Neuromuscular dysfunction in burns and its relationship to burn size, hypermetabolism, and immunosuppression.

The etiology of neuromuscular (NM) dysfunction following burn injury has not been characterized. NM deficits, together with hypermetabolism and immunosuppression, are debilitating processes which play a key role in the morbidity and mortality of burned patients. This study examined the usefulness of the murine model to replicate clinically observed NM dysfunction. Systemic effects of graded increases in burn size were studied in the acute phase (3 weeks) of burn trauma. Metabolic rates, immune response to dinitrofluorobenzene (DNFB), maximum tension developed by gastrocnemius muscle, and the response of its NM junction to d-tubocurarine (dTc) were the parameters analyzed. Groups of male CF1 mice were given a 20%, 30%, and 50% total body surface area burn and compared to controls. By Day 21 postburn, all the burn groups showed elevated metabolic rates and immunosuppression to the inflammatory antigen DNFB. NM dysfunction evidenced as a significant depression of maximal tension development was observed in the 30% and 50% groups. A threefold increase in the effective dose (ED95) values of dTc was seen only in the 50% burn group. No NM junctional changes were seen in the 20% burn group. These findings are consistent with clinical observations. We conclude that the mouse is a useful model for evaluating NM dysfunction of burns.