Preulcerative Cutaneous Changes

Inflammation dominates the early skin changes that precede venous ulceration. Increased leukocyte activation and an increased expression of soluble adhesion molecules have been demonstrated. There is a perivascular infiltration of the papillary plexus capillaries. Granulation tissue composed of lymphocytes, plasma cells, macrophages, histiocytes, and fibroblasts invades the subepithelial layer. This granulation tissue is responsible for the deposition of collagen fibers.13 Collagen fibers appear to have completely lost their normal orientation in the cutaneous tissue. These lesions account for the inflammatory and post-inflammatory process of tissue fibrosclerosis: lipodermatosclerosis.

When skin at the border of chronic venous insufficiency is compared to normal skin in the same individual, the strong expression of ICAM-1 is seen in addition to a dense infiltration by T lymphocytes and macrophages. In some instances, the tissue also is infiltrated by an increased number of mast cells.14 This is the typical picture of a chronic inflammatory reaction with an upregulation of endothelial adhesion molecules and dermal infiltration by T lymphocytes and macrophages in the skin of patients with CVI.

The Perforating Veins

Incompetent perforating veins are strongly associated with superficial venous reflux, and it is still controversial whether incompetent perforating veins are the primary cause of skin changes of chronic venous insufficiency or whether the incompetent perforating veins and skin changes are the result of superficial reflux. The cause of valvular dysfunction in perforating veins is not yet fully understood (see Figure 58.1).

Despite the classic studies of Linton15 and Cockett,16 it is still not known what the exact role of incompetent perforating veins is in the development of venous ulceration. Our observations suggest that venous hypertension is closely associated with valve damage and remodeling, which produces subsequent valve incompetence.17 Therefore, it is useful to relate these findings to the valves in perforating veins.

It is well known that muscle contraction produces muscular compartment pressures in the range of 100 mm mercury

FIGURE 58.1 This reproduction of an ultrasound scan shows a perforating vein penetrating the deep fascia and refluxing into a nonsaphenous varix. It is calf muscle contraction that provides the pressure that is transmitted through a failed valve and elongates and dilates the superficial vein thus converting it into a varix.

FIGURE 58.1 This reproduction of an ultrasound scan shows a perforating vein penetrating the deep fascia and refluxing into a nonsaphenous varix. It is calf muscle contraction that provides the pressure that is transmitted through a failed valve and elongates and dilates the superficial vein thus converting it into a varix.

and higher.18 Such pressures exerted over time could initiate the cascade of molecular events, which eventuate in valvular incompetence. This valve incompetence would then produce the cutaneous "blow out" described as "spherical dilatations on veins under the skin" by Dodd and Cockett.19 Failure of perforating vein valves due to their remodeling caused by repetitive compartment pressure elevation induced by normal exercise would lead to the skin changes described earlier.

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