Normal hemostasis requires an intact interrelating mechanism composed of vascular and tissue components, platelets, and coagulation proteins. Deficiency or disease of any of these components may cause either spontaneous or trauma-related hemorrhage. The intensive care setting, by definition, involves a population that is characterized by multiorgan failure, polypharmacy, and multiple wounds of both accidental or iatrogenic variety. Such pathophysiology significantly stresses even an initially normal hemostatic mechanism. It is not surprising, then, that bleeding is a frequent complication encountered in the intensive care setting. A thorough history, physical findings as well as a broad battery of laboratory tests, often serves to differentiate the different bleeding dyscrasias.
KeywordsFactor VIII Platelet Function Disseminate Intravascular Coagulation Disseminate Intravascular Coagulation Bleeding Time
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- Addonizio VP. Platelet function in cardiopulmonary bypass and artificial organs. Hem Oncol Clin North Am 1990; 4: 31–51.Google Scholar
- Furlan M, Rodolfo R, Galbusera M, Remuzzi G, et al. Von Willebrand factor-cleaving protease in thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome. N Engl J Med 1998; 339: 1578 1584.Google Scholar
- Mammen E. Coagulation defects in liver disease. Med Clin North Am 1994; 78: 544–545.Google Scholar
- Wandt H, Frank M, Ehninger G, Schneider C et al. Safety and cost-effectiveness of a 10 X 10/L trigger for prophylactic platelet transfusions compared with the traditional 20 X 10/L trigger: a prospective comparative trial in 105 patients with acute myeloid leukemia. Blood 1998; 91: 3601–3606.PubMedGoogle Scholar