Claudication, critical limb ischaemia and diabetic peripheral vascular disease
THE CONTEXT
Lower-limb peripheral arterial disease (PAD) commonly presents with intermittent claudication. Critical limb ischaemia and diabetes-associated vascular and neurological abnormalities have additional clinical implications.
Intermittent claudication
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Intermittent claudication is the most common presentation of lower-limb PAD and consists of ischaemic pain in leg muscles.
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Calf pain is usual because the superficial femoral artery is most commonly affected. Iliac artery involvement may produce thigh or buttock pain.
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Pain typically starts after walking, often after a reproducible distance, rapidly subsides with rest, and returns when walking resumes.
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Symptoms may follow cycles of exacerbation and resolution as disease progresses and collateral vessels subsequently develop.
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Upper-limb PAD can cause arm claudication, although this is uncommon.
Critical limb ischaemia
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Critical limb ischaemia is defined by rest pain requiring opiate analgesia, or ulceration or gangrene present for more than 2 weeks, in the presence of an ankle blood pressure below 50 mmHg.
Vascular and infective difficulties in diabetes
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Arterial calcification makes ankle vessels incompressible and can produce a spuriously high ankle–brachial pressure index. It can prevent arterial clamping for bypass surgery and is resistant to angioplasty.
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Immunocompromise predisposes to rapidly spreading cellulitis, gangrene and osteomyelitis.
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Coexisting coronary and cerebral arterial disease increases the risks of intervention.
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Diabetic vascular disease preferentially affects calf vessels. Foot vessels are often spared, but bypass or angioplasty involving these small vessels is technically challenging.
Neuropathy and foot damage
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Sensory neuropathy can make even severe ischaemia or tissue loss completely painless, contributing to late presentation with extensive foot destruction.
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Loss of proprioception causes abnormal pressure loading and worsens joint destruction, producing Charcot joints.
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Motor neuropathy weakens the long and short flexors and extensors, causing abnormal foot architecture, abnormal pressure loads, callus formation and ulceration.