Handbook of Clinical Anesthesia

Chapter 39

Anesthesia for Neurosurgery

An understanding of neuroanatomy and neurophysiology is requisite knowledge for the anesthetic management of patients with disease of the central nervous system (CNS), including the brain and the spine (M Sean Kincaid, Lam AM: Anesthesia for neurosurgery. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1003–1031).

  1. Neuroanatomy
  2. The brain and spinal cord are surrounded by protective but nondistensible bony structures that surround them and provide protection.
  3. The intracranial volume is fixed, thereby providing little room for anything other than the brain, cerebrospinal fluid (CSF), and blood contained in the cerebral vasculature. It is in the context of the restrictive nature of the space in which the CNS is housed that all interventions must be considered.
  4. The anterior cerebral circulation originates from the carotid artery, the posterior circulation results from the vertebral arteries, and the system of collateralization is known as the circle of Willis (Fig. 39-1).
  5. The spinal column is the bony structure made up of the seven cervical, 12 thoracic, and five lumbar vertebrae, as well as the sacrum.
  6. The spinal cord exits the skull through the foramen magnum and enters the canal formed by the vertebral bodies. In adults, the spinal cord typically ends at the lower aspect of the first lumbar vertebral body.
  7. The anterior spinal artery arises from the vertebral arteries and supplies the anterior two thirds of the spinal cord. This vessel runs the length of the cord,

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receiving contribution from radicular arteries via intercostal vessels. The artery of Adamkiewicz is the most important radicular vessel.

 

Figure 39-1. The circle of Willis, which supplies blood flow to the brain.

  1. The posterior third of the cord is supplied by two posterior spinal arteries, which arise from the vertebral arteries and also receive contribution from radicular arteries.

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  1. Neurophysiology
  2. 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.
  3. 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.
  4. 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. 39-2).
  5. 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.)
  6. A number of other factors govern CBF directly without changing metabolism.
  7. A potent determinant of CBF is PaCO2. CBF changes by approximately 3% of baseline for each 1 mm Hg of change in PaCO2(Fig. 39-3).
  8. 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.
  9. In contrast to PaCO2, PaO2has little effect on CBF except at abnormally low levels (Fig. 39-4). When PaO2 decreases below 50 mm Hg, CBF begins to increase sharply.
  10. CBF remains approximately constant despite modest swings in arterial blood pressure (autoregulation) (Fig. 39-5).
  11. 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.

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Figure 39-2. Intracranial compliance (elastance) curve.

  1. 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.
 

Figure 39-3. Cerebrovascular response to change in arterial carbon dioxide partial pressure (PaCO2) from 25 to 65 mm Hg.

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Figure 39-4. Cerebrovascular response to change in arterial oxygen partial pressure (PaO2). The response of cerebral blood flow to change in PaO2 is flat until the PaO2decreases below about 50 mm Hg.

 

Figure 39-5. Cerebral autoregulation maintains cerebral blood flow constant between 60 to 160 mm Hg. These are average values, and there is considerable variation in both the lower and upper limit of cerebral autoregulation among normal individuals.

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  2. At the low end of the plateau, CVR is at a minimum, and any further decrease in CPP compromises CBF.
  3. At the high end of the plateau, CVR is at a maximum, and any further increase in CPP results in hyperemia.
  4. Anesthetic Influences
  5. Anesthetic agents have a variable influence on CBF and metabolism, carbon dioxide reactivity, and autoregulation.
  6. 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.
  7. The resultant effect is that during low-dose inhalation anesthesia, CBF is either unchanged or slightly increased.
  8. Intravenous (IV) agents, including thiopental and propofol, cause vasoconstriction coupled with a reduction in metabolism. Ketamine, on the other hand, increases CBF and metabolism.
  9. 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 39-1).

Table 39-1 Events That May Interrupt Homeostatic Mechanismsfor Brain Protection

Traumatic Insults Contusion with edema formation
Depressed skull fractures
Rapid deceleration
Mass Lesions
Tumors (compress adjacent structures, increase ICP, and obstruct normal flow of CSF)
Hemorrhage (spontaneous or traumatic)

CSF = cerebrospinal fluid; ICP = intracranial pressure.

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Table 39-2 Monitoring Central Nervous System Function

Electroencephalography (depolarization of cortical neurons provides a pattern of electrical activity that can be measured on the scalp)
Evoked potential monitoring (detect signals that result from a specific stimuli)
   GSSEP (requires intact sensory pathway, spine surgery when dorsal column of the spinal cord may be at risk)
   BAEP (acoustic neuroma surgery)
   VEP (difficult to record during anesthesia)
   MEP (monitors descending motor pathways, complements SSEP during spine surgery, signals sensitive to volatile anesthetics and intravenous may be preferred)
sEMG (detects injury to nerve roots in the surgical area; muscle relaxants must be avoided)
Electromyography (cranial nerve monitoring)

BAEP = brainstem auditory evoked potential; MEP = motor evoked potential; sEMG = spontaneous electromyography; SSEP = somatosensory evoked potential; VEP = visual evoked potential.

  1. Monitoring

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

  1. Central Nervous System Function(Tables 39-2, 39-3 and 39-4)
  2. Influence of Anesthetic Technique(Table 39-5)

Table 39-3 Electroencephalogram Frequencies

 

Frequency (Hz)

Description

Delta

0–3

Low frequency, high amplitude
Present in deep coma, encephalopathy, deep anesthesia

Theta

4–7

Not prominent in adults
May be seen in encephalopathy

Alpha

8–12

Prominent in the posterior region during relaxation with the eyes closed

Beta

>12

High frequency, low amplitude Dominant frequency during arousal

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Table 39-4 Indications for Electroencephalographic Monitoring

During anesthesia

Carotid endarterectomy
Cardiopulmonary bypass
Cerebrovascular surgery (temporary clipping, vascular bypass)

Intensive care unit

Barbiturate coma for patients with traumatic brain injury
Subclinical seizures suspected

Table 39-5 Influence of Anesthetic Technique on Central Nervous System Monitoring

Inhalation agents (including nitrous oxide) generally have more depressant effects on evoked potential monitoring than IV agents.
Whereas cortical evoked potentials with long latency involving multiple synapses (SSEP, VEP) are exquisitely sensitive to the influence of anesthetic, short-latency brainstem (BAEP) and spinal components are resistant to anesthetic influence.
Monitoring of MEP and cranial nerve EMG in general preclude the use of muscle relaxants. Use of a short-acting neuromuscular blocking agent for the purpose of tracheal intubation is acceptable.
MEP is exquisitely sensitive to the depressant effects of inhalation anesthetics, including nitrous oxide. Total IV anesthesia without nitrous oxide is the recommended anesthetic technique for monitoring of MEP.
Opioids and benzodiazepines have negligible effects on recording of evoked potentials.
Propofol and thiopental attenuate the amplitude of virtually all modalities of evoked potentials but do not obliterate them.
During crucial events when part of the central neural pathway is specifically placed at risk by surgical manipulation, as in placement of a temporary clip during aneurysm surgery, change in “anesthetic depth” should be minimized to avoid misinterpretation of the changes in evoked potential.

BAEP = brainstem auditory evoked potential; IV = intravenous; MEP = motor evoked potential; SSEP = somatosensory evoked potential; VEP = visual evoked potential.

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  1. Cerebral Perfusion

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

  1. Laser Doppler flowmetryrequires a burr hole and measures flow in only a small region of the brain.
  2. 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. 39-6).
  3. In addition to the measurement of flow velocity, TCD is useful for detecting emboli (Fig. 39-7).
  4. Specific applications for intraoperative use of TCD include carotid endarterectomy (CEA), non-neurologic surgery in patients with traumatic brain injury (TBI), and surgical procedures requiring cardiopulmonary bypass.
  5. Intracranial Pressure Monitoring
  6. Although monitoring ICP does not provide direct information about CBF, it allows calculations of CPP (the difference between MAP and ICP).
  7. Within a physiologic range of CPP, CBF should remain approximately constant. A CPP that is too

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low results in cerebral ischemia, and a CPP that is too high causes hyperemia.

 

Figure 39-6. Transcranial Doppler tracing with release of the cross-clamp during carotid endarterectomy. The resultant hyperemia is accompanied with evidence of air embolism (vertical streaks in the tracing). ICA = internal carotid artery; MCA = middle cerebral artery; RT = right.

 

Figure 39-7. Particulate emboli seen on transcranial Doppler in a patient with symptoms of transient ischemic attacks consistent with right carotid artery territory embolization. The emboli are denoted by the arrows. L = left; MCA = middle cerebral artery; R = right.

  1. 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 39-6 and 39-7). MAP is increased via adequate intravascular

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resuscitation and with a vasopressor as needed. The goal CPP in TBI is greater than 50 to 60 mm Hg.

Table 39-6 Interventions to Lower Intracranial Pressure

Suppression of cerebral metabolic activity
Positional changes to decrease cerebral venous blood volume
Drainage of CSF
Removal of brain water with osmotic agents (mannitol)
Mild to moderate hyperventilation to further decrease cerebral blood volume

CSF = cerebrospinal fluid.

Table 39-7 Interventions for Management of Inadequate Cerebral Perfusion Pressure

Reduce brain water

Mannitol
Hypertonic saline
Furosemide

Remove CSF

External ventricular drain
Lumbar drain

Decrease CBV

Head-up tilt
Neutral neck position
Metabolic suppression (propofol, barbiturate)
Mild to moderate hyperventilation

Elevate MAP

Adequate intravascular volume resuscitation
Vasopressor

CBV = cerebral blood volume; CSF = cerebrospinal fluid; MAP = mean arterial pressure.

  1. Cerebral Oxygenation and Metabolism Monitors(Table 39-8)
  2. 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

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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.)

Table 39-8 Monitors of Cerebral Oxygenation and Metabolism

Near-infrared spectroscopy is a noninvasive method of evaluating the oxygenation of cerebral blood and balance between flow and metabolism.
Brain tissue PO2 probe is placed through a burr hole. It is commonly used in patients with traumatic brain injury (<15 mm Hg who warrant intervention, including treatment of anemia.)
Jugular venous oximetry provides the same information as the brain tissue PO2 probe but over a larger portion of the brain. Normal jugular venous saturation is 65% to 75%; saturation below 50% in traumatic brain injury is associated with a poor outcome.

  1. Ischemia and Reperfusion
  2. It is reasonable to attempt to minimize ischemic insult by lowering cerebral metabolic rate, thus decreasing the likelihood of exhausting adenosine triphosphate reserves during the period of ischemia (traditional paradigm for approaching the subject of intraoperative neuroprotection).
  3. Unfortunately, further damage occurs as a result of processes that are initiated during the reperfusion stage.
  4. A shift in the focus of neuroprotection from metabolic suppression to targeting ischemic cascades has recently been advocated.
  5. Hypothermia
  6. Profound hypothermia is well known for its neuroprotective effects. When core body temperature decreases below 20°C, circulatory arrest of less than 30 minutes appears to be well tolerated.
  7. Mild hypothermia (33° to 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.
  8. There is ample evidence that hyperthermia is associated with worse outcome in the setting of ischemic stroke, subarachnoid hemorrhage, cardiac arrest, and TBI.
  9. In the operating room during neurosurgical procedures during which the brain is at risk for ischemic insult, a goal temperature of 35° to 36°C is reasonable. Mild hypothermia (33° to 35°C) may be appropriate in many patients, recognizing that there may be no benefit to this therapy.

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  1. Medical Therapy for Cerebral Protection
  2. 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.
  3. Barbiturates, such as thiopental, have been shown to have at least short-term benefits on focal cerebral ischemia, but the benefit in global ischemia remain controversial. Propofol likely has similar protective effects.
  4. 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).
  5. Clinically, barbiturates and propofol are used intraoperatively to achieve burst suppression on the electroencephalogram (EEG), although its neuroprotective action does not appear to be metabolically mediated.
  6. Glucose and Cerebral Ischemia
  7. Although considerable evidence has accumulated suggesting harm from hyperglycemia, evidence for benefit with normalization of serum glucose concentrations using insulin has been controversial.
  8. 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.)
  9. A Practical Approach
  10. 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.
  11. Euglycemia before vessel occlusion is desirable, but frequent glucose checks are essential during anesthesia

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to avoid episodes of hypoglycemia if insulin is administered.

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

VII. Anesthetic Management

  1. Preoperative Evaluation
  2. 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.
  3. 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.
  4. Many patients presenting for spine surgery have weakness or paralysis that may present a contraindication to the use of succinylcholine (Sch).
  5. Many neurosurgical patients have been exposed to antiepileptic medications. Previous allergies or reactions to these medications, especially phenytoin, should be elucidated.
  6. Induction and Airway Management
  7. During induction of anesthesia, three iatrogenic consequences (hypotension, hypertension, apnea) may be significant hazards for neurosurgical patients.
  8. Hypertension caused by laryngoscopy is poorly tolerated by patients after aneurysmal subarachnoid hemorrhage because systolic hypertension is thought to be a cause of recurrent hemorrhage from the aneurysm.
  9. Hypertension may worsen elevated ICP and possibly lead to herniation of cranial contents into the foramen magnum.
  10. Apnea results in a predictable increase in PaCO2and corresponding cerebral vasodilation.
  11. 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.
  12. Because patients with subarachnoid hemorrhage are at risk for harm from hypertension, it is reasonable to

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place an arterial catheter for hemodynamic monitoring before induction of anesthesia.

  1. Many neurosurgical and spine surgery patients have conditions in which Sch is contraindicated.
  2. 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.
  3. Alternatively, a rapid-acting nondepolarizing muscle relaxant is appropriate in many neurosurgical patients to achieve acceptable intubating conditions.
  4. Maintenance of Anesthesia
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. Ventilation Management
  10. Hypocapnic cerebral vasoconstriction provides anesthesiologists with a powerful tool for manipulating CBF and CBV.
  11. Hyperventilation is routinely used to provide brain relaxation and optimize surgical conditions.
  12. 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.
  13. During neurosurgical procedures, it is reasonable to maintain the PaCO2between 30 and 35 mm Hg. Further brain relaxation should be accomplished with

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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.

  1. 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.
  2. Fluids and Electrolytes
  3. To maintain adequate cerebral perfusion, adequate intravascular volume should be maintained (euvolemia to slight hypervolemia).
  4. 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.)
  5. 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.)
  6. Glucose Management
  7. The combination of hyperglycemia and cerebral ischemia appears to be particularly deleterious. Although a paucity of evidence addresses the topic of intraoperative glucose management, logic dictates that glucose concentrations should be normalized before periods of iatrogenic ischemia.
  8. The presumed risk of tight glycemic control is inadvertent episodes of hypoglycemia.
  9. A target glucose concentration above 180 mg/dL is adequate in most patients.
  10. Emergence
  11. 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.
  12. 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

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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.

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

VIII. Common Surgical Procedures

  1. Surgery for Intracranial Tumors
  2. 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.
  3. 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.
  4. Adequate brain relaxation is typically achieved with a standard anesthetic including sub-MAC volatile anesthesia, an opioid infusion, mild to moderate hyperventilation, and mannitol.
  5. Pituitary Surgery
  6. 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.
  7. Small pituitary tumors can be resected by a transsphenoidal approach, but larger tumors may require a craniotomy.
  8. 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.
  9. DI is a common complication of pituitary surgery because of the loss of antidiuretic hormone production. It may be temporary or permanent and

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may occur either in the intraoperative or postoperative period.

  1. 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.
  2. Arteriovenous Malformations
  3. Cerebral angiography remains the “gold standard” for diagnosis of arteriovenous malformations (AVMs).
  4. 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.
  5. After resection of large AVMs or those in the posterior fossa, it may be appropriate to take the patient to the intensive care unit (ICU) 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.
  6. Cerebral Aneurysm Surgery and Endovascular Treatment
  7. For patients who survive hemorrhage, surgical or endovascular intervention to secure the aneurysm is essential to prevent further hemorrhage.
  8. Patients with aneurysmal subarachnoid hemorrhage 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.
  9. 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.
  10. Carotid Surgery
  11. Carotid stenosis is a common cause of transient ischemic attack and ischemic stroke. It is amenable to surgical intervention and endovascular stenting.
  12. 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

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antihypertensive therapy, the margin of benefit of surgery may be even lower.

  1. Both general and regional anesthesia may be used for CEA. Regional anesthesia is accomplished with a superficial cervical plexus block or a combination of superficial and deep cervical plexus block.
  2. Several CNS monitors may be used during CEA under general anesthesia.
  3. Rapid emergence and tracheal extubation at the end of the procedure are desirable because they allow immediate neurologic assessment.
  4. Epilepsy Surgery and the “Awake” Craniotomy
  5. 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).
  6. Patients with a difficult airway, obstructive sleep apnea, or orthopnea may present a relative contraindication to an “awake” craniotomy. Patients with severe anxiety, claustrophobia, or other psychiatric disorders may be particularly inappropriate candidates for this type of procedure.
  7. For suitable candidates, spontaneous ventilation with propofol anesthesia is an attractive option because it allows emergence with minimal coughing, gagging, or straining. In addition, propofol provides an acceptable anesthetic for these patients because of its low incidence of nausea and vomiting during the awake period. Benzodiazepines should be avoided because they may interfere with electrocorticography during epilepsy surgery. Allowing the patient to emerge during an infusion of low-dose remifentanil or dexmedetomidine may facilitate extubation with little movement.
  8. Anesthesia and Traumatic Brain Injury
  9. Overview of Traumatic Brain Injury
  10. The presence of TBI is the primary determinant in quality of outcome for patients with traumatic injuries.
  11. 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.

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  1. Patients with TBI have a 5% to 6% incidence of an unstable cervical spine injury.
  2. Risk factors include a motor vehicle accident and Glasgow Coma Score (GCS) 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.
  3. 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 efficacy of application of cricoid pressure has not been demonstrated, and it may displace cervical fractures; nevertheless, it may be considered the standard of care during rapid sequence intubation.
  5. An important consideration is the choice of drugs to facilitate tracheal intubation. Hypotension is extremely detrimental to the injured brain.
  6. Administering muscle relaxants prevents coughing and the resultant spikes of ICP. The main choice is between Sch and rocuronium. The main drawback to rocuronium is the prolonged effect when a rapid sequence dose (1.2 mg/kg) is used. The argument against Sch is the potential increase in ICP (this is not supported by clinical data).
  7. The overwhelming evidence of harm from hypotension necessitates restoration of intravascular volume. The goal is to maintain CPP in the range of 50 to 70 mm Hg.
  8. In the absence of ICP monitoring but with known TBI, an ICP of at least 20 mm Hg should be assumed, and MAP should be kept above 60 mm Hg.
  9. Patients with TBI are typically described by their GCS (see Table 39-9). This simple test provides prognostic information and facilitates communication between providers.
  10. The presence of a unilateral dilated pupil suggests brainstem compression and is a surgical emergency. The presence of bilateral dilated pupils portends a dismal prognosis.
  11. Intracranial hypertension predisposes patients to poor outcomes, and elevated ICP refractory to therapy is associated with a worse prognosis.

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Table 39-9 Glasgow Coma Scale

Eyes

1

No eye opening

2

Opens to painful stimulation

3

Open to voice

4

Spontaneous eye opening

Verbal

1

No sounds

2

Incomprehensible sounds

3

Inappropriate words

4

Confused conversation

5

Normal speech

Motor

1

No movement

2

Extension to painful stimulus

3

Abnormal flexion to painful stimulus

4

Withdrawal from painful stimulus

5

Localization of painful stimulus

6

Follows commands

  1. CPP goals are 50 to 70 mm Hg.
  2. Reduction of ICP in patients with head injuries can be accomplished effectively using osmotic diuretics.
  3. Mannitol is the most commonly used agent and is available for IV administration in either a 20% or 25% solution. Common doses range from 0.25 to 1 g/kg of body weight. Mannitol may be used on a repeated schedule, but the serum osmolarity should not be allowed to exceed 320 mOsm. Intravascular volume depletion should be avoided.
  4. The mechanism of ICP reduction by mannitol may be related to its osmotic effect in shifting fluid from the brain tissue compartment to the intravascular compartment as well as its ability to decrease blood viscosity.
  5. Hyperventilation is an effective way to reduce ICP. It is useful in the setting of an acutely increased ICP that needs to be controlled until more definitive therapy can be initiated. Current recommendations are that patients with TBI should be maintained at normocapnia except when hypocapnia is necessary to control acute increases in ICP. Chronic hyperventilation should be avoided if possible.
  6. Given the rather limited situation in which hypothermia appears to be beneficial in patients with head injury, it is not recommended for routine use.

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  1. Barbiturates may be used as an adjunct to other therapy for controlling ICP. Barbiturate therapy is appropriate only in patients who are hemodynamically stable and have been adequately resuscitated. Propofol is a reasonable alternative to barbiturates for ICP management. Prolonged use of high-dose propofol is not recommended because it may cause a propofol infusion syndrome.
  2. Anesthetic Management.Patients with TBI requiring surgery can be subdivided into those who require emergent surgery and those who require non-emergent surgery.
  3. Emergent Neurosurgical Surgery.These patients commonly arrive in the operating room with an endotracheal tube in place. The neurologic condition of the patient can be determined rapidly by obtaining the GCS, examining the pupils, and reviewing the computed tomography (CT) scan.
  4. The patient's hemodynamic status is also extremely important. Patients may demonstrate a Cushing's response (hypertension and bradycardia), which signifies brainstem compression from increased ICP. These classic findings may be masked by hypovolemia, and their absence does not rule out brainstem compression.
  5. These patients usually do not have ICP monitors in place, but one can assume the presence of intracranial hypertension. The presence of midline shift on CT scan and pupillary abnormalities on physical examination reinforce this diagnosis.
  6. Moderate hyperventilation should be used in these patients until the dura is opened because the elevation in ICP is likely more detrimental than short-term hyperventilation.
  7. Blood pressure management is critical in these patients.
  8. Emergent Non-Neurosurgical Surgery.Trauma patients presenting for emergent surgical management of noncranial injuries who also have a concurrent TBI are complex to manage. The most immediately life-threatening condition must take priority, but the presence of TBI should be considered, particularly in patients with a depressed level of consciousness or abnormal pupil examination results.
  9. Non-Emergent Neurosurgical Surgery.Patients with TBI frequently have other injuries, especially fractures

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requiring operative fixation. The timing of surgery in these patients remains a controversial issue. In the setting of refractory elevations in ICP or very labile ICP, only emergent surgery should be performed.

  1. Anesthesia for Spine Trauma and Complex Spine Surgery

Surgery on the spinal column has become increasingly complex and lengthy, with multilevel fusions, combined anterior and posterior approaches to the spine, and staged procedures.

  1. Spinal Cord Injury
  2. Primary Injury.SCI can occur without radiographic abnormality, and damage to the spinal column may occur without injury to the spinal cord. Unstable SCI puts the neural elements at risk and necessitates some intervention to provide stability, which may be application of a brace or surgical intervention.
  3. Secondary injuryto the spinal cord is mediated through a cascade of deleterious events similar to those seen in TBI. Secondary injury may be exacerbated by hypotension caused by hemorrhage or neurogenic shock.
  4. Central, Anterior, Brown-Séquard, and Cauda Equina Injuries.Although a complete cord transection results in disruption of afferent and efferent signals, many injuries damage only a portion of the spinal cord.
  5. Central cord syndromeis characterized by greater severity of paresis in the upper extremities than the lower, as well as bladder dysfunction and variable loss of sensation below the lesion.
  6. Anterior cord syndromeis generally caused by disruption of blood flow through the anterior spinal artery at the level of the injury. The anterior portion of the cord becomes ischemic, disrupting motor function below the level, with a variable effect on sensation. Pain and temperature tracts are typically interrupted as well, but proprioception remains intact.
  7. Brown-Séquard syndromeis characterized by interruption of the lateral half of the spinal cord, typically through penetrating trauma. However, patients may not display all the classic findings of Brown-Séquard syndrome, which include loss of

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motor and touch sensation ipsilateral to the lesion with pain and temperature sensation lost contralateral to the lesion.

  1. Cauda equina syndromeis the result of injury below the level of the conus, or caudal end of the cord, typically below L2. Compression of the cauda equina results in perineal anesthesia, urinary retention, fecal incontinence, and lower extremity weakness.
  2. Comorbid Injuries
  3. Cervical spine trauma is associated with blunt cerebrovascular injury, TBI, and facial fractures.
  4. Thoracic trauma is also associated with vascular injury; in addition, one must consider the possibility of pneumothorax, myocardial contusion, and pulmonary contusion.
  5. Lumbar spine fractures may be associated with bowel and solid viscus injury.
  6. Initial Management
  7. Urgent Airway Management.Endotracheal intubation can be particularly difficult in patients with SCI, especially if the lesion is in the cervical spine. Cervical spine injury should be presumed in any trauma patient requiring intubation before complete physical and radiographic evaluation. Intubation should proceed with little movement of the cervical spine. A rapid sequence induction (which may include cricoid pressure) and manual in-line stabilization are appropriate unless a difficult airway is anticipated.
  8. Hemodynamic Stabilization.Restoration of intravascular volume is the first step in treatment of hypotension in patients with SCI. After euvolemia has been achieved, support of blood pressure with inotropic agents, vasopressors, or both may be required because of loss of sympathetic nervous system control below the level of the lesion (spinal shock).
  9. Role of Steroids.Methylprednisolone has become a common therapy for patients with neurologic deficit after SCI, although not all practitioners agree steroids are the standard of care.
  10. Timing of Surgical Intervention.The purpose of surgical intervention is to decompress the neural structures and stabilize the spinal column to prevent further injury to the spinal cord. Persistent hemodynamic instability or severe acute respiratory distress syndrome may impose a significant delay on surgical intervention.

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  1. Intraoperative Management
  2. Anesthetic Induction and Airway Management.If the patient's cervical spine has been radiographically and clinically “cleared” before arrival in the operating room, then the technique for induction of anesthesia and endotracheal intubation should be determined by the patient's other injuries, comorbidities, and airway examination results.
  3. Patients with a confirmed cervical spine injury should be immobilized in either a cervical collar or Halo device. A rapid sequence induction remains a viable option, particularly in patients who are unable to cooperate with an awake procedure.
  4. The most conservative approach to airway management in the presence of known cervical spine injury is awake fiberoptic endotracheal intubation (which requires thorough application of topical anesthesia to the airway).
  5. Anesthetic Technique
  6. Complex spine and trauma surgery imposes a significant risk of blood loss. An arterial catheter is essential for continuous hemodynamic monitoring and intermittent arterial blood gas and hematocrit analysis.
  7. In large thoracic or lumbar spine surgeries, particularly in the prone position, central venous access may be appropriate. The value of central venous pressure monitoring is controversial, however, because it is neither a good indicator of end-diastolic volume nor a predictor of volume responsiveness in patients with hypotension.
  8. Placement of a pulmonary artery catheter can be justified in sick patients with poor cardiac function, especially those in whom fluid management is difficult and vasopressor therapy is required.
  9. Neuromonitoring.The goals of spine surgery, whether for trauma or other spine disease, are typically to decompress the cord and stabilize the spinal column. These goals must be accomplished without inflicting further injury to the spinal cord. Monitoring spinal cord function is appropriate for many surgical procedures. The anesthetic plan must be tailored to accommodate these monitors.
  10. Patient Positioning.The prone position provides unique challenges to the anesthesiologist with respect

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to achieving adequate protection of the patient from pressure points (eyes, face, breasts, genitals, knees, toes). Frequent confirmation that the eyes are free from contact is important. The slight reverse Trendelenburg position may facilitate venous drainage from the head and reduce congestion and intraocular pressure. Padding on the chest should not compress the neck because this may also obstruct venous drainage.

  1. Glucose Management.There is little evidence to guide the management of glucose in patients with disease of the spine, particularly in the intraoperative setting.
  2. It is reasonable to continue tight glycemic control in patients who arrive in the operating room from the ICU, and it is reasonable to start tight glycemic control on patients who will be admitted to the ICU after surgery.
  3. These recommendations assume that frequent glucose monitoring is an integral part of the anesthetic procedure.
  4. In patients who are administered methylprednisolone, glucose control may be more difficult to achieve.
  5. Complications of Anesthesia for Spine Surgery
  6. Autonomic Hyperreflexia.Patients with chronic spinal cord lesions above T7 may develop autonomic reflexia when stimulated below the site of the lesion (intense vasoconstriction below the site of the lesion accompanied by cutaneous vasodilation above, hypertension, and bradycardia). To reduce the incidence of this complication, suppression of the afferent pathway by “deepening” anesthesia is necessary. A spinal anesthetic, if possible, may be ideal.
  7. Postoperative Visual Loss.The visual loss is commonly bilateral and caused by ischemic optic neuropathy (which has a multifactorial etiology), although retinal artery occlusion and cortical blindness may also occur.
  8. Postoperative visual loss may occur despite the absence of pressure on the eyes from positioning errors, which would result in central retinal artery thrombosis rather than anterior or posterior ischemic optic neuropathy.
  9. Ischemic optic neuropathy is associated with blood loss and a long operative duration.
  10. Given the increasing recognition of this problem, it may be a preoperative consideration to inform

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high-risk patients (those in whom blood loss and long surgeries are anticipated) of this rare event.

  1. There is no proven method to prevent ischemic optic neuropathy nor is there a reliable method to monitor visual function during these procedures.
  2. Staging of a complex spine procedure may be the most effective means of preventing this devastating complication because limiting the duration of the procedure would also limit the risk of hypotension and blood loss.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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