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CONSULTANT ANAESTHETIST
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
He underwent carotid endarterectomy(CEA) two weeks later and was admitted to the
He was discharged from the intensive care unit on the third postoperative day with no
HISTORY
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
6.1
Following admission to the surgical ward he was treated with aspirin 150mg/nocte,
improved within three days of commencing treatment and was investigated further to arrive
at a diagnosis.
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.
EXAMINATION
He was averagely built with a body weight of 42.5kg and a height of 157cm.
Angle of the mouth was deviated to the left but there was no dribbling.
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CARDIOVASCULAR SYSTEM
Both first and second heart sounds could be heard along with a systolic murmur well
BP was 170/80 on both arms. Pulse rate was 62/minute, with a good volume and was regular.
RESPIRATORY SYSTEM
He had a respiratory rate of 14/ breaths per minute and on auscultation there was vesicular
CNS EXAMINATION
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
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AIRWAY ASSESMENT
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,
Haemoglobin = 9.3gm/dl
PCV = 27.4
WBC = 9,500
INR = 0.91
Diastolic Dysfunction
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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.
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.
PERIOPERATIVE MANAGEMENT
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
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Thiopental Sodium 250mg
Morphine 7mg
Atropine 0.2mg/ml along with ephidrine 6mg/ml solutions were also prepared in noted
concentrations .
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
An arterial line was inserted into the right forearm under strict sterile aseptic conditions and
6.6
He was placed supine with a slight head up tilt and turned to the right. Both arms were tucked
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
Warm intravenous fluids were transfused at 65ml per hour as maintenance and a deficit of
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
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
6.7
Estimated blood loss was 300ml.
At the end of a four and a half hour surgery the inhalational agents were turned off and with
was administered. Once the tidal volume was adequate he was extubated in the lateral
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
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
complications.
On the 7th postoperative day he was discharged from the surgical ward with clear instructions
DISCUSSION
6.8
This patient presented with a 70 to 80% stenosis as a result of which he developed a transient
ischaemic attack.
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
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
patient had no other comorbid factors he obviously had age related atherosclerosis as was
6.9
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
*The asymptomatic group who have demonstrable disease at the carotid bifurcation but no
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
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
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
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GOALS OF MANAGEMENT
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
increased heart rate, systemic vascular resistance and myocardial oxygen consumption which
6.11
Therefore the patient was prescribed an oral benzodiazepine the day prior to surgery in the
INTRAOPERATIVE MANAGEMENT
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
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
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
experience.
6.12
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.
NEUROLOGICAL MONITORING
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
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
CEREBRAL PROTECTION
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.
6.13
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.
HAEMODYNAMIC INSTABILITY
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
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
carotid body and sympathetic stimulation. However his heart rate was stable throughout
surgery.
Hypotension is observed because of the direct vasodilating and negative inotropic effects of
protective process and this was appreciated in this patient during the procedure.
6.14
Cerebral autoregulation protects the brain from reperfusion by reducing cerebral production
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
fixed dose of heparin may be given as 5000 units or dosing may be on weight based. This
Both postoperative hypertension and hypotension are common after CEA. Hypertension is
6.15
Patients with poorly controlled preoperative hypertension often have severe hypertension
postoperatively.
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.
POST-OPERATIVE COMPLICATIONS
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
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.
6.16
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
CONCLUSION
Carotid endarterectomy is a valuable operation which has a firm evidence base and can
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
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REFERENCES:
*Edward j Norris, Steven M Frank, Anaesthesia for vascular surgery, Anaesthesia 5th edition
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