ANAESTHESIA FOR CAROTID ARTERY SURGERY

British Journal of Anaesthesia 1993; 7 1 : 569-579

ANAESTHESIA FOR CAROTID ARTERY SURGERY M. A. GARRIOCH AND W. FITCH

THE OPERATION

The first operation for carotid occlusive disease was carried out by Eastcott, Pickering and Robb at St Mary's Hospital, London in 1954 [28]. Since then, carotid endarterectomy has become relatively frequently performed in the U.K. [56] and is one of the commonest vascular procedures in the U.S.A. where it is performed between 19 and 27 times more

frequently in that country than in the U.K. [10, 70]. The differences in practice on either side of the Atlantic probably derive from differences in the referral mechanism: most British surgeons receive patients from neurologists, who are more likely to evaluate medical therapy first, whereas direct referral from a general practitioner to a vascular surgeon is commoner in the U.S.A. American surgeons are also more likely than their British counterparts to operate for asymptomatic bruit or frank stroke. As with every operation, it is important to take all risks to the patient into account and weigh them against the advantages of a successful procedure. If the operation is to be undertaken, the ultimate goal of surgery and anaesthesia is maintenance or improvement of oxygen delivery to potentially ischaemic brain tissue. Currently, no surgical technique prevents the transient occlusion of the blood flow to the brain. During unilateral carotid occlusion, the delivery of oxygen to the compromised hemisphere can be maintained only by collateralflowvia the Circle of Willis or the vertebral arteries. Minimal amounts of flow also arise from meningeal arterial branches that originate from the external carotid and the ophthalmic artery. Studies in primates suggest that unilateral carotid occlusion decreases perfusion pressure in the ipsilateral middle cerebral artery by only 14% [83]. However, this does not provide comfort for the anaesthetist during carotid endarterectomy, as the circulation under consideration is often that of an elderly atherosclerotic patient in whom collateral flow is poor. Cerebral autoregulation is the ability of the brain to maintain constant cerebral blood flow over a wide range of perfusion pressures. With intact autoregulation, total cerebral blood flow approaches 50 ml min~yi00 g of brain. Critical blood flow, less than that at which damage occurs to cerebral tissue, has been shown to be 18-24 ml min~V100 g. Over a range of mean arterial pressure of 60-180 mm Hg, flow greater than this critical value provides the oxygen necessary for adequate cerebral metabolism— 3 ml min~7100 g of brain. The surgical technique associated with carotid

MAGNUS A. GARRIOCH*, M.B., CH.B., F.R.C.A., Division of Anaes-

thesia, Glasgow Royal Infirmary, Glasgow G31 2ER. WILLIAM

(Br. J. Anaesth. 1993; 71: 569-579) KEY WORDS Surgery: carotid endarterectomy.

FITCH, B.SC, M.B., CH.B., PH.D., F.R.C.A., F.R.C.P. (GLAS.).,

University Department of Anaesthesia, Glasgow Royal Infirmary, 8-16 Alexandra Parade, Glasgow G31 2ER. *Present address: Department of Anaesthesia, Royal Infirmary, Edinburgh EH3 9YW. Correspondence to W.F.

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Transient ischaemic attack, reversible ischaemic neurological deficit and progressive or complete stroke are leading causes of morbidity and mortality in the Western World. In the United Kingdom, stroke accounts for an annual mortality of 10 deaths per 100000 of population at age 40 yr, increasing to 1000 deaths per 100000 at age 75 yr. Transient ischaemic attacks are estimated to affect, on average, 0.5 per 1000 of the general population at any age, becoming more common in the elderly. Commonly, these focal ischaemic events are the result of artery-to-artery embolization of aggregates of platelets and fibrin, or of cholesterol and atheromatous debris. Stenotic arterial lesions and ulcerated atheromatous plaques, at sites of predilection for atherosclerotic lesions in the cervico-cranial arteries, are the commonest sources of such emboli. Other causes of cerebral ischaemia include emboli from the heart and lacunar infarcts in the brain [8]. The endothelial surfaces of the heart which may be damaged include congenital bicuspid aortic valves and surgically-placed prosthetic valves. Mural thrombus, endocarditic vegetations or atrial myxoma may produce similar effects. Atrial fibrillation associated with any of the former greatly increases the frequency of cerebrovascular events. Lacunar infarcts occurring within the brain are solely attributable to atherosclerotic, hypertensive and vascular disease [32]. Stenosis of the internal carotid artery is one of the primary sources of cerebral emboli [9, 37] and removal of the atheromatous plaque without leaving loose arterial intima distally is the aim of surgical reconstruction of the artery. The end result of surgery should be a smooth arterial wall and blood-tight closure [76], thereby preventing future embolic phenomena.

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incentive spirometry and techniques to aid expectoration of secretions. Appropriate use of bronchodilators and antibiotics and the cessation of smoking also help to improve postoperative recovery. Diabetes Diabetic patients have a high incidence of vascular disease. Preoperative assessment should establish the diabetic type and current medical treatment (diet alone, oral hypoglycaemic agents or insulin). Diabetic control should be evaluated and, where necessary, stabilized—as should the complications of chronic diabetes such as peripheral neuropathy, renal insufficiency or cardiomyopathy. Diabetic patients may require the use of glucose-containing solutions for intraoperative management of bloodsugar concentration, although these solutions should be avoided in other patients, for reasons explained later.

Patients presenting for carotid artery surgery are frequently elderly and may be expected to have coexisting medical problems common to patients with vascular disease: chronic obstructive airway disease and diabetes. An increase in systemic arterial pressure is found in up to 70 % of patients presenting for carotid endarterectomy and is the major risk factor in stroke [27], even if the hypertension is minimal or only systolic in nature [42]. The pathophysiology of hypertension also leads to an impairment of cerebral autoregulation [80] and a decrease in regional cerebral blood flow [68]. Not surprisingly, it has been shown that control of hypertension in the preoperative period reduces the incidence of postoperative hypertension and neurological deficit [6]. In addition to hypertension, the presence of cardiac disease should be suspected and sought. Silent cardiac disease, complicated by transient ischaemic attacks, has an annual mortality rate of 5 % which nearly equals the mortality from asymptomatic three-vessel coronary artery disease (6%) [1]. Myocardial infarction is a major complication of carotid endarterectomy and is the most frequent cause of perioperative mortality [13, 24, 40]. Other medical problems frequently complicate the management of carotid endarterectomy.

Other factors Preoperative evaluation should be thorough, with particular emphasis on the nature, frequency and date of onset of the patient's symptoms, if any, of carotid arterial insufficiency. A drug history and general review of systems should be undertaken. Particular attention should be devoted to the measurement of systemic arterial pressure. Values should be obtained in both arms, and with the patient supine and standing. A cardiac history and extensive cardiac evaluation should be undertaken whether or not the patient is symptomatic. ECG and chest x-ray are mandatory. An exercise ECG is of additional value. If general anaesthesia is being considered, positioning of the patient's head is an important consideration. Many patients have cervical spondylosis, vertebro-basilar insufficiency, or both, and inappropriate operative positioning may exacerbate or cause neurological damage. Preoperative neurological examination of the patient facilitates early recognition of postoperative central nervous system dysfunction which may necessitate prompt pharmacological or surgical intervention. In summary, adequate control of arterial pressure and an optimal general medical status should be obtained as far as possible before elective carotid surgery. In most instances, the patient's routine medication should be continued on the morning of surgery. This applies especially to beta-adrenoceptor blockers, calcium antagonists and centrally acting antihypertensive drugs, as these agents are associated with rebound hypertension if stopped abruptly.

Smoking Many patients who present for carotid endarterectomy are, or were, smokers. They may be expected to have some degree of airway obstruction and suffer from postoperative ventilatory difficulty because of reactive airways, excess secretions and lung closing volumes which exceed tidal volumes—thus leading to atelectasis and secondary ventilation/perfusion mismatch. Correct preoperative preparation of such patients is important and the physiotherapist can help by teaching breathing exercises, the use of

Premedication Good rapport should be established with the patient in the preoperative period when possible. An adequate and sensitive preoperative interview including an open, non-technical explanation of the perioperative events should help to alleviate preoperative anxiety. This is important, as anxiety in this patient population exacerbates the potential hazards of surgery such as perioperative hypertension, myocardial ischaemia, cardiac arrhythmia and potentially fatal myocardial infarction. In the

ANAESTHETIC CONSIDERATIONS

Preoperative Assessment

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endarterectomy has improved steadily. Most surgeons make a skin incision anterior to the sternocleidomastoid muscle. The carotid artery is dissected carefully, with as little manipulation as possible, and systemic heparin is given by the anaesthetist. The vessel is then occluded above and below the lesion, with careful protection of the vagus and hypoglossal nerves. A longitudinal arteriotomy is made extending above and below the plaque, which is then dissected away from the intima or adventia. The use of systemic heparin, a heparinimpregnated shunt, or both, provides the surgeon with adequate time for endarterectomy. The use of a shunt is controversial, as good results have been reported both with [84] and without its use [62]. Those favouring a shunt argue that it maintains blood flow to an already compromised cerebrovascular bed. The procedure does, however, add to operative time and complexity, may not be performed easily, and carries a risk of inducing embolization. The shunt may lead to further intimal damage to the vessel wall and may obstruct surgical access.

ANAESTHESIA FOR CAROTID ARTERY SURGERY opinion of the authors, light premedication with benzodiazepines is also justified to ameliorate anxiety and consequent tachycardia and hypertension. A delicate balance must be maintained, however, as oversedation may depress the neurological status of the patient leading to hypotension, hypercapnia, or both, with consequent detrimental effects on the cerebral circulation [18, 31]. Intraoperative Management

In the unconscious patient, other less reliable methods of assessing cerebral perfusion must alert the anaesthetist and surgical team to impending neurological deficit. No single technique is perfect, but those available include the electro-encephalograph (EEG) [5], evoked potential monitoring [43], measurement of regional cerebral blood flow by intra-arterial injection of xenon-133 and subsequent scintillation counting over the brain [73], measurement of distal carotid stump pressure to assess adequacy of cross-over flow from the contralateral carotid artery [47], and those tests which may also be used in preoperative carotid evaluation, namely, oculoplethysmography [63], angiography [57,69] and Doppler ultrasound [92].

The variable measured most commonly is the perfusion pressure as reflected by the stump, or carotid occlusion, pressure [82]. Stump pressure is that pressure measured distal to the surgically occluded carotid artery and is thought to equal the collateral perfusion pressure via the Circle of Willis. Critical stump pressure (the minimum required to avoid inadequate collateral flow) is considered to be in the range 50-60 mm Hg. At values smaller than this, most surgeons who make this measurement consider a bypass shunt necessary to maintain perfusion. EEG changes indicative of ischaemia lasting 10 min or more have been shown to correlate with new postoperative cerebral ischaemic changes [65]. Problems with the EEG primarily involve interpretation, as most anaesthetists are not skilled in this technique. Also, by the time that an EEG trace shows an abnormality, it may no longer be possible to correct the neurological deficit by restoration of cerebral perfusion. The monitoring of somatosensory evoked potentials (SSEP) has been shown to be as sensitive and specific as the EEG in detecting cerebral ischaemia during carotid endarterectomy; a decrease in SSEP amplitude (greater than 50 %) may be a better indicator of ischaemia than an increase in latency [66]. Delayed detection of neurological damage is obviously a major drawback of general anaesthesia. Cerebral Protection

Any anaesthetic technique should attempt to protect the brain from hypoxic damage. This may be achieved under general anaesthesia by decreasing the cerebral metabolic rate for oxygen. The administration of a barbiturate is still the only proven mechanism allowing this to occur in humans by depression of metabolism in actively metabolizing brain [48]. Thiopentone has the effect of reducing intracranial pressure [46], which may be of benefit in carotid endarterectomy. Other cerebroprotective advantages of barbiturates include inhibition of oxygen free radical formation [78], reduction of cerebral oedema [77] and a more recently discovered sodium channel blocking action [34]. Barbiturates do not, however, provide protection from global ischaemia—as recent evidence from post cardiac arrest victims shows. When ischaemia is present, barbiturates do not aid resuscitation [17]. Of the other induction agents, ketamine should be avoided as it increases both flow and CMRo2. Etomidate reduces CMRo2 and may be cerebroprotective but, unfortunately, acts as a cerebral vasoconstrictor before suppressing CMRo2 [89]; it also suppresses the adrenocortical axis. Midazolam reduces CMRo2 and has demonstrated cerebroprotective qualities in animals [11]. As it has relatively mild haemodynamic effects if used correctly, it may well have a place, in conjunction with barbiturates, as a useful induction agent. Propofol still remains to be fully evaluated in this setting, but early laboratory evidence is not encouraging [90]. Recent work evaluating the effect of propofol infusions on cerebral circulation and autoregulation in anaesthetized baboons showed that a dosedependent decrease in cerebral blood flow occurred.

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Myocardial and cerebral ischaemia must be prevented. While most cerebral morbidity is thought to be caused by emboli either resulting from the disease itself or associated with the surgical intervention, the anaesthetist can greatly influence the overall success of the procedure. Optimizing cerebral perfusion, manipulating cardiovascular physiology and monitoring the patient appropriately to allow early intervention to prevent potential neurological or cardiovascular mishaps are vital functions performed by the anaesthetist. Adequate monitoring is of crucial importance. Continuous ECG is mandatory, with the ability to record from limb and precordial leads an advantage. An indwelling arterial catheter should be used for direct monitoring of systemic arterial pressure and collection of blood for measurement of arterial blood-gas tensions and other laboratory tests. The pulse oximeter provides not only a continuous estimate of blood oxygen saturation, but also the detection of a peripheral pulse. Temperature monitoring is a useful aid to maintenance of cardiovascular stability and also to estimation of appropriate timing of awakening and antagonism of neuromuscular block. As large blood losses or fluid loads are not usually associated with the procedure, central venous or pulmonary artery catheterization is unnecessary unless the cardiovascular system is unstable (recent myocardial infarction [66]) or there is a history of congestive heart failure or poor left ventricular function (ejection fraction less than 0.5) [49]. Several monitoring techniques to assess the adequacy of cerebral perfusion have been used during anaesthesia. However, neurological well-being can only be demonstrated fully if the entire procedure is conducted using a regional anaesthetic technique. This allows continuous monitoring of cerebral function by observation of, and verbal communication with, an awake patient.

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leak is induced, albeit to a much lesser degree [54]. The attainment of hypothermia is also difficult without the facility of cardiopulmonary by-pass and adds significantly to the duration of anaesthesia. Thus, on balance, deep hypothermia is of little benefit. In contrast, mild hypothermia (temperature about 35 °C) may be achieved easily and may decrease cerebral metabolism sufficiently (in this particular context) with no obvious disadvantages. Hyperglycaemia worsens ischaemic brain damage and should be avoided [64]. Laboratory evidence suggests that even mild increases in blood-sugar concentration worsen the prognosis for the ischaemic brain [44]; thus maintenance of normoglycaemia during surgery is important. The use of glucosecontaining fluids during operation should be considered with this in mind. Obviously, the diabetic patient represents a class of subject in whom meticulous blood-glucose control is mandatory and the use of glucose-containing solutions may be necessary. Choice of Technique

It is the aim of the anaesthetist to maintain normocapnia, normotension or slight hypertension, mild anticoagulation and normovolaemia by careful choice of drugs and fluids. Regional anaesthesia

Several authors have reported low morbidity and mortality associated with the use of regional anaesthesia for carotid endarterectomy [15, 19, 22, 36, 81]. Two different methods may be used: combined deep and superficial cervical block or cervical extradural anaesthesia. Both of these techniques are unfamiliar to most anaesthetists, leading to a natural reluctance to perform either. Identification of the second, third and, occasionally, fourth cervical roots is needed to perform deep cervical block. In addition, superficial block is necessary because of communication between the trigeminal nerve and the lower cervical plexus. Unfortunately, even in experienced hands, the block is associated with a high failure rate (20%) [12]. In addition, discomfort may still be felt by the patient because of difficulty in anaesthetizing the carotid sheath—leading to a requirement for additional infiltration during the operation. An alternative regional technique is that of cervical extradural block. Originally performed by Dogliotti [25] in 1933 for thoracic surgery, this block has been used most frequently for chronic head or neck pain associated with Pancoast syndrome. Bonnet and colleagues [15] reported a series of 394 consecutive patients (undergoing carotid artery surgery) operated on under cervical extradural block with apparently good results. Patients in the sitting position had an 18-gauge Tuohy needle placed by the midline approach into the C6-7 or C7-T1 interspace and the extradural space identified by the hanging drop method. Bupivacaine (0.37-0.4%) 15 ml (and in most patients fentanyl 50—100 ug also) was administered into the extradural space, after negative aspiration for blood and a lignocaine test dose. The majority of patients needed supplementary sedation during the procedure but a large proportion (46%) found the technique satisfactory. Complications in

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This may be of advantage in carotid artery surgery; however, the effect on cerebral metabolism was more equivocal and the authors suggested that further studies are needed to evaluate the influence of propofol on the coupling between metabolism and blood flow [87]. The rapid awakening associated with propofol anaesthesia is also an attractive feature of the drug, but further information is needed before the use of propofol can be endorsed. In addition to the above "anaesthetic" drugs, several other drugs are currently being evaluated for use as cerebroprotective agents. Nimodipine, a calcium channel blocker, has been shown to be efficacious in this regard. It has been of proven benefit in the treatment of vascular spasm after subarachnoid haemorrhage [4]. Interestingly, it is not clear if this agent acts by an effect on the vascular smooth muscle or if its primary mechanism of action is directly on the neurone. Whether prophylactic use of nimodipine is warranted in patients undergoing carotid endarterectomy has still to be investigated and it is likely that evidence will derive from neurosurgical observations. Other drugs potentially offering pharmacological brain protection act via a variety of means and still remain experimental. Antagonists of excitatory neurotransmitters (e.g. dizocilipine maleate) are cerebroprotective in lower mammals (e.g. rats, mice), but their effect is insufficient to allow the more complex areas of primate brain, exquisitely dependent on adequate oxygenation, to be protected. Dizocilipine maleate may, however, have a place in regional incomplete ischaemia such as may occur in carotid endarterectomy, although much work remains to be done before this agent can be recommended clinically [51]. Free radical scavenging may provide a means of defence against ischaemic brain damage. Methylprednisolone has recently been suggested to improve outcome in spinal cord injury if given within 8 h of the injury [16]. Whether this drug has a place in cerebral protection has yet to be demonstrated. Proven laboratory evidence shows the free radical scavenger U74006F, a 21-amino steroid, to have marked cerebroprotective properties in dogs, but only if given before the period of ischaemia [51]. As yet, no clinical use of this product has been permitted, but it is interesting to speculate about its future place in cerebroprotection. Non-pharmacological means of cerebroprotection worthy of discussion include hypothermia and control of blood-glucose concentration. Hypothermia (to temperatures less than 32 °C) has found a place in the management of cardiopulmonary bypass by reducing cerebral metabolic rate and thus increasing the tolerance of the brain to ischaemia. This mechanism differs from barbiturate-induced reduction of CMRo2 as the effect of decreased metabolism is global, barbiturates affecting primarily the metabolic rate of the actively working brain. Why, therefore, is hypothermia not utilized more often for carotid surgery? Unfortunately, the integrity of neuronal membranes is not guaranteed with deep hypothermia. In fact, a hypo thermic brain is similar to a hypoxic brain in that intracellular ionic

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General anaesthesia

General anaesthesia is undoubtedly more familiar ground for the majority of anaesthetists. The choice of a specific technique is less important than the maintenance of adequate cerebral and coronary blood flows; this can be achieved by a variety of means. Oxygenation, the airway, systemic arterial pressure and blood carbon dioxide tensions may be controlled effectively under general anaesthesia, allowing the anaesthetist considerable influence over factors which improve surgical outcome; namely, cerebral blood flow and cerebral metabolism. Some degree of cerebral protection is another benefit of the carefully managed general anaesthetic. In the 1960s and early 1970s it was believed that general anaesthesia with hypercapnia and induced hypertension was the preferred technique for carotid endarterectomy. The rationale for this approach was that general anaesthesia reduced CMRo2 and increased the blood oxygen content by delivery of large inspired concentrations of oxygen. The increase in arterial pressure was thought to increase collateral blood flow and the hypercapnia to increase global cerebral blood flow. These factors, combined, were thought to provide cerebral protection. This technique has now been shown to be undesirable for two reasons. First, intracerebral steal may occur with the diversion of blood supply from compromised tissue to relatively normal tissue, leading to worsening hypoxic brain damage. Second, by the effects on the heart of increased carbon dioxide tensions concurrent cardiac work, myocardial compromise and arrhythmias may develop [7]. The control of arterial pressure, however, is important. Both hypotension and excess hypertension should be avoided during carotid endarterectomy. The former obviously leads to malperfusion of what could be critically perfused cerebral tissue with consequent neurological damage. This complication may be avoided by ensuring adequate hydration before and throughout the operation and avoiding the clumsy use of agents known to decrease arterial

pressure. Extreme hypertension is also dangerous because of its deleterious demands upon the heart. Attainable goals during surgery should be no systolic arterial pressure less than lOOmmHg or a decrease greater than 40 mm Hg from the smallest preoperative systolic pressure in patients with known hypertension. Increased arterial pressure can be manipulated during operation by various means. Infusions of the ultra short-acting beta-adrenoceptor blocker, esmolol, have been used in the U.S.A. to control the hypertensive response to intubation, thus decreasing the need for increases in the concentration of anaesthetic agents which may then cause a precipitous decrease in arterial pressure when intubation has been accomplished [23]. A short-acting opioid, for example alfentanil, may also be used for this effect [52]. Because of the brief action of these drugs, decreases in arterial pressure encroaching into the intraoperative period are unlikely. During operation, application of a local anaesthetic to the carotid sinus prevents the hypertensive response to clamping of the vessel, but the anaesthetist should be prepared for a possible surge in arterial pressure and have the appropriate agents available. What of induced hypertension? Blood vessels in ischaemic regions are thought to be in a maximally dilated state; thus they do not display autoregulation and are, therefore, "pressure dependent" and exquisitely sensitive to inadequate arterial pressure. There is, therefore, an argument that induced hypertension ensures a margin of safety for perfusion of these regions. Unfortunately, utilizing vasopressors to induce hypertension in this patient population increases cardiac afterload and myocardial oxygen consumption; we do not recommend that this technique be used. "Light" anaesthesia to achieve the same increases in arterial pressure is not associated with the same incidence of myocardial ischaemia and may be used by those in favour of the above rationale [79]. Occasionally, of course, unexpected decreases in arterial pressure occur despite adequate fluid volume and appropriate anaesthetic depth. Under these circumstances, the alpha-adrenoceptor stimulant, methoxamine, is probably the drug of choice as it vasoconstricts with minimal concurrent tachycardia and may be used to return the arterial pressure to the normal range. Other anaesthetic techniques

Inhalation agents. All three volatile anaesthetics commonly in use today, halothane, enflurane and isoflurane, increase cerebral blood flow in man. Halothane suppresses EEG activity only at doses not tolerated by the cardiovascular system. It is known also to increase the cerebral lactate: pyruvate ratio [53]. For these reasons, which together show halothane to be a poor suppressor of CMRo2, it is better avoided for carotid endarterectomy. Enflurane may, in large doses, and in the presence of hypocapnia, cause spike and dome complexes similar to those of clinical seizure activity so is better avoided, especially when EEG monitoring is in use. Investigations undertaken in the U.S.A. assessing critical regional cerebral blood flow during carotid endarterectomy with differing concentrations of

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these experienced hands appeared to be few, the most frequent being cardiovascular: hypotension (affecting 10.9% of patients), bradycardia (2.8%) and extradural venepuncture (1.5%). The first two complications were treated with a vasopressor or atropine, respectively; the third led to one grand mal convulsion. Neurological deficit also occurred in a significant proportion of patients, but was detected very early and the incidence of permanent neurological deficit was correspondingly very low (3%). The mortality of the series was 2.3%, which compares well with North American statistics indicating a perioperative mortality of 2.8% [26]. Cervical extradural block does, therefore, appear to have a place in the performance of carotid endarterectomy. However, it should be stressed that experience of the technique is essential to prevent the highly dangerous complications which may occur occasionally. According to a recent survey [56], most British anaesthetists do not make use of this method of anaesthesia, but perhaps its use may increase in the future.

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has a long duration of action and is associated with cardiovascular stability [74]. Postoperative Considerations The postoperative sequelae of carotid endarterectomy may be varied and multiple. A physiological approach to understanding potential complications assists when considering their clinical management. This is never more important than for the cardiovascular system. The complications of the pre- and perioperative periods pertaining to the heart and vascular tree apply equally to the postoperative phase. Lability of arterial pressure may lead to myocardial infarction, stroke or, less commonly, the hyperperfusion syndrome. The detection of myocardial infarction in the postoperative period relies on vigilance of the surgical team and some have advocated "myocardial surveillance" by serial ECG over the first 3 days after operation for early detection and subsequent management of myocardial infarction or ischaemia [20]. Hypertension Neurological deficits are undoubtedly more common in the patient in whom control of arterial pressure is poor [72]. In the postoperative period, this may occur for a variety of reasons. Hypertension, defined as a systolic arterial pressure greater than 180 mm Hg or 40 mm Hg greater than preoperative values, or a diastolic arterial pressure greater than 100 mm Hg, may occur because of "wearing off" of preoperative medications, pain, agitation, new neurological deficit or dysfunction of the carotid sinus baroreceptor reflexes. The last of these results from interruption of carotid sinus innervation of the medullary vasomotor centre, which falsely indicates systemic hypotension. The reflex arc then results in an increase in sympathetic nervous activity and a vagolytic effect on the heart, with resulting hypertension and tachycardia. Neurogenic hypertension may also occur, and is believed to be caused by deteriorating neurological state of the patient. In one study [45], 69% of patients with neurological deficits developed hypertension, whereas only 28% of neurologically intact patients did so. Thus hypertension occurring after carotid endarterectomy may serve as the first sign of impending deterioration in neurological function. Several hypotheses exist. Surgical manipulation of the carotid bulb may lead to a humoral influence on arterial pressure in addition to the reflex arc described above. Hodge, Lowe and Vane [41] noted increased angiotensin concentrations in dogs after bilateral carotid occlusion, presumably because of stimulation of renin release by sympathetic discharge. Total extradural anaesthesia, but not bilateral nephrectomy, blocked this increase in arterial pressure [55], suggesting that the sympathetic discharge was unrelated to the kidneys. Another possible mechanism accounting for a surge in arterial pressure in the postoperative period is that related to centrally acting sympathetic neuroamines such as noradrenaline or adrenaline. Ann, Marcus and Moore investigated this issue [3] and found

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halothane and 50 % nitrous oxide in oxygen revealed that ischaemia occurred at flows less than 1820 ml min"V100 g [75]. Similar critical flows were shown to exist for enflurane used in the same way [52]. Isoflurane, however, has been shown to allow a greater decrease in regional cerebral blood flow than the other two agents [52]. Patients anaesthetized with isoflurane, in appropriate concentrations, showed no evidence of cerebral ischaemia on the intraoperative EEG, and developed no new neurological deficits after operation when measured flows as small as 10 ml mkrVlOO g were shown to have occurred [50]. In addition, isoflurane at concentrations less than 1.5 MAC in an animal model produced less cerebral vasodilatation than halothane [86] and did not increase cerebral blood flow at 1.0 MAC in man [58], thus avoiding the problems associated with cerebral dilatation during carotid endarterectomy: increased intracranial pressure, cerebral steal phenomenon, or both. By decreasing the probability of awareness during surgery and reducing requirements for long acting opioids, isoflurane, in concentrations less than 1.0 MAC, is the inhalation agent of choice. It would be tempting also to extrapolate from the above information that it has some cerebroprotective effects, but the belief that isoflurane protects the brain in a manner similar to barbiturate drugs is now considered unlikely [86, 88]. Nitrous oxide has been shown to have several deleterious effects in the setting of carotid surgery. An increase in intracranial pressure secondary to metabolic activation is associated with its use [39], the potential for air embolism is aggravated and it may negate the cerebroprotective effects of thiopentone [38]. These three factors suggest that an air-oxygen mixture combined with low-dose isoflurane may be the inhalation anaesthetic combination associated with fewest complications. Interestingly, propofol may obtund these metabolic effects of nitrous oxide [33] but, as discussed previously, has not been fully evaluated in the context of carotid surgery. Opioid analgesics. The use of opioid analgesics is essential in the light of the previous discussion. The agents of choice are the newer synthetic opioids (fentanyl and alfentanil). Fentanyl, in particular, has a mild vasoconstrictive effect with an accompanying reduction in CMRo2. Alfentanil may also have these effects, but must be titrated carefully to avoid unexpected hypotension when combined with other i.v. agents. Neuromuscular blocking agents. Intubation of the trachea is essential, in order to guarantee security of the airway and permit mild hyperventilation. Either depolarizing or non-depolarizing neuromuscular blocking drugs may be used for tracheal intubation but, if suxamethonium is used, the possibility of hyperkalaemia in the paraplegic patient must not be overlooked [21]. Atracurium and vecuronium are the non-depolarizing drugs of choice as they are associated with greater cardiovascular stability than other agents. The new agent pipecuronium bromide may also be ideal for carotid endarterectomy, as it

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Hypotension

Unexpected hypotension may occur and is equally as hazardous as hypertension. It may result from relative hypovolaemia, oversedation or a differing response of the carotid sinus to increased flow (stretching of the receptors with a resulting hypotensive reflex). Baroreceptor function does, however, decrease with increasing age and cerebrovascular disease and may not affect postoperative arterial pressure as much as expected. A simple test to evaluate baroreceptor function, performed easily before operation, is to ask the patient to perform a Valsalva manoeuvre. If no brady-tachycardiac response occurs, baroreceptor function is obviously not nor-

mal. In any event, hypotension can be treated satisfactorily by ensuring absence of hypovolaemia, myocardial ischaemia and oversedation and then by treating with a stimulant drug such as methoxamine, phenylephrine or ephedrine in incremental bolus doses until vasoconstriction restores a reasonable cerebral perfusion pressure. Neurological deficit

Postoperative neurological deficit occurs in 1-7 % of patients after carotid endarterectomy, regardless of anaesthetic technique [6]. Patients who are neurologically unstable before surgery or who have angiography which demonstrates soft thrombus, contralateral stenosis or extensive disease do suffer more frequent neurological problems. Treatment of a new neurological deficit may require immediate return to the operating theatre without performance of angiography [45]. Otherwise, management is by prevention: control of arterial pressure, good surgical technique, heparinization and avoidance of prolonged intraoperative clamping. Hyperperfusion syndrome

The hyperperfusion syndrome is another complication of carotid endarterectomy. Because of the stenotic nature of the diseased carotid artery, the intracranial blood vessels supplied by that vessel are conditioned to receive minimal blood flow and are chronically vasodilated to maintain adequate cerebral perfusion. Their ability to autoregulate is lost. After carotid endarterectomy has restored normal perfusion pressure, a state of hyperperfusion exists at least until autoregulation is regained after some days [14]. This may present as migrainous type headache, seizures or unexpected intracerebral haemorrhage. Unfortunately, CT scan, angiography and clinical examination may demonstrate no abnormality in the early phases, but complaints of severe unilateral headache, with or without neurological deficit occurring up to 5 days after operation, should be taken seriously and control of arterial pressure commenced [67]. This is particularly important in those patients known to have high-grade stenosis, severe hypertension, or both, before operation, as they are at risk of this complication. Patients who have seizures without evidence of focal ischaemia (on CT scan) should be treated with anticonvulsants. Anticoagulation is contraindicated, as it may precipitate intracerebral haemorrhage. Perioperative antiplatelet therapy should also be used with caution for the same reasons. Postoperative haemorrhage

Postoperative haemorrhage causing swelling of the neck may occur. Difficult intubation may result from this complication and the unwary may mismanage these patients with catastrophic results [61]. Clinical assessment of the airway can underestimate the potential hazard of a rapid sequence induction technique. Thus the necessity for general anaesthesia must be defined. Could surgical evacuation of the haematoma be performed under local anaesthesia ? If a general anaesthetic is necessary, an

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statistically significant increases in cerebral noradrenaline concentrations. They postulated that these existed as a result of increased release from intracranial capillary and arterial endplates in response to the hypoperfusion occurring during carotid cross-clamping. The same authors suggested that this central response may be inadequately treated by peripherally acting antihypertensive drugs. The aetiology of hypertension in the postoperative period should, therefore, be considered before selection of a suitable therapeutic agent. Management. Most clinicians appear to favour use of a short-acting antihypertensive given by infusion. Alteration of infusion according to response and rapid discontinuation of therapy if hypotension should occur unexpectedly are advantages of this approach. Sodium nitroprusside is an obvious drug of choice. By acting as both an arterial and venous vasodilator, and because of its extremely short onset and duration of action, it can be carefully titrated to effect by infusion. It does, however, suffer the disadvantages of association with tachyphylaxis and possible accumulation of thiocyanate if used for prolonged periods, and should therefore be replaced with longer acting vasodilators if required other than for 24-72 h control of arterial pressure. The short acting beta-blocker, esmolol, also may be given by infusion for rapid control of heart rate and arterial pressure [23]. This drug may also be of benefit in counteracting the increases in renin, and consequently angiotensin, concentration as hypothesized by some authors [41]. Esmolol infusion should be replaced by longer acting oral or i.v. agents if prolonged medication is deemed necessary, as infusions of this agent are currently very expensive. Although less controllable than esmolol, labetalol (a combined alpha-and-beta adrenoceptor antagonist) is favoured by many for the short-term control of arterial pressure in the immediate postoperative period. It is usually given i.v. in repeated (if required) bolus doses. Calcium channel blockers also may be used to achieve control of hypertension, particularly in the presence of myocardial ischaemia. Finally, the central sympathomimetic theory of postoperative hypertension warrants trial of clonidine as a suitable antihypertensive drug [3]. This would be an interesting adjunct to current therapy, but remains to be thoroughly evaluated.

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inhalation induction or a fibreoptic awake intubation are the methods of choice. RECOMMENDED GENERAL ANAESTHETIC TECHNIQUE

discontinued to allow a smooth but rapid awakening for evaluation of neurological status. Transfer to a neurosurgical intensive care unit would be undertaken when awakening is satisfactory. Supplementary oxygen should be given during transfer and continued into the postoperative period. The intensive care staff should be alerted to observe closely for fluctuations in arterial pressure outside pre-set limits, neurological deterioration, hypersomnolence, unilateral headache and presence of wound haematoma. In addition to the basic technique of anaesthesia, it would be customary to consider techniques of monitoring directed specifically to the central nervous system or deliberate manipulation of cerebral metabolism. The advisability of this would depend on the individual patient, the extent of the disease process and the surgical technique used (e.g. shunt or no shunt). COMMENT

The place of carotid endarterectomy as a surgical procedure is currently under scrutiny [35,71,84]. Medical therapy and the decreasing incidence of stroke in the general population have called into question the relevance of the operation. For example, Winslow and colleagues [91] concluded from their study in a random sample of 1302 patients undergoing carotid endarterectomy that only 35% had the procedure for an appropriate reason. In their view, the reasons were equivocal in 32 % of patients and inappropriate in 32%. However, the picture is now becoming clearer: several large-scale trials of carotid endarterectomy have recently issued preliminary reports. The European Carotid Surgery Trial (ECST) [30], which began in 1981, has studied the results from 2518 patients over the past 10 years. In those patients in whom there was a 30-69% stenosis of the carotid artery, the balance of surgical risk and eventual benefit remains uncertain. The benefits of surgery were outweighed by the risks in patients with mild degrees of carotid stenosis (< 29 %). In contrast, however, the immediate risks of operation were significantly outweighed by the later benefits in the group of patients with severe stenosis (70-99%). The North American Symptomatic Carotid Endarterectomy Trial (NASCET) [59, 60] began in 1988 and, after allocating more than 1000 patients randomly between surgery and non-surgery, has produced findings similar to those in the ECST investigation. In particular, NASCET demonstrated statistically definitive benefits of surgery in those patients with "severe" stenosis (70-99%). The results for patients with moderate (30-69%) stenosis remain unclear (as in ECST); however, random allocation of treatment for such patients is continuing. The implications of these findings for the anaesthetist are clear. First, it is likely that only those patients with the "severest" degree of stenosis will be submitted for surgery. Obviously, this is a group of patients in whom the alterations to cerebrovascular physiology, and the results of anaesthetic manipulation, will be the most marked.

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Anaesthesia for carotid endarterectomy presents a challenge for the anaesthetist. An understanding of the nature of the disease process, the surgical technique and the physiology of the cardiovascular and neurological systems is mandatory. Thorough cardiovascular and neurological preoperative assessment and management must take place and a suitable anaesthetic technique be considered. Two options are available—regional or general anaesthesia. In the opinion of the authors, a suitable basic general anaesthetic technique would be as follows. The patient should be seen by the anaesthetist before surgery for full preoperative evaluation and discussion of the forthcoming procedure. Benzodiazepine premedication should be prescribed in a low dose; for example, diazepam 5-10 mg 1.5-2 h before the start of surgery or temazepam 20-30 mg by mouth 1-2 h before surgery. Aids to intraoperative monitoring should be commenced in the anaesthetic room: ECG, noninvasive measurement of arterial pressure, intraarterial catheter placement under local anaesthesia and all other monitors recommended by the Association of Anaesthetists of Great Britain and Ireland [2]. Induction should commence after 3 min of preoxygenation supplemented with i.v. midazolam through a large-gauge, free-flowing infusion, to produce a state of light sedation. Induction is then completed with thiopentone 5—7 mg kg"1 followed by an intubating dose of non-depolarizing neuromuscular blocker (suitable examples are vecuronium 0.1 mg kg"1 or atracurium 0.5 mg kg"1). Tracheal intubation may be undertaken after adequate time for relaxation and after pretreatment with lignocaine 1 mg kg"1 i.v. or an infusion of esmolol commenced at 500 ug kg"1 min"1 or pretreatment with alfentanil 10 ug kg"1. In this way surges in arterial pressure or intracranial pressure may be avoided. Anaesthesia should be maintained with an oxygen-air mixture, isoflurane 1.0 MAC or less and supplementary doses of opioids such as fentanyl or alfentanil to provide a stable intraoperative course. Normocapnia (end-tidal carbon dioxide and confirmatory blood-gas measurement), normotension or hypertension within 20 % of the preoperative arterial pressure (not exceeding 200 mm Hg) and avoidance of hypovolaemia by adequate transfusion of colloids or blood are all desirable goals. Mild hypothermia to 34 °C may be an advantage. If a shunt is used, it may be worth considering the administration of thiopentone by infusion during the periods of clamping before insertion and removal of the shunt. Ideally, a burst suppression pattern should be obtained on the EEG. However, in practice, it may be better to ensure that arterial pressure is not compromised. At the conclusion of surgery, antagonism of neuromuscular block should be achieved with neostigmine and glycopyrronium, and inhalation anaesthesia

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ANAESTHESIA FOR CAROTID ARTERY SURGERY Second, at least as far as the U.K. is concerned, the results of the ECST study could suggest that there will be a 3—5-fold increase per annum in the number of carotid endarterectomies over the next decade [29].

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