Anesthetic Considerations for Carotid Endarterectomy
Author: Shilpa Rao MD
Case: A 76 year old female patient was admitted with symptoms of left sided weakness, speech difficulties and multiple episodes of blurry vision which has spontaneously resolved over the last two weeks.
PMH: History of myocardial infarction 2 years ago with placement of a drug eluting stent (DES),
Medications: aspirin, metoprolol, lisinopril, atorvastatin
Physical Examination: Patient is awake, alert and oriented. Mild left hand and foot weakness.
Denies any chest pain, shortness of breath or any other symptoms. However, she is very anxious about her acute onset of symptoms. She has intermittent slurred speech.
Cardiovascular Examination: S1, S2 present, no murmurs.
Respiratory System: clear to auscultation bilaterally
Central Nervous System: as above. No other focal neurological deficits
Vital signs: Pulse: 92; Blood Pressure (BP): 190/85, Temperature: 36.5 C, Respiratory Rate: 14,
SpO2 98% on room air
Height: 155 cm, Weight: 65 kg, BMI 27
Airway: Mallampati-2, adequate mouth opening of > 3 finger breadths, some missing teeth, normal c-spine range of movement
Laboratory studies: Hemoglobin 12 g/dl, Sodium 137 mmol/L, K: 3.2 mmol/L, Glucose: 125 mg/dl
Electrocardiogram: Sinus rhythm, occasional premature ventricular complexes, non-specific STT
Echocardiogram: Ejection Fraction: 55%, No Regional Wall Motion Abnormalities, Normal
Imaging: Ultrasound of the carotid reveals 80% stenosis of the right internal carotid artery and <
50% stenosis of the left internal carotid artery
She is now scheduled for an urgent right carotid endarterectomy.
1. What are the indications and contra indications of carotid endarterectomy?
2. Does this patient need any further pre-operative work up?
3. Does the anesthetic technique (general anesthesia vs. local anesthesia) affect outcome?
4. What monitors would you like to use?
5. After a stable induction of general anesthesia, the BP increases to 220/110 mmHg during
laryngoscopy and intubation, HR: 104. What is the next step in the management?
6. During dissection around the carotid artery, you notice the HR suddenly drop to 25 b/min.
What is the differential diagnosis and management approach?
7. Following the application of carotid cross clamp, it is noticed that there is diffuse slowing
of the EEG signals across the cerebral cortex. What is the etiology and management?
8. Immediately in the post-operative period, the patient complains of pain around the incision
site as well as moderate headache. The BP is now 190/110 and HR is 98/min. Does this
need to be treated and why?
9. You examine the patient and you notice a tongue deviation to the right side. What is the
10. Forty-five minutes into the post-operative period, she complains of nausea and starts to
retch. You also notice a right sided neck swelling which is increasing in size. Discuss the
etiology and management.
Indications of Carotid Endarterectomy
• Carotid Endarterectomy (CEA) should be considered for any patient with carotid artery
stenosis in whom surgery will improve the natural history of the disease to a greater degree
than the corresponding medical treatment would.1
• In symptomatic low-risk patients with surgical morbidity and mortality (stroke and death)
of less than 6%, proven indications for CEA include the following:
• One or more transient ischemic attacks (TIAs) in the preceding 6 months and carotid artery
stenosis exceeding 50% 2
• The 2014 American Heart Association (AHA)/American Stroke Association (ASA)
guidelines for the prevention of stroke in patients with stroke or TIA contained the
following new or updated recommendations relevant to CEA3:
• Carotid angioplasty and stenting (CAS) is indicated as an alternative to CEA for
symptomatic patients at medium or low risk for complications associated with
endovascular intervention when the diameter of the lumen of the internal carotid artery is
reduced by >70% by noninvasive imaging or >50% by catheter-based imaging or
noninvasive imaging with corroboration and the anticipated rate of peri-procedural stroke
or death is <6% (class IIa; evidence level B).
• It is reasonable to consider the patient’s age in choosing between CAS and CEA; for
patients older than about 70 years, CEA may be associated with improved outcome
compared to CAS, particularly when the arterial anatomy does not favor endovascular
intervention; for younger patients, CAS is equivalent to CEA in terms of risk for periprocedural
complications and long-term risk for ipsilateral stroke (class IIa; evidence level
• CAS and CEA in the above settings should be performed by operators with established
peri-procedural stroke and mortality rates of < 6% for symptomatic patients (class I;
evidence level B).
• Routine, long-term follow-up imaging of the extracranial carotid circulation with carotid
duplex ultrasonography is not recommended (class III; evidence level B)
• There are relatively few contraindications for CEA, which include any associated acute life
threatening illness / condition which poses an imminent threat to life, or any other
immediate condition which requires prioritization in terms of surgery.
Pre-operative risk stratification:
• According to the ACC/AHA perioperative risk assessment:
Active Cardiac Conditions
Unstable coronary syndromes:
• Acute or recent myocardial infarction
• Unstable or severe angina (Canadian class III or IV)
Decompensated heart failure
• High-grade atrioventricular block
• Symptomatic ventricular arrhythmias in the presence of underlying heart disease
• Supraventricular arrhythmias with uncontrolled ventricular rate
Severe valvular heart disease
Clinical Risk Factors
History of ischemic heart disease
History of cerebrovascular disease
Compensated or prior heart failure
• The American College of Cardiology National Database Library has defined recent
myocardial infarction as >7 days but ≤1 month (30 days); acute myocardial infarction is
within 7 days
Cardiac Risk* Stratification for Non-cardiac Surgical Procedures4
High Risk (reported cardiac risk >5%)
Emergent major operations, particularly in older patients
Aortic and other major vascular surgeries
Peripheral vascular surgery
Anticipated prolonged surgical procedures associated with large fluid shifts, blood loss, or both
Intermediate Risk (reported cardiac risk >1% but <5%)
Head and neck surgery
Intraperitoneal and intrathoracic surgery
Low Risk (reported cardiac risk <1%)
• If the patient belongs to the intermediate-risk group, he or she should be managed
aggressively with lipid-lowering agents and tight BP control. The class I recommendations
are to continue perioperative beta blockers in patients who are already on beta blockers pre
• Much debate is ongoing concerning the use of noninvasive stress testing in this patient
subgroup. In any case, there is little evidence supporting the use of revascularization before
non-cardiac surgery. The role of preoperative PCI in reducing untoward perioperative
cardiac complications is uncertain given the available data. Performing PCI before noncardiac
surgery should be limited to 1) patients with left main coronary artery disease
whose comorbidities preclude coronary artery bypass surgery without undue risk and 2)
patients with unstable coronary artery disease who would be appropriate candidates for
emergency or urgent revascularization.
• Patients with ST-elevation MI or non–ST-elevation acute coronary syndrome benefit from
early invasive management (if non-cardiac surgery is time sensitive in these patients
despite an increased risk in the perioperative period, a strategy of balloon angioplasty or
bare-metal stent (BMS) implantation should be considered. Retrospective data analyses of
patients who have undergone coronary artery bypass grafting (CABG) or percutaneous
coronary intervention (PCI) months to years before non-cardiac surgery have shown a
lower incidence of perioperative complications compared with patients who had medical
Retrospective data analyses of patients who have undergone coronary artery bypass
grafting (CABG) or percutaneous coronary intervention (PCI) months to years before noncardiac
surgery have shown a lower incidence of perioperative complications compared
with patients who had medical therapy alone.7
Anesthetic Technique (General Anesthesia vs. Local Anesthesia):
• Most available evidence suggests that the choice of anesthetic technique has no significant
impact on major adverse primary outcomes (eg: death and stroke) after CEA. However, the
length of stay in the intensive care unit and hospital and certain adverse outcomes (eg,
hemodynamic instability, delirium) may be reduced in patients receiving local/regional
anesthesia compared with general anesthesia, and some centers have reported a lower
incidence of perioperative myocardial infarction (MI) when local/regional anesthesia is
• The major advantage of local/regional anesthesia is the ability to continuously monitor an
awake and conscious patient for neurological function. This approach requires extensive
pre-operative patient preparation and cautious use of sedation so as not to excessively
sedate the patient. In patients with possible difficult airway or obstructive sleep apnea, one
needs to weigh the risks and benefits of regional anesthesia vs general anesthesia, keeping
in mind that there is always a possibility to convert to general anesthesia during the surgery.
• Regional anesthesia is predominantly performed with superficial cervical plexus block and
additional local anesthesia infiltration as needed. In addition, a low dose of infusion of
dexmedetomidine (at 0.3-0.5 mcg/kg/hour and titrated to effect)[ML1] may be employed for
sedation as well as to maintain spontaneous ventilation. The risks associated with this
technique include local anesthetic toxicity, complications associated with the block such
as vessel or nerve injury, and the necessity to convert to general anesthesia, should the
block prove to be inadequate.
• The major advantage of general anesthesia is the ability to control the airway and have a
patient without movement. The risks associated with general anesthesia include
hemodynamic instability during induction, laryngoscopy, intubation and emergence, as
well as reliance on indirect monitors of neurological function which will be discussed
• The GALA trial by Gough et al. in 2008 was a multicenter, randomized controlled trial
which enrolled 3500 patients undergoing CEA from 90 centers between 2001 and 2007.
They compared general anesthetic versus local anesthesia technique for these patients.
They concluded that there was no major difference in 30 day mortality in either groups and
that the choice of anesthetic does not affect the perioperative outcome.9
Hence, in summary, although the type of anesthesia does not influence the outcome nor
does it influence the incidence of perioperative strokes, an awake and co-operative patient
is considered the “gold standard” in early diagnosis of stroke or other neurological events.
• As discussed above, an awake patient is considered the “gold standard” for neurological
monitoring, allowing for early detection of ischemic events. This also allows for the
continuous use of sensory and motor function monitoring in an awake patient.
• However, indirect monitors of cerebral function need to be used if general anesthesia is
employed. Some of these are listed below in Table 1.10
|Using simple tasks for
the patient to perform to
assess the signs for
|Direct monitor of
|As stated above for
performing CEA under
| A Doppler probe is
placed on the petrous
temporal bone allowing
measurement of middle
cerebral artery flow
| Monitors both flow
and emboli, used
during intra- and
| • Operator-dependent
• Placement is
found in 10–
20% of patients
| The stump pressure
distal to the carotid
clamp reflects the
around the circle of
| Specific measure of
|EEG|| EEG is affected by
Raw and processed
(spectral array) datacan be used
cortical and not
• Difficult to
• GA can alter the
• Cannot identify
| EEG is recorded
after a stimulus, thus
reflects the cortex
and deeper structure
| Maybe useful
| • GA can alter the
• Thought to be no
more sensitive or
• Cannot identify
arterial venous and
producing a regional
|• Poor positive
• Frontal lobe
• Interference from
blood flow and
• Cannot identify
• The use of each of the above monitors or a combination of the above is operator and
facility-dependent. When selecting an anesthetic technique, one should take into
consideration their effect on monitoring. (eg. inhalational anesthetics increase latency and
decrease the amplitude of SSEP in high concentrations. Propofol infusion titrated to burst
suppression will essentially abolish EEG signals. Dexmedetomidine generally has minimal
effect on EEG monitoring).
Potential Intraoperative Complications:
• Hemodynamic instability: Dissection around the carotid sinus can cause heart rate and blood
pressure variations, which may be acute in onset. The carotid sinus baroreceptors are located
close to the bifurcation of the common carotid artery. Any surgical manipulation in this area
may lead to acute onset bradycardia / sinus arrest (afferent limb: glossopharyngeal nerve,
efferent nerve: vagus nerve). Treatment involves prompt cessation of stimulation, and
sometimes intravenous atropine.
• Intra-operative change in the quality of EEG signals in a patient under GA: Multiple factors
can contribute to the diffuse slowing in the quality of EEG signals. These include anesthetic
factors such as: excessive anesthetic depth / hypothermia / excessive hyperventilation
/hypotension etc. The most concerning factor, however, is stroke. Stroke is the second most
common cause of death following carotid endarterectomy (CEA). Stroke rates associated with
CEA in large randomized trials are generally <3 percent for asymptomatic patients and <5
percent for symptomatic patients.11,12 The treatment involves ensuring adequate anesthetic
depth and normothermia, and possibly placing a shunt if the patient is not tolerating cross
clamping of the carotid artery. In addition, hypotension should be aggressively treated as
appropriate during the period of cross clamping to aid perfusion.
• Myocardial ischemia: In one systematic review that collected data on over 60,000 patients
who underwent CEA, the pooled absolute risk of perioperative (30 day) myocardial infarction
was 0.87 percent. Risk factors for myocardial infarction included older age, coronary heart
disease, peripheral artery disease, and carotid restenosis.13
• Other complications: Major blood loss can occur, particularly during the dissection phase,
especially if the dissection around the major vessels is technically challenging.
• Delay in emergence: Delayed emergence can be due to multiple factors including but not
limited to residual anesthetic, residual narcotic, stroke, hypoglycemia and electrolyte
Potential Postoperative Complications:
• Post-operative reperfusion injury: Cerebral hyperperfusion syndrome (CHS) is an extreme
form of cardiovascular instability which occurs in 1% of patients undergoing CEA,
typically 2–7 days after surgery. Patients usually present with a hypertensive
encephalopathy, that is, severe headache, variable neurological deficits, blurry vision,
seizures, and marked hypertension. The etiology is probably an ischemia–reperfusion
injury with impaired cerebral autoregulation in areas of the brain which were previously
under-perfused. CHS can lead to cerebral edema and cerebral hemorrhage.14,15
• Treatment of CHS include strict blood pressure control and treatment of associated signs
of increased intracranial pressure, if present.
• Cervical Hematoma: Blood pressure control is extremely important in the postoperative
period as well. Uncontrolled hypertension can lead to a rapid development of a neck
hematoma which has the potential for airway compromise. In addition, associated
anticoagulation can exacerbate the situation. The treatment involves emergent
decompression in the operating room, reversal of anticoagulation (where deemed
appropriate) and securing the airway as quickly as possible.
• Nerve Injuries: Cranial nerve or other nerve injuries occur in about 5 percent of patients
following CEA.16-18 Most of the nerve injuries are transient and temporary, likely due to
neurapraxia / retraction or surgical manipulation, and they tend to improve and completely
resolve over time. The hypoglossal nerve is one of the most common nerves affected, and
is manifested by ipsilateral tongue deviation. In addition, the glossopharyngeal and vagus
nerves may also be affected due to their close proximity to the carotid bifurcation. The
treatment involves supportive care and follow up to ensure improvement.
• Other complications include post-operative wound infection, and the potential need for reexploration.
1) Ricotta JJ, Aburahma A, Ascher E, Eskandari M, Faries P, Lal BK, et al. Updated Society
for Vascular Surgery guidelines for management of extracranial carotid disease. J Vasc
Surg. 2011 Sep. 54 (3):e1-31
2) Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade
carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial
Collaborators. N Engl J Med. 1991 Aug 15. 325(7):445-53.
3) Kernan WN, Ovbiagele B, Black HR, et al, American Heart Association Stroke Council,
Council on Cardiovascular and Stroke Nursing, et al. Guidelines for the prevention of
stroke in patients with stroke and transient ischemic attack: a guideline for healthcare
professionals from the American Heart Association/American Stroke Association. Stroke.
2014 Jul. 45 (7):2160-236
4) Fleisher LA, et al. 2014 ACC/AHA Perioperative Guideline: Executive Summary
5) Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA Guideline for Coronary Artery
Bypass Graft Surgery. A report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. Developed in
collaboration with the American Association for Thoracic Surgery, Society of
Cardiovascular Anesthesiologists, and Society of Thoracic Surgeons. J Am Coll Cardiol.
6) Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guideline for
Percutaneous Coronary Intervention. A report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines and the
Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol.
7) Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 guidelines on perioperative
cardiovascular evaluation and care for noncardiac surgery: a report of the American
College of Cardiology/American Heart Association task force on practice guidelines.
8) Leichtle SW, Mouawad NJ, Welch K, et al. Outcomes of carotid endarterectomy under
general and regional anesthesia from the American College of Surgeons’ National Surgical
Quality Improvement Program. J Vasc Surg 2012; 56:81.
9) Hye RJ, Voeks JH, Malas MB, et al. Anesthetic type and risk of myocardial infarction after
carotid endarterectomy in the Carotid Revascularization Endarterectomy versus Stenting
Trial (CREST). J Vasc Surg 2016; 64:3.
10) Gough MJ, Bonham A, Horrocks M, Colam B, Lewis SC, Rothwell PM, et al. GALA: An
international multicentre randomised trial comparing general anesthesia versus local
anesthesia for carotid surgery. Trials. 2008;9:28
11) General or local anaesthesia for carotid endarterectomy? Nadia Ladak, MB ChB FRCA ,
Jonathan Thompson, BSc (Hons) MD FRCA. Contin Educ Anaesth Crit Care Pain (2012)
12) Wu TY, Anderson NE, Barber PA. Neurological complications of carotid
revascularisation. J Neurol Neurosurg Psychiatry 2012; 83:543.
13) Hill MD, Brooks W, Mackey A, et al. Stroke after carotid stenting and endarterectomy in
the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST). Circulation
14) Boulanger M, Camelière L, Felgueiras R, et al. Periprocedural Myocardial Infarction After
Carotid Endarterectomy and Stenting: Systematic Review and Meta-Analysis. Stroke
15) Stoneham MD, Thompson JP .Arterial pressure management and carotid endarterectomy
Br J Anaesth 2009 vol. 102 (pg. 442 – 52)
16) Fokkema M, de Borst GJ, Nolan BW, et al. Clinical relevance of cranial nerve injury
following carotid endarterectomy. Eur J Vasc Endovasc Surg 2014; 47:2.
17) Cunningham EJ, Bond R, Mayberg MR, et al. Risk of persistent cranial nerve injury after
carotid endarterectomy. J Neurosurg 2004; 101:445.
18) Kakisis JD, Antonopoulos CN, Mantas G, Moulakakis KG, Sfyroeras G, Geroulakos G
Cranial Nerve Injury After Carotid Endarterectomy: Incidence, Risk Factors, and Time
Trends Eur J Vasc Endovasc Surg. 2017 Mar;53(3):320-335. doi:
10.1016/j.ejvs.2016.12.026. Epub 2017 Jan 21.