Pericapillary fibrin cuffs in venous disease. A reappraisal.

Abstract

Over the last several years, a number of hypotheses have been proposed to explain the pathogenesis of venous ulceration. According to an early model suggested by Browse and Burnand, pericapillary fibrin cuffs, developing as a result of venous hypertension and extravasation of fibrinogen, act as a barrier to the diffusion of oxygen and nutrients; ultimately, tissue anoxia, cell death, and ulceration would follow. More recent hypotheses include the idea that macromolecules leaking from the vasculature trap growth factors and adhesion molecules, and the notion that white blood cells adhere to and damage endothelial cells in the microcirculation. To review the available evidence for or against a pathogenic role of fibrin cuffs, and hope to provide a useful perspective for this controversial topic. We have reviewed the different hypotheses for venous ulceration and the evidence for and against fibrin cuffs acting as a barrier. Venous ulceration is likely to be the result of a number of distinct pathogenic events. Pericapillary fibrin cuffs remain a prominent feature, whether they act as a barrier, a marker for endothelial cell damage, or as part of an overall mechanism of macromolecular leakage and trapping.