DIFFUSE ALVEOLAR HEMORRHAGE RESULTING FROM RIVAROXABAN USE: A RARE COMPLICATION IN A PATIENT WITHOUT PREDISPOSING CONDITIONS

Abstract

TOPIC: Diffuse Lung Disease TYPE: Fellow Case Reports INTRODUCTION: Diffuse alveolar hemorrhage (DAH) is a rare complication of direct oral anticoagulant (DOAC) use with few reported cases in patients with predisposing conditions or underlying lung disease. DAH results from disruption of the alveolar-capillary interface. Infectious, autoimmune, and drug mediated conditions may lead to DAH. Rivaroxaban is a DOAC used to treat venous thromboembolism (VTE) and non-valvular atrial fibrillation (NVAF). We present a case of a patient who developed DAH one month after starting rivaroxaban. CASE PRESENTATION: A 43-year-old female with a past medical history of hyperlipidemia and tobacco use disorder presented with frank hemoptysis and shortness of breath. She was diagnosed with lower extremity deep vein thrombosis (DVT) and was started on rivaroxaban. Vitals were stable without hypoxia. Hemoglobin dropped from 14 to 7 g/dL (normal 12.3-15.3 g/dL) requiring 2 units of blood. Prothrombin Complex Concentrate was given. Computed tomography angiogram of the chest showed bilateral lung fields with patchy ground-glass opacities with peripheral sparing, without significant intra-lobular septal thickening and no pulmonary embolus. Infectious work up was negative. Rheumatological workup with anti-glomerular basement antibodies, anti-double stranded DNA antibodies, lupus anticoagulant, antinuclear antibody, rheumatoid factor, anti-neutrophilic cytoplasmic antibody, proteinase-3 antibody, myeloperoxidase antibody, C-reactive protein and erythrocyte sedimentation rate was negative. Bronchoscopy confirmed the diagnosis of DAH. Hemoptysis resolved after discontinuing rivaroxaban, repeat lower extremity dopplers were negative for DVT. She was discharged home without anticoagulation. DISCUSSION: DAH occurs from direct injury or inflammation of the pulmonary arterioles, venules, or alveolar septal capillaries causing bleeding into the lung. It presents with non specific symptoms including cough, chest pain, hemoptysis, and dyspnea. It is life threatening with fast clinical deterioration leading to respiratory failure. The underlying vascular injury of DAH is based on histological appearance and is divided into pulmonary capillaritis, bland pulmonary hemorrhage, and diffuse alveolar damage. The diagnosis is usually made clinically and supported with imaging and bronchoscopic findings. There are few cases of rivaroxaban induced DAH in the literature. The majority of the cases report patients with an underlying medical conditions such as autoimmune disease, lung cancer, interstitial lung disease and pulmonary hypertension, predisposing them to DAH. Our patient had no predisposing factors that put her at risk of developing DAH. CONCLUSIONS: Oral anticoagulants are a under-recognized cause of DAH with limited literature on the incidence of DAH with the use of these medications. This case illustrates that patients with no underlying risk factors can develop DAH with the use of rivaroxaban. REFERENCE #1: Collard HR, Schwarz MI. Diffuse alveolar hemorrhage. Clinics in Chest Medicine 2004; 25(3): 583-92. REFERENCE #2: Park MS. Diffuse alveolar hemorrhage. Tuberc Respir Dis (Seoul) 2013; 74(4): 151-62. REFERENCE #3: Chen A, Stecker E, Warden BA. Direct Oral Anticoagulant Use: A Practical Guide to Common Clinical Challenges. Journal of the American Heart Association 2020; 9(13): e017559 DISCLOSURES: No relevant relationships by Ahmad Alhajhusain, source=Web Response No relevant relationships by Stephanie Baltaji, source=Web Response No relevant relationships by Helene Rovnan, source=Web Response