The fate of the leg: The clinical course of intermittent claudication is largely benign. Three quarters of patients either stay the same or improve their walking distance. Only 5–10% with claudication will need endovascular or surgical intervention by 5 years for worsening claudication or severe limb ischaemia. Only 2% with claudication progress to needing major amputation. Smoking increases the risk of reconstructive surgery or major amputation. Patients with diabetes have a higher risk of major amputation in part due to small and 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 the overall mortality rate. Some 10% of claudicants have a non-fatal cardiovascular event (myocardial infarction or stroke) within 5 years and the 5-year mortality rate is 30% with ¾ being cardiovascular. Smoking increases mortality rates amongst claudicants by 1.5–3.0 times.

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 artificially elevate pressures).

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.

Duplex ultrasonography: This combines greyscale ultrasound imaging (GSUS) and colour Doppler blood 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 non-invasive and rarely requires intravenous contrast media. There is substantial user dependency in the results.

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.

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.

Mild to moderate claudication: Most patients are optimally treated with best medical management and lifestyle advice. Symptoms often improve spontaneously over 6–18 months, especially if the patient stops smoking, exercises regularly and loses excess weight. Simple advice to walk more slowly and use a walking stick often greatly extends the claudication distance. Supervised exercise programmes produce a sustained increase in walking distance but need to continue for at least 3 months to show benefit—there is often a problem with compliance. These programmes are not yet offered in the NHS.

Disabling claudication: Disabling claudication usually requires treatment unless the patient is too unfit even for angiography. Symptoms may include severe exercise restriction in younger patients or markedly worsening symptoms, especially if proximal arterial obstruction is the cause (shown by absent femoral pulses), which is often easily treated by angioplasty. Reconstructive surgery is sometimes needed.