Diffuse alveolar haemorrhage and pulmonary-renal syndromes — Rapid

Synopsis

Recognise diffuse alveolar haemorrhage with or without glomerulonephritis, secure respiratory and renal support, and obtain urgent multidisciplinary diagnosis before irreversible lung or kidney injury.

Diffuse alveolar haemorrhage is bleeding into the alveolar space from pulmonary microvasculature; haemoptysis may be absent, especially in intubated or severely ill patients.
The core pattern is acute breathlessness or hypoxaemia, new bilateral ground-glass or air-space opacity, falling haemoglobin and bloodier sequential lavage aliquots when bronchoscopy is safe.
Pulmonary–renal syndrome combines alveolar haemorrhage with glomerulonephritis, classically from ANCA-associated vasculitis, anti-GBM disease or systemic lupus erythematosus.
Urinalysis is a rapid high-value test: blood, protein and casts with rising creatinine make a capillaritic pulmonary–renal process much more likely.
Normal coagulation or absent haemoptysis does not exclude haemorrhage. Anticoagulation and thrombocytopenia may cause bland bleeding but do not explain active urinary sediment.
Send PR3-ANCA, MPO-ANCA, anti-GBM antibodies, ANA, dsDNA and complement early, but interpret them with phenotype and tissue because false-positive and seronegative disease occur.
Bronchoscopy supports diagnosis and infection sampling but can destabilise severe hypoxaemia; do not require it before urgent expert treatment when the clinical picture is compelling.
Kidney biopsy often provides safer and more specific tissue than lung biopsy when glomerulonephritis is present.
Severe ANCA-associated disease is induced with glucocorticoids plus rituximab or cyclophosphamide under specialist guidance. Anti-GBM disease often requires urgent plasma exchange as part of a distinct protocol.
Infection, drug toxicity and immune haemorrhage can coexist. Immunosuppression demands active microbiological assessment and prophylaxis planning.

Key red flags

Diffuse alveolar haemorrhage

Acute hypoxaemia, diffuse or patchy bilateral ground-glass opacity and a falling haemoglobin suggest DAH; haemoptysis strengthens but is not required for the diagnosis.

Pulmonary–renal syndrome

Haematuria, proteinuria, red-cell casts or rapidly rising creatinine alongside pulmonary haemorrhage indicates glomerulonephritis and needs immediate nephrology and vasculitis assessment.

ANCA-associated vasculitis

ENT disease, mononeuritis multiplex, purpura, constitutional symptoms, orbital inflammation or pulmonary nodules accompany capillaritis in granulomatosis with polyangiitis or microscopic polyangiitis.

Anti-GBM disease

Abrupt severe alveolar haemorrhage with rapidly progressive glomerulonephritis, sometimes after smoking or hydrocarbon exposure, requires immediate anti-GBM testing and specialist plasma-exchange consideration.

Bland or medicine-related haemorrhage

Anticoagulation, thrombocytopenia, coagulopathy, severe left-sided filling pressure or selected drugs may cause bleeding without systemic capillaritis; active urinary sediment argues for an immune process.

Mimic or coexisting infection

Severe bilateral pneumonia, oedema and ARDS can look identical. Fever, immunosuppression and focal consolidation require broad microbiological sampling even when immune disease is likely.

Investigation priorities

FBC, serial haemoglobin, platelets and coagulation screenFirst step

Detect blood loss, thrombocytopenia and a reversible haemostatic contributor.

Management branches

First hoursStabilise and recognise the syndrome

Hypoxaemia with bilateral opacities, haemoptysis or unexplained haemoglobin fall.

Use ABCDE care, controlled oxygen and early critical-care support; crossmatch blood and assess the need for invasive ventilation.
Stop or reverse anticoagulation and correct severe haemostatic defects when clinically justified, balancing thrombosis risk.
Send FBC, coagulation, renal profile, urinalysis, ANCA, anti-GBM, lupus tests and microbiology immediately.
Involve respiratory, renal and rheumatology teams together and treat severe infection in parallel when plausible.

Key medicines

Systemic glucocorticoid inductionUse a specialist acute regimen followed by a protocolised reduction, selected for disease severity, age, infection risk and the current BSR recommendation.High exposure increases infection, hyperglycaemia, delirium, myopathy, gastrointestinal and bone harm. Obtain microbiology promptly and use prophylaxis and monitoring rather than prolonging empirically.

RituximabGive only through the vasculitis service using a licensed or commissioned induction schedule, with pre-infusion screening and current product information.Screen hepatitis B, immunoglobulins, infection and vaccination status; infusion reactions, late neutropenia and hypogammaglobulinaemia require monitoring. It is not immediate mechanical haemostasis.

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