Abstract Introduction Diffuse alveolar hemorrhage (DAH) is a life-threatening syndrome with a reported inpatient mortality of 20-50%. It typically presents with hemoptysis, new pulmonary infiltrates, and anemia; however, one-third patients lack hemoptysis, delaying diagnosis. Early identification of underlying etiology is essential to prevent worsening respiratory failure and mortality. Case Presentation 74-year-old female with uncontrolled hypertension, coronary artery disease, congestive heart failure, CKD-4, and permanent pacemaker for heart block presented with progressive dyspnea, dry cough, chest tightness, and weakness for one week. She denied fevers, chills, hemoptysis, or smoking history. On presentation, she was hypoxic despite BiPAP, requiring intubation. Laboratory workup revealed leukocytosis (19.1 K/μL) with neutrophilic predominance, hemoglobin 6.4 g/dL, BUN 78 mg/dL, creatinine 7.68 mg/dL (baseline 3.5 mg/dL), lactic acid 2.8 mmol/L. ESR and CRP were mildly elevated (25 mm/hr and 15.5 mg/dL, respectively). Arterial blood gas showed pH 7.51, pCO2 23 mmHg, and pO2 61mmHg. Chest X-ray demonstrated diffuse bilateral patchy infiltrates. Broad-spectrum antibiotics and blood transfusions were initiated. Urgent bronchoscopy with BAL was performed, given rapid clinical deterioration and radiographic findings. Sequential aliquots became progressively bloody, confirming DAH. Initial infectious workup, including bacterial, fungal, and viral studies from BAL and blood cultures, was negative. CT Chest demonstrated extensive bilateral ground-glass opacities with patchy consolidation. Given concurrent AKI on CKD, and concern for pulmonary-renal syndrome, an autoimmune etiology was suspected, specifically. Collateral personal and family history was negative for autoimmune symptoms or diseases, and no eosinophilia, asthma, or established granulomatous disease was noted. Emperic therapy with pulse-dose methylprednisolone (500 mg IV daily × 3 days) and plasmapheresis was initiated. Autoimmune testing revealed ANA (1:1280, homogeneous), elevated SSA antibodies, and markedly positive MPO-ANCA (222.4 U/mL). Other serologies were negative. Rituximab (1 gm IV) was initiated in collaboration with rheumatology; meanwhile, kidney biopsy showed MPO+ crescentic glomerulonephritis along with ATN. Her respiratory status improved with extubation on day 6 of admission. Discussion ANCA-associated vasculitides (AAV) are a known cause of pulmonary capillaritis leading to DAH. However, DAH as the predominant or initial manifestation, particularly in MPO-ANCA vasculitis, remains uncommon. This case also highlights the importance of recognizing DAH as an ARDS mimic, where overlapping radiographic findings and the absence of hemoptysis can obscure the diagnosis. Early diagnostic bronchoscopy and autoimmune testing should be pursued in patients with unexplained diffuse infiltrates and concomitant renal dysfunction. Timely initiation of corticosteroids, immunosuppressive therapy, and plasmapheresis can help prevent irreversible respiratory and renal failure. This abstract is funded by: None
Zubairi et al. (Fri,) studied this question.