neumonia eosinifilica

Idiopathic acute eosinophilic pneumonia (AEP) typically presents with an acute febrile illness of less than four weeks duration (often less than seven days), a nonproductive cough, and progressively worsening dyspnea. Associated symptoms and signs may include malaise, myalgias, night sweats, and pleuritic chest pain. (See 'Introduction' above and 'Clinical features' above.)

●AEP has been associated most often with new onset or resumption of cigarette smoking. Heavy inhalational exposure to smoke, fine sand, and dust has also been associated with AEP. (See 'Etiology' above.)

●Lung histopathology obtained in a small number of patients reveals extensive abnormality with marked eosinophilic infiltration in the interstitium and alveolar spaces, acute and/or organizing diffuse alveolar damage, and absence of granulomas or hemorrhage. (See 'Pathology' above.)

●At presentation, the peripheral blood count usually shows a neutrophilic leukocytosis without eosinophilia, although peripheral blood eosinophilia may develop over the course of the disease. (See 'Laboratory studies' above.)

●The initial chest radiograph may show only subtle reticular or ground glass opacities, often with Kerley B lines. As the disease progresses, bilateral diffuse mixed ground glass and reticular opacities develop. Typical findings on high resolution computed tomography (HRCT) scans include bilateral, random, and patchy ground-glass or reticular opacities and also small bilateral pleural effusions. (See 'Imaging' above.)

●A confident diagnosis of AEP can usually be made on the basis of the combination of an acute febrile illness of short duration (one month or less), hypoxemic respiratory failure, diffuse pulmonary opacities on chest radiograph, and bronchoalveolar lavage eosinophilia (>25 percent), after exclusion of infection, vasculitis, or other known precipitants (eg, drugs, irradiation) (table 1). (See 'Diagnosis' above and "Causes of pulmonary eosinophilia".)

●For the majority of patients with AEP, we recommend treatment with systemic glucocorticoids after exclusion of infection (Grade 1B). This recommendation is due to the severity and progressive nature of respiratory impairment and the dramatic response to glucocorticoids. The optimal dose of glucocorticoids is not known, but a reasonable course is to select the dose based upon the severity of respiratory impairment. (See 'Treatment'above.)

•In the presence of severe hypoxemia or respiratory failure requiring mechanical ventilation, methylprednisolone (60 to 125 mg every six hours) is given until respiratory failure resolves (usually within one to three days).

•In the absence of respiratory failure (eg, pulse oxygen saturation >92 percent on room air), initial treatment with oral prednisone (40 to 60 mg daily) is reasonable.

●Oral prednisone is continued at a dose of 40 to 60 mg per day for two weeks beyond the complete resolution of symptoms and conventional chest radiograph abnormalities. Prednisone is then tapered over approximately four weeks and discontinued. (See 'Treatment' above.)

●As cigarette smoking initiation or increase in amount are often associated with AEP and as relapses have been associated with resumption of smoking, complete smoking cessation should be strongly encouraged. (See'Treatment' above.)

●Symptomatic and radiographic improvement is usually rapid and progressive with complete radiographic clearing over one to two months. Relapse is uncommon and is usually attributable to resumption of cigarette smoking after initial cessation. (See 'Outcomes' above.)

RAPHICS

Known causes of acute eosinophilic pneumonia

Drug or toxin reactions

Nitrofurantoin

Phenytoin

L-tryptophan

Ampicillin

Minocycline

Acetaminophen

Inhaled pentamidine isethionate

Ranitidine

GM-CSF

Oxaliplatin

Trazodone (overdose)

Inhalation of heroin

Inhalation of crack cocaine

Inhalation of Scotchguard

Inhalational injury following building collapse

Infections

Human immunodeficiency virus

Parasitic infections (Toxocara, filaria, Strongyloides, Ascaris, and Paragonimus)

Fungal infections (Coccidioides immitis, Trichosporon terrestre, Trichosporon cutaneum, Trichoderma viride)

Aspergillus sp*

Coxsackie A2 virus*

Stenotrophomonas maltophilia*

Other associations

Chronic myelogenous leukemia

Guillain-Barré syndrome

Hypersensitivity to "red spider" allergens

Postoperative respiratory failure of unknown etiology

* Following lung transplantation.

Graphic 65178 Version 1.0

Acute eosinophilic pneumonia

Low power photomicrograph from a patient with acute eosinophilic pneumonia illustrates air space exudate and alveolar septal thickening resembling that seen in the organizing phase of diffuse alveolar damage.

Courtesy of Jeffrey L Myers, MD.

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Normal lung

Low power photomicrograph of normal lung tissue shows open alveoli with thin, capillary- containing interstitial spaces. An artery (A) is identifiable by its thick, muscular wall; the accompanying bronchus (B) contains mucoid material and is lined by columnar respiratory epithelial cells.

Courtesy of Steven E Weinberger, MD.

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Acute eosinophilic pneumonia

High power photomicrograph of acute eosinophilic pneumonia shows a mixed inflammatory infiltrate expanding the alveolar septa and spilling into adjacent air spaces. The inflammatory infiltrate contains numerous eosinophils and mononuclear cells and is accompanied by a fibrinous exudate resembling hyaline membranes (arrow).

Courtesy of Jeffrey L Myers, MD.

Graphic 58648 Version 2.0

Normal lung

High power photomicrograph shows alveoli containing capillaries within a narrow interstitium. The alveoli are lined with thin, elongated type I pneumocytes (arrow) and smaller numbers of cuboidal type II pneumocytes (dashed arrow).

Courtesy of Steven E Weinberger, MD.

Graphic 80140 Version 2.0

Acute eosinophilic pneumonia

Posteroanterior chest radiograph of a patient with idiopathic acute eosinophilic pneumonia demonstrating bilateral mixed alveolar and reticular opacities.

Courtesy of Steven E Weinberger, MD.

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Acute eosinophilic pneumonia

Chest CT scan of a patient with idiopathic acute eosinophilic pneumonia demonstrating bilateral patchy ground-glass opacities.

CT: computed tomography.

Courtesy of Steven E Weinberger, MD.

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Acute eosinophilic pneumonia on radiography and CT

These images were obtained from a 42-year-old man with progressive dyspnea over one month; acute eosinophilic pneumonia was diagnosed based on the clinical presentation, a bronchoalveolar lavage showing 51 percent eosinophils, and response to therapy. An anteroposterior radiograph (A) shows patchy opacities predominantly involving the lower lobes, middle lobe, and lingual (arrows). This pattern is unlike heart failure since the left atrium is not enlarged, there is no vascular redistribution, and the opacities are diffuse in nature and not perihilar. A CT with coronal reconstruction (B) shows patchy opacities involving all segments of the lung (arrows). An axial CT at the level of the carina (C) shows a combination of ground glass and consolidative opacities in the anterior segments of both upper lobes (arrows). A CT scan through the mid chest (D) shows pulmonary opacities centered along thickened broncho-vascular bundles (arrows).

CT: computed tomography.