Vascular and endovascular surgery

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13 Vascular and endovascular surgery

Atherosclerosis

Atherosclerosis is a disease affecting arteries of all sizes and means literally ‘hardening of the arteries’. Large elastic arteries (aorta, iliac, carotid) and medium-sized muscular arteries (coronary, femoral and popliteal) are most commonly affected. The basic lesion of atherosclerosis is a localised fibrofatty plaque in the wall of the artery causing narrowing of the lumen. The plaque is often calcified and contains a core of cholesterol covered with a fibrous cap.

Atherosclerosis is a multifocal condition. A patient with peripheral vascular disease is highly likely to have coronary disease or cerebrovascular disease and vice versa.

The pathogenesis of atherosclerosis is complex and not fully understood. The development of atheromatous lesions is aggravated by risk factors including smoking, hypercholesterolaemia, hypertension and diabetes mellitus (see ‘Vascular risk factors and their modification’, below). Low-density lipoproteins and monocyte-derived macrophages accumulate in the tunica intima, forming a fatty streak. In certain susceptible arteries, smooth muscle and inflammatory cells are recruited into the intimal fatty streak, promoting the development of the fibrofatty plaque covered by a collagen fibrous cap.

The symptoms caused by atherosclerotic disease depend on the arteries affected. Thus coronary artery disease gives rise to angina and myocardial infarction; cerebrovascular disease leads to strokes and transient ischaemic attacks (TIAs); and peripheral vascular disease results in limb ischaemia. Most deaths and serious morbidity in the Western world are due to these conditions resulting from atherosclerosis.

Atherosclerosis causes symptoms via three mechanisms:

• limitation of blood flow

• embolisation

• thrombosis.

An atheromatous plaque may allow sufficient flow through a vessel to satisfy end-organ demands at rest but cause problems when the flow needs to increase, for example angina on exertion due to stable coronary artery disease. Another example is intermittent claudication (see p. 210). Such symptoms may be unpleasant but not necessarily imminently dangerous.

Embolisation and thrombosis are related in that they both depend on plaque stability. Their consequences are much more serious. The fibrous cap covering an atherosclerotic plaque may be quite smooth and covered by endothelial cells. In an unstable plaque, the cap may fissure or rupture, exposing the highly thrombogenic core of the plaque causing immediate platelet activation and formation of thrombus. A small thrombus may break off and embolise. More major plaque disruption may cause complete thrombosis and occlusion of the artery. In the carotid circulation this is a common cause of TIAs and strokes. In the heart this may cause unstable angina or myocardial infarction. In the peripheral circulation, acute limb ischaemia results.

The beneficial effects of statin therapy for individuals with coronary and peripheral artery disease extend beyond their lipid-lowering properties. In addition to lowering blood cholesterol concentration, statins have plaque-stabilising effects that greatly reduce the likelihood of stroke and myocardial infarction.

Vascular risk factors and their modification

Fixed (non-modifiable) risk factors

These are of limited interest since no-one can alter their age, the population into which they were born or the age at which a parent had a heart attack or stroke.

Vascular disease in any one arterial territory is an important risk factor for adverse events in others. Patients surviving strokes are more likely to die of a heart attack than another stroke. Similarly, intermittent claudication is a major risk factor for stroke and ischaemic heart disease.

Major modifiable risk factors

Smoking, hypertension, hypercholesterolaemia and sedentary lifestyle each increase the risk of acute myocardial infarction. When two or more are present, the risk is multiplied, not added. The benefit of removing a risk factor by lifestyle changes or treatment depends on the background risk set by an individual’s fixed risk factors.

Smoking

There is a dose-response relationship between smoking and atherosclerotic disease in all arterial territories. This is complicated by the fact that some individuals may smoke heavily without obvious ill effects, while others are much more susceptible to harm from smoking even a few cigarettes. The excess risk reduces rapidly when an individual stops smoking.

Hypertension

Hypertension is a progressive cardiovascular syndrome which may cause organ damage before blood pressure elevation is substantial. Hypertension cannot therefore be classified solely by strict blood pressure thresholds.

The International Society of Hypertension defines hypertension as systolic pressure over 140 mmHg and diastolic pressure over 90 mmHg. These levels are arbitrary, since the risk of ischaemic heart disease and stroke rises steadily across the whole range of blood pressure and only around one-third of strokes occur in patients with ‘hypertension’. The effect of the entire population lowering their blood pressure by only 5 mmHg by lifestyle changes would be dramatic, reducing heart attacks by nearly a quarter and strokes by a third.

Cholesterol

Like hypertension, the definition of hypercholesterolaemia is arbitrary and the risk of vascular disease rises steadily across the whole range of blood cholesterol concentrations. Treating patients with established vascular disease with statins provides protection against heart attack and stroke even for patients with normal cholesterol levels, an effect mediated by stabilisation of atherosclerotic plaque.

Exercise

Regular aerobic exercise confers considerable protection against myocardial infarction. Thirty minutes of moderate activity most days of the week is the current recommendation. Cardiac arrest is five times more likely during vigorous exercise but individuals who regularly undertake such activity still have only half the risk of fatal heart attack compared to those who remain sedentary.

Diabetes

Patients with diabetes are at greatly elevated risk of vascular disease in all territories (cardiac, carotid and peripheral). Good diabetic control improves prognosis.

Alcohol

Heavy drinkers tend to have higher blood pressure but those who consume modest quantities of alcohol on a regular basis have lower mortality rates than teetotallers (the J-shaped curve).

Homocysteine

The blood level of this amino acid is an independent risk factor for arterial disease and increasing intake of vitamin B₆ and folate effectively reduce homocysteine concentrations. It is not yet clear whether this will be an important way of reducing atherosclerotic disease.

Aneurysms

An aneurysm is an abnormal dilatation of a blood vessel. They may either rupture causing bleeding, or thrombose causing distal ischaemia. The two commonest sites for aneurysms are the infrarenal aorta (often in association with iliac aneurysm) and the popliteal artery.

Thoracoabdominal aortic aneurysms (TAAAs)

The aetiology of TAAAs is different from infrarenal AAAs, with medial degeneration and dissection being more common. Patients are often symptomatic with back pain due to compression of surrounding structures. Prognosis for large or symptomatic TAAAs is poor with only about 25% 5-year survival without treatment.

Surgery is high risk, especially for extensive aneurysms. Open repair involves an extensive thoracoabdominal exposure. Spinal cord ischaemia due to damage to intercostal vessels and the artery of Adamkiewicz may cause paraplegia. Manoeuvres such as reimplantation of the larger intercostal vessels, intraoperative hypothermia and CSF drainage may protect the spinal cord from ischaemia.

Endovascular repair is the preferred treatment for aneurysms of the thoracic aorta. Branched and fenestrated stents grafts allow endovascular grafting of complete aneurysms involving visceral branches of the aorta. Hybrid surgical/endovascular procedures are increasingly used for aneurysms of the aortic arch.

Infrarenal abdominal aortic aneurysms

The infrarenal aorta is considered aneurysmal if its diameter exceeds 3 cm. The natural history of AAAs is gradual enlargement until rupture occurs. Ruptured AAA accounts for around the same number of deaths per year as upper GI malignancies. Males are eight times more likely to be affected (1 in 20 men over 65 have an AAA) but females with an aneurysm are more prone to rupture.

The main risk factors are age, male gender, smoking and family history. The aneurysm wall becomes chronically inflamed, elastin and collagen are degraded and vascular smooth muscle cells are lost, leading to weakening and dilatation of the aorta. The risk of rupture rises sharply once the diameter exceeds 6 cm; therefore repair is advised for aneurysms over 5.5 cm in all but very unfit patients.

Most AAAs are asymptomatic until they rupture. Screening programmes reduce deaths due to aneurysms. Many AAAs are detected incidentally during investigation for other problems.

Clinical examination is unreliable for diagnosing and measuring AAAs. Ultrasound is highly sensitive and specific, and is used to diagnose and monitor aneurysm growth. Once an aneurysm has reached 5.5 cm and repair is indicated, CT scanning is vital to define aneurysm anatomy and determine whether endovascular or open repair is appropriate.

Open repair comprises replacement of the aneurysmal aorta with a Dacron graft sutured into place just below the renal arteries (p. 376). Mortality for elective surgery is around 5–10%, higher for less fit patients. Smoking, reduced FEV, impaired renal function and female gender are adverse risk factors.

Endovascular aneurysm repair (EVAR) allows a stent-graft to be delivered inside the aneurysm via the femoral artery, then expanded and fixed in position under fluoroscopic guidance (Fig. 13.1). The whole procedure is performed via small groin incisions, or even percutaneously in some cases. Recovery is quicker than for open repair and less fit patients can be treated. The mortality for EVAR is less than 2%, one third of that for open repair. Long term complications of EVAR include endoleaks, graft migration, iliac limb occlusion and aneurysm rupture. Long term surveillance with duplex scanning ± CT is required.

Figure 13.1 Schematic depiction of an endovascular repair of an abdominal aortic aneurysm with a bifurcated stent-graft.

(© 2012 W L Gore & Associates, Inc, with permission.)

Ruptured AAA (p. 96)

The presentation of a ruptured aortic aneurysm is very variable depending on the size and site of the rupture. This commonly leads to diagnostic confusion. Misdiagnoses such as ureteric colic and pancreatitis may lead to delayed diagnosis with disastrous results.

A large leak, especially one which ruptures into the peritoneal cavity, causes a swift death. Other patients have a contained retroperitoneal bleed causing pain of sudden onset which is severe and continuous, in the central abdomen and radiates to the back. The site of pain may be very variable and may be felt only in the back, or one or other flank. The signs of acute haemorrhage; tachycardia, hypotension, vasoconstriction and depressed conscious level, depend on the size of leak. In many patients the initial rupture is contained and tamponaded by the periaortic tissue and posterior peritoneum to the extent that no haemodynamic disturbance occurs, indeed the patient may even be hypertensive during this early stage. The aneurysm may be palpable as a pulsatile expansile mass in the epigastrium, but even a large aneurysm may be difficult to feel, and haematoma surrounding the aorta may mask the aortic pulsation. For these reasons, the abdominal signs of aortic aneurysm rupture are not as clear-cut as might be expected.

Immediate management of suspected ruptured AAA

The diagnosis is made on clinical grounds. Call the duty vascular surgeon and anaesthetist immediately. Give 100% oxygen, put up two large-bore IVs and take blood for FBC, U&E, amylase, clotting and cross-match. Request at least 10 units of blood and inform the haematologist that fresh frozen plasma and platelets are likely to be required urgently. Pass a urinary catheter. Do not give excessive IV fluids to patients who are conscious: a systolic pressure of 80 mmHg is more than adequate. Excessive fluid at this stage only increases bleeding into the abdomen and makes the operation more difficult. Treatment is immediate aneurysm repair and nothing should delay transfer to the operating theatre. Time spent in A&E doing X-rays, ECGs, and central lines may be lethal; these can be done in theatre.

For open repair, the anaesthetic must be induced on the operating table after preparing and draping the abdomen. As soon as the muscle relaxant is given, the abdominal muscles become paralysed and the blood pressure may collapse. It is then a race against time to get a clamp on the aorta above the leak. The rest of the operation proceeds along the same lines as for elective repair.

For emergency endovascular repair, the procedure is performed using local anaesthetic infiltration of the groins for femoral artery exposures.

In stable patients where the diagnosis is not clear, a CT scan is crucial. This confirms or excludes the presence of a ruptured aorta and may also detect pancreatitis or ureteric obstruction, the two main differential diagnoses.

An ultrasound scan is not sufficient to exclude a rupture in patients who have an AAA.

Popliteal aneurysms

The popliteal artery is usually considered aneurysmal if its diameter exceeds 1 cm. The risk factors are the same as for AAAs, indeed around 20% of individuals with a popliteal aneurysm also have an AAA, and vice versa. Rupture is rare (under 4%) but embolisation (causing chronic critical limb ischaemia) and thrombosis (causing acute limb ischaemia) are common. Mural thrombus lining the aneurysm sac leads to chronic microembolisation over many years causing severe damage to the distal small arteries. When the patient finally presents with critical limb ischaemia the situation may be difficult to salvage since successful bypass requires a patent distal vessel to accept a graft. For this reason popliteal aneurysms greater than 2–3 cm in diameter should be treated with femoropopliteal vein bypass with ligation of the proximal and distal ends of the aneurysm. Such surgery for asymptomatic popliteal aneurysms is very successful with 5-year graft patency of around 80% and limb preservation of over 95%. If treatment is delayed until the aneurysm becomes symptomatic, the outcome is poor, with nearly 20% of limbs requiring amputation.

Endovascular covered stenting is an alternative for patients with no suitable vein for bypass, or who are unfit for surgery.

Other peripheral aneurysms

True aneurysms of the femoral artery are much less common than the popliteal variety. Rupture is rare but symptoms result from local compression or distal ischaemia due to embolisation. Treatment is usually surgical reconstruction.

Visceral artery aneurysms

Aneurysms involving the splenic, hepatic and mesenteric arteries are rare. Splenic aneurysms are four times commoner in females and hepatic aneurysms more frequent in men. Multiple aneurysms in the same patient are usually associated with a connective tissue abnormality such as Ehlers–Danlos syndrome. Rupture is uncommon but may be fatal. Endovascular coil embolisation is the treatment of choice.

Mycotic aneurysms

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