• Marcus Timlin, Deirdre Toomey, Claire Condron, Colm Power, John Street, Paraic Murray, and David Bouchier-Hayes.
• Departments of Orthopaedics, Royal College of Surgeons in Ireland, Education & Research Centre, Beaumont Hospital, Dublin, Ireland. marcustimlin@eircom.net
• J Trauma. 2005 Jun 1; 58 (6): 1223-9.

BackgroundPatients with multiple skeletal injuries are susceptible to acute respiratory distress syndrome and multiple organ failure, which result from hyperactivation of the immune system. This study was designed to evaluate in vitro the proinflammatory properties of fracture hematoma (FH).MethodsFH was isolated from patients undergoing emergent open reduction and internal fixation for isolated closed fractures. Neutrophils (PMNs), isolated from healthy volunteers, were exposed to the FH supernatant and activation was examined (CD11b and CD18 adhesion receptor expression and respiratory burst). PMN phagocytosis, apoptosis, and transmigration across an endothelial barrier were also assessed.ResultsFH increased PMN respiratory burst (control, 100; FH-treated, 186) and phagocytosis (control, 100; FH-treated, 172) but had no effect on adhesion receptor expression. Transendothelial migration of PMNs was unaffected, although FH was toxic to endothelial cells. In contrast, apoptosis of FH-treated PMNs was delayed (control, 46; FH-treated, 8).ConclusionThese effects, although beneficial at the site of injury in the context of antibactericidal function, may cause PMN-mediated tissue injury systemically.

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