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RATIONALE: A significant body of data clearly supports the efficacy of HBO2 in the treatment of thermal injury. A reduction in fluid requirements, less conversion of partial to full thickness injury, preservation of marginally viable tissue, improved microcirculation, reduction in edema, faster epithelialization, less inflammatory response, enhancement of PMN killing, preservation of tissue creatine phosphate, adenosine triphosphate, and decreased wound lactate have all been reported. Infection remains the leading cause of death from burn injuries that are treated at burn centers. Therefore, control of infection is a major goal of therapy. Present evidence indicates that brief HBO2 exposures (2 ATA for 2 hrs) inhibit Pseudomonas aeruginosa both in vitro and in vivo. An intact microvasculature is a critical factor in the ability to provide cellular and humeral elements to the site of the injury. Any improvement in the microvasculature, whether it be preservation of intact capillaries or control of interstitial edema, would favorably influence the burn outcome. In human studies, HBO2 therapy has been shown to exert a positive, beneficial effect on the burn wound by: (1) reducing edema and plasma extravasation, (2) preserving the microcirculation, (3) preventing the conversion of partial to full thickness injury, and (4) maintaining the viability of the dermal elements which lead to a more rapid epithelialization. This has lead to a reduced need for surgery, a reduced length of hospital stay, and a reduced mortality rate. HBO2 therapy, used as an adjunct to traditional burn care, demonstrates greatest effects when initiated within the first 4 hours following the injury, or as quickly as possible. Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision. Telephone: Email: Chico Hyperbaric Center Web Site Developed & Hosted by Access Now 2000. Copyright © 1999-2001. All Rights Reserved. # |