Carotid Endarterectomy – General Anesthesia

Version 1.0 ; 1/8/2024

Andrew Schober & Dylan Masters & Michael Bokoch

Note : these guidelines apply to vascular surgery cases. The protocol is slightly different for neurosurgery.

Carotid stenosis refers to narrowing of the common or internal carotid artery. It is most commonly due to progressive atherosclerotic plaque buildup, but it can also be due to a number of other etiologies including trauma, prior surgical manipulation, radiation, or congenital lesions such as carotid webs. Carotid endarterectomy (CEA) is indicated for the treatment of high-grade or symptomatic carotid stenosis, largely to prevent embolic complications / ischemic strokes. While open repair via endarterectomy is considered the gold standard, it is now considered one of a number of treatment options including optimal medical management, trans-femoral stenting, and trans-carotid stenting (TCAR).

1. Procedure description

The carotid artery is exposed, in an area typically spanning the carotid bifurcation, to obtain proximal and distal control. After heparinization, the carotid artery is clamped above and below the lesion to exclude it during the repair. A stump pressure is measured distal to the upper clamp to determine whether there is adequate collateral flow to the ipsilateral hemisphere via the Circle of Willis. If stump pressure is insufficient (see below), a shunt is performed to maintain blood flow during repair. Patients with significant contralateral carotid and/or vertebral artery stenosis are higher risk for having inadequate collateral flow via the Circle of Willis, thus needing a shunt.

A longitudinal incision is then made in the vessel. If a shunt is used, it is placed within the surgical field, directly bypassing the clamped area. After a dissection plane is developed, the atheromatous material is removed. The vessel is then closed with an eye-shaped bovine pericardial patch. If a shunt was used, it is removed prior to completion of the vessel closure. The carotid clamp is then removed and adequacy of flow assessed by ultrasound. Heparinization is reversed with protamine and hemostasis achieved, followed by closure of the incision.

2. Patient demographics

Risk factors for carotid stenosis are similar to those for atherosclerotic heart disease including older age, hypertension, diabetes, obesity, metabolic syndrome, hyperlipidemia, smoking, sedentary lifestyle, and family history of atherosclerosis. As such, there is considerable comorbid cardiovascular disease including hypertension, coronary artery disease, heart failure, valvular disease, and peripheral vascular disease, all of which can affect the ability to effectively manage hemodynamics and put the patient at elevated risk of cardiovascular complications (including hemodynamic instability / vasoplegia, MI, stroke, arrhythmia, etc).

Indications for carotid surgery include :
Symptomatic : stroke or TIA referable to the appropriate carotid artery distribution within the previous six months AND carotid stenosis > 50%.
Asymptomatic : atherosclerotic narrowing of the extracranial ICA (>80%) without recent stroke or TIA (Of note, vertigo and syncope are not typical manifestations).

Of the patients eligible for carotid surgery, the decision to stent as opposed to open repair is based on anatomy and the level of either surgical or cardiovascular risk. If the patient has an acceptable level of risk and a longer life expectancy, then CEA provides a more durable option.

3. Preoperative Assessment

This should focus on evaluation of comorbid disease, as described above, which could negatively impact effective blood pressure management and result in an elevated risk of cardiovascular complications. Carotid surgery falls into the moderate-risk category. Pre-surgical testing should follow AHA/ACA guidelines for intermediate risk noncardiac surgery.

• 12 lead EKG, standard
• Labs (including CBC, electrolytes, creatinine, coags)
• CT angiogram vs. carotid ultrasound to define anatomy (surgeon’s purview)
• Consider exercise or pharmacologic stress test if functional status is poor or unknown and patient is at elevated risk (>1%) of MACE based on VQI or NSQIP calculator
• Consider TTE if concerned for heart failure, pulmonary hypertension, or valvular disease as these may impair the ability to effectively induce hypertension required during carotid clamping

The urgency of the procedure, based on whether the patient is symptomatic or not, should also factor into the decision to obtain additional testing. As is often the case, one needs to weigh the benefits of additional diagnostic information against the cost of delaying the procedure. Preoperative studies showing high cardiovascular or pulmonary risks generally indicate a patient may be a better candidate for TCAR than for open CEA.

4. Preoperative Preparations

• Clopidogrel and oral anticoagulants (i.e. warfarin, DOACs) are generally held for the appropriate washout period according to the particular agent and GFR. Aspirin and statins are usually continued.
• Continue any previously prescribed beta blockers.
• Carefully consider continuing vs. discontinuing other anti-hypertensives; consider stopping ACEi / ARBs as refractory post-induction hypotension can compromise cerebral perfusion and make induced hypertension during carotid cross clamp difficult.

5. Access / Fluids

• Generally, 2 good PIVs are adequate, but one should be confident in the integrity of those lines as vasopressors / vasodilators will likely be required during critical portions of the procedure when the arms are tucked.
• If central access is needed, recommend contralateral IJ / subclavian vs. femoral access.
• No restrictions / requirement for fluids per se. Carefully assess volume status as many of these patients are on diuretics / hemodialysis for concomitant renal and cardiovascular disease. Relative hypovolemia may adversely affect the ability to achieve induced hypertension required during carotid clamping.
• Patients should be type & crossed for at least 2 units of PRBCs ; can consider more depending on the preoperative Hgb.

6. Monitors

• Standard ASA monitors plus…
• Pre-induction arterial line for strict blood pressure monitoring
• Second (or double) transducer for measuring stump pressure ; surgeon will pass sterile tubing off the field which should be connected to this transducer (must be zeroed and display SBP / DBP / MAP).
• Cerebral oximetry to monitor adequacy of collateral circulation via the Circle of Willis during carotid clamping (trend more important than absolute value)
• Consider processed EEG monitoring with SedLine.
• For higher risk cases, the surgeon may choose to monitor SSEPs and EEG via neuromonitoring in addition to stump pressure (which has implications for the choice of anesthetic).
• ACT monitoring during heparinization (target 280-340 seconds)

7. Anesthetic Technique

While CEA can be performed under MAC with a cervical plexus block, at UCSF, the overwhelming majority are done under general anesthesia. Choice of agents for both induction and maintenance are at the discretion of the anesthesia provider and should be based on comorbidities in order to achieve stable hemodynamics throughout. Of note, if monitoring SSEPs, consideration should be given to using a predominantly IV anesthestic with propofol as the primary maintenance agent. Adjustments should be made when a TIVA in used to appropriately time emergence as the goal is for assessment of a neurologic exam as soon as possible following completion of the case.

Awake CEA is a viable option, particularly for those who are poor candidates for general anesthesia. However, information regarding MAC for CEA is beyond the scope of this reference document and can be found elsewhere.

Superficial Cervical Plexus Block

Can be used either as the primary anesthetic in awake CEA or as an adjunct to GA to improve pain control and limit the dose of general anesthesia. We recommend performing this as a field block by landmarks since it is faster and equally as effective as ultrasound-guided. Consider use of ultrasound when there is significant distortion of anatomy by prior surgery / radiation or electively to give trainees a better understanding of underlying anatomic structures.

1. Control syringe, ~25g needle
2. 10mL of 0.5% Ropiv or 0.25% Bupiv (consider adding mepivacaine if case done under MAC, for faster block onset)
3. Locate posterior border of sternocleidomastoid (SCM)
4. Mark mid-point between mastoid process and clavicle
5. Enter posterior to SCM, 0.5-1 cm deep, aspirate
6. Inject 4 mL, fan cephalad (3 mL), fan caudad (3 mL)

Deep cervical plexus block is not recommended, even for awake cases, due to the risk of inadvertent vascular or dural puncture. Supplementation of the superficial block by local infiltration in the surgical field is generally safer and equally effective.

8. Key procedure related points

• Titration of vasopressors during periods of variable surgical stimulation is often necessary to maintain BP goals. During exposure, stimulation is high and it is relatively low during the clamp / vessel repair period.
• After dissection and immediately prior to carotid clamping, the surgeon will request IV heparin (usually approx. 100mg/kg). An ACT should be checked 3-4min after the initial dose of heparin, followed by every 20min thereafter. Target ACT is usually 280-350s
• During carotid clamping, maintain blood pressure at least 15-20% above baseline to aid in perfusion via Circle of Willis (typically requires use of vasopressors).
• Inadequacy of collateral flow during carotid clamping is typically defined by one or more of the following : lack of pulsatility ; MAP < 40 (some surgeons prefer a higher MAP goal) ; and/or a significant decline in cerebral saturation (usually a relative decrease of > 20% or an absolute decrease of > 15%).
• Although less than TCAR, there is a risk of acute bradycardia during surgical manipulation due to stimulation of the carotid sinus reflex. Not usually premedicated with glycopyrrolate. Treat with cessation of surgical pressure, antimuscarinics (i.e. glycopyrrolate / atropine), and/or BP support with vasopressors. The surgeon can also infiltrate with lidocaine to prevent recurrence, but this is rarely done.
• Monitor rSO2 (cerebral oximeter) and/or raw EEG (via SedLine) for e/o frontal lobe hypoperfusion during the clamp period. Notify the surgeon of any changes. If this occurs early, it may be an indication to shunt. The trend is more important than the raw number.
• Stump pressure will be measured immediately after carotid clamping. A second a.line transducer will be attached to sterile pressure tubing which is passed off the field. This should be set to display SBP / DBP / MAP and zeroed after tubing is connected. Prior to measurement, this should be flushed / de-aired, which the surgeon will prompt.
• Respond to e/o cerebral hypoperfusion during clamping by increasing the FiO2 to 1.0, incrementally increasing systemic BP (increasing the gradient across the Circle of Willis), bolusing IVFs, and decreasing ventilation / increasing PaCO2 (to facilitate cerebral vasodilation).
• Goal after unclamping is tighter control of SBP (110-140mmHg) to maintain perfusion but avoid cerebral hyperperfusion from relief of stenosis
• Protamine is usually given to reverse heparinization. Dose depends on ACT prior to reversal but is usually 30-50mg. Give slowly and monitor EtCO2 and blood pressure closely for signs of protamine reaction. Recheck ACT 3-4min after protamine is all in to confirm return to baseline.
• Significant coughing / transient hypertension during emergence / extubation risks injury or rupture at the new carotid suture lines. Usually mitigated by careful titration of opiates and direct counterpressure on the neck by the surgeons during emergence. Consider a deep extubation only in patients with a low risk airway and with elevated surgical risk of hematoma. This may be at odds with the goal of an immediate postop neurological exam.
• Admission is generally to PACU and then TCU. However, will admit to neuro ICU for close neurologic and hemodynamic monitoring if bed is available or if vasopressors are needed postop.

9. Potential complications

• Embolic stroke : during exposure or due to manipulation of plaque material outside of clamp area.
• Stroke due to hypoperfusion / insufficient collateral flow via Circle of Willis ; watershed infarct.
• Bleeding due to shunt / clamp dislodgement : higher risk during MAC as opposed to GA.
• Cerebral hyperperfusion syndrome : after unclamping, ipsilateral ACA/MCA distribution now seeing higher pressure and flow since no longer obstructed by stenotic segment of carotid artery. Stroke like syndrome, due to reperfusion-type physiology, which can manifest as encephalopathy or unilateral sensory / motor deficits, seizure, or rarely, intracranial hemorrhage.
• Neck hematoma / airway compromise : an expanding surgical site hematoma can compromise surrounding structures including patency of the airway ; should prompt emergent return to OR for exploration ; opening of the incision at bedside may be necessary in the case of impending airway compromise (prior to induction / securing the airway in rapidly evolving hematomas).

10. Positioning / ergonomic considerations

• supine, ipsilateral neck prepped
• consider taping endotracheal tube to the contralateral side; angle circuit away from surgical field
• neck extended with shoulder roll and head rotated away from surgical side to improve exposure

11. Duration of case

Surgical time : 90-120 min
Total OR time : 180-240 min