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Bleeding during Thrombolytic Therapy for Acute Myocardial Infarction: Mechanisms and Management

David C. Sane, MD; Robert M. Califf, MD; Eric J. Topol, MD; David C. Stump, MD; Daniel B. Mark, MD, MPH; and Charles S. Greenberg, MD
[+] Article, Author, and Disclosure Information

Grant Support: Supported in part by training grant 5T32 HL-07101-14 from the National Institutes of Health; research grants HL-17670, HL-36587, and HL-35058 from the National Heart, Lung, and Blood Institute; research grant HS-05635 from the National Center for Health Services Research; training grant LM-07003 and grant LM-03373 from the National Library of Medicine; and grants from the Andrew W. Mellon Foundation and the Robert Wood Johnson Foundation. Drs. Stump and Greenberg are Established Investigators, American Heart Association.

Requests for Reprints: David C. Sane, MD, Box 3360, Duke University Medical Center, Durham, NC 27710.

Current Author Addresses: Dr. Sane: Box 3360 Duke University Medical Center, Durham, NC 27710.

Dr. Califf: Box 31123, Duke University Medical Center, Durham, NC 27710.

Dr. Topol: 1500 East Medical Center Drive, Ann Arbor, MI 48109.

Dr. Stump: Department of Medicine, University of Vermont, Burlington, VT 05405.

Dr. Mark: Box 3485, Duke University Medical Center, Durham, NC 27710.

Dr. Greenberg: Box 3934, Duke University Medical Center, Durham, NC 27710.

© 1989 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1989;111(12):1010-1022. doi:10.7326/0003-4819-111-12-1010
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Hemorrhage is the major adverse effect of thrombolytic therapy, but its incidence can be reduced by careful selection of patients and avoidance of unnecessary invasive procedures. More than 70% of bleeding episodes occur at vascular puncture sites. Hypofibrinogenemia and elevation of fibrinogen degradation products have been weakly correlated with the risk of hemorrhage. Although depletion of factors V and VIII may occur, the role of such depletion in bleeding is unknown. Several in-vitro studies have shown plasmin-induced platelet dysfunction, but clinical data are limited. Nevertheless, the role of platelet inhibition should be considered because many patients are treated with antiplatelet agents. Most patients who have bleeding can be managed by interruption of thrombolytic and anticoagulant therapy, volume replacement, and manual pressure applied to an incompetent vessel. Protamine should be considered if heparin has been administered within 4 hours of the onset of bleeding. In the few patients who fail to respond to these conservative measures, judicious use of transfusion products may be indicated. Transfusion of cryoprecipitate, fresh frozen plasma, and platelets should be considered with clinical and laboratory reassessment after each administration. A target fibrinogen level of 1 g/L is desirable with cryoprecipitate infusion. Antifibrinolytic agents are available as a last alternative. We have developed an algorithm for using these products.





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