Hyperbaric oxygen therapy (HBOT) is an important adjunct in the management of problem wounds which exist in chronic oxygen deficiency and in which the local oxygen tension is below optimal for healing. In the treatment of hypoxic and ischemic wounds, the most important effects of hyperbaric oxygenation are the stimulation of fibroblast proliferation and differentiation, increased collagen formation and cross-linking, augmented neovascularization, and the stimulation of leukocyte microbial killing. Ischemic soft tissues also benefit from hyperoxygenation through improved preservation of energy metabolism and reduction of edema. Hyperbaric oxygen is administered in either a multiplace or a monoplace hyperbaric chamber. Normally, pressures of 2 to 2.5 ATA are used for a period of 90 minutes once or twice daily. For an objective assessment of wound perfusion and oxygenation, transcutaneous oximetry provides a simple, reliable, noninvasive, diagnostic technique. It can be used for assessment of tissue perfusion in the vicinity of the problem wound. Transcutaneous oximetry may be used in the assessment of wound healing potential, selection of amputation level, and patient selection for HBOT. In diabetic patients with chronic foot ulcers peri-wound transcutaneous oxygen tensions (TcP(O2)) over 400 mmHg in 2.5 ATA hyperbaric oxygen or over 50 mmHg in normobaric pure oxygen predict healing success with adjuncted HBOT with high accuracy.

To reduce mortality and morbidity, effective treatment of Fournier's gangrene should be started promptly. Debridement and antibiotics combined with surgical intensive care must be started as soon as possible. Hyperbaric oxygen is both life and tissue saving. It is an important adjunct that prevents extension of necrosis and reduces systemic toxicity.

The effects of epidermal growth factor (EGF) on granulation-tissue formation and collagen-gene expression were studied in experimental sponge-induced granulomas in rats. After daily administration of 5 micrograms of EGF into the sponge, total RNA was extracted from the ingrown granulation tissue at days 4 and 7 and analysed by Northern hybridization for the contents of mRNAs for types I and III procollagens. EGF treatment increased procollagen mRNA, particularly at day 4. To determine whether this elevation was due to increased proliferation of collagen-producing fibroblasts or to activation of collagen-gene expression in these cells, fibroblast cultures were started from granulation tissue and treated with EGF. These experiments confirmed that EGF is a potent mitogen for granuloma fibroblasts in a dose-dependent manner. The effect of EGF treatment on radioactive hydroxyproline production in cultured cells was inhibitory. The decreased rate of collagen synthesis was also indicated by decreased amounts of procollagen mRNAs. The results suggest that the stimulation of wound healing and collagen production by EGF is due to increased fibroblast proliferation, and not to increased expression of type I and III procollagen genes.

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This work was undertaken to study the effects of tumor necrosis factor-α (TNF-α/cachectin) on developing granulation tissue in rats. Cylindrical hollow sponge implants were used as an inductive matrix for the growth of granulation tissue. In the two test groups the implants were injected daily for 4 days with a solution containing either 50 or 200 ng of TNF-α, while the implants of the control group were treated correspondingly with phosphate-buffered saline solution only. Analyses of granulation tissue and wound fluid in the sponge implants were carried out 7, 14 and 21 days after implantation. In histological specimens the ingrowth rate of granulation tissue into the sponge was significantly lower after 7 days in the group treated with 200 ng of TNF-α. No such an effect was observed after 14 or 21 days. After 7 days, the mean amounts of nucleic acids reflecting cellularity in the granulation tissue decreased dose-dependently, but nonsignificantly, in the groups treated with TNF-α. Simultaneously, the accumulation of collagen hydroxyproline of the sponge was significantly lower in the group treated with 200 ng of TNF-α than in the controls (–30%, one-way analysis of variance). This effect was not observed after 14 or 21 days. No significant differences were detected in the amounts of nitrogen, hexosamines and uronic acids between the groups, reflecting unchanged accumulation of glycosaminoglycans in the developing granulation tissue. No difference was detected in interleukin-1 activity of the wound fluid between the control and TNF-α-treated groups. These findings demonstrate that TNF-α treatment inhibits wound healing during its inflammatory phase by decreasing production of new granulation tissue. However, this effect disappears at later phases of healing.

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