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.

Schematic representation of various herniation pathways.

(1) Sub-falcine, (2) uncal (transtentorial), (3) cerebellar, and (4) transcalvarial.

From Fishman RA. Brain edema. N Engl J Med. 1975;293:706–711.

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.

Computed tomography scan depicting normal (left) and compressed (right) basal cisterns. The basal, or perimesencephalic, cerebrospinal fluid space consists of the interpeduncular cistern (anterior), the ambient cisterns (lateral), and the quadrigeminal cisterns (posterior). In the right panel, the cisterns have been obliterated in a patient with diffuse cerebral swelling (caused by sagittal sinus thrombosis).

Courtesy Ivan Petrovitch, MD.

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.

The intracranial volume-pressure relationship.

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

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.

• 1.
  

  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.

  
  
• 2.
  

  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.

  
  
• 3.
  

  The fluid compartment. This compartment can be addressed with steroids and osmotic/diuretic agents. The use of these agents is discussed later.

  
  
• 4.
  

  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.

The pathophysiology of intracranial hypertension.

The figure depicts the manner in which increases in the volumes of any or all of the four intracranial compartments, blood, cerebrospinal fluid (CSF) , fluid (interstitial or intracellular), and cells, result in intracranial pressure (ICP) increases and eventual neurologic damage. The elements that are most readily under the control of the anesthesiologist are indicated with asterisks (∗) . (Control of CSF volume requires the presence of a ventriculostomy catheter.) BP, Blood pressure; Pa CO _2, partial pressure of carbon dioxide in the arterial blood; PaO ₂ , partial pressure of oxygen in the arterial blood.

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.

The effect of cerebral venous outflow obstruction on intracranial pressure (ICP) in a patient with an intracerebral hematoma.

Bilateral jugular compression was applied briefly to verify the function of a newly placed ventriculostomy. The ICP response illustrates the importance of maintaining unobstructed cerebral venous drainage.

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 .

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 .

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.

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.

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.

Partial pressure of carbon dioxide in the arterial blood (Pa CO ₂ ), cerebral blood flow (CBF) , and cerebrospinal fluid (CSF) pH changes with prolonged hyperventilation. Although the decreased arterial Pa CO ₂ (and the systemic alkalosis) persists for the duration of the period of hyperventilation, the pH of the brain and CBF return toward normal over 8 to 12 hours.

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.

Normal and absent autoregulation curves.

The “absent” curve indicates a pressure-passive condition in which cerebral blood flow (CBF) varies in proportion to cerebral perfusion pressure (CPP). This curve is drawn to indicate subnormal CBF values during normotension, as have been shown to occur immediately after head injury ²⁶ and subarachnoid hemorrhage. ³⁰ The potential for modest hypotension to cause ischemia is apparent. MAP, Mean arterial 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.

Steroids

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.

Anticonvulsants

The general principle is that any acute irritation of the cortical surface has the potential to result in seizures. This includes acute neurologic events such as 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.

Positioning

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 ).

Sitting

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.

The sitting position.

(A) The head-holder support is correctly positioned so that the head can be lowered without the necessity to first detach the head holder. (B) This configuration, with the support attached to the thigh portion of the table, should be avoided.

From Martin JT. Positioning in Anesthesia and Surgery . Philadelphia: Saunders; 1988, with permission.

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.

Macroglossia

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.

Quadriplegia

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 ).

Pneumocephalus

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.

Postoperative computed tomographic scan demonstrating a large pneumocephalus after a subfrontal approach to a suprasellar glioma. Immediately postoperatively, the patient was confused and agitated, and he complained of a severe headache.

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.

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

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.

The relative sensitivity of various monitoring techniques to the occurrence of venous air embolism.

BP , Blood pressure; CO , cardiac output; CVP , central venous pressure; ECG , electrocardiogram; ET-CO ₂ , end-tidal carbon dioxide; PAP , pulmonary artery pressure; Stetho , esophageal stethoscope; T-echo , transesophageal echo; VAE , venous air embolism.

Fig. 57.12 presents the physiologic and monitor response to an air embolic event, and Box 57.6 offers an appropriate management response to such an event.

The responses of the electrocardiogram (ECG) , arterial pressure, pulmonary artery pressure (PAP) , pan-tidal CO ₂ concentration, a precordial Doppler and central venous pressure (CVP) to the intravenous administration of 10 mL of air over 30 seconds to an 11-kg dog. BP , Blood pressure.

Box 57.6

Management of an Acute Air Embolic Event

• 1.
  

  Prevent further air entry

  
  
  
  
  • ▪
    

    Notify surgeon (flood or pack surgical field)

    
    
  • ▪
    

    Jugular compression

    
    
  • ▪
    

    Lower the head

  
  
  
  
• 2.
  

  Treat the intravascular air

  
  
  
  
  • ▪
    

    Aspirate right heart catheter

    
    
  • ▪
    

    Discontinue N ₂ O

    
    
  • ▪
    

    Fi O ₂ : 1.0

    
    
  • ▪
    

    Pressors, inotropes

    
    
  • ▪
    

    Chest compression

  
  

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.

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

Monitoring

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 .

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.

Glucose Management

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.

Hypothermia

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.

Supratentorial Tumors

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.

Pituitary tumor with suprasellar extension.

The left panel shows the proximity of the tumor to the carotid arteries (which lie within the cavernous sinuses) and the potential for distortion of the ventricular system. The optic chiasm (not seen) lies above the sella in the path of the upwardly expanding tumor. The right panel shows that tumors that lie above the sella (including craniopharyngiomas, which arise in this location) abut and can invade the hypothalamus. The more radio-dense (whiter) cap over the superior and anatomic right lateral aspects of the tumor mass is a normal pituitary gland.

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.

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).

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.

Preoperative Evaluation

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.

Vasospasm

The anesthesiologist should determine whether vasospasm has occurred and what, if any, therapies for it have been undertaken. Vasospasm is thought to be caused by the breakdown products of 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

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

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.

Electrocardiogram abnormalities associated with subarachnoid hemorrhage.

The canyon T waves that may be seen after subarachnoid hemorrhage are evident.

Head Injury

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.

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