Carotid and Intracranial Surgery

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.

Carotid Endarterectomy

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.

Preoperative Assessment

Cardiovascular System

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 .

Box 21.1

Preoperative risk factors for perioperative stroke.

Medical risk factors

▪
Female sex
▪
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
▪
Obesity
▪
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

Anesthetic Management

Physiologic Management

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.

General Anesthesia

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.

Regional Anesthesia

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 .

Box 21.2

Cerebral monitoring to detect ischemia during carotid endarterectomy.

Cerebral functions

▪
Clinical neurological monitoring of the awake patient
▪
Electroencephalography (EEG)
▪
Somatosensory evoked potentials (SSEP)
▪
Motor evoked potentials (MEP)

Cerebral blood flow

▪
Transcranial Doppler ultrasound
▪
Stump pressure
▪
Xenon 133 washout

Cerebral metabolism

▪
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.

Postoperative Management

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 Evaluation

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.

Anesthesia Induction

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.

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