Anaesthesia for Vascular, Endocrine and Plastic Surgery

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Anaesthesia for Vascular, Endocrine and Plastic Surgery

MAJOR VASCULAR SURGERY

Many aspects of vascular surgery have changed during the last two decades, largely as a result of advances in radiological practice and cardiology. Examples include improvements in the treatment of myocardial infarction, the development of endovascular aortic surgery and lower limb angioplasty; such progress is likely to continue. However, anaesthesia for major vascular surgery remains a challenging area of practice. In addition to general considerations, the specific features of the commoner vascular procedures are described in this chapter: elective and emergency repair of abdominal aortic aneurysm (AAA), endovascular AAA repair, lower limb revascularization and carotid endarterectomy.

General Considerations

Peripheral vascular disease is a manifestation of generalized cardiovascular disease, and therefore coronary artery disease is present to some degree in almost all patients presenting for major vascular surgery. Most patients are elderly and have a high incidence of other coexisting medical disease, in particular:

Most of these are considered independent risk factors for perioperative cardiac complications after major surgery (see Ch 18).

The broad aims of preoperative evaluation before vascular surgery are to:

Vascular surgery is associated with a high morbidity and mortality, resulting mostly from cardiac complications (myocardial infarction, arrhythmias and cardiac failure) (see Chs 18 and 43). It is therefore vital that cardiac function is assessed preoperatively and that the risks of surgery are evaluated and discussed with the patient. Although the outcome of subsequent vascular surgery is improved in those who have previously undergone coronary revascularization by coronary artery bypass grafting (CABG), this is associated with additional risks. Percutaneous coronary interventions (insertion of bare metal or drug-eluting intracoronary stents (ICS)) are being used increasingly as an alternative to CABG in suitable patients. There is a risk of stent thrombosis after ICS so patients receive dual antiplatelet therapy (aspirin and clopidogrel) for 6 weeks after bare metal and 1 year after drug-eluting stent insertion. The risks of perioperative cardiac events or stent thrombosis are very high if surgery is performed during the period when dual antiplatelet drugs are needed because of increased haemorrhage if antiplatelet therapy is continued, or acute thrombotic events if it is interrupted. The most recent guidelines suggest that elective surgery should be postponed for at least 4–6 weeks after bare metal stent insertion (and ideally delayed for 3 months) and for 1 year after drug-eluting stent insertion, unless surgery is more urgent. It should be remembered that coronary revascularization should be performed only if indicated because of the severity of coronary disease and is not justified simply to improve outcome from subsequent vascular surgery.

Preoperative Medical Therapy in Vascular Surgical Patients

The preoperative assessment clinic is an ideal opportunity to assess concurrent medication. Drugs particularly relevant to the patient with vascular disease are β-blockers, antiplatelet drugs and statins.

β-Blockers are used extensively in patients with angina, and improve the long-term survival after myocardial infarction and in patients with heart failure. Some studies have shown beneficial effects of perioperative β-blockade in high-risk patients undergoing major vascular surgery although the benefits in lower risk patients are less clear. Current guidelines suggest that β-blockers may be commenced in patients with inducible ischaemia (documented on preoperative stress testing), or proven coronary artery disease, who are undergoing major vascular surgery. The optimum duration, dose and role of individual regimens for β-blockade are not established, but if they are used, bisoprolol 2.5–10 mg or atenolol 25–100 mg daily should be started 1–2 weeks preoperatively, titrated towards a heart rate of 60–70 beats min–1. Conversely, the perioperative discontinuation of β-blockers may be harmful, and they should be continued when already being used to control angina, arrhythmias or hypertension.

Current UK recommendations are that all patients undergoing major vascular surgery should be receiving antiplatelet therapy with aspirin unless there is a contraindication. Clopidogrel or dipyridamole are alternatives. Some clinicians consider that clopidogrel should be stopped 5 days before aortic surgery, but this should be discussed with the surgeon and prescribing physician. Aspirin should be continued throughout the perioperative period. Statin therapy should also be considered in all vascular surgical patients, and if prescribed it should be continued throughout the perioperative period.

Minimum investigations before major vascular surgery should include ECG, chest X-ray, full blood count and serum urea and electrolyte concentrations, but more invasive or specialized tests may be required (see Ch 18), including cardiopulmonary exercise testing where available. Some assessment of exercise tolerance should be made in all patients because it is a useful indicator of functional cardiac status, although many vascular patients are limited by intermittent claudication or old age and may have a sedentary lifestyle. In this case, a patient with severe coronary artery disease may have no symptoms of angina and a normal resting ECG. In some patients (e.g. those with limited functional capacity or life expectancy because of severe intractable coexistent medical conditions), the risks of elective vascular surgery may outweigh the overall potential benefits and invasive surgery may not be appropriate.

Abdominal Aortic Aneurysm

Abdominal aortic aneurysms (AAAs) occur in 2–4% of the population over the age of 65 years, predominantly in males. Approximately 90% of AAAs arise below the origin of the renal arteries and they tend to expand over time. The risk of rupture increases exponentially when the aneurysm exceeds 5.5 cm in diameter and elective surgery is then indicated. The mortality from elective AAA repair is decreasing and is now 5–8%, but overall mortality from a ruptured AAA is up to 90%, and is 50% in those who survive until emergency surgery can be performed. Consequently, screening programmes are in place to identify patients with a small asymptomatic aneurysm and to offer intervention when the aneurysm reaches a diameter of 5.5 cm. Open surgery involves replacing the aneurysmal segment with a tube or bifurcated prosthetic graft, depending on the extent of iliac artery involvement. In all cases, the aorta must be cross-clamped (see below) and a large abdominal incision is required. Surgery is prolonged and blood loss may be substantial. Patients are usually elderly, with a high incidence of coexisting disease. These factors contribute to the high morbidity and mortality of this procedure. Endovascular aortic aneurysm surgery avoids some of these problems (see below).

Elective Open AAA Repair

Preoperative evaluation and risk assessment are paramount. All vasoactive medication (except perhaps ACE inhibitors and angiotensin-II receptor blockers) must be continued up to the time of surgery and an anxiolytic premedication may be advantageous. The patient may have recently undergone arteriography and the injection of large volumes of radiopaque dye may cause renal dysfunction. Maintenance of hydration with intravenous crystalloids is advisable the night before surgery. Some patients with severe chronic obstructive pulmonary disease may benefit from regular nebulizers and chest physiotherapy before surgery to decrease the incidence of respiratory complications.

An intra-arterial and two large intravenous cannulae should be inserted before induction of anaesthesia, with monitoring of ECG and pulse oximetry. Cardiovascular changes at induction may be diminished by preoperative hydration and careful titration of the intravenous induction agent. After neuromuscular blockade, the trachea is intubated (see below) and anaesthesia continued using a balanced volatile/opioid technique. Perioperative epidural analgesia is useful and may be undertaken before or after induction of anaesthesia.

Several important considerations apply to patients undergoing aortic surgery (Table 31.1). The following are required:

TABLE 31.1

Major Anaesthetic Considerations for Patients Undergoing Aortic Surgery

High incidence of coexisting cardiovascular and respiratory disease

Cardiovascular instability during induction of anaesthesia, aortic cross-clamping and declamping

Large blood loss and fluid shifts during and after surgery

Prolonged major surgery in high-risk patients

Marked heat and evaporative fluid losses from exposed bowel

Potential postoperative impairment of respiratory, cardiac, renal and gastrointestinal function

In the more compromised patient, e.g. with ischaemic heart disease and poor left ventricular function, an additional cardiac output monitor (e.g. transoesophageal echocardiography or other non-invasive device) should be used to monitor cardiac index and guide fluid management. A pulmonary artery catheter may be indicated in some patients. All possible measures should be undertaken to maintain body temperature, including heated mattress and overblanket, warmed intravenous fluids, and warmed and humidified inspired gases. The ambient temperature should be warm and the bowel may be wrapped in clear plastic to minimize evaporative losses.

Three specific stimuli may give rise to cardiovascular instability during surgery:

image Tracheal intubation. Laryngoscopy and tracheal intubation may be accompanied by marked increases in arterial pressure and heart rate which may precipitate myocardial ischaemia in susceptible individuals. This response may be attenuated by the i.v. administration of a β-blocker (e.g. esmolol 1.5 mg kg–1) or a rapidly-acting opioid (e.g. alfentanil 10 μg kg–1) before intubation.

image Cross-clamping of the aorta. Clamping of the aorta causes a sudden increase in aortic impedance to forward flow and hence left ventricular afterload. This increases cardiac work and may result in myocardial ischaemia, arrhythmias and left ventricular failure. Arterial pressure proximal to the clamp increases acutely even though left ventricular ejection fraction and cardiac output are reduced. The effects on preload are variable. The degree of cardiovascular disturbance is greater when the clamp is applied more proximally (greater at the supracoeliac > suprarenal > infrarenal levels). A vasodilator, e.g. glyceryl trinitrate (GTN), is often infused just before clamping (and continued up to clamp release) to obviate these problems. Deepening of volatile anaesthesia or an additional dose of an opioid may also be used at aortic clamping. While the aorta is clamped, blood flow distal to the clamp decreases, and distal organ perfusion is largely dependent on the collateral circulation. The lower limbs, pelvic and abdominal viscera suffer variable degrees of ischaemia during which inflammatory mediators are released from white blood cells, platelets and capillary endothelium. These mediators include oxygen free radicals, neutrophil proteases, platelet activating factor, cyclo-oxygenase products and cytokines.

image Aortic declamping. Declamping of the aorta causes sudden decreases in aortic impedance, systemic vascular resistance and venous return with reperfusion of the bowel, pelvis and lower limbs and redistribution of blood. Inflammatory mediators are swept into the systemic circulation causing vasodilatation, metabolic acidosis, increased capillary permeability and sequestration of blood cells in the lungs. This is a critical period of anaesthesia and surgery because hypotension after aortic declamping may be severe and refractory unless circulating volume has been well maintained. If relative hypervolaemia is produced during the period of clamping by infusion of fluids to produce a CVP of greater than 12–14 mmHg (and perhaps administration of GTN until shortly before clamp release), declamping hypotension is less of a problem and metabolic acidosis may be diminished. Declamping hypotension usually resolves within a few minutes but vasopressors or positive inotropes are often required; these can be given before clamp release in anticipation. Good communication with the surgeon and slow or sequential clamp release helps the anaesthetist to manage aortic declamping. Renal blood flow decreases even when an infrarenal cross-clamp is used, and steps to maintain renal function are often required. The single most important measure is the maintenance of extracellular fluid volume (i.e. CVP > 12–14 mmHg). Prophylactic mannitol 0.5–1.0 g kg–1 i.v. or furosemide may also be administered, although the evidence for their efficacy is conflicting.

Bleeding is a problem throughout the operation, often after aortic clamping when back bleeding from lumbar vessels occurs, but may be particularly severe at aortic declamping as the adequacy of vascular anastomoses is tested. A red cell salvage device should be used routinely in aortic surgery when it is available, but other modes of autologous blood transfusion (predonation, normovolaemic haemodilution) may be valuable. In addition to red cells, specific clotting factors are often required. It is often preferable to reserve the use of clotting factors until the anastomoses are complete and most of the anticipated blood loss has occurred. Many surgeons request the administration of heparin (usually 5000 units i.v.) before insertion of the graft and occasionally it may be appropriate to reverse its effects with protamine (0.5 mg per 100 units of heparin). Point-of-care haemostatic testing (thromboelastography or thromboelastometry) are very useful to diagnose coagulopathy and guide the use of clotting products.

Epidural analgesia is usually provided through a catheter placed at the mid-thoracic level, unless there is a contraindication. There is some debate as to whether epidural local anaesthetics are best administered during surgery (to attenuate cardiovascular and stress responses) or at the end of surgery (because sympathetic blockade may cause hypotension and make cardiovascular management more difficult during the procedure). A popular technique is to use combined volatile general anaesthesia with boluses of fentanyl or an infusion of remifentanil for intraoperative analgesia; epidural analgesia is then established after aortic declamping and once cardiovascular stability is ensured, using a combination of local anaesthetic and fentanyl.

Most patients are elderly and are unable to tolerate the large heat loss occurring through the extensive surgical exposure, which necessitates displacement of the bowel outside the abdominal cavity. Hypothermia causes vasoconstriction, which may cause myocardial ischaemia, delayed recovery and difficulties with fluid management during rewarming, because large volumes of intravenous fluid may be required. Therefore, all measures should be taken to prevent hypothermia.

Emergency Open Repair

The principles of management are similar to those discussed above. However, the patient may be grossly hypovolaemic and arterial pressure is often maintained only by marked systemic vasoconstriction and the action of abdominal muscle tone acting on intra-abdominal capacitance vessels. Resuscitation with intravenous fluids before the patient reaches the operating theatre should be judicious; permissive hypotension (maintaining systolic pressure at 80–100 mmHg) limits the extent of haemorrhage and improves outcome. The patient is prepared and anaesthesia induced on the operating table. While 100% oxygen is administered by mask, an arterial and two large-gauge i.v. cannulae are inserted under local anaesthesia. The surgeon then prepares and towels the patient ready for surgery and it is only at this point that anaesthesia is induced using a rapid-sequence technique. When muscle relaxation occurs, systemic arterial pressure may decrease precipitously and immediate laparotomy and aortic clamping may be required. Thereafter, the procedure is similar to that for elective repair.

The prognosis is poor for several reasons. There has been no preoperative preparation and most patients have concurrent disease. There may have been a period of severe hypotension, resulting in impairment of renal, cerebral or myocardial function. Blood loss is often substantial and massive transfusion of red cells and clotting factors is usually required. Postoperative jaundice is common because of haemolysis of damaged red cells in the circulation and in the large retroperitoneal haematoma which usually develops after aortic rupture. In addition, postoperative renal impairment and prolonged ileus often occur. Artificial ventilation and organ support are required for several days and the cause of death is usually multiorgan failure.

Endovascular Aortic Aneurysm Repair

Endovascular aortic aneurysm repair (EVAR) is now an established alternative to open surgery. A balloon-expandable stent-graft is inserted under radiological guidance via the femoral or iliac arteries into the aneurysm to exclude it from the circulation. It is performed via groin incisions and the aortic lumen is temporarily occluded from within, rather than being cross-clamped. The cardiovascular, metabolic and respiratory consequences are reduced in comparison with conventional open surgery. Perioperative blood loss, transfusion requirements, postoperative pain, hospital stay and morbidity are lower compared with open surgery. Perioperative morbidity is 1–2% although long-term (> 8 years) survival after EVAR is similar to that after open surgery because of deaths from cardiovascular and respiratory diseases. Despite advances in stent-graft technology, the morphology of the aneurysm in some patients renders it unsuitable for EVAR (based on the site, shape, degree of angulation and the size of iliac arteries). Repeated radiological procedures (e.g. angioplasty) are required in up to 20% of patients. The procedure usually takes 1–2 h and may be performed by radiologists and/or surgeons but the patients have the same coexisting diseases and some of the anaesthetic considerations are similar. In some cases, EVAR may be preferred as a less invasive technique in patients judged unfit for open surgery. Access to the iliac vessels is often possible using infra-inguinal incisions in the groin and postoperative pain is therefore minimal compared to open surgery. In many centres, EVAR is performed in the radiology suite, in which case the anaesthetist must ensure that anaesthetic facilities for high-risk patients are adequate.

EVAR may be performed under general, regional or local anaesthesia with or without sedative adjuncts. In all cases, direct arterial pressure monitoring is mandatory because rapid fluctuations in arterial pressure may occur during stent-graft deployment. In awake patients, hyoscine 20 mg i.v. may be useful to decrease bowel motility during stent-graft placement. CVP monitoring is not usually necessary unless dictated by the patient’s medical condition (e.g. moderate/severe cardiac disease). Short periods of apnoea are needed during insertion of the device; this is easy when ventilation is controlled but requires the patient’s co-operation if a regional or local anaesthetic technique is used. The devices are positioned under angiographic control and large volumes of radiocontrast may be used, predisposing to contrast-induced nephropathy (CIN). It is important to avoid hypotension and hypovolaemia, both of which can contribute to CIN; sodium bicarbonate, N-acetylcysteine or mannitol may be administered, although the evidence of their benefit is limited. Brisk haemorrhage is unusual during EVAR and, although bleeding may be significant, it is usually insidious. However, large-diameter cannulae should be inserted and vasoactive drugs readily available because if endovascular repair is not technically feasible, conversion to open surgery may be required. EVAR may also be used to repair contained ruptured or leaking AAAs, and has an increasing role in the management of thoracic aortic aneurysms.

Surgery for Occlusive Peripheral Vascular Disease

Peripheral reconstructive surgery is performed in patients with severe atherosclerotic arterial disease causing ischaemic rest pain, tissue loss (ulceration or gangrene), severe claudication with disease at specific anatomical sites (aorto-iliac, femoropopliteal, popliteal or distal) or failure of nonsurgical procedures. Most patients are heavy smokers, suffer from chronic pulmonary disease and have widespread arterial disease. Most patients present with intermittent claudication. Consequently, exercise tolerance is limited and severe coronary artery disease may be present despite few symptoms. Surgical revascularization is performed to salvage the ischaemic limb, but arterial angioplasty is a less invasive alternative and is increasingly performed as a first-line procedure in suitable patients. Patients presenting for surgical reconstruction are often those in whom angioplasties have failed and who may have more severe vascular disease. Short-term mortality after lower limb revascularization is comparable to that following AAA repair and long-term outcome is worse as a consequence of associated cardiovascular disease. Acute limb ischaemia which threatens limb viability requires rapid intervention comprising full anticoagulation, intrathrombus thrombolysis after arteriography, analgesia and revascularization via embolectomy, angioplasty or bypass surgery as indicated. The clinical findings of sensory loss and muscle weakness necessitate intervention within 6 h and therefore preoperative evaluation and correction of risk factors may be limited.

Peripheral Arterial Reconstruction

The commonest procedures involve the insertion of an autologous vein or synthetic vascular graft between axillary and femoral, or femoral and popliteal, arteries. Axillofemoral bypass surgery is performed in those not considered fit for open aortic surgery, and these patients are often particularly frail. All these operations are prolonged and an IPPV/relaxant balanced anaesthetic technique is suitable. A meticulous anaesthetic technique is paramount, with particular attention to the maintenance of normothermia and administration of i.v. fluids. Hypothermia or hypovolaemia may cause peripheral vasoconstriction, compromising distal perfusion and postoperative graft function. Blood loss through the walls of open-weave grafts may continue for several hours after surgery and cardiovascular status should be monitored closely during this time. Epidural analgesia may be used alone or as an adjunct to general anaesthesia for lower limb procedures. Despite theoretical advantages, epidural anaesthesia has no effect on graft function per se but it does provide effective postoperative analgesia. However, i.v. heparin is usually administered during and after surgery (see below) and the risks of epidural haematoma should be considered. Oxygen therapy should be continued for at least 24 h after surgery, and monitoring in a high-dependency unit is often required.

Carotid Artery Surgery

Despite advances in the medical treatment of patients with stroke, it remains a significant cause of death and disability. Carotid endarterectomy is performed to prevent disabling embolic stroke in patients with atheromatous plaques in the common carotid bifurcation, or internal or external carotid arteries. Most patients are elderly, with generalized vascular disease. Cerebral autoregulation may be impaired and cerebral blood flow is therefore much more dependent upon systemic arterial pressure. The main risk of surgery is the production of a new neurological deficit (which may be fatal or cause permanent disability), although cardiovascular complications account for 50% of the overall morbidity and mortality.

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