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

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 [1].

Transpulmonary passage of helminth larvae (Löffler syndrome)

  • Three types of helminths, Ascaris (A. lumbricoidesA. suum), hookworms (Ancylostoma duodenaleNecator americanus), and Strongyloides stercoralis, have larvae that reach the lungs, penetrate into alveoli, and ascend the airways then reach the gastrointestinal tract. [10]
  • Ascaris is the most common cause of Löffler syndrome worldwide. [11]

Tropical pulmonary eosinophilia

  • Tropical pulmonary eosinophilia is immune response to the bloodborne microfilarial stages of the lymphatic filariae and Wuchereria bancrofti. [16-18].
  • 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. [18]

Eosinophilic granulomatosis with polyangitis

  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) is a vasculitic disorder often characterized by sinusitis, asthma, and prominent peripheral blood eosinophilia. [49]
  • 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. [51]
  • 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) [26]
  • anticonvulsants
  • antidepressants
  • angiotensin converting enzyme inhibitors
  • beta blockers
  • hydrochlorothiazide
  • sulfa-containing compounds [27]

Differential Diagnosis

Clinical Picture Laboratory diagnosis Imaging Pulmonary function tests Treatment
Acute eosinophilic pneumonia Onset <1 month
Chronic eosinophilic pneumonia Onset >2–4 week
Transpulmonary passage of helminth larvae
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
  • mucous plugging: “finger-in-glove” pattern
  • ground-glass attenuation
  • airspace consolidation.
  • Bronchiolitis: tree-in-bud pattern
  • centrilobular nodules and
  • 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

  • BAL 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
  • 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 manifestations.159,162  

References

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