Synopsis
Recognise eosinophilic pulmonary syndromes, distinguish isolated pneumonia from systemic vasculitis or secondary causes, and escalate hypoxaemia and organ-threatening disease safely.
- Pulmonary eosinophilia means eosinophils are implicated in lung disease; the task is to identify whether disease is primary, vasculitic, allergic, parasitic or drug induced.
- Acute eosinophilic pneumonia presents over days with fever, diffuse infiltrates and hypoxaemia; blood eosinophilia may be absent initially.
- Chronic eosinophilic pneumonia usually evolves over weeks with cough, breathlessness, constitutional symptoms, asthma and peripheral-predominant air-space opacity.
- EGPA combines eosinophilic inflammation with variable necrotising small-vessel vasculitis, often in an adult with asthma and chronic rhinosinusitis.
- Cardiac involvement, mononeuritis multiplex, renal injury, gastrointestinal ischaemia or CNS disease makes suspected EGPA urgent regardless of the chest radiograph.
- ABPA should be considered when asthma or bronchiectasis coexists with high total IgE, Aspergillus sensitisation, eosinophilia and mucus plugging or central bronchiectasis.
- Build a medicine and travel timeline: daptomycin and other drugs can cause eosinophilic pneumonia, while helminth infection changes both diagnosis and steroid safety.
- Bronchoalveolar lavage eosinophilia supports acute disease when peripheral counts lag, but lavage findings still require exclusion of infection and other causes.
- Corticosteroid response is often dramatic yet not diagnostic; relapse after taper is more typical of chronic disease than a completely treated acute episode.
- Benralizumab is a NICE-approved add-on option for eligible relapsing or refractory adult EGPA, delivered through specialist vasculitis services rather than general eosinophilic pneumonia care.
Key red flags
Days of febrile respiratory illness, diffuse bilateral opacity, severe hypoxaemia and often pleural fluid occur in a previously healthy person; recent smoking or inhalational change may be reported.
Chest pain, heart failure, arrhythmia, syncope, foot or wrist drop, asymmetric painful neuropathy, seizures or encephalopathy in suspected EGPA requires emergency organ-specific assessment.
Cough, fever, dyspnoea and infiltrates begin after a plausible medicine, sometimes weeks into treatment; daptomycin is a recognised trigger and blood eosinophilia can initially be normal.
Investigation priorities
Quantify eosinophilia and observe its trajectory before treatment.
Management branches
Pulmonary infiltrates coexist with blood or lavage eosinophilia, or acute disease remains strongly suspected.
- Assess respiratory severity and systemic organ danger first, obtaining urgent cardiac, neurological or renal input when features suggest EGPA rather than isolated pneumonia.
- Map onset against asthma, sinonasal disease, new smoking, medicines, travel, parasites, fungal sensitisation and systemic symptoms; repeat the eosinophil count if initially normal.
- Use HRCT, lavage and cause-directed blood, urine and microbiology tests to distinguish acute or chronic eosinophilic pneumonia, EGPA, ABPA and secondary disease.
- Discuss uncertain or organ-threatening cases with respiratory, vasculitis, infectious-disease and radiology specialists before defining the long-term treatment label.