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82 year old male patient presented with a history of faintishness and deviation of mouth to the

left associated with difficulty in speaking which was sudden in onset. On investigation the

carotid duplex revealed a 70 to 80 percent stenosis at the origin of the left internal carotid

artery as a result of an atheromatous plaque.

He underwent carotid endarterectomy(CEA) two weeks later and was admitted to the

intensive care unit postoperatively.

He was discharged from the intensive care unit on the third postoperative day with no

residual neurological symptoms and a well controlled blood pressure.

He was discharged from hospital after a period of 7 days.


Mr.X 82 years of age was admitted to the surgical proffesorial unit at the National Hospital of

Sri Lanka with a history of sudden onset of faintishness followed by difficulty in speaking

and deviation of the mouth to the left. He also complained of a transient attack of monocular

blindness(Amaurosis Fugax).He had no upper or lower limb weakness nor did he give a

history of faecal or urinary incontinence.

Following admission to the surgical ward he was treated with aspirin 150mg/nocte,

dipyridamole 100mg/bd, captopril 12.5mg/tds and simvastatin 10mg/nocte. His speech

improved within three days of commencing treatment and was investigated further to arrive

at a diagnosis.

He had been apparently well prior to this with no comorbid factors.

He had not undergone any surgeries in the past nor was he allergic to food or drugs .He had

been a farmer by occupation and a farther of three children with adequate family support.

He was a non alcoholic, non smoker but chews beetle 3 to 4 times a day.


He was averagely built with a body weight of 42.5kg and a height of 157cm.

He had a mild pallor and was afebrile.

Angle of the mouth was deviated to the left but there was no dribbling.

He was not dyspnoeic and his effort tolerance was good.

There was no pedal oedema.

Carotid bruit could be heard on auscultation over the left carotid.


Both first and second heart sounds could be heard along with a systolic murmur well

appreciated at the apex.

BP was 170/80 on both arms. Pulse rate was 62/minute, with a good volume and was regular.


He had a respiratory rate of 14/ breaths per minute and on auscultation there was vesicular

breathing and air entry was bilaterally equal.

There were no crepitations nor rhonchi


Mouth was deviated to the left. There was no dribbling of saliva from the angle of the mouth.

He was able to close his eyes tight. His power and reflexes were normal in both upper and

lower limbs. There was no gait disturbance.


His mouth opening was satisfactory. There was no limitation of neck movements and the

thyromental distance was more than 6cm. Mallampati was Class 2. He had no dentures,

crowns or caps nor loose teeth.

The following Investigations were done.

Haemoglobin = 9.3gm/dl

PCV = 27.4

WBC = 9,500

Neutrophils 75%, Lymphocytes 10%, Eosinophils 1%

Prothrombin Time = 10.5 seconds

INR = 0.91

Serum Na+ = 136 Meq/l

Serum K + = 5.6 Meq/l

Blood Urea = 6.2 mmol/l

Blood Sugar = 4.3 mmol/l

Serum Creatinine = 134 Meq/l

2D ECHO : Concentric LVH

Ejection Fraction 60%

Diastolic Dysfunction

Carotid Duplex : 70- 80% stenosis of the left Internal carotid artery at it’s origin due to an

atheromatous plaque. Bilateral common carotid, external carotid and right internal carotid

appears normal.

12 lead ECG : Sinus rhythm with no evidence of ischaemia. There was evidence of left

ventricular hypertrophy.

Telechest : Revealed mild cardiomegaly.

Following the diagnosis a left sided carotid endarterectomy was planned two weeks later. An

intensive care unit (ICU) bed was reserved for postoperative care.

On the day prior to surgery he was kept fasting for liquids and solids for 6 hours and was

instructed to continue his oral antihypertensives including the morning dose with a sip of

water. He had been advised to discontinue dipyridamole for 10 days prior to surgery and

aspirin was continued. He was prescribed oral diazepam 10mg at night day prior to surgery

and 5 mg on the morning of surgery. Three units of blood was reserved for him.


On the day of surgery the anaesthetic machine, suction apparatus, breathing circuits and

equipment necessary for maintenance of airway and intubation was checked and the

following drugs were prepared according to the patient’s body weight.

Thiopental Sodium 250mg

Morphine 7mg

Atracurium 25mg for intubation and 10mg boluses for maintenance

Atropine 0.2mg/ml along with ephidrine 6mg/ml solutions were also prepared in noted

concentrations .

Prior to induction the baseline values of vital parameters was obtained.

Non invasive blood pressure 170/100 mmHg (Rt.upper arm)

Pulse rate 68 beats per minute

ECG showed sinus rhythm

O2 saturation on air 99% and with O2 it was 100%

18G cannula was inserted under aseptic conditions to the right upper forearm after explaining

to the patient the procedure. One pint of warm 0.9% normal saline was commenced .

He was pre-oxygenated with 100% O2 with a well fitting face mask for 3 minutes via the

circle circuit.

7mg of intravenous morphine followed by 250mg of thiopentone was given. Once the ability

to ventilate was verified 25mg of atracurium was given. He was initially ventilated with 2L

of O2, 4L of N2O and 2% halothane. 3 minutes later he was intubated with a size 8mm

reinforced endotracheal tube. Air entry was checked, tube cuffed until the air leak

disappeared and the lip level was noted. Tube placement was confirmed by auscultation and

by capnography. Tube was well secured.

An arterial line was inserted into the right forearm under strict sterile aseptic conditions and

connected to a pressure transducer for continuous invasive blood pressure monitoring.

He was placed supine with a slight head up tilt and turned to the right. Both arms were tucked

to the patients side.

He was connected to the ventilator which was set to deliver a tidal volume of 400ml, a

respiratory rate of 10 breaths per minute ( which was adjusted according to the end tidal

CO2) and an inspiratory to expiratory ratio of 1:2. Airway pressure was 18cm of water.

He was maintained on 1L O2, 2L N2O and 0.6% halothane which was adjusted according to

the blood pressure. Intravenous co-amoxyclavulinic acid 1.2gm was given before the

commencement of surgery.

Non invasive and invasive blood pressure, pulse rate, body temperature, O2 saturation, end

tidal CO2, airway pressure and lead two on ECG for rhythm disturbances and ST segment

changes were monitored every 10 minutes.

Boluses of atracurium were repeated every 20 to 30 minutes.

Warm intravenous fluids were transfused at 65ml per hour as maintenance and a deficit of

650ml was replaced with 0.9% saline.

4000 IU of intravenous heparin was given slowly before cross clamping to reduce the risk of

thromboembolic complications.

The fluctuations in blood pressure, hypertension following clamping and hypotension with

unclamping was noted and treated with increasing the volatile agent concentration and

increasing the infusion rate of fluids respectively. Since hypotension responded well to

intravenous fluids ephedrine was not used.

The atheromatous plaque was removed from the internal carotid artery. The internal carotid

artery was clamped, opened and the plaque stripped off and a carotid shunt was placed and

the artery closed.

Estimated blood loss was 300ml.

At the end of a four and a half hour surgery the inhalational agents were turned off and with

the commencement of spontaneous breathing 1.2mg of atropine with 2.5mg of neostigmine

was administered. Once the tidal volume was adequate he was extubated in the lateral

position after suctioning of the pharynx.

He was admitted to the recovery unit following surgery for observation.

2 to 3 hours later his Blood pressure kept increasing and an infusion of glyceryl trinitrate was

started and titrated accordingly. Blood pressure was aggressively controlled to near

preoperative levels. 6 hours later oral antihypertensives were commenced.

24 hours following surgery his blood pressure was within normal limits. He was discharged 3

days later from the intensive care unit with no residual neurological sequele nor cardiac


On the 7th postoperative day he was discharged from the surgical ward with clear instructions

to return for clinic follow up.


Carotid endarterectomy (CEA) is an operation to reduce the incidence of embolic stroke in

symptomatic (transient ischaemic attack/ cerebrovascular accident) patients with a 70% or

greater carotid stenosis due to atheromatous disease at the carotid bifurcation.

This patient presented with a 70 to 80% stenosis as a result of which he developed a transient

ischaemic attack.

There is substantial evidence to support early operation in symptomatic patients ideally

within two weeks of the last neurological symptoms. And this patient was one such candidate

who was scheduled for surgery within two weeks of presentation which resulted in an

excellent outcome.

Carotid endarterectomy has a combined mortality and major stroke incidence of 2-5%.

Patients who present for surgery are usually elderly such as this patient and are arteriopaths.

This patient had no postoperative residual neurological sequele except for the deviation of the

mouth to the left which was present prior to surgery.

The principal cause of occlusive disease is atherosclerosis which commonly involves the

bifurcation of the common carotid artery with frequent extension into both internal and

external carotid arteries. Cerebrovascular sequele is a result of either embolization of

thrombus and or atheromatous debris or hypoperfusion secondary to stenosis. Though this

patient had no other comorbid factors he obviously had age related atherosclerosis as was

evident from the carotid duplex.

The American Academy of Neurology considers 2 groups of patients for CEA.

They are:

*The symptomatic patients who have active plaques giving rise to emboli that enter the

cerebral circulation and causes TIA like in our patient

*The asymptomatic group who have demonstrable disease at the carotid bifurcation but no

history of recent neurological event


The perioperative stroke rate for CEA is between 3-5%. The incidence is heighest for patients

diagnosed with stroke and lower for patients with TIA’s and lowest in the asymptomatic

group which was evident in this patient. Neurological deficits occur mostly in the poorly

controlled perioperative hypertensives and in those with postoperative

hypertension/hypotension. This patient was diagnosed to have high blood pressure only at the

time of admission, which was treated aggressively thus preventing him from developing

further neurological deficits. More than half these deficits occur more than 4 hours

postoperatively. Myocardial infarction is the leading cause of both perioperative and late

mortality following CEA.

Coronory artery disease (CAD) is common in patients for CEA and is a leading cause of both

early and late mortality. However this patient had no evidence suggestive of CAD. The

second major perioperative complication of CEA is cerebrovascular accident.


Anaesthetic management goals for CEA include

*Protection of the heart and brain from ischaemic injury

*Control of heart rate and blood pressure

*Ablation of surgical pain and stress response

It is equally important to have an awake patient at the end of surgery for the purpose of

neurological examination, and the same was demonstrated in this patient who responded to

command and moved all four limbs prior to transfer to the recovery unit.


In the preoperative visit the patient was instructed to continue all the medication until the

morning of surgery. Current recommendations are that all patients with carotid artery disease

should be on aspirin 75-325mg on a regular basis. Aspirin should be continued through the

perioperative period. The patient was on Aspirin 150mg daily along with dipyridamole

100mg twice daily. Discontinuation of aspirin therapy may be related to an increased rate of

MI and transient ischaemic events in patients undergoing CEA.

Patient reassurance is particularly important in this population as anxiety is associated with

increased heart rate, systemic vascular resistance and myocardial oxygen consumption which

could precipitate significant cardiac morbidity.

Therefore the patient was prescribed an oral benzodiazepine the day prior to surgery in the

night, as well as in the morning two hours prior to surgery.


CEA may be performed under general anaesthesia which was the method employed in our

patient or it could be the “awake carotid” where the cervical dermatomes C2-C4 is blocked

by deep and or superficial cervical plexus block. Regional anaesthesia allows continuous

neurological assessment of the awake patient which is the most sensitive method for

detecting inadequate cerebral perfusion and function . Since this patient underwent general

anaesthesia intraoperative neurological assessment was not possible.

Carotid shunt is essentially a length of plastic tubing to carry the blood from the common

carotid artery to the internal carotid artery thereby maintaining the blood flow during the

course of surgery. Some surgeons routinely insert shunts in all patients.

Acute complications of shunt insertion include air or plaque embolization, intimal tears,

carotid dissection, haematoma , nerve injury, infection and late carotid re-stenosis.

While the use of local anaesthetics has the merit that it allows direct neurological monitoring

of the conscious patient general anaesthesia also has laudable qualities. Patients can find CEA

under regional anaesthesia stressful and a patient who was 82 years of age would have found

it extremely difficult to lie still under the drapes and it would have being an unpleasant


Access to the airway during surgery can be difficult with the head turned to one side.

Therefore airway control offered by endotracheal intubation was what was preferred.


When the carotid is cross clamped the ability to identify inadequate cerebral circulation in the

ipsilateral hemisphere is critical. In the awake patient the anaesthetist shoud remain in

constant verbal contact with the patient during and after cross clamping.

When the patient is under general anaesthesia the decision as to whether or not to perform

shunting is more difficult. Therefore a number of neurological monitoring techniques are

made available to assist with the decision. However intraoperative monitoring for cerebral

ischaemia and or hypoperfusion could not be done for this patient as there were no facilities

for such procedures.


In the management of cerebral ischaemia, the primary intervention is insertion of a shunt. It

is appropriate to maintain the mean arterial pressure 20% above the preoperative level to

maintain the perfusion pressure across the circle of willis, which was done in our patient .

Both induced hypocarbia and hypercarbia augments ipsilateral cerebral blood flow.

Hypocarbia may cause ipsilateral vasoconstriction and extend the area of cerebral ischaemia.

Hypercarbia may produce contralateral vasodilatation and cause a steal phenomenon.

Normocarbia is the best policy. The capnograph was used to assist in monitoring the end tidal

CO2 levels and the intraoperative blood gas analysis revealed normocarbia.


During carotid clamping and immediately afterwards in the recovery patients are often

haemodynamiclly labile. Bradycardia can develop during surgical manipulation of the carotid

sinus because of direct stimulation of the vagus nerve. Tachycardia may be due to stress or

pain or as a result of direct manipulation of the carotid sinus with the release of

catecholamines into the circulation. Many patients have hypertension as a co-morbid

condition which is further exacerbated during surgery. Carotid cross clamping is frequently

associated with marked increase in arterial pressure and which was evident in this patient

who exhibited high blood pressure during the application of the second clamp and this rise in

blood pressure, was treated with deepening of the level of anaesthesia by increasing the

volatile agent concentration. Hypertension is a result of surgical stress, manipulation of the

carotid body and sympathetic stimulation. However his heart rate was stable throughout


Hypotension is observed because of the direct vasodilating and negative inotropic effects of

anaesthetic agents. Hypotension following carotid unclamping could be due to a cerebral

protective process and this was appreciated in this patient during the procedure.

Cerebral autoregulation protects the brain from reperfusion by reducing cerebral production

of renin, vasopressin and norepinephrine which results in hypotension.

Because of the nature of the problems and wide swings in blood pressure and heart rate many

anaesthesiologists place a triconnector (“crows foot”) in the IV line at the site of entry of the

indwelling venous cannula so that a vasoconstrictor and a vasodilator along with

maintenance fluid can be manipulated immediately should any haemodynamic changes

require treatment. Since vasodilators or vasoconstrictors were used in the intraoperative

period a triconnector was not used.


The use of intravenous heparin is to reduce the risk of thromboembolic complications. A

fixed dose of heparin may be given as 5000 units or dosing may be on weight based. This

patient recieved 4000 units of IV heparin.


Both postoperative hypertension and hypotension are common after CEA. Hypertension is

seen in 25-58% of patients after endarterectomy and hypotension in 8-10% as suggested by

O’Conner and Tuman.

Patients with poorly controlled preoperative hypertension often have severe hypertension


Surgical denervation of the carotid sinus baroreceptors is contributory. . Blood Pressure

should be aggressively controlled near preoperative values after surgery. Short acting drugs

are the safest and most effective. This patient had to be started on glyceryl trinitrate

postoperatively as his blood pressure was high at the intensive care unit and he responded to

treatment well.


Since 1-3% of patients develop very dramatic increase in cerebral blood flow with middle

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

the patient was monitored continuously at the ICU for symptoms suggestive of

hyperperfusion syndrome such as ipsilateral headache, hypertension, seizures and focal

neurological deficits. If not treated properly it can result in cerebral oedema, intracerebral

(most occur 1-5 days after surgery) or subarachnoid haemorrhage and death.

CEA may also be associated with cranial nerve injury ( recurrent laryngeal nerve, superior

laryngeal, hypoglossal, marginal mandibular nerve), bleeding , airway swelling and oedema.

Many if not all these injuries can be attributed to surgical traction. The operation is performed

on an artery embedded among vascular tissues and postoperative bleeding leading to neck

haematoma (occurs in 5-10%), airway compression and respiratory compromise are possible.

Fortunately this patient did not develop such complications. Hence the importance of patient

monitoring in the immediate postoperative period in the HDU or in an ICU.


Carotid endarterectomy is a valuable operation which has a firm evidence base and can

reduce the incidence of stroke in vulnerable patients.

It remains unclear if general or local anaesthesia offer particular benefits in this setting.

All patients should be monitored in an intensive care setting for the first 16-24 hours after

CEA because most events requiring intervention occur within this time frame.

CEA is a prophylactic operation which only yields benefits if the risks of surgery are less

than the risks of medical management.


*S J Howell, Carotid endarterectomy, British Journal of Anaesthesia 2007; 1: 119-31

*Edward j Norris, Steven M Frank, Anaesthesia for vascular surgery, Anaesthesia 5th edition

volume 2- Ronald D Miller, 51: 1878-1883

*G Edward Morgan, Maged S Mikkhail, Michael J Murray, Neurophysiology & Anaesthesia,

Clinical Anaesthesiology 4th edition 25: 626-629

*Mark Stoneham, Carotid endarterectomy , Vascular surgery, Oxford Handbook of

Anaesthesia 2nd edition, 17:434-436