from a hypocoagulable state on admission toward a hypercoagulable
state later during the hospital stay, which may predispose
to MOF. Immediately after tissue injury,thrombomodulin
complexes and extracellular histones activate protein C, which leads
to hypocoagulopathy due to the inhibition of FVa and FVII and
hyperfibrinolysis(28, 37, 74, 75). Activation of protein C results
in utilization of protein C.If protein C levels are consumed and
patients do not recover their protein C levels, inhibition of FVa
and VII will not occur, causing ahypercoagulablestate.This may
be followed by the formation of vascular thrombi leading to cell
damage in organs and eventually MOF (Figure5). Further studies
are required to confirm this hypothesis.
Risk factors for transfusion-associated MOF are administration
of crystalloids, transfusion of RBCs, the age of RBCs >14 days and
an FFP:RBC ratio 1:1. When transfusion of fluids and blood
products is inevitable a limited amount of fluid and blood
products is recommended. We found that a high FFP : RBC ratiois
an independentriskfactorforMOF.However,sincetransfusion
with a low FFP : RBC ratio of