Anesthesia for Carotid

Endarterectomy
Robert Y. Gumnit, MD
Director of Clinical Education
Burlington Anesthesia Associates
 Carotid Endarterectomy
• Prophylactic
intervention to
prevent cerebral
infarction and
relieve symptoms of
carotid
artherosclerosis
• Stroke incidence in
USA- 160/100,000
people
 Etiologies of Ischemic Stroke
• Thromboembolism from atherosclerotic
large extracranial or intracranial arteries
• Embolism from a cardiac source
• Atherosclerotic disease in small
cerebral vessels
 Location of Carotid Disease
• Most likely site is at the
carotid bifurcation with
proximal internal carotid
involvement
• Carotid circulation
supplies 80 to 90% of
cerebral blood supply
• Vertebral circulation
supplies 10 to 20% of
cerebral blood supply
 Distal Circulation
• Internal carotid
contributes to
anterior and middle
cerebral arteries
• 1st intracranial
branch of ICA is the
ophthalmic artery
 Important Anatomic Structures
Near Carotid Dissection
• Hypoglossal nerve
• Vagus Nerve
• Recurrent Laryngeal
Nerve
• Mandibular Branch of
Facial Nerve
• Important to document
preoperative neurologic
examination
 Clinical Presentation of Carotid
Disease
• Varies by site of stenosis and distal
embolization
• Part of a generalized vascular disease
• Transient Ischemic Event (TIA)/
Reversible Ischemic Neurologic
Deficit(RIND)
 Transient Ischemic Events
• Sudden onset of focal neurologic deficit
which resolves within 24 hours
• Contralateral motor or sensory deficits
• Amaurosis Fugax
 RIND’s
• Neurologic dysfunction greater than 24
hours but less than 2 weeks
• Important to differentiate between
carotid disease and posterior vertebro-
basilar artery disease
 Posterior Circulation Symptoms
• Binocular vision loss
• Vertigo
• “Drop Attacks”
 Differential Diagnosis of TIA
• Intracranial mass
• Cardiac Disease- e.g. Atrial Fibrillation,
Valvular Heart Disease,
Cardiomyopathy)
• Metabolic Encephalopathy/
Hyperglycemia
 Risk Factors for Carotid Disease
• Advanced age
• Hypertension
• Diabetes
• Hyperlipidemia
• Hypercoagulable states
• Smoking
 Diagnostic Imaging
• Ultrasound- 89%
detection rate
• Gold standard is
cerebral
angiography but
there is a 1%
chance of a
neurologic deficit
 Choice of Therapy
• Individualized assessment of stroke risk
weighing medical management versus
risk of perioperative stroke, death, or
cardiac event
• Large multicenter trials comparing
medical versus surgical management
comparing anti-platelet therapy versus
surgery
Summary of Large Clinical Trials
• Depending on particular series, patients
with between a minimum of 50% to 70%
stenosis are candidates with ipsilateral
disease and acceptable surgical risk
• The greater the degree of stenosis, the
greater the difference in outcome
statistics compared to medical therapy
 Preoperative Evaluation
• Comorbidities including advanced
vascular disease, coronary artery
disease- leading causes of
perioperative death
• Testing is useful if the only if results will
impact on actual perioperative care
 Conditions Requiring Some
Workup
• Orthostatic hypotension
• Coronary artery disease
• Myocardial infarction
• Congestive heart failure
• Dysrhythmias, Implanted pacer, AICD’s
 Assessment of Functional
Capacity
• DM
• Renal Insufficiency
• Pulmonary disease
 ACC/AHA Guidelines
• Stepwise approach to risk assessment
• Functional capacity
• Major markers: unstable coronary
syndromes, MI, unstable angina,
uncompensated CHF, severe valvular
lesions
 Intermediate Markers
• Mild angina
• Previous MI
• Compensated CHF
• DM
• Renal Insufficiency
 Minor Clinical Predictors
• Advanced age
• Abnormal EKG
• Non-sinus rhythm
• Low functional capacity
• History of stroke
• Uncontrolled hypertension
• Cardiac and Long-term risks are increased in
patients unable to meet a 4-MET demand
 Surgery Specific Risks
• ACC/AHA define CEA as an
intermediate risk procedure
• Risk of cardiac death or non-fatal MI
generally less than 5%
• If surgery is to be performed in
presence of high risk indicators, ACC
recommends delaying surgical for
further evaluation and treatment
 Elective CEA with Intermediate
Risk Predictors
• Consider functional capacity
• Consider non-invasive testing
 Indications for Further Testing
• Exercise tolerance < 4 METS
• Symptomatic valvular lesions
• Dilated or Hypertrophic Cardiomyopathy
• Hemodynamically significant
dysrhythmias
 Simple Conservative Approach
• Assume presence of CAD
• Treat with medically appropriate therapy
• Coronary angiography and prophylactic
revascularization has not been shown to
reduce cardiac morbidity and should
only be used in high risk cases
 Hypertension
• Most treatable preoperative risk factor for
stroke
• Reduced blood pressure decreases
probability of perioperative stroke
• Poorly controlled BP increases risk of
perioperative hemodynamic instability and
significant neurologic events
• BP meds continued right up to time of surgery
• Rapid correction of BP preoperatively not
advised
 Delay Surgery if Not Emergent
• Uncontrolled hypertension
• Uncontrolled diabetes
• Uncontrolled coronary disease
Goals of Anesthetic Management
• Protect brain and heart
from ischemic injury
• Maintain hemodynamic
stability
• Ablate stimulatory and
stress response to
surgery
• Awake, cooperative
patient at end of
procedure allowing
clear neurologic
evaluation
 Standard Monitoring
• ECG- Leads II, V4-5 for rhythm and S-T
segments
• Continuous arterial pressure monitoring,
arterial line
• Pulse oximetry
• Central lines generally not necessary
but should not be placed in jugular area
 Perioperative ß-Blockade
• Continue for patients already on this
therapy
• Those who are not already on ß-
blockers can be started on them
immediately if there is no
contraindication for reduction of
perioperative myocardial ischemia
 Choice of Anesthetic Technique
• Largely dependent on preferences of:
1. Surgeon
2. Patient
3. Anesthesia Team
• No strong data to clearly mandate any
particular method or agents
 General Anesthesia for CEA
• Maintain cerebral perfusion
• Minimize myocardial work
• Rapid and smooth emergence to allow
immediate postoperative neurologic
assessment
 Advantages of GA
• Allows for still, motionless patient
• Early control of airway and ventilation
• Ability to protect brain if ischemia
develops
 Blood Pressure Management
• Best range is individualized to each
patient
• Risk of either myocardial or cerebral
ischemia is minimized if perfusion
pressures are maintained in the
patient’s high normal range
 Choice of Induction Agent
• All available agents reduce cerebral
metabolic rate in excess of reduction of
cerebral blood flow
• Pentothal provides best protection against
focal ischemia
• Most rapid awakening with Propofol
• Etomidate has most favorable hemodynamic
profile but may worsen ischemic neurologic
injury (animal data)
 Hemodynamic Response to
Intubation/ Hypertension
• Short acting narcotic

• Short acting beta-

blocker

• Nitroglycerin or
Nitroprusside
 Maintenance with a
Volatile Agent
• All presently clinical available agents reduce
cerebral metabolic rate
• Isoflurane has the most pronounced effect
with a minimum of myocardial depression
• Newer agents allow for more rapid
emergence ( Sevoflurane, Desflurane)
• Maintain at a lighter plane to allow rapid
emergence and an easily interpretable EEG
 Hypotensive Response to
Induction
• Hypertensive patients often present in a
mildly hypovolemic state

• Small fluid boluses

• Phenylephrine
 Maintenance Events
• Cervical incision not especially
stimulating
• Rapid changes in pulse rate and blood
pressure/ hemodynamic instability can
be frequent
• Role of short acting agents/ vasoactive
drugs
 Blood Pressure Management
• Phenylephrine- α-agonist with no
direct effect on cerebral vasculature;
cerebral perfusion increased by
elevating perfusion pressure

• Ephedrine- Mixed α and β activity

 Stimulation of Carotid
Baroreceptor
• Manipulation can
result in sustained
bradycardia
• Infiltration with local
agent in carotid
sinus area
• atropine
 Tachycardia
• Not well tolerated in
the beta-blocked
patient

• Short acting beta-

blocker – e.g.
esmolol
 Management of Ventilation
• Maintain
normocarbia
• Hypercapnea may
cause cerebral steal
syndrome
• Hypcapnea may
decrease cerebral
perfusion
• LMA vs. ETT?
 Emergence Issues
• Coughing
• Hyperdynamic circulation
• Stress on suture lines
• Deep extubation?
• Airway topicalization?
 Neurologic Monitoring During
GA
• No monitoring modality is as effective
as watching an awake patient

• Rational for monitoring is to identify

which patients need shunting or
selective blood pressure augmentation
 Carotid Shunts Problems
• Carotid emboli
• Intimal dissection
• Limited surgical
exposure
 Commonly Used Monitors
• EEG
• Somatosenory-evoked potentials
SSEP’s
• Transcranial Doppler
• Internal carotid artery stump pressure
 EEG Monitoring

•Measures electrical activity of cortical neurons

•Cortical ischemia is manifested as ipsilateral cortical

slowing, attenuation, or both

•EEG signal is usually diminished when cerebral blow

flow < 15 ml/ 100 gm of brain tissue

•Below 12-15 ml/ 100 gm brain tissue there is the

beginning of cortical ischemia
 Causes of EEG Changes
• Ischemia from cross clamping
• Shunt Malfunction
• Hypotension
• Contralateral carotid stenosis
• Cerebral Emboli
 Limits of EEG Monitoring
• Inability to detect subcortical injury
• High false positive rate
• Diminished sensitivity in patients with
prior stroke
• Majority of intraoperative strokes are
embolic in nature
• Most strokes occur postoperatively
 SSEP’S
• Unlike EEG, it can detect deep brain
and brainstem ischemia
• Ischemia causes a detectable decrease
in signal amplitude with a concomitant
increase in signal latency
• Data is unclear whether this is actually
more sensitive than EEG
 Transcranial Doppler
• Allows continuous noninvasive
assessment of blood flow velocity
• Can detect emboli in ipsilateral middle
cerebral artery
• In presence of a shunt, can determine
shunt adequacy
 Carotid Artery Stump Pressure
• Mean arterial pressure cephalad to
carotid cross clamp
• Needle artery and connect to pressure
transducer
• Pressure is generated by back pressure
from Circle of Willis
• Minimal pressures believed to be in the
25 to 70 mm Hg range
 Other Neuro-Monitors
• Jugular bulb oxygen saturation
• Cerebral blood flow measurements
using injection of xenon-133 and
calculation done with scintilography
Regional Anesthesia Techniques
• Requires the correct combination of
surgeon, anesthesiologist and patient to
be successful
• Deep and Superficial Cervical Plexus
Block
• Epidural anesthesia
• Local infiltration
 Advantages of Regional
Anesthesia
• Awake patient- allowing for repeated
neurologic evaluations
• Can avoid complicated neurologic monitors
• Greater hemodynamic stability
• Improved cross clamp tolerance
• Reduced hospital stay and costs
• Lower (?) incidence of stroke and cardiac
morbidity
 Disadvantages of Regional
Anesthesia
• Inability to use pharmacologic cerebral
protection
• Requires a cooperative, non-claustrophobic
patient
• Possibility of seizures
• Poor access to the airway if GA becomes
necessary
• Phrenic and superior laryngeal nerve block is
common
 Other Problems
• Conversion rate to GA reported to be
around 3%
• Patients who undergo CEA and develop
neurologic changes under Cervical
Plexus Block are 6 times more likely to
suffer a stroke
 Relevant Anatomy
• Cervical Plexus is formed by the 1st 4
cervical nerves
• Nerves pass laterally along respective
vertebral transverse processes
• At the tips of C-2 to C-4 the nerves
divide into ascending and descending
branches and form loops before uniting
into deep and superficial branches
 Anatomy Continued
• The plexus is situated in front of the
levator scapulae and scalenus medius and
covered by the sternocleidomastoid
muscle
• The deep branches are purely motor
• The superficial branches are sensory and
supply the skin and subcutaneous tissues
of the neck and posterior aspect of the
head
 Sensory Anatomy
• The side of the neck may also derive
sensation from the trigeminal nerve
• The platysma receives some sensory
innervation from cervical branches of
the facial nerve
Cervical Plexus
Plexus Diagram
 Technique of Cervical Plexus
Block
• Superficial block requires infiltration
along posterior border of
sternocleidomastoid muscle
• Deep plexus requires block of the nerve
roots are they pass through the
intervertebral foramina of C-2,C-3,& C-4
Superficial Plexus Block
Deep Plexus Block
 Materials for Block
• Regular length #25 spinal needle
• Short (1-1.5 inch) spinal needle
• Intermediate acting local anesthetic- 1%
lidocaine, 0.5% bupivicaine, etc.
• Use 10 to 20 cc of anesthetic for
superficial plexus
• 3 to 5 cc at C-2, C-3, C-4
 Superficial vs. Deep Plexus
Block
• 3 different randomized trials (205 patients)
could not demonstrate clear benefit if deep
block was done with superficial block or
not
• Same VAS scores
• Same need for additional supplementation
• Some authors question if there is a real
anatomic basis for any difference
 Supplemental Block
• Manibular branch of
trigeminal nerve
 Surgical Approach
• Ventrojugular approach is standard
surgical technique
• This approach improves patient tolerance
• This technique is associated with a higher
transient incidence ipsilateral vocal cord
motility impairment because of a need for
greater vagal nerve mobilization
 Cervical Plexus Complications
• Deep plexus block:
• Intravascular injection
• Subarachnoid injection with brain stem
anesthesia
• Phrenic nerve block
• Recurrent laryngeal nerve block
• Vagus nerve block
• Horner’s syndrome
 Cervical Plexus Complications
• Superficial plexus block
• Intravascular injection
• Recurrent laryngeal nerve block if injection
is made deeper than the inferior border of
the SCM muscle
• Partial brachial plexus block has been
reported
 Incidence of Problems
• Pandit et al did not find a single incidence of
serious complications related to superficial
block in a review of 2500 cases collected from
several publications
• In this review serious complications defined as
life threatening occurred in only 0.25% of
patients (inadvertent subarachnoid injection,
respiratory distress from phrenic or laryngeal
nerve block)

• Br J Anaesth 2007,99:159-169
 Additional Problems
• Deep blocks done alone are associated
with a higher conversion rate to GA
(2.1% vs. 0.4%)
• When deep and superficial blocks are
done together the incidence of
ipsilateral hemidiaphragmatic paralysis
is 55 to 61%
 Choice of Local Anesthetic
• Bupivicaine 0.5% provides the longest
time to request for first analgesia
• Ropivicaine is probably the least
cardiotoxic
• Use the least possible amount of total
anesthetic in any case.
 Outcomes: Local vs. GA
• One series of 548 cases
• Local was 10 cc lidocaine for skin, 10 cc
for platysma
• GA was thiopental with isoflurane, nitrous-
oxide/oxygen, fentanyl maintenance
• No differences in postoperative stroke or
death rate

• Watts et al Am. J Surg 2004; 188:741-747

 Outcomes: Patient Satisfaction
Local vs. GA
• Prospective randomized study of 176
patients comparing CEA under local or GA
• Only the recovery was significantly better
with the local group
• No differences in anxiety or satisfaction

• McCarthy et al. Eur J Vasc Endovasc Surg 2001;

27:654-659
 Anesthetic Technique and
Surgical Stress Response
• Prospective trial of 109 patients
• Cortisol, ACTH, prolactin, and C-reactive
protein were measured before and after carotid
cross clamping and then daily for 3 days after
• Cortisol and ACTH levels were higher in the
regional group but this effect was abolished if a
shunt was used

• Marrocco-Trischitta et al. J Vasc Surg 2004; 39:1295-

1304
 Conclusions: Regional vs. GA
• No clear data to suggest improved
outcome in perioperative neurologic
problems
• GA can be combined with plexus block
and can result in greater hemodynamic
stability and shorter operating times

• Reg Anesth Pain Med 2008;33:340-345

 Complications:
PACU Issues/ Postoperative Care
• Hypertension
• Hypotension
• Myocardial ischemia or infarct
• Cranial nerve injury
• Recurrent Laryngeal Nerve injury
• Stroke
• Bleeding
 Postoperative Hypertension
• Can be secondary to local infiltration
around the carotid sinus or its nerve-
can be profound in 20% of patients
• Patients with poorly controlled BP are at
risk
• Severe hypertension is associated with
increased mortality, increased cardiac
and neurologic morbidity
 Management Options for
Postoperative Hypertension
• Short acting agents such as esmolol
and nitroglycerin are considered 1st line
agents
• IV titration of labetolol or hydralazine
• Nitroprusside infusion
• Nicardipine infusion
 Postoperative Hypoperfusion
Syndrome
• Somewhat uncommon
• Results from impaired cerebral
autoregulation in the surgically reperfused
hemisphere
• Manifested as headache, seizure,
neurologic deficit, cerebral edema, or
hemorrhage.
• CT scan- intracerebral hemorrhage, white
matter edema
 Hypotension
• May be related to carotid baroreceptor
hypersensitivity after plaque removal
• Can result in myocardial or cerebral
ischemia
• Consider judicious amounts of fluid
replacement and sympathomimetic
agents for support
 Postoperative Respiratory
Insufficiency
• Massive hematoma formation (active
bleeding, coagulopathy)
• Bilateral recurrent laryngeal nerve injury
• Soft tissue swelling, supraglottic
mucosal edema
 Carotid Body Denervation
• Secondary to surgical manipulation
• Results in impaired response to hypoxia
• Can be clinically significant in presence
of agents which depress respiration
• May be exaggerated with moderate to
severe COPD
• Consider using non-narcotic analgesia
 Cranial Nerve Dysfunction
• Generally secondary to surgical traction
not transection
• Generally transient- resolution within 6
months
• Dysphagia/ Hoarseness- recurrent
laryngeal nerve injury
• Tongue deviation – hypoglossal nerve
injury
 Myocardial Infarction
• A major cause of morbidity
• Symptoms and EKG changes should be
investigated promptly
• Hemodynamic instability
• Arrhythmia
• Maximize the balance between
myocardial oxygen supply and demand
 Parting Thoughts
• CEA requires a multi-disciplinary team
approach from the pre-op period through
convalescence
• CEA is a prophylactic procedure requiring
careful patient selection
• Close intraoperative communication
• There is no data to strongly support any
specific anesthetic approach as long as
CBF is maintained and hemodynamic
stress is limited