The CEAP classification for chronic venous disease categorises disease severity. A patient with active venous ulceration at the medial malleolus is classified as CEAP class C6. The pathophysiological mechanism most specific to ulcer formation in chronic venous insufficiency is:
- A Leucocyte trapping in the microcirculation causing fibrin cuffs and pericapillary inflammation ✓
- B Arterial insufficiency causing tissue ischaemia at the malleolus
- C Lymphatic obstruction causing lipodermatosclerosis
- D Deep vein thrombosis causing acute limb ischaemia
Explanation
The Browse-Burnand hypothesis explains venous ulceration: sustained venous hypertension causes leucocyte (neutrophil and monocyte) trapping in dermal capillaries, release of proteases and free radicals, and deposition of fibrin as a diffusion barrier (pericapillary fibrin cuff). This creates local tissue hypoxia and ulceration. The fibrin cuff theory has partially been superseded but leucocyte-mediated microvascular injury remains central. Lymphoedema causes skin changes but not the typical venous ulcer mechanism. Arterial insufficiency produces pale, painful, non-dependent ulcers.
Reference: Bailey & Love's Short Practice of Surgery, 27th ed.
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Written and medically reviewed by the StethoPrep medical team.