• Pain—severe but variable in intensity; affects distal part of limb

• Pallor—the ischaemic area is initially white but later becomes mottled (marbling) due to stagnation of deoxygenated blood. If this blanches on pressure, the limb is still viable. If the mottling does not blanch (fixed staining) then the limb is non-viable

• Pulselessness— foot pulses are absent and popliteal and femoral pulses may be lost, depending on level of arterial occlusion

• Perishing coldness—most extreme at foot (or hand)

• Paraesthesia (reduced sensation) or anaesthesia of the periphery. This only occurs if ischaemia is severe

• Paralysis of calf muscles. The patient is unable to flex or extend toes or ankle. This only occurs if ischaemia is extreme. Pain may disappear at this stage

The acutely cold white foot: The main cause is a sudden complete arterial occlusion by thrombosis or embolism. This is usually spontaneous but precipitating events such as trauma or frostbite will be evident from the history. Ischaemia is usually unilateral unless the abdominal aorta or both iliac arteries become obstructed. Ischaemic tissue changes reach a variable distance up the leg.

Colour change in venous thrombosis: Noticeable colour change is unusual in deep venous thrombosis but massive pelvic vein thrombosis may cause changes sometimes mistaken for arterial occlusion. Massive thrombosis was once more common, especially during late pregnancy. The condition was known as white leg of pregnancy or phlegmasia alba dolens. The whole lower limb is painful, pale and massively swollen. In contrast to arterial occlusion, the limb is warm and pulses are detectable despite the oedema. A more serious variant is blue leg or phlegmasia caerulea dolens, which represents incipient venous infarction.

The chronically cold foot:

The warm foot: Inflammatory dilatation of the microcirculation causes redness, and the skin is warm and slightly swollen because of enhanced blood flow. An example is low-grade bacterial cellulitis which may be seen in diabetes or chronic venous insufficiency or may arise unexpectedly. Note that if a severely ischaemic limb becomes infected, the usual signs of inflammation may not develop and the extent of infection may be underestimated. If blood supply is later restored, signs of inflammation appear.

Abnormal pigmentation: Brown pigmentation around the gaiter area is often caused by superficial or deep chronic venous insufficiency due to gross reflux in varicose veins or a post-thrombotic limb. In the latter, deep vein valves have been disrupted by inflammation, organisation and recanalisation following DVT. Valves thus become incompetent and allow deep venous reflux. This prevents an effective muscle pump and leads to chronic venous insufficiency. In gross superficial or deep venous reflux, standing causes venous stagnation, increased venous pressure in the leg (venous hypertension) and chronic leg swelling. Red cells extravasate into the tissues and form haemosiderin deposits which cause brown pigmentation. This, accompanied by dry, scaly, atrophic skin, is described as varicose or venous eczema (see Fig. 40.4).

History of the ulcer: Details of the initial skin lesion and how it occurred may provide clues. Minor trauma or an insect bite may initiate it but failure to heal can usually be attributed to abnormal skin nutrition. The common causes include chronic venous insufficiency, arterial ischaemia and diabetic neuropathy. The ulcer often begins insidiously with minor breakdown in a patch of atrophic skin. In venous insufficiency, the leg is often oedematous and the skin may ‘weep’ plasma.

The ulcer duration, its healing, and recurrences or change in extent or distribution give further clues. Ischaemic ulcers present early because pain becomes intolerable (except in diabetics with coexisting neuropathy and ischaemia)—see Table 40.8. In contrast, post-thrombotic and varicose ulcers are not severely painful and fluctuate between healing and breakdown. Very rarely, squamous carcinoma develops in a longstanding ulcer and is recognised by proliferative change at the ulcer margin. These are sometimes known as Marjolin’s ulcers and were first described following burns which failed to heal (Fig. 40.5). Primary skin malignancies on the leg may ulcerate, but these usually begin as a cutaneous lump.

If the patient has claudication or rest pain, this suggests an ischaemic cause (Fig. 40.6). Neuropathic or mixed diabetic ulcers tend to be painless because of sensory neuropathy (which may be the main predisposing cause). Neuropathic changes to motor nerves affect small muscles of the foot, altering its shape and pressure areas, and autonomic dysfunction results in dryness, both predisposing to ulceration. A history or strong suspicion of previous deep venous thrombosis makes venous insufficiency the likely cause.

Site of the ulcer: Post-thrombotic and varicose ulcers typically arise just above the medial malleolus and may extend circumferentially (Fig. 40.7). They rarely occur elsewhere. Diabetic neuropathic ulcers always occur on the foot either as perforating ulcers on the sole beneath metatarsal heads or at other bony prominences; these include the toes, the ball of the great toe and the malleoli (see Fig. 41.8, p. 507), but ischaemia must always be excluded first.

Arterial ulcers may occur anywhere below mid-calf. Pressure ulcers occur mainly in debilitated, elderly or unconscious patients, especially at the heel (see Fig. 12.8). Even a few minutes resting on a hard casualty trolley or operating table may initiate necrosis in an ischaemic limb. Pressure ulcers usually begin as a circumscribed patch of discolouration, becoming necrotic and later ulcerating. The heels of vulnerable patients should be nursed carefully and regularly inspected to avoid this. Treatment of pressure ulcers is difficult and prolonged and it is best to prevent them.

Characteristics of the ulcer: Most ulcers are shallow, involving only skin and subcutaneous fat. Diabetic ulcers tend to penetrate deeply into the foot, where there is necrotic and infected tissue. The base of any ulcer usually contains slough and fibrin but granulation tissue may be visible beneath. Slough should not be removed unless arterial insufficiency can be excluded. If there is proliferating tissue in the ulcer, this should be biopsied.

The edge of most chronic lower limb ulcers slopes towards the base with no diagnostic features, although epithelial proliferation growing inwards from the edge suggests healing. Diabetic foot ulcers have a characteristic ‘punched-out’ edge with abrupt transition from normal skin to the necrotic crater. On the sole, diabetic ulcers have a hyperkeratinised edge in response to excess pressure during walking caused by foot distortion and loss of sensation. Malignant ulcers may have a raised margin.

Nature of the surrounding tissues: The surrounding tissues indicate the background on which the ulcer has formed. These include colour, e.g. chronic venous pigmentation, texture, e.g. induration, and perfusion (shown by temperature, blanching response, venous filling and Buerger’s test), as well as swelling.

Regional features: Regional examination should search for diagnostic clues, e.g. peripheral pulses, inguinal lymphadenopathy (infection or malignancy), varicose veins and deep or superficial venous thrombosis.