Diffuse Alveolar Haemorrhage — Written Clinical Reasoning

Model answer — Part A: the haemoptysis-absent pulmonary-renal presentation

Frame the problem. Falling haemoglobin, new diffuse ground-glass infiltrates and worsening hypoxaemia are diffuse alveolar haemorrhage until proven otherwise — and the absence of haemoptysis does not argue against it, because up to a third of DAH presents without it. The active urine sediment makes this a pulmonary-renal syndrome, which shortens the differential to the immune causes: ANCA-associated vasculitis, anti-GBM disease and SLE ^{[1] [2]}.

Confirm the bleeding. The diagnostic move is bronchoscopy with serial bronchoalveolar lavage: three sequential aliquots from the same segment becoming progressively bloodier confirms DAH, and haemosiderin-laden macrophages on Prussian blue staining confirm bleeding of at least 48–72 hours' duration. Lavage also samples for infection, the main mimic ^[1].

Hunt the cause in parallel, same day. ANCA by ELISA with MPO and PR3 specificity, anti-GBM antibody, ANA with dsDNA, complement C3/C4, and antiphospholipid antibodies if the story suggests; urine microscopy for dysmorphic red cells and red-cell casts with protein:creatinine ratio; creatinine trend; and an echocardiogram to exclude mitral stenosis before any idiopathic label. In a 28-year-old woman, SLE and MPO-ANCA disease (MPA) lead the pre-test probabilities ^{[1] [7]}.

Renal biopsy once stable: pauci-immune necrotising crescentic GN (ANCA), linear IgG (anti-GBM) or full-house immune-complex GN (lupus) — the pattern determines both treatment and prognosis. Tissue must never delay emergency treatment in a deteriorating patient ^[7].

Close the loop: the differential also includes bland causes (coagulopathy, toxins) and idiopathic pulmonary haemosiderosis — but IPH is a diagnosis of exclusion and is untenable here because the urine is active ^[2].