Anesthesia for Neurologic Surgery and Neurointerventions PDF

57 Anesthesia for Neurologic Surgery and Neurointerventions BRIAN P. LEMKUIL, JOHN C. DRUMMOND, PIYUSH M. PATEL, and ARTHUR LAM KEY POINTS □ □ □ □ □ □ □ □ □ □ □ □ F or the purposes of planning a strategy for controlling intracranial pressure (ICP), the four subcompartments of the intracranial space...

57 Anesthesia for Neurologic Surgery and Neurointerventions BRIAN P. LEMKUIL, JOHN C. DRUMMOND, PIYUSH M. PATEL, and ARTHUR LAM KEY POINTS □ □ □ □ □ □ □ □ □ □ □ □ F or 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 C ­ hapter 56. 1868 Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 57 Anesthesia for Neurologic Surgery and Neurointerventions 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. BOX 57.1 Recurrent Issues in Neuroanesthesia □ □ □ □ □ □ □ □ □ □ □ □ □ □ □  ontrol of intracranial pressure/brain relaxation C Management of PaCO2 Management of arterial blood pressure Use of steroids Use of osmotherapy Use of diuretics Use of anticonvulsants Patient positioning Pneumocephalus Venous air embolism Monitoring Intravenous fluid management Hypothermia Glucose management Emergence from anesthesia 1 4 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).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. 1869 2 3 Fig. 57.1 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.) 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.    Volume compensation mechanisms reaching exhaustion CPP reduction Herniation risk SECTION IV Adult Subspecialty Management Intracranial pressure 1870 Volume compensation (CSF, blood) Fig. 57.2 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.) Intracranial volume Fig. 57.3 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. Airway or intrathoracic pressure* Intracranial volume ICP Jugular venous pressure* PaCO2* Pao2 Some anesthetics* Blood volume CSF volume* Cellular Compartment Fluid* Compartment Mass Lesions Edema Neurologic injury Herniation or perfusion pressure BP Arterial pressure* Vasodilators* Seizures BP Tumor Hematoma subdural extradural intracerebral Mechanical injury or ischemia (If autoregulation defective) Fig. 57.4 The pathophysiology of intracranial hypertension. The figure depicts the manner in which increases in the volumes of any or all of the four intracranial compartments, blood, cerebrospinal fluid (CSF), fluid (interstitial or intracellular), and cells, result in intracranial pressure (ICP) increases and eventual neurologic damage. The elements that are 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; PaCO2, partial pressure of carbon dioxide in the arterial blood; PaO2, partial pressure of oxygen in the arterial 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. Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 57 Anesthesia for Neurologic Surgery and Neurointerventions 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.    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 TABLE 57.1 Intracranial Compartments and Techniques for Manipulation of Their Volume Volume Control Methods 1. Cells (including neurons, glia, tumors, and extravasated blood) Surgical removal 2. Fluid (intracellular and extracellular) Diuretics osmotic/diuretic agents Steroids (principally tumors) 3. Cerebral spinal fluid Drainage 4. Blood Arterial side Venous side Decrease cerebral blood flow Improve cerebral venous drainage 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).2-4 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. BOX 57.2 Factors that Influence Cerebral Blood Flow See effects of anesthetics on cerebral blood flow and cerebral metabolic rate in Chapter 11 for detailed discussion. □ PaO 2 □ PaCO 2 □ Cerebral metabolic rate □ Arousal/pain □ Seizures □ Temperature □ Anesthetics □ Blood pressure/status of autoregulation □ Vasoactive agents □ Anesthetics □ Pressors □ Inotropes □ Vasodilators □ Blood viscosity □ Neurogenic pathways (intra- and extra-axial) BP (mm Hg) ICP (mm Hg) Compartment 1871 Fig. 57.5 The effect of cerebral venous outflow obstruction on intracranial pressure (ICP) in a patient with an intracerebral hematoma. Bilateral jugular compression was applied briefly to verify the function of a newly placed ventriculostomy. The ICP response illustrates the importance of maintaining unobstructed cerebral venous drainage. 1872 SECTION IV Adult Subspecialty Management 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 (CO2) 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 (PaCO2) acting in conjunction with any disease-related impairment in CO2 responsiveness. Nitrous oxide (N2O) can also be a cerebral vasodilator. The CBF effect of N2O 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 N2O 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 N2O 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,” N2O and volatile anesthetics5,6 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).7,8 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 BOX 57.3 High Intracranial Pressure (“Tight Brain”) Checklist 1. Are the relevant pressures controlled? a. Jugular venous pressure i. Extreme head rotation or neck flexion? ii. Direct jugular compression? iii. Head-up posture? b. Airway pressure i. Airway obstruction? ii. Bronchospasm? iii. Straining, coughing; adequately relaxed? iv. Pneumothorax? v. Excessive PEEP or APR ventilation? c. Partial pressure of CO2 and O2 (PaCO2, PaO2) d. Arterial pressure 2. Is the metabolic rate controlled? a. Pain/arousal? b. Seizures? c. Febrile? 3. Are any potential vasodilators in use? a. N2O, volatile agents, nitroprusside, calcium channel blockers? 4. Are there any unrecognized mass lesions? a. Hematoma b. Air ± N2O c. CSF (clamped ventricular drain) APR, Airway pressure release; CSF, cerebrospinal fluid; PEEP, positive end-expiratory pressure. BOX 57.4 Methods for Rapid Reduction of Intracranial Pressure and Brain Volume (After Review of the Checklist in Box 57.3) □ □ □ □ □ □ F urther reduction of PaCO2 (to 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,66,67 although severe clinical occurrences have been very infrequent.68 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 extubation69 (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. Sitting There have been several reviews of numerous experiences with the sitting position.70-74 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, 57 Anesthesia for Neurologic Surgery and Neurointerventions 1877 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. 57.8A) rather than to the portions under thighs or legs75 (see Fig. 57.8B). 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* 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.76 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 77 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 * A column of blood 32 cm high exerts a pressure of 25 mm Hg. A B Fig. 57.8 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.) 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.39,69,78 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 hypothesized79 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 1878 SECTION IV Adult Subspecialty Management 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 headup posture.80,81 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 N2O because any N2O 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 N2O may result in an effect comparable with that of an expanding mass lesion. We do not view N2O as absolutely contraindicated because, before dural closure, intracranial gas is probably only rarely trapped. Nonetheless, attention to this possibility is important when one is presented with the problem of an increasingly tight brain during a posterior fossa craniotomy.82,83 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, N2O should be omitted because of the possibility of contributing to a tension pneumocephalus. Note that the use of N2O up to the point of dural closure may actually represent a clinical advantage,84 as in rabbits the gas pocket has been shown to shrink more rapidly because of the presence of N2O (because N2O diffuses much more quickly than nitrogen). Tension pneumocephalus is often naively viewed as exclusively a function of the use of N2O. However, tension pneumocephalus can most certainly occur as a complication of intracranial neurosurgery entirely unrelated to the use of N2O.85 It is one of the causes of delayed awakening or nonawakening after both posterior fossa and supratentorial procedures (Fig. 57.9).85,86 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 Fig. 57.9 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 pneumatocele. We doubt that the possible occurrence of this phenomenon represents a contraindication to N2O. However, withdrawal of N2O 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.87 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.88 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%.89-92 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 72), 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 procedures91). 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 57 Anesthesia for Neurologic Surgery and Neurointerventions 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 CO2 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,97 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 VAE98 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.99 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. 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 Fig. 57.10 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). No physiol changes Modest physiol changes Clinically apparent changes Cardiovascular collapse PAP ET-CO2 CO CVP BP ECG STETHO VAE volume 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.93,94 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.95 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 evidence96 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. 1879 T-echo Doppler Decreasing sensitivity Fig. 57.11 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-CO2, end-tidal carbon dioxide; PAP, pulmonary artery pressure; Stetho, esophageal stethoscope; T-echo, transesophageal echo; VAE, venous air embolism. 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 1880 SECTION IV Adult Subspecialty Management 10 mL Air Injection ECG 11 kg. dog mm Hg BP 200 Doppler 0 %CO2 8 0 PAP 40 CVP 0 10 0 30sec. Fig. 57.12 The responses of the electrocardiogram (ECG), arterial pressure, pulmonary artery pressure (PAP), pan-tidal CO2 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 O 2 □ FiO : 1.0 2 □ Pressors, inotropes □ Chest compression 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 singleorificed catheter with the tip 3 cm above the superior vena caval-atrial junction.100 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),101 or (3) TEE.102 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 57 Anesthesia for Neurologic Surgery and Neurointerventions P Bi-phasic P Fig. 57.13 Electrocardiogram (ECG) configurations observed at various locations when a central venous catheter is used as an intravascular ECG electrode. The configurations in the figure 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.101 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.103 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 1881 of the occurrence of PAE.104 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 gradient105 and generous fluid administration (e.g., 2800 mL/patient vs. 1220 mL/control patient106) 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.107 Some centers have advocated performing bubble studies preoperatively with echocardiography92 or transcranial Doppler (TCD),108 or intraoperatively using TEE prior to positioning109 to identify patients with a PFO with a view to using alternatives to the sitting position in this subpopulation.91,110 Some centers thereafter advocate the use of TEE to identify paradoxical embolization intraoperatively.91,111 However, none of these practices has become a communitywide 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 procedure74 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.112-114 Transpulmonary passage is more likely to occur when large volumes of air are presented to the pulmonary vascular filter.115,116 In addition, pulmonary vasodilators, including volatile anesthetics, may decrease the threshold for transpulmonary passage.115-117 The magnitude of differences among anesthetics does not appear to mandate any related “tailoring” of anesthetic techniques. However, N2O 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 105 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.118,119 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 1882 SECTION IV Adult Subspecialty Management 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. 120 Nitrous Oxide Nitrous oxide diffuses into air bubbles trapped in the vascular tree and, accordingly, N2O should be eliminated after a clinical VAE event to avoid aggravating the cardiovascular impact. As noted earlier, the PAE phenomenon adds an additional reason for eliminating N2O after the occurrence 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,121 and major VAE results in an acutely increased risk of PAE in patients with a PFO.104 Should N2O be used in patients at risk for VAE? Some clinicians may decide to simply avoid it. However, N2O can be used with the knowledge that it neither increases the incidence of VAE122 nor aggravates the hemodynamic response to VAE provided that it is eliminated when VAE occurs.123 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 BOX 57.7 Relative Indications for Intraarterial Pressure Monitoring □ □ □ □ □ □ □ □ □ □ □ E levated 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 Circulatory instability □ Trauma □ Spinal cord injury (spinal shock) □ Sitting position □ Possible barbiturate coma Possibility of induced hypotension Possibility of induced hypertension Anticipated or potential major blood loss □ Aneurysm clipping □ Arteriovenous malformations □ Vascular tumors □ Tumors involving or adjacent to major venous sinuses □ Craniofacial reconstruction □ Extensive craniosynostosis procedures Anticipated light anesthesia without paralysis Brainstem manipulation, compression, dissection Anticipated CN manipulation (especially CN V) Advantageous for postoperative intensive care □ Hypervolemic therapy □ Head injury □ Diabetes insipidus Incidental cardiac disease CN, Cranial nerve. 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.124,125 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.126 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 surgery127 and critically ill intensive care patients128 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. 57 Anesthesia for Neurologic Surgery and Neurointerventions 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.125 In the setting of largevolume 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.129 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.130 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.131 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.132 Second, the 4% albumin solution used was hypoosmolar (274 mOsm/L) and might have been expected to aggravate edema.133 Furthermore, there is no 1883 compelling physiologic explanation for an albumin-specific hazard. The formation of cerebral edema that is more difficult to clear is an inevitable suspicion.134 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.135,136 In contrast to alleged adverse effects in the context of TBI, there are potential beneficial effects in SAH.137,138 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.139 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.140 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 exceeded141 or in which the starch was administered up to the recommended limit on successive days, probably resulting in an accumulation effect.142 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 143 and have been administered uneventfully to patients with severe TBI.144 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.145 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 1884 SECTION IV Adult Subspecialty Management 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.146-149 This may be because injury can produce a state of hyperglycolysis.147,150 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” 151 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).152 The NICE-Sugar study’s control group range of 144 to 180 mg/dL (7.8-10 mmol/L) 153 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.154 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,26,155 hypothermia was also studied in laboratory models of TBI.156 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.157 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.158 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.159 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.160,161 A subsequent randomized trial reported similar outcomes in patients treated with targeted temperature management at either 33°C or 36°C.162 Widespread clinical application of targeted temperature management has been advocated by an international task force and other groups.163,164 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.165 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.166-171 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 57 Anesthesia for Neurologic Surgery and Neurointerventions 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.170,171 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.167 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.172 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 emergence173 and hypertension in the postanesthesia care unit.174 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 1885 BOX 57.8 Specific Procedures □ □ □ □ □ □ □ □ □ □ □ □ Supratentorial tumors Aneurysms and arteriovenous malformations Traumatic brain injury Posterior fossa procedures Transsphenoidal surgery Awake craniotomy/seizure surgery Stereotactic procedures Neuroendoscopic procedures Neuroradiologic procedures Cerebrospinal fluid shunting procedures Pediatric neurosurgery Spinal surgery 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. Specific Procedures 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). 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. 1886 SECTION IV Adult Subspecialty Management 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. Preoperative Preparation 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 CO2 retention in patients whose intracranial compliance is already abnormal, sedative premedication outside of the operating room is usually avoided. Monitoring 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.175 That intervention may entail either operative clipping or an endovascular approach.175 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.175 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 176). 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 TABLE 57.2 World Federation of Neurosurgeons Subarachnoid Hemorrhage Scale WFNS Grade GCS Score Motor Deficit I 15 Absent II 14-13 Absent III 14-13 Present IV 12-7 Present or absent V 6-3 Present or absent GCS, Glasgow Coma Scale; WFNS, World Federation of Neurosurgeons. TABLE 57.3 Hunt-Hess Classification of Neurologic Status After Subarachnoid Hemorrhage Category Criteria* 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. 57 Anesthesia for Neurologic Surgery and Neurointerventions 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.175,177-180 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.181,182 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.183 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.184-186 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.186,187 When there is a clinical suspicion of vasospasm (typically because of a change in sensorium or new neurologic deficit), 1887 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),175,188 hypertension, and sometimes balloon angioplasty or intraarterial vasodilators.189 For patients proceeding to surgery, hypotension should be avoided175 and CPP should usually be maintained intraoperatively at values near the waking normal range. The association of hypotension with poor outcome,190 and the potential for hypotension to cause or aggravate cerebral ischemia in patients with some degree of vasospasm, is well recognized.191-193 This concern should extend even to patients classified as World Federation of Neurosurgeons grade I who may have regions of cerebral ischemia30 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.188,194-196 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.187,196-199 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.196 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,200 although it was not associated with any reduction in the incidence of vasospasm as detected by angiography.201 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 trial202,203 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, nimodipine204-207) are also used intraarterially as a primary treatment for medically-refractory vasospasm. Milrinone and papaverine are similarly administered.206,208 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 1888 SECTION IV Adult Subspecialty Management magnesium, a larger randomized, placebo-controlled trial reported no improvement in outcome among patients in whom magnesium was initiated within 4 days of SAH.209 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.210 A subsequent large RCT (STASH) failed to demonstrate either short-term or long-term outcome benefits related to statin administration.211 The phosphodiesterase inhibitor cilostazol (a platelet inhibitor as well as vasodilator) was reported to reduce symptomatic vasospasm,212,213 new cerebral infarctions,213 and improve outcome212 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.175 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 214 and is sometimes sufficient to require pressor support.215 The mechanism is uncertain but is thought to be catecholamine mediated.216 Troponin elevation occurs commonly, though typically reaching levels less than the diagnostic threshold for myocardial infarction.217 Peak troponin levels correlate with the severity of both neurologic injury and echocardiographic myocardial dysfunction.215,218 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.217 ECG abnormalities do not herald evolving or impending cardiac disease.219 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,218 and has been associated with an increased incidence of malignant ventricular rhythms including torsades de pointes.220 Anesthetic Technique Important considerations include the following:    1. Absolute avoidance of acute hypertension with its attendant risk of rerupture. 2. Achievement of intraoperative brain relaxation to facilitate surgical access to the aneurysm. 3. 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. 4. 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. Monitoring An arterial line is invariably appropriate. A central venous catheter may be appropriate if peripheral access is inadequate. Anesthetic Selection. 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.176 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). Induced Hypotension. 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. Induced Hypertension. 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. 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 PaCO2). 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 57 Anesthesia for Neurologic Surgery and Neurointerventions 1889 Fig. 57.14 Electrocardiogram abnormalities associated with subarachnoid hemorrhage. The canyon T waves that may be seen after subarachnoid hemorrhage are evident. 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.221-224 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.45 Surgeons who believe in its CBF-enhancing effect may request a second 1 g/kg approximately 15 minutes before an anticipated temporary occlusion. Temporary Clipping. 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.225 In another institution, the threshold 1890 SECTION IV Adult Subspecialty Management for ischemic injury was 20 minutes of occlusion.226 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. Brain Protection. 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.227 Furthermore, a clinical investigation during aneurysm clipping revealed decreases in brain tissue PO2 in association with administration of etomidate, which contrasted with the brain PO2 increases that occurred with the introduction of desflurane. During subsequent temporary vessel occlusion, tissue pH decreased alarmingly in patients receiving etomidate and was unchanged with desflurane.228 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.227,229-231 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.231,232 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.230,231,233 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 N2O-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.234 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.199,235 Hypothermia. As noted in the previous section Hypothermia, a prospective trial of mild hypothermia in patients undergoing aneurysm surgery revealed no improvement in neurologic outcome.154 Nonetheless, some neurosurgical teams that were already using mild hypothermia (32°C-34°C) are continuing its use for proce