SOME ASPECTS OF THE PATHOGENESIS OF TROPHIC VENOUS ULCERS

P.G. Shvalb, S.V. Gryaznov, A.P. Shvalb
Course of Vascular Surgery, I.P. Pavlov Ryazan State Medical University,
Ryazan, Russia

This paper deals with essentials of trophic venous ulcer pathogenesis, their criticism as well as with the treatment of some phenomena which should be taken into account when creating any new theory of the pathogenesis and essentials of the treatment of trophic ulcers. Basically, this concerns inflammation as a general biological reaction. Chronic venous insufficiency (CVI) changes capillary permeability. The paravasal space is invaded by red blood cells. On break down they secrete hemosiderin, protein molecules and lipid complexes. All this is denaturated to form substances liable to resorption. According to the biological laws resorption may be brought about only by means of inflammatory reaction, more exactly, through its cellular phases – acute (leucocytic) and chronic (macrophagal). It is assumed that the main signal for activation of leucocytes is accumulation of the above-indicated decomposition products rather than hypertension which, in non-occlusive CVI forms, cannot be proven numerically.

The basic cause of trophic ulcers lies in the permanent cellular phase of the common defence inflammatory reaction because of the presence of the non-transient injurious factor. The permanently repeated cycles of the inflammatory trio (vascular, cellular and reparative phases), being in different correlation, form in the ulcer itself an unusual system which is not governed by the regularities of wound process.

Bacterial contamination and colonization of trophic ulcer occur without fail but this process bears secondary character after impairment of barrier skin function and emergence of skin defects. At the same time different processes may take place in trophic ulcer such as exudation in the form of serous and seropurulent discharge, formation of the fibrinonecrotic deposit, formation of granulation tissue, and appearance of islets of unstable epithelialization. From the conceptual viewpoint such a state can be regarded as a system marked by closed pseudochaotic activity. To start up healing, this self-reproducing system must be destroyed while ulcer must transform to a wound with the linear sequence of processes.

KEY WORDS: chronic venous insufficiency, trophic ulcer.

P. 64

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