Editorial I

‘It ain’t what you do; it’s the way that you do it ...’: reducing haemodynamic instability during carotid surgery

Mark D. Stoneham1

1 Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford OX3 9DU, UK E-mail: mark.stoneham{at}nda.ox.ac.uk

Some 10% of patients with a symptomatic internal carotid artery stenosis greater than 70% suffer a stroke every year. Of these, approximately one-third die, one-third recover, and one-third suffer significant residual neurological impairment.1 Carotid endarterectomy (CEA) reduces the risk of stroke in such symptomatic patients,2 although not in those with lesser stenoses, or near-occluded carotid disease. Thus, rather like the management of hypertension, the operation does not cure the patient of their disease, but is performed to prevent a life-threatening complication. Additionally, the complication rate of the procedure is high, so the stakes are high and, perhaps more than many other procedures, clinicians involved in carotid surgery tend to have dogmatic views regarding the anaesthetic and surgical techniques they are prepared to use.

Whilst the primary indication for surgery is neurological symptoms, much of the morbidity and mortality of the operation is cardiovascular in origin. Overall, the incidence of serious cardiac and neurological complications (stroke, myocardial infarction, or death) is estimated at 5–8%,2 with almost 50% of the mortality being cardiovascular rather than neurological in origin.3 However, even the neurological sequelae of CEA may themselves be caused by haemodynamic instability. For example, hypertension may lead to headache, seizures and ultimately subarachnoid haemorrhage, hypotension may lead to cerebral hypoperfusion or ischaemia, and cardiac arrhythmias may lead to thrombus formation and embolic stroke. Another significant fraction of the mortality of carotid surgery is postoperative airway obstruction caused by wound haematoma or arteriotomy dehiscence. This may be exacerbated—or even caused—by arterial (or venous) hypertension. In the NASCET trial, this pathophysiological mechanism was responsible for all non-stroke related fatal surgical complications.4 Thus, overall, haemodynamic stability is of paramount importance in preventing complications of carotid surgery. It is, after all, the only factor within the direct influence of the anaesthetist.

In this edition of the journal, Godet and colleagues5 demonstrate that an opioid-based anaesthetic technique for CEA using a target-controlled infusion (TCI) of remifentanil provides less haemodynamic stability than an hypnotic-based technique using TCI propofol in terms of causing more hypotension and hypertension, although, perhaps predictably, less tachycardia. It is worth mentioning that their study population is unrepresentative of UK practice, as 28 out of 46 of their patients (61%) had asymptomatic carotid disease and the benefits of surgery in this group of patients are less clear.6 Otherwise, the study is applicable to current UK practice. Alteration of remifentanil and propofol TCI concentration was used to maintain a constant Bispectral Index, thus controlling for anaesthetic depth as a variable affecting haemodynamic parameters.

If one accepts that haemodynamic instability during CEA is more likely to result in cardiac and neurological complications, the results of this study have implications for vascular anaesthetic practice. Indeed, it may come as a surprise to many anaesthetists who rely on the haemodynamic stability which remifentanil affords in other types of surgery.7 8 However, there are other factors, particularly with respect to concomitant medications, that could partially explain these results. First, a third of the patients (15/46) were receiving beta-blockers. The combination of remifentanil and beta-blockade may have profound, unpredictable effects on heart rate and arterial pressure control,9 although, on their own, perioperative administration of vasoactive drugs like beta-blockers,10 or alpha-2 agonists11 may help to maintain haemodynamic stability and reduce myocardial ischaemia in major vascular surgery. Thus, it would appear that it is the combination of the vagotonic effects of remifentanil and other vasoactive drugs that may be the cause of the haemodynamic disturbance. Second, 19/46 (41%) of the patients were receiving angiotensin converting enzyme inhibitors or angiotensinogen II antagonists. Although these were omitted on the day of surgery, there may still have been residual haemodynamic effects from these drugs.12 13 It is not stated whether the patients suffering haemodynamic disturbance were predominantly those still receiving these vaso-active medications, although one might suspect this. Third, perioperative manipulation of the carotid sinus, which is within the operating field, can itself cause considerable haemodynamic fluctuations.14 Fourth, head and neck manipulation, which sporadically happens during CEA, can cause movement of the tracheal tube,15 which may itself cause catecholamine release and subsequent hypertension and tachycardia. Of course, whilst any of these factors alone might not be clinically significant, the combination of two or more of them may interact to exaggerate the effects.

Another possible influence on cardiovascular complications during carotid surgery is the use of nitrous oxide. Intraoperative use of nitrous oxide has been shown to result in postoperative increases in plasma homocysteine concentration,16 which were associated with an increase in postoperative myocardial ischaemia as defined by ST segment elevation in a 3-channel, 7-lead Holter monitor. These findings could change contemporary practice as nitrous oxide is currently used in the majority of patients undergoing CEA under general anaesthesia.17 Indeed, patients in the Godet study in this issue received nitrous oxide 50% in addition to the remifentanil/propofol TCI combination.5

The choice of regional or general anaesthesia may itself have considerable influence on the haemodynamic control and cardiovascular complications of carotid surgery.18 An often-quoted systematic review of prospective and retrospective CEA studies found that in 17 non-randomized studies looking at nearly 6000 patients, the use of regional anaesthesia was associated with a 50% reduction in death, stroke, myocardial infarction, and pneumonia.19 This initiated the GALA trial for CEA: a multicentre study of general vs local anaesthesia in 5000 patients undergoing CEA, organized by the Department of Clinical Neurosciences of Western General Hospital, Edinburgh. The GALA results are eagerly awaited to answer the fundamental question of whether anaesthetic technique can influence outcome in carotid surgery. The trial eventually should have enough patients to detect a significant difference in outcome if one exists, although the trial protocol does allow any regional or general anaesthetic technique to be used, which could dilute any potential difference in outcome between the two groups. A preliminary analysis of the first 600 patients of the GALA trial (without breaking the code) showed that the overall incidence of stroke in both groups together was 34/600=5.7%, myocardial infarction 5/600=0.8%, and death from any cause was 2.5% (personal communication, Professor Charles Warlow, GALA trial office).

Even if the apparent reduction in morbidity and mortality of regional anaesthesia is not borne out by the results of the GALA trial, it is certainly true that there are differences in the haemodynamic profile during CEA between regional and general anaesthesia. Under general anaesthesia, events such as tracheal intubation, surgical incision, emergence, and extubation may all cause catecholamine release leading to hypertension and tachycardia, whilst opioids, volatile and i.v. anaesthetic agents tend to cause vasodilatation and depression of myocardial contractility, resulting in hypotension. In contrast, under regional anaesthesia, cerebral autoregulation and baroreceptor function are relatively preserved, leading to a tendency to hypertension during the period of carotid cross-clamping and subsequent hypotension in recovery,20 commonly requiring treatment with vasopressors.21 Peroperative pain, which may occur in 50% or more of patients undergoing awake carotid surgery,22 and which may be a result of additional afferent sympathetic innervation of the carotid sheath, will also tend to cause hypertension and tachycardia.

Some clinicians utilising general anaesthetic techniques for CEA routinely augment arterial pressure pharmacologically by up to 25% to maintain cerebral perfusion in the face of the negative inotropic effect of general anaesthetic drugs.23 Arterial pressure augmentation has also been used more selectively in patients undergoing CEA under regional anaesthesia to reverse neurological deficit developing following carotid cross-clamping.24 There are also indications that the incidence of myocardial ischaemia may not only be reduced with the use of regional anaesthesia,25 but detected at an earlier stage than under general anaesthesia.24 Further evidence of differences in haemodynamic profiles of regional and general anaesthetic techniques come from vasoactive drug use during CEA, which is greater in patients receiving general anaesthesia.26

The tendency toward individual sub-specialization in anaesthesia is nowhere more appropriate than in vascular anaesthesia. There is evidence that individual surgeon and institutional experience and expertise can influence outcome following CEA.27 Logically, this should apply to anaesthetists too. Thus, vascular anaesthetists should, perhaps, not be anaesthetizing less than, for example, 10 or 20 carotid cases per annum. Finally, carotid angioplasty and stenting is becoming more common as an alternative to CEA. Rather like aortic stenting, patients deemed inappropriate for surgery because of their co-morbid condition or extent of their disease may have their carotid stenosis treated radiologically rather than surgically. The perioperative morbidity and mortality is similar to that of CEA;28 anaesthetists will therefore be required to be involved fully with the management of these high risk patients.

In conclusion, the Godet study5 once again confirms that patients undergoing CEA are prone to considerable haemodynamic instability. Whilst CEA may be safely performed using a wide variety of anaesthetic techniques, it is probably more important to pay attention to the ‘small print’ of one’s technique. Anaesthetising patients for CEA, particularly under regional anaesthesia, requires constant clinical vigilance, maintaining pulse and arterial pressure within narrow ranges, and reacting expediently to changes in neurological status or cardiovascular variables. Further studies on the use of protocol-driven anaesthesia, including the use of beta-blockers, or perhaps, alpha-2 agonists, may help to maintain haemodynamic stability and reduce cardiac, and therefore neurological, complications. The maintenance of haemodynamic stability, thus optimizing cerebral and myocardial perfusion, is the single most important role of the anaesthetist in reducing the morbidity and mortality of this procedure.

References

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