Peripheral vascular disease

Epidemiology, pathogenesis and pathology

The prevalence of peripheral arterial disease increases with age (most symptomatic patients are over 60 years old); although it is twice as high in men as in women between the ages of 50 and 70 years, it almost identical after the age of 70 at around 15% to 20%.

Peripheral arterial disease is usually due to atherosclerosis of the lower abdominal aorta or the iliac, femoral and/or popliteal arteries. In common with carotid and coronary artery disease, the disease processes that exacerbate peripheral arterial disease include diabetes mellitus, hypertension, smoking, hyperlipidaemia and previous limb surgery or trauma. A significant collateral circulation may develop. If so, it is made up of pre-existing pathways arising from the distributing branches of large and medium-sized arteries. It develops over time when there is an increase in the velocity of flow through these arteries secondary to arterial occlusion that has developed in a main vascular pathway. Collateral flow can usually provide an adequate supply to the resting limb but may be insufficient to meet additional requirements associated with moderate exercise.

Clinical features

Presentation may be acute or chronic. Symptoms consist of pain, ulceration or changes in appearance, with swelling or discoloration. Lower limb ischaemia usually manifests as claudication, the most important symptom of extremity arterial occlusive disease. Chronic critical lower limb ischaemia is defined by either of the following two criteria:

• Recurring ischaemic rest pain persisting for more than 2 weeks and requiring regular analgesics. This is diagnosed with an ankle systolic pressure of below 50 mm Hg and a toe systolic pressure of less than 30 mm Hg or both.

• Ulceration or gangrene of the foot or toes, with similar haemodynamic parameters.

The classic description of claudication is of pain in a functional muscle unit that occurs as a result of a consistent amount of exercise and is promptly relieved by rest. Limp may also be pronounced. The commonest site of occlusion leading to claudication is the superficial femoral artery, resulting in pain in the calf. This occurs on walking upstairs or slopes and is relieved by rest. Less commonly, occlusive aortoiliac disease produces symptoms of pain in the thigh or buttock. Night pain experienced in the foot, relieved by either dependency or, paradoxically, by walking around, implies a reduction in blood flow to a level below that required for normal resting tissue metabolism. Typically rest pain tends to be distal to the metatarsals, severe, persistent and worsened by elevation.

Detailed examination of the peripheral vascular system is essential. Abnormalities tend to be related to changes in the peripheral arteries and tissue ischaemia. Distal pulses may be absent or diminished in amplitude and bruits (commonly femoral) may be present. Capillary return, atrophic changes and foot colour are poorly discriminatory for the diagnosis of peripheral vascular disease. Pallor may be apparent on exercise and is usually associated with pain. There may be pallor on elevation of the foot, with reactive hyperaemia on dependency: the more limited the elevation resulting in pallor, the greater the degree of stenosis (Buerger test).

As ischaemia becomes more advanced, the skin often becomes shiny and scaly, with associated atrophy of the subcutaneous tissues and muscle. In advanced stages of ischaemia, there may be red discoloration, caused by capillary blood stasis and high oxygen extraction. There may also be tissue necrosis and non-healing wounds or ulcers secondary to trauma, which may progress to gangrene.

Clinical investigations

Routine blood tests should be carried out to derive baselines for renal and hepatic function as well as to exclude anaemia, polycythaemia, hyperglycaemia, thrombocythaemia and hyperlipidaemia. In patients below 50 years of age, a thrombophilia screen should be done.

The ankle–brachial pressure index (ABPI) should be measured to confirm the clinical diagnosis. This is calculated (for each leg) by dividing the highest systolic pressure recorded at the respective ankle by the highest systolic brachial pressure obtained in recordings from both arms. Resting ABPI is normally greater than 1 and a figure of less than 0.9 indicates arterial disease. Values between 0.5 and 0.9 may be associated with claudication and below 0.5 with rest pain. Normal ABPI values may be recorded in diabetic patients, even though they have claudication, owing to the presence of medial arterial calcification and small vessel rather than large vessel disease.

Duplex ultrasound is initially used to assess the vascular tree non-invasively. Digital subtraction angiography (DSA) has now been superseded by computed tomography angiography (CTA) or magnetic resonance angiography (MRA), as they are both non-invasive and give a three-dimensional image of the disease extent. MRA is generally considered a first-line investigation if available, with CTA being used if there is a contraindication to MRA; DSA is still required if intervention (e.g. angioplasty) is planned.

Treatment

In patients with chronic stable disease, treatment is focused on preventing progression of the disease. This is usually co-ordinated by the patient’s primary care physician and consists of regular exercise (ideally a supervised exercise program), control of associated medical diseases and cessation of smoking, which is absolutely essential. Specific measures should be taken to address hyperlipidaemia, diabetes mellitus and hypertension. A low-dose antiplatelet agent (usually aspirin) should be given if there is no contraindication, but there is no benefit from warfarin therapy or dual antiplatelet therapy. Statins should be given to all patients with arterial disease. Beta blockers have been shown to be safe in patients with peripheral arterial disease.

In more advanced progressive disease, strategies to minimize other complications, including lower limb ulcers and gangrene, should also be considered. Patients presenting to the emergency department (ED) at this stage or with debilitating symptoms merit early referral for a multidisciplinary vascular assessment with a view to operative or radiological (endovascular) intervention.

Pathogenesis and pathology

Acute lower limb ischaemia, or ‘limb-threatening’ ischaemia, is associated with significant morbidity and mortality. Early recognition of the signs and symptoms is critical. Arterial occlusion will cause symptoms most obviously when there is inadequate collateral circulation. Causes may be embolic, thrombotic, traumatic or iatrogenic in nature, of which emboli are the most common. Most arterial emboli originate from thrombus formed in the heart (85%), the vast majority of these from left atrial or atrial appendage thrombus related to chronic atrial fibrillation. Other uncommon causes include arterial thrombosis due to endothelial injury or alterations in the blood flow to the limb. Iatrogenic causes may be secondary to intra-arterial cannulation, recent cardiac catheterization or angiography or ischaemic limb anaesthesia (such as a Bier block).

Clinical features

Sudden occlusion of a previously patent artery is a dramatic event. Unfortunately recognition can be difficult, particularly in the elderly or those with chronic cognitive impairment or dementia; careful examination is therefore essential. Occlusion may be portrayed by one or more of the classic signs of pulselessness, pain, pallor, paraesthesia, paralysis and ‘perishing cold’ (the ‘6 Ps’). However, none of these, either alone or in combination, is sufficient to establish or exclude the diagnosis of an acutely ischaemic limb. Loss of a palpable pulse in the symptomatic limb compared with the other side should raise significant concern.

The pain is a severe, constant ache that requires intravenous opiates for relief. The ischaemic periphery is pale, white or cadaveric in appearance and feels cold to the touch. Progression occurs with blotchy areas of cyanosis and further discoloration. Pain, tense swelling and acute tenderness of a muscle belly are late findings. If these findings persist for longer than 12 hours, irreversible ischaemia with gangrene is highly likely.