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Acute eosinophilic pneumonia — SCE Respiratory MCQ

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HardACEPAcute eosinophilic pneumoniaSCE Respiratory

A 24-year-old man is admitted with 5 days of fever, pleuritic chest pain and rapidly progressive breathlessness. He has no history of asthma, atopy or systemic disease and takes no medication. Three weeks earlier, he began vaping nicotine frequently, having never previously smoked or vaped. He requires invasive ventilation for severe hypoxaemic respiratory failure. CT shows diffuse bilateral ground-glass opacification, smooth interlobular septal thickening and small bilateral pleural effusions. His admission eosinophil count is 0.1 × 10^9/L. Bronchoalveolar lavage contains 38% eosinophils. BAL bacterial, fungal and mycobacterial cultures, respiratory viral PCR and Pneumocystis jirovecii PCR are negative. There is no relevant travel or parasite exposure. ANCA is negative, urinalysis is normal, and there are no cutaneous, neurological or upper-airway manifestations. Which management plan is most appropriate?

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Correct answer: C — Stop vaping and give intravenous corticosteroid, followed by oral prednisolone to complete approximately 2 weeks

Explanation lettering: D = shown as A · A = shown as B · B = shown as D

This is smoking-related acute eosinophilic pneumonia (AEP). The decisive features are an acute febrile illness of less than 1 month, diffuse bilateral infiltrates, BAL eosinophilia above 25%, exclusion of infection and a recent change in inhalational exposure. Peripheral eosinophilia is commonly absent initially, particularly in smoking-related AEP, and its absence should not delay treatment. Severe hypoxaemic respiratory failure is a recognised presentation. The inciting exposure should be withdrawn and systemic corticosteroids started promptly. Intravenous treatment is appropriate while the patient is ventilated, followed by oral prednisolone as he improves. Unlike chronic eosinophilic pneumonia, AEP usually resolves completely without relapse; cohort evidence supports a total corticosteroid course of approximately 2 weeks even in respiratory failure. A is inappropriate because pulmonary eosinophilia already establishes the relevant eosinophilic process after infection has been excluded; waiting for blood eosinophilia risks delay. B reflects treatment for chronic eosinophilic pneumonia, which has a subacute course and frequent relapse during tapering. D would be appropriate for organ-threatening eosinophilic granulomatosis with polyangiitis, but there is no asthma, vasculitic organ involvement or supporting serology. E is plausible because some mild AEP cases improve after exposure cessation alone, but observation is inappropriate in severe respiratory failure requiring invasive ventilation.

Reference: Idiopathic eosinophilic pneumonias (2023) — https://publications.ersnet.org/binary/ersworks/4adeb01c44df48b9/82abe59b7e94b9c0d18454de0b53f351189c25ab67dec5f7e5463818253329d4/9781849841672_chapter_20.pdf Clinical characteristics and corticosteroid treatment of acute eosinophilic pneumonia (2013) — https://publications.ersnet.org/content/erj/41/2/402 Acute Eosinophilic Pneumonia: Causes, Diagnosis, and Management (2018) — https://pubmed.ncbi.nlm.nih.gov/29206477/