• B Wenz.
• Albert Einstein College of Medicine, Bronx, NY 10461.
• Transfus Sci. 1993 Oct 1; 14 (4): 353-9.

AbstractThe pathophysiology and support of the massively transfused patient from the vantage of a blood banker is reviewed. Hypothermia, acidosis and shock must be reversed if blood component therapy is to be effective. Algorithms which employ ratios of various blood components have not proved themselves, nor are screening coagulation tests of value until they are remarkably abnormal. Thrombocytopenia, thrombocytopathy, and hypofibrinogenemia appear to be the parameters which predispose to continued bleeding and microvascular hemorrhage in these patients. A large part of the impaired hemostasis is due to a consumption coagulopathy rather than the anecdotal assumption that dilution of the hemostatic elements is to blame. Hypocalcemia, hypomagnesemia and hyperkalemia are rarely observed nor do they pose a problem for this group of individuals. The logistics of blood supply to the clinical areas are addressed by describing one system that has proved itself.

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