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Potential for Bleeding with the New Beta-Lactam Antibiotics

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▸Requests for reprints should be addressed to Fred R. Sattler, M.D.; Los Angeles County-University of Southern California Medical Center, 1200 North State Street—5P21; Los Angeles, CA 90033.

Hershey, Pennsylvania

© 1986 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1986;105(6):924-931. doi:10.7326/0003-4819-105-6-924
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Several new beta-lactam antibiotics impair normal hemostasis. Hypoprothrombinemia has occurred frequently with cephalosporins that possess a methylthiotetrazole substitution (cefamandole, moxalactam, and cefoperazone). The incidence ranges from 4% to 68%, and the risk is greatest in debilitated patients with cancer, intra-abdominal infection, or renal failure. Impaired platelet function caused by perturbation of agonist receptors on the platelet surface has occurred primarily with beta-lactam antibiotics having an alphacarboxyl substitution (moxalactam, carbenicillin, and ticarcillin). These antibiotics often cause the template bleeding time to be markedly prolonged (> 20 minutes). Acylureidopenicillins, which lack the alpha-carboxyl marker, impair platelet function less frequently and only modestly prolong the bleeding time. If serious hemorrhage occurs, hypoprothrombinemia associated with methylthiotetrazole-substituted cephalosporins should be treated with fresh frozen plasma. Likewise, dangerous bleeding due to impaired platelet aggregation requires treatment with platelet concentrates.





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