Managing lower limb arterial insufficiency, the diabetic foot and major amputations

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Managing lower limb arterial insufficiency, the diabetic foot and major amputations

Chronic lower limb ischaemia

Intermittent claudication


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. 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 also 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 often 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 as for any atherosclerotic disease and patients often have ischaemic heart disease (angina, previous MI, coronary artery bypass grafting) or cerebrovascular disease (previous stroke or transient ischaemic attack). Intermittent claudication is about twice as common in diabetic patients as in non-diabetics. Nearly all have smoked cigarettes at some stage. The severity of PAD increases with the number of cigarettes smoked, with heavy smokers having a four-fold risk of claudication. Non-smokers affected invariably have other risk factors; most are hypertensive, with a two and a half to four-fold 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 thrombotic risk factors clustering in healthy male relatives of men with PAD.

Natural history of intermittent claudication

Severe ischaemia

Severe lower limb ischaemia most commonly presents without claudication but sometimes manifests after a period of deteriorating claudication. In general, these patients are older and less physically active than typical claudicants.

The first manifestations of severe ischaemia develop in the foot and include:

If untreated, a very small proportion improve and lose their pain, but most smoulder on 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 multi-organ 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.

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 alone, is not an indication for treatment. All patients with critical limb ischaemia should be considered for revascularisation.

The ankle brachial pressure index (ABPI): All claudication patients should have resting ankle systolic pressures measured in clinic to confirm the diagnosis, plus a full blood count to exclude polycythaemia and thrombocythaemia. Pressure is measured using a Doppler ultrasound flow detector (see Fig. 5.9, p. 72). 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 ankle brachial pressure index (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 patients with diabetes owing to calcification in the arterial media which prevents cuff compression. In non-classical exercise-induced leg pain or those with a good history of claudication but normal resting ABPI, a treadmill test with pre- and post-exercise 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.

Arteriography (see Ch. 5): Arteriography should be reserved for patients thought to require angioplasty or reconstructive surgery. It maps the arterial system (see 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, see Fig. 41.2). Arteriography is sometimes used wrongly by non-specialists to assess chronic arterial insufficiency but it cannot measure blood flow to the tissues or dynamic circulatory responses to exercise; it helps only with the mechanics of revascularisation. Traditional arteriography is performed via direct arterial puncture but carries risks of vessel trauma and high doses of contrast aggravating chronic renal impairment. It is being replaced by less invasive CT and MR angiography which use lower doses of intravenous contrast media.

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.

Conservative management: In intermittent claudication, management starts with lifestyle measures such as stopping smoking, attention to diet (reduced fat, more fruit and vegetables, weight reduction) and systematic exercise. Cigarette smoking is a primary risk factor in causing atherosclerosis and a secondary risk factor in causing deterioration, as well as causing occlusions or stenoses of angioplasty or graft after reconstruction. Symptoms are more likely to resolve (by collateral development) if the patient stops smoking. Giving up is difficult as nicotine is highly addictive but smoking cessation programmes can help as well as pharmacological aids such as nicotine replacement therapy, bupropion (Zyban) and varenicline (Champix). All family members need to give up together to reinforce the message.

Medical management is important, with blood pressure control and regular anti-platelet agents (usually aspirin) and a statin (even if cholesterol levels are normal). These measures aim to reduce mortality by treating systemic atherosclerosis, as well as encourage collateral vessels to develop. Treatment with the phosphodiesterase inhibitor cilostazol provides a small increase in walking distance but does have significant side-effects.

The degree of handicap in claudication is assessed clinically by careful history-taking and perhaps by walking with the patient. There is a marked trend towards conservative treatment these days, now we know many patients recover function and this recovery is more durable than intervention. The choice of active treatment depends on the handicap, the patient’s willingness to give up smoking, the potential for treating the pattern of atherosclerosis and the patient’s overall preference. Severe and critical ischaemia are clear indications for revascularisation (or amputation) since the symptoms cannot be tolerated in the long term.

Techniques of revascularisation for chronic arterial insufficiency

Percutaneous transluminal angioplasty (PTA): PTA involves cannulating an artery (usually the common femoral but occasionally the brachial), introducing a guide-wire into this remote artery and advancing it to lie across the stenosis. A balloon catheter is passed over the wire and into position (see Fig. 41.3) and the balloon inflated to a high pressure (5–15 atmospheres), crushing the atheroma into the arterial wall to relieve the obstruction. Success is very operator-dependent and also depends upon the site, length and nature of the diseased artery. PTA is most effective for isolated short stenoses in iliac arteries. With increasing experience, longer stenoses and occlusions in smaller vessels can be tackled, avoiding the need for major surgery. The method is less successful for distal calf arteries. Angioplasty often provides symptom improvement for a few years but disease progression (and failure to modify lifestyle) is a limiting factor.


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