Diffuse Alveolar Haemorrhage (DAH)
🩸 Diffuse Alveolar Haemorrhage (DAH) is a rare but life-threatening condition where blood acutely fills the alveoli.
A retrospective review of 34 cases revealed that ~30% were due to granulomatosis with polyangiitis (GPA, formerly Wegener’s).
🚨 Rapid recognition is essential because untreated DAH carries a high risk of respiratory failure and death.
ℹ️ About
- DAH: Acute bleeding into multiple alveolar spaces caused by capillary disruption. 🫁
- Unlike haemoptysis from airway disease, DAH originates from the pulmonary microvasculature (arterioles, venules, capillaries).
- Represents a pulmonary emergency often associated with systemic disease.
🧬 Aetiology & Pathophysiology
- Disruption of the alveolar–capillary basement membrane → leakage of blood into alveoli.
- Triggered by inflammation (e.g. vasculitis), immune injury, toxins, or hypertension.
- Bleeding arises from pulmonary (not bronchial) circulation, explaining diffuse involvement.
- Key mechanisms:
• Capillaritis (vasculitis, SLE, ANCA)
• Bland haemorrhage (anticoagulation, mitral stenosis, toxins)
• Diffuse alveolar damage (ARDS, infection, transplantation).
🤝 Associations
- ANCA-associated vasculitides:
• Microscopic polyangiitis
• Granulomatosis with polyangiitis (GPA)
• Eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss)
- Autoimmune: Goodpasture (anti-GBM), SLE, mixed connective tissue disease, antiphospholipid syndrome.
- Other: HSP, cryoglobulinaemia, coagulopathy, HIV, Kaposi sarcoma, inhaled toxins, drugs (e.g. amiodarone, nitrofurantoin), mitral valve disease, pulmonary veno-occlusive disease, malignancy.
- Post allo-HSCT: DAH can complicate engraftment or GVHD.
🔺 Classical Triad
- Symptoms: Dyspnoea, haemoptysis (may be absent in 30%), anaemia.
- Imaging: CXR/CT → bilateral ground-glass opacities ± “bat-wing” alveolar infiltrates, usually no effusion, heart size normal.
- Bronchoscopy with BAL: Progressively bloodier aliquots on lavage = diagnostic. 🧪
👩⚕️ Clinical Features
- Rapid onset hypoxaemia, cough, haemoptysis (may be subtle or occult).
- Constitutional features if vasculitis/SLE present (fever, arthralgia, rash, renal disease).
- Severe cases: shock, acute respiratory failure, acute renal failure (pulmonary–renal syndrome).
🧪 Investigations
- Bloods: Falling Hb/Hct, ↑LDH.
- Serology: ANCA, anti-GBM, ANA, dsDNA, antiphospholipid antibodies.
- Clotting screen: Rule out coagulopathy.
- CXR: Diffuse bilateral alveolar infiltrates.
- CT Chest: Patchy or diffuse ground-glass opacities; sometimes “crazy-paving.”
- ABG: Hypoxaemia, possible Type I respiratory failure.
- Echo: Exclude cardiac cause (mitral stenosis, LV dysfunction).
- Bronchoscopy: Bloody BAL fluid diagnostic.
⚠️ Complications
- Acute respiratory failure requiring mechanical ventilation.
- Disseminated intravascular coagulation (DIC).
- Progression to organising pneumonia and pulmonary fibrosis.
💊 Management
- Stabilisation: ABC protocol, high-flow O₂, ventilatory support if required. Treat superadded infection with broad-spectrum antibiotics if suspected.
- Stop offending agents: Withdraw anticoagulants, offending drugs, correct coagulopathy.
- Immunosuppression: High-dose IV corticosteroids (methylprednisolone). Add cyclophosphamide or rituximab for vasculitis.
- Plasma exchange: Indicated in anti-GBM (Goodpasture) and severe vasculitis with pulmonary–renal syndrome.
- Targeted therapy:
• ANCA vasculitis → Cyclophosphamide/Rituximab
• Anti-GBM → PLEX + Cyclophosphamide
• SLE/APL → Steroids ± Rituximab, anticoagulation balancing bleeding risk
📚 References
