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Acute Eosinophilic Pneumonia

By

Joyce Lee

, MD, MAS, University of Colorado Denver

Last full review/revision Sep 2019| Content last modified Sep 2019
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Acute eosinophilic pneumonia (AEP) is a disorder of unknown etiology characterized by rapid eosinophilic infiltration of the lung interstitium.

In contrast to chronic eosinophilic pneumonia, acute eosinophilic pneumonia is an acute illness that does not usually recur. Incidence and prevalence are unknown. Acute eosinophilic pneumonia can occur at any age but most often affects patients between 20 and 40 years, with a male-to-female ratio of 2:1.

The cause is unknown, but acute eosinophilic pneumonia may be an acute hypersensitivity reaction to an unidentified inhaled antigen in an otherwise healthy person. Cigarette or other smoke exposure may be involved.

Symptoms and Signs

Acute eosinophilic pneumonia causes an acute febrile illness of short duration (usually < 7 days). Symptoms are nonproductive cough, dyspnea, malaise, myalgias, night sweats, and pleuritic chest pain.

Signs include tachypnea, fever (often > 38.5° C), and bibasilar inspiratory crackles and, occasionally, rhonchi on forced exhalation.

Patients with acute eosinophilic pneumonia frequently present with acute respiratory failure requiring mechanical ventilation. Rarely, distributive (hyperdynamic) shock can occur.

Diagnosis

  • High-resolution CT (HRCT)

  • Usually complete blood count (CBC), pleural fluid analysis, and pulmonary function testing

  • Bronchoscopy for lavage and, sometimes, biopsy

The diagnosis of acute eosinophilic pneumonia is suspected in patients with symptoms of acute pneumonia that progress to respiratory failure and do not respond to antibiotics. Diagnosis is based on findings from routine testing and is confirmed by bronchoscopy.

Acute eosinophilic pneumonia is a diagnosis of exclusion and requires the absence of known causes of eosinophilic pneumonia (eg, drug- and toxin-induced, helminthic and fungal infection–related, eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, tumors).

The CBC often fails to demonstrate markedly elevated eosinophil counts, unlike in chronic eosinophilic pneumonia. Erythrocyte sedimentation rate (ESR) and IgE levels are high but are nonspecific.

The chest x-ray initially may show only subtle reticular or ground-glass opacities, often with Kerley B lines. Isolated alveolar (about 25% of cases) or reticular (about 25% of cases) opacities may also be observed. Unlike in chronic eosinophilic pneumonia, in acute eosinophilic pneumonia opacities are not characteristically localized to the lung periphery. Small pleural effusions occur in two thirds of patients and are frequently bilateral.

HRCT is always abnormal with bilateral, random, patchy ground-glass or reticular opacities.

Pleural fluid examination shows marked eosinophilia with high pH.

Pulmonary function tests often show a restrictive process with reduced diffusing capacity for carbon monoxide (DLCO).

Bronchoscopy should be done for lavage and, occasionally, biopsy. Bronchoalveolar lavage fluid often shows a high number and percentage (> 25%) of eosinophils. The most common histopathologic features on biopsy include eosinophilic infiltration with acute and organizing diffuse alveolar damage, but few patients have undergone lung biopsy.

Treatment

  • Systemic corticosteroids

Some patients with acute eosinophilic pneumonia improve spontaneously. Most are treated with prednisone 40 to 60 mg orally once a day. In patients with respiratory failure, methylprednisolone 60 to 125 mg IV every 6 hours is preferred.

The prognosis of acute eosinophilic pneumonia is usually good; response to corticosteroids and complete recovery are common. Pleural effusions resolve more slowly than parenchymal opacities.

Drugs Mentioned In This Article

Drug Name Select Trade
MEDROL
RAYOS
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