Pneumonia eosinofílica aguda idiopática: aspectos clínicos e diagnóstico

Abstract

Introduction: Idiopathic acute eosinophilic pneumonia (AEP) typically presents with an acute febrile illness lasting less than four weeks (usually 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. PEA has been most frequently associated with new initiation or resumption of smoking. Heavy inhalational exposure to smoke, fine sand, and dust has also been linked to ASD. Lung histopathology obtained in a small number of patients reveals extensive abnormality with marked eosinophilic infiltration in the interstitial and alveolar spaces, acute alveolar damage and/or diffuse organization, and absence of granulomas or hemorrhage. Objectives:discuss the clinical and diagnostic aspects of acute eosinophilic pneumonia.  Methodology: Integrative literature review based on scientific databases from Scielo, PubMed and VHL, from January to April 2024, with the descriptors "Acute Eosinophilic Pneumonia", "Clinical" AND "Diagnostic". Articles from 2019-2024 (total 83) were included, excluding other criteria and choosing 5 full articles. Results and Discussion: 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.  The initial chest x-ray 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) examinations include bilateral, random, irregular ground-glass or reticular opacities and small bilateral pleural effusions. A confident diagnosis of PEA can usually be made based on the combination of an acute febrile illness of short duration (one month or less), hypoxemic respiratory failure, diffuse pulmonary opacities on chest x-ray, and bronchoalveolar lavage eosinophilia (>25%), after exclusion of infection, vasculitis, or other known precipitants (e.g., medications, irradiation). For most patients with ASD, we recommend treatment with systemic glucocorticoids after ruling out infection. This recommendation is due to the severity and progressive nature of the respiratory deficiency and the dramatic response to glucocorticoids. The optimal dose of glucocorticoids is not known, but a reasonable course is to select the dose based on the severity of respiratory impairment. In the presence of severe hypoxemia or respiratory failure requiring mechanical ventilation, methylprednisolone (60 to 125 mg every six hours) is administered until respiratory failure resolves (usually within one to three days). In the absence of respiratory failure (SatO2>92%), initial treatment with oral prednisone (40 to 60 mg per day) is reasonable. Oral prednisone is continued at a dose of 40 to 60 mg per day for two weeks beyond complete resolution of symptoms and conventional chest x-ray abnormalities. It is then tapered over approximately four weeks and discontinued. Because initiation of smoking or an increase in the amount of smoking are often associated with ASD and because relapses have been associated with resumption of smoking, complete smoking cessation should be strongly encouraged. Relapses have not been well documented in other cases of acute exposures, but avoidance is prudent when an etiology can be identified. Conclusion: Symptomatic and radiographic improvement is generally rapid and progressive, with complete radiographic clearance over one to two months. Relapse is uncommon and is usually attributable to resumption of smoking after initial cessation.