Infection Of Post Burn

By Author: sudarshan singh
Total Articles: 327
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Burn injury leads to suppression of nearly all aspects of immune response. Post-burn serum levels of immunoglobulins, fibronectin, and complement levels are reduced, as well as a diminished ability for opsonization. Chemotaxis, phagocytosis, and killing function of neutrophils, monocytes, and macrophages are impaired. Granulocytopenia is common following burn injury. Cellular immune response is impaired, as evidenced by delayed allograft rejection, anergy to common antigens, impaired lymphocyte mitogenesis, and altered mixed lymphocyte responsiveness. Burn injury results in reductions of interleukin-2 (Il-2) production, T-cell and NK cell cytotoxicity, and helper to suppressor T-cell ration (HSR). Furthermore, infusion of serum from burned to normal patients or animals can transmit some of these immunosuppressive effects.Before embarking on the antimicrobial therapeutic approach in the treatment of burn wound sepsis, it is important to establish certain consistencies in terminology.

Bacteremia: The transient presence of bacteria or other microorganisms in the blood. (e.g. bacteria in the blood after brushing one's ...
... teeth)

Septicemia: The invasion of the blood stream by pathologic microbes from a focus of infection or a locus minoris resistentiae and an active proliferation of these microbes accompanied by hyperthermia, hypothermia and/or prostration. Frequently, it is diagnosed clinically by the presence of any 3 of the cardinal signs: obtundation, hyperventilation, ileus, thrombocytopenia, hyperglycemia, leucocytosis or leukopenia.

Colonization: The mere presence of bacteria, establishment of a colony;bacterial counts of
105 bacteria/gm of tissue with no evidence of invasion into viable tissue.

Infection is the most common and most serious complication of a major burn injury related to burn size. Sepsis accounts for 50-60% of deaths in burn patients today despite improvements in antimicrobial therapies. Sepsis in burns is commonly due to bronchopneumonia, pyelonephritis, thrombophlebitis, or invasive wound infection. The burn wound is an ideal substrate for bacterial growth and provides a wide portal for microbial invasion. Microbial colonization of the open burn wounds, primarily from an endogenous source, is usually established by the end of the first week. Infection is promoted by loss of the epithelial barrier, by malnutrition induced by the hypermetabolic response to burn injury, and by a generalized post-burn immunosuppression due to release of immunoreactive agents from the burn wound.

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