Information of Post Burns

Published: 23rd January 2012
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First and superficial second degree burns are partial thickness burns which may heal without skin grafting as there is still healthy skin at the bottom of the burn to heal the skin from the bottom up. Full thickness or 3rd degree burns and deep 2nd degree burns most often require surgery in the form of skin graft to restore skin coverage. Patients who burn large parts of their body will often need more than one trip to the operating room for the plastic surgeon to remove the nonviable skin and replace it with skin grafts.

When people are burned across joints, the burns may heal by tightening the skin and restricting joint movement. This is called joint contracture. Joint contracture occurs quite frequently in poorer countries Plastic surgeons are often called upon to provide reconstruction after burn injuries even when skin grafting is available and performed. Combinations of skin flaps and grafts are used to provide additional skin when it is required.
Where skin grafting is not available.


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 minors 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, illus., thrombocytopenia, hyperglycemia, leucocytosis or leucopenia.

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 hyper metabolic response to burn injury, and by a generalized post-burn immunosuppressant due to release of immunoreactive agents from the burn wound.

Burn injury leads to suppression of nearly all aspects of immune response. Post-burn serum levels of immunoglobulin, fibronectin, and complement levels are reduced, as well as a diminished ability for opsonization. Chemo taxis, 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, energy 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.

Control of Infection
Although care of the burn wound is not the initial priority, subsequent survival depends upon it. The avascular burn eschar is rapidly colonized by 5 days post-burn, despite the use of antimicrobial agents. If the bacterial density exceeds the immune defenses of the host, then invasive burn sepsis may ensue. When bacterial wound counts are >105 microorganisms per gram of tissue, risk of wound infection is great, skin graft survival is poor, and wound closure is delayed.

The goals of local wound management are the prevention of desiccation of viable tissue and the control of bacteria. These are achieved by use of topical antimicrobial agents and/or biological dressings. It is unrealistic to expect to keep a burn wound sterile. Bacterial counts of less than 103 organisms/gm are not usually invasive and allow skin graft survival rates of >90%.

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