Early excision of a full-thickness burn prevents peripheral nerve conduction deficits in mice

Background: A full-thickness 20 percent body surface area burn in mice produces a significant decrease in tibial motor nerve conduction velocity within 6 hours of the burn and in sensory conduction velocity within 7 days. This suggests that cutaneous burn injury produces a systemic response that affects peripheral motor and sensory nerve function at a distance from the burn site. The authors tested the hypothesis that burn wound excision either 30 minutes or 3 hours after burn would prevent neuropathy. Methods: A 20 percent body surface area third-degree burn was applied to the backs of anesthetized mice using procedures that followed National Institutes of Health guidelines. Motor nerve conduction velocity and sensory conduction velocity were determined in intact, anesthetized mice by percutaneous nerve stimulation. Burn wounds were excised and closed at 30 minutes or 3 hours after burn. Motor nerve conduction velocity and sensory conduction velocity were measured before burn and 1, 3, 7, 14, and 21 days after a burn or sham procedure. The number of circulating neutrophils and serum concentrations of tumor necrosis factor-a, nitrite, and electrolytes were also determined in each group. Results: Motor nerve conduction velocity and sensory conduction velocity in the 30-minute excision (n = 10) and sham group (n = 5) were not significantly different. Motor nerve conduction velocity and sensory conduction velocity in the nonexcised group (n = 10) and 3-hour excision group (n = 10) were significantly decreased. Serum tumor necrosis factor-a concentration was elevated 6 hours after burn in nonexcised animals (n = 9) and in 3-hour excision mice (n = 8) but was not significantly different in the sham (n = 8) and the 30-minute excision group (n = 7). Conclusion: The authors conclude that burn wound excision at 30 minutes but not at 3 hours prevents the nerve conduction deficits measured in mice with 20 percent body surface area burns. The cellular basis of burn-induced neuropathy is unknown, but nitric oxide and tumor necrosis factor alpha-α appear to play a role.