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Anesthesia for carotid endarterectomy and carotid stenting

Anesthesia for carotid endarterectomy and carotid stenting
Authors:
John Augoustides, MD, FASE, FAHA
Jacob T Gutsche, MD, FASE, FCCM
Jared W Feinman, MD, FASE
Section Editor:
Peter D Slinger, MD, FRCPC
Deputy Editors:
Nancy A Nussmeier, MD, FAHA
Kathryn A Collins, MD, PhD, FACS
Literature review current through: Jan 2024.
This topic last updated: Nov 16, 2022.

INTRODUCTION — Carotid atherosclerosis is a common cause of stroke. Carotid endarterectomy (CEA) and carotid artery stenting (CAS; percutaneous, transcarotid artery revascularization [TCAR]) are both established revascularization options [1-3]. This topic will review the anesthetic management of patients undergoing elective CEA or CAS, utilizing the options of either general anesthesia or local/regional anesthesia [4,5].

The indications for carotid revascularization and the selection of CEA or CAS, and when CAS is selected between percutaneous CAS or TCAR, are reviewed elsewhere [1,2,6].

●(See "Management of asymptomatic extracranial carotid atherosclerotic disease" and "Management of symptomatic carotid atherosclerotic disease".)

●(See "Carotid endarterectomy".)

●(See "Overview of carotid artery stenting" and "Percutaneous carotid artery stenting" and "Transcarotid artery revascularization".)

PREANESTHETIC MANAGEMENT

Assessment of cardiopulmonary comorbidities — Assessment for cardiovascular comorbidities is a focus of the preanesthesia evaluation since coexisting coronary atherosclerosis increases risk for perioperative morbidity due to myocardial ischemia [7]. A 12-lead electrocardiogram is routinely performed for all patients undergoing carotid endarterectomy (CEA) or carotid artery stenting (CAS; percutaneous CAS, transcarotid artery revascularization [TCAR]). Further consultation with a cardiologist may be warranted in patients with severe or unstable heart disease. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Noncardiac surgery in adults with aortic stenosis".)

Medication management — Appropriate perioperative medication management reduces cardiovascular risk and minimizes perioperative thrombotic complications.

●Statins and beta blockers should be continued in patients already receiving these therapies. (See "Management of cardiac risk for noncardiac surgery", section on 'Statins' and "Management of cardiac risk for noncardiac surgery", section on 'Beta blockers'.)

●Specific recommendations regarding preoperative administration of aspirin or dual antiplatelet therapy, as well as statin therapy, prior to CEA, CAS, or TCAR are noted in other topics:

•(See "Carotid endarterectomy", section on 'Antiplatelet therapy' and "Carotid endarterectomy", section on 'Statins'.)

•(See "Percutaneous carotid artery stenting", section on 'Antiplatelet/statin therapy'.)

•(See "Transcarotid artery revascularization", section on 'Dual antiplatelet therapy and statins'.)

●Management of other perioperative medications is discussed in a separate topic. (See "Perioperative medication management".)

INTRAOPERATIVE MANAGEMENT: GENERAL CONSIDERATIONS

Anesthetic goals — Regardless of surgical technique (open carotid endarterectomy [CEA], percutaneous carotid artery stenting [CAS], or transcarotid artery revascularization [TCAR]) or anesthetic technique (general anesthesia or local/regional anesthesia), anesthetic goals are to:

●Ensure prompt awakening and ability to fully cooperate with a neurologic examination for early stroke detection at the end of the procedure, as well as during the procedure if a local/regional anesthetic technique is used.

●Avoid wide variations in heart rate (HR) and/or blood pressure (BP) by maintaining maintain systolic BP in a range from the patient's baseline BP to 20 percent above that baseline. (See 'Hemodynamic management during CEA' below and 'Hemodynamic management during CAS or TCAR' below.)

Hemodynamic monitoring — Extreme perioperative lability of BP and/or HR may occur during CEA, percutaneous CAS, or TCAR due to altered baseline carotid baroreceptor function and intraoperative manipulation of these baroreceptors [8]. (See "Carotid endarterectomy", section on 'Location and influence of the carotid baroreceptor' and "Percutaneous carotid artery stenting", section on 'Stent positioning and dilation' and "Transcarotid artery revascularization", section on 'Establishing flow reversal and carotid stenting'.)

For this reason, direct intra-arterial BP monitoring is employed to rapidly detect and treat hypotension or hypertension. An intra-arterial catheter is also useful to guide management of vasoactive drugs (ie, vasopressors and vasodilators) and to obtain blood gas measurements if necessary. (See "Anesthesia for open abdominal aortic surgery", section on 'Monitoring' and "Anesthesia for endovascular aortic repair", section on 'Cardiovascular monitoring'.)

We insert the intra-arterial catheter before induction of anesthesia. Typically, we monitor BP contralateral to surgical site. Particularly during right-sided CEA, the left radial artery is preferred because the surgical procedure may interfere with the right radial arterial pulse due to the common brachiocephalic arterial origin of the right common carotid artery and the right subclavian artery on the right side.

Patients with carotid disease have systemic atherosclerotic disease and may have a discrepancy in the systolic blood pressure from one arm to the other because of concomitant subclavian artery disease [9]. In such cases, the arm with the higher BP is usually selected for arterial cannulation. If the cuff BP is suspiciously low in both arms, the surgeon is notified, and BP in the legs is checked and femoral arterial cannulation may be selected. For CAS, the surgeon should be consulted regarding their plans for access for stent placement before final selection of the artery to be cannulated for direct intra-arterial BP monitoring [10]. Arterial BP may be monitored during CAS by transducing the femoral arterial access catheter placed by the vascular team for the stenting procedure.

Hemodynamic management

Preparation and use of pharmacologic agents — Control of BP is necessary throughout the perioperative period. Pharmacologic management includes preparation of sympathomimetic, vasodilator, and short-acting beta blocker medications to rapidly treat hypotension, hypertension, tachyarrhythmias, or bradyarrhythmias. In our center, bolus doses of the following drugs are immediately available:

●Vasopressor and inotropic agents – Phenylephrine, ephedrine, vasopressin (table 1)

●Agents to lower BP and/or treat tachycardia – Nicardipine, labetalol, esmolol (table 2)

●Agents to treat or prevent bradycardia – Atropine, glycopyrrolate

In addition, we prepare infusion solutions of phenylephrine (table 1) and of nitroglycerin (table 2) so that these are immediately available for administration.

While a bolus of fluids may help achieve normovolemia and normotension, carotid surgery is not usually associated with excessive blood or fluid loss or fluid extravasation. Thus, volume resuscitation with large amounts of fluid is rarely appropriate during either CEA or CAS.

Hemodynamic management during CEA — If general anesthesia is selected, induction and emergence are periods of risk for hemodynamic instability. (See 'Induction, maintenance, and emergence' below.)

Other periods of high risk for hemodynamic instability and/or myocardial or cerebral ischemia during CEA include:

●Surgical manipulation of the carotid sinus and carotid artery – During carotid dissection and surgical manipulation of the carotid sinus, sympathetic stimulation may result in tachycardia and hypertension, or may increase parasympathetic outflow with resultant bradycardia and hypotension. Injection of local anesthetic has been proposed as a method to minimize the bradycardic reflex and reduce hemodynamic lability due to carotid manipulation, either into the carotid body [11,12], or into the periadventitial area around the carotid sinus [13]. However, there are insufficient data to endorse routine practice. (See "Carotid endarterectomy", section on 'Endarterectomy procedure'.)

●Carotid cross-clamping and unclamping – We control and maintain systolic BP in a range from the patient's baseline BP to 20 percent above that baseline in order to optimize collateral cerebral perfusion while the cross-clamp is applied, typically using a continuous infusion of phenylephrine (table 1) [14,15]. Some centers monitor and maintain a higher mean arterial BP (rather than systolic BP) to achieve this goal. (See 'Prevention of cerebral ischemia during CEA' below.)

After carotid unclamping, the BP is allowed to return to baseline values. However, the ensuing period of reperfusion after unclamping may be complicated by hypotension, which is treated to maintain baseline BP [15].

Hemodynamic management during CAS or TCAR — During percutaneous CAS or TCAR, the period of highest risk for hemodynamic instability and/or myocardial or cerebral ischemia is during balloon inflation. We control and maintain systolic BP in a range from the patient's baseline BP to 20 percent above that baseline to optimize collateral cerebral perfusion, similar to management of systolic BP during carotid cross-clamping for CEA [14,15]. After balloon deflation, BP is allowed to return to baseline values. (See 'Hemodynamic management during CEA' above and 'Prevention of cerebral ischemia during CAS or TCAR' below.)

In addition, the endovascular pressure on the baroreceptors during balloon inflation can reduce sympathetic activity and increase parasympathetic outflow, which may cause bradycardia and hypotension [16]. These effects usually resolve with administration of atropine (0.2 to 0.4 mg increments). In some centers, a prophylactic dose of glycopyrrolate 0.2 mg is administered prior to balloon dilation, and a repeat dose of 0.2 mg is administered if necessary [17]. (See "Percutaneous carotid artery stenting", section on 'Stent positioning and dilation' and "Transcarotid artery revascularization", section on 'Pretreatment to prevent hypotension'.)

ANESTHETIC MANAGEMENT FOR CAROTID ENDARTERECTOMY

Selection of the anesthetic technique — Carotid endarterectomy (CEA) can be performed using general anesthesia or local/regional anesthetic techniques. Selection of a technique is determined in consultation with the surgeon, considering the approach to carotid revascularization, the individual patient's characteristics and preferences, and surgeon preferences. Specific medical, surgical, or patient-centered factors may influence the choice in an individual patient [14]. Ideally, surgical and anesthetic teams should be experienced using both general and local/regional techniques. (See "Carotid endarterectomy", section on 'Anesthesia'.)

A 2021 Cochrane meta-analysis that included 16 randomized trials (4839 participants) noted that neither the incidence of stroke or death were significantly different between local/regional versus general anesthesia [18]. Other evidence also suggests that the choice of anesthetic technique has no significant impact on symptomatic stroke or mortality, although there may be differences in rates of silent cerebral events and local complications (eg, nerve injury) [19-22]. (See "Complications of carotid endarterectomy".)

In an analysis of 26,070 cases in the American College of Surgeons (ACS) National Surgical Quality Improvement Program (NSQIP) database, general anesthesia was used in 84.6 percent of patients undergoing CEA, while local/regional anesthesia was used in 15.4 percent of cases [23]. There are distinct advantages for each technique (table 3):

●Advantages of local/regional anesthesia

•Neurologic monitoring ease – The major advantage of using a local/regional anesthetic technique in an awake patient is the ability to continuously monitor neurologic function by simply talking to the awake patient and asking him to perform basic tasks with the contralateral hand, rather than using EEG or other continuous neuromonitoring techniques to detect brain ischemia during a carotid intervention [14,15]. If the patient develops a new neurologic deficit, the surgeon or interventionalist can intervene to mitigate neurologic injury. However, sedation must be minimized so that the patient is able to give a reliable neurologic response. (See 'Neuromonitoring in the awake patient' below.)

•Hemodynamic stability – Local/regional anesthesia incurs a lower incidence of hypotension during and after the procedure. A 2009 meta-analysis identified nine trials that recorded BP during and after CEA [24]. Significant decreases in BP were noted in the general anesthesia group after induction. In one trial, more patients in the general anesthesia group had significant hypotension during or after the operation (25 versus 7 percent). Similarly, the general anesthesia versus local anesthesia (GALA) trial found that more patients undergoing general anesthesia required manipulation of BP compared with patients receiving local anesthetic (72 versus 54 percent) [25]. However, intraoperative and postoperative blood pressure (BP) responses were highly variable, and both hypotension and hypertension were reported for both anesthetic techniques.

•Selective shunt placement – Use of local/regional anesthesia allows for selective surgical placement of a carotid shunt during CEA, rather than the routine shunting that many surgeons employ during general anesthesia. However, selective shunting based on continuous neuromonitoring techniques is also possible with general anesthesia [26,27].

•Costs – Evidence suggests that there may be a cost benefit to the use of local/regional anesthesia. In a post-hoc analysis of the GALA trial [25], local/regional anesthesia was found to be more cost effective than general anesthesia [28]. The difference in cost was primarily due to differences in the length of intensive care unit stay and the use of consumables, with a mean cost difference of ₤178 ($285 US). Two other nonrandomized studies have also suggested a cost difference between the two anesthesia techniques [29,30]. The larger of these evaluated 24,716 patients from the NSQIP database, finding modestly shorter operative and anesthesia times, and a larger proportion of patients discharged on the first postoperative day in the local/regional compared with general anesthesia groups (77 versus 64 percent) [29].

●Advantages of general anesthesia – Although local/regional anesthesia has some advantages, general anesthesia is more commonly used in the United States for open CEA [23,31].

•Patient comfort – General anesthesia is more comfortable for the patient and may be favored if the preoperative assessment reveals anxiety, reluctance to be awake, inability to cooperate or communicate, neurocognitive dysfunction, or inability to lie supine comfortably (eg, congestive heart failure or severe chronic obstructive pulmonary disease).

•Avoidance of urgent conversion to general anesthesia – Use of general anesthesia at the outset avoids the need for urgent conversion from a local/regional to a general anesthetic technique, which can be problematic for the patient undergoing CEA.

General anesthesia techniques — CEA is typically a relatively short procedure lasting less than 90 minutes. In general, short-acting medications are selected to facilitate rapid emergence and prompt awakening for participation in a neurologic examination [4].

Induction, maintenance, and emergence

●Induction – Similar to other patients with cardiovascular disease, induction with a short-acting hypnotic such as etomidate or low titrated doses of propofol is typically combined with a small dose of an opioid such as fentanyl or remifentanil and/or lidocaine 50 to 100 mg so that the sympathetic responses to laryngoscopy and intubation are blunted [32,33]. Neuromuscular blocking agents (NMBAs) are generally administered during anesthetic induction to facilitate intubation. These can be allowed to wear off as the case progresses, especially if a total intravenous anesthesia (TIVA) technique is selected that includes a remifentanil dose sufficient to produce akinesia. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Induction' and "General anesthesia: Intravenous induction agents".)

Administration of induction agents may cause hypotension by removing sympathetic tone, directly decreasing systemic vascular resistance, directly depressing the myocardium, reducing venous return, or inducing bradycardia. Subsequent endotracheal intubation may induce sympathetic stimulation resulting in tachycardia and hypertension. These hemodynamic aberrations are managed by administering vasoactive agents (table 1 and table 2) (see 'Preparation and use of pharmacologic agents' above), as well as by deepening (or lightening) anesthetic depth.

●Maintenance – Either a volatile anesthetic technique or TIVA, or a combination of these may be used to maintain anesthesia [34]. (See 'Neuromonitoring modalities' below and "Neuromonitoring in surgery and anesthesia", section on 'Anesthetic strategy'.)

•Volatile anesthetic technique – When a volatile anesthetic is selected for carotid revascularization, we suggest desflurane or sevoflurane because the low solubility of these agents facilitates more rapid emergence compared with isoflurane when the duration of the revascularization procedure is short [35,36]. If neuromonitoring is used, the neuromonitoring team may request a ceiling concentration for a volatile inhalation anesthetic. Typically, the selected volatile anesthetic is typically administered at a dose that is ≤0.5 to 1 minimum alveolar concentration (MAC) to avoid signal suppression that may interfere with detection of brain ischemia, and such low concentrations are maintained without significant adjustments [37]. (See "Inhalation anesthetic agents: Clinical effects and uses" and "Neuromonitoring in surgery and anesthesia", section on 'Volatile inhalation agents'.)

•TIVA technique – A TIVA technique (eg, propofol and remifentanil in combination) is a reasonable alternative to maintain general anesthesia during carotid revascularization [34,38-41]. If neuromonitoring is employed, the neuromonitoring team may request dosing limits during a TIVA technique. (See "Neuromonitoring in surgery and anesthesia", section on 'Intravenous agents'.)

•Use of nitrous oxide – While nitrous oxide (N2O) is employed by some clinicians as an adjunct for general anesthesia in patients undergoing carotid revascularization, the following clinical issues have limited its use [42-44] (see "Inhalation anesthetic agents: Clinical effects and uses", section on 'Nitrous oxide'):

-N2O may increase risk of postoperative nausea and vomiting, which may increase the risk of postoperative neck hematoma (see 'Hematoma' below). However, this risk is reduced by limiting its total dose and use of nausea and vomiting prophylaxis. (See "Maintenance of general anesthesia: Overview", section on 'Nitrous oxide gas' and "Postoperative nausea and vomiting", section on 'Anesthetic factors'.)

-The effect of N2O on the EEG is usually to increase frequency, but the effects vary depending on the other agents also being administered. The effect of N2O on other neuromonitoring modalities is similar to that of the volatile inhalation agents, but it is synergistic when coadministered with a volatile agent. (See "Neuromonitoring in surgery and anesthesia", section on 'Nitrous oxide'.)

●Emergence – Coughing due to tracheal irritation during extubation should be avoided. One of the advantages of a TIVA technique with propofol and remifentanil is a typically smooth emergence with little to no coughing. Alternatively, coughing can be minimized by administration of small boluses of remifentanil as the volatile anesthetic is eliminated, or IV lidocaine can be administered immediately before emergence. Also, sympathetic stimulation due to tracheal irritation may cause severe hypertension, which is treated with agents to lower BP and/or treat tachycardia (eg, nicardipine, labetalol, esmolol (table 2)).

Airway management — For patients undergoing CEA with general anesthesia, we usually prefer endotracheal intubation.

●An endotracheal tube (ETT) secures the airway and enables reliable controlled mechanical ventilation throughout the procedure despite limited access to the airway. However, placement of an ETT, as well as manipulation of the head during surgery in an intubated patient, may induce sympathetic stimulation and consequent tachycardia, hypertension, and myocardial ischemia in patients at high risk [7]. Furthermore, during anesthetic emergence and tracheal extubation, coughing and hypertension may cause suture line disruption, carotid hematoma, and life-threatening airway compression after CEA [45]. Hemodynamic lability during anesthetic emergence can be minimized by extubating the patient under deep anesthesia, followed by gentle mask ventilation during emergence, and continuing until return of full consciousness with adequate spontaneous ventilation.

●An LMA is an alternative airway management device for CEA. This technique has been associated with less hemodynamic lability during anesthetic induction and emergence compared with endotracheal intubation because the supraglottic position of the LMA minimizes tracheal irritation [46]. However, there is a greater chance of dislodging a LMA during CEA compared with using an ETT, and airway access is limited if conversion to general anesthesia should become necessary.

Conversely, during carotid artery stenting procedures, an LMA is often used since the anesthesiologist has free access to the airway. (See 'Anesthetic management for carotid artery stenting' below.)

Ventilation management — Normocapnia should be maintained during general anesthesia.

●Permissive hypercapnia is avoided. Permissive hypercapnia, achieved by hypoventilating patients under general anesthesia, has been associated with adverse reactions in patients who experienced intracerebral vascular "steal," due to increased blood flow to normally perfused brain tissue [47,48]. In addition, the cerebral vasodilation caused by hypercapnia may increase the risk of cerebral embolization.

●Hypocapnia is also avoided because it increases cerebrovascular tone, thereby adversely decreasing cerebral blood flow.

Neuromonitoring modalities — Several techniques have been used to monitor and detect decreased cerebral perfusion due to carotid artery clamping or embolic phenomena during general anesthesia for CEA. A 2022 meta-analysis of 236,983 patients undergoing CEA (27 studies) with various neuromonitoring techniques including electroencephalography (EEG), stump pressure (SP), somatosensory evoked potentials (SSEPs), transcranial Doppler (TCD), and cerebral oximetry and various shunting strategies if probable cerebral ischemia was identified with neuromonitoring [49]. These investigators did not find differences in stroke incidence that were associated with any specific neuromonitoring modality. However, in the 17 randomized controlled trials included in this meta-analysis, a trend towards increased risk for stroke was noted in patient groups randomized to receive no shunt regardless of whether evidence of cerebral ischemia was noted with a neuromonitoring modality. (See 'Prevention of cerebral ischemia during CEA' below.)

●Electroencephalography – Continuous electroencephalography (EEG) is the most commonly used neuromonitoring technique during CEA with general anesthesia [50-52]. Since anesthetic agents may impact the EEG, monitoring is initiated before induction of anesthesia. A second baseline EEG is obtained under general anesthesia before any carotid manipulation has occurred. Subsequently, EEG waveforms obtained from scalp electrodes in multi-channel sets are continuously evaluated by trained neuromonitoring personnel [37,51]. Frequent communication between the anesthesiologist and the neuromonitoring team is necessary to minimize anesthetic interference with the neuromonitoring goals for an individual patient.

Changes in EEG related to ischemia during CEA are classified as mild, moderate, or severe (ie, a greater than 50 percent decrease in waveform amplitude in a generalized or lateralized distribution) [51]. Severe changes indicate a need for safe augmentation of the systemic BP and/or insertion of a shunt by the surgeon. (See 'Prevention of cerebral ischemia during CEA' below.)

Limitations of EEG monitoring in this setting include the inability to monitor subcortical structures, difficulties with interpretation, and limited sensitivity [40]. In particular, monitoring processed EEG (eg, the bispectral index [BIS]) rather than raw EEG data has limited ability to detect cerebral ischemia because only the frontal cortex is monitored [53]. Further details regarding EEG monitoring are available in a separate topic. (See "Neuromonitoring in surgery and anesthesia", section on 'Electroencephalography'.)

●Somatosensory evoked potential (SSEP) monitoring – SSEP monitoring has been studied during CEA, but the sensitivity of this modality for detection of cerebral ischemia is not consistent [40,54-58]. (See "Neuromonitoring in surgery and anesthesia", section on 'SSEP Monitoring'.)

●Cerebral perfusion monitoring

•Carotid stump pressure – Carotid stump pressure is measured by transducing a needle inserted into the distal common carotid artery after clamping. Only a single pressure is obtained with each measurement, rather than continuous pressure monitoring. However, there is no consensus regarding standards or a cut-off for stump pressure to decide when to place a shunt, and its use as a neuromonitoring technique during CEA is operator specific. (See "Carotid endarterectomy", section on 'General conduct of operation'.)

•Transcranial Doppler (TCD) – Specialized TCD monitoring techniques have been used to detect and quantify emboli [59], with studies noting that a higher embolic burden detected by TCD correlates with increased stroke risk after CEA [60-62]. Also, the instantaneous audio feedback that occurs during embolization provides guidance during surgical manipulation of the carotid artery [63,64]. (See "Evaluation of carotid artery stenosis", section on 'Transcranial Doppler'.)

Although TCD monitoring has also been used to measure blood flow velocities in the middle cerebral artery during CEA, no data support improved outcomes with its use. Sensitivity and specificity of TCD monitoring are unreliable to detect cerebral ischemia because changes in blood flow velocity may reflect changes in arterial diameter rather than actual changes in blood flow.

A disadvantage of using TCD monitoring during CEA is the position of the probes, which may interfere with the surgeon's access to the neck and the anesthesiologist's access to the airway.

●Cerebral oximetry – Cerebral oximetry utilizes near-infrared spectroscopy to detect regional cerebral oxygen saturation (rSO2) via an adhesive pad applied to the forehead [65-67]. In one study of 466 patients undergoing CEA, a decrease in rSO2 ≥20 percent below baseline during temporary carotid clamping predicted perioperative stroke in seven patients, with a sensitivity of 86 percent and a specificity of 57 percent [67]. In that study, absolute baseline rSO2 values that were ≤50 percent before induction of anesthesia also predicted stroke after CEA with a sensitivity of 91 percent and a specificity of 67 percent [67].

However, there is lack of agreement about the threshold decrease in rSO2 indicating need for carotid shunt placement or other interventions [68]. Other limitations include poor sensitivity due to the small sampling window in a region of the frontal lobe cortex, wide individual and interpatient variations in baseline readings, and the multiple factors that may cause a decrease in rSO2 (eg, systemic and regional hemodynamics, blood oxygen transport, tissue metabolism) [66-69].

Local/regional anesthetic techniques — Local/regional anesthesia is performed with or without a nerve block. Although usually supplemented with intravenous (IV) sedation to maintain patient comfort during the procedure, doses are minimized to allow neurologic exams to be performed at frequent intervals during and at the end of the procedure.

Regional nerve block — The most commonly used nerve block techniques for CEA are superficial or deep cervical plexus blocks [4,70]. We recommend a superficial cervical plexus block rather than a deep plexus block. We do not typically add fentanyl or clonidine to the local anesthetic, although limited data suggest that the quality and duration of a cervical plexus block may be enhanced with such additives [71,72]. Evidence from randomized and non-randomized trials suggests that superficial plexus blocks provide adequate anesthesia for CEA while avoiding potentially serious complications associated with a deep plexus block (eg, subarachnoid injection, Horner syndrome, unwanted blockade of the phrenic, recurrent laryngeal or vagus nerves) [4,73-75]. A 2007 systematic review of 69 studies noted a higher risk of need to convert to general anesthesia (see 'Conversion from local/regional to general anesthesia' below), as well as a higher risk of serious complications (eg, intravascular injection, respiratory distress [due to presumed or confirmed diaphragmatic or vocal cord paralysis]) in patients who had a deep plexus block (157/7558; 2.08 percent) compared with those who had superficial plexus block (10/2533; 0.39 percent) [74]. Details regarding placement of these blocks, including use of ultrasound guidance, are found in a separate topic [76,77]. (See "Scalp block and cervical plexus block techniques", section on 'Superficial cervical plexus block technique' and "Scalp block and cervical plexus block techniques", section on 'Deep cervical plexus block technique'.)

Local anesthetic infiltration — Local anesthesia is typically infiltrated in the skin prior to making the incision (longitudinal, transverse) for CEA, with additional local anesthesia infiltrated into the subcutaneous tissues after skin incision. Local anesthesia is readministered as needed, typically into the peri-incisional tissues just prior to skin closure. Placement of a superficial cervical plexus block minimizes the need for local anesthesia.

Use of sedation — Sedation is minimized to allow performance of serial neurologic examinations, and only short-acting agents are employed.

We typically administer dexmedetomidine to provide supplemental sedation during CEA performed with local/regional anesthesia [78-81]. An initial loading dose of 1 mcg/kg is administered, followed by infusion at 0.3 mcg/kg per hour. Lower doses are used in older or frail patients to avoid the potential for prolonged sedation due to the relatively long duration of action of dexmedetomidine. In such cases, a low dose of the ultra-short-acting opioid remifentanil (ie, 0.01 to 0.03 mcg/kg per minute) can be added to augment sedation if necessary. (See "Monitored anesthesia care in adults", section on 'Dexmedetomidine'.)

Although dexmedetomidine theoretically decreases cerebral blood flow by inducing a degree of vasoconstriction within the brain [82], clinical evidence suggests its use during CEA is safe and effective [78-81]. Also, dexmedetomidine may cause hypotension, which should be treated with a vasopressor (eg, phenylephrine or ephedrine). (See 'Preparation and use of pharmacologic agents' above.)

In other centers, a propofol infusion is used to provide sedation and attenuate the stress response during CEA performed with local/regional anesthesia [83] (see "Monitored anesthesia care in adults" and "Monitored anesthesia care in adults", section on 'Propofol'). Other agents that provide sedation during monitored anesthesia care are also reasonable, as described separately. (See "Monitored anesthesia care in adults", section on 'Drugs used for sedation and analgesia for monitored anesthesia care'.)

Neuromonitoring in the awake patient — The gold standard for assessment of brain perfusion is serial neurologic examination, which is possible only in an awake patient (ie, a patient receiving little or no sedation). A baseline assessment is performed at the beginning of the procedure and repeated every 10 to 15 minutes during exposure and dissection of the carotid arteries, as well as immediately prior to carotid clamping, and continuously during carotid clamping. This assessment consists of noting the answers to simple questions directed to the patient and simple commands such as asking to squeeze a team member's hand or to squeeze a noise-making toy with the contralateral hand to ensure that grip strength is normal [14,15,84]. Agitation, slurred speech, disorientation, or extremity weakness indicate possible cerebral ischemia and the need for shunt placement if not already in place, or assessment of the shunt if already in use, or reassessment of the endarterectomy site if carotid repair has been completed.

Conversion from local/regional to general anesthesia — Indications for conversion from local/regional anesthesia to general anesthesia include patient request, severe agitation, or seizure. The need to convert is a relatively uncommon event, occurring in 4 percent of the patients undergoing CEA in the general anesthesia versus local anesthesia (GALA) trial [25]. In a systematic review, the risk of conversion to general anesthesia was significantly higher when a deep rather than a superficial cervical plexus block was used (odds ratio [OR] 5.35), possibly due to inadequate analgesia and/or a higher risk of complications with the deep plexus block [74]. (See 'Local/regional anesthetic techniques' above.)

Airway access may be initially limited by head positioning required CEA and by surgical drapes that partially cover the head and neck. The surgeon or surgical assistant may aid the anesthesiologist by returning the head to a neutral position and partially lifting the drape while maintaining surgical site sterility.

Prevention of cerebral ischemia during CEA — Neurologic injury from stroke associated with CEA may be minimized if ischemia is anticipated or immediately detected as noted above (see 'Neuromonitoring modalities' above and 'Neuromonitoring in the awake patient' above), and treated as discussed below [85,86]:

●BP management – Ipsilateral cerebral ischemia may occur during carotid cross-clamping due to decreased carotid blood flow. We maintain systolic BP in a range from the patient's baseline BP to 20 percent above that baseline while the carotid cross-clamp is applied, typically using a continuous infusion of phenylephrine (table 1), with the goal of optimizing collateral cerebral perfusion [14,15] (see 'Hemodynamic management during CEA' above). This is necessary, even if a shunt is used. If cerebral ischemia is noted, BP may be increased further. Some centers monitor and maintain a mean arterial BP that is higher than the patient's baseline, rather than using the systolic BP to achieve this goal.

After carotid unclamping, we allow BP to return to baseline values. However, the ensuing period of reperfusion after unclamping may be complicated by hypotension, which is treated to maintain baseline BP [15].

●Carotid shunting – Surgical management of cerebral ischemia detected during CEA may include placement of a carotid shunt if one is not already in place, or assessment of the integrity of the carotid shunt if already in use. (See "Carotid endarterectomy", section on 'Carotid shunting'.)

Anticoagulation during CEA — Anticoagulation is recommended during CEA. A bolus of IV heparin is administered before clamping the carotid artery. Typically, the heparin dosing strategy is guided by activated clotting time (ACT) values, with a target ACT of 200 to 250 seconds [87,88]. However, there are few data supporting specific ACT targets for CEA or other major vascular procedures, and the anesthesiologist is often not required to monitor ACT values since the duration of carotid clamping is generally short [89]. At the completion of a CEA procedure, reversal of heparin with protamine is left to the discretion of the surgeon depending on the risk of potential bleeding. When protamine reversal is selected, the anesthesiologist should always administer protamine slowly, while monitoring for an adverse reaction (eg, hypotension due to histamine-induced vasodilation or a more severe anaphylactic reaction) [90,91]. (See "Carotid endarterectomy", section on 'Endarterectomy procedure' and "Protamine: Administration and management of adverse reactions during cardiovascular procedures", section on 'Prevention and mitigation of protamine reactions' and "Protamine: Administration and management of adverse reactions during cardiovascular procedures", section on 'Adverse effects of protamine: Recognition and management'.)

ANESTHETIC MANAGEMENT FOR CAROTID ARTERY STENTING

Anesthetic techniques

For percutaneous carotid artery stenting — For percutaneous carotid artery stenting (CAS), most procedures are performed with local anesthesia at the arterial puncture site, typically the femoral artery [14,15,23,31,92-94]. In a review of more than 10,000 CAS procedures performed between 2005 and 2017, the Society for Vascular Surgery (SVS) Vascular Quality Initiative (VQI) reported that only 11.5 percent were performed under general anesthesia [92]. (See 'Conversion from local/regional to general anesthesia' above.)

During CAS procedures performed using local/regional anesthesia, we typically provide sedation with a dexmedetomidine infusion, as with use of sedation during local/regional anesthesia for carotid endarterectomy (CEA) [95]. (See 'Use of sedation' above.)

During CAS procedures performed using general anesthesia, the anesthesiologist has free access to the airway if conversion to general anesthesia becomes necessary, unlike conversion during CEA (see 'Airway management' above). Furthermore, during anesthetic emergence and tracheal extubation, coughing and hypertension may cause femoral hematoma at the percutaneous insertion site [45]. Thus, a laryngeal mask airway (LMA) is typically selected during general anesthesia.

For transcarotid artery revascularization — For transcarotid artery revascularization (TCAR), which requires a small incision low in the neck, either general anesthesia or local/regional anesthesia can be used, similar to anesthetic techniques used for open CEA. (See 'General anesthesia techniques' above and 'Local/regional anesthetic techniques' above.)

Early in the experience with TCAR, local anesthesia predominated [94]. In later reviews from the SVS VQI database, general anesthesia predominated with only about 20 percent performed under local/regional anesthesia [92,96]. In an early National Surgical Quality Improvement Program (NSQIP) study that include procedures performed between 2012 and 2016, mortality and pulmonary complications were significantly reduced for local/regional anesthesia compared with general anesthesia and procedure length and duration of hospital stay were shorter. However, in a later review of 2609 TCAR patients from the VQI database, perioperative outcomes for local/regional anesthesia (17.7 percent) and general anesthesia (82.3 percent) were similar [96]. The authors concluded that surgical teams should perform TCAR under the anesthesia type with which they are most comfortable.

Neuromonitoring — For patients who are awake, the clinical exam is tracked very closely for neuromonitoring, as noted above. (See 'Neuromonitoring in the awake patient' above.)

For TCAR patients undergoing general anesthesia, neuromonitoring techniques are similar to those used for patients undergoing CEA (see 'Neuromonitoring modalities' above). In one retrospective review of TCAR procedures, 80 percent were monitored using intraoperative electroencephalography (EEG) [97]. The rate of EEG changes was 13 percent, which is like that reported for carotid endarterectomy.

Prevention of cerebral ischemia during CAS or TCAR

●Surgical techniques – During carotid stenting procedures, specific techniques are used to prevent cerebral events. These include:

•Placement of an embolic protection device during transfemoral CAS. (See "Percutaneous carotid artery stenting", section on 'Embolic protection devices'.)

•Establishing flow reversal during TCAR. Flow reversal to prevent cerebral emboli is also integral to the TCAR technique [98]. (See "Transcarotid artery revascularization", section on 'Establishing flow reversal and carotid stenting'.)

●Blood pressure (BP) management – During balloon inflation, we maintain systolic BP in a range from the patient's baseline BP to 20 percent above that baseline to optimize collateral cerebral perfusion, similar to management during carotid cross-clamping for CEA [14,15]. The BP is allowed to return to baseline after balloon deflation. (See 'Prevention of cerebral ischemia during CEA' above.)

●Cerebral angiography – If cerebral ischemia occurs due to carotid vasospasm, emboli, or dissection during manipulation or inflation of the carotid artery stent balloon, the interventionalist performs cerebral angiography to identify any potentially treatable condition that may respond to neurovascular intervention (eg, thrombus that can be aspirated). (See "Percutaneous carotid artery stenting", section on 'Completion arteriography' and "Transcarotid artery revascularization", section on 'Completion'.)

Anticoagulation during CAS or TCAR — During CAS or TCAR, the patient is anticoagulated to prevent thrombosis, typically with unfractionated heparin administered prior to advancing wires into the carotid artery. The activated clotting time (ACT) should be confirmed to be between 250 and 300 seconds before manipulation of the carotid artery. Subsequently, the ACT is maintained at this level until all wires and cerebral protection devices have been removed. Heparin is not reversed after CAS or TCAR. (See "Percutaneous carotid artery stenting", section on 'Anticoagulation' and "Transcarotid artery revascularization", section on 'Anticoagulation'.)

MANAGEMENT IN THE EARLY POSTOPERATIVE PERIOD — Management of the patient in the post-anesthesia care unit is similar regardless of the technique used for carotid revascularization. Goals include pain control, hemodynamic management, and recognition and treatment of early postoperative complications.

Pain management — Mild to moderate pain is experienced at the incision site in the neck for carotid endarterectomy (CEA) or transcarotid artery revascularization (TCAR), and in the groin for transfemoral carotid artery stenting (CAS). The level of pain in the immediate postoperative period may be even less when the incision site or puncture site is infiltrated with a longer acting local anesthetic near the end of the procedure. Increasing or severe pain may indicate a developing complication (eg, hematoma). (See 'Management of early postoperative complications' below.)

Opioids are often unnecessary and administration of acetaminophen may avoid their use. If an opioid is necessary, dosing is minimized to reduce side effects such as respiratory depression and somnolence, which interferes with postoperative neurologic assessments [99,100].

We avoid nonsteroidal antiinflammatory drugs (NSAIDs) for pain control after carotid revascularization, as their safety in this setting has not been established. (See "NSAIDs: Adverse cardiovascular effects".)

Management of early postoperative complications

Blood pressure control — Disruption of baroreceptor function during CEA or CAS may result in labile blood pressure (BP) and heart rate (HR) necessitating ongoing management in the early postoperative period [16,101]. We continue invasive monitoring of arterial BP during the initial post-anesthesia care unit stay and administer vasoactive medications if necessary.

●Hypotension – Persistent hypotension may occur after CEA due to residual carotid hypersensitivity after plaque excision [102]. Systolic BP should be maintained at 100 to 150 mmHg to provide adequate cerebral perfusion pressure and cerebral blood flow, and thus avoid cerebral ischemia. If necessary, an infusion of phenylephrine is administered (table 1). Postoperative hypotension after stenting (transfemoral CAS, TCAR) has been associated with adverse neurologic and cardiac events as well as mortality and prolonged length of stay [103].

●Hypertension – Conversely, postoperative hypertension can also occur after carotid revascularization, resulting in abnormally increased cerebral blood flow due to disruption of cerebral autoregulation. Labetalol, nicardipine, or esmolol may be administered in bolus doses to strictly control postoperative hypertension and maintain systolic BP at 100 to 150 mmHg. Furthermore, postoperative pain must be promptly treated. (See 'Pain management' above.)

When necessary, a continuous intravenous infusion of labetalol, nitroprusside, nitroglycerin, nicardipine, or esmolol is administered (table 2).

Occasionally, postoperative hypertension is a predecessor of a condition known as cerebral hyperperfusion syndrome, characterized by cerebral edema, petechial or frank intracerebral hemorrhage, and seizures [104]. (See "Complications of carotid endarterectomy", section on 'Hyperperfusion syndrome'.)

Delayed emergence or stroke — Potential causes of slow emergence from general anesthesia include residual anesthetic effects, hypothermia, hypercarbia, or stroke. A basic neurologic examination is performed, and possible causes are assessed (see "Delayed emergence and emergence delirium in adults", section on 'Delayed emergence'). An urgent neurologic consultation and computed tomography (CT) scanning may be requested to evaluate the possibility of stroke since neurologic changes after CEA must be considered related to problems at the endarterectomy site (eg, thrombosis, intimal flap) until proven otherwise. Details regarding evaluation and management of perioperative stroke after CEA are described separately. (See "Delayed emergence and emergence delirium in adults", section on 'Consider neurologic disorders' and "Complications of carotid endarterectomy", section on 'Perioperative stroke'.)

Hematoma

●Neck hematoma after CEA or TCAR – Postoperative bleeding resulting in neck hematoma occasionally occurs after CEA or TCAR, and is more likely in patients with poorly-controlled postoperative hypertension or ongoing anticoagulation [105-107]. Most hematomas are mild and require no treatment. However, a significant wound hematoma may compromise the patient's airway, resulting in a need for emergency airway management and reoperation. This event is associated with higher risk of in-hospital mortality, stroke, and myocardial infarction [107,108]. (See "Complications of carotid endarterectomy", section on 'Cervical hematoma' and "Transcarotid artery revascularization", section on 'Complications'.)

Emergency airway management may be challenging after carotid revascularization because the neck hematoma typically compresses and displaces upper airway structures. It may be necessary to reopen the incision prior to intubation to acutely decompress the trachea and improve glottic visualization for intubation. Visualization of upper airway anatomy may be further complicated by multiple intubation attempts resulting in oropharyngeal and laryngeal edema or bleeding. The American Society of Anesthesiologists (ASA) has developed guidance for airway management in this setting (table 4). (See "Complications of carotid endarterectomy", section on 'Cervical hematoma' and "Anesthesia for adult trauma patients", section on 'Airway management'.)

●Groin hematoma after percutaneous CAS – Following percutaneous CAS, inadequate closure of the femoral artery puncture site used to obtain percutaneous access may lead to bleeding and hematoma, in part because of concomitant administration of antiplatelet therapy and ongoing anticoagulation. (See "Percutaneous carotid artery stenting", section on 'Complications'.)

Vocal cord paralysis or other nerve injury — Injury to the recurrent laryngeal nerve during CEA (traction, compression) may result in paralysis of the ipsilateral vocal cord. This typically presents as new-onset hoarseness. In rare cases, contralateral recurrent laryngeal nerve injury related to prior neck surgery may not have been recognized preoperatively, and this combined with new ipsilateral recurrent laryngeal nerve injury during CEA may require emergency endotracheal intubation if adduction of both vocal cords causes closure of the glottic aperture and laryngeal obstruction. (See "Carotid endarterectomy", section on 'Otolaryngologic examination' and "Complications of carotid endarterectomy", section on 'Nerve injury'.)

Cranial nerve injury can also occur with TCAR, but is very rare (0.4 percent in one review [105]).

SUMMARY AND RECOMMENDATIONS

●Preanesthesia consultation – Preanesthesia consultation for carotid artery procedures (ie, carotid endarterectomy [CEA], percutaneous carotid artery stenting [CAS], transcarotid artery revascularization [TCAR]) identifies comorbidities and ensures that perioperative medication management reduces cardiovascular risk and minimizes perioperative thrombotic complications. (See 'Preanesthetic management' above.)

●Anesthetic goals – Regardless of surgical procedure or anesthetic technique, goals are to (see 'Anesthetic goals' above):

•Ensure prompt awakening and ability to fully cooperate with neurologic examinations during local/regional anesthesia and at the end of the procedure after any anesthetic technique

•Avoid wide variations in blood pressure (BP) and/or heart rate (HR)

●Hemodynamic monitoring – Intra-arterial BP monitoring is used to rapidly detect and treat hypotension or hypertension; the intra-arterial catheter is inserted before anesthetic induction. (See 'Hemodynamic monitoring' above.)

●Hemodynamic management – Intra-arterial BP is controlled using vasoactive agents as needed (table 1 and table 2). Periods of highest risk for hemodynamic instability include induction and emergence from general anesthesia, and surgical manipulation of the carotid sinus and carotid artery (including cross-clamping and unclamping during CEA or balloon inflation and deflation during CAS). (See 'Hemodynamic management' above.)

●Choice of anesthetic technique – Ideally, surgical and anesthetic teams should be competent in techniques for either general anesthesia or local/regional anesthesia since specific medical, surgical, or patient-centered factors may influence the choice. (See 'Selection of the anesthetic technique' above.)

•Local/regional anesthesia – Advantages of local/regional anesthetic technique include the ability to continuously monitor neurologic function in an awake patient, hemodynamic stability, selective shunt placement, and possibly cost.

•General anesthesia – Advantages of general anesthesia include greater patient comfort for those who are anxious, reluctant to be awake, unable to lie supine comfortably, or cooperate or communicate, and avoidance of the need for urgent conversion from local/regional to general anesthesia.

●General anesthesia techniques – (See 'General anesthesia techniques' above.)

•Induction and maintenance – General anesthesia is induced with a short-acting agent such as etomidate or propofol, typically with addition of a low-dose, short-acting opioid (eg, fentanyl or remifentanil) and/or lidocaine to blunt responses to sympathetic stimulation during endotracheal intubation. Either a volatile anesthetic (eg, sevoflurane or desflurane) or total intravenous anesthesia (TIVA; eg, propofol and remifentanil in combination) may be used to maintain anesthesia. If neuromonitoring is employed, dosing limits for volatile or intravenous anesthetics are typically necessary. (See 'Induction, maintenance, and emergence' above.)

•Airway management – Endotracheal intubation is preferred for CEA because access to the airway is generally limited after surgical positioning and draping. (See 'Airway management' above.)

•Ventilation management – Maintain normocapnia; avoid hypocapnia or permissive hypercapnia. (See 'Ventilation management' above.)

•Neuromonitoring modalities – Neuromonitoring techniques to detect cerebral ischemia during general anesthesia include continuous electroencephalography (EEG), cerebral perfusion monitoring (eg, measurement of carotid stump pressure during CEA, transcranial Doppler [TCD]), and cerebral oximetry. (See 'Neuromonitoring modalities' above.)

●Local/regional anesthesia techniques

•Regional block – When regional anesthesia is selected for carotid revascularization procedures that require a neck incision (ie, CEA, TCAR), we recommend a superficial cervical plexus block, rather than deep cervical plexus block (Grade 1B). Superficial cervical plexus block provides adequate anesthesia while avoiding complications associated with a deep block. (See 'Regional nerve block' above.)

•Local anesthesia – Local anesthesia is typically injected at the neck incision site for CEA or TCAR or at the arterial puncture site for CAS (typically femoral access site in the groin). (See 'Local anesthetic infiltration' above.)

•Sedation – Sedation is minimized to allow performance of serial neurologic examinations. (See 'Use of sedation' above.)

•Neuromonitoring with neurologic examinations – (See 'Neuromonitoring in the awake patient' above.)

●Prevention of cerebral ischemia – (See 'Prevention of cerebral ischemia during CEA' above and 'Prevention of cerebral ischemia during CAS or TCAR' above.)

•BP management – We suggest maintaining systolic BP in a range from the patient's baseline BP to 20 percent above baseline to optimize collateral cerebral perfusion during carotid cross-clamping for CEA or balloon inflation for CAS (Grade 2C).

•During CEA – A carotid shunt may be placed to manage cerebral ischemia.

•During CAS

-An embolic protection device employed to prevent cerebral ischemia.

-Cerebral angiography is used to identify potentially treatable conditions (eg, thrombus that can be aspirated) if cerebral ischemia is detected

•During TCAR – Flow reversal is employed to prevent cerebral emboli.

●Management of anticoagulation

•CEA – During CEA, the patient is systemically anticoagulated prior to carotid artery clamping with a target activated clotting time (ACT) of 200 to 250 seconds. Reversal of anticoagulation at the completion of the procedure is at the discretion of the surgeon. (See "Carotid endarterectomy", section on 'Endarterectomy procedure'.)

•CAS or TCAR – During CAS or TCAR, the patient is anticoagulated with heparin to maintain ACT at 250 to 300 seconds prior to any manipulation of guidewires and catheters within the carotid artery. However, anticoagulation is generally not reversed. (See "Percutaneous carotid artery stenting", section on 'Anticoagulation'.)

●Postoperative problems – Problems in the immediate postoperative period requiring urgent treatment include hypotension, hypertension, pain, hematoma at the surgical site, slow emergence from anesthesia that may indicate new stroke, or rarely, evidence of vocal cord paralysis. (See 'Management in the early postoperative period' above.)

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  78. Bekker A, Gold M, Ahmed R, et al. Dexmedetomidine does not increase the incidence of intracarotid shunting in patients undergoing awake carotid endarterectomy. Anesth Analg 2006; 103:955.
  79. Bekker AY, Basile J, Gold M, et al. Dexmedetomidine for awake carotid endarterectomy: efficacy, hemodynamic profile, and side effects. J Neurosurg Anesthesiol 2004; 16:126.
  80. McCutcheon CA, Orme RM, Scott DA, et al. A comparison of dexmedetomidine versus conventional therapy for sedation and hemodynamic control during carotid endarterectomy performed under regional anesthesia. Anesth Analg 2006; 102:668.
  81. Gallego-Ligorit L, Vives M, Vallés-Torres J, et al. Use of Dexmedetomidine in Cardiothoracic and Vascular Anesthesia. J Cardiothorac Vasc Anesth 2018; 32:1426.
  82. Prielipp RC, Wall MH, Tobin JR, et al. Dexmedetomidine-induced sedation in volunteers decreases regional and global cerebral blood flow. Anesth Analg 2002; 95:1052.
  83. Szabó P, Mayer M, Horváth-Szalai Z, et al. Awake Sedation With Propofol Attenuates Intraoperative Stress of Carotid Endarterectomy in Regional Anesthesia. Ann Vasc Surg 2020; 63:311.
  84. McCleary AJ, Maritati G, Gough MJ. Carotid endarterectomy; local or general anaesthesia? Eur J Vasc Endovasc Surg 2001; 22:1.
  85. Krul JM, van Gijn J, Ackerstaff RG, et al. Site and pathogenesis of infarcts associated with carotid endarterectomy. Stroke 1989; 20:324.
  86. Krul JM, Ackerstaff RG, Eikelboom BC, Vermeulen FE. Stroke-related EEG changes during carotid surgery. Eur J Vasc Surg 1989; 3:423.
  87. Goldhammer JE, Zimmerman D. Pro: Activated Clotting Time Should Be Monitored During Heparinization For Vascular Surgery. J Cardiothorac Vasc Anesth 2018; 32:1494.
  88. Apinis A, Sehgal S, Leff J. Intraoperative management of carotid endarterectomy. Anesthesiol Clin 2014; 32:677.
  89. Wolo E, Herman C. Con: Activated Clotting Time Should Not Be Monitored During Heparinization for Vascular Surgery. J Cardiothorac Vasc Anesth 2018; 32:1497.
  90. Weiss ME, Nyhan D, Peng ZK, et al. Association of protamine IgE and IgG antibodies with life-threatening reactions to intravenous protamine. N Engl J Med 1989; 320:886.
  91. Comunale ME, Maslow A, Robertson LK, et al. Effect of site of venous protamine administration, previously alleged risk factors, and preoperative use of aspirin on acute protamine-induced pulmonary vasoconstriction. J Cardiothorac Vasc Anesth 2003; 17:309.
  92. Malas MB, Dakour-Aridi H, Wang GJ, et al. Transcarotid artery revascularization versus transfemoral carotid artery stenting in the Society for Vascular Surgery Vascular Quality Initiative. J Vasc Surg 2019; 69:92.
  93. Mas JL, Chatellier G, Beyssen B, et al. Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis. N Engl J Med 2006; 355:1660.
  94. Burton BN, Finneran Iv JJ, Harris KK, et al. Association of Primary Anesthesia Type with Postoperative Adverse Events After Transcarotid Artery Revascularization. J Cardiothorac Vasc Anesth 2020; 34:136.
  95. Wu LP, Kang WQ. Effect of dexmedetomidine for sedation and cognitive function in patients with preoperative anxiety undergoing carotid artery stenting. J Int Med Res 2020; 48:300060520938959.
  96. Mukherjee D, Collins DT, Liu C, et al. The study of transcarotid artery revascularization under local versus general anesthesia with results from the Society for Vascular Surgery Vascular Quality Initiative. Vascular 2020; 28:784.
  97. Healy LC, Gifford E, Shah P, et al. Intraoperative electroencephalographic changes during transcarotid artery revascularization are more frequent than previously reported. J Vasc Surg 2021; 74:922.
  98. Kashyap VS, Schneider PA, Foteh M, et al. Early Outcomes in the ROADSTER 2 Study of Transcarotid Artery Revascularization in Patients With Significant Carotid Artery Disease. Stroke 2020; 51:2620.
  99. Toung TJ, Sieber FE, Grayson RF, Derrer SA. Chemoreceptor injury as probable cause of respiratory depression after a simultaneous, bilateral carotid endarterectomy. Crit Care Med 1990; 18:1290.
  100. Lee JK, Hanowell S, Kim YD, Macnamara TE. Morphine-induced respiratory depression following bilateral carotid endarterectomy. Anesth Analg 1981; 60:64.
  101. Mylonas SN, Moulakakis KG, Antonopoulos CN, et al. Carotid artery stenting-induced hemodynamic instability. J Endovasc Ther 2013; 20:48.
  102. Rubio G, Karwowski JK, DeAmorim H, et al. Predicting Factors Associated with Postoperative Hypotension following Carotid Artery Stenting. Ann Vasc Surg 2019; 54:193.
  103. Noori VJ, Aranson NJ, Malas M, et al. Risk factors and impact of postoperative hypotension after carotid artery stenting in the Vascular Quality Initiative. J Vasc Surg 2021; 73:975.
  104. Biller J, Feinberg WM, Castaldo JE, et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation 1998; 97:501.
  105. Sagris M, Giannopoulos S, Giannopoulos S, et al. Transcervical carotid artery revascularization: A systematic review and meta-analysis of outcomes. J Vasc Surg 2021; 74:657.
  106. Treiman RL, Cossman DV, Foran RF, et al. The influence of neutralizing heparin after carotid endarterectomy on postoperative stroke and wound hematoma. J Vasc Surg 1990; 12:440.
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  108. Ferguson GG, Eliasziw M, Barr HW, et al. The North American Symptomatic Carotid Endarterectomy Trial : surgical results in 1415 patients. Stroke 1999; 30:1751.
Topic 90608 Version 34.0

References

1 : Clinical practice. Carotid stenosis.

2 : Advances in the management of carotid artery disease: focus on recent evidence and guidelines.

3 : Carotid Endarterectomy and Carotid Artery Stenting in the US Medicare Population, 1999-2014.

4 : General versus regional anesthesia for carotid endarterectomy.

5 : Local versus general anaesthesia for carotid endarterectomy.

6 : 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, Congress of Neurological Surgeons, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, Society for Vascular Medicine, and Society for Vascular Surgery.

7 : 2009 ACCF/AHA focused update on perioperative beta blockade incorporated into the ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American college of cardiology foundation/American heart association task force on practice guidelines.

8 : Incidence, predictors, and outcomes of hemodynamic instability following carotid angioplasty and stenting.

9 : Right- and left-arm blood pressure discrepancies in vascular surgery patients.

10 : Initial Experience of a Novel Sheath Guide Specifically Designed for Transradial Approach for Carotid Artery Stenting.

11 : Carotid sinus nerve blockade to reduce blood pressure instability following carotid endarterectomy: a systematic review and meta-analysis.

12 : Effect of carotid sinus nerve blockade on hemodynamic stability during carotid endarterectomy under local anesthesia.

13 : Effect of lignocaine injection in carotid sinus on baroreceptor sensitivity during carotid endarterectomy.

14 : Carotid endarterectomy.

15 : Intraoperative management: carotid endarterectomies.

16 : Cardiac autonomic control during balloon carotid angioplasty and stenting.

17 : Improved hemodynamic outcomes with glycopyrrolate over atropine in carotid angioplasty and stenting.

18 : Local versus general anaesthesia for carotid endarterectomy.

19 : General Anesthesia Versus Local Anesthesia in Carotid Endarterectomy: A Systematic Review and Meta-Analysis.

20 : Anesthesia Type is Associated with Decreased Cranial Nerve Injury in Carotid Endarterectomy.

21 : Anesthesia type determines risk of cerebral infarction after carotid endarterectomy.

22 : Associations of Perioperative Variables With the 30-Day Risk of Stroke or Death in Carotid Endarterectomy for Symptomatic Carotid Stenosis.

23 : Outcomes of carotid endarterectomy under general and regional anesthesia from the American College of Surgeons' National Surgical Quality Improvement Program.

24 : Routine or selective carotid artery shunting for carotid endarterectomy (and different methods of monitoring in selective shunting).

25 : General anaesthesia versus local anaesthesia for carotid surgery (GALA): a multicentre, randomised controlled trial.

26 : Intraoperative Cerebral Monitoring During Carotid Surgery: A Narrative Review.

27 : Shunting during carotid endarterectomy.

28 : Cost-effectiveness analysis of general anaesthesia versus local anaesthesia for carotid surgery (GALA Trial).

29 : Regional versus general anesthesia for carotid endarterectomy: the American College of Surgeons National Surgical Quality Improvement Program perspective.

30 : Patient and hospital benefits of local anaesthesia for carotid endarterectomy.

31 : Anesthetic type and risk of myocardial infarction after carotid endarterectomy in the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST).

32 : Low-dose fentanyl blunts circulatory responses to tracheal intubation.

33 : Efficacy of intravenous lidocaine versus placebo on attenuating cardiovascular response to laryngoscopy and tracheal intubation: a systematic review of randomized controlled trials.

34 : A comparison of sevoflurane, target-controlled infusion propofol, and propofol/isoflurane anesthesia in patients undergoing carotid surgery: a quality of anesthesia and recovery profile.

35 : Comparison of induction, maintenance, and recovery characteristics of sevoflurane-N2O and propofol-sevoflurane-N2O with propofol-isoflurane-N2O anesthesia.

36 : Isoflurane, desflurane and sevoflurane for carotid endarterectomy.

37 : Guidelines for intraoperative neuromonitoring using raw (analog or digital waveforms) and quantitative electroencephalography: a position statement by the American Society of Neurophysiological Monitoring.

38 : Meta-analysis of desflurane and propofol average times and variability in times to extubation and following commands.

39 : Hemodynamic stability, myocardial ischemia, and perioperative outcome after carotid surgery with remifentanil/propofol or isoflurane/fentanyl anesthesia.

40 : Monitoring electrophysiologic function during carotid endarterectomy: a comparison of somatosensory evoked potentials and conventional electroencephalogram.

41 : Haemodynamic instability and myocardial ischaemia during carotid endarterectomy: a comparison of propofol and isoflurane.

42 : Outcomes after neuroanesthesia and neurosurgery: what makes a difference.

43 : The perioperative use of nitrous oxide: renaissance of an old gas or funeral of an ancient relict?

44 : Nitrous oxide and perioperative cardiac morbidity (ENIGMA-II) Trial: rationale and design.

45 : Difficult airway management after carotid endarterectomy: utility and limitations of the Laryngeal Mask Airway.

46 : Cardiovascular stability during carotid endarterectomy: endotracheal intubation versus laryngeal mask airway.

47 : Cerebral blood flow during carotid endarterectomy.

48 : Cerebral blood flow measurements and electroencephalograms during carotid endarterectomy.

49 : A Systematic Review and Meta-Analysis on Perioperative Cerebral and Hemodynamic Monitoring Methods during Carotid Endarterectomy.

50 : Anesthesia for carotid endarterectomy: a survey.

51 : Computer-derived density spectral array in detection of mild analog electroencephalographic ischemic pattern changes during carotid endarterectomy.

52 : Neuromonitoring in carotid surgery: are the results obtained in awake patients transferable to patients under sevoflurane/fentanyl anesthesia?

53 : Bispectral index monitoring may not reliably indicate cerebral ischaemia during awake carotid endarterectomy.

54 : Somatosensory evoked potentials sensitivity relative to electroencephalography for cerebral ischemia during carotid endarterectomy.

55 : Monitoring of brain function during carotid endarterectomy: an analysis of contemporary methods.

56 : The role of somatosensory evoked potentials in detecting cerebral ischaemia during carotid endarterectomy.

57 : Monitoring of median nerve somatosensory evoked potentials in carotid surgery.

58 : Multimodal Neurophysiological Monitoring Reduces Shunt Incidence during Carotid Endarterectomy.

59 : Detection of middle cerebral artery emboli during carotid endarterectomy using transcranial Doppler ultrasonography.

60 : Transcranial Doppler monitoring during carotid endarterectomy: is it appropriate for selecting patients in need of a shunt?

61 : The value of transcranial Doppler in predicting cerebral ischaemia during carotid endarterectomy.

62 : Stump pressure and transcranial Doppler for predicting shunting in carotid endarterectomy.

63 : Association of intraoperative transcranial doppler monitoring variables with stroke from carotid endarterectomy.

64 : Carotid endarterectomy with transcranial Doppler and electroencephalographic monitoring. A prospective study in 130 operations.

65 : Comparison of electroencephalography and cerebral oximetry to determine the need for in-line arterial shunting in patients undergoing carotid endarterectomy.

66 : Transcranial cerebral oximetry in random normal subjects.

67 : Brain Oxygen Supply Parameters in the Risk Assessment of Cerebral Complications During Carotid Endarterectomy.

68 : Outcome of Near-Infrared Spectroscopy-Guided Selective Shunting During Carotid Endarterectomy in General Anesthesia.

69 : The value of near-infrared spectroscopy measured cerebral oximetry during carotid endarterectomy in perioperative stroke prevention. A review.

70 : Examination of regional anesthesia for carotid endarterectomy.

71 : Does clonidine 50 microg improve cervical plexus block obtained with ropivacaine 150 mg for carotid endarterectomy? A randomized, double-blinded study.

72 : The addition of fentanyl to local anesthetics affects the quality and duration of cervical plexus block: a randomized, controlled trial.

73 : Comparison of intermediate vs subcutaneous cervical plexus block for carotid endarterectomy.

74 : Superficial or deep cervical plexus block for carotid endarterectomy: a systematic review of complications.

75 : Regional anesthesia for carotid surgery.

76 : Ultrasound-guided intermediate cervical plexus and additional peripheral facial nerve block for carotid endarterectomy : A prospective pilot study.

77 : Cervical plexus block.

78 : Dexmedetomidine does not increase the incidence of intracarotid shunting in patients undergoing awake carotid endarterectomy.

79 : Dexmedetomidine for awake carotid endarterectomy: efficacy, hemodynamic profile, and side effects.

80 : A comparison of dexmedetomidine versus conventional therapy for sedation and hemodynamic control during carotid endarterectomy performed under regional anesthesia.

81 : Use of Dexmedetomidine in Cardiothoracic and Vascular Anesthesia.

82 : Dexmedetomidine-induced sedation in volunteers decreases regional and global cerebral blood flow.

83 : Awake Sedation With Propofol Attenuates Intraoperative Stress of Carotid Endarterectomy in Regional Anesthesia.

84 : Carotid endarterectomy; local or general anaesthesia?

85 : Site and pathogenesis of infarcts associated with carotid endarterectomy.

86 : Stroke-related EEG changes during carotid surgery.

87 : Pro: Activated Clotting Time Should Be Monitored During Heparinization For Vascular Surgery.

88 : Intraoperative management of carotid endarterectomy.

89 : Con: Activated Clotting Time Should Not Be Monitored During Heparinization for Vascular Surgery.

90 : Association of protamine IgE and IgG antibodies with life-threatening reactions to intravenous protamine.

91 : Effect of site of venous protamine administration, previously alleged risk factors, and preoperative use of aspirin on acute protamine-induced pulmonary vasoconstriction.

92 : Transcarotid artery revascularization versus transfemoral carotid artery stenting in the Society for Vascular Surgery Vascular Quality Initiative.

93 : Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis.

94 : Association of Primary Anesthesia Type with Postoperative Adverse Events After Transcarotid Artery Revascularization.

95 : Effect of dexmedetomidine for sedation and cognitive function in patients with preoperative anxiety undergoing carotid artery stenting.

96 : The study of transcarotid artery revascularization under local versus general anesthesia with results from the Society for Vascular Surgery Vascular Quality Initiative.

97 : Intraoperative electroencephalographic changes during transcarotid artery revascularization are more frequent than previously reported.

98 : Early Outcomes in the ROADSTER 2 Study of Transcarotid Artery Revascularization in Patients With Significant Carotid Artery Disease.

99 : Chemoreceptor injury as probable cause of respiratory depression after a simultaneous, bilateral carotid endarterectomy.

100 : Morphine-induced respiratory depression following bilateral carotid endarterectomy.

101 : Carotid artery stenting-induced hemodynamic instability.

102 : Predicting Factors Associated with Postoperative Hypotension following Carotid Artery Stenting.

103 : Risk factors and impact of postoperative hypotension after carotid artery stenting in the Vascular Quality Initiative.

104 : Guidelines for carotid endarterectomy: a statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association.

105 : Transcervical carotid artery revascularization: A systematic review and meta-analysis of outcomes.

106 : The influence of neutralizing heparin after carotid endarterectomy on postoperative stroke and wound hematoma.

107 : Wound hematomas after carotid endarterectomy.

108 : The North American Symptomatic Carotid Endarterectomy Trial : surgical results in 1415 patients.

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