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Are Antibiotics Helping or Hurting?

Rodney Hochman, MD; Jeffrey Clark, MD; Arturo Rolla, MD; Spiros Thomas, DPharm; Antoine Kaldany, MD; John A. D'Elia, MD

Arch Intern Med. 1982;142(8):1440-1442.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

An accurate and timely diagnosis is crucial when serious bleeding occurs in critically ill patients who are receiving broad-spectrum antibiotics. The appropriate therapy might be radically different if the bleeding were caused by the antibiotics rather than the underlying disease process. Bleeding secondary to antibiotics may occur through several of the following mechanisms: (1) bone marrow suppression and aplasia with resultant thrombocytopenia, (2) immunologic platelet destruction, (3) inhibition of circulating platelet function, (4) potentiation of the effects of warfarin sodium (Coumadin), and (5) interruption of the vitamin K-dependent clotting apparatus.

Bone marrow suppression and aplasia are most frequently associated with chloramphenicol. While aplasia is an idiosyncratic occurrence, reversible bone marrow suppression is dose related and is characterized by anemia and neutropenia both with and without thrombocytopenia. A plasma level of 25 µg/mL or greater of chloramphenicol is often associated with bone marrow suppression that is characterized by the following: (1) . . . [Full Text PDF of this Article]

Author Affiliations
Department of Internal Medicine New England Deaconess Hospital Harvard Medical School Boston, MA 02215

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