epilepsy. J Neurosurg Anesthesiol 19:195-199, 2007.

309. Bustillo MA, Lazar RM, Finck AD, et al: Dexme-detomidine may impair cognitive testing during endovascular embolization of cerebral arteriov-enous malformations: A retrospective case report series. J Neurosurg Anesthesiol 14:209-212, 2002.

310. Sarang A, Dinsmore J: Anaesthesia for awake crani-otomy—evolution of a technique that facilitates awake neurological testing. Br J Anaesth 90:161-165, 2003.

311. Cascino GD: Pharmacological activation. Electroen-cephalogr Clin Neurophysiol Suppl 48:70-76, 1998.

312. Cascino GD, So EL, Sharbrough FW, et al: Alfen-tanil-induced epileptiform activity in patients with partial epilepsy. J Clin Neurophysiol 10:520-525, 1993.

313. McGuire G, El-Beheiry H, Manninen P, et al: Acti-vation of electrocorticographic activity with remifentanil and alfentanil during neurosurgical excision of epileptogenic focus. Br J Anaesth 91:651-655, 2003.

314. Ebrahim ZY, DeBoer GE, Luders H, et al: Effect of etomidate on the electroencephalogram of patients with epilepsy. Anesth Analg 65:1004-1006, 1986.

324. Campi A, Ramzi N, Molyneux AJ, et al: Retreatment of ruptured cerebral aneurysms in patients rand-omized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT). Stroke 38:1538-1544, 2007.

325. Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 351:1493-1501, 2004.

326. Mas JL, Chatellier G, Beyssen B, et al: Endarterec-tomy versus stenting in patients with symptomatic severe carotid stenosis. N Engl J Med 355:1660-1671, 2006.

327. Ringleb PA, Allenberg J, Bruckmann H, et al: 30 day results from the SPACE trial of stent-protected angioplasty versus carotid endarterectomy in symp-tomatic patients: A randomised non-inferiority trial. Lancet 368:1239-1247, 2006.

328. Hobson RW 2nd, Howard VJ, Roubin GS, et al: Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase. J Vasc Surg 40:1106-1111, 2004.

329. Bracken MB, Shepard MJ, Collins WF: A rand-omized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury: Results of the second National Acute Spinal Cord Injury Study. N Engl J Med 322:1405-1411, 1990.

330. Bracken MB, Shepard MJ, Holford TR, et al: Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treat-ment of acute spinal cord injury. JAMA 277:1597-1604, 1997.

331. Rosner MJ, Daughton S: Cerebral perfusion pres-sure management in head injury. J Trauma 30:933-941, 1990.

315. Gancher S, Laxer KD, Krieger W: Activation of epi-leptogenic activity by etomidate. Anesthesiology 61:616-618, 1984.

316. Wass CT, Grady RE, Fessler AJ, et al: The effects of remifentanil on epileptiform discharges during intraoperative electrocorticography. Epilepsia 42:1340-1344, 2001.

317. Perlmutter JS, Mink JW: Deep brain stimulation. Annu Rev Neurosci 29:229-257, 2006.

318. Hammond C, Bergman H, Brown P: Pathological synchronization in Parkinson’s disease: Networks, models and treatments. Trends Neurosci 30:357-364, 2007.

319. Rozet I, Muangman S, Vavilala MS, et al: Clinical experience with dexmedetomidine for implantation of deep brain stimulators in Parkinson’s disease. Anesth Analg 103:1224-1228, 2006.

320. Young W: Anesthesia for endovascular neurosur-gery and interventional neuroradiology. Anesthe-siol Clin 25:391-412, 2007.

321. Pile-Spellman J, Young WL, Joshi S, et al: Adeno-sine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malforma-tions: Technical case report. Neurosurgery 44:881-886, 1999.

322. International Subarachnoid Aneurysm Trial Col-laborative Group, Molyneux A, Kerr R, et al: Inter-national Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneu-rysms: A randomised trial. Lancet 360:1267-1274, 2002.

323. Lanzino G, Fraser K, Kanaan Y, et al: Treatment of ruptured intracranial aneurysms since the Interna-tional Subarachnoid Aneurysm Trial: Practice uti-lizing clip ligation and coil embolization as individual or complementary therapies. J Neuro-surg 104:344-349, 2006.

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