Vascular and endovascular surgery

Chemical injury

The main risk factor for the development of atherosclerosis is smoking. Hypercholesterolaemia and hypertriglyceridaemia are also important risk factors. Arterial disease is more common in patients with diabetes, who have disordered glucose and lipid metabolism.

Physical injury

Atheroma often appears first where blood flow exerts high levels of shear stress on the arterial wall, for example, at vessel bifurcations. Hypertension, which increases this stress, is an important predisposing factor for arterial disease.

Lipid deposition

Injury increases the permeability of the endothelium to lipids and inflammatory cells, which become deposited in the subendothelial layer. At this point, atheroma forms a discoloured but flat yellow patch (fatty streak).

Inflammatory cell infiltrate

Leucocytes adhere to the overlying damaged endothelium, migrate into the subendothelial space, digest lipid to become ‘foam’ cells and liberate free radicals and proteases that destroy the arterial wall. They also liberate cytokines, which attract further leucocytes and smooth muscle cells from the media. The overlying endothelium becomes increasingly ‘sticky’, leading to platelet deposition and thrombosis.

Smooth muscle cells

Smooth muscle cells migrate from the media into the subendothelial space and begin to proliferate. They take on the properties of fibroblasts and lay down collagen. At this stage, the atheroma is raised and encroaches upon the lumen of the artery.

Plaque rupture

At this point, the plaque comprises a thin ‘cap’ of endothelium stretched over a mass of lipid and inflammatory and smooth muscle cells. Intraplaque haemorrhage from immature new blood vessels that infiltrate the lesion (angiogenesis) weakens the plaque. Further chemical and/or physical injury can lead to rupture and the exposure of highly thrombotic plaque contents to the flowing blood. This results in acute thrombotic occlusion of the vessel and/or distal embolisation. It is this sudden decompensation that leads to the most serious and dramatic clinical presentations of arterial disease. Rupture can also occur in a plaque that has hitherto been completely asymptomatic.

Haemodynamic mechanism

An atheromatous plaque must reduce the cross-sectional area of an artery by about 70% to cause an appreciable drop in flow at rest, a so-called ‘critical stenosis’. However, on exertion—for example, walking—a much lesser stenosis may become flow limiting. The reason for this is that the pressure drop across a stenosis is proportional to the square of the velocity of the blood entering that stenosis; on exercise, blood velocity increases markedly. The clinical consequence of this is that the lesion only becomes symptomatic on exertion. This type of mechanism tends to have a relatively benign course; IC as a result of SFA stenosis is a common example.

Thrombosis

By the time a ‘critical’ stenosis occludes, the collateral supply may be so well developed that the event is clinically silent. However, if a plaque that has been causing little or no haemodynamic impairment suddenly ruptures, then acute thrombosis of the vessel can have severe consequences. Such an event can cause MI (coronary arteries) or stroke (internal carotid artery) in a previously asymptomatic patient.

Atheroembolism

The effect that embolising plaque contents (predominantly cholesterol) or adherent thrombi (predominantly platelets) have upon the distal circulation depends on the factors outlined previously, in addition to the embolic load. Perhaps the best-known example is atheroembolism from an internal carotid artery plaque, which can cause small, discrete and temporary areas of cerebral and retinal ischaemia that manifest clinically as TIA and amaurosis fugax. If the embolic load is high, however, these emboli may cause irreversible occlusion of major distal vessels, leading to stroke and retinal infarction (monocular blindness).

Thromboembolism

The most common source of thromboembolism in high-economic countries is from the left atrial appendage in association with atrial fibrillation (AF). Historically, and in low- and middle-economic countries, valvular heart disease, usually from rheumatic heart disease, was the predominant source of cardiac thromboemboli. The clinical consequences are usually dramatic because the thrombus load is often large and tends to suddenly and completely occlude a large or medium-sized vessel that has previously been healthy and around which there is therefore no collateral supply. This is an important cause of stroke and acute limb ischaemia.

Symptoms

Chronic lower-limb ischaemia presents as two distinct clinical entities, IC and CLTI, which have different epidemiologies, natural histories, treatments and prognoses (see following discussion).

Examination findings

On examination, the chronically ischaemic limb is usually characterised by the following:

• Skin that is thin and dry

• Pallor, particularly on elevation. Upon dependency, the foot becomes bright red; this is known as dependent rubor or ‘sunset foot’ and is a result of reactive hyperaemia—the microcirculation of a severely, chronically ischaemic limb is vasodilated to maximise extraction of oxygenated blood (Buerger’s test).

• Superficial veins that fill sluggishly in the horizontal position and empty upon minimal elevation (venous guttering)

• Nails that are brittle and crumbly

• Muscle wasting

• Reduced temperature

• Pulses that are weak or absent and sometimes associated with thrills on palpation and bruits on auscultation

Ankle-to-brachial pressure index

The ratio between the ankle and brachial blood pressures is a simple method of diagnosing peripheral arterial disease. An ankle-to-brachial pressure index (ABPI) of <0.9 is 90% sensitive and 95% specific for diagnosing lower-limb arterial disease. The latter is recorded in the normal way, the former using an ankle cuff and a handheld Doppler device ( Fig. 22.4 ).

22.1 Summary

Intermittent claudication

• IC is the most common manifestation of peripheral arterial disease, affecting up to 1 in 20 people over 60 years of age.

• Limb loss is uncommon (1–3% over 5 years), but myocardial infarction and stroke are 3 times more common than in a nonclaudicant population (up to 5–10% per year).

• The mainstays of treatment are risk-factor modification (most importantly, complete and permanent smoking cessation), statin and antiplatelet (aspirin, clopidogrel) therapy and (supervised) exercise. This so-called best medical therapy (BMT) leads to a clinically significant improvement in walking distance in the majority of patients; more importantly, it improves health-related quality of life and increases longevity.

• Normally, patients should not be considered for surgical or endovascular intervention until they have been compliant with BMT for at least 6 months; intervention in the face of continued smoking is very unlikely to produce meaningful or durable benefit and is cost-ineffective.

• Intervention includes angioplasty, stenting and bypass surgery. Long-term results are generally much better in the larger-sized vessels of the aorto-iliac segment than below the inguinal ligament.

Clinical features

Because lower-limb arterial disease most frequently affects the SFA ( Fig. 22.5 ), IC is usually characterised by pain on walking in the muscles of one or both calves. If the iliac arteries are affected, then that pain may also be felt in the thigh and even the buttock (internal iliac disease). The pain comes on after a reasonably constant ‘claudication distance’ and usually subsides rapidly and completely on cessation of walking. Resumption of walking causes the pain to return. These and other features distinguish it from neurogenic and venous claudication ( Table 22.1 ).

Typically, the SFA first becomes narrowed at the adductor canal ( Fig. 22.6A ). Ankle pulses may be palpable but are diminished, and a bruit may be heard at or below the stenosis. The ABPI is often (near) normal at rest but falls after exercise.

With time, collateral arteries arising from the PFA enlarge and elongate so that they carry a higher proportion of the blood flow to the lower leg. As a result, in the majority of patients, symptoms gradually improve or even disappear. However, very occasionally, the stenosed SFA undergoes an acute thrombotic occlusion (see Fig. 22.6B ). This may lead to a sudden deterioration in walking distance or even an acutely ischaemic limb. Ankle and popliteal pulses will be absent at this stage.

The evolution of the collateral circulation may lead to an improvement in symptoms and walking distance. This phase of moderate claudication can remain stable for several years. However, without BMT (see following discussion) and risk-factor modification, the atherosclerosis will progress to involve other segments, such as the aortoiliac, PFA, and tibial vessels (see Fig. 22.6C ). The IC will progress to become severe, restricting the patient’s ability to walk to less than 100 m; the scope for spontaneous improvement diminishes steadily. As the disease progresses further in site and severity, symptoms may worsen to a point where chronic limb-threatening ischaemia (CLTI) develops as a result of multilevel disease (see Fig. 22.6D ). Such patients will often go on to develop night/rest pain and are at risk of limb loss (see following discussion).

An understanding of this cyclical pattern of exacerbation and resolution in IC is important because spontaneous improvement may mislead the patient into thinking all is well and that there is no longer a need to comply with medical advice (see following discussion)—and in particular, that they can continue to smoke.

Epidemiology

IC affects up to 5% of people aged over 60 years. Provided patients comply with BMT, only a small proportion (1–2%) of those affected by IC will deteriorate to a point where amputation and/or revascularisation to prevent amputation is required. However, the annual mortality rate is 5% to 10% per year, which is 2 to 3 times higher than the rate for an age- and sex-matched nonclaudicant population. A diagnosis of claudication is associated with a 5-year risk of death of 25%, similar to a diagnosis of breast cancer or lymphoma. This is because IC is a marker of widespread atherosclerosis, with the attendant risk of cardiovascular events and deaths from MI, stroke and limb loss. The emphasis is therefore on the prolongation of life; in most patients, measures to reduce cardiovascular events will also improve the functional performance of the patient.

Night and rest pain

Ischaemic ‘night pain’ typically develops in the forefoot a few hours after going to bed. The pain results from the accumulation of anaerobic metabolites (acidosis) as a result of inadequate delivery of oxygenated blood to the distal foot. Hypoperfusion develops from the loss of the beneficial effects of gravity and from normal circadian physiology that causes cardiac output to fall at night. The pain is extreme and wakes the patient from sleep. At first the pain may be relieved by dangling the leg out of bed to restore the advantage of gravity, but as the disease progresses, the patient has to get up and walk about to gain relief. Patients typically resort to sleeping seated in a chair. This causes dependent oedema and increases interstitial tissue pressure, further reducing arterial perfusion. The patient is then in a vicious cycle of increasing pain and sleep loss. At this point, even a minor injury to the foot will fail to heal, and the entry of bacteria leads to infection and an increase in the metabolic demands of the foot. The result is the rapid formation of ulcers, gangrene and, without treatment, limb loss and death.

Diabetic vascular disease

Approximately 40% of patients with CTLI have diabetes, and such patients pose a number of unique problems for vascular specialists:

• Arteries are often calcified, leading to vessel incompressibility, which results in spuriously high ankle pressures and inaccurate ABPI measurements and also impairs imaging with duplex ultrasound or computed tomography (CT) angiogram.

• Calcified vessels make surgery and angioplasty technically difficult.

• Impaired immune responses to foot infections

• Severe multisystem arterial disease (coronary, cerebral and peripheral), which increases the risks of intervention

• In the lower limbs, diabetic vascular disease has a predilection for the infrapopliteal vessels. Although vessels in the foot may be spared, the technical challenge of performing a satisfactory bypass or angioplasty to these small-calibre vessels is considerable.

• Altered foot biomechanics and frequent coexisting neuropathy may lead to altered distribution of forces through the foot, resulting in ulceration in its own right (see following discussion).

The diabetic foot

The term diabetic foot refers to the combination of ischaemia, neuropathy, biomechanical change and immunocompromise that renders the feet of diabetic patients vulnerable to ulceration, sepsis and gangrene. Diabetic neuropathy affects motor, sensory and autonomic nerves.

Sensory neuropathy

Sensory neuropathy renders the patient incapable of feeling pain. Minor trauma—for example, from a stone in the shoe—remains unnoticed. Even severe ischaemia and/or tissue loss that would prompt a patient with intact sensation to seek urgent medical advice may be completely painless in individuals with diabetes. For this reason, patients with diabetes often present late, with extensive destruction of the foot. Sensory neuropathy also affects proprioception such that, when walking, pressure is applied at unusual sites. This leads to ulcer formation and even joint disruption (Charcot’s joint).

Motor neuropathy

The normal structure and function of the foot depend not only on ligaments but also on the long and short flexors and extensors of the calf and foot. The former is affected more than the latter by motor neuropathy, leading to weakness and atrophy. The result is that the long extensors of the toes are unopposed, and the toes become increasingly dorsiflexed. This exposes the metatarsal heads to abnormal pressure, and they are a frequent site of callus formation and ulceration ( Fig. 22.7 )

Autonomic neuropathy

Autonomic neuropathy leads to a dry foot deficient in the sweat that normally lubricates the skin and contains antibacterial properties. The result is scaling and fissuring of the skin and the creation of a portal of entry for bacteria. Abnormal blood flow in the bones of the ankle and foot resulting from a loss of autonomic control may also contribute to osteopenia and bony collapse (Charcot’s foot).

Management

If the blood supply to the foot is adequate, dead tissue can be excised in the expectation that healing will occur, provided infection is controlled and the foot is protected from pressure (so-called off-loading ). If there is ischaemia as well, the priority is to revascularise the foot, if possible. Sadly, many patients with diabetes present late, with extensive tissue loss and ‘unreconstructable’ disease, which accounts for the very high amputation rate.

Medical management

All patients with atherosclerotic vascular disease should be strongly urged to comply with BMT, which comprises the following:

• Immediate, absolute and permanent cessation from smoking. This is by far the most important intervention and prognostic factor. In the face of continued smoking, other treatments are rendered largely ineffective, and disease progression, limb loss and death (usually from cardiovascular causes) within a few years are the likely outcome.

• Control of hypertension according to current guidelines (e.g., see the National Institute for Health and Care Excellence (NICE) guideline at https://www.nice.org.uk/guidance/ng136 ).

• Control of hypercholesterolaemia according to current guidelines (e.g., see the NICE guideline at https://www.nice.org.uk/guidance/cg181 ).

• All vascular patients should be prescribed lipid-lowering drugs, usually a statin. Ideally, their baseline total cholesterol will be reduced by a third (ideally to below 4 mmol/L). Statins also stabilise atheromatous plaques and may prevent the development and progression of aneurysmal disease through as-yet incompletely understood antiinflammatory mechanisms.

• Prescription of an antiplatelet agent (for guidance, see the NICE Clinical Knowledge Summary at https://cks.nice.org.uk/antiplatelet-treatment ). This is either aspirin (75 mg daily) or clopidogrel (75 mg daily); the latter is a more effective. Anticoagulation with warfarin or direct-acting oral anticoagulants should normally be reserved for patients with AF or ischaemic heart disease.

• Regular exercise. It is widely accepted that supervised exercise in a healthcare environment is more effective than (unsupervised) simple advice to exercise.

• Control of obesity. This will help bring down blood pressure, cholesterol and the ‘strain’ of walking; diabetes will also be easier to control. Surgical and endovascular intervention are much more difficult and morbid in obese patients.

• The identification and active treatment of patients with diabetes. This includes foot care (for further information, see the guidelines of the International Working Group on the Diabetic Foot at https://iwgdfguidelines.org ).

Compliance with BMT not only increases walking distance but also affords very significant protection against cardiovascular events and improves quality of life and life expectancy. Unfortunately, many patients fail to comply and, in particular, continue to smoke. Endovascular or open surgery for IC should not normally be considered until the patient is fully compliant with BMT and that therapy has been given an adequate chance to effect symptomatic improvement. Intervention in the face of continued smoking is usually clinically and cost-ineffective and represents a poor use of healthcare resources. Revascularisation is in addition to, not instead of, BMT, a point that often has to be emphasised to patients anxious to return to their previous lifestyle-related risk factors.

By the time a patient develops CLTI, it is often the case that, without surgical or endovascular revascularisation, the limb will be lost. However, this does not in any way detract from the value of instituting BMT in such patients. On occasion, BMT may improve the condition of the leg such that intervention is not required or a lesser procedure becomes an option. In those undergoing intervention, BMT undoubtedly reduces the overall risks and increases procedural success.

Endovascular management

Balloon angioplasty (BAP), with or without stenting, can be used in the iliac, femoral, popliteal and crural arteries and is usually performed under local anaesthesia ( Fig. 22.8 ). An endovascular wire is used to navigate across a stenosis or burrow through an occluded artery. A balloon catheter is introduced over the wire, and the balloon is inflated. This enlarges the lumen by disrupting the atheromatous plaque. In occlusions and complex disease, metal stents may be deployed across the lesion to improve patency and reduce emboli from the fractured plaque. Sometimes these balloons and stents are coated with antiproliferative drugs (so-called drug-eluting balloons and stents ) that can reduce the inflammatory arterial scarring

(neo-intimal hyperplasia) that follows any intervention and can lead to restenosis and reocclusion. The success and durability of endovascular intervention diminish with distal progression down the arterial tree. Endoluminal repair of the aortoiliac segment has become the treatment of choice in most vascular units because of its high patency rates and low morbidity compared with open surgery. Infrainguinal BAP and, less commonly, stenting are also widely used in the management of IC and CLTI. The evidence base for infrapopliteal BAP is less well developed.

Intermittent claudication

Endoluminal treatment (BAP, stent) should be used selectively in patients with IC because it is associated with a 1% to 2% morbidity rate and rarely mortality. There is some evidence that patients who have intervention for claudication have poorer long-term outcomes than those who are managed with BMT and exercise. There is controversy with regard to its role in the femoropopliteal and infrapopliteal segments because of a perceived lack of durability of benefit as a result of restenosis. By contrast, most vascular specialists believe that endoluminal therapy should be considered in patients with IC resulting from aortoiliac disease (absent or reduced femoral pulses) because patients

• tend to be younger, so that their symptoms have a greater impact on their quality of life and livelihood;

• often have short-segment disease that is amenable to BAP, with or without a stent;

• often have (relatively) normal infrainguinal arteries, so that restoring flow in the aortoiliac segment effects a dramatic improvement in the perfusion to their legs;

• tend to be more symptomatic, with shorter walking distances and bilateral symptoms; and

• the long-term patency of BAP and stenting is optimal in high-flow, large-calibre vessels, leading to a durable clinical benefit in many patients.

Critical limb ischaemia

A UK randomised controlled trial comparing BAP and bypass surgery (BSX) ( http://basiltrial.com ) showed that although BAP is safer and less expensive than BSX in the short term (12–18 months), BSX (with vein) offers a more durable and complete revascularisation in the longer term (3–5 years; EBM 22.1 ). At the present time, patients with CLTI expected to only live 1 to 2 years and who do not have a suitable vein for the construction of a bypass are probably best treated by BAP where technically possible; all other patients with CLTI are probably best served by BSX. The role for endovascular therapy may increase in the future as technology improves.

Intermittent claudication

Many surgeons are reluctant to perform infrainguinal bypass surgery for IC because of the following:

• The risk of limb loss is very low with BMT.

• Those patients who fail to comply with BMT (fail to stop smoking) are those most likely to press for surgery because of ongoing symptoms. However, they are also those at greatest operative risk and those least likely to gain durable benefit from their bypass.

• Surgery is associated with a significant risk of mortality and major morbidity, with the size of that risk depending on the procedure and the patient but probably approaching 3% to 5% for infrainguinal bypass and 5% to 10% for aorto-bifemoral bypass.

• Because most patients have bilateral disease, even if they have unilateral symptoms, successful infrainguinal surgery on one side often reveals limiting IC symptoms on the other, requiring a second operation (the same for endoluminal treatment).

• Grafts have a finite patency, especially in those who fail to comply with BMT and, in particular, continue to smoke (the same for endoluminal treatment).

• As soon as a bypass graft is inserted, collaterals circumventing the original lesion shrink down. For this reason, when the graft occludes, usually suddenly, the patient is normally returned to a worse situation than before the operation. A patient who was previously a claudicant may now have acute limb-threatening ischaemia, which then forces the surgeon or radiologist to reintervene. Secondary interventions are technically more difficult and are associated with higher risk and a lower patency rate.

As with BAP and stenting, the balance of risks and benefits for open surgery is different in patients with aorto-iliac disease. Although the risk of surgery is higher, the long-term patency rates of such grafts are excellent, and one operation deals with both legs. Whatever the treatment being considered, patients must be made fully aware of the risks and benefits to enable fully informed shared decision making. These discussions must always be accurately recorded in the clinical records; it is good practice to send copies of this to the patient and the primary care doctor.

Endarterectomy

Endarterectomy involves the direct removal of atherosclerotic plaque and thrombus, and in modern vascular practice, it is largely reserved for carotid and femoral bifurcations ( Fig. 22.9 ).

Bypass grafting

For a surgical bypass operation ( Fig. 22.10 ) to be successful in the long term, three conditions must be fulfilled:

• There must be widely open high-flow arteries to act as a source for the graft (inflow).

• There must be a suitable conduit to carry blood.

• There must be widely open arteries for blood to travel into when it leaves the graft (outflow or runoff).

Two main types of conduits are available:

• Autogenous material, most commonly the ipsilateral great saphenous vein (GSV).

• Prosthetic material, most commonly expanded polytetrafluoroethylene (ePTFE) or Dacron.

The main advantage of vein is that it is lined by endothelium that is actively antithrombotic and profibrinolytic and therefore much less liable to induce coagulation than even the most inert of human-made materials. This translates into much better long-term graft patency. Vein is also much more resistant to infection (see following discussion) and less expensive. It is generally agreed that wherever possible, vein from the leg or arm should be used for infrainguinal reconstruction.

Amputation

Level of amputation

The level of amputation is determined by local blood supply, the status of the joints, the patient’s general health and the patient’s age. The broad principle is to amputate at the lowest level consistent with healing and preserving function ( Fig. 22.13 ). The more proximal an amputation, the better the arterial perfusion and healing potential. It is useful to conserve the knee joint if at all possible because the energy required to walk on a below-knee prosthesis is much less than that required to walk on an above-knee prosthesis. However, if the patient has another comorbidity or disability that would make walking with a prosthesis impossible, there is no point in attempting to conserve the knee joint at the expense of healing. A common situation is where a patient presents with a fixed flexion contracture of the knee. A below-knee amputation in such a patient is usually ill-advised because the contracture will prevent the patient from ever walking and will also result in the stump wound resting on the bed or chair, leading to poor healing and wound breakdown.

Definitions

Pathophysiology

In the UK, approximately 80% of strokes are ischaemic, and about 40%% of these are thought to be a result of atheroembolism from the carotid bifurcation. The origin of the internal carotid artery is particularly prone to atherosclerosis. The tighter the degree of stenosis, the more likely it is to cause symptoms. Athero-emboli entering the ophthalmic artery lead to amaurosis fugax or permanent monocular blindness on the same side (ipsilateral). If they enter the middle cerebral artery, they may cause hemiparesis and hemisensory loss on the opposite side (contralateral). If the dominant hemisphere is affected, there may also be dysphasia.