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Bleeding Diathesis

  • Ronald Rubin

Abstract

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.

Keywords

Factor VIII Platelet Function Disseminate Intravascular Coagulation Disseminate Intravascular Coagulation Bleeding Time 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Suggested Reading

  1. Addonizio VP. Platelet function in cardiopulmonary bypass and artificial organs. Hem Oncol Clin North Am 1990; 4: 31–51.Google Scholar
  2. Alving BM, Krishnamurti C. Recognition and management of heparin-induced thrombocytopenia (HIT) and thrombosis. Semin Thromb Hemost 1997; 23: 569–575.PubMedCrossRefGoogle Scholar
  3. Furie B, Limentani S, Rosenfeld CG. A practical guide to the evaluation and treatment of hemophilia. Blood 1994; 84: 3–9.PubMedGoogle Scholar
  4. 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
  5. George JN, Shattil SJ. The clinical importance of acquired abnormali- ties of platelet function. N Engl J Med 1994; 331: 1207–1211.PubMedCrossRefGoogle Scholar
  6. George JN, Woolf SH, Raskob GE, Wasser JS, et al. Idiopathic thrombocytopenic purpura: a practice guideline developed by explicit methods for the American Society of Hematology. Blood 1996; 88: 3–40.PubMedGoogle Scholar
  7. George JN, Raskob GE, Shah SR, Rizvi MA. Drug-induced thrombocytopenia: a systemic review of published case reports. Ann Intern Med 1998; 129: 886–890.PubMedGoogle Scholar
  8. Mammen E. Coagulation defects in liver disease. Med Clin North Am 1994; 78: 544–545.Google Scholar
  9. Penner JA. Managing the hemorrhagic complications of heparin administration. Hematol Oncol Clin North Am 1993; 7: 1281–1289.PubMedGoogle Scholar
  10. Rubin RN, Colman RW. Disseminated intravascular coagulation: approach to treatment. Drugs 1992; 44: 963–971.PubMedCrossRefGoogle Scholar
  11. 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
  12. Woodman RC, Harker LA. Bleeding complications associated with cardiopulmonary bypass. Blood 1990; 76: 1680–1697.PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2002

Authors and Affiliations

  • Ronald Rubin

There are no affiliations available

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