J. Paul Waymack

Cultured epithelial autografts have been advocated for permanent closure of skin surfaces after massive thermal injuries. A 10-year-old boy sustained a nearly 100% total body surface area burn (98% full-thickness) in an explosion accident. Cultured epithelial autograft was used to cover 70% of the total body surface area on postburn day 26. In spite of early success of coverage, 60% of cultured epithelial autograft areas blistered and sloughed over the ensuing weeks. Electron microscopic examination of a biopsy specimen of the healed cultured epithelial autograft (80 days after placement) revealed a lack of dermal attachments of the anchoring fibrils. Additionally, blister fluid that was taken from the bullae of the cultured epithelial autograft revealed levels of 18 ng/ml thromboxane and 24 ng/ml prostaglandin E2. These levels are significantly higher than those seen in acute burn blister fluid and indicate an ongoing inflammatory process. Cultured keratinocytes, although they provide early wound closure, may not provide adequate long-term coverage for patients with massive burns.

Blood transfusions have been shown to prevent allograft rejection, to increase the rate of tumor growth, and to increase susceptibility to infectious complications. We evaluated the mechanism of this immunosuppression by studying the effect of transfusions on macrophage function in a Lewis rat model. Allogeneic transfusions were found to decrease macrophage migration in response to inflammatory stimuli and to increase their production of the strongly immunosuppressive arachidonic acid metabolite prostaglandin E. Syngeneic transfusions did not alter macrophage migration or arachidonic acid metabolism. The immunosuppression seen following transfusions appears to be related to an increased synthesis of prostaglandin E.

This article reviews the scientific and clinical evidence that supports trauma and shock as potential etiologies for translocation of intestinal microorganisms and their by-products. The potential for loss of intestinal barrier function to cause the eventual septic deaths observed in such patients, as well as possible mechanisms for preventing and treating this entity is also discussed.

Blood transfusions repeatedly have been shown to prolong allograft survival, probably by stimulating suppressor T lymphocytes. The effects of transfusions on immune function in traumatized patients has not previously been investigated. We investigated the effects of transfusions on the immune system using a burned rat model. The transfusions were found to have no effect on the white blood cell counts, differential cell count, or neutrophil migration and bactericidal index. Those animals that received transfusion did exhibit impaired cell-mediated immunity and macrophage migration. Blood transfusions seem to increase further the immunosuppression seen with trauma and surgery.

The enterococcus has been relegated to a position of unimportance in the pathogenesis of surgical infections. However the increasing prevalence and virulence of these bacteria prompt reconsideration of this view, particularly because the surgical patient has become increasingly vulnerable to infectious morbidity due to debility, immunosuppression, and therapy with increasingly potent antibiotics. The enterococcus is a versatile opportunistic nosocomial pathogen, causing such diverse infections as wound, intra-abdominal, and urinary tract infections; catheter-associated infection; suppurative thrombophlebitis; endocarditis; and pneumonia. Although surgical drainage remains the cornerstone of therapy for enterococcal infections involving a discrete focus, in the circumstances typified by the compromised surgical patient, specific antibacterial therapy directed against the enterococcus is warranted. Recent evidence indicates that parenteral antibiotic therapy for enterococcal bacteremia is mandatory and that appropriate therapy clearly reduces the number of deaths.