Medication Summary

Research into the pathophysiology of primary blast injury (PBI) continues. On a cellular level, shock waves produce an inflammatory response. Interleukin 8 is released, causing mobilization of polymorphonuclear leukocytes (PMNs) into the systemic circulation. The release of proinflammatory cytokines induces the expression of the CD11b receptor complex on the PMN surface, leading to adhesion at the site of injury. Select free-radical scavengers and inhibitors of inflammatory pathways are promising in phase I animal trials. In addition, blast injury to the lungs causes levels of inducible nitric oxygen synthase (iNOS) to increase in the brain, causing brain injury. The iNOS inhibitor aminoguanidine appears to be effective when administered to mice either before or 1 hour after the blast, but human data are lacking.

Although animal models suggest that bradycardia and hypotension observed in primary blast injury may be vagally mediated, it would be premature to recommend atropine at this time.

Broad-spectrum prophylactic antibiotics should be considered for patients with open wounds from blasts. Tetanus immunization status should be confirmed, and tetanus toxoid should be provided as required.

Use of copper sulfate solution for management of burns contaminated with the military munition WP is described in Emergency Department Care.

Committee on Gulf War and Health: Long-Term Effects of Blast Exposures; Board on the Health of Select Populations; Institute of Medicine. Gulf War and Health, Volume 9: Long-Term Effects of Blast Exposures. The National Academies Press. Available at http://www.nap.edu/catalog.php?record_id=18253. Accessed: February 19, 2014.