Case Presentation:

Pulmonary infiltrates with eosinophilia (PIE syndrome) is characterized by eosinophilic pulmonary infiltrates and peripheral blood eosinophilia. We describe clinical,radiological and histological presentation of a patient with chronic eosinophilic pneumonia.55–year–old lady with a h/O asthma complained of cough,fever and night sweats for 2 weeks. It started with a mild runny nose and sore throat with body aches. She denied any medication intake or travel outside US. Her CXR showed RUL infiltrate and was treated with avelox for 10 days. She continued with fevers and drenching night sweats. PE showed rales in right chest. CT chest showed worsening of patchy peripheral pulmonary infiltrates involving right upper, middle, and bilateral lower lobes. Labs revealed CBC with 44% peripheral eosinophilia, negative ANCA and negative stool ova and parasite. Bronchoscopy and biopsy revealed BAL with 85% eosinophils, eosinophilic infiltration of alveoli consistent with eosinophilic pneumonia. She responded well to steroids with complete resolution of symptoms and CXR findings in 2 weeks.

Discussion:

PIE syndrome is classified as medications induced, Loeffler’s syndrome related to Ascaris, Strongyloides infections, tropical pulmonary eosinophilia related to microfilaria infections, Churg–Strauss syndrome(CSS), allergic bronchopulmonary aspergillosis(ABPA), Bronchocentric granulomatosis(BCG), acute and chronic eosinophilic pneumonias(CEP). Medications causing PIE syndrome include NSAIDS, abx notably daptomycin among others. Loeffler’s syndrome is caused by helminths migrating through the lungs causing transient pulmonary infiltrates. CSS is an ANCA positive vasculitic disorder characterized by sinusitis, asthma, and pulmonary eosinophilia. ABPA presents with sinusitis, bronchiectasis, elevated IgE levels and radiologic finding of central bronchiectasis. BCG presents with granulomatous destruction of the bronchi and has eosinophilic infiltration. Clinically resembles ABPA. Acute eosinophilic pneumonia (AEP) presents as acute onset of respiratory failure, fever, and pulmonary infiltrates. Peripheral eosinophilia is rare. Characteristic CT findings include bilateral ground glass opacities and consolidations. BAL shows eosinophilia >25% but less than that seen in CEP. AEP responds well to steroids. CEP presents with the insidious onset of dyspnea, fever, cough, and pulmonary infiltrates. It affects predominantly middle aged women and 50% are asthmatics. A CXR finding consists of peripheral patchy pulmonary infiltrates although classic “photographic negative” of pulmonary edema is seen in only 1/3rd of patients. BAL shows eosinophilia >40%.

Conclusions:

Patients presenting with cough, fever, peripheral pulmonary infiltrates with peripheral and BAL eosinophilia without parasitic, helminthic risk factors is highly suggestive of CEP. Exquisite response to steroids is seen in CEP though recurrence is common.