Acute eosinophilic pneumonia (AEP) is a disorder of varied etiology characterized by rapid eosinophilic infiltration of the lung interstitium. Respiratory distress and rapid progression to respiratory failure is common. Diagnosis is based on imaging (radiography and high-resolution computed tomography) and bronchoalveolar lavage demonstrating eosinophils. Treatment almost always involves systemic glucocorticoids and sometimes mechanical ventilation. Prognosis is generally good.
In contrast to chronic eosinophilic pneumonia, acute eosinophilic pneumonia is an acute illness that does not usually recur. There are limited data about the frequency of the disease, but it is thought to be rare. One study of deployed U. S. military personnel reported an incidence rate of approximately 9 per 100,000 person-years (1). 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 unclear, but acute eosinophilic pneumonia may be an acute hypersensitivity reaction to certain triggers such as inhaled toxic fumes, medications, or infections (2). Cigarette or other smoke exposure, particularly among new smokers, as well as fine airborne desert sand or dust appear to be triggers (1). However, in many cases, no cause can be identified and it is idiopathic. A history of asthma and allergic disease may be present. Because of its rarity, it is often a diagnosis of exclusion.
General references
1. Shorr AF, Scoville SL, Cersovsky SB, et al. Acute eosinophilic pneumonia among US Military personnel deployed in or near Iraq. JAMA 2004;292(24):2997-3005. doi:10.1001/jama.292.24.2997
2. Allen J, Wert M. Eosinophilic Pneumonias. J Allergy Clin Immunol Pract. 2018;6(5):1455-1461. doi:10.1016/j.jaip.2018.03.011
Symptoms and Signs of Acute Eosinophilic Pneumonia
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), hypoxia, and bibasilar inspiratory crackles and, occasionally, rhonchi on forced exhalation.
Acute eosinophilic pneumonia can rapidly progress to acute respiratory failure, requiring mechanical ventilation. Rarely, distributive (hyperdynamic) shock can occur.
Diagnosis of Acute Eosinophilic Pneumonia
High-resolution CT (HRCT)
Usually complete blood count (CBC) with differential and pleural fluid analysis (if effusion present)
Exclusion of other autoimmune or infectious causes of acute pneumonia
Bronchoscopy for lavage and, rarely, biopsy
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 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.
The CBC with differential often fails to demonstrate markedly elevated eosinophil counts, unlike in chronic eosinophilic pneumonia. Erythrocyte sedimentation rate (ESR) and IgE levels can be high but are nonspecific.
The chest radiograph initially may show only subtle reticular or ground-glass opacities (or attenuation), 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 and high pH.
Pulmonary function testing is not diagnostic but often shows a restrictive process with reduced diffusing capacity of the lung for carbon monoxide (DLCO).
Bronchoscopy should be performed for lavage if patients are clinically stable enough to tolerate the procedure. Bronchoalveolar lavage (BAL) fluid often shows a high number and percentage (> 25%) of eosinophils. Biopsy is rarely needed and typically reserved for patients who do not respond adequately to systemic glucocorticoids or in whom an infectious etiology cannot be excluded by BAL. The most common histopathologic features on biopsy include eosinophilic infiltration with acute and organizing diffuse alveolar damage.
Treatment of Acute Eosinophilic Pneumonia
Systemic glucocorticoids
Sometimes mechanical ventilation
Some patients with acute eosinophilic pneumonia improve spontaneously. However, most require treatment with high doses of oral prednisone. In patients with respiratory failure, intravenous methylprednisolone is preferred. Some patients with acute eosinophilic pneumonia improve spontaneously. However, most require treatment with high doses of oral prednisone. In patients with respiratory failure, intravenous methylprednisolone is preferred.Mechanical ventilation is initiated if hypoxemic respiratory failure is present; choice of ventilatory modality (such as intubation) depends on extent of involvement.
The prognosis of acute eosinophilic pneumonia is usually good if treatment is initiated immediately; response to glucocorticoids within 1 to 2 days and complete recovery within 4 to 8 weeks are common. Radiographic improvement lags behind clinical response. Pleural effusions resolve more slowly than parenchymal opacities.
