The effects of early excision and grafting on myocardial inflammation and function after burn injury

Sepsis is a frequent complication of burn injury despite absence of confirmed infection. Numerous investigators have proposed that the burn wound itself is a primary stimulus for postburn inflammation, and that early excision of the burn wound attenuates the hypermetabolic and inflammatory responses to burn injury. However, others have suggested that aggressive fluid resuscitation and correction of postburn fluid and electrolyte deficits should be the primary focus of intervention in the first 24 hours postburn. This present study determined whether excision and grafting of the burned wound within 30 minutes after injury abrogated myocardial inflammation and contractile defects that occur after burn injury.

In group 1, Sprague Dawley rats were given a third-degree burn over 20% total body surface area (TBSA), whereas rats in group 2 had burns over 30% TBSA and no wound excision. Rats in groups 3 and 4 had burn over 20% and 30% TBSA, respectively, followed by-wound excision and grafting (WE/G) within 30 minutes after completing burn injury. Group 5 included sham burn with no excision, whereas rats in groups 6 and 7 included shams that had either 20% or 30% normal skin excised and grafted to provide appropriate surgical controls. All rats received lactated Ringer's (4 mL/kg/% burn or percent wound excision). Twenty-four hours postburn, hearts were perfused (Langendorff) to assess ventricular function; myocytes were isolated to examine cytokine secretion and Ca2+/Na+ homeostasis.

Burn in the absence of wound excision produced myocardial inflammation and contractile defects as indicted by a lower left ventricular pressure and lower rate of left ventricular pressure rise (+dP/dt) and fall (-dP/dt) response to maximal increases in preload or perfusate Ca2+ compared with responses measured in sham hearts. WE/G within 30 minutes after burn injury reduced myocyte secretion of proinflammatory cytokines and improved left ventricular pressure and +/-dP/dt responses to inotropic challenge.

Cutaneous burn injury and the loss of the skin barrier function contribute, in part, to the myocardial inflammation which, in turn, contributes to myocardial contractile dysfunction that is characteristic of major burn injury.