Reversal of cocaine-induced diffuse alveolar hemorrhage in a patient on rivaroxaban with activated prothrombin complex concentrate.

Document Type

Conference Proceeding

Publication Date

2015

Publication Title

Am J Respir Crit Care Med

Abstract

Diffuse alveolar hemorrhage (DAH) is a well described complication of cocaine abuse. We present a unique case of cocaine-induced DAH in a patient on anticoagulation with rivaroxaban successfully treated with activated prothrombin complex concentrate (aPCC). Case Report A 29 year-old African-American male presented to the emergency department with hemoptysis. His past medical history remarkable for hypertension, heart failure and atrial fibrillation on rivaroxaban. He smoked 0.5 packs of cigarettes daily for 13 years and he denied illicit drugs. On examination, the respiratory rate 18 per minute with a pulse of 81 per minute, blood pressure of 119/75 mmHg and a temperature of 37.0°C. Chest auscultation was significant for coarse breath sounds. The white blood cell count was 5,400 cells/mm3, hemoglobin was 9.9 mg/dL from a baseline of 12 mg/dL and platelets were 205,000 cells/mm3. The serum creatinine was 1.14 mg/dL, blood urea nitrogen was 19 mg/dL and the INR was 2.07. Urine toxicology was positive for cocaine and marijuana. The antinuclear antibody and neutrophil cytoplasmic antibody were undetectable. A chest radiograph showed evidence of cardiomegaly with no infiltrates. Fiberoptic bronchoscopy demonstrated no evidence of active bleeding but blood throughout the airways. Serial lavages showed progressively more hemorrhagic fluid with analysis of the bronchial lavage fluid showing hemosiderin-laden macrophages. Given persistent hemoptysis, hypotension and active bleeding from the endotracheal tube, the decision was made to start aPCC. Hemoptysis improved significantly after initiation of therapy and the patient became hemodynamically stable. He was successfully extubated and discharged home. Discussion We present a case of cocaine-induced DAH complicated by rivaroxaban-induced anticoagulation. The new oral anticoagulants including Factor Xa inhibitors (rivaroxaban) are proven to be as effective as vitamin K antagonists in preventing cardio-embolic events in nonvalvular atrial fibrillation and have the advantages of decreased need for laboratory monitoring and fewer drug interactions, making them attractive options for patients and physicians. Therefore, understanding their mechanism of action and potential reversal options are essential in the case of life-threatening bleeding. Recent studies in vitro and in healthy individuals showed that prothrombin complex concentrates, aPCC, and recombinant activated factor VII have a role in reversing the effects of factor Xa inhibitors (1,2). Similarly, after therapy with aPCC our patient showed significant improvement in hemoptysis with stabilization of hemoglobin and resolution of hypotension. Conclusion Patients with severe life-threatening bleeding and hemodynamic instability on anticoagulation with factor Xa inhibitors may benefit from reversal with aPCC.

Volume

191

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