Anesthesia for Carotid Surgery
In the United States, each year approximately 795,000 people experience a new or recurrent stroke. Approximately 610,000 of these were first attacks and 185,000 were recurrent attacks. In 2016 the age-adjusted death rate for stroke as an underlying cause of death was 37.3 per 100,000.
The risk of stroke in the hyperacute period after the index TIA in patients with 50%–99% carotid stenoses is: 5%–8% at 48 hours, 17% at 72 hours, 8%–22% at 7 days, and 11%–25% at 14 days. Clinical predictors of increased late stroke in patients with 50%–99% stenoses are: male gender, age > 75 years, hemispheric symptoms, increasing comorbidity. Clinical/imaging parameters associated with a lower risk of stroke are: female gender especially those with 50%–99% stenoses, ocular symptoms/lacunar strokes, smooth stenoses, chronic subocclusion. Imaging features associated with increased late stroke in patients with 50%–99% stenoses are: irregular stenoses, contralateral occlusion, increasing stenosis severity but not subocclusion, tandem intracranial disease, failure to recruit intracranial collaterals, low gray-scale median (GSM) measurement on carotid ultrasound, magnetic resonance imaging (MR) diagnosis of intraplaque hemorrhage, spontaneous embolization on transcranial doppler (TCD), increased fluorodeoxyglucose (FDG) uptake in the carotid plaque on positron emission tomography (PET).
A number of interventions exist potentially to prevent recurrent stroke. Carotid surgery is one such intervention. Carotid surgeries performed for prevention of strokes are carotid endarterectomy (CEA), carotid angioplasty/stenting, and transcarotid artery revascularization. CEA is the most frequently performed surgical procedure to prevent stroke in the United States. In 2014, an estimated 86,000 inpatient CEA procedures were performed in the United States.
CEA is recommended for symptomatic patients (e.g., with ipsilateral transient ischemic attacks [TIAs] or nonprogressing, nondisabling stroke within the previous 6 months) who have 70% to 99% angiographic stenosis of the internal carotid artery.
CEA can be considered for men with 50% to 69% symptomatic stenosis, especially men older than 75 years, but additional clinical and angiographic variables that might alter the risk-to-benefit ratio should be considered. For symptomatic patients, life expectancy should be at least 5 years and perioperative stroke or death rate should be less than 6%. CEA should not be considered for symptomatic patients when stenosis is less than 50%. Symptomatic patients with near occlusion angiographically also do not derive any long-term benefit from CEA. CEA can be considered for asymptomatic patients between the ages of 40 and 75 years with stenosis of 60% to 99%. Life expectancy should be at least 5 years and the perioperative stroke or death rate should be less than 3%. Notably, women with symptomatic stenosis of 50% to 69% did not show clear benefit in any of the large trials. Patients presenting with retinal ischemia (amaurosis fugax or retinal infarction) have a lower risk of subsequent stroke compared with patients with hemispheric events. However, CEA may be beneficial when other risk factors for stroke are also present.
Up to 28% of patients presenting for CEA have severe angiographic coronary artery disease and myocardial infarction is a leading cause of death after CEA. However, the overall incidence of perioperative myocardial infarction is low (0.3% from North American Symptomatic Carotid Endarterectomy Trial [NASCET] data).
Medical complications occur in 8.1% of patients within 30 days after CEA with symptomatic stenosis (30% to 99%): 1% myocardial infarctions, 7.1% other cardiovascular disorders (arrhythmia, congestive heart failure, angina pectoris, hypertension, hypotension, sudden death), 0.8% respiratory complications, 0.4% transient confusions, 0.7% other complications. CEA was approximately 1.5 times more likely to trigger medical complications in patients with a history of myocardial infarction, angina, or hypertension. In patients with 50%–99% stenosis, 11%–25% will suffer stroke within 14 days of index symptoms. Based on this, delaying CEA for those who fit the criteria is not recommended. Identification and optimization of modifiable risk factors such as hypertension, coronary artery disease, diabetes mellitus, and renal insufficiency should occur in accordance with the guidelines for perioperative evaluation for noncardiac surgery. Patients with major clinical predictors, such as suspected unstable coronary syndrome, may require cardiac catheterization independent of the need for CEA. In the unusual cases of patients requiring coronary revascularization, staged or combined operations may be necessary, depending on the severity of the coronary and carotid disease.
Preoperative Risk Factors for Perioperative Stroke
Risk factors for stroke resulting from CEA can be divided into preoperative medical, neurologic, and radiographic risk factors. Based on these factors, a risk stratification system was proposed and has been validated as a valuable tool in predicting adverse neurologic outcome after CEA. An adaptation of this risk stratification is presented in Box 21.1 .
Medical risk factors
Chronic renal insufficiency (creatinine > 1.5 mg/dL)
Active coronary artery disease (unstable angina or angina with minimal activity in the past 12 months)
Diabetes mellitus, on insulin
Congested cardiac failure
Severe, poorly controlled hypertension
Advanced age (> 70 years) with comorbidities
Chronic obstructive airways disease
Neurologic risk factors
Crescendo transient ischemic attacks (TIAs) (i.e., more than one TIA per day)
TIA while anticoagulated with heparin
Multiple completed strokes
Ischemic symptoms less than 24 hours before the surgical procedure
Symptom status of the patient: asymptomatic patients and patients with only ocular ischemic events < patients with TIA < patients with stroke
Radiographic risk factors
Occlusion of the contralateral internal carotid artery
Near occlusion on the operative side
Lack of angiographic collateral blood flow
Ipsilateral intracranial stenosis
Plaque extension more than 3 cm distal to the origin of the internal carotid artery or 5 cm proximal to the common carotid artery
High bifurcation of the carotid artery
Thrombus extending from the operative lesion
Perioperative stroke risk stratification
Group 1: no preoperative risks
Group 2: angiographic risks only
Group 3: medical risks with or without angiographic risks
Group 4: neurologic risks with or without medical or angiographic risks
As part of the preoperative assessment, a series of blood pressure and heart rate measurements should be obtained to define patient-specific acceptable ranges for perioperative management. Blood pressure should be maintained in the high–normal range throughout the procedure, particularly during the period of carotid clamping, in an attempt to increase collateral blood flow to prevent cerebral ischemia.
Hemodynamic fluctuations are common during CEA. Hypotension is more common under general anesthesia and often occurs immediately after the induction of anesthesia or after carotid unclamping and cerebral reperfusion. In patients with contralateral internal carotid artery occlusion or severe stenosis, induced hypertension to approximately 10% to 20% above baseline may be helpful during carotid clamping when neurophysiologic monitoring is not used. Blood pressure preservation or augmentation can be accomplished by appropriate intravascular hydration, avoiding unnecessarily deep levels of general anesthesia, and vasopressor therapy, such as phenylephrine and ephedrine. In the absence of severe left ventricular systolic dysfunction, phenylephrine may be preferred over ephedrine because increased contractility and heart rate associated with ephedrine increases myocardial oxygen consumption to a greater extent than the increase in wall stress caused by phenylephrine.
Because intraoperative hypertension and tachycardia can increase myocardial oxygen consumption, blood pressure elevations above 20% of the baseline and tachycardia should be avoided. Furthermore, such increases in blood pressure might put the patient with a recent stroke at risk of hemorrhagic conversion of the infarcted brain tissue. Hypertension should be treated appropriately, taking into account the stage of the operation, the level of anesthesia, and the patient’s heart rate. Deepening the anesthetic, beta-blocker therapy, nicardipine, and clevidipine are commonly used. Agents with a short half-life are preferred.
Bradycardia might occur during surgical manipulation of the carotid sinus or direct stimulation of the vagus nerve during dissection. Prophylactic injection of local anesthetic between the internal and external carotid arteries before manipulation of these vessels can attenuate bradycardia. However, local anesthetic infiltration may increase intraoperative and postoperative hypertension. Administration of anticholinergic drugs can result in tachycardia, excessive hypertension, and increased myocardial oxygen requirements, and their use should therefore be avoided.
Severe carotid stenosis, in particular during cross-clamping, represents a state of gross regional flow inequality and collateral dependence. The vessels supplying ischemic areas are usually maximally vasodilated and blood flow could be diverted from these vascular beds to those already adequately perfused by cerebral vasodilators such as carbon dioxide, volatile anesthetic agents, and nitrates (i.e., cerebral steal). The reverse may occur in hypocapnia or as a result of intravenous anesthetic agents such as thiopental and propofol (i.e., inverse steal). On balance, normocarbia is recommended and low levels of volatile anesthetic agents are acceptable.
There is sufficient evidence that hyperglycemia in nondiabetic patient is associated with poor outcome. Persistent hyperglycemia, defined as hyperglycemia within 6 hours of stroke and at 24 hours, is inversely associated with neurological improvement, 30-day favorable functional outcome, and 90-day negligible dependence.
There is no difference in outcome between general and regional anesthesia for carotid surgery. The choice of anesthesia should be determined by patient and surgical team preference and a specific patient’s comorbidities and risk factors. General anesthesia can offer ideal operating conditions. Provided that close attention is paid to the physiologic variables and a rapid, controlled emergence from anesthesia is ensured, no outcome-based evidence favors one anesthetic over another. Although it would seem logical that isoflurane or even barbiturate pretreatment would offer cerebral protection during carotid cross-clamping, no outcome data suggest reduction in either the incidence or severity of intraoperative stroke during CEA.
Remifentanil infusion (0.05 to 0.2 μg/kg/min) ablates the sympathetic response to surgery, although phenylephrine infusion may be needed to maintain perfusion pressure. For amnesia, a low dose of volatile anesthetic (isoflurane or sevoflurane, usually between 0.3 and 0.5 of the minimum alveolar concentration [MAC]), or less commonly a propofol infusion, is titrated using electroencephalogram (EEG) based hypnotic monitors such as bispectral index (BIS). Muscle relaxation can be maintained with a nondepolarizing agent. This approach provides hemodynamic stability and stable conditions for EEG monitoring. Nitrous oxide can be safely used during CEA. Nitrous oxide decreases the MAC of volatile agents and may decrease vasopressor requirement. In a secondary analysis of the general anesthesia versus local anesthesia for carotid surgery (GALA) trial, patients who received nitrous oxide were more likely to have coronary artery disease, peripheral vascular disease, and atrial fibrillation, but intraoperative nitrous oxide exposure was not associated with an increased risk of perioperative stroke, myocardial infarction, or death.
After closure of the deep fascial layers, volatile anesthetic can be discontinued and neuromuscular reversal agents administered. On skin closure, the remifentanil infusion rate is reduced to 0.02 to 0.05 μg/kg/min, allowing the patient to emerge gently from anesthesia. This approach can allow a neurologic assessment while the patient is still intubated. Hypertension on emergence usually responds well to labetalol, and in some instances infusion of nicardipine, clevidipine, or nitroprusside may be required.
Superficial cervical plexus block, in combination with additional local anesthetic infiltration by the surgeon, can achieve required sensory blockade of C2 to C4 dermatomes. Deep cervical plexus blockade can also be performed safely but adds risks, such as inadvertent intravascular or intrathecal injections, paralysis of the ipsilateral diaphragm, and local anesthetic toxicity, without reducing the need for intraoperative local anesthetic supplementation. Sedation should be kept to a minimum to allow continuous neurologic assessment, in particular during carotid cross-clamping. Levels of consciousness, speech, and contralateral handgrip are assessed throughout the procedure. Patient refusal, language barriers, and difficult surgical anatomy, such as a high carotid bifurcation, may be contraindications to regional techniques.
Cerebral Monitoring to Detect Ischemia During CEA
Clamping of the carotid artery during CEA and balloon insufflation during carotid angioplasty/stenting can lead to cessation of blood flow in an already stenosed artery. Perfusion of the brain ipsilateral to the side of occlusion depends on perfusion from collateral circulation. Brain ipsilateral to the side of procedure is at risk of ischemia from poor collateral circulation and thromboembolic stroke from ruptured atherosclerotic plaque and/or surgical debris. The incidence of periprocedural stroke in the stenting group is 4.1% and in the endarterectomy group 2.3%. Therefore it is important to monitor for signs of ischemia during carotid surgery. Commonly used monitors are listed in Box 21.2 .
Clinical neurological monitoring of the awake patient
Somatosensory evoked potentials (SSEP)
Motor evoked potentials (MEP)
Cerebral blood flow
Transcranial Doppler ultrasound
Xenon 133 washout
Near infra-red spectroscopy (NIRS)
Jugular venous oxygen saturation
Conjunctival oxygen tension
Monitoring of neurological and cognitive functions in awake patients is very reliable in detecting cerebral ischemia during CEA performed under regional or local anesthesia. In a study of 314 awake patients undergoing CEA under regional anesthesia, neurological monitoring in awake patients was found to be more sensitive and specific in identifying patients requiring shunt placement compared with EEG and measurement of carotid artery stump pressure. Awake monitoring under regional anesthesia requires the patient to be cooperative, which might not be possible in all cases. The GALA trial did not show any definite difference in outcomes between general and local anesthesia for carotid surgery.
In patients undergoing CEA, intraoperative EEG and somatosensory evoked potential (SSEP) monitoring with selective carotid artery shunting had a stroke rate lower than that of the routine shunting group. Stump pressure of 25 mmHg and either transcranial Doppler (TCD) or EEG was found to have best results in detecting brain ischemia during carotid artery cross-clamping. EEG has a sensitivity of 70% and a specificity of 96% and diagnostic odds ratio increase with a high number of channels. Sensitivity and specificity for SSEP (amplitude reduction greater than 50%) in detecting postoperative neurologic deficits were 100% and 94% when compared with EEG of 50% and 92% respectively in 64 patients undergoing CEA under anesthesia with isoflurane or halothane-nitrous oxide. SSEP is a highly specific test and patients with perioperative neurological deficits are 14 times more likely to have had changes in SSEPs during the procedure. Transcranial motor evoked potentials (MEP) can be an adjunct to SSEP to avoid a false-negative of 1.5% from SSEP.
During CEA, TCD changes of middle cerebral artery velocity (MCAV) or cerebral microembolic signals showed specificity of 72.7% and sensitivity of 56.1% in predicting perioperative strokes. Intraoperative MCAV showed strong specificity of 84.1% and sensitivity of 49.7% for predicting perioperative strokes.
Carotid stump pressure is the measurement of internal carotid artery back pressure at distal end after cross-clamping. Stump pressure reflects adequacy of collateral circulation and is used to determine selective shunt placement during CEA. Carotid stump pressure of < 50 mmHg and abnormal EEG changes is indicated for selective shunting in patients undergoing CEA under general anesthesia. In a series of 474 CEA under cervical plexus block, shunting was required because of neurologic changes in 7.2% of all CEA; 0.9% had stump pressure ≥ 50 mmHg systolic versus 1.0% with stump pressure ≥ 40 mmHg systolic. Stump pressure threshold of 40 mmHg systolic would have resulted in shunting in 15% with the false-negative rate of 1.0% if CEA had been performed under general anesthesia (GA). These results were similar to CEA performed under GA with EEG monitoring.
Near infrared spectroscopy (NIRS) is a noninvasive continuous cerebral oximetry measuring hemoglobin oxygen saturation of the frontal region of the brain from the measurements of near infrared light backscattered from the brain. Cerebral oximetry has shown an ipsilateral decrease in regional cerebral tissue oxygenation (rSCO 2 ) during carotid cross-clamp or balloon occlusion as a result of a decrease in cerebral perfusion and oxygen delivery. In patients undergoing CEA under regional anesthesia, a 20% decrease in rSCO 2 from the preclamp baseline as a predictor of neurologic compromise has shown sensitivity of 80% and specificity of 82.2%. The false-positive rate was 66.7%, the false-negative rate was 2.6%, positive predictive value was 33.3%, and a negative predictive value of 97.4%. In patients undergoing CEA under GA, greater than 25% reduction rSCO 2 from baseline resulted in sensitivity of 100%, specificity of 90.6%, positive predictive value of 9%, and negative predictive value of 100%. A 20% reduction in rSCO 2 persistent for more than 4 minutes resulted in sensitivity of 100%, specificity of 82.83%, positive predictive value of 2.26%, and a negative predictive value of 100% respectively.
Blood pressure may continue to be labile for several days postoperatively, sometimes requiring continued use of vasoactive drugs. Untreated hypertension in the postoperative period may lead to cerebral hyperperfusion syndrome, myocardial ischemia, and neck hematoma. Hypertension unresponsive to labetalol may require a nicardipine infusion.
In patients with severe carotid stenosis, regional intracranial circulation may be unable to autoregulate blood flow and remain maximally vasodilated in the postoperative period. Sudden increase in cerebral perfusion pressure (CPP) and blood flow may lead to edema formation, termed “perfusion breakthrough.” This typically occurs within the first few hours after surgery and may manifest as a severe headache, seizure, or even intracranial hemorrhage. Intracranial hemorrhage after CEA has high mortality and blood pressure should therefore be carefully controlled in these patients.
Wound hematoma is one of the more common early postoperative complications, occurring in about 4% of patients. Because of increased risk of airway obstruction, these patients have to be intubated for emergent surgical exploration. Tracheal deviation caused by the hematoma and pharyngeal edema caused by venous and lymphatic obstruction may complicate mask ventilation and intubation. Furthermore, pharyngeal edema may not resolve immediately after hematoma evacuation and patients should be extubated with great care if this was present at the time of intubation.
Endovascular Carotid Artery Angioplasty and Stenting for Carotid Stenosis
Endovascular carotid artery angioplasty and stenting (CAS) is gaining popularity. Advantages of CAS are minimal invasiveness, relatively short operative time, performance under MAC, and accommodation of patient’s comorbid conditions that increase risk with CEA. CAS may also be performed when CEA is technically or anatomically difficult, including challenging neck anatomy, carotid stenosis located too high or too low in the neck, restenosis after CEA, or radiation in the cervical area.
Endovascular treatment for carotid stenosis is associated with an increased risk of periprocedural stroke or death compared with endarterectomy in patients > 70 years of age, despite lower risks of myocardial infarction, cranial nerve palsy, and access site hematomas when compared with CEA.
Anesthesia for Intracranial Surgery
Anesthesia for intracranial surgery requires detailed discussion between anesthesiologist, surgeon, and attendants regarding patient positioning, intraoperative use of steroids, diuretics and anticonvulsants, anticipated blood loss, appropriate intraoperative management of blood pressure, PaCO 2 and temperature. Special considerations should be given for intracranial pressure and volume management, control of hemodynamic response to endotracheal intubation and Mayfield pin placement, and smooth emergence from anesthesia. The brain is enclosed in a rigid skull and may be intolerant of volume increases, but it is a highly vascular organ and has the potential for massive hemorrhage. Tolerance to interruption of substrate delivery is minimal and the brain is therefore equipped with a highly developed and responsive ability to autoregulate regional blood flow. Anesthetics and physiologic factors controlled by the anesthesiologist have profound effects on the brain and it is reasonable to expect an anesthesiologist who is providing care for patients undergoing craniotomy to understand these interactions.
There is increase use of intraoperative neurophysiological monitoring such as MEP, SSEP, brain stein auditory evoked potentials (BAEP), cranial nerve monitoring, and electromyogram (EMG) during intracranial surgery. Detailed discussion with surgeons regarding intraoperative neurophysiological monitoring dictates anesthetic selection during intracranial surgery.
Preoperative considerations for neurosurgical patients are similar to those for all surgical patients, with some significant adjuncts. Of primary importance is the baseline neurologic evaluation. At emergence from anesthesia, failure to recover baseline neurologic function can be attributed to a number of surgical or anesthetic-related factors of varying degrees of urgency. First, the anesthesiologist must recognize changes from baseline and participate in the decision-making process. Second, the anesthesiologist must recognize the magnitude of preoperative intracranial pressure (ICP) and intracranial compliance, and the potential for intraoperative intracranial hypertension. Third, the anesthesiologist should be familiar with the location and size of the lesion because this has a bearing on the surgical approach and patient positioning, the potential for intraoperative hemorrhage, the effects of cerebral edema, and possible postoperative neurologic deficits, including airway protection and arousal difficulties. Finally, the list of preoperative medications is important for a variety of reasons. During the course of surgery, scheduled doses of antiepileptics, steroids, and antibiotics may be missed, which could result in postoperative complications. High-dose steroid requirements may require intensive insulin regimens to maintain normal serum glucose and patients receiving antihypertensive therapy may exhibit exaggerated hemodynamic responses to anesthetic agents. A focused history and brief physical examination should incorporate all these issues and adequately prepare the anesthesiologist for the neurosurgical procedure.
In addition to preoperative evaluation, the anesthesiologist should consider any necessary premedication. As a general rule, long-acting preoperative medications that might result in an alteration of the postoperative neurologic status should be minimized or avoided. Premedications for prophylaxis against postoperative nausea and vomiting is reasonable, given its frequency.
Concerns unique to induction of anesthesia for craniotomy are principally related to maintaining cerebral perfusion pressure and preventing intracranial hypertension. To maintain cerebral perfusion in the presence of impaired autoregulation, hypotension or intracranial hypertension must be avoided. Early studies recognized that induction of anesthesia for craniotomies is associated with major increases in ICP and techniques evolved to minimize this. Sympathetic responses and associated increases in ICP caused by noxious stimuli such as endotracheal intubation, line placement, and surgical stimulation can be effectively blunted with an adequate depth of anesthesia. Complete muscle relaxation should be achieved and maintained to avoid coughing and straining and use of opioids and intravenous lidocaine prior to intubation is common. In addition to blunting responses to intubation, intravenous anesthetic agents decrease cerebral metabolic rate, cerebral blood flow (CBF), intracranial volume, and ICP. Volatile anesthetic agents are potent cerebrovascular vasodilators that overcome blood flow reduction caused by metabolic suppression and result in dose-dependent increase in CBF, blood volume, and ICP. Increase in ICP can be blunted by simultaneous moderate hyperventilation. Use of specific anesthetics for ICP control has unclear effects on outcome after craniotomy and advocating any specific anesthetic or technique for ICP control during induction is difficult.
Maintenance of neurosurgical anesthesia, like that of other surgeries, is usually uncomplicated. However, two special considerations exist: attendance to intracranial volume and necessity for rapid emergence. ICP and intracranial volume are usually managed by careful head positioning to avoid neck vein compression, maintaining normocapnia and normotension, avoiding high dosages of volatile anesthetic (greater than 1 MAC), and administering routine osmotic diuretics, such as mannitol. Occasionally, problems arise, particularly when the dura mater is opened or during the posterior fossa procedures. A “swollen” brain can herniate through dural defects, prohibiting further dural incision or adequate surgical field visualization. Management of acute intracranial hypertension is discussed later.
Rapid emergence is required for quickly and fully assessing patients for any postoperative neurologic deficit related to treatable causes (e.g., hematoma or cerebral edema). If the patient does not return to preoperative neurologic function, brain imaging and possible empiric treatment may be required. Therefore, it is imperative that residual anesthetics play no role in altered levels of consciousness or postoperative neurologic deficit. Methods that result in a fully awake, cooperative patient after anesthesia include lower doses of volatile agent (0.5 to 0.7 MAC) supplemented by remifentanil infusion. This technique allows excellent hemodynamic control through titration of remifentanil doses during the stimulating portions of the surgery, with rapid awakening at its end. All volatile anesthetic agents except nitrous oxide suppress cerebral metabolic rate for oxygen (CMRO 2 ) in a dose-dependent manner. All volatile anesthetic agents are also intrinsic cerebral vasodilators. The order of vasodilating potency is approximately halothane >> enflurane > desflurane > isoflurane > sevoflurane. Volatile agents (except nitrous oxide) at a dose of 0.5 MAC cause predominant reduction in CMRO 2 with net reduction in CBF. At 1.0 MAC, CBF is unchanged, and decrease in CBF due to CMRO 2 suppression is balanced by vasodilatory effects of volatile agents (increase in CBF). Above 1.0 MAC, flow-metabolism uncoupling occurs with vasodilatory activity of volatile agents and subsequent CBF increase.
For surgical procedures where neurophysiological monitoring is used, volatile anesthetic agents can be replaced by propofol infusion. Neuromuscular blockage can be avoided with the use of remifentanil infusion when monitoring MEP and EMG.
Management of Arterial Blood Pressure
In general, normotension is maintained in craniotomy patients. However, at times either low or high blood pressure may be more suitable. Blood pressure management can usually be accomplished by adjusting the anesthetic level. However, anesthetic techniques based largely on high-dose remifentanil infusion may induce more pronounced vasodilation and hypotension, and alpha agonism via phenylephrine may be used to offset hypotension caused by the anesthetic. When increased arterial blood pressure may be of benefit (e.g., in a patient with a high ischemic risk), phenylephrine is, again, in common use. However, patients who might be in a low cardiac output state may derive more benefit from appropriate intravascular volume therapy and inotropic support in the form of mixed alpha–beta agonism (i.e., norepinephrine). When strict blood pressure maintenance is essential to avoid even minimal amounts of hypertension (e.g., at induction during aneurysm clipping and at emergence from anesthesia), infusion of a calcium channel blocker, nicardipine or clevidipine generally provides adequate control. Either agent rapidly and effectively treats increased systemic blood pressure and allows blood pressure to be maintained within a very strict range. The choice of agent depends primarily on provider preference, although clevidipine pharmacokinetics may be more favorable as a result of rapid onset of action and ease of titration. The use of nitroprusside may interfere with brain autoregulation of blood flow and cause increased intracranial pressure via increased blood volume in the arterial vasculature; this concern is not present with the use of nicardipine. When less precise control is acceptable, longer-acting agents, such as labetalol or clonidine, may be used.
Management of Ventilation
Alteration of PaCO 2 , within the range of approximately 20 to 80 mmHg causes a parallel change in CBF, which is a surrogate for cerebral blood volume (CBV). Because of the rigid structure of the skull and the relatively unchangeable volume outside the intravascular space, CBV is a direct determinant of ICP. Although CBF is easy to measure, CBV is not (particularly in humans). Given constant mean arterial pressure (MAP), PaCO 2 -induced changes in CBF correlate with reproducible changes in CBV. Indeed, abundant clinical evidence in patients with ICP monitors shows that reduction of PaCO 2 results in transient reduction in ICP and vice versa. Historically, large reductions in PaCO 2 were common practice. However, use of techniques to measure retrograde jugular venous hemoglobin O 2 saturation in patients with traumatic head injury has repeatedly shown that reduction in PaCO 2 can exacerbate cerebral hypoperfusion, presumably as a result of vasoconstriction. As a result, it is no longer advocated that major reductions in PaCO 2 be made in patients undergoing craniotomy for space-occupying lesions. Modest reductions in PaCO 2 remain valuable, however, to counteract vasodilatory effects of volatile anesthetics. Finally, it is important to measure arterial to end-tidal CO 2 gradients in all neurosurgical patients, because physiologic dead space variability can be unpredictable.
Intraoperative Fluid Management
The goals of intraoperative fluid management for patients undergoing craniotomy includes maintenance of euvolemia and avoidance of reduction in serum osmolarity. The induction of hyperosmotic therapy for the treatment of brain edema results in a predictable diuresis. Despite this, euvolemia should be maintained because both hypervolemia and hypovolemia are detrimental in some forms of brain injury. Euvolemia promotes improved osmotic diuresis and hypovolemia results in hypoperfusion, especially with sudden large surgical blood loss. Therefore, preoperative fluid deficit should be replaced and once hyperosmotic therapy has been instituted, euvolemia should be maintained by replacing urine volume. Because urine output should be replaced with the solution that most closely approximates the goal osmolality of 310 mM/dL, normal saline (with an osmolality of 308 mM/dL) should be considered over hypo-osmolar lactated Ringer’s solution, although no outcome data exist to support any particular fluid choice. In the setting of major blood loss, fluid management becomes more challenging. Because of osmotic diuresis, urine output cannot be used as a gauge for intravascular volume and surgical loss should be carefully estimated while observing the patient closely for signs of hypovolemia. Coagulopathy should be anticipated and treated early with appropriate products, as indicated by coagulation studies. Controversy exists over the use of colloid to replace surgical blood loss because of concern over potential bleeding diathesis with the use of synthetic colloids. There is increasing evidence that synthetic colloids starches are associated with increased bleeding diathesis, requirement of blood transfusion, and renal replacement therapy (RRT) in critically ill patients. Human albumin and fresh frozen plasma when compared with crystalloids were not associated with increased requirement for RRT. Although albumin has little effect on coagulation and RRT, fluid resuscitation with albumin in critically ill patients with traumatic brain injury (TBI) was associated with higher mortality than resuscitation with normal saline. Human albumin use for resuscitation in patients with severe TBI is associated with increased ICP and most likely mechanism of increased mortality in these patients.
Succinylcholine has received special consideration in the context of craniotomy. In both experimental animals and humans, succinylcholine can increase ICP when intracranial compliance is poor, although the increase is typically small and transient. Animal evidence supports the idea that fasciculation plays a role in the ICP effects of succinylcholine and there are data in humans that ICP changes caused by this drug can be prevented by preadministration of a defasciculating dose of nondepolarizing relaxants. A probable mechanism is that the massive fasciculation-induced afferent barrage from muscle spindles to the brain causes transient increases in metabolic rate and coupled increases in CBF. As with any decision, the risk-to-benefit ratio must be weighed when deciding whether succinylcholine is the appropriate agent. In controlled settings for nonemergent craniotomy, the ICP effects of succinylcholine can easily be offset by pretreatment with a nondepolarizing agent. At the same time, emergency airway management and the need to minimize hypercapnia and hypoxemia in patients with low intracranial compliance dictate that succinylcholine can be an appropriate adjunct for tracheal intubation.
The majority of patients undergoing craniotomy have been recently exposed to anticonvulsant agents. There is clear evidence that the duration of action of nondepolarizing muscle relaxants is reduced by anticonvulsant medications and even limited exposure can elicit this change. The mechanism for this remains unclear, but nondepolarizing agents that are metabolized by Hoffman elimination (e.g., atracurium and cis atracurium) are largely resistant to the effects of anticonvulsants.
Management of Emergence
With neurosurgical procedures involving craniotomy, planning for emergence from anesthesia begins with induction. The goals of emergence are a predictable recovery to allow testing of neurologic function in the context of stable hemodynamics and airway. A unique concern is that failure to emerge may be attributable to either anesthesia or surgery, which drastically alters subsequent treatment. If failure to emerge is attributable to surgery, a computerized tomographic (CT) scan is usually obtained to rule out hematoma formation or malignant cerebral edema. In contrast, if residual anesthesia is the issue, the use of opioid antagonists or additional reversal of neuromuscular blockade may be necessary. Therefore, when planning the anesthetic, it is helpful to restrict the use of agents to those that can be monitored for concentration or to those for which sufficient knowledge of pharmacodynamics allows highly probable and predictable clearance or reversal for emergence. It is best to keep the anesthetic simple so that each compound can be independently ruled out as an etiology for failure to emerge.
Although the magnitude of surgical stimulation after dural opening is minimal, patients undergoing craniotomy experience significant postoperative pain. Fear about delayed emergence and sedating effects of opioids analgesics frequently leads to emergence hypertension, tachycardia, coughing, straining, and inadequate post-craniotomy pain control. Ultra-short-acting opioid remifentanil as a sole analgesic agent may provide stable hemodynamics and rapid and smooth emergence but lacks postoperative analgesic effect. Compared with fentanyl infusion, patients receiving remifentanil infusion during craniotomy often have higher postoperative systolic blood pressure and earlier analgesic requirement. When used as a useful adjuvant, dexmedetomidine has been shown to reduce anesthetic requirement and to delay postoperative analgesic use.
A practical approach is to assume that the anesthesiologist needs 5 to 10 minutes after completion of the head dressing to allow a controlled emergence. Thus, neuromuscular blockade may be maintained until completion of the head dressing, elimination of volatile anesthetics should be complete by the time of head dressing, and anesthesia is maintained by either residual concentration of opioid (e.g., fentanyl or sufentanil) or continued infusion of remifentanil. Additionally, nitrous oxide can be used to supplement other volatile anesthetics. Compared with using intravenous anesthetic agents, nitrous oxide concentration can be defined by end-tidal gas analysis, which aids in defining failure to emerge. However, although nitrous oxide is usually well tolerated, the anesthesiologist should be vigilant in monitoring for a clinically apparent expanding pneumocephalus. Furthermore, rapidly cleared intravenous agents such as lidocaine can be of value in sustaining anesthesia for a few additional minutes. Finally, if remifentanil is used, the rate of infusion can remain unchanged until the dressing is complete. It is important, however, to provide transitional analgesia (typically 50–100 μg/kg morphine or 1–2 μg/kg fentanyl in adults) before discontinuation of remifentanil.
After the need for a predictable emergence, the second concern is hypertension. For reasons not yet understood, patients undergoing craniotomy often exhibit extreme hypertension during emergence that is sustained through the early phases of recovery. Because of possible intracranial hemorrhage, a plan for treatment of hypertension before it manifests is imperative. Aside from ensuring adequate analgesia, prophylactic doses of labetalol may be helpful (typically, 40 to 60 mg). Additionally, nicardipine or clevidipine infusion is rapidly and easily titratable and does not contribute to increases in ICP (see earlier section “Management of Arterial Blood Pressure”). While patients who develop postoperative hematomas have episodes of hypertension during emergence or early recovery, the source of hemorrhage is almost always within the surgical field, and thus the quality of hemostasis is undoubtedly important. However, because the mortality associated with postoperative hematoma formation requiring emergent evacuation is high, mitigating hypertension during emergence is suggested.
Finally, postoperative nausea and vomiting (PONV) is a frequent problem after craniotomy. In addition to being uncomfortable, it can contribute to postoperative hypertension. Several studies have shown that more than 50% of patients suffer this complication. Its incidence appears to be independent of anesthetic technique (awake or general) or opioid dose, suggesting that surgery itself is contributory. Women, younger patients, and those undergoing infratentorial craniotomy are at greater risk, but prophylactic antiemetic therapy markedly reduces the magnitude of this problem. Droperidol (0.625 mg) appears to be at least as effective as 4 mg ondansetron without causing detectable sedation. Many patients require multiple agents to control nausea and emesis. Combination of aprepitant 40 mg and dexamethasone 10 mg is found to be more effective than was the combination of ondansetron 4 mg and dexamethasone 10 mg for prophylaxis against postoperative vomiting but did not affect the incidence or severity of nausea or the need for rescue antiemetic. Regardless, some form of prophylaxis is generally warranted in patients undergoing craniotomy.
Although brain scanning modalities (magnetic resonance imaging [MRI] and PET) can identify the speech-dominant cerebral hemisphere noninvasively, intraoperative mapping of the eloquent cortex is still the most reliable method to ensure preservation of speech function when the speech center is close to the surgical field. Mapping the speech cortex, originally developed to allow maximal resection of epileptic foci in the dominant hemisphere, is equally useful for safely maximizing the extent of other cortical resections near language cortex, especially resections for low-grade gliomas and vascular malformations. Neuroleptanalgesia with intermittent periods of general analgesia has been the technique most often utilized in the past. The development of short-acting titratable anesthetics and narcotics has led to an “asleep-awake-asleep” technique (e.g., spontaneously ventilating general anesthesia with intraoperative wakeup) for use during craniotomy when the eloquent cortex is at risk. The combined use of narcotics and intravenous anesthetics can result in decreased respiratory drive, hypercarbia, and elevated intracranial pressure. Patients with reflux risk, morbid obesity, chronic obstructive airways disease, or a tendency to airway obstruction pose a particular challenge, and these risk factors might even prohibit the use of this technique.
The Wada Test: Determining Whether Speech Mapping Is Required
Because the speech cortex is a unilateral structure, preoperative identification by a Wada test of the hemisphere containing it may be required. The Wada test is advocated as a preliminary to operations in the vicinity of the Sylvan area in left-handed and ambidextrous patients, and also in the right-handed patient if any doubt exists as to which cerebral hemisphere is dominant for speech. The test is performed by intracarotid amytal injection. This results in immediate speech disruption, contralateral hemiparesis, and maintenance of consciousness when the injected carotid supplies the speech-dominant hemisphere. The nondominant hemisphere is identified by speech preservation and contralateral hemiparesis after carotid amytal injection.
Intraoperative Electrophysiologic and Anatomic Components of Speech Mapping
Electrical stimulation of the cortex allows mapping for speech. Language function is measured by showing the patient pictures of objects with common names. While the patient names the pictures, cortical sites are stimulated. Three sets of sites have been identified. At one set of sites, repeated errors are evoked; a second set shows only single errors on multiple samples, and the third group shows no effect of stimulation at all. Regions in which repeated errors are evoked seem to be essential for a particular language function because when the cortical resection encroaches on these sites, aphasia commonly occurs. However, regions in which stimulation produces only occasional errors do not seem to be essential for that particular language function, and at least some of these sites can be included in a resection without producing aphasia. Too low a current may not adequately block local cortical function, whereas too large a current is likely to evoke seizures.
Thus, it is essential to determine the after-discharge threshold on electrocorticography and to use a current just below that threshold to identify language cortex with stimulation mapping while decreasing the chance of inducing a generalized seizure. Alteration of the seizure threshold by pharmacologic agents should be minimal and ideally the seizure threshold should be constant during the period of testing. Intraoperative seizures may be aborted by irrigating the stimulated cortex with iced solution. Alternatively, a small dose of a short-acting sedative (e.g., barbiturate, benzodiazepine, or propofol) may be required.
Comparing Neurolept and General Anesthesia for Awake Cortical Mapping
The technique of neuroleptanalgesia, also called conscious-sedation analgesia, relies on the titration of fentanyl and droperidol to a specific endpoint rather than administration of a dose based on bodyweight. The goals of neuroleptanalgesia technique are to enable the patient to tolerate surgical discomfort during prolonged immobility while maintaining verbal responsiveness. Short periods of unconsciousness were induced to complete painful portions of the procedure by increasing doses of fentanyl. The neurolept craniotomy technique is therefore more accurately described as neuroleptanalgesia with intermittent periods of general anesthesia. Loss of consciousness could be accompanied by hypoventilation or airway obstruction, leading to hypoxia, hypercarbia, and elevation of the intracranial pressure. These complications would occasionally necessitate the conversion to general anesthesia with endotracheal intubation and controlled ventilation.
Although the majority of patients undergoing awake cortical testing can be managed successfully with a conscious sedation technique, a small percentage of patients (2% to 16%) are unable to tolerate the conditions of the surgery and require conversion to general anesthesia. In these patients, gaining control of the airway can be a challenge. Intubation by direct laryngoscopy necessitates rapid uncovering of the drapes and, if applicable, removing the fixation holder from the patient’s head. Emergency blind nasal intubation may be an option, although it is not always fast or successful. Alternative options include the use of a fiberoptic bronchoscope or an intubating laryngeal mask airway (LMA), or the combined use of these two devices.
In a series of 140 patients, LMA (classic, Proseal or Igel) were used. All patients were placed in lateral position and ventilation was controlled with pressure-controlled ventilation. The anesthetic maintenance included target-controlled infusion of propofol and remifentanil. All patients received a lidocaine scalp block before placing the Mayfield head holder and making the incision. All patients awoke smoothly for awake mapping and neurological testing. During the second asleep phase, LMA was inserted in 54 patients with no failure or technical difficulty in 46 patients and difficult placement in eight patients. Orotracheal intubation was attempted in 91 patients using video laryngoscopy or a Fastrach LMA, with five failures with intubation and no failure of airway control with LMA. One patient had a severe pulmonary complication related to aspiration of gastric contents.
To minimize coughing and Valsalva associated with airway instrumentation or at the time of emergence, techniques relying on spontaneous ventilation through a natural or splinted airway continue to evolve. Careful titration of remifentanil and propofol infusions in an asleep-awake-asleep technique produced good results, with only 2% of cases requiring conversion to general anesthesia during cortical mapping. Airway support was dictated by the patient’s ability to maintain airway patency and sufficient respiratory drive and, when required, established with positive-pressure ventilation through nasal trumpets or LMA. Adverse side effects were equivalent to previously reported rates using a neurolept technique. Some degree of hypercarbia (median PaCO 2 , 50; range, 47 to 55 mmHg) was seen and the incidence of apnea was high, underscoring the importance of an available method to offer positive-pressure ventilation.
Table 21.1 summarizes anesthesia techniques for craniotomy with awake intraoperative language testing and illustrates that no single method for the anesthetic management of awake testing during craniotomy is perfect. The choice of technique and the management of intraoperative complications are directed by patient and surgical requirements (patient position, duration of surgery, duration of wakefulness, and multiple periods of wakefulness). Close communication (both preoperative and intraoperative) between surgeon, patient, anesthesiologist, and the electrophysiologists is critical. Focus on details of patient comfort, details of patient monitoring, and requirements for patient wakefulness are necessary to increase the rate of successful procedures.