Managing Lower Limb Arterial Insufficiency, the Diabetic Foot and Major Amputations

Introduction

The specialty of vascular surgery has evolved over the last 60 or so years, with a move towards more noninvasive imaging and greater use of endovascular revascularisation.

Peripheral atherosclerosis is well recognised as a marker for coronary and cerebrovascular atherosclerosis (approximately 30% 5-year mortality in intermittent claudication and 50% in patients with critical limb ischaemia), and best medical therapy (antiplatelet agent, statins, optimal blood pressure treatment and diabetic control, smoking cessation, exercise) is often more important than dealing with the leg problem in claudicants.

Chronic lower limb arterial insufficiency can cause mild to severe intermittent claudication or when more advanced, rest pain/ulceration/distal gangrene. It can also be asymptomatic or picked up on screening (e.g., for diabetic foot).

Chronic Lower Limb Ischaemia

Intermittent Claudication

Symptoms

Intermittent claudication is the usual presentation of lower limb peripheral arterial disease (PAD). It more often affects men and is present in 5% of the male population over 65 years. The patient experiences cramping pain in leg muscles on walking, which is relieved by rest. The calf is involved first because the superficial femoral artery is the most commonly affected with atherosclerosis. If arterial disease is mainly more proximal (i.e., iliac artery), the pain may ascend to the thigh or the buttock if walking continues. The distance before onset of pain is remarkably reproducible and is reduced by walking uphill.

Symptom onset is usually insidious and often attributed to musculoskeletal causes. The patient seeks medical advice only when symptoms have lasted a few months without improving. Risk factors for intermittent claudication are the same as any atherosclerotic disease, and patients often also have ischaemic heart disease (angina, previous myocardial infarction [MI], coronary artery bypass grafting [CABG]) or cerebrovascular disease (previous stroke or transient ischaemic attack). Intermittent claudication is about twice as common in diabetic patients as in nondiabetics. Nearly all have smoked cigarettes at some stage. The severity of PAD increases with the number of cigarettes smoked, with heavy smokers having a fourfold risk of claudication. Even one cigarette a day has been shown a significant risk factor for atherosclerosis, as is passive smoking. Nonsmokers affected invariably have other risk factors; most are hypertensive, who have a 2.5- to fourfold age-adjusted risk of developing PAD, depending on gender. The presence of coexisting risk factors increases the risk exponentially, particularly cigarette smoking. Polycythaemia is a rarer causative factor. There is also some evidence of genetic prothrombotic disorders clustering in male relatives of men with PAD.

Physical Signs of Intermittent Claudication

Peripheral pulses are usually absent or reduced on the affected side but local examination is otherwise unremarkable. The dorsalis pedis, posterior tibial and popliteal pulses are almost invariably absent; the femoral pulse is weak or absent in about 30%. Trophic (nutritional) skin changes are rarely present. General systematic examination should seek other signs of atherosclerosis likely to bear on management and prognosis.

Natural History of Intermittent Claudication

The Fate of the Leg

The clinical course of intermittent claudication is largely benign. Three-quarters of patients either stay the same or spontaneously improve their walking distance. Only 2% with claudication later progress to major amputation. Continued smoking increases the risk of needing reconstructive surgery or major amputation. Patients with diabetes have a higher risk of major amputation in part because of significant distal vessel atherosclerosis.

The Fate of the Patient

Lower limb PAD is a marker of systemic atherosclerosis. The severity of PAD (as estimated by ankle brachial pressure index, ABPI) is associated with increasing coronary artery disease and overall mortality rate. Some 10% of claudicants have a nonfatal cardiovascular event (MI or stroke) within 5 years and the 5-year mortality rate is 30%, with three quarters being cardiovascular events. Smoking increases mortality amongst claudicants by 1.5 to 3.0 times.

Severe Ischaemia

Severe lower limb ischaemia most commonly presents in patients who are generally older and less physically active than typical claudicants.

The first manifestations of severe ischaemia develop in the foot (most distal from the heart) and can include:

intolerable rest pain initially at night, later becoming continuous during the day;
trophic skin changes—atrophic shiny red skin of the leg; ischaemic ulcers between toes, in foot pressure areas or on the leg;
patchy necrosis of the toes or skin of the foot;
positive Buerger test;
failure of trivial injuries to heal;
extreme vulnerability of feet to pressure sores.

If untreated, a very small proportion improve and lose their pain, but most continue with intolerable pain or progress to necrosis. Once the deep tissues of the foot become necrotic, local defences are overwhelmed and infection spreads widely in vulnerable ischaemic tissue, especially in diabetics. This causes wet gangrene and, ultimately, death from sepsis and multiorgan dysfunction. This sequence rarely runs its course since rest pain is so severe and signs of sepsis so obvious that vascular reconstruction or amputation becomes unavoidable.

Critical Ischaemia

Critical ischaemia occurs when arterial insufficiency is so severe that it threatens the viability of foot or leg. This is formally defined by a European consensus document as follows: persistently recurring rest pain requiring regular analgesia for more than 2 weeks, or ulceration or gangrene affecting the foot, plus an ankle systolic pressure of less than 50 mmHg ( Note : in diabetics, absent ankle pulses on palpation replace pressure, as calcification may give falsely high pressure readings).

Managing Lower Limb Ischaemia

Investigation of Chronic Lower Limb Arterial Insufficiency

How far to investigate a patient with symptomatic ischaemia depends on the clinical picture (claudication vs. critical ischaemia) and, in claudication, whether it seriously impairs quality of life. Note that patient-reported claudication distance is unreliable and is not alone an indication for treatment. All patients with critical limb ischaemia should be considered for revascularisation.

Ankle Systolic Pressure and the Ankle Brachial Pressure Index

Patients with claudication should have resting ankle systolic pressures measured in clinic to confirm the diagnosis. Pressure is measured using a Doppler ultrasound flow detector (see Fig. 5.8 , p. 67). Normal pressure is slightly above brachial systolic, whilst patients with claudication usually range between 50 and 120 mmHg. Results are often expressed as a ratio, the ABPI , with normal values from 0.9 to 1.2. Note that Doppler pressures can be misleading; experience is needed in taking and interpreting measurements, and radical treatment should not be based on random pressure measurements. Values may be spuriously elevated in diabetics owing to calcification in the arterial media which prevents cuff compression. In nonclassical exercise-induced leg pain or those with a good history of claudication, but normal resting ABPI, a treadmill test with pre- and postexercise pressure or ABPI helps the diagnosis. A drop in ankle pressure after exercise gives an indication of arterial disease severity and the recovery rate an indication of collateral compensation.

Duplex Ultrasonography

This combines greyscale ultrasound imaging (GSUS) and colour Doppler flow estimation. GSUS allows estimation of plaque narrowing and colour Doppler allows estimation of flow velocities, which increase in areas of stenosis. These methods provide a ‘road map’ of atherosclerosis in the arterial tree and are usually performed in a vascular laboratory by specialist ultrasonographers. It is noninvasive and does not require intravenous contrast media. There is a high degree of operator dependency in the results. Other noninvasive imaging modalities include computed tomography (CT) and magnetic resonance (MR) angiography.

Arteriography (See Ch. 5 )

Arteriography should be reserved for patients thought to require angioplasty or reconstructive surgery. It maps the arterial system ( Fig. 41.1 ), showing sites and severity of stenoses and occlusions, the quality of inflow (arteries feeding the area of concern) and the runoff (arteries beyond the main obstruction, Fig. 41.2 ). Arteriography is sometimes used wrongly by nonspecialists to assess chronic arterial insufficiency, but it does not measure blood flow to the tissues or dynamic circulatory responses to exercise; it helps only with the mechanics of revascularisation. Traditional arteriography was performed via direct arterial puncture, but carries risks of vessel trauma, and high doses of contrast aggravate chronic renal impairment. It is being replaced by less invasive CT and MR angiography, which use lower doses of intravenous contrast.

Fig. 41.1, Typical Patterns of Lower Limb Arterial Disease.

Fig. 41.2, Arteriograms Comparing the Normal With Typical Patterns of Arterial Obstruction Affecting the Lower Limbs.

Approach to Management of Chronic Lower Limb Arterial Insufficiency

Treatment options range from conservative or ‘expectant’ treatment for most, to reconstructive procedures for the few with severe ischaemia. Treatments are summarised in Box 41.1 .

BOX 41.1

Treatment Options for Chronic Lower Limb Ischaemia

Mild to Moderate Claudication

No active treatment except advice to stop smoking, exercise regularly, take statin and aspirin, lose weight
Endovascular management

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