Severe limb ischaemia: nocturnal pain, tissue loss and diabetic autonomic neuropathy
THE CONTEXT
The passage explains progressive night pain and tissue loss in limb ischaemia, alongside the effects of autonomic neuropathy on the diabetic foot.
Autonomic neuropathy and the foot
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Autonomic neuropathy produces a dry foot deficient in sweat, which normally lubricates the skin and has antibacterial effects.
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Scaling and fissuring provide a portal of entry for bacteria.
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Abnormal blood flow in the ankle and foot bones may contribute to osteopenia and bony collapse.
Development of nocturnal ischaemic pain
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Pain typically develops in the forefoot about an hour after going to bed. Lying down removes the beneficial effect of gravity on perfusion, while blood pressure and cardiac output fall during sleep.
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Severe pain awakens the patient and is relieved by hanging the limb out of bed.
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Eventually, the patient must get up and walk about, causing loss of sleep.
Progression to tissue loss
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Sleeping in a chair leads to dependent oedema. The resulting increase in interstitial tissue pressure further reduces arterial perfusion, creating a cycle of worsening pain and sleep loss.
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A trivial injury may fail to heal. Bacterial entry causes infection and increases the metabolic demands of the foot, followed by rapid development of ulcers and gangrene.
Severe limb ischaemia
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Severe limb ischaemia includes critical and subcritical limb ischaemia.
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Intermittent claudication is usually associated with a single-segment plaque, whereas severe limb ischaemia is always associated with multilevel disease.
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Some patients have not previously sought advice because other illnesses prevent them from walking far enough to develop claudication.
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Without surgical bypass or endovascular revascularisation by angioplasty or stenting, patients risk losing their limb, and sometimes their life, within weeks or months.
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Treatment is difficult because most affected patients are older adults with extensive severe disease and major multisystem comorbidities.