title: Early burn excision attenuates the postburn lung and systemic response to endotoxin.
abstract: The lung and systemic physiologic response to endotoxin is markedly accentuated in the presence of a body burn. Our purpose was to determine whether early burn excision and closure would decrease this response. We compared the endotoxin (2 micrograms/kg)-induced response in 10 adult sheep with lung and soft-tissue lymph fistulas 3 days after a 15% total-body surface full-thickness burn that was excised immediately with that of sheep without burn excision and nonburned sheep. No infection was present in the burn wound. Early excision prevented the ongoing postburn lipid peroxidation and lung inflammation seen 3 days after burn before endotoxemia in animals with 15% total body surface burn wound not excised. Sheep that underwent excision demonstrated significantly less pulmonary hypertension and hypoxia after endotoxin than did either endotoxin-treated and intact burned sheep or endotoxin-treated nonburned sheep. Lung inflammatory changes as determined by neutrophil content of lung tissue and the increase in lung tissue malondialdehyde in the group that underwent burn excision after endotoxin were comparable to those seen with endotoxin alone, as was the lung lymph-flow response. Also, the systemic response was nearly identical to that seen with endotoxin alone with no increase in soft-tissue permeability as measured by lymph flow. Oxygen consumption (VO2) remained unchanged from baseline. In contrast, VO2 doubled in burn-intact animals initially after endotoxin, after which VO2 decreased to levels below baseline. An increase in soft-tissue vascular permeability was also noted. We can conclude that early burn excision and closure prevent the accentuated response to endotoxin that is seen when the burn wound is left intact, even if it is uninfected.
authors.affiliation: Longwood Area Trauma Center, Brigham and Women's Hospital, Boston, MA 02115.
authors.forename: R H
authors.initials: RH
authors.lastname: Demling
authors.forename: C
authors.initials: C
authors.lastname: LaLonde
mesh_terms: D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002056:Burns / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery; D002199:Capillary Permeability / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D015227:Lipid Peroxidation / Q000187:drug effects*; D008168:Lung / Q000378:metabolism* / Q000503:physiopathology; D008315:Malondialdehyde / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D011651:Pulmonary Artery / Q000502:physiology; D012756:Sheep; D013997:Time Factors
chemical_list: D001427:Bacterial Toxins; D008315:Malondialdehyde