Severe heart failure secondary to 5-fluorouracil and low-doses of folinic acid: usefulness of an intra-aortic balloon pump.

David, J S; Gueugniaud, P Y; Hepp, A; Gaussorgues, P; Petit, P · Crit Care Med · 2000

case_report · Level V

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Abstract

To report 5-fluorouracil in combination with folinic acid as a cause of severe nonischemic heart failure and to demonstrate the potential usefulness of an intra-aortic balloon pump. Case report. An adult, 19-bed medical/surgical intensive care unit of a university hospital. A patient, who developed severe heart failure secondary to 5-fluorouracil infusion with low-dose folinic acid, which was introduced to treat a rectal cancer, was transferred from a cancer institute to our intensive care unit 4 days after the treatment was initiated. Electrocardiography, determination of level of cardiac enzymes, echocardiography, radial arterial catheterization, mechanical ventilatory support, continuous venovenous hemodialysis, vasopressors, and secondary intra-aortic balloon pump. During shock, the patient's systolic blood pressure progressively decreased to 70 mm Hg, despite inotropic agents and vasopressors. Transesophageal echocardiography showed a calculated left ventricular ejection fraction within 20% with global hypokinesia. Electrocardiography showed sinus tachycardia with only nonspecific ST-T changes. Results of serial determination of levels of cardiac enzymes were not significant for myocardial infarction. Treatment with an intraaortic balloon pump was initiated and resulted in a dramatical improvement within 48 hrs. The patient was gradually weaned from vasopressors and the intra-aortic balloon pump. By the tenth day, echocardiography showed a septoapical hypokinesia with a 50% left ventricular ejection fraction. On the 30th day, the echocardiography was considered normal. Intravenous 5-fluorouracil in combination with low doses of folinic acid can induce severe nonischemic heart failure. In such a case, an intra-aortic balloon pump could be useful by providing left ventricular function support when inotropic agents and vasopressors fail to restore normal hemodynamics.

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