Anaesthesia for carotid endarterectomy

Dr. S. Parthasarathy MD., DA., DNB, MD (Acu),

Dip. Diab.DCA, Dip. Software statistics PhD (physio)

Mahatma Gandhi Medical college and research institute ,puducherry- India

Why of it ??

• Stroke is the third largest cause of death

• Carotid artery disease occurs in 30 % of stroke patients

• TIA is followed by stroke in almost all cases of thrombotic stroke

Circle of Willis

80-90 %

Normal CBF

• Normal CBF is approximately 50 mL/100 g/minute for the entire brain.

• blood flow is about four times higher in gray matter than it is in white matter, with the flows being 80 and 20mL /100 g/minute

• Neuronal destruction occurs with CBF less than 10 mL/100 g/minute.

Regulation of CBF• Cerebral autoregulation is the tendency of the tissue to

maintain normal blood flow despite variations in blood pressure.

• In normotensive individuals, cerebral blood flow (CBF) is constant between mean arterial pressures of 50 and 150 mm Hg.

• this means is that cerebrovascular resistance increases, through vasoconstriction, as mean arterial pressure increases from 50 to 150 mm Hg.

• THEN ?? • At pressures less than 50 mm Hg, cerebral vessels are

maximally vasodilated, so that as mean arterial pressure falls CBF decreases

In hypertension

PCO2 --- 20 -80 mmHg

• Hypercarbia results in cerebral vasodilation

and hypocarbia in cerebral vasoconstriction.

CBF changes approximately 4% for each mm

Hg increase or decrease in arterial PCO2

• pH and PaO2 and neurogenic – also influence

PaCO2 and PaO2

What is that ??

• In carotid artery disease, atherosclerotic plaques develop at the lateral aspect of the bifurcation of the carotid artery.

• In addition to traditional CEA, carotid angioplasty and stenting (CAS) is increasingly used.

Why at carotid bifurcation

• Impedance mismatch, • altered hemodynamic conditions that

accompany division of a vessel into vessels of substantially different sizes,

• be implicated in the vessel injury

Luxury perfusion

• blood flow that is in excess of metabolic need (increased cerebral blood flow [CBF] relative to cerebral metabolic rate for O2).

• It is most frequently observed in tissues surrounding tumors or areas of infarction.

• It has also been described in tissues that have been manipulated during surgery.

Steal and inverse steal

• Intra cerebral steal is a paradoxical response to carbon dioxide in which hypercapnea decreases the blood flow in an ischemic area.

• Inverse steal is the effect of hypo capnea producing increased blood flow to ischemic regions of the brain.

Procedure

• occluding the common, external, and internal carotid arteries, isolating the diseased segment, opening the vessel wall, and removing the plaque.

• The vessel is then closed. If the remaining intima is too thin, the vessel is closed with a vein graft or a synthetic (Dacron) patch.

• Shunt or no

Symptoms

• TIA • Asymptomatic bruit • Amaurosis fugax • Posterior • Binocular vision loss• Vertigo• “Drop Attacks”

Diagnosis

• duplex scan, which combines B-mode anatomic imaging and pulse Doppler spectral analysis of blood flow velocity. The accuracy of duplex scanning reaches 95% in experienced hands when compared with angiography.

• magnetic resonance angiography

Indications

• symptomatic, high-grade carotid stenoses (70%

to 99%)

• 50 – 70 % stenosis but – recents stroke, males

hemisphere symptoms

• Surgically accessible stenosis

• Stable medical and neurologic condition

Inappropriate candidate for CEA

• Asymptomatic 50 - 60% stenosis

• Symptomatic or asymptomatic with Intracranial stenoses more severe than the extracranial stenosis

• Uncontrolled diabetes mellitus, hypertension, congestive heart failure, or unstable angina pectoris

• A major neurologic deficit or decreased level of consciousness

Preanaesthesia

• Basic health • Chart review • Head and neck – • airway • Coexisting disease (CAHD,COPD)• Neuro status

Risks ??

Risks

• Medical risk • angina , MI within 6 months ,CCF , Severe HT,

COPD, >70 years • Neurological risk • Multiple cerebral infarcts, progressive deficit,

newer deficit in 24 hours, frequent daily TIA

Angiographic risk

• Other side carotid occlusion • Siphon stenosis • Bifurcation • Soft thrombus

• All risks – I to IV ---- 1 – 10 % mortality

Preop stabilization

• Hypertension - > 150 greater risk • Diabetes – 150 -180 mg% • CAHD – adequate medical control • Special investion – depend on the original

disease and urgency of surgery • COPD, parkinsons, renal, hepatic etc. • Dangers – uncontrolled systemic diseases

Nerves close to dissection of surgery

• Hypoglossal nerve• Vagus Nerve• Recurrent Laryngeal Nerve• Mandibular Branch of Facial Nerve• Important to document preoperative

neurologic examination

Most feared complications

• CVA 4.5%• BP to be maintained• higher side

• Myocardial Infarct 2.2%• BP to be maintained • lower side

Anaesthesia

• Ablate stimulatory and stress response to surgery

• Awake, cooperative patient at end of procedure allowing clear neurologic evaluation

GA Vs LA

• A meta-analysis of the randomized studies

showed that the use of local anaesthetic was

associated with a reduction in the risk of local

haemorrhage within 30 days of surgery, but

there was no evidence of a reduction in the

odds of operative stroke.

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

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

may worsen ischemic neurologic injury (animal data)

Hemodynamic Response to Intubation/ Hypertension

• Short acting narcotic

• Short acting beta-blocker

• Nitroglycerin or Nitroprusside

Armoured

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

• Maintain at a lighter plane to allow rapid emergence and an easily interpretable EEG

Plus and minus

• The response of the cerebral circulation to carbon dioxide is maintained with sevoflurane

• Nitrous oxide should be avoided if possible. It increases the cerebral metabolic rate and produces a concomitant increase in middle cerebral artery blood flow velocity

• While cerebral autoregulation is impaired with sevoflurane, it is preserved under propofol–

remifentanil anaesthesia

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

Intra op events and monitors

• Maintain normocarbia• SPO2 • Urine • IBP

EEGs

• 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 < 10 ml/ 100 gm of brain tissue

Antiplatelets – Slowing and ischemia

• Aspirin to continue

• Heparin 100 units / kg

• No protamine

Limitations of EEG

• deep brain structures are not monitored by EEG.

• patients with pre-existing or fluctuating neurologic deficits the EEG may be false-negative;

• In these patients, there may be cell populations that are electrically silent

Somatosensory evoked potentials

• Stimulation to see response • deeper structures of the brain• Suppressed brain • Infarcted brain • BIS monitor is not suitable for cerebral

monitoring in this setting as it primarily detects frontal lobe activity and cannot be relied upon to detect localized changes elsewhere in the brain

stump pressure

• Once the common and external carotid arteries are clamped, the pressure measured in the internal carotid artery reflects the perfusion pressure transmitted around the Circle of Willis.

• This is the stump pressure.• A number of thresholds for the stump

pressure, ranging between 25 and 70 mm Hg , have been proposed below which shunting would be appropriate.

Near infrared spectroscopy

• Near infrared spectroscopy (NIRS) gives a value for regional cerebral oxygenation (rSO2) which is a composite measure of arterial venous and capillary oxygenation

• Cross clamping decrease rSo2 but ? Predictable

Transcranial Doppler

• Petrous part of temporal bone - thin acoustic window - doppler of MCA

• Decrease to 15 % - post op stroke • But difficult acoustic window in 10 – 20 %

patients

Emergence Issues

• Coughing• Hyperdynamic circulation• Stress on suture lines• Deep extubation?• Airway topicalization?• Deal for the needs of the situation

Regional

• 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

Regional

• Deep and Superficial Cervical Plexus Block• Epidural anesthesia• Local infiltration

Problems with RA

• 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

GA Vs RA

• Reg Anesth Pain Med 2008;33:340-345• Marrocco-Trischitta et al. J Vasc Surg 2004;

39:1295-1304• McCarthy et al. Eur J Vasc Endovasc Surg

2001; 27:654-659• Watts et al Am. J Surg 2004; 188:741-747

Conclusions of RA 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

• We can do whichever technique we are familiar with understanding the disease and drugs

Problems are plenty after also

Postoperative problems

• Hypertension• Hypotension• Myocardial ischemia or infarct• Cranial nerve injury• Recurrent Laryngeal Nerve injury• Stroke• Bleeding

Hypertension – 25 – 58 %

• poorly controlled BP• Carotid sinus local infiltration

• esmolol and nitroglycerin• Nicardipine and SNP next

Hypotension - 8-10 %

• May be related to carotid baroreceptor hypersensitivity after plaque removal

• Can result in myocardial or cerebral ischemia

• Consider judicious amounts of fluid sympatho mimetics for support

Other causes of haemodynamic instability

• Pneumothorax • Pain • Bladder distension • Arrhythmias • Hypoxemia

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

Hyperperfusion syndrome

• 1 and 3% of patients develop very dramatic increases in cerebral blood flow with middle

cerebral artery blood flow velocities more than 100% above the preoperative value

Why ?? Treat BP aggresively

Myocardial Infarction

• A major cause of morbidity 0.5 % - 4%• Symptoms and EKG changes should be

investigated promptly• Hemodynamic instability, Arrhythmia to be

treated • Maximize the balance between myocardial

oxygen supply and demand• 40 % of the perioperative mortality

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

Carry home message

• Circle of willis • Cerebral blood flow • Carotid endarterectomy • Neurological monitoring

• Thank you all