Eosinophilic pneumonia differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Acute eosinophilic pneumonia may be differentiated from other causes of pulmonary eosinophilia such as acute eosinophilic pneumonia, the transpulmonary passage of helminth larvae (Löffler syndrome), tropical pulmonary eosinophilia, eosinophilic granulomatosis with polyangiitis, allergic bronchopulmonary aspergillosis, and drugs and toxins.

Differential Diagnosis

Acute eosinophilic pneumonia may be differentiated from other causes of pulmonary eosinophilia.

Acute eosinophilic pneumonia (AEP)

• The cause of acute eosinophilic pneumonia is unknown.
• Some investigators have suggested that AEP is an acute hypersensitivity reaction to an unidentified inhaled antigen in an otherwise healthy individual.

Transpulmonary passage of helminth larvae (Löffler syndrome)

• Three types of helminths, Ascaris (A. lumbricoides, A. suum), hookworms (Ancylostoma duodenale, Necator americanus), and Strongyloides stercoralis, have larvae that reach the lungs, penetrate into alveoli, and ascend the airways then reach the gastrointestinal tract.
• Ascaris is the most common cause of Löffler syndrome worldwide.

Tropical pulmonary eosinophilia

• Tropical pulmonary eosinophilia is immune response to the bloodborne microfilarial stages of the lymphatic filariae and Wuchereria bancrofti.
• The typical symptoms are cough, breathlessness, wheezing, fatigue, and fever. Pulmonary function tests may show a mixed restrictive and obstructive abnormality with a reduction in diffusion capacity.

Eosinophilic granulomatosis with polyangitis

• Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) is a vasculitic disorder often characterized by sinusitis, asthma, and prominent peripheral blood eosinophilia.
• It is the sole form of vasculitis that is associated with both eosinophilia and frequent lung involvement. In addition to the lungs, the skin and the cardiovascular, gastrointestinal, renal, and neurologic systems may also be involved.

Allergic bronchopulmonary aspergillosis

• Allergic bronchopulmonary aspergillosis (ABPA) is a complex hypersensitivity reaction that occurs when airways become colonized by Aspergillus. 
• Repeated episodes of bronchial obstruction, inflammation, and mucoid impaction can lead to bronchiectasis, fibrosis, and respiratory compromise.
• Immunologic responses elicited by Aspergillus fumigatus are responsible for this syndrome.

Drugs and toxins

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a drug-induced hypersensitivity reaction that includes skin eruption, eosinophilia, atypical lymphocytosis, lymphadenopathy, and kidney involvement. Drugs causing DRESS are:

• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Anticonvulsants
• Antidepressants
• Angiotensin converting enzyme inhibitors
• Beta blockers
• Hydrochlorothiazide
• Sulfa-containing compounds

	Clinical Picture	Laboratory diagnosis	Imaging	Pulmonary function tests	Treatment
Acute eosinophilic pneumonia	Onset <1 month Acute onset of dyspnea Fever Cough Pleuritic pain Myalgias Acute respiratory distress syndrome	Bronchoalveolar lavage showing eosinophilia is often the key to the diagnosis of IAEP. Bronchoalveolar lavage showing eosinophilia may persist for several weeks.	Bilateral infiltrates Poorly defined nodules Ground-glass attenuation Interlobular septal thickening Bilateral pleural effusion Thickening of bronchovascular bundles	A mildly restrictive ventilatory defect Reduced carbon monoxide transfer capacity Hypoxemia A PaO2/FiO2 300 mm Hg)	Systemic corticosteroids for 2 weeks A starting dose of oral prednisone of 30 mg per day, or 1 to 2 mg/kg per day IAEP does not relapse
Chronic eosinophilic pneumonia	Onset >2–4 week Dyspnea Cough Rhinitis or sinusitis Wheezes Fatigue Malaise Fever	Peripheral blood eosinophilia 6000/mm3	Bilateral alveolar infiltrates with ill-defined margins Ground-glass opacities Septal line thickening Mediastinal lymphadenopathy Pleural effusion	Airflow obstruction, and the other half have a restrictive ventilatory defect Mild hypoxemia	Oral corticosteroids Initial dose of 0.5 mg/kg per day of oral prednisone for 2 weeks Relapses occur in more than half the patients while decreasing or after stopping corticosteroids
Allergic bronchopulmonary aspergillosis	Stages of ABPA: Acute Remission Recurrent exacerbations Corticosteroid-dependent asthma Fibrotic end stage RF Chronic cough Dyspnea Low-grade fever Chronic rhinitis	Eosinophils greater than 1000/ mm Total and Aspergillus-specific IgE levels increase sputum examination Fungal mycelia can be found Sputum cultures often positive for Pseudomonas aeruginosa if bronchiectasis occurs	Central cylindrical bronchiectasis Bronchial wall thickening Mucus plugging: “finger-in-glove” pattern Ground-glass attenuation Airspace consolidation Bronchiolitis: tree-in-bud pattern Centrilobular nodules		The mainstay of treatment for ABPA is the use of corticosteroids Oral prednisolone: 0.5 mg kg per day for 2 weeks Followed by 0.5 mg kg per day on alternate days for 8 weeks High-dose methylprednisolone may be used in refractory ABPA Oral itraconazole for 16 to 32 weeks Omalizumab with difficult asthma
Eosinophilic granulomatosis with polyangitis	3 phases: Rhinosinusitis and asthma Blood and tissue eosinophilia, Systemic vasculitis Asthma is always present in EGPA Chronic rhinitis in 75% of cases Chronic paraseptal sinusitis and nasal polyposis Asthenia, weight loss, fever, arthralgias Glomerulonephritis Eosinophilic myocarditis and coronary arteritis may cause heart failure	Peripheral blood eosinophilia: Between 5 and 20,000/mm Bronchoalveolar lavage showing eosinophilia greater than 25% and usually greater than 40% Increase in serum IgE and C-reactive protein ANCAs are found in only 40% of patients	Pulmonary infiltrates: ill-defined opacities with peripheral predominance Ground-glass opacities Airspace consolidation Centrilobular nodules Bronchial wall thickening Interlobular septal thickening Hilar or mediastinal lymphadenopathy Pleural effusion	Airflow obstruction is present in 70% of patients Mild airflow obstruction may persist in 30% to 40% of patients	Corticosteroids A dose of 1 mg/kg per day for 3 to 4 weeks An initial methylprednisolone bolus (15 mg/kg per day for 1–3 days) may be indicated in the most severe cases. Subcutaneous interferon High-dose intravenous immunoglobulins Plasma exchange Cyclosporine Rituximab Approximately 25% of patients experience at least 1 relapse The 5-year overall survival in EGPA is currently greater than 95 Cardiac involvement “Poor prognostic” criteria: Age older than 65 years; cardiac symptoms; gastrointestinal involvement; renal insufficiency with serum creatinine greater than 150 mg/L; and absence of ear, nose, and throat manifestation