II. NEUROPHYSIOLOGY

A. Cerebral metabolism is directly related to the number and frequency of neuron depolarizations (activity or stimulation increases the metabolic rate). Cerebral blood flow (CBF) is tightly coupled to metabolism.

B. The CSF occupies the subarachnoid space, providing a protective layer of fluid between the brain and the tissue that surrounds it. It maintains a milieu in which the brain can function by regulating pH and electrolytes, carrying away waste products, and delivering nutrients.

C. Intracranial pressure (ICP) is low except in pathologic states. The volume of blood, CSF, and brain tissue must be in equilibrium. An increase in one of these three elements, or the addition of a space-occupying lesion, can be accommodated initially through displacement of CSF into the thecal sac but only to a small extent. Further increases, as with significant cerebral edema or accumulation of an extradural hematoma, quickly lead to a marked increase in ICP because of the low intracranial compliance (Fig. 36-2).

D. Many factors affect CBF because of their effect on metabolism. (Stimulation, arousal, nociception, and mild hyperthermia elevate metabolism and flow, and sedative–hypnotic agents and hypothermia decrease metabolism and flow.)

E. A number of other factors govern CBF directly without changing metabolism.

1. A potent determinant of CBF is PaCO₂. CBF changes by approximately 3% of baseline for each 1 mm Hg of change in PaCO₂ (Fig. 36-3).

2. As CBF changes, so does cerebral blood volume (CBV), which is the reason hyperventilation can be used for short periods of time to relax the brain or to decrease ICP. This effect is thought to be short lived (minutes to hours) because the pH of CSF normalizes over time and vessel caliber returns to baseline.

F. In contrast to PaCO₂, PaO₂ has little effect on CBF except at abnormally low levels (Fig. 36-4). When PaO₂ decreases below 50 mm Hg, CBF begins to increase sharply.

G. CBF remains approximately constant despite modest swings in arterial blood pressure (autoregulation) (Fig. 36-5).

1. As cerebral perfusion pressure (CPP), defined as the difference of mean arterial pressure (MAP) and ICP, changes, cerebrovascular resistance (CVR) adjusts in order to maintain stable flow.

2. The range of CPP over which autoregulation is maintained is termed the autoregulatory plateau. Although this range is frequently quoted as a MAP range of 60 to 150 mm Hg, there is significant variability between individuals, and these numbers are only approximate.

a. At the low end of the plateau, CVR is at a minimum, and any further decrease in CPP compromises CBF.

b. At the high end of the plateau, CVR is at a maximum, and any further increase in CPP results in hyperemia.

H. Anesthetic Influences

1. Anesthetic agents have a variable influence on CBF and metabolism, carbon dioxide reactivity, and autoregulation.

2. Inhalation anesthetics tend to cause vasodilation in a dose-related manner but do not per se uncouple CBF and metabolism. Thus, the vasodilatory influence is opposed by a metabolism-mediated decrease in CBF.

3. The resultant effect is that during low-dose inhalation anesthesia, CBF is either unchanged or slightly increased. Compared with other inhaled agents, sevoflurane in clinically relevant doses does not increase CBF. Furthermore, sevoflurane is associated with profound regional and global reductions in cerebral metabolic rate.

4. Intravenous (IV) agents, including thiopental and propofol, cause vasoconstriction coupled with a reduction in metabolism. Ketamine, on the other hand, increases CBF and metabolism.

5. Cerebrovascular carbon dioxide reactivity is a robust mechanism and is preserved under all anesthetic conditions. Cerebral autoregulation, on the other hand, is abolished by inhalation agents in a dose-related manner but is preserved during propofol anesthesia.

III. PATHOPHYSIOLOGY. The homeostatic mechanisms that ensure protection of the brain and spinal cord, removal of waste, and delivery of adequate oxygen and substrate to the tissue can be interrupted through a multitude of mechanisms (Table 36-1).

IV. MONITORING. The integrity of the CNS needs to be evaluated intraoperatively with monitors that specifically detect CNS function, perfusion, or metabolism.

A. Central Nervous System Function (Tables 36-2 to 36-4)

B. Influence of Anesthetic Technique (Table 36-5)

V. CEREBRAL PERFUSION. Although adequate CBF does not guarantee the well-being of the CNS, it is an essential factor in its integrity.

A. Laser Doppler flowmetry requires a burr hole and measures flow in only a small region of the brain.

B. Transcranial Doppler ultrasonography (TCD) is a noninvasive monitor for evaluating relative changes in flow through the large basal arteries of the brain (often flow velocity in the middle cerebral artery) (Fig. 36-6).

1. In addition to the measurement of flow velocity, TCD is useful for detecting emboli (Fig. 36-7).

2. Specific applications for intraoperative use of TCD include carotid endarterectomy (CEA), nonneurologic surgery and cerebral autoregulation in patients with traumatic brain injury (TBI), and surgical procedures requiring cardiopulmonary bypass.

3. An important use of TCD is to monitor the development of vasospasm in patients who have experiences a subarachnoid hemorrhage (SAH).

C. Intracranial Pressure Monitoring

1. Although monitoring ICP does not provide direct information about CBF, it allows calculations of CPP (the difference between MAP and ICP).

2. Within a physiologic range of CPP, CBF should remain approximately constant. A CPP that is too low results in cerebral ischemia, and a CPP that is too high causes hyperemia.

3. When ICP is high and CPP is low, interventions can target either ICP (maintain <20 mm Hg) or MAP to restore a favorable balance of the two (Tables 36-6 and 36-7). MAP is increased via adequate intravascular resuscitation and with a vasopressor as needed. The goal CPP in TBI is >50 to 60 mm Hg.

D. Cerebral Oxygenation and Metabolism Monitors (Table 36-8)

VI. CEREBRAL PROTECTION. Efforts to avert neurologic insult using medications or through the manipulation of physiologic parameters have met with meager results. Although recent advances are intriguing, no maneuver matches the cerebral protection provided by mild to moderate hypothermia. The operating room is unique in that an opportunity exists to intervene before the ischemic event occurs. (Use of a temporary aneurysm clip on the middle cerebral artery is an example of a focal ischemic insult that could be predicted; a brief period of circulatory arrest induced with adenosine to facilitate clipping of a basilar artery aneurysm is an example of a global insult.)

A. Ischemia and Reperfusion

1. It is reasonable to attempt to minimize ischemic insult by lowering the cerebral metabolic rate, thus decreasing the likelihood of exhausting adenosine triphosphate reserves during the period of ischemia (the traditional paradigm for approaching the subject of intraoperative neuroprotection).

2. Unfortunately, further damage occurs as a result of processes that are initiated during the reperfusion stage.

3. A shift in the focus of neuroprotection from metabolic suppression to targeting ischemic cascades has recently been advocated.

B. Hypothermia

1. Profound hypothermia is well known for its neuroprotective effects. When core body temperature decreases below 20°C, circulatory arrest of <30 minutes appears to be well tolerated.

2. Mild hypothermia (33°C–35°C) not only decreases cerebral metabolism but likely also modulates the immune and inflammatory response to ischemia, thus affecting the reperfusion portion of the injury as well. Although considerable evidence in rats suggests that mild hypothermia is beneficial, there is a paucity of evidence in humans. Nevertheless, hypothermia remains the most promising intervention for cerebral protection.

3. There is ample evidence that hyperthermia is associated with worse outcome in the setting of ischemic stroke, SAH, cardiac arrest, and TBI.

4. In the operating room during neurosurgical procedures during which the brain is at risk for ischemic insult, a goal temperature of 35°C to 36°C is reasonable. Mild hypothermia (33°C–35°C) may be appropriate in many patients, recognizing that there may be no benefit to this therapy.

C. Medical Therapy for Cerebral Protection

1. Volatile and IV anesthetic agents decrease cerebral metabolism. Animal studies have found protective effects of volatile anesthetics, particularly isoflurane, in mitigating a mild to moderate ischemic insult, although this effect may only be short lived.

2. Barbiturates, such as thiopental, have been shown to have at least short-term benefits on focal cerebral ischemia, but the benefit in global ischemia remains controversial. Propofol likely has similar protective effects.

3. Current opinion is that anesthetic neuroprotection is primarily mediated through prevention of excitotoxic injury, not through termination of apoptotic pathways. (It thus delays neuronal death and leaves a greater temporal window for intervention.)

4. Clinically, barbiturates and propofol are used intraoperatively to achieve burst suppression on the electroencephalogram, although their neuroprotective action does not appear to be metabolically mediated.

D. Glucose and Cerebral Ischemia

1. Although considerable evidence has accumulated suggesting harm from hyperglycemia, evidence for benefit with normalization of serum glucose concentrations using insulin has been controversial.

2. Despite a reluctance to embrace intraoperative tight glycemic control given the current literature, it is worthwhile to consider for patients undergoing cerebrovascular surgery. Given the preponderance of evidence that hyperglycemia and cerebral ischemia in combination are harmful, changing practice in these patients may be warranted. Tight glycemic control is a reasonable goal in these patients. (It cannot be stated that this intervention is neuroprotective.)

E. A Practical Approach

1. For patients undergoing surgical procedures with an anticipated period of cerebral ischemia such as cerebral aneurysm surgery or cerebrovascular bypass procedures, either volatile anesthesia or an IV technique is appropriate. It is reasonable to administer additional propofol or thiopental before vessel occlusion.

2. Euglycemia before vessel occlusion is desirable, but frequent glucose checks are essential during anesthesia to avoid episodes of hypoglycemia if insulin is administered.

3. Hyperthermia should be avoided during this time, with the temperature kept at or below 36°C.

VII. ANESTHETIC MANAGEMENT

A. Preoperative Evaluation

1. It is prudent to consider the nature of the patient’s disease that brings him or her to the operating room in the context of the patient’s medical and surgical history.

2. Preoperative risk stratification for a cardiac complication is important to consider. Current guidelines include delaying surgery for at least 2 weeks after simple balloon angioplasty, 4 to 6 weeks after placement of a bare metal stent, and 1 year after placement of a drug-eluting stent.

3. Many patients presenting for spine surgery have weakness or paralysis that may present a contraindication to the use of succinylcholine (Sch).

4. Many neurosurgical patients have been exposed to antiepileptic medications. Previous allergies or reactions to these medications, especially phenytoin, should be elucidated.

B. Induction and Airway Management

1. During induction of anesthesia, three iatrogenic consequences (hypotension, hypertension, apnea) may be significant hazards for neurosurgical patients.

a. Hypertension caused by laryngoscopy is poorly tolerated by patients after aneurysmal SAH because systolic hypertension is thought to be a cause of recurrent hemorrhage from the aneurysm.

b. Hypertension may worsen elevated ICP and possibly lead to herniation of cranial contents into the foramen magnum.

c. Apnea results in a predictable increase in PaCO₂ and corresponding cerebral vasodilation.

2. A cervical collar for known or suspected cervical spine injury may make tracheal intubation more difficult. These patients are also particularly harmed by periods of hypotension or hypertension.

3. Because patients with SAH are at risk for harm from hypertension, it is reasonable to place an arterial catheter for hemodynamic monitoring before induction of anesthesia.

4. Many neurosurgical and spine surgery patients have conditions in which Sch is contraindicated.

a. In the setting of acute stroke or spinal cord injury (SCI), it remains safe to use Sch for approximately 48 hours from the time of injury.

b. Alternatively, a rapid-acting nondepolarizing muscle relaxant is appropriate in many neurosurgical patients to achieve acceptable intubating conditions.

C. Maintenance of Anesthesia

1. The primary considerations for maintenance of anesthesia include the type of monitoring planned for the procedure, brain relaxation, and the desired level of analgesia at the end of the surgical procedure.

2. Remifentanil is appropriate for neurosurgical procedures in which tracheal extubation is planned at the end of the surgery and minimal residual sedation is desired to facilitate the neurologic examination.

3. Replacement of a volatile anesthetic with a continuous infusion of propofol is desirable with motor evoked potential (MEP) monitoring and when brain relaxation is inadequate with a volatile anesthetic.

4. The use of intraoperative muscle relaxants should be avoided during MEP, spontaneous electromyography, and cranial nerve monitoring. Muscle relaxants may be used during isolated somatosensory evoked potential monitoring.

D. Ventilation Management

1. Hypocapnic cerebral vasoconstriction provides anesthesiologists with a powerful tool for manipulating CBF and CBV.

2. Hyperventilation is routinely used to provide brain relaxation and optimize surgical conditions.

3. Because hyperventilation decreases CBF, it has the theoretical potential for causing or exacerbating cerebral ischemia. Clinically, hyperventilation has been associated with harm only in the early period of TBI, but it is still recommended to be avoided in all patients with TBI except when necessary for a brief period to manage acute increases in ICP.

4. During neurosurgical procedures, it is reasonable to maintain the PaCO₂ between 30 and 35 mm Hg. Further brain relaxation should be accomplished with other modalities, such as mannitol, hypertonic saline, or IV anesthesia. If hyperventilation to a PaCO₂ below 30 mm Hg is required, it is appropriate to guide this therapy with jugular venous oximetry and the arterial–jugular lactate gradient.

5. The duration of effectiveness of hyperventilation is limited. Normalization of CBF and consequently CBV has been reported to occur within minutes. Clinically, the beneficial effects of hyperventilation appear to be sustained during most neurosurgical procedures of modest duration.

E. Fluids and Electrolytes

1. To maintain adequate cerebral perfusion, adequate intravascular volume should be maintained (euvolemia to slight hypervolemia).

2. To minimize brain edema, it is important to maintain serum tonicity. It is prudent to check serum sodium levels on a regular basis in prolonged surgical procedures in which mannitol has been given.

3. In addition to osmotic dehydration of the brain interstitium, other proposed benefits of hypertonic solutions include a reduction in blood viscosity, increasing erythrocyte deformability, and improving cardiac output and microcirculatory flow.

F. Transfusion Therapy. The lower limit of acceptable hemoglobin or hematocrit has not been well defined. (Evidence supports avoidance of transfusion for a hematocrit above 21% except in the context of ongoing hemorrhage and possibly the early phase of resuscitation for septic patients.)

G. Glucose Management

1. The combination of hyperglycemia and cerebral ischemia appears to be particularly deleterious. Nevertheless, tight glycemic control (80–110 mg/dL) with insulin may be associated with an increased mortality rate at 90 days.

2. In the neurosurgical population, intensive insulin treatment results in increased variability in the blood glucose concentration, leading to cerebral osmotic shifts and higher incidences of hypoglycemia, leading to worse outcomes.

H. Emergence

1. The decisions that need to be made regarding emergence from anesthesia for neurosurgical and spine surgery patients hinge on whether the patient is an appropriate candidate for tracheal extubation.

2. For extensive spine surgeries in the prone position, significant dependent edema frequently occurs. Although the predictive value of an air leak from around the endotracheal tube cuff is poor, the combination of pronounced facial edema and an absent cuff leak after prone surgery should make one suspicious of upper airway edema. Delaying extubation of the trachea under these circumstances may be appropriate.

3. Avoiding coughing and hemodynamic changes with emergence is important for all neurosurgical patients.

VIII. COMMON SURGICAL PROCEDURES

A. Surgery for Tumors

1. The fundamental anesthetic considerations in tumor surgery are proper positioning of the patient to facilitate the surgical approach; providing adequate relaxation of the brain to optimize surgical conditions; and avoiding well-known devastating complications, such as venous air embolism.

2. Preoperative assessment of the level of consciousness and a review of relevant radiologic studies should be performed, and the results should be taken into consideration in the anesthetic plan.

3. Adequate brain relaxation is typically achieved with a standard anesthetic, including sub-MAC volatile anesthesia, an opioid infusion, mild to moderate hyperventilation, and mannitol.

B. Pituitary Surgery

1. These patients should undergo a preoperative evaluation of their hormonal function to detect hypersecretion of pituitary hormones, which is common in patients with pituitary adenomas, as well as panhypopituitarism. Patients with panhypopituitarism need hormone replacement, including cortisol, levothyroxine, and possibly desmopressin. These medications should be continued in the perioperative period.

2. Small pituitary tumors can be resected by a transsphenoidal approach, but larger tumors may require a craniotomy.

3. Intraoperative monitoring of glucose and electrolytes is essential, particularly if the patient has pre-existing diabetes insipidus (DI) or if the patient develops signs of DI during surgery.

a. DI is a common complication of pituitary surgery because of the loss of antidiuretic hormone production. It may be temporary or permanent and may occur either in the intraoperative or postoperative period.

b. DI is initially suspected on the basis of copious urine output, as well as increased serum sodium concentration. A urine specific gravity 1.005 or below is confirmative.

C. Cerebral Aneurysm Surgery and Endovascular Treatment

1. For patients who survive hemorrhage, surgical or endovascular intervention to secure the aneurysm is essential to prevent further hemorrhage.

2. Patients with aneurysmal SAH are at risk for numerous complications that may affect the anesthetic plan. These complications include cardiac dysfunction, neurogenic or cardiogenic pulmonary edema, and hydrocephalus, as well as further hemorrhage from the aneurysm.

3. A patient presenting for the elective correction of an intracranial aneurysm typically has good brain condition, with easily achievable relaxation using mannitol (0.5–1.0 g/kg), mild to moderate hyperventilation, and administration of a low concentration of volatile anesthetic combined with an opioid infusion.

D. Arteriovenous Malformations

1. Cerebral angiography remains the “gold standard” for diagnosis of arteriovenous malformations (AVMs).

2. Although embolization of the AVM is commonly performed, either radiosurgery or an open surgical procedure is typically required subsequent to the embolization to cure the lesion.

3. After resection of large AVMs or those in the posterior fossa, it may be appropriate to take the patient to the intensive care unit mechanically ventilated and sedated. If the decision is made by the surgeon and anesthesiologist to allow emergence and extubation of the trachea, aggressive management of blood pressure should be instituted, and coughing should be avoided.

E. Carotid Surgery

1. Carotid stenosis is a common cause of transient ischemic attack and ischemic stroke. It is amenable to surgical intervention and endovascular stenting.

2. Surgery is associated with a risk of stroke, myocardial infarction, and wound infection. With recent advances in medical therapy, including more effective lipid-lowering drugs, antiplatelet agents, and antihypertensive therapy, the margin of benefit of surgery may be even lower.

3. Both general and regional anesthesia may be used for CEA. (There is no difference in outcomes based on the anesthetic technique.) Regional anesthesia is accomplished with a superficial cervical plexus block or a combination of superficial and deep cervical plexus block.

4. Several CNS monitors may be used during CEA under general anesthesia.

5. Rapid emergence and tracheal extubation at the end of the procedure are desirable because they allow immediate neurologic assessment.

6. Carotid artery stenting (CAS) is minimally invasive and may be performed under sedation (may need to convert to general anesthesia). There is no difference in outcome (stroke, myocardial infarction, death) comparing CAS and CEA.

F. Epilepsy Surgery and Awake Craniotomy. Some intracranial neurosurgical procedures are performed on “awake” (sedated and pain free yet able to respond to verbal or visual command) patients to facilitate monitoring of the region of the brain on which the surgeon is operating (epileptic focus). Patients with a difficult airway, obstructive sleep apnea, or orthopnea may have relative contraindications to an “awake” craniotomy. Patients with severe anxiety, claustrophobia, or other psychiatric disorders may be particularly inappropriate candidates for this type of procedure.

1. Intraoperative Management. Direct visual and verbal contact with the patient should be maintained throughout the procedure.

2. Conscious Sedation Technique. Propofol is one of the most frequently used drugs either alone or in combination with remifentanil. Dexmedetomidine may be the ideal sedative (minimal respiratory depression) for awake procedures (0.3–0.6 μg/kg/hr).

3. “Asleep–Awake–Asleep” Technique. This is often the preferred method for epilepsy surgery (general anesthesia for the initial craniotomy and closure and awake in the middle to identify the precise location of the epileptic focus).

4. General anesthesia is selected for children, patients with continuous movement disorders, and patients with an increased ICP.

IX. ANESTHESIA AND TRAUMATIC BRAIN INJURY

A. Overview of Traumatic Brain Injury

1. The presence of TBI is the primary determinant in quality of outcome for patients with traumatic injuries.

2. Airway and breathing are of paramount importance in any critically ill patient but even more so in patients with head injuries given the sensitivity of the brain to hypoxemia and hypercapnia.

3. Patients with TBI have up to a 10% incidence of an unstable cervical spine injury.

a. Risk factors include a motor vehicle accident and Glasgow Coma Scale (GCS) score below 8 (Table 36-9). Therefore, all attempts at intubation should include in-line neck stabilization to decrease the chance of worsening a neurologic injury.

b. Patients with TBI should generally be intubated orally because the potential presence of a basilar skull fracture may increase the risk associated with a nasal intubation.

4. Minimizing the risk of aspiration during airway procedures is essential. The effectiveness and correct application of cricoid pressure have been questioned.

5. An important consideration is the choice of drugs to facilitate tracheal intubation. Hypotension is extremely detrimental to the injured brain.

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