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CAROTID ENDARTERECTOMY
JYOTI D BORKAR*, ROCHANA G BAKHSHI **
*Associate Professor; **Lecturer, Department of Anaesthesiology, Seth GS Medical College and KEM Hospital, Mumbai 400012.
A carotid endarterectomy is a surgical procedure which re-tunnels the narrowed or blocked lumen (space within the blood vessel) of the carotid artery. Risk factors include smoking, high levels of blood cholesterol, diabetes mellitus, saturated animal fats and hypertension. The major causes of mortality and morbidity for carotid endarterectomy surgery are myocardial infarction, stroke, neurological deficit (transient and permanent), temporary loss of certain cranial nerve function (resulting in notable paralysis to muscles in the mouth, throat, neck and shoulders), permanent vocal cord paralysis and neck haematoma. As the surgery is performed under a general anaesthetic, patients will show usual post-operative side effects and undergo risks associated with that form of anaesthesia. We present three cases of carotid endarterectomy under general anaesthesia.
INTRODUCTION
Since the 1950s carotid endarterectomy has been performed in patients with symptomatic carotid artery stenosis, based on suggestive but inconclusive evidence for its effectiveness. Only during the last 5 years have randomized studies clarified the indications for surgery. The object of surgical correction of carotid artery stenosis is to remove the atheromatous lesion(s) and to restore the patency of the vessel to near-normal. These patients frequently have multiple problems including coronary artery disease, peripheral vascular diseases, diabetes, hypertension, or a combination of many of the above. There is no clear-cut evidence that any one anaesthetic technique is superior. While a regional anaesthetic technique may be associated with less extensive postoperative haemodynamic instability, and carry some benefit for the patient with severely compromised cardiac function, it has not been uniformly proven to be of benefit. It can be accomplished either by a superficial cervical plexus block, interscalene cervical plexus block or specific cervical plexus block of the C2-C4 nerve roots. General anaesthesia provides some advantages as well. It offers better control and the possibility of a "baseline anaesthetic" level of brain protection. We present 3 cases of carotid endarterectomy under general anaesthesia.
CASE REPORTS
A 66 year old female patient presented with history of transient ischaemic attacks since last 9 months characterized by slurring of speech, giddiness and numbness of tongue. Each of these attacks resolved within few hours. The last attack was four months back and since then patient has decreased vision in the right eye. Patient was a known case of hypertension since two years on treatment with capsule Depin 10 mg three times a day and aspirin half tablet once a day. The carotid angiography report showed 85% stenosis of right carotid artery with 60% luminal narrowing. Colour Doppler showed a calcific plaque in proximal Internal carotid artery. Patient was started on Ticlopidine 250 mg once a day and lovastatin 10 mg once a day. A right carotid endarterectomy was planned for this patient.
On the morning of surgery patient’s usual dose of antihypertensive was given with sips of water. High risk consent was taken. Cardioscope and pulse oximeter probe were attached. Blood pressure was recorded as 130/80 mm Hg and pulse rate was 86/min regular rhythm and rate. IV line was secured in the left upper limb with 16 gauge venflon.
Intra arterial cannula was placed in the right dorsalis pedis artery. CVP line was secured via right antecubital vein.
Induction agent used was Thiopentone sodium 5 mg/kg. Relaxant used was vecuronium as an infusion. Analgesia and sedation was achieved with 0.5 mg/kg pentazocine and 0.05 mg/kg midazolam. Intubation was with No. 34 flexometallic cuffed endotracheal tube. Injection xylocard 2 mg/kg was given just prior to intubation. Maintenance was with Oxygen and Nitrous oxide in the ratio of 40:60 with intermittent isoflurane and propofol infusion in the dose of 4 to 5 mg/kg. Continuous endtidal carbondioxide monitoring was done and maintained between 25 and 30 mm Hg. Blood pressure, ECG and saturation was maintained within normal limits. Continuous arterial pressure monitoring was done.
Normotension was maintained throughout the procedure. During carotid clamping the blood pressure was maintained between 140 - 150 mm Hg systolic. Patient was given injection heparin 7000 units prior to clamping. The clamp time was 45 minutes. After completion of procedure heparin was reversed with 70 mg of protamine.
The surgery lasted for 3.5 hours. Patient was reversed with injection Atropine 0.02 mg/kg and Neostigmine 0.05 mg/kg. She had good breathing attempts, was responsive to oral commands, had good tone and power and was extubated. Postoperatively patient recovered completely and was asymptomatic.
A 56 year old female patient presented with history of giddiness followed by right sided facial nerve palsy and slurring of speech. She had suffered from stroke 2 years back with complete recovery after 2 months treatment in a private hospital. She was a known case of hypertension on amlodipine 5 mg OD, aspirin half tablet OD and ticlopidine 1 tablet OD. Carotid angiography revealed 85% stenosis in the left carotid artery, right side being normal. CT scan showed lacunar infarcts in the right basal ganglion with mild cerebral cortical atrophy. 2D echocardiography revealed an ejection fraction of 65%.
A 60 year old male patient presented with repeated episodes of transient ischaemic attacks since 1 year. He was a known case of hypertension on tablet atenolol 50 mg OD and amlodipine 5 mg BD and ticlopidine 1 OD. Carotid angiography revealed 75% left carotid stenosis. 2D echocardiography revealed ejection fraction of 60%.
The anaesthetic management remained same for all patients as mentioned in case 1. The clamp time was 30 minutes and 35 minutes for case 2 and case 3, respectively.
DISCUSSION
The strong association between stroke and carotid artery occlusive disease is well known.[1] The principal cause of occlusive disease is atherosclerosis which most commonly involves the bifurcation of the common carotid artery with frequent extension into both internal and external carotid artery. Endarterectomy of the carotid bifurcation has been used to reduce symptoms and prevent stroke for nearly 40 years.[3]
Anaesthetic management goals for carotid endarterectomy include protection of heart and brain from ischaemic injury,[2] control of heart rate and blood pressure and ablation of surgical pain and stress responses. The ultimate goal is to have an awake patient at the end of surgery for the purpose of neurological examination. Most prudent approach to the ventilatory management of patients undergoing carotid endarterectomy appears to be maintenance of normocapnia. This is accomplished with reference to preoperative arterial blood gas, if this is not available, by ventilating to a PaCO2 that produces a normal pH in a patient who does not have a coexisting metabolic acidosis. Thus a balance between optimization of cerebral blood flow (CBF) and avoidance of cerebral steal is to be achieved. Cerebral blood flow is remarkably maintained constant within the range of mean arterial pressure (MAP) from 50 to 150 mm Hg. Beyond this range, the limit of vasomotor activity is exceeded and cerebral blood flow becomes directly dependent on changes in cerebral perfusion pressure (CPP).
CBF = CPP/CVR
i.e. cerebral blood flow = cerebral perfusion pressure/cerebral vascular resistance
Hypertension during the perioperative period will maintain normal cerebral blood flow in areas of healthy brain while flow will be increased in areas of brain that are hypoperfused because of vasomotor paralysis or atherosclerotic vascular narrowing.
Hypertension may produce cerebral haemorrhage and can increase oedema formation in regions of the brain that have lost the ability to autoregulate.
Patients with cerebrovascular disease have been shown to have a relative depression of the cerebral blood flow response to changes in PaCO2, that blood vessels distal to regions of atherosclerotic narrowing are operating near the limits of autoregulatory vasodilatation. Under these conditions improvement in cerebral blood flow is likely to largely depend on increases in cerebral perfusion pressure. Indeed, higher stump pressures and reversal of ischaemic EEG recordings after cross clamping have been recorded in some patients in response to induced hypertension.
Hypotension is detrimental because it can promote intravascular thrombosis and may render marginally adequate collaterals inadequate.
Hence best policy is not to use routine intraoperative elevation of blood pressure more than the patient’s normal level but careful maintenance of blood pressure within the normal preoperative range. Spontaneous increases in systolic blood pressure of upto 20% above normal at the time of cross are acceptable. In each of the above cases, blood pressure was maintained 10-15 mm Hg more than the initial systolic pressure during the clamp time.
Prophylactic barbiturates reduce the size of cerebral infarction under conditions of focal ischaemia.[2] Each of the above cases received 10 mg/kg of Thiopentone sodium just before clamping.
The internal carotid artery stump pressure represents the back pressure resulting from collateral flow through the circle of Willis via the contralateral carotid artery and the vertebrobasilar system. Although the critical stump pressure is unknown, pressures below 50 mm Hg are thought to be associated with hypo perfusion.[3]
ACKNOWLEDGEMENT
Acknowledgement to Dean and Dr. LD Naik Head Department of Anaesthesiology, Seth GS Medical College and KEM Hospital, Mumbai-400012
REFERENCES
1. Moore WS, Barnett HJM, Beebe HG, Bernstein EF, Brener BJ, Brott T, Caplan LR, Day A, Goldstone J, Hobson RW II, Kempczinski RF, Matchar DB, Mayberg MR, Nicolaides AN, Norris JW, Ricotta JJ, Robertson JT, Rutherford RB, Thomas D, Toole JF, Trout HH III, Wiebers DO. Guidelines for carotid endarterectomy: a multidisciplinary consensus statement from the Ad Hoc Committee, American Heart Association. Stroke 1995; 26 : 188-201. Review.
2.Youngberg JA, Gold MD. Carotid artery surgery: Perioperative anaesthetic considerations. In Kaplan JA(ed): Vascular Anaesthesia. New York, Churchill Livingstone, 1991, p349.
3. Edward JN, Steven MF. Anaesthesia for Vascular Surgery. In Miller RD(ed): Anaesthesia. New York, Churchill Livigstone, 2000, p1878.
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