Humorally mediated thrombocytosis in major lower extremity trauma.

Abstract

Thrombocytosis in patients undergoing free tissue transfer for coverage of posttraumatic lower extremity defects may be associated with an increased incidence of microvascular thrombosis. Patients with isolated lower extremity trauma have an elevated platelet count that peaks approximately 2 weeks after injury. It is our theory that a humoral component of trauma sera is responsible for the induction of this thrombocytosis. Eight patients with isolated soft-tissue and bony trauma were included in the study. Serum was collected at baseline and throughout the study period. Platelet count, leukocyte count, hemoglobin concentration, and hematocrit were determined. Immunoassay for human interleukin-3 (IL-3), IL-6, and IL-11 as well as granulocyte macrophage colony stimulating factor (GM-CSF) were performed by solid-phase enzyme-linked immunosorbent assay. Balb-C mice were then injected intraperitoneally with the human trauma sera from all time points. Blood was collected at baseline and throughout the study period for determination of platelet count, hemoglobin, and hematocrit. Mean initial platelet count in the 8 human subjects was 152,000 per cubic millimeter with an average peak to 642,000 per cubic millimeter. IL-3, IL-11, and GM-CSF were not detectable in the serum of any patient. Elevated levels of IL-6 were detected in all patients in a nonspecific pattern. In the murine model, an early and late thrombocytosis was elicited. The early peak averaged 78.6% over baseline whereas the late peak average 81.0% over baseline. The induction by human trauma sera of an early and late thrombocytosis in this mouse bioassay supports the theory of humoral mediators. The humoral mediators are yet to be determined but may include IL-6.