Thrombocytosis in patients undergoing free tissue transfer for coverag
e of posttraumatic lower extremity defects may be associated with an I
ncreased incidence of microvascular thrombosis. Patients with isolated
lower extremity trauma have an elevated platelet count that peaks app
roximately 2 weeks after injury. It is our theory that a humoral compo
nent of trauma sera is responsible for the induction of this thrombocy
tosis, Eight patients with isolated soft-tissue and bony trauma were i
ncluded in the study. Serum was collected at baseline and throughout t
he study period. Platelet count, leukocyte count, hemoglobin concentra
tion, and hematocrit were determined. Immunoassay for human interleuki
n-3 (IL-3), IL-6, and IL-11 as well as granulocyte macrophage colony s
timulating 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 plate
let 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 averag
ed 78.6% over baseline whereas the late peak average 81.0% over baseli
ne. The induction by human trauma sera of an early and late thrombocyt
osis in this mouse bioassay supports the theory of humoral mediators.
The humoral mediators are yet to be determined but may include IL-6.