For the purposes of planning a strategy for controlling intracranial pressure (ICP), the four subcompartments of the intracranial space should be considered: cells, interstitial and intracellular fluid, cerebrospinal fluid (CSF), and blood.
The clinician should make a preoperative assessment of the probable intracranial compliance reserve as the basis for selection of appropriate anesthetic drugs and techniques.
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.
Cerebral perfusion pressure (CPP) should be supported at or near normal waking levels in patients with recent cerebral injuries (e.g., traumatic brain injury [TBI], subarachnoid hemorrhage [SAH], and spinal cord injury [SCI]) because of low resting cerebral blood flow and impaired autoregulation.
When neurosurgical procedures are performed 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.
Monitoring for venous air embolism (VAE) in at-risk situations includes the precordial Doppler and end-tidal carbon dioxide analysis.
Despite encouraging preclinical data, therapeutic mild hypothermia cannot be advocated in the care of head-injured patients in the intensive care unit (ICU) or during the operative management of patients with intracranial aneurysms because of negative human trial results for those patient groups.
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 during management of a cerebral aneursym.
Although induced hypotension is rarely used electively in aneurysm surgery, the clinician must be ready to reduce blood pressure immediately and accurately in the event of aneurysm rupture.
Tracheal intubation of a head-injured patient with an undefined cervical spine injury can be accomplished using rapid sequence induction with manual in-line stabilization (the occiput held rigidly to the backboard), with only a very small risk of injury to the spinal cord.
CPP (CPP = MAP – ICP) should be supported to a target range of 60 to 70 mm Hg in the first 48 to 72 hours after TBI in adults.
Hypocapnia has the potential to cause cerebral ischemia, particularly in a recently injured brain and in a 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. Issues that arise in connection with a wide variety of neurosurgical procedures—those constituting a checklist that the practitioner should review before undertaking anesthesia for any neurosurgical procedure—are reviewed first, followed by procedure-specific discussions. This chapter assumes familiarity with the cerebral physiology and effects of anesthetics as described in Chapter 11 , and with neurologic monitoring as described in Chapter 39 . Carotid endarterectomy (CEA) and carotid angioplasty and stenting are discussed in Chapter 56 .
Recurrent Issues in Neuroanesthesia
Several basic elements of neurosurgical and neuroanesthetic management are recurrent and, in the absence of an established understanding between surgeon and anesthesiologist, should be discussed and agreed upon at the outset of every neurosurgical procedure ( Box 57.1 ). The list varies by procedure and may include the intended surgical position and requisite positioning aids; intentions with respect to the use of steroids, osmotic agents/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 pressure, carbon dioxide tension, 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, sometimes, the perceived risk of air embolism. The considerations driving the decisions made about these issues are presented in this section. One additional recurrent issue, brain protection, is discussed briefly in the section on aneurysms and arteriovenous malformations (AVMs) and in detail in Chapter 11 .
Control of intracranial pressure/brain relaxation
Management of Pa CO 2
Management of arterial blood pressure
Use of steroids
Use of osmotherapy
Use of diuretics
Use of anticonvulsants
Venous air embolism
Intravenous fluid management
Emergence from anesthesia
Control of Intracranial Pressure and Brain Relaxation
The necessity of preventing increases in intracranial pressure (ICP) or reducing ICP that is already increased is recurrent in neuroanesthesia. When the cranium is closed, the objectives are 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. 57.1 ). When the cranium is open, the issue may be to provide relaxation of the intracranial contents to facilitate surgical access or, in extreme circumstances, reverse ongoing brain herniation through the craniotomy site. 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. Computed tomography (CT) findings suggestive of either increased ICP or reduced intracranial compliance reserve include midline shift, obliteration of the basal cisterns, loss of sulci, ventricular effacement (or enlarged ventricles in the event of hydrocephalus or ventricular trapping), and edema. Edema appears on a CT scan as a region of hypodensity. The basal cisterns appear on CT as a dark (hypodense fluid) halo around the upper end of the brainstem ( Fig. 57.2 ). 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.
Fig. 57.3 presents the volume-pressure relationship of the intracranial space. The plateau phase occurring at low volumes reveals that the intracranial space is not completely closed, which confers some compensatory latitude. Compensation is accomplished principally by the translocation of cerebrospinal fluid (CSF) and venous blood to the spinal CSF space and the extracranial veins, respectively. Ultimately, when the compensatory potential is exhausted, even tiny incremental increases in volume can substantially increase 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. 57.1 ), with resultant mechanical injury to brain tissue, or in reduction of perfusion pressure, leading to ischemic injury.
Several variables can interact to cause or aggravate intracranial hypertension ( Fig. 57.4 ). 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 57.1 ): cells (including neurons, glia, tumors, and extravasated collections of blood), fluid (intracellular and interstitial), CSF, and blood.
The cellular compartment. This compartment is largely the province of the surgeon. However, it may be the anesthesiologist’s responsibility to pose a well-placed diagnostic question. When the brain is bulging into the surgical field at the conclusion of evacuation of an extra-axial hematoma, the clinician should ask whether a subdural or extradural hematoma is present on the contralateral side that warrants either immediate burr holes or immediate postprocedure radiologic evaluation.
The CSF compartment. There is no pharmacologic manipulation of the CSF space with a time course and magnitude that is relevant to the neurosurgical operating room. The only practical means of manipulating the size of this compartment is by drainage. A tight surgical field can sometimes 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 situations with no substantial hazard of uncal or transforamenal magnum herniation.
The fluid compartment. This compartment can be addressed with steroids and osmotic/diuretic agents. The use of these agents is discussed later.
The blood compartment. This compartment receives the anesthesiologist’s greatest attention because it is the most amenable to rapid alteration. The blood compartment should be viewed as having two separate components: venous and arterial.
|Compartment||Volume Control Methods|
|Diuretics osmotic/diuretic agents |
Steroids (principally tumors)
|Decrease cerebral blood flow|
|Improve cerebral venous drainage|
With respect to the blood compartment, the venous side of the circulation should initially be considered. It is largely a passive compartment and is often overlooked. Despite this passivity, engorgement of this compartment is a common cause of increased ICP or poor conditions in the surgical field ( Fig. 57.5 ). A head-up posture to ensure good venous drainage is the standard in neurosurgical anesthesia and critical care. Obstruction of cerebral venous drainage by extremes of head position or circumferential pressure (cervical collars, endotracheal tube ties) should be avoided. Anything that causes increased intrathoracic pressure can also result in obstruction of cerebral venous drainage. Relevant phenomena include kinking or partial obstruction of endotracheal tubes, tension pneumothorax, coughing or straining against the endotracheal tube, or gas trapping as a result of bronchospasm. Neuromuscular blockade is usually induced during craniotomies unless a contraindication is present. Such a blockade would prevent a sudden cough that can cause a dramatic herniation of cerebral structures through the craniotomy.
Thereafter, the arterial side of the circulation should be considered. Attention to the effect of anesthetic drugs and techniques on cerebral blood flow (CBF) (see Chapter 11 ) is an established part of neuroanesthesia because, in general, increases in CBF are associated with increases in cerebral blood volume (CBV). The notable exception to this rule occurs in the context of cerebral ischemia caused by hypotension or vessel occlusion, at which times CBV may increase as the cerebral vasculature dilates in response to a sudden reduction in CBF. However, the relationship generally applies, and attention to the control of CBF is relevant in situations in which intracranial volume compensation mechanisms are exhausted or ICP is already increased. The general approach is to select anesthetics and to control physiologic variables in a manner that avoids unnecessary increases in CBF. The variables that influence CBF are listed in Box 57.2 and are discussed in Chapter 11 .
See effects of anesthetics on cerebral blood flow and cerebral metabolic rate in Chapter 11 for detailed discussion.
Pa O 2
Pa CO 2
Cerebral metabolic rate
Blood pressure/status of autoregulation
Neurogenic pathways (intra- and extra-axial)
Selection of Anesthetics
The question of which anesthetics are appropriate, especially in the context of unstable ICP, arises frequently. Chapter 11 provides relevant information in detail, and only broad generalizations are described here.
In general, intravenous anesthetic, analgesic, and sedative drugs are associated with parallel reductions in CBF and cerebral metabolic rate (CMR) and consequently will not have adverse effects on ICP. Ketamine, given in large doses to patients with a generally normal level of consciousness before anesthesia, is the exception. Autoregulation and carbon dioxide (CO 2 ) responsiveness are generally preserved during the administration of intravenous anesthetics (see Chapter 11 ).
By contrast, all the volatile anesthetics can be, depending on physiologic and pharmacologic circumstances, dose-dependent cerebral vasodilators. The order of vasodilating potency is approximately halothane → enflurane → desflurane → isoflurane → sevoflurane. As noted in Chapter 11 , the CBF differences among desflurane, isoflurane, and sevoflurane are unlikely to be clinically significant. The net CBF effect of a volatile anesthetic depends on the interaction of several factors: the concentration of the anesthetic, the extent of previous CMR depression, simultaneous blood pressure changes acting in conjunction with previous or anesthetic-induced autoregulation abnormalities, and simultaneous changes in partial pressure of carbon dioxide in the arterial blood (Pa CO 2 ) acting in conjunction with any disease-related impairment in CO 2 responsiveness.
Nitrous oxide (N 2 O) can also be a cerebral vasodilator. The CBF effect of N 2 O is greatest when it is administered as a sole anesthetic; least when it is administered against a background of narcotics, propofol, or benzodiazepines; and intermediate when it is administered in conjunction with volatile anesthetics (see Chapter 11 ).
Despite the vasodilatory potential of both N 2 O and volatile anesthetics, experience dictates that both, with the latter in concentrations less than the minimum alveolar concentration (MAC), can be used in most elective and many emergent neurosurgical procedures when administered as part of a balanced anesthetic technique in combination with opioids. However, there are exceptions. Because both N 2 O and volatile anesthetics can be vasodilators in some circumstances, when the compensatory latitude of the intracranial space has been exhausted and physiology is abnormal, omitting them on a just-in-case basis may be prudent. In a somnolent, vomiting patient with papilledema, a large tumor mass, and compressed basal cisterns; or in a traumatic brain injury (TBI) victim with an expanding mass lesion or obliterated cisterns and sulci on CT, a predominantly intravenous technique should be used until the cranium and dura are open. Thereafter, the effect of the anesthetic technique can be assessed by direct observation of the surgical field. Although inhaled anesthetics are entirely acceptable components of most anesthetics for neurosurgery, in circumstances in which ICP is persistently increased or the surgical field is persistently “tight,” N 2 O and volatile anesthetics should be replaced by intravenous anesthetics.
Neuromuscular blockers that can release histamine (e.g., atracurium) should be given in small, divided doses. Although succinylcholine can increase ICP, the increases are small and transient. Moreover, the increases can be blocked by a preceding dose of nondepolarizing neuromuscular blocking drugs and, in at least some instances, are not evident in patients with common emergency neurosurgical conditions (TBI, SAH). Succinylcholine in conjunction with proper management of the airway and MAP can be used when rapid endotracheal intubation is needed.
From the material just presented and from the discussion of cerebral physiology in Chapter 11 , a systematic clinical approach should follow easily. A schema for approaching the problem of an acute increase in ICP or acute deterioration in conditions in the surgical field is presented in Box 57.3 .
Are the relevant pressures controlled?
Jugular venous pressure
Extreme head rotation or neck flexion?
Direct jugular compression?
Straining, coughing; adequately relaxed?
Excessive PEEP or APR ventilation?
Partial pressure of CO 2 and O 2 (Pa CO 2 , PaO 2 )
Is the metabolic rate controlled?
Are any potential vasodilators in use?
N 2 O, volatile agents, nitroprusside, calcium channel blockers?
Are there any unrecognized mass lesions?
Air ± N 2 O
CSF (clamped ventricular drain)
APR, Airway pressure release; CSF, cerebrospinal fluid; PEEP, positive end-expiratory pressure.
If the problem has not resolved satisfactorily after following the approach in Box 57.3 , Box 57.4 presents options for resolution. CSF drainage was discussed earlier. Additional hyperosmolar solutions are frequently used (see the subsequent section Osmotherapy and Diuretics). Barbiturates have long been the most widely used drugs for inducing reduction in CMR, with the objective of causing a coupled reduction in CBF and CBV. Propofol has gained popularity for this application. However, although the use of barbiturates is supported by ICU experience demonstrating efficacy in ICP control (if not outcome), little such evidence has been accumulated for propofol. Furthermore, a frequently fatal syndrome of metabolic acidosis and rhabdomyolysis has been recognized in patients who have received prolonged propofol infusions in the ICU setting.
Further reduction of Pa CO 2 (to not <23-25 mm Hg)
CSF drainage (ventriculostomy, brain needle)
Diuresis (usually mannitol)
CMR suppression (barbiturates, propofol)
MAP reduction (if dysautoregulation)
Surgical control (i.e., lobectomy or removal of bone flap)
CMR , Cerebral metabolic rate; MAP , mean arterial pressure.
Management of PaCO2
The anesthesiologist and the surgeon should agree on the objectives with respect to Pa co 2 . Induction of hypocapnia was once a routine part of the management of intracranial neurosurgical procedures. The rationale is principally that the concomitant reduction in CBF (see Chapter 11 , Fig. 11.9) and CBV will result in a reduction in ICP, or “brain relaxation.” The rationale is valid. However, two considerations should influence the clinician’s use of hyperventilation. First, the vasoconstrictive effect of hypocapnia can cause ischemia in certain situations. Second, the CBF-lowering and ICP-lowering effect is not sustained for prolonged time periods.
Hypocapnia-Induced Cerebral Ischemia
A normal brain is unlikely to be damaged by the typical clinical use of hyperventilation. However, this may not be the case in certain pathologic conditions.
Available data indicate that in normal subjects, ischemia will not occur at a Pa CO 2 greater than 20 mm Hg. However, in one investigation, electroencephalogram (EEG) abnormalities and paresthesia occurred in volunteers hyperventilating to Pa CO 2 values less than 20 mm Hg, and these effects were reversed by hyperbaric oxygenation, suggesting that they may truly have been caused by ischemia. Accordingly, given that a Pa CO 2 of less than 20 to 25 mm Hg offers very little additional benefit in terms of improvement in intracranial compliance, acute reduction of Pa CO 2 should be no more than 22 to 25 mm Hg in previously normocapnic persons.
Preventing herniation, maintaining ICP less than 20 mm Hg, minimizing retractor pressure, and facilitating surgical access remain priorities that may justify hypocapnia. Yet hyperventilation is potentially deleterious and should not be overused. Hyperventilation can result in ischemia, especially when baseline CBF is low, as is commonly the case in the first 24 hours after injury. An increased frequency of brain regions with very low CBF has been demonstrated in head-injured patients who were acutely hyperventilated. In addition, low levels of jugular venous oxygen saturation (SjvO 2 ) can be increased by reducing the degree of hyperventilation.
The deleterious effect of hyperventilation is difficult to prove. Muizelaar and colleagues performed a study that included a near normocapnic group in which Pa CO 2 was maintained at approximately 35 mm Hg, and a hypocapnic group in which Pa CO 2 was maintained in the vicinity of 25 mm Hg. Outcomes at 3 and 6 months after injury were not different. However, in a subset of patients with the best initial motor scores, outcome was better in the normocapnic group. These patients with good motor scores probably represented a subgroup in which the severity of injury was such that, although they needed tracheal intubation, hyperventilation was not necessarily required for control of ICP and who therefore had little to gain from hyperventilation. Thus, prophylactic hyperventilation seemed inadvisable. That conclusion has been extrapolated far beyond the circumstances of relatively mild TBI.
Hyperventilation should not be an automatic component of every neuroanesthetic. There should be an indication for its institution (usually increased or uncertain ICP or the need to improve conditions in the surgical field, or both). Hyperventilation has the potential to cause an adverse effect and should be withdrawn as the indication for it subsides. The concern regarding the hazards of hypocapnia, which evolved in the context of TBI, has influenced all of neurosurgery. In particular, it is now widely avoided in the management of SAH because of the low CBF state that is known to occur. In addition, brain tissue beneath retractors can have a similarly reduced CBF. However, hyperventilation, used as briefly as possible, is still very much a component of rescue therapy, when herniation is imminent or in progress, or when conditions in the surgical field are too difficult to allow surgery to proceed.
Duration of Hypocapnia-Induced Reduction in Cerebral Blood Flow
The effect of hypocapnia on CBF is not sustained. Fig. 57.6 is a nonquantitative representation of changes in CBF and CSF pH occurring in association with a sustained period of hyperventilation. With the onset of hyperventilation, the pH of both CSF and the brain’s extracellular fluid space increases, and CBF decreases abruptly. However, the cerebral alkalosis is not sustained. By alterations in function of the enzyme carbonic anhydrase, the concentration of bicarbonate in CSF and the brain’s extracellular fluid space is reduced, and with a time course of 8 to 12 hours, the pH of these compartments returns to normal. Simultaneously, CBF returns toward normal levels. The implications are twofold. First, patients should be hyperventilated for only as long as a reduction in brain volume is required. Prolonged, unnecessary hyperventilation can lead to a circumstance wherein subsequent events call for additional maneuvers to reduce the volume of the intracranial contents, and then incremental hyperventilation is not efficacious. If, after adaptation, Pa CO 2 is already in the 23 to 25 mm Hg range, additional hyperventilation may risk pulmonary barotrauma. Second, in a patient who has been hyperventilated for a sustained period (e.g., 2 days in an ICU setting), restoration of Pa CO 2 from values in the vicinity of 25 mm Hg to typical normal values (e.g., 40 mm Hg) should ideally be accomplished slowly. A sudden increase in Pa CO 2 from 25 to 40 mm Hg in a patient who has been chronically hyperventilated will have the same physiologic effect that a rapid change from 40 to 55 mm Hg would have in a previously normocapnic patient.
If hypocapnia has been required as an adjunct to brain relaxation during craniotomy, Pa CO 2 should also be allowed to increase once the retractors are removed (if dural closure requirements permit) to minimize the residual intracranial pneumatocele (see the section on Pneumocephalus).
Management of Arterial Blood Pressure
Acceptable arterial blood pressure limits should similarly be agreed on at the beginning of a neurosurgical procedure. One of the prominent themes of contemporary neurosurgery is that CPP should be maintained at normal or even high-normal levels after acute central nervous system insults and during most intracranial neurosurgical procedures. This concept has evolved from the growing appreciation that CBF is frequently very low in some brain regions after acute neurologic insults, in particular TBI 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. Fig. 57.7 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. In addition, maintenance of arterial pressure is also relevant to brain compressed under retractors because the effective perfusion pressure is lowered by increased local tissue pressure.
Although the only supportive data are anecdotal, we believe that an aggressive attitude toward arterial blood pressure support should also be given to patients who have sustained a recent spinal cord injury (SCI). This also applies to a spinal cord that is under compression, at risk for compression or vascular compromise because of a disease process (most commonly cervical spinal stenosis with or without ossification of the posterior longitudinal ligament) or an intended surgical procedure, and to those patients undergoing surgery involving retraction of the spinal cord. We believe that arterial blood pressure during anesthesia in these patients should be maintained as closely as possible to, and certainly within, 10% of average awake values.
The administration of steroids for the purpose of reducing or limiting the formation of edema has a well-established place in neurosurgery. The efficacy of steroids in reducing edema associated with tumors and radiation-induced necrosis is well confirmed, but not the edema associated with any other intracranial pathology. Although the time course of this effect is relatively rapid, it is too slow for the management of acute intraoperative events. However, administration beginning 48 hours before an elective surgical procedure has the potential to reduce edema formation and improve the clinical condition by the time of craniotomy. Although clinical improvement occurs within 24 hours, a reduction in ICP may not occur for 48 to 72 hours after the initiation of therapy. Steroids somehow improve the viscoelastic properties of the intracranial space before a reduction in edema occurs, although the mechanism remains undefined. The practice of administering steroids to patients with TBI has been abandoned as a result of controlled trials that demonstrated either no benefit or deleterious effects.
Osmotherapy and Diuretics
Hyperosmolar agents and diuretics are used widely in neurosurgery and neurocritical care to reduce the volume of the brain’s intracellular and extracellular fluid compartments. Both osmotic and loop diuretics have been used. Although loop diuretics can be effective, hyperosmolar agents are more widely used.
Mannitol is used most commonly intraoperatively because of its long history of rapid and effective reduction of brain volume. The doses vary from 0.25 g/kg to 100 g, with 1.0 g/kg the most common dose. A systematic study in TBI demonstrated that an equivalent initial ICP-reducing effect can be achieved with 0.25 g/kg, although the duration of effect is reduced compared to larger doses. More recent studies reported better surgical brain relaxation scores with higher doses (1-1.5 g/kg) of mannitol compared to a dose of 0.25 g/kg. Mannitol should be administered by infusion (e.g., over 10-15 minutes). Sudden exposure of the cerebral circulation to extreme hyperosmolarity can have a vasodilatory effect, which can produce brain engorgement and increased ICP, both of which do not occur with slower administration.
Mannitol enters the brain and, over a reasonably short time course, appears in the CSF space. 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. Most clinicians nonetheless find it to be a mainstay of ICP management. There is the concern that it will only be effective when some degree of blood-brain barrier (BBB) integrity is preserved in a significant portion of the brain. Clinicians respond to this concern by making empiric use of this agent; that is, if it is effective in reducing ICP or improving conditions in the surgical field, repeated doses are administered. The use of hyperosmolar agents is theoretically limited by an upper acceptable osmolarity limit of approximately 320 mOsm/L (although the data supporting the validity of that limit are soft ). However, in life-threatening situations, the use is frequently empiric, and incremental doses (e.g., 12.5 g of mannitol) are administered until a clinical response is no longer observed.
In the critical care environment, the use of hypertonic saline (HTS) in place of mannitol is increasing. Although the initial ICP effects of equiosmolar doses of mannitol and HTS are very similar, HTS may have some advantages in the ICU, where repeated administration makes the adverse effects (e.g., diuresis, renal injury) more likely to have clinical significance. In addition, there are anecdotal reports of HTS being effective in patients who were refractory to mannitol. Although there is enthusiasm for HTS, supporting data are limited. Furthermore, because of the variations in HTS concentrations (3%, 7.5%, 15%, 23.4%) and osmolar loads in the various studies, it is difficult to make specific recommendations.
The combination of a loop diuretic (usually furosemide) and an osmotic diuretic is sometimes used. The superficial rationale is that mannitol establishes an osmotic gradient that draws fluid out of brain parenchyma and that the furosemide, by hastening excretion of water from the intravascular space, facilitates the maintenance of that gradient. A second mechanism may add additional justification for the practice of combining the two diuretics. Neurons and glia have homeostatic mechanisms to ensure regulation 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 , which serve to minimize the gradient between the internal and external environments. One of those idiogenic osmoles is chloride. Loop diuretics inhibit the chloride channel through which this ion must pass and thereby retard the normal volume-restoring mechanism. These diuretic combinations may cause hypovolemia and electrolyte disturbances.
The normal volume regulatory mechanisms of neurons and glia may also 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 possible, the rebound may in fact 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 osmolarity decreases rapidly toward normal levels. Rebound cerebral swelling can certainly occur after an episode of extreme increase in blood glucose concentration. The use of HTS rather than mannitol will not obviate this phenomenon.
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 TBI and SAH. Cortical incisions and brain surface irritation by retractors may similarly be potential foci. Given the relatively benign nature of contemporary anticonvulsants (e.g., levetiracetam), routine administration to patients undergoing most supratentorial craniotomies seems appropriate in the absence of a contraindication. There is no necessity for rapid administration because the intention is to prevent seizures during the postoperative period.
The intended surgical position and the necessary positioning aids should be agreed upon at the outset. The commonly used positions and positioning aids and supports are listed in Box 57.5 (see Chapter 34 ).
Lateral (park bench)
Pin (“Mayfield”) head holder
Radiolucent pin head holder
Horseshoe head rest
Foam head support (e.g., Voss, O.S.I., Prone-View)
Vacuum mattress (“bean bag”)
Andrews (“hinder binder”)-type frame
Relton-Hall (four-poster) frame
The 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 complications in neurosurgical patients, precautions including graduated compression stockings and sequential compression devices are warranted. For cranial procedures, some component of head-up posturing (e.g., 15-20 degrees) is used to ensure optimal venous drainage. The conspicuous exception occurs with evacuation of a chronic subdural hemorrhage, after which patients are usually nursed flat to discourage reaccumulation of fluid. Patients are occasionally also maintained flat after CSF shunting to avoid overly rapid collapse of the ventricles.
The 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 longue (lawn chair) position (hip flexion, pillows under the knees, slight reverse Trendelenburg). This orientation, in addition to promoting cerebral venous drainage, decreases back strain.
The semilateral position, also known as the Jannetta position, named 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. Again, extreme head rotation, sufficient to cause compression of the contralateral jugular vein by the chin, should be avoided.
The 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 vertebral and basilar arteries. An axillary roll is important for preventing brachial plexus injury.
The prone position is used for spinal cord, occipital lobe, craniosynostosis, and posterior fossa procedures. For cervical spine and posterior fossa procedures, the final position commonly entails neck flexion, reverse Trendelenburg, and elevation of the legs. This orientation serves to bring the surgical field to a horizontal position. There should be a plan for detaching and reattaching monitors in an orderly manner to prevent an excessive monitoring window. Awake tracheal intubation and prone positioning may be warranted in patients with an unstable cervical spine in whom an unchanged neurologic status should be confirmed before induction of anesthesia in the final surgical position. This approach is also sometimes performed in obese patients.
The head can be secured in a pin head holder (applied before the turn) or positioned on a disposable foam head rest or, less frequently, a horseshoe head rest. A complication of the prone position, which requires constant attention, is retinal ischemia and blindness caused by orbital compression causing central retinal vessel occlusion. It must be intermittently confirmed (e.g., every 15 minutes) and after any surgery-related head or neck movement that pressure has not come to bear on the eye. However, not all postoperative vision loss (POVL) is a result of direct orbital compression. Ischemic optic neuropathy actually appears to be a more frequent cause of POVL than pressure-causing occlusion of central retinal vessels. The cause-and-effect relationships associated with ischemic optic neuropathy are uncertain, but low arterial pressure, low hematocrit level, lengthy surgical procedures, and large intravascular volume fluid administration are statistically associated with the phenomenon .
Direct pressure can also result in various degrees of pressure necrosis of the forehead, maxillae, and chin, especially with prolonged spinal procedures. Pressure should be distributed as evenly as possible over facial structures. Other pressure points to check include the axillae, breasts, iliac crests, femoral canals, genitalia, knees, and heels. Traction on the brachial plexus must be avoided and can usually be accomplished by not exceeding a “90-90” position (arms abducted not >90 degrees; elbows extended not >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 antisialagogue (e.g., glycopyrrolate) and an adhesive (e.g., benzoin) may help reduce loosening of the 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 cava return diverts blood to the epidural plexus and increases the potential for bleeding during spinal surgery. Minimizing vena cava pressure is an objective of all spinal surgery frames and is accomplished effectively by the Wilson, Andrews, and Jackson variants. However, this does introduce a risk of air embolism, although severe clinical occurrences have been very infrequent.
Attention should be paid to preventing injury to the tongue in the prone position. With both cervical and posterior fossa procedures, it is frequently necessary to flex the neck substantially to facilitate surgical access. This reduces the anterior-posterior dimension of the oropharynx, and compression ischemia of the base of the tongue (as well as the soft palate and posterior wall of the pharynx) can occur in the presence of foreign bodies (endotracheal tube, esophageal stethoscope, oral airway). The consequence can be macroglossia, caused by accumulation of edema after reperfusion of the ischemic tissue causing airway obstruction of rapid onset after extubation (discussed later). Accordingly, placing unnecessary adjuncts 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 oropharynx.
There have been several reviews of numerous experiences with the sitting position. All concluded that the sitting position can be used with acceptable rates of morbidity and mortality. However, these reports were prepared by groups that perform 50 to 100 or more of these procedures per year, and the hazards of the sitting position may be more frequent for teams who have fewer occasions to use it. The sitting position can be avoided by using one of its alternatives (prone, semilateral, lateral). However, this position will continue to be used because even surgeons who are inclined to use alternative positions may opt for it when access to midline structures (e.g., the quadrigeminal plate, the floor of the fourth ventricle, the pontomedullary junction, and the vermis) is required. Nonetheless, alternative positions for posterior fossa surgery are available and should be considered when contraindications to the sitting position exist.
Achieving the Sitting Position
The properly positioned patient is more commonly in a modified recumbent position as shown in Fig. 57.8 rather than truly sitting. The legs should be kept as high as possible (usually with pillows under the knees) to promote venous return. The head holder should be attached to the back portion of the table (see Fig. 57.8 A ) rather than to the portions under thighs or legs (see Fig. 57.8 B ). This permits lowering of the head and closed chest compressions, 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 level of the external auditory canal. If a manual blood pressure cuff on the arm is used, a correction ∗
∗ A column of blood 32 cm high exerts a pressure of 25 mm Hg.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 discussed in this section. Pneumocephalus is discussed in its own section. Venous air embolism (VAE) and paradoxical air embolism (PAE) are discussed in the section Venous Air Embolism. Several of these hazards are also relevant when cervical spine and posterior fossa procedures are performed in non-sitting positions but occur with greater frequency in the sitting position.
Cardiovascular Effects of the Sitting Position
Hypotension should be avoided. Prepositioning hydration, compressive stockings, and slow, incremental adjustment of table position are appropriate. Intravenous vasopressor administration may be required in some patients. However, in most healthy patients the hemodynamic changes are of a nonthreatening magnitude. In a study of healthy anesthetized adults aged 22 to 64 years old, relatively modest changes were observed. MAP was relatively unaffected, whereas wedge pressure, stroke volume, and cardiac index decreased—the latter by approximately 15%—although there was some variation with the anesthetics used. The combination of an unchanged MAP (which in general requires the use of a light, high sympathetic tone anesthetic) and a reduced cardiac index implies that systemic vascular resistance (SVR) increased. Their calculations and the observations of other investigators reveal significant increases in SVR. For patients in whom an abrupt increase in SVR may be poorly tolerated, the sitting position may represent a physiologic threat and alternative positions should be considered.
During procedures performed in the sitting position, MAP should be transduced at or corrected to head level to provide a meaningful index of CPP. Specifically, CPP (MAP – estimated ICP) should be maintained 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 raised for elderly patients, for those with hypertension or known cerebral vascular disease, or for those 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.
There have been sporadic reports of upper airway obstruction after posterior fossa procedures in which swelling of pharyngeal structures, including the soft palate, posterior pharyngeal wall, and base of the tongue, has been observed. 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 pressure on these structures in the circumstances of lengthy procedures with sustained neck flexion (which is usually required to improve access to posterior structures). It is customary to maintain at least two fingerbreadths between the chin/mandible and the sternum/clavicle to prevent excessive reduction of the anterior-posterior diameter of the oropharynx. Consideration of the macroglossia phenomenon may also be relevant as clinicians contemplate the use of transesophageal echocardiography (TEE) in the neurosurgery suite. The centers that routinely use TEE in neurosurgery mostly use pediatric diameter probes to avoid trauma to pharyngeal and perilaryngeal structures.
The sitting position has been implicated as a cause of rare instances of unexplained postoperative quadriplegia. It has been hypothesized that neck flexion, a common concomitant of the seated position, may result in stretching or compression of the cervical spinal cord. This possibility may represent a relative contraindication to the use of this position in patients with significant degenerative disease of the cervical spine, especially when there is evidence of associated cerebral vascular disease. The arterial blood pressure management implications are mentioned in the preceding section on cardiovascular effects. It may also represent a justification for evoked response monitoring during the positioning phase of a sitting procedure for patients perceived to be at high risk (also see Chapter 39 ).
The issue of pneumocephalus arises most often in connection with posterior fossa craniotomies performed with a head-up posture. During these procedures, air may enter the supratentorial space, much as air enters an inverted pop 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 N 2 O because any N 2 O that enters a trapped gas space augments the volume of that space. In those (probably uncommon) intraoperative circumstances where there is, in fact, a completely closed intracranial gas space, the use of N 2 O may result in an effect comparable with that of an expanding mass lesion. We do not view N 2 O 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.
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 atmosphere, N 2 O should be omitted because of the possibility of contributing to a tension pneumocephalus. Note that the use of N 2 O up to the point of dural closure may actually represent a clinical advantage, as in rabbits the gas pocket has been shown to shrink more rapidly because of the presence of N 2 O (because N 2 O diffuses much more quickly than nitrogen). Tension pneumocephalus is often naively viewed as exclusively a function of the use of N 2 O. However, tension pneumocephalus can most certainly occur as a complication of intracranial neurosurgery entirely unrelated to the use of N 2 O. It is one of the causes of delayed awakening or nonawakening after both posterior fossa and supratentorial procedures ( Fig. 57.9 ). It occurs because air enters the cranium when the patient is in a head-up position at a time when the volume of the intracranial contents has been reduced because 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, and extracellular fluid return or reaccumulate and the air pocket becomes an unyielding mass lesion (because of the very slow diffusion of nitrogen). It may cause delayed recovery of consciousness or severe headache. Among supratentorial craniotomies, the largest residual air spaces occur after frontal skull base procedures in which energetic brain relaxation measures are used to facilitate subfrontal access (see Fig. 57.9 ). At the end of these procedures, typically done in a supine/brow-up position, the intracranial dead space cannot be filled with normal saline as is commonly done with smaller craniotomy defects, and there may be a large residual pneumatocele. We doubt that the possible occurrence of this phenomenon represents a contraindication to N 2 O. However, withdrawal of N 2 O may be appropriate at the time of scalp closure. The diagnosis of pneumocephalus is established by a brow-up lateral radiography or, more commonly, a 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, both neurosurgical and nonneurosurgical. Air frequently remains evident on CT scan for more than 7 days after a craniotomy. Pneumocephalus can also develop de novo in the postoperative period in patients who have a residual dural defect and a communication between the nasal sinuses and the intracranial space.
Venous Air Embolism
The incidence of VAE varies according to the procedure, the intraoperative position, and the detection method used. During posterior fossa procedures performed in the sitting position, VAE is detectable by precordial Doppler in approximately 40% of patients and by TEE in as many as 76%. 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 colleagues ), and it is probable but unproven that the average volume of air entrained per event is also smaller. The incidence of VAE is apparently lower with cervical laminectomy (25% using TEE in the sitting position versus 76% for posterior fossa procedures ). 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 parasagittal or falcine meningiomas, that encroach on the posterior half of the sagittal sinus ( Fig. 57.10 ) and craniosynostosis procedures, typically performed in children. Pin sites can also serve as VAE access sites. Accordingly, pin head holders should be removed after the patient has been taken out of significant degrees of the head-up positioning. Spontaneous ventilation (with the attendant intermittent negative intrathoracic pressure) will increase the risk of air entrainment. A 6% incidence of Doppler-detectable VAE was reported in a series of deep-brain stimulator placement procedures performed in spontaneously breathing patients.
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 noncollapsible because of their dural attachments. Air entry may also occur via emissary veins, particularly from suboccipital musculature, via the diploic space of the skull (which can be violated by both the craniotomy and pin fixation) and the cervical epidural veins. It is believed (but not confirmed by systematic study) that the VAE risk associated with cervical laminectomy is more likely 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 is also anecdotal evidence that air under pressure in the ventricles or subdural space can occasionally enter the venous system, perhaps along the normal egress route of the CSF.
Detection of Venous Air Embolism
The monitors used 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 CO 2 monitoring meets these criteria and is the current practice in many institutions. 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, and when good heart tones are heard, maneuvers to confirm adequate placement appear to be unnecessary. The TEE is more sensitive than the precordial Doppler ( Fig. 57.11 ) to VAE and offers the advantage of also identifying right-to-left shunting of air. However, its safety during prolonged use (especially with pronounced neck flexion) is not well established. Expired nitrogen analysis is theoretically attractive. However, the expired nitrogen concentrations involved in anything less than catastrophic VAE are very small and push the available instrumentation to the limits of its sensitivity.
Prevent further air entry
Notify surgeon (flood or pack surgical field)
Lower the head
Treat the intravascular air
Aspirate right heart catheter
Discontinue N 2 O
Fi O 2 : 1.0
Which Patients Should Have a Right Heart Catheter?
All patients who undergo sitting posterior fossa procedures should have a right heart catheter placed. Although life-threatening VAE is relatively uncommon, a catheter permits immediate evacuation of an air-filled heart. With the nonsitting positions, it is frequently appropriate, after a documented discussion with the surgeon, to omit the right heart catheter. The perceived risks of VAE associated with the intended procedure and the patient’s physiologic reserve are the variables that contribute to the decision. Microvascular decompression of the fifth or seventh cranial nerves are examples of procedures for which the right heart catheter is usually omitted. The essentially horizontal semilateral position and the very limited retromastoid craniectomy that is required have resulted (at our institution) in a very low incidence of Doppler-detectable VAE. One should know the local surgical practices, particularly with respect to the degree of head-up posture, before deciding to omit a right atrial catheter. With regard to the Jannetta 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 limited number of patients, high ICP may make the head-down posture undesirable. In others, unfavorable anatomy with an increased likelihood of a difficult cannulation and hematoma formation may also encourage the use of alternate access sites.
Positioning the Right Heart Catheter
The investigation by Bunegin and colleagues suggested that a multiorificed catheter should be located with the tip 2 cm below the superior vena caval-atrial junction and a single-orificed catheter 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. Confirmation of right heart placement can be accomplished by (1) radiography, (2) intravascular electrocardiography (ECG), or (3) TEE. Although there is no literature to support the practice, with catheter access via the right internal jugular vein, a measured placement to the level of the second or third right intercostal space should suffice when the catheter passes readily. The intravascular electrocardiography technique makes use of the fact that an ECG “electrode” placed in the middle of the right atrium will initially “see” an increasing positivity as the developing P-wave vector approaches it ( Fig. 57.13 ), and then an increasing negativity as the wave of atrial depolarization passes and moves away from it. The resultant biphasic P wave is characteristic of an intraatrial electrode position. The technique requires that the central venous pressure (CVP) catheter become an exploring ECG electrode. This is accomplished by filling the catheter with an electrolyte solution (bicarbonate 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 will be observed at various intravascular locations are shown in Fig. 57.13 . To minimize the microshock hazard, a battery-operated ECG unit is preferable, and any unnecessary electrical apparatus should be detached from the patient during catheter placement.
Paradoxical Air Embolism
The possibility of the passage of air across the interatrial septum via a patent foramen ovale (PFO), which is known to be present in approximately 25% of adults, is a concern. The risk is major cerebral and coronary morbidity. However, the precise definition of the morbidity that can actually be attributed to PAE is not clear. Although the minimal pressure required to open a probe PFO is not known with certainty, the necessary gradient may be as much as 5 mm Hg. In a clinical investigation, Mammoto and colleagues observed that PAE occurred only in the context of major air embolic events, suggesting that significant increases in right heart pressures are an important predisposing 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 positive end-expiratory pressure (PEEP) increases the incidence of a positive RAP to pulmonary wedge pressure gradient and generous fluid administration (e.g., 2800 mL/patient vs. 1220 mL/control patient ) reduces it. As a result, the use of PEEP, which was once advocated as a means of preventing air entrainment, was abandoned. Subsequently, the practice of more generous fluid administration for patients undergoing posterior fossa procedures evolved. However, 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.
Some centers have advocated performing bubble studies preoperatively with echocardiography or transcranial Doppler (TCD), or intraoperatively using TEE prior to positioning to identify patients with a PFO with a view to using alternatives to the sitting position in this subpopulation. Some centers thereafter advocate the use of TEE to identify paradoxical embolization intraoperatively. However, none of these practices has become a community-wide standard of care. Furthermore, because the morbid events attributable to PAE have been relatively infrequent, surgeons who are convinced that the sitting position is optimal for a given procedure are loath to be dissuaded 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 Air
Air can sometimes traverse the pulmonary vascular bed to reach the systemic circulation. Transpulmonary passage is more likely to occur when large volumes of air are presented to the pulmonary vascular filter. In addition, pulmonary vasodilators, including volatile anesthetics, may decrease the threshold for transpulmonary passage. The magnitude of differences among anesthetics does not appear to mandate any related “tailoring” of anesthetic techniques. However, N 2 O should be discontinued promptly after even apparently minor VAE events because of the possibility that air may reach the left-sided circulation either via a PFO or the pulmonary vascular bed.
Box 57.6 presents an approach for responding to an acute VAE event. It includes raising venous pressure by direct compression of the jugular veins. PEEP and the Valsalva maneuver were once advocated. However, both PEEP and the release of a Valsalva maneuver increase the risk of PAE, and the relative superiority of jugular venous compression in raising cerebral venous pressures has been confirmed. Furthermore, 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 recommended 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 will remain in the right atrium, where it will not contribute to an air lock in the right ventricle and where it will remain amenable 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.
Nitrous oxide diffuses into air bubbles trapped in the vascular tree and, accordingly, N 2 O 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 N 2 O after the occurrence of VAE. When major VAE occurs, no matter how the RAP-LAP gradient was manipulated before the event, RAP increases abruptly with respect to LAP, and major VAE results in an acutely increased risk of PAE in patients with a PFO. Should N 2 O be used in patients at risk for VAE? Some clinicians may decide to simply avoid it. However, N 2 O can be used with the knowledge that it neither increases the incidence of VAE nor aggravates the hemodynamic response to VAE provided that it is eliminated when VAE occurs.
Neurologic monitoring techniques are discussed in Chapter 39 . Invasive monitoring is frequently appropriate in neurosurgery. Some of the numerous indications for an arterial catheter are listed in Box 57.7 .
Elevated intracranial pressure
Ischemia or incipient ischemia of neural tissue
Recent subarachnoid hemorrhage
Recent head injury
Recent spinal cord injury
Intended or possible temporary vessel occlusion
Spinal cord injury (spinal shock)
Possible barbiturate coma
Possibility of induced hypotension
Possibility of induced hypertension
Anticipated or potential major blood loss
Tumors involving or adjacent to major venous sinuses
Extensive craniosynostosis procedures
Anticipated light anesthesia without paralysis
Brainstem manipulation, compression, dissection
Anticipated CN manipulation (especially CN V)
Advantageous for postoperative intensive care
Incidental cardiac disease
CN, Cranial nerve.
Patients with increased ICP may be intolerant of the vascular engorgement associated with sudden hypertension occurring 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 depth of anesthesia monitor and as an early neurologic injury warning system. Much of the brain is insensate. As a consequence, the intradural portion of many neurosurgical procedures is not very stimulating and, to achieve circulatory stability, relatively light anesthesia is often necessary. There should be constant attention to 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 motor-evoked potential monitoring or electromyographic recording from facial muscles to monitor cranial nerve integrity. Blood pressure responses may reveal imminent arousal; they may also serve to warn a surgeon of excessive or unrecognized irritation, traction, or compression of neurologic tissue. 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 VAE. In the absence of VAE risk and in the presence of good peripheral venous access, we rarely place right heart catheters for neurosurgical procedures. Antecedent cardiac disease may justify a pulmonary arterial catheter. The use of the precordial Doppler is also described in the section VAE.
Intravenous Fluid Management
The general principles of fluid management for neurosurgical anesthesia are (1) maintain normovolemia and (2) avoid reduction of serum osmolarity. The first principle is a derivative of the concept presented in the section Management of Arterial Blood Pressure, which is that it is generally ideal to maintain a normal MAP in patients undergoing most neurosurgical procedures and neurosurgical critical care. Maintaining normovolemia is simply one element of maintaining a normal MAP. The second principle is a derivative of the observation that lowering serum osmolarity results in edema of both normal and abnormal brain. 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) lowers serum osmolarity if the amount of free water administered is in excess of that required to maintain ongoing free water loss. Normal saline and balanced salt solutions 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 large volumes can cause hyperchloremic metabolic acidosis. The physiologic significance of this acidosis, which involves the extracellular but not the intracellular fluid space, is unclear. At a minimum, it has the potential to confuse the diagnostic picture when acidosis is present. Comparisons between normal saline and balanced crystalloid solutions in the setting of cardiac surgery and critically ill intensive care patients did not reveal any adverse events (acute kidney injury, mortality, length of hospital stay) attributable to administration of normal saline. Nonetheless, to avoid hyperchloremic metabolic acidosis, many clinicians use lactated Ringer solution. Although lactated Ringer solution (273 mOsm/L) is in theory not ideal for replacement of blood and third-space loss or insensible losses, it serves as an entirely reasonable compromise for meeting both needs simultaneously and is very suitable in most instances. It is a hypoosmolar fluid, and in a healthy experimental animal, it is possible to reduce serum osmolarity and produce cerebral edema with a large volume of lactated Ringer solution. In the setting of large-volume fluid administration (e.g., significant blood loss, multiple trauma), it is the authors’ practice to alternate, liter by liter, lactated Ringer solution and normal saline. Alternatively, Plasma-Lyte (Baxter International Inc.; Deerfield, IL), a buffered crystalloid solution (pH 7.4) with physiochemical properties similar to plasma, may be considered, if available. Plasma-Lyte is considered isotonic with a calculated in vivo osmolality range of approximately 270 to 294 mOsmol/kg (depending on the manufacturing country). Although there may be advantages to the use of a physiologically balanced solution such as Plasma-Lyte, there remains insufficient clinical evidence to advocate for one fluid over another at the present time.
The crystalloid versus colloid discussion is a recurrent one. It arises most commonly in the context of the patient with TBI. Although views differ, there has in fact been only a single demonstration that the reduction of colloid oncotic pressure (COP) in the absence of a change of osmolarity can actually contribute to an augmentation of cerebral edema in the setting of experimental head injury. The transcapillary membrane pressure gradients that can be produced by reduction of COP are in fact very small by comparison of those created by changes in serum osmolarity. Nonetheless, it appears that those small gradients, probably in the setting of an experimental BBB injury of intermediate severity, have the potential to augment edema. A fluid administration pattern should be selected that, in addition to maintaining normal serum osmolarity, prevents substantial reductions in COP. For most elective craniotomies, which entail only modest fluid administration, this does not require the administration of colloid solutions. However, in situations requiring substantial volume administration (e.g., multiple trauma, aneurysm rupture, cerebral venous sinus laceration, filling pressure support during barbiturate coma), a combination of isotonic crystalloid and colloid may be appropriate.
Which Colloid Solutions Should Be Used?
Colloid administration has created increasing concern about not only its efficacy but also its safety. Based on empirical local experience, we view albumin to be a reasonable choice. However, there are conflicting opinions and cross-currents in the literature. An analysis of the subset of patients in the SAFE (Saline vs. Albumin Fluid Evaluation) trial with severe TBI (Glasgow Coma Scale [GCS] score 3-8) revealed increased mortality among those who received albumin. However, there are several reasons to be suspicious of that conclusion. First, SAFE trial patients were not originally randomized on the basis of TBI characteristics and, by chance, there were imbalances in TBI-related characteristics that appear to have placed the albumin group at greater risk. Second, the 4% albumin solution used was hypoosmolar (274 mOsm/L) and might have been expected to aggravate edema. Furthermore, there is no compelling physiologic explanation for an albumin-specific hazard. The formation of cerebral edema that is more difficult to clear is an inevitable suspicion. However, if valid, that should be a class effect relevant to all colloids (including fresh frozen plasma and starches) rather than being albumin specific. Furthermore, albumin has been used in TBI by others with no evidence of adverse effects. In contrast to alleged adverse effects in the context of TBI, there are potential beneficial effects in SAH. The ALIAS phase III clinical trial evaluated the use of albumin in acute stroke patients. Although albumin administration was associated with increased rate of symptomatic intracranial hemorrhage (ICH) and congestive heart failure (CHF), no negative impact was detected in the primary outcome measure—the rate of favorable neurologic outcome at 90 days. At best, the existing literature may justify consideration of limiting albumin volumes in patients with severe head injury. The indications and concerns for colloids, and especially albumin administration, have been recently expressed (see Chapter 47 ).
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 both platelets and the factor VIII complex. The coagulation effects are proportional to the average molecular weight and the hydroxyethyl group substitution ratio of the starch preparation. There have been several reported instances of bleeding in neurosurgical patients that were attributed to hydroxylethyl starch administration. However, all of those have involved circumstances in which the manufacturer’s recommended dosage limit was exceeded or in which the starch was administered up to the recommended limit on successive days, probably resulting in an accumulation effect. The latitudes are wider with the subsequent availability of small molecule/lower substitution ratio preparations. These preparations have a record of safety when used in the operating room in general and have been administered uneventfully to patients with severe TBI. The decision about whether to use these products is frequently a matter of local practice. Although hydroxylethyl starch solutions can be used in neuroanesthesia, clinicians 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. Recent concern about adverse effects on renal function in patients who have received starches in critical care situations have made some reluctant to use these compounds in any setting. The dextran-containing solutions are generally avoided because of their effects on platelet function.
There is longstanding interest in the use of hypertonic fluids for the resuscitation of polytrauma victims in general, and of patients with TBI in particular. However, there has yet to be a scientifically convincing demonstration of outcome improvement associated with hypertonic solution administration.
There is a widespread notion that increased plasma glucose aggravates a cerebral ischemic insult. This may be true for an acute ischemic event in a previously normal brain, but that should not be extrapolated to the idea that all “neuro patients” should be submitted to very tight glycemic control. The potential benefits of a lower plasma glucose concentration in the event of an acute ischemic episode (which have not been well confirmed in humans) should be outweighed by the very clear demonstrations that the injured brain (e.g., TBI, SAH) becomes “hypoglycemic” and suffers metabolic distress at plasma glucose levels that are satisfactory for a normal brain. This may be because injury can produce a state of hyperglycolysis. Although severe hyperglycemia should be treated to reduce infection rates, patients with acute injuries (e.g., TBI, SAH) should not be submitted to very tight control. As one reviewer said, “extra sweetness [is] required” by the injured brain. The authors’ intraoperative intervention threshold is 250 mg/dL (14 mmol/L), the objective being to reduce plasma glucose to less than 200 mg/dL (11 mmol/L). One published guideline recommends an ICU objective of less than 180 mg/dL (10 mmol/L) in patients with cerebral injuries but cautions that plasma glucose not be allowed to decrease to less than 100 mg/dL (5 mmol/L). The NICE-Sugar study’s control group range of 144 to 180 mg/dL (7.8-10 mmol/L) is probably also a reasonable target. However, control should only be undertaken when processes to prevent hypoglycemia are firmly in place, and the lower the targets, the more comprehensive the hypoglycemia prevention processes must be.
The effects of hypothermia on cerebral physiology and its potential cerebral protective mechanisms are presented in Chapter 11 . There have been numerous laboratory demonstrations on the efficacy of mild hypothermia (32°C-34°C) in reducing the neurologic injury occurring after standardized cerebral and spinal cord ischemic insults. On that basis, the use of induced hypothermia in the management of cerebral vascular procedures, in particular aneurysms and sometimes AVMs, became widespread. However, an international multicenter trial of mild hypothermia in 1001 relatively good-grade patients undergoing aneurysm surgery revealed no improvement in neurologic outcome. Thus, the routine use of intraoperative hypothermia has inevitably diminished.
Because ischemia is recognized to make a post-insult contribution to neuronal injury after TBI, hypothermia was also studied in laboratory models of TBI. Hypothermia was effective and resulted in a prospective multicenter trial in which hypothermia (33°C) was induced within 8 hours of injury and was maintained for 48 hours. No outcome benefit was evident. Post hoc subgroup analysis indicated that patients younger than 45 years old 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 second trial in which more rapid induction of hypothermia was accomplished (35°C by 2.6 hours, 33°C by 4.4 hours) was undertaken. However, the results were similarly negative. Hypothermia has also been evaluated as a neuroprotective strategy in pediatric TBI. The largest randomized controlled trial (RCT) failed to demonstrate improved outcome at 6 months and in fact, demonstrated a trend toward worse outcomes in the hypothermia group.
Based on a lack of demonstrated efficacy in humans, routine use of hypothermia in neurosurgery cannot be advocated in a standard textbook. The decision to use it, usually in the context of aneurysm surgery, is local. The authors continue to use mild hypothermia selectively, most commonly in patients perceived to be at an especially high risk of intraoperative ischemia. If hypothermia is used, cardiac dysrhythmia and coagulation dysfunction can occur if body temperatures become too low. Patients should be rewarmed adequately before emergence to avoid shivering, hypertension, or delayed awakening.
By contrast with clinical neurosurgery, the use of hypothermia after cardiac arrest is now practiced widely. Two multicenter trials demonstrated improved neurologic outcome among survivors of witnessed cardiac arrest cooled to 32 to 34°C within 4 hours and maintained at that temperature for 12 to 24 hours. A subsequent randomized trial reported similar outcomes in patients treated with targeted temperature management at either 33°C or 36°C. Widespread clinical application of targeted temperature management has been advocated by an international task force and other groups.
Although mild hypothermia is perceived to convey the hazard of coagulation dysfunction and dysrhythmia, neither has been evident in elective neurosurgery in the temperature ranges typically used (32°C-34°C). The issue of where body temperature should be recorded to best reflect brain temperature has been addressed. It appears that esophageal, tympanic membrane, pulmonary arterial, and jugular bulb temperature are all very similar and provide a reasonable reflection of deep brain temperature, whereas bladder temperature does not. During craniotomies, superficial layers of cortex may be substantially cooler than deep brain and central temperatures.
Emergence from Anesthesia
Most practitioners of neuroanesthesia feel that there is a premium on a smooth emergence—that is, one free of coughing, straining, and arterial hypertension. The avoidance of arterial hypertension is desired because arterial hypertension can contribute to intracranial bleeding and increased edema formation. In the face of poor cerebral autoregulation, hypertension also has the potential, through vascular engorgement, to contribute to an increase in ICP. Much of the concern with coughing and straining has a similar basis. The sudden increases in intrathoracic pressure are transmitted to both arteries and veins, producing transient increases in both cerebral arterial and venous pressure, with the same potential consequences: edema formation, bleeding, and elevation of ICP. Coughing is a specific concern with certain individual procedures. In the circumstances of transsphenoidal pituitary surgery in which a surgeon has opened, and subsequently taken pains to close, the arachnoid membrane to prevent CSF leakage, there is a belief that coughing has the potential to disrupt this closure because of the sudden and substantial increases in CSF pressure. Opening a pathway from the intracranial space to the nasal cavity conveys a substantial risk of postoperative meningitis. In other procedures, notably those that have violated the floor of the anterior fossa, air can be driven into the cranium and, in the event of a flap-valve mechanism, cause a tension pneumocephalus. This latter event can only happen 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 associated with emergences that are not considered smooth. Two retrospective studies have revealed that increased postoperative arterial blood pressure was associated with intracerebral bleeding after craniotomy. However, whether hypertension occurring at emergence causes postoperative intracerebral bleeding is not clear. Also, the relationship between hypertensive transients at emergence and edema formation is unconfirmed. In anesthetized animals, sudden and very substantial increases in arterial pressure can result in a breach of the BBB with extravasation of tracers. However, there are no data to confirm that the pressure transients associated with the typical coughing episode or common emergence are in fact 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 the management of systemic hypertension during the last stages of a craniotomy is the expectant and/or reactive administration of lidocaine and vasoactive agents, most commonly labetalol and esmolol. Other drugs, including hydralazine, enalapril, diltiazem, nicardipine, and clevidipine have been used to good effect. Administration of dexmedetomidine during the procedure or just prior to its conclusion also reduces the hypertensive response to emergence and hypertension in the postanesthesia care unit.
There are also many approaches to the prevention of coughing and straining. The authors encourage trainees to include in their anesthetic technique as much narcotic as is consistent with spontaneous ventilation at the conclusion of the procedure, as opioids are antitussive and depress airway reflexes. Patients may also emerge more rapidly and smoothly when the last inhaled anesthetic to be withdrawn is nitrous oxide. This can be supplemented, if necessary, with propofol by either bolus increments or infusion at rates in the range of 12.5 to 25 μg/kg/min.
An additional principle relevant to the emergence from neurosurgical procedures 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. Many a good anesthetic for neurosurgery has been spoiled by severe coughing and straining that occurs in association with endotracheal tube motion during the application of the head dressing. Another nuance of our practice has been to withhold administration of neuromuscular antagonists as long as possible in the later stages of the procedure. The administration of lidocaine is another apparently effective technique for reducing airway responsiveness and the likelihood of coughing/straining as the depth of anesthesia is reduced in anticipation of emergence. We commonly administer 1.5 mg/kg of intravenous lidocaine just before the head movement associated with applying the dressing.
Because of the premium placed on minimizing coughing and straining and hypertension, there may be a temptation to extubate from the trachea before complete recovery of consciousness. This may be acceptable in some circumstances. However, it should be undertaken with caution when the circumstances of the surgical procedure make it possible that neurologic events have occurred that will delay recovery of consciousness, or when there may be cranial nerve dysfunction. In these circumstances, it would, in general, be best to wait until the likelihood of the patient’s recovery of consciousness is confirmed or until patient cooperation and airway reflexes are likely to have recovered.
Many of the considerations relevant to individual neurosurgical procedures are generic ones that have already been presented in the preceding section on Recurrent Issues in Neuroanesthesia. The descriptions that follow will highlight only procedure-specific issues ( Box 57.8 ).
Aneurysms and arteriovenous malformations
Traumatic brain injury
Posterior fossa procedures
Awake craniotomy/seizure surgery
Cerebrospinal fluid shunting procedures
Craniotomies for excision or biopsy, or both, of supratentorial tumors are among the most common neurosurgical procedures. Gliomas and meningiomas are among the most frequent tumors. The relevant preoperative considerations include the patient’s ICP status, and the location and size of the tumor. Location and size of the tumor give the anesthesiologist an indication of the surgical position, the potential for blood loss, and will sometimes reveal a risk of air embolism. VAE is infrequent for the majority of supratentorial tumors. However, lesions (usually convexity meningiomas) that encroach upon the sagittal sinus may convey a substantial risk of VAE. Full VAE precautions, including a right atrial catheter, are usually reserved for only the 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 (see Fig. 57.18 ). Irritation of the hypothalamus can elicit sympathetic responses including hypertension. Damage to the hypothalamus can result in a spectrum of physiologic disturbances, notably water balance. Diabetes insipidus is the most likely, although the cerebral salt-wasting syndrome can infrequently occur. The various disturbances of water balance typically have a delayed onset, beginning 12 to 48 hours postoperatively, rather than in the operating room. Postoperative temperature homeostasis may also be disturbed.
Patients who undergo a craniotomy involving a subfrontal approach sometimes manifest a disturbance of consciousness in the immediate postoperative period. Retraction and irritation of the inferior surfaces of the frontal lobes can result in a patient who exhibits either delayed emergence or some degree of disinhibition, or both. The phenomenon is more likely to be evident when there has been bilateral frontal lobe retraction. The anesthetic implication is that the clinician should be more inclined to confirm return of consciousness before extubating the patient rather than to extubate expectantly. A further implication taken by these authors (though not confirmed by any systematic study) is that a less liberal use of intravenous anesthetic drugs (e.g., fentanyl, propofol infusion) may be appropriate when there is to be bilateral subfrontal retraction. This is based on the rationale that low residual concentrations of these anesthetics that are compatible with reasonable recovery of consciousness in most patients may be less well tolerated in this population. Subfrontal approaches are most commonly used in patients with olfactory groove meningiomas and patients with suprasellar tumors including craniopharyngiomas and pituitary tumors with suprasellar extension.
Patients with a significant tumor-related mass effect, especially if there is tumor-related edema, should receive preoperative steroids. A 48-hour course is ideal (see the previous discussion of steroids), 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 CO 2 retention in patients whose intracranial compliance is already abnormal, sedative premedication outside of the operating room is usually avoided.
Institutional practices vary; however, we almost invariably place arterial catheters for craniotomies under general anesthesia (GA). Preinduction placement may be appropriate in patients with severe mass effect and little residual compensatory latitude. At a minimum, we achieve intraarterial monitoring before pin placement. It is the period of induction and pinning during which hypertension, with its attendant risks in a patient with impaired compliance and autoregulation, is most likely to occur. Arterial lines also facilitate careful management of blood pressure during emergence. Procedures with a substantial blood loss potential (e.g., tumors encroaching on the sagittal sinus, large vascular tumors) may also justify central venous catheters when peripheral venous access is limited. If not already present for other indications, ICP monitoring is rarely warranted for induction, given our understanding of the potential impact of anesthetics and associated procedures. Once the cranium is open, observation of conditions in the surgical field provides equivalent information.
Management of Anesthesia
The principles governing the choice of anesthetic drugs are presented in the previous section, Control of Intracranial Pressure and Brain Relaxation.
Aneurysms and Arteriovenous Malformations
Contemporary management and current recommendations regarding ruptured intracranial aneurysms call for intervention as early as feasible to reduce the rate of rebleeding. That intervention may entail either operative clipping or an endovascular approach. The latter is discussed in the subsequent section Neurointerventional Procedures.
Early intervention was originally undertaken only in patients in the better neurologic grades—that is, grades I-III and perhaps IV of the World Federation of Neurosurgeons classification ( Table 57.2 ) or grades I-III of the Hunt-Hess classification ( Table 57.3 )—but is now recommended for the majority of patients. If early intervention is not feasible and a surgical approach is intended, surgery may be delayed for 10 to 14 days to be safely beyond the period of maximal vasospasm risk (i.e., days 4-10 post-SAH).
|WFNS Grade||GCS Score||Motor Deficit|
|IV||12-7||Present or absent|
|V||6-3||Present or absent|
|Grade I||Asymptomatic, or minimal headache and slight nuchal rigidity|
|Grade II||Moderate to severe headache, nuchal rigidity, no deficit other than cranial nerve palsy|
|Grade III||Drowsiness, confusion, or mild focal deficit|
|Grade IV||Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances|
|Grade V||Deep coma, decerebrate rigidity, moribund appearance|
∗ Serious systemic disease, such as hypertension, diabetes, severe arteriosclerosis, chronic pulmonary disease, and severe vasospasm seen on arteriography, results in placement of the patient in the next less favorable category.
The rationale for early intervention is several-fold. The sooner the aneurysm is clipped or obliterated, the less the likelihood of rebleeding (and rebleeding is the principal cause of death for patients hospitalized after SAH ). Second, the management of the ischemia caused by vasospasm involves fluid resuscitation and induced hypertension. Early occlusion of the aneurysm eliminates the risk of rebleeding associated with this therapy. Prior surgical practices entailed maintaining the patient on bed rest until approximately day 14, when the period of spasm risk had passed. Early aneurysm clipping reduces the period of hospitalization and reduces the incidence of the medical complications (i.e., deep vein thrombosis, atelectasis, pneumonia) associated with a lengthy period of enforced bed rest.
Early intervention makes the surgeon’s task more difficult. The brain in the early post-SAH period is likely to be more edematous than after a 2-week delay. Furthermore, some degree of hydrocephalus is very common after blood contaminates the subarachnoid space. In fact, about 9% to 19% of aneurysmal SAH victims eventually require permanent CSF diversion. Early intervention may also enhance the risk of intraoperative aneurysmal rupture because of the lesser period of time for a clot to organize over the site of the initial bleed. All this places a substantial premium on techniques designed to reduce the volume of the intracranial contents (see Control of Intracranial Pressure and Brain Relaxation earlier in this chapter) to facilitate exposure and minimize retraction pressures.
Many patients scheduled for intracranial aneurysm clipping will come directly from the ICU, and elements of their critical care management may influence their immediate preoperative status.
Intravenous 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 that probably occurs as a result of the release of a natriuretic peptide by the brain. Cerebral salt-wasting syndrome is characterized by the triad of hyponatremia, volume contraction, and high urine sodium concentrations (>50 mmol/L), and its occurrence is correlated with the occurrence of symptomatic vasospasm. The distinction between cerebral salt-wasting syndrome and SIADH is important. SIADH, which is characterized by normovolemia or mild hypervolemia, is treated by volume restriction. Cerebral salt-wasting syndrome is associated with a contracted intravascular volume. Fluid restriction and further volume contraction may be especially deleterious in the post-SAH patient and should be avoided. Although the clinical distinction between these two causes of hyponatremia (SIADH and cerebral salt-wasting syndrome) may be difficult, management of both is relatively simple: administration of isotonic and/or hypertonic fluids using intravascular normovolemia and normonatremia as the end point.
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 the hemoglobin that have accumulated around the vessels of the circle of Willis after SAH. A specific mechanism/mediator has not been identified. Calcium channels are thought to be involved, and there is also suspicion that the nitric oxide and endothelin systems may be contributory.
When there is a clinical suspicion of vasospasm (typically because of a change in sensorium or new neurologic deficit), surgery is usually deferred and TCD, angiography, or other imaging is performed. Symptomatic vasospasm has historically been treated with “Triple H” therapy (hypervolemia, hypertension, and hemodilution). Current management has shifted toward fluid resuscitation to euvolemia (rather than hypervolemia), hypertension, and sometimes balloon angioplasty or intraarterial vasodilators.
For patients proceeding to surgery, hypotension should be avoided and CPP should usually be maintained intraoperatively at values near the waking normal range. The association of hypotension with poor outcome, and the potential for hypotension to cause or aggravate cerebral ischemia in patients with some degree of vasospasm, is well recognized. This concern should extend even to patients classified as World Federation of Neurosurgeons grade I who may have regions of cerebral ischemia that are subclinical when the patient is normotensive.
In the ICU, the regimens used to treat vasospasm usually involve some combination of fluid resuscitation and blood pressure augmentation. The science behind hypervolemic-hypertensive therapy is soft and the efficacy of neither Triple H therapy nor volume expansion in isolation has been proved by prospective study. The relative importance of the rheologic and blood pressure effects is undefined, although there is evidence for the relevance of blood pressure elevation in isolation. Phenylephrine and dopamine are the most commonly used pressors; exact pressor choice should be primarily governed 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 systolic pressure. However, it has been reported that augmentation of cardiac output with dobutamine, without simultaneous MAP increase, augments CBF in ischemic territories. It is also believed that a hematocrit in the low 30s is optimal for cerebral perfusion, but this is not a therapeutic target that is directly manipulated.
Calcium-channel blockers are an established part of the management of SAH. Administration of nimodipine decreases the incidence of morbidity caused by cerebral ischemia after SAH, although it was not associated with any reduction in the incidence of vasospasm as detected by angiography. Patients presenting to the operating room after SAH should already be receiving nimodipine. Because nimodipine must be administered orally in North America, nicardipine has been evaluated as an intravenous alternative. The multicenter nicardipine trial revealed a reduced incidence of symptomatic vasospasm but no improvement in outcome. As a consequence, nimodipine remains the standard. Calcium-channel blockers (i.e., verapamil, nicardipine, nimodipine ) are also used intraarterially as a primary treatment for medically-refractory vasospasm. Milrinone and papaverine are similarly administered.
Other Pharmacologic Therapies
Several other agents/drug classes have been considered for the prevention of vasospasm and delayed ischemic deficits. None of them is approaching the status of standard therapy. A study of the endothelin antagonist clazosentan revealed improved mortality without improvement in the outcome of survivors. After several small trials suggested a beneficial effect of magnesium, a larger randomized, placebo-controlled trial reported no improvement in outcome among patients in whom magnesium was initiated within 4 days of SAH. Several small trials have examined the post-SAH administration of statins. Meta-analysis revealed only nonsignificant trends toward reduced incidence of delayed cerebral ischemia and death. A subsequent large RCT (STASH) failed to demonstrate either short-term or long-term outcome benefits related to statin administration. The phosphodiesterase inhibitor cilostazol (a platelet inhibitor as well as vasodilator) was reported to reduce symptomatic vasospasm, new cerebral infarctions, and improve outcome following SAH. Although promising, a larger study to confirm the safety and efficacy of cilostazol is anticipated.
Antifibrinolytics have been administered in an attempt to reduce the incidence of rebleeding. Although they accomplish this end, long courses do so at the cost of an increased incidence of ischemic symptoms and hydrocephalus, with an overall adverse effect on outcome. However, early, brief courses of antifibrinolytics that are continued until the aneurysm is secured may have a net favorable effect on outcome.
Subarachnoid Hemorrhage-Associated Myocardial Dysfunction
SAH can result in a largely reversible myocardial “stunning” injury. The severity of the dysfunction correlates best with the severity of the neurologic injury and is sometimes sufficient to require pressor support. The mechanism is uncertain but is thought to be catecholamine mediated. Troponin elevation occurs commonly, though typically reaching levels less than the diagnostic threshold for myocardial infarction. Peak troponin levels correlate with the severity of both neurologic injury and echocardiographic myocardial dysfunction.
ECG abnormalities are common after SAH. In addition to the classic canyon T waves ( Fig. 57.14 ), 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 dysfunction. ECG abnormalities do not herald evolving or impending cardiac disease. Accordingly, when ventricular function is adequate and ECG patterns other than those that are typical of myocardial ischemia are observed, no specific interventions or modifications of patient management are warranted, other than attention to the possibility of dysrhythmias. In particular, an increased Q-T interval (>550 ms) occurs frequently after SAH, especially in patients with more severe SAH, and has been associated with an increased incidence of malignant ventricular rhythms including torsades de pointes.
Important considerations include the following:
Absolute avoidance of acute hypertension with its attendant risk of rerupture.
Achievement of intraoperative brain relaxation to facilitate surgical access to the aneurysm.
Maintenance of a high-normal MAP to prevent critical reduction of CBF in recently insulted and now marginally perfused areas of brain, or in regions critically dependent on collateral pathways.
Preparedness to perform precise manipulations of MAP as the surgeon attempts to clip the aneurysm or to control bleeding from a ruptured aneurysm or during periods of temporary vascular occlusion.
An arterial line is invariably appropriate. A central venous catheter may be appropriate if peripheral access is inadequate.
Any technique that permits proper control of MAP is acceptable. However, in the face of increased ICP or a tight surgical field, an inhaled anesthetic technique may be less suitable. The prevention of paroxysmal hypertension is the only absolute requirement in patients undergoing aneurysm clipping. The poorly organized clot over the aneurysms 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 penetrate 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).
The routine use of induced hypotension has essentially vanished (see previous section Management of Arterial Blood Pressure). Nonetheless, the anesthesiologist should be prepared to reduce blood pressure immediately and precisely if called upon to do so. Preparation of an appropriate hypotensive agent must occur before the episode of bleeding. There are theoretical pros and cons for various hypotensive agents. However, the choice should ultimately be made based on which regimen, in the hands of the individual practitioner, results in the most precise control of MAP. There are rare occasions when the anesthesiologist is asked to control MAP in the range of 40 to 50 mm Hg in the face of 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.
Relative hypertension may be requested during periods of temporary arterial occlusion (see the later section Temporary Clipping) to augment collateral CBF. In addition, after clipping of the aneurysm, some surgeons will 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 has traditionally been used as an adjunct to brain relaxation. However, the practice has been questioned on the basis of the concern that it will aggravate ischemia (see the earlier section Management of PaCO 2 ). It is now generally avoided unless ICP/brain relaxation circumstances demand it.
Lumbar Cerebrospinal Fluid Drainage
CSF drainage has been used to facilitate exposure. However, its use appears to be diminishing because surgeons have appreciated that the same brain-relaxing effect can be achieved by release of CSF from the basal cisterns. If a lumbar CSF drain is placed, it is appropriate to avoid excessive loss of CSF. A sudden reduction in the transmural pressure gradient across the dome of the aneurysm (by sudden reduction of ICP consequent upon substantial CSF drainage) should be avoided because of the theoretical concern that this decompression might encourage rebleeding. Having verified the patency of the drainage system, it is usual to leave it closed until the surgeon is opening the dura. The drain is then opened and allowed to drain freely to floor level. Drainage should be discontinued promptly after final withdrawal of the retractors to allow CSF to reaccumulate and to thereby reduce the size of the potential pneumocephalus.
Some surgeons use mannitol relatively aggressively (e.g., 2 g/kg). In part, it is used to facilitate exposure and reduce retractor pressures, but there is evidence that it may have additional benefits. Specifically, there are data derived in both animals and man indicating that mannitol may have a CBF-enhancing effect in regions of moderate CBF reduction. The mechanism is not defined. Reduction of interstitial tissue pressure around capillaries and/or an alteration of blood rheology have been proposed as contributors. Typically, mannitol administered in a dose of 1 g/kg just before dural opening provides satisfactory brain relaxation. Surgeons who believe in its CBF-enhancing effect may request a second 1 g/kg approximately 15 minutes before an anticipated temporary occlusion.
Many surgeons limit inflow to an aneurysm during application of the permanent clip by placing a temporary clip proximally on the feeding vessel. It is occasionally necessary to trap the aneurysm (i.e., to temporarily occlude the vessel on both sides of the aneurysm) to complete the dissection of the neck and apply the clip. This 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 of the neurologic outcome after temporary occlusion in normothermic, normotensive adults revealed that occlusions of fewer than 14 minutes were invariably tolerated. The likelihood of an ischemic injury increased with longer occlusions and reached 100% with occlusions in excess of 31 minutes. In another institution, the threshold for ischemic injury was 20 minutes of occlusion. An informal 7-minute rule is sometimes applied to individual periods of temporary occlusion. Typically, MAP should be sustained at high-normal levels during periods of occlusion to facilitate collateral CBF.
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 temporary occlusion, and perhaps mild hypothermia are the important brain protection techniques. Specific anesthetic drugs have been promoted as brain protectants, but evidence is limited (see the discussion in Chapter 11 ). There have been no convincing laboratory demonstrations that propofol provides any greater tolerance to a standardized ischemic insult than does anesthesia with a volatile anesthetic. Attempts to demonstrate protection by etomidate in an animal model of focal ischemia actually demonstrated an adverse effect of etomidate. Furthermore, a clinical investigation during aneurysm clipping revealed decreases in brain tissue PO 2 in association with administration of etomidate, which contrasted with the brain PO 2 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. Etomidate probably should not be used because of a lack of sufficient data regarding its efficacy. With respect to the volatile anesthetics, attempts in the laboratory to confirm the once proclaimed protective efficacy of isoflurane have demonstrated that there are no differences among the various volatile anesthetics in terms of their influence on outcome after focal or global ischemia in the laboratory. Nor has there been any demonstration of greater protective efficacy with concentrations of volatile anesthetics sufficient to cause EEG suppression as opposed to more modest (e.g., 1.0 MAC) levels. Nonetheless, these animal investigations suggest that a standardized experimental ischemic insult is better tolerated, relative to the awake state, by animals receiving a volatile anesthetic. In addition, data derived in animals also suggest that there may also be a relative protective advantage to an anesthetic that includes a volatile anesthetic compared with a strict N 2 O-narcotic technique. 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 important anesthetic objectives are precise hemodynamic control and timely wake-up, and those two constraints should dictate the choice of the anesthetic regimen for most aneurysm procedures. Among anesthetics, it is only the barbiturates for which additional protective efficacy has been demonstrated convincingly. Because of their potentially adverse effects on hemodynamics and wake-up, they are not ideal for routine use. They should probably be reserved for situations in which a prolonged 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.
The patient with, or at substantial risk for, vasospasm probably benefits from a minimum hemoglobin greater than that which is commonly accepted in stable ICU patients (i.e., >7 g/dL). The best available information suggests a minimal hemoglobin value of 9 g/dL.
As noted in the previous section Hypothermia, a prospective trial of mild hypothermia in patients undergoing aneurysm surgery revealed no improvement in neurologic outcome. Nonetheless, some neurosurgical teams that were already using mild hypothermia (32°C-34°C) are continuing its use for procedures in which temporary vessel occlusion may occur. The institutions that use the lower temperatures are those in which the team is willing to accept a delay in emergence from anesthesia to achieve sufficient rewarming to avoid the extreme hypertension that can occur when a patient is awakened at low body temperatures.
Evoked responses and EEG have been used for monitoring. EEG monitoring can be used as a guide to management during the period of flow interruption or to guide the administration of CMR-reducing anesthetic agents given before occlusion. At some institutions, the surgeon places an electrode strip 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. In most circumstances, if occlusion is deemed necessary, a temporary occlusion is performed, and the EEG is observed. If the EEG shows significant slowing, the common practice is to raise the MAP and proceed with as brief as possible a period of occlusion or intermittent episodes of temporary occlusion. If the necessity for a sustained period of occlusion seems likely, it may be appropriate to administer barbiturates (discussed earlier) to produce burst suppression. These events are very infrequent (see also Chapter 39 ).
Intraoperative angiography is an increasingly common component of the management of intracranial aneurysm surgery. It does not have substantial implications for the anesthesiologist except with respect to placement of the radiographic equipment.
Special Considerations for Specific Aneurysms
The most common procedures are performed for aneurysms arising in or close to the circle of Willis. The vessels 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; and, less frequently, the posterior cerebral artery. These procedures are relatively 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 proximal to the origin of the posterior communicating artery. A catheter is placed in the excluded segment and put to suction. Blood loss, which is usually minimal, should be monitored.
These procedures are typically performed in the lateral position. The exposure may involve a combined middle and posterior fossa approach, with some attendant, although minor, risk of VAE. Cortical or skin surface EEG monitoring is of less relevance with vertebrobasilar aneurysms. Auditory, somatosensory, and motor-evoked responses have been used to monitor for vascular compromise. As with any other procedure 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.
Vein of Galen Aneurysms
Vein of Galen aneurysms are congenital dural arteriovenous fistulas, usually treated in the neonate using endovascular methods, and share considerations relevant to AVMs. These include anticipation of the possibility of the cerebral dysautoregulation phenomenon and are considered subsequently.
For the majority of intracranial AVMs, the general considerations are similar to those appropriate to aneurysm surgery: avoidance of acute hypertension and the capability to accurately manipulate arterial blood pressure in the event of bleeding. A problem specific to AVMs is the phenomenon of perfusion pressure breakthrough, or cerebral dysautoregulation. It is characterized by an often sudden engorgement and swelling of the brain, sometimes with a relentless cauliflower-like protrusion from the cranium. It tends to occur in the advanced stages of lengthy procedures on large AVMs, or it may be the cause of otherwise unexplained postoperative swelling and hemorrhage. The phenomenon is not entirely understood. An AVM provides a high-volume, low-resistance pathway that chronically diverts blood from adjacent and therefore marginally perfused vascular territories. Perhaps these tissues have long been maximally vasodilated and are incapable of vasoconstricting when exposed to a higher-pressure head after acute obliteration of the AVM. Although this explanation superficially fits the clinical occurrence, experimental data are not entirely consistent with this mechanism. At least some component of the hyperemia is not passive, and neurogenic or paracrine mechanisms may be involved.
The management constraints are essentially the same as those relevant to aneurysm surgery, although the risk of intraoperative rupture is much less. Institutional practices will vary. We do not use induced hypotension unless it is necessitated by bleeding. We reason that the effects on the surrounding brain of devascularizing the AVM would be best appreciated if the devascularization occurs at normal pressures. If refractory brain swelling occurs, tight blood pressure control is essential, and reducing MAP may be of use to control swelling. The latter is based on the notion that CBF through the involved area is pressure-passive and will decrease as MAP is reduced. With severe episodes of swelling, we have used (in addition to hypotension, which we use cautiously because of the associated ischemia risk) hypocapnia, hypothermia, and barbiturates. The latter three techniques probably serve to 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 is also 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 the greatest care because of the concern that the dysautoregulating brain adjacent to the resected AVM will develop edema or hemorrhage if hypertension occurs.
Intubating the Trachea of a Head-Injured Patient
Patients with GCS scores of 7 to 8 ( Table 57.4 ) or less require tracheal intubation and controlled ventilation for ICP or airway control, or both. Patients with less severe TBI may also require intubation because of trauma-related cardiopulmonary dysfunction or, when uncooperative, to facilitate diagnostic procedures. The anesthesiologist, in choosing the intubation technique, may encounter a number of conflicting constraints ( Box 57.9 ). These include: (1) elevated ICP; (2) a full stomach; (3) uncertain cervical spine status; (4) uncertain airway status (e.g., presence of blood, possible laryngotracheal injury, possible skull base fracture); (5) an uncertain volume status; (6) an uncooperative or combative patient; and (7) hypoxemia. The best approach is determined by the relative weight of these various factors along with the degree of urgency. The anesthesiologist must not be 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 priorities than ICP. Do not risk losing the airway or causing severe hypotension for the sake of preventing coughing on the tube or brief hypertension with intubation.
|Best verbal responses|
|Garbled or incomprehensible sounds||2|
|Confused but conversant||4|
|Best motor responses|
|Extension (decerebrate rigidity)||2|
|Abnormal flexion (decorticate rigidity)||3|
Uncertain cervical spine stability
Airway injury (larynx, cricoarytenoid cartilage)
Uncertain volume status
Increased intracranial pressure
The Cervical Spine
The possibility of causing or aggravating an injury to the cervical spine is a relevant concern. Approximately 2% of blunt trauma victims who reach a hospital, and 8% to 10% of TBI victims with GCS scores less than 8, have a fracture of the cervical spine. Those incidences suggest 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 contradictions, several published series have concluded that rapid-sequence induction does not convey significant risk of neurologic injury. However, it is possible that the incidence of intubation-related neurologic injury is underreported. An informal survey indicated that there have been more such events than one can infer from the published literature. Nonetheless, the majority of patients with TBI requiring airway control are intubated using a hypnotic-relaxant-laryngoscopy sequence. In our opinion, the possibility of devastating spinal cord injury may be higher with injuries in the atlanto-occipital region, which are also difficult to identify radiologically, and that the anesthesiologist 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 when the exigencies of the situation do not require an immediate rapid-sequence induction. The nasal route can be considered if the clinical context warrants it, bearing in mind that risk of infection may be increased with skull base fracture and CSF leak. The anesthesiologist should use discretion (e.g., in the presence of an obvious facial injury, the nasal route should be avoided) and be sensitive to unusual resistance in passing the endotracheal tube.
When a hypnotic-relaxant sequence is used (and the exigencies of airway control will frequently demand it), the standard approach includes the use of cricoid pressure and in-line axial stabilization. In-line traction was once 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 intubation with anesthesia and relaxation is reasonable used in-line stabilization with the patient’s occiput held firmly on the backboard, limiting the amount of “sniff” that was feasible ( Fig. 57.15 ). There is no question that in-line stabilization, properly performed, makes laryngoscopy somewhat more difficult; however, it serves to decrease the amount of atlanto-occipital extension necessary to achieve visualization of the glottis. This is probably because performing the laryngoscopy against the assistant’s counterpressure 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 cervical collar in place during laryngoscopy (see Fig. 57.15 ) because it functions as a strut between the shoulder and the occiput and serves to further limit atlanto-occipital extension.