pulmonary hemorrhage

Diffuse alveolar hemorrhage (DAH) results from disruption of the alveolar-capillary basement membrane, allowing red blood cells to leak into alveolar spaces. This can occur due to immune-mediated capillaritis (e.g., ANCA-associated vasculitides like granulomatosis with polyangiitis and microscopic polyangiitis, anti-GBM disease/Goodpasture syndrome, SLE), bland pulmonary hemorrhage without capillaritis (e.g., mitral stenosis, anticoagulant use, idiopathic pulmonary hemosiderosis), infections (invasive aspergillosis, leptospirosis), or trauma/iatrogenic causes (bronchoscopy, pulmonary artery catheter rupture). Clinical presentation includes hemoptysis (though absent in up to a third of cases due to alveolar clearance), dyspnea, cough, and hypoxemia; anemia may be significant due to blood sequestration in the lungs. Chest imaging typically shows bilateral, patchy or diffuse ground-glass opacities/infiltrates. Bronchoalveolar lavage (BAL) is diagnostic, revealing progressively bloodier return with sequential aliquots and hemosiderin-laden macrophages on staining, confirming chronic or recurrent hemorrhage. Diagnostic workup includes ANCA, anti-GBM antibodies, ANA, complement levels, coagulation studies, echocardiography (to assess for mitral stenosis or cardiac causes), and renal function tests (given frequent pulmonary-renal syndrome overlap, e.g., Goodpasture syndrome causing rapidly progressive glomerulonephritis plus DAH). Management involves supportive care (oxygen, mechanical ventilation if needed, correction of coagulopathy), treating the underlying cause, and immunosuppression (corticosteroids, cyclophosphamide, rituximab) for autoimmune causes; plasmapheresis may be added for anti-GBM disease. Prompt recognition is critical, as DAH can rapidly progress to respiratory failure and death if untreated.