Therapy For Venous Ulcers Research Articles

Venous ulcers

Successful therapy of venous ulcers combines local wound treatment modalities and ambulatory hemodynamic support to control the underlying disease. Compression bandaging reduces or eliminates edema, and a moist wound environment not only debrides necrotic tissue but also aids development of granulation tissue, a prerequisite for epidermal repair. We have occluded chronic wounds, known to be heavily colonized, with a hydrocolloid dressing for up to 7 days and found that soft-tissue infections occurred in only 1% of all dressing changes in our clinic, compared with 6.5% generally reported in the literature. In venous ulcers, resident bacteria may be beneficial in that their proteolytic activity assists with autolysis of fibrinopurulent wound exudate. The importance of lysing fibrin and reducing the number of existing fibrin “cuffs,” thereby improving local tissue oxygenation and nutrient/waste exchange, is not completely understood; however, this phenomenon, in part, may explain the excellent clinical results obtained with one type of hydrocolloid dressing (DuoDERM), which has been shown to lyse fibrin more effectively than other types of moisture-retentive and hydrocolloid dressings.

Clinical parameters and transcutaneous oxygen measurements for the prognosis of venous ulcers

Few data exist on the prognosis of venous ulcers. We therefore prospectively studied 14 patients with severe venous ulcers for up to 18 months and examined various possible prognostic factors, including transcutaneous oxygen tension (TcPO 2) measurements of skin next to the ulcers. The ulcers had been present for a mean duration of 15.6 months before referral to our clinic. During the study only four patients (29%) had ulcers that were healed with conservative management consisting of topical and systemic antibiotics and conventional and occlusive dressings. We observed that the number of ulcers, their duration before admission to the study, and the extent of lipodermatosclerosis were more pronounced in the unhealed group. For all patients the mean ulcer TcPO 2 level (5.6±1.5 mm Hg, mean ± standard error) was significantly reduced when compared with the control chest site (62.4±2.1 mm Hg) ( p<0.001; paired t test). The mean ulcer TcP0 2 was not significantly different between the healed (4.5±2.0 mm Hg) and unhealed groups (6.1±2.0 mm Hg). We conclude that TcPO 2 levels may not be predictive of the response to therapy in venous ulcers. TcP0 2 levels may be markedly reduced, but even extremely low levels are not incompatible with healing.