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A6645 - Apixaban, an Infrequent Cause of Diffuse Alveolar Hemorrhage
Author Block: J. Cantu-Clatza1, T. Abdo2, H. A. Jaliawala1, K. R. Jones2; 1Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States, 2Pulmonary and Critical Care Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.
Introduction: Apixaban is a direct factor Xa inhibitor, with a better side-effect profile compared to warfarin, favoring its use for the treatment of non-valvular atrial fibrillation and venous thromboembolism. Albeit rare, major bleeding does occur with apixaban. Herein, we present a case of diffuse alveolar hemorrhage (DAH), where apixaban was the presumable culprit.
Case Presentation: A 65-year-old man with a history of bilateral lung transplantation for alpha-1-antitrypsin deficiency, chronic kidney disease, atrial fibrillation, and a newly diagnosed left ventricular thrombus, anti-coagulated with apixaban, was admitted to the hospital for symptomatic bradycardia. Cardiac workup was unremarkable, and bradycardia was deemed secondary to diltiazem. On the day of discharge, he developed hypoxemic respiratory failure, requiring high-flow nasal cannula, with increase in FiO2 requirement to 100% within less than 24h. He had atrial fibrillation with rapid ventricular response. Chest X-ray showed bilateral diffuse airspace disease. Since there was no clinical evidence of cardiogenic pulmonary edema, DAH was highly suspected, and apixaban was held. He was also started on antibiotics and antifungals to cover possible opportunistic infections. Elective intubation was performed, followed by flexible bronchoscopy showing increasingly bloody aliquots on sequential bronchoalveolar lavages, and confirming the diagnosis of DAH. Infectious and autoimmune workup was negative. He improved with supportive management and was successfully extubated after 3 days.
Discussion: DAH is characterized by bleeding into the alveolar spaces, originating from the pulmonary microcirculation. Various conditions are associated with DAH. These are histologically divided into three distinguishing patterns: pulmonary capillaritis, diffuse alveolar damage, and bland pulmonary hemorrhage. DAH secondary to anticoagulants follows the bland pattern, characterized by hemorrhage in the absence of inflammation or alveolar damage. Contrary to cases secondary to pulmonary capillaritis, pulse steroids and immunosuppressive therapies have no role in this population. Treatment is mainly supportive with invasive or non-invasive ventilation, and correction of bleeding disorder whenever possible. In apixaban related life-threatening bleeds i.e. DAH, administration of four-factor prothrombin complex concentrate and anti-fibrinolytic agents may be considered. In our patient, we elected not to do so in light of clinical improvement, and increased risk for thromboembolic disease secondary to the left ventricular thrombus.
Conclusions: DAH related symptoms are not specific and can masquerade as cardiac/infectious-related, especially when hemoptysis is absent (~ 33%). Despite its rarity, DAH should be considered in the differential diagnosis of anticoagulated patients with hypoxemia and bilateral infiltrates since the delay in the diagnosis can be life-threatening.