C48-01 Warfarin-Induced Diffuse Alveolar Hemorrhage

Abstract Introduction Diffuse alveolar hemorrhage (DAH) is a rare, life-threatening syndrome characterized by bleeding into the alveolar spaces. Anticoagulation-induced DAH is an uncommon but essential etiology. We present a case of warfarin-induced DAH in a patient with a left ventricular assist device (LVAD), developing persistent hemoptysis despite normalization of coagulopathy. Case Presentation A 34-year-old male with heart failure with reduced ejection fraction with an LVAD on warfarin presented to the emergency room for evaluation of a supratherapeutic INR of 26. He subsequently developed hemoptysis requiring intubation for airway protection. Initial laboratory findings revealed PT 320, PTT 92.5, fibrinogen 479mg/dL, D-dimer 0.784ug/ml, hemoglobin 13g/dL, creatinine 1.6mg/dL. He received 4-factor prothrombin complex concentrate, intravenous vitamin K, and tranexamic acid. Despite INR normalization, episodes of hemoptysis continued. Computed tomography demonstrated multinodular opacities bilaterally (Figure 1). Bronchoalveolar lavage (BAL) revealed increasingly bloody return, consistent with DAH. Empiric broad-spectrum antibiotics and pulse dose steroids were initiated. Autoimmune work-up returned negative, leading to suspicion of DAH secondary to supratherapeutic INR. His hemoptysis resolved over time, and once stable, he was successfully extubated. Discussion DAH is a rare, life-threatening syndrome of pulmonary hemorrhage arising from injury to the alveolar microcirculation. Various etiologies have been identified, autoimmunity being most common. It typically presents with hemoptysis, anemia, and hypoxemia. Progression to respiratory failure may occur, thus entailing a high mortality rate. Radiologic findings are often non-specific with patchy/diffuse groundglass opacities, “crazypaving” pattern, or frank consolidation. Diagnosis is confirmed with bronchoscopy and BAL, demonstrating increasingly bloody return on sequential BAL samples plus hemosiderinladen macrophages on cytology. Anticoagulation-induced DAH is a relatively rare phenomenon. The first known case was published by Brown et al in 1965, with possible DAH secondary to accidental excess warfarin ingestion. There have been isolated case reports of anticoagulation-induced DAH since, with and without concurrent autoimmunity. Treating the underlying cause of DAH is the mainstay of treatment, whilst using immunosuppressive agents to address autoimmune alveolar destruction. In anticoagulation-induced DAH, immediate steps should be taken to stop the offending agent, initiate anticoagulation reversal, and closely monitor coagulation parameters. Immediate ventilatory and hemodynamic support should be implemented. Conclusion This case illustrates the challenges in diagnosing and managing DAH. Anticoagulation-induced DAH should be considered in patients taking these medications, with careful attention to potential interacting agents and the possibility of excess ingestion. Appropriate supportive therapy should not be delayed, with close monitoring of ventilatory and hemodynamic status, regardless of INR normalisation. This abstract is funded by: None