Morphology of chronic venous insufficiency--light and electron microscopic examinations.
The morphology of chronic venous insufficiency (cvi) as seen by light and by electron microscopy with additional immunohistological examinations is described. The course of events follows the well-known pattern of "injury and repair". The tissue injury is due to an increased capillary permeability induced by rise of the intravenous ambulatory pressure. This results in the formation of a pericapillary edema ("halo"). No evidence of a pericapillary fibrin deposition could be found, but fibrinogen might well be extravasated together with erythrocytes. The accumulation of cell debris and metabolites around the capillaries induces a secondary ("resorptive") inflammation with mobilisation of white blood cells and formation of a granulation tissue. Occlusion of small blood vessels is responsible for the development of micronecroses. These lesions have to be repaired by a new granulation tissue. Finally a fibrous scar tissue with impaired microcirculation results. Persistence of the venous stasis prevents a restitution of the tissue. Only by permanent elimination of the venous stasis, a restitution of the scar tissue may be achieved.
Leu
H J
HJ
Institute of Pathology, University of Zürich, Switzerland.
D002196:Capillaries / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology; D004907:Erythrocyte Deformability / Q000502:physiology; D006801:Humans; D008854:Microscopy, Electron; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D012867:Skin / Q000098:blood supply*; D014647:Varicose Ulcer / Q000473:pathology*; D014689:Venous Insufficiency / Q000473:pathology*