Fracture hematoma is a potent proinflammatory mediator of neutrophil function.
BACKGROUND
Patients 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).


METHODS
FH 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.


RESULTS
FH 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).


CONCLUSIONS
These effects, although beneficial at the site of injury in the context of antibactericidal function, may cause PMN-mediated tissue injury systemically.
Departments of Orthopaedics, Royal College of Surgeons in Ireland, Education & Research Centre, Beaumont Hospital, Dublin, Ireland. marcustimlin@eircom.net
Marcus
M
Timlin
Deirdre
D
Toomey
Claire
C
Condron
Colm
C
Power
John
J
Street
Paraic
P
Murray
David
D
Bouchier-Hayes
D000328:Adult; D017209:Apoptosis / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005596:Fractures, Closed / Q000150:complications / Q000503:physiopathology / Q000601:surgery*; D006406:Hematoma / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology*; D014471:Umbilical Veins / Q000166:cytology; D015854:Up-Regulation
D018799:Intercellular Adhesion Molecule-1