263

Page 1

Anesthesia for Carotid Surgery

Daniel J. Cole, M.D.

Loma Linda, California

OBJECTIVES
Participants will learn pathophysiologic principles of carotid artery disease, understand effective strategies for
anesthetic evaluation and perioperative management of carotid artery surgery and its complications, and consider
different methods of neurophysiologic monitoring for carotid artery surgery.
CASE PRESENTATION
There are about 1.2 million strokes or transient ischemic attacks each year in the United States; and with more than
150,000 deaths each year, stroke is the third leading cause of death in the United States.
Medical therapy for stroke is directed at prevention by correcting modifiable risk factors, and by utilizing
antiplatelet and anticoagulant agents for patients whom have suffered cerebral ischemia of atherothrombotic origin.
Carotid endarterectomy was introduced in 1954 as a preventive measure for occlusive stroke, and has proved to be
of benefit for selected patients. For symptomatic patients, carotid endarterectomy is indicated if the carotid artery
stenosis is greater than 70 percent; and provided the surgical risk is low, for patients with carotid artery stenosis of
50-69 percent. For asymptomatic patients, carotid endarterectomy is beneficial if the carotid artery stenosis is greater
than 60 percent; however, the benefit is considered marginal, and the surgical risk should be favorable.1-5
Currently, there are ongoing trials evaluating carotid stenting and angioplasty. This procedure involves placement of
a saline filled balloon, preloaded with a stent, under angiographic guidance and occluding the carotid artery for 1-3
minutes with 15 atmospheres of pressure. The anesthetic technique for this procedure involves minimal sedation.
This procedure can cause severe bradycardia and hypotension. The complications associated with angioplasty are
less clear and more randomized trials with strict enrollment criteria are required. Criticisms of this nonsurgical
approach to carotid artery disease include a high rate of stroke due to angiography alone.
Physiologic Considerations
Carotid artery disease is usually the result of atherosclerosis at the bifurcation of the common carotid artery or origin
of the internal carotid artery. Ischemia is most often due to embolic phenomenon, but may also be due to local
hemodynamic factors. During ischemia, collateral flow is a cornerstone of cerebral blood flow (CBF) compensation.
The principal pathways of collateral flow are the Circle of Willis, extracranial anastomotic channels, and
leptomeningeal communications that bridge watershed areas between major arteries.
During carotid endarterectomy, the risk of ischemia is related to the dependency of the cerebral circulation on the
ipsilateral internal carotid artery, and the cerebrovascular reserve of the contralateral hemisphere. This concept is
supported by data that has demonstrated an increased incidence of stroke in patients with carotid artery cross-clamp
related changes suggestive of ischemia. Moreover, there is a fivefold increase in the incidence of perioperative
stroke associated with carotid endarterectomy for patients without adequate collateral blood flow.6,7
Preoperative Evaluation
Carotid endarterectomy has an inherent risk of perioperative stroke and cardiovascular events. Approximately of
strokes associated with carotid endarterectomy occur intraoperatively; and about 1/3 of these stroke are
hemodynamic versus embolic in origin.8-10 Recent data from the North American Symptomatic Carotid
Endarterectomy Trial report a 6.5% rate of stroke and death (1.1% rate of death, 0.9% disabling stroke, and 4.5%
non-disabling stroke) associated with carotid endarterectomy.8,9 Increased risk for stroke following a carotid
endarterectomy is most strongly associated with an active neurologic process prior to surgical intervention. Other
factors which have been reported to increase neurological risk include:
hemispheric versus retinal transient ischemic attack
a left sided procedure
ipsilateral ischemic lesion on computerized tomography
contralateral carotid occlusion
impaired consciousness
poor collaterals
an irregular or ulcerated ipsilateral plaque
endarterectomy done in conjunction with coronary artery bypass graft surgery.

263
Page 2
Medical complications occur about 10% of the time following carotid endarterectomy.
Hypertension-the incidence of a neurologic deficit is greater in patients with postoperative hypertension, and the
incidence of both postoperative hypotension and hypertension is greater in patients who have uncontrolled
hypertension preoperatively. In a multicenter study11 diastolic hypertension (>110 mmHg) was found to be a
predictor of adverse events. Although it seems reasonable that hypertension should be controlled before surgery,
there is an absence of prospective data to confirm this logic. A reasonable recommendation is to delay elective
surgery if the diastolic blood pressure is greater than 110 mmHg. A less firm recommendation would be to delay
elective surgery if the systolic blood pressure is greater than 180 mmHg.
Cardiac-carotid artery disease is typically a manifestation of systemic vascular disease. Accordingly, a cardiac
assessment is indicated in all patients who present for carotid endarterectomy surgery. This should include a history
that emphasizes previous myocardial infarction, angina, exercise tolerance, congestive heart failure, and rhythm
disorders. An electrocardiogram and chest radiograph should be routine; and other tests including echocardiography,
a stress test, and rhythm monitoring may be indicated.9
Diabetes-diabetic patients have increased cardiac related death, but data seems to indicate that carotid
endarterectomy can be performed safely in patients with diabetes.12
Renal insufficiency-patients with renal insufficiency have an overall increased risk for stroke and death, and
cardiac morbidity, associated with carotid endarterectomy.13
Monitoring
A continuous lead II and V5 ECG and an arterial catheter are considered routine; a PA catheter or TEE may be
considered in patients with symptomatic cardiac disease or a recent myocardial infarction. There is considerable
variability in brain monitoring during carotid endarterectomy (see Table 1). Some centers would not change therapy
based on any index and do not monitor. Most centers use some means of monitoring and selectively shunt during
cross clamping if signs of inadequate perfusion appear. Two standard of care monitors are an awake patient and
the EEG.14-16
Table 1-cerebral ischemia monitors for carotid endarterectomy.
EEG-electroencephalogram; TCD-transcranial Doppler.
Comment
likely the gold standard for neurologic monitoring. However, there is an absence of
Awake Patient
prospective data that would compel one to chose this method of neurologic monitoring
neurologic changes may correlate with the EEG. However, there is a fairly high rate of
EEG
"false-positives" for discriminating ischemia with the EEG
probably not any better than the EEG, but more complex. May be a better indicator of
SSEPs
subcortical ischemia
Stump Pressure poor sensitivity/specificity
TCD may be beneficial for assessing hemodynamic ischemia, shunt function, embolic
TCD
phenomenon, and the hyperperfusion syndrome
Oximetry
high false positive rate
JvO2
sensitivity, specificity, and intervention thresholds not determined

Anesthetic Management
No compelling advantage has been demonstrated with either regional or general anesthesia, and accordingly, a
technique that optimizes perfusion to the brain, minimizes myocardial stress, and allows for a rapid anesthetic
recovery is suggested.
Anesthetic choice is often strongly influenced by surgeon preference and the anesthesiologists familiarity with a
specific technique. General anesthesia is preferred in patients with anatomy or pathology that may make the surgical
conditions difficult. One caveat regarding general anesthesia that is often not appreciated regards nitrous oxide. It is
very difficult to place a shunt in the carotid artery, or to release the carotid artery cross-clamp, without exposing the

263
Page 3
distal cerebral circulation to arterial air. Accordingly, it is recommended that, if used, nitrous oxide be discontinued
at the time of carotid artery cross-clamp.
In a recent published study, sevoflurane and desflurane provided quicker extubation times and recovery profiles
after carotid endarterectomy, compared to isoflurane, with no significant perioperative difference in cardiac index or
ST segment analysis. Propofol and narcotics may be associated with systemic hypotension in patients undergoing
carotid endarterectomy surgery.
A regional technique for carotid endarterectomy necessitates the correct combination of patient, surgeon, and
anesthesiologist. Carotid endarterectomy requires a block of cervical nerves 2-4. Superficial cervical plexus block,
deep cervical plexus block, epidural anesthesia, straight local, and combinations of these techniques have all been
used successfully. Tangkanakul et al16 performed a meta-analysis of studies evaluating the safety and efficacy of
regional anesthesia for carotid endarterectomy. The non-randomized studies suggested that the use of a regional
technique may be associated with reductions (approximately 50%) in the odds of stroke, death, myocardial
infarction and pulmonary complications, and with reductions in hospital stay. There were far too little data from the
randomized trials to confirm or refute these findings.
Local infiltration alone requires a motivated patient and surgeon. A cervical epidural block is achieved via a
catheter, placed in the cervical epidural space, with injection of 10-15 ml of a solution such as 0.5% bupivacaine. All
cervical and many thoracic nerve roots are potentially affected. Morbidity includes hypotension, bradycardia,
inevitable changes in pulmonary function, frank respiratory failure, dural puncture, and bloody tap.
Superficial and deep cervical plexus block can be utilized to carry out both superficial and deep operations within
the region of the neck. As a motor block is not required, lower concentrations of a local anesthetic can be used such
as 1% lidocaine or mepivacaine, or 0.25% bupivacaine.
Superficial cervical plexus block can be performed with the patient in the supine position and the head slightly
rotated to the side opposite of the block. A 22-gauge, 4-cm needle is inserted at the midpoint of the
sternocleidomastoid muscle in the subcutaneous region immediately posterior to the muscle. Approximately 5 ml of
a local anesthetic solution is injected, and the needle is repositioned in a fan-like fashion in order to perform a field
block by injecting an additional 5 ml of local anesthetic both superiorly and inferiorly along the posterior border of
the sternocleidomastoid muscle.
A deep cervical plexus block is technically more difficult to place but provides a more reliable analgesic pattern.
This can be performed with the neck slightly extended and head turned away from the block site. A line should be
drawn from the mastoid process to Chassaignacs tubercle of the C6 transverse vertebrae. A second line should be
drawn 1 cm posteriorly and parallel to the first line. The C2 transverse process is approximately 1-2 cm caudad to
the mastoid process, and C3 and C4 approximately 1.5 and 3.0 cm caudad to C2, respectively. A 22-gauge, 5-cm
needle, is then inserted over the C4 transverse process until contact with the transverse process is achieved at a depth
of 1.5 to 3 cm. When paresthesias are obtained, inject 10-12 ml of the desired local anesthetic solution. If
paresthesias are not elicited on the first pass, then redirect the needle in a step-wise pattern in an anterior-posterior
fashion. Conversely, a more traditional block may be achieved by injecting approximately 5 ml of local anesthetic at
each of the transverse processes (C2, C3, and C4). During a deep cervical plexus block, the phrenic nerve is usually
partially or completely blocked, therefore, bilateral blocks should be avoided.
There is an expected rate of supplementation required in most regional techniques.21 This may be due to crossover
fibers from the contralateral side or to sympathetic innervation of the carotid sheath; in these instances the surgeon
can simply supplement the anesthetic. Conversely, a high carotid artery lesion may require aggressive retraction of
the mandible; in this instance an intraoral mandibular nerve block may be helpful.

263
Page 4
Modalities of Cerebral Protection
Surgical: a shunt can be placed to maintain CBF during carotid artery cross-clamping. Most often, placement of the
shunt is dependent upon the data one obtains from some monitor of cerebral function. However, a shunt entails the
risks of embolization and carotid intimal dissection, and limits surgical exposure.
Physiologic:
1. Hypothermia-much has been studied about the profound beneficial effect mild hypothermia (33-34C) has upon
cerebral infarction. Although this degree of hypothermia has appeal for carotid endarterectomy, the therapeutic
sequence of normothermiahypothermia normothermia is not a simple maneuver that one turns on or off.
Accordingly, is the concern that if mild hypothermia is employed as a cerebral protectant for carotid endarterectomy
surgery, many patients may suffer from shivering in the recovery phase and a consequent increase in myocardial
oxygen consumption which may precipitate myocardial ischemia. Thus, routine employment of mild hypothermia is
not recommended for patients undergoing carotid endarterectomy. Conversely, hyperthermia should be avoided.
2. Hyperglycemia-should be treated and avoided when possible. This is generally accomplished by eliminating
glucose-containing intravenous solutions, when possible, and by judiciously treating hyperglycemia with small
doses of insulin. A more severe neurologic injury has been shown to result in animal models of ischemia if
hyperglycemia is present. This may be due to higher tissue lactate levels.
3. Hypertension-during ischemia, autoregulation is impaired and CBF become exquisitely dependent on perfusion
pressure. Increasing perfusion by augmenting mean arterial blood pressure should open collateral vessels, effecting
an increase in flow to the area of ischemia. Hypertensive therapy has consistently decreased injury in animals;
however, clinical efficacy has not been definitively established. However, there is evidence of an ischemic blood
pressure threshold in patients suffering from stroke. i.e., above this threshold neurologic symptoms subsided, and
below this threshold neurologic symptoms were manifest. Thus, it is advisable to maintain normal to high mean
arterial pressure in most situations.
4. Hemodilution-the technique of hemodilution to improve CBF is dependent upon the rationale that CBF is
inversely related to hematocrit. Although the optimal hematocrit during cerebral ischemia seems to be about 30%,
the data are not compelling. It is, however, recommended to avoid a high hemocrit level in patients whom are
scheduled for carotid endarterectomy.
5. Carbon Dioxide-normocarbia should be the goal. There is no advantage to hypercarbia, and extreme levels of
hypocarbia may precipitate cerebral ischemia, per se.
Anesthetic Methods:17-22
1. Barbiturates-as a whole, the evidence does not support the use of barbiturates as a cerebral protectant for
permanent focal ischemia. However, during transient focal ischemia there is evidence to support barbiturate therapy.
One point for barbiturates is just prior to carotid artery cross-clamp, however significant cardiovascular depression
and delayed awakening can occur.
2. Volatile Anesthetics-general anesthesia with isoflurane and sevoflurane is associated with a lower critical CBF
(that at which electroencephalographic evidence of ischemia was present) compared to halothane and enflurane.17
3. Etomidate-because of its short duration of action, hemodynamic profile, and cerebral metabolic properties
etomidate has been used during neurovascular procedures. However, there is evidence in animals that etomidate
worsens ischemic injury while thiopental improved injury.22 Accordingly, etomidate is not recommended for use as
a cerebral protectant.
4. Propofol-animal studies have produced conflicting results.

263
Page 5
The Postoperative Period
The objective is a smooth and prompt emergence with optimal systemic and cerebral hemodynamics. Additional
concerns in the immediate postoperative period include:
1. Hypertension-may occur as a result of damage or local anesthesia to the carotid sinus or its nerve and is profound
in 20% of patients in the immediate recovery period. Patients who have systolic hypertension are at greater risk of
developing a neurologic deficit than those patients who remain normotensive. Hypertension may worsen neurologic
outcome by exacerbating the hyperperfusion syndrome with resultant intracerebral hemorrhage.23 Hyperperfusion is
most likely to occur in patients with high grade stenosis who develop >100% increase in CBF after carotid
endarterectomy.23,24 To minimize the risk of hemorrhage, normotension should be maintained in patients at risk for
the hyperperfusion state.
2. Hypotension-after the removal of atheromatous plaques, increased stimulation to baroreceptors may result in
bradycardia and hypotension. Regional anesthesia may be associated with a higher incidence of postoperative
hypotension while general anesthesia is more often associated with postoperative hypertension.
3. Myocardial Infarction-the most frequent cause of morbidity and mortality.
4. Stroke-most often embolic in origin.
5. Bleeding-airway obstruction has been attributed to neck hemotoma that may be worsened by hypertension. Recent
data demonstrated that soft tissue swelling with edematous supraglottic mucosal folds compromising the airway
occurs in patients after carotid endarterectomy.25,26
6. Cranial Nerve Injury-occurs in 10% of patients. Damage to the recurrent laryngeal nerve may compromise
protective reflexes as well as cause airway obstruction. The most commonly injured nerves are the hypoglossal,
vagus, recurrent laryngeal, and accessory nerves. Unilateral injury to any of the above nerves is unlikely to cause
symptomatology requiring intervention in the immediate postoperative period. Bilateral injuries can result in upper
airway obstruction (beware in patients with preexisting neck surgery).
7. Carotid Body Damage-results in reduced ventilatory response to hypoxemia and hypercapnia. Patients undergoing
second-side carotid endarterectomy merit close observation.
Carotid Endarterectomy and Coronary Artery Bypass Graft Procedures
One of the more difficult decision matrices regards the patient who presents with simultaneous disease of the carotid
artery and the coronary arteries. The best available evidence would suggest that a patients risk of death or stroke is
almost doubled if the procedures are performed during a single anesthetic as opposed to a staged procedure.
Additional evidence would suggest, that when performing the procedures in a staged sequence, that risk is related to
which procedure is performed first (i.e., if a carotid endarterectomy is performed first, the risk of myocardial
infarction increases; while if a coronary artery bypass graft(s) is performed first the risk of stroke increase).
Timing of Carotid Endarterectomy After Stroke
Presently, there is insufficient information to establish definitive guidelines for the timing of carotid endarterectomy,
or other surgery, after an ischemic episode. Recent data suggests that there is a small but real increase in morbidity if
carotid endarterectomy is performed shortly after the onset of symptoms.27 Risk may be associated with the presence
of a low density lesion on the CT scan, vascular territory of the infarct, brain shift, and level of consciousness.28
Short-stay Carotid Endarterectomy
In the 1980s a carotid endarterectomy patient typically was sent to the ICU for 1-2 days and a general floor for 3-5
days to follow. With pressure to decrease cost it is inevitable that the length of stay for carotid endarterectomy be
scrutinized. Indeed there are several recent publications which are advocating the safety and cost-effectiveness of a
24 hour non-ICU stay for low risk patients following CEA.29 Most of the perioperative strokes following carotid
endarterectomy occur in the first 24 hours.

263
Page 6
Conclusions
The key points when managing a patient for carotid endarterectomy are summarized in Table 2. Several multicenter,
randomized, trials have validated the efficacy of carotid endarterectomy. Approximately one third of strokes that
occur perioperatively are hemodynamic in nature. It is reasonable that tight physiologic management might affect
this subset of patients. Most strokes however, are embolic in nature. Patients who have undergone carotid
endarterectomy have increased risk of a perioperative myocardial event; in fact, this is the most common morbid
event.
Table 2-key points of anesthetic management of carotid endarterectomy surgery.
Comment
Symptomatic patients-indicated if the carotid artery stenosis is greater than 70 percent; and
Indications
for selected patients if the carotid artery stenosis is 50-69 percent.
Preoperative
Hypertension
Concerns
Regional anesthesia may be associated with a decrease in stroke and cardiac morbidity of
Anesthetic 50%, a shorter operating room time, fewer shunts, quicker recognition of shunt dysfunction, a
Technique lower incidence of perioperative hypertension, and a shorter postoperative hospital stay and
lower costs.
Cerebral
Neurologic status in the awake patient, and the electroencephalogram may be considered
Monitoring close to a "gold" standard.
Postoperative
Hypertension
Concerns
There is no demonstrable advantage of a specific general anesthetic technique for patients undergoing carotid
endarterectomy. Whichever anesthetic technique is employed, it is imperative that CBF is optimized, there is
minimal cardiac stress, and that anesthetic recovery is rapidin order to evaluate neurologic status. During the crossclamp period, the risk of ischemia may be decreased by maintaining normal to high perfusion pressure.
Additional concerns in the immediate postoperative period are tight hemodynamic control. It may be necessary to
add a vasodilator for hypertensive patients to prevent hyperperfusion syndrome. In the other spectrum some patients
may become hypotensive due to stimulation to the baroreceptors. Persistent, hypotensive patients may require an
addition of vasopressors.

References
1. NASCET. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med
325:445-453, 1991
2. Barnett HJM, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med
339:141-1425, 1998
3. ECSTs Collaborative Group. Endarterectomy for moderate symptomatic carotid stenosis: interim results from the MRC
European Carotid Surgery Trial. Lancet 347:1591-1599, 1996
4. Executive Committee for the ACAS. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 273:1421-28, 1995
5. National Institutes of Health. Clinical advisory: carotid endarterectomy for patients with asymptomatic internal carotid artery
stenosis. Stroke 25:2523-2524, 1994
6. Perkins WJ, et al. Low regional cerebral blood flow during carotid cross clamping is correlated with an increased risk of
perioperative stroke. Anesthesiology 85:A1183, 1996
7. Davies MJ, et al. Neurologic changes during carotid endarterectomy under cervical block predict a high risk of postoperative
stroke. Anesthesiology 78:829-833, 1993
8. Ferguson GG, et al. The North American Symptomatic Carotid Endarterectomy Trial. Surgical results in 141 patients. Stroke
30:1751-1758, 1999
9. Paciaroni M, et al. Medical complications associated with carotid endarterectomy. Stroke 30:1759-1763, 1999
10. Perkins WJ, et al. Timing and etiology of perioperative stroke following carotid endarterectomy. J Neurosurg Anesthesiol
7:301, 1995
11. McCrory DC, et al. Predicting complications of carotid endarterectomy. Stroke 24:1285-1291, 1993
12. Ballotta E, et al. Is diabetes mellitus a risk factor for carotid endarterectomy? A prospective study. Sugery 129:146-152, 2001

263
Page 7
13. Hamdan AD, et al. Renal insufficiency and altered postoperative risk in carotid endarterectomy. J Vasc Surg 29:1006-1011,
1999
14. Evans WE, et al. Optimal cerebral monitoring during carotid endarterectomy: neurologic response under local anesthesia. J
Vasc Surg 2:775-780, 1985
15. Spencer MP, et al. Transcranial Doppler monitoring and causes of stroke from carotid endarterectomy. Stroke 28:685-691,
1997
16. Tangkanakul C, et al. Local versus general anaesthesia in carotid endarterectomy: a systematic review of the evidence. Eur J
Vasc Endovasc Surg 13:491-499, 1997
17. Messick JM, et al. Correlation of regional cerebral blood flow (rCBF) with EEG changes during isoflurane anesthesia for
carotid endarterectomy: critical rCBF. Anesthesiology 66:344-349, 1987
18. Mutch WA, et al. Haemodynamic instability and myocardial ischaemia during carotid endarterectomy: a comparison of
propofol and isoflurane. Can J Anaesth 42:577-587, 1995
19. Allen BT, et al. The influence of anesthetic technique on perioperative complications after carotid endarterectomy. J Vasc
Surg 19:834-843, 1994
20. Bonnet F, et al. Cervical epidural anaesthesia for carotid artery surgery. Can J Anaesth 37:353-358, 1990
21. Davies MJ, et al. Superficial and deep cervical plexus block for carotid artery surgery: a prospective study of 1000 blocks.
Reg Anesth 22:442-446, 1997
22. Drummond JC, et al. Focal cerebral ischemia during anesthesia with etomidate, isoflurane or thiopental: a comparison of the
extent of cerebral injury. Neurosurgery 37:742-749,1995
23. Schroeder T, et al. Cerebral hyperperfusion following carotid endarterectomy. J Neurosurg 66:824-829, 1987
24. Powers AD, et al. Hyperperfusion syndrome following carotid endarterectomy: a transcranial Doppler evaluation.
Neurosurgery 26:56-59, 1990
25. Carmichael FJ, et al. Computed tomographic analysis of airway dimensions after carotid endarterectomy. Anesth Analg
83:12-17, 1996
26. Hughes R, et al. Upper airway edema after carotid endarterectomy: the effect of steroid administration. Anesth Analg 84:475478, 1997
27. Paty PSK, et al. Timing of carotid endarterectomy in patients with recent stroke. Surgery 122:850-855, 1997
28. Pritz, MB. Timing of carotid endarterectomy after stroke. Stroke 28:2563-2567, 1997
29. Kaufman JL, et al. Feasibility and safety of 1-day postoperative hospitalization for carotid endarterectomy. Arch Surg
131:751-755, 1996