Chemical burns are slow healing injuries and their depth is difficult to assess. Tissue destruction continues as long as active material is present in the wound site. The routine therapy for treatment of full thickness chemical burns is early excision; it shortens hospitalization and reduces morbidity. However, presently there is no specific treatment for chemical burns of partial thickness. This study examined several treatment modalities for partial thickness chemical burns: surgical excision; laser ablation and chemical debridement with Debridase or trypsin-linked to gauze. Chemical burns were inflicted with nitrogen mustard (NM -- a nitrogen analog to sulfur mustard -- mustard gas) in an experimental guinea pig model. Debridase was most effective and reduced significantly lesion area of burns after 'humid' exposure to 2 mg NM. The healing action of Debridase was also evident in the significantly higher histopathological score of biopsies from local tissue obtained on day 5. Laser ablation was most effective and accelerated healing of burn lesions after 'dry' exposure to 5 mg NM. The histopathology score of the laser treated burns was higher on day 4 compared to untreated controls. It is concluded that for partial thickness chemical burns early nonsurgical removal of the damaged tissues accelerates wound healing.

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Sulfur mustard (SM) is a powerful vesicant used as an agent of chemical warfare. The severity of lesions incurred after exposure to SM reiterated the need for an efficient and rapid neutralizing agent against SM. Previous studies have shown that postexposure treatment with iodine is effective against SM lesions in rodents. In the current study we used the pig model to emulate SM-induced burn lesions, and observed the immediate effect of a single dose of iodine formulation treatment on these burns. SSD, a common agent recommended for use in both chemical and thermal burns was used as control. Results indicated that 1.27 mg of SM caused deep lesions and histopathological changes in the pig skin as scored in the biopsies obtained. A single application of an iodine formulation 20 minutes from exposure to SM exhibited no protective action on the skin as evident in the biopsies obtained 1, 3, 5, 10, and 21 days after treatment. SSD treatment induced the least protective action. The SSD-treated wounds also took the longest to heal. Attempts to neutralize the SM action with iodine compounds were not successful in the pig model. Currently, other compounds are being investigated. Attention must be drawn to the adverse effect of SSD on SM-induced wounds. Further studies must be initiated to elucidate this phenomenon.