Phys · respiratory
Diffuse Alveolar Haemorrhage and Pulmonary-Renal Syndromes
Also known as DAH · diffuse alveolar hemorrhage · alveolar haemorrhage · pulmonary-renal syndrome · pulmonary renal syndrome · lung-kidney syndrome · Goodpasture syndrome · anti-GBM disease · pulmonary capillaritis · idiopathic pulmonary haemosiderosis
Consultant-physician-depth guide to diffuse alveolar haemorrhage — the haemoptysis-absent trap, capillaritis versus bland versus diffuse alveolar damage mechanisms, serial BAL diagnosis, the ANCA/anti-GBM/SLE pulmonary-renal differential, and evidence-based severe DAH management from pulse methylprednisolone to plasma exchange — structured for FRACP DWE and DCE preparation.
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Red flags
- Falling haemoglobin + new diffuse infiltrates + worsening hypoxaemia is DAH until proven otherwise — up to a third of patients have NO haemoptysis
- Haemoptysis with haematuria or red-cell casts — pulmonary-renal syndrome: same-day ANCA, anti-GBM, ANA, complement and urine microscopy
- Young smoker with DAH and acute kidney injury — anti-GBM disease: start plasma exchange on suspicion, not on biopsy
- SLE with new infiltrates and falling Hb — lupus DAH carries high mortality; escalate early
- New infiltrates in an anticoagulated patient — bland DAH from over-anticoagulation, not pneumonia
Diffuse Alveolar Haemorrhage and Pulmonary-Renal Syndromes
The answer first
Diffuse alveolar haemorrhage (DAH) is bleeding into the alveolar spaces from the pulmonary microcirculation — a syndrome, not a diagnosis. The job is never just to recognise it; it is to find which of the immune, cardiac, toxic or coagulopathic causes is bleeding, because the treatments are opposites [1] [2]. Three rules carry you through the DWE and the DCE:
- Haemoptysis is not required. Up to a third of DAH episodes present without any haemoptysis. The real triad is a falling haemoglobin, new diffuse pulmonary infiltrates, and worsening hypoxaemia — in a ventilated ICU patient that combination, unexplained by pneumonia or pulmonary oedema, is DAH until bronchoscopy proves otherwise [1] [2].
- Bronchoscopy with serial lavage is the diagnostic move. Not another CT, not empiric antibiotics: bronchoalveolar lavage aliquots that become progressively bloodier, later confirmed by haemosiderin-laden macrophages [1].
- The urine finishes the examination. DAH plus an active urinary sediment (haematuria, red-cell casts, rising creatinine) is the pulmonary-renal syndrome — and the shortlist is ANCA-associated vasculitis, anti-GBM disease and SLE. Same-day serology decides the treatment: plasma exchange is the cornerstone for anti-GBM, while rituximab or cyclophosphamide anchors ANCA vasculitis — and after PEXIVAS, plasma exchange is no longer routine for ANCA disease [7] [12] [16].
References19ShowHide
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