UC Irvine

Within a span of four months at a 550 bed community hospital, four elderly patients who had been taking cefamandole for various infections developed a severe coagulopathy within 10 days after initiation of cefamandole. All patients had a prolonged prothrombin time and activated partial thromboplastin time with a marked decrease of the vitamin K dependent clotting factors II, VII, IX, X, and also were found to have mild to moderate renal function impairment. The coagulopathy was promptly corrected to normal with or without treatment of vitamin K and/or fresh frozen plasma when the drug was discontinued. Treatment with vitamin K while on cefamandole also corrected the coagulation abnormalities and in vitro cefamandole had no direct effect on prothrombin time and activated partial thromboplastin time in therapeutic concentrations. These clinical and laboratory observations and the nature of high excretion rate of cefamandole in bile suggest cefamandole induced coagulopathy is caused by decreased vitamin K synthesis, probably secondary to rapid depletion of vitamin K producing intestinal organisms.