How to recognize acute eosinophilic pneumonia

  Eosinophilic infiltrative lung diseases (EIDs) are a group of lung diseases characterized by eosinophilia in blood or/and lung tissue, and their clinical manifestations and prognosis vary widely. Among them, acute eosinophilic pneumonia (AEP) has not been reported in China.  Case presentation: The patient, female, 77 years old, hospitalization number 257075, was admitted to a hospital on March 4, 2000 with fever, cough and shortness of breath after activity for 4 days. She was admitted to a hospital on March 4, 2000 with fever, cough and shortness of breath after activity for 4 days. He was given prednisone 30 mg/d for 7 days, and then gradually reduced to 10 mg/d; cyclosporine A 300 mg/d, and then reduced to 100 mg/d after 2 weeks, and the rash basically disappeared. In the last 4 days, fever, dry cough and mild dyspnea after physical activity appeared. Out-of-hospital blood tests: WBC 5.0G/L, neutrophilic 0.85, lymphatic 0.09, mononuclear 0.05; Hb 10.8g/L; PLT 181G/L. Blood sedimentation 40mm/h, blood C-reactive protein 91.1mmol/L. Blood gas analysis: pH 7.494, PaCO 234.3mmHg, PaO 246.6mmHg, HCO3- 26.6mmol/L. Liver and kidney function, blood glucose, electrolytes and muscle enzyme profile were in normal range. Sputum culture was free of pathogenic bacteria growth, and sputum was negative for antacid bacilli 5 times. Chest X-ray showed blurred texture in both lungs, reduced translucency and small patchy shadow. Electrocardiogram, echocardiogram and abdominal ultrasound showed no abnormalities. He was treated with Rohypnol 2.0/d, Rifaximin 0.4/d, oxygen, prednisone 10 mg and symptomatic treatment. The disease gradually worsened and severe respiratory distress appeared and he was transferred to our department on March 14.  On admission: temperature 38.5℃, pulse 126/min, respiration 40/min, blood pressure 110/70mmHg. mental clarity. The skin and mucous membranes were cyanotic, and the superficial lymph nodes were not large. The trachea was centered, both lungs were clear on percussion, breath sounds were decreased, and popping sounds were heard in both lower lungs. The heart rate was 126/min, the heart rhythm was uniform, the heart sounds were acceptable, and a class III systolic murmur was heard in the apical part of the heart. Mild sunken edema in both lower extremities. Blood gas analysis (nasal catheter oxygen 5L/min) pH 7.498, PaCO 229.7mmHg, PaO 238.9mmHg, SaO 278.6%. The chest X-ray showed blurred texture in both lungs, and patchy shadows were visible with markedly reduced translucency, and a small amount of pleural effusion on the right side. At FiO20.8, PaO2 was only 65.3mmHg and oxygenation index (PaO2/FiO2) was 81. blood WBC 5.3G/L, neutrophil 0.75, lymph 0.2, Hb10.2g/L, PLT 163G/L. 2 bronchoalveolar lavage (BAL) cell classification: eosinophils accounted for 80%, neutrophils 10%, lymphocytes 10%; no pathogenic bacteria growth in tracheal aspirate culture; no acid-fast bacilli found. Acute eosinophilic pneumonia was considered, and methylprednisolone 500 mg/d for 3 days was given, followed by prednisone 60 mg/d with gradual reduction. Pulmonary function improved significantly on day 2 after hormone shock. at FiO2 0.3, PaO2 rose to 75.3 mmHg and oxygenation index rose to 250. chest X-ray of both lungs had enhanced translucency compared with the previous one, and dot film shadow was significantly absorbed. On the 7th day of mechanical ventilation, the patient became febrile again, with a temperature of 38°C. The sputum volume increased and turned yellow, and the WBC rose to 15.0 G/L with a neutrality of 0.90. The tracheal aspirates were repeatedly cultured with Pseudomonas aeruginosa, Xanthomonas maltophilia and methicillin-resistant Staphylococcus aureus (MRSA). Blood gas indicators deteriorated further and there was another significant increase in dotted film shadow in both lungs. Despite strong antibiotic therapy and hormone reduction, the pulmonary infection further worsened and the patient died on April 19, 2000.  DISCUSSION: AEP was first reported in 1989 and has distinctly different clinical features from other eosinophilic lung diseases. Little is known about the pathogenesis of AEP, which may be an overreaction of the organism to an unknown antigen. The pathological changes are mainly eosinophilic infiltration of the alveolar space, bronchial wall and interstitial lung. It can develop at all ages without gender differences. The main clinical manifestations are acute fever, dyspnea, bilateral lung bursting sounds, normal blood eosinophils and diffuse infiltrative shadow in both lungs on chest X-ray. The diagnosis is based on eosinophils greater than 25% in BAL and normal blood eosinophils, with the exception of various infectious lung diseases and ARDS. After glucocorticoid shock therapy, the disease can be completely relieved, and it is not easy to relapse after stopping the drug. The commonly used drugs and doses are methylprednisolone 240~500mg/d, reduced to 40~60mg after 1~3d, and the course of treatment is 2~4 weeks. The patient presented with fever, progressive dyspnea, severe respiratory failure, low total blood leukocytes and eosinophils, diffuse infiltrative shadow of both lungs on X-ray, eosinophils up to 90% in BAL, no pathogenic bacteria cultured in sputum before admission and tracheal aspirate after admission, ineffective treatment with various antibacterial drugs, and significant relief after glucocorticoid shock therapy, which could be diagnosed as AEP. The patient died of refractory pneumonia due to the complication of ventilator-associated pneumonia during mechanical ventilation and the culture of various refractory bacteria such as Pseudomonas aeruginosa, Xanthomonas maltophilia and MRSA in the tracheal aspirate.  Due to the lack of specificity of clinical manifestations of AEP, it is easily misdiagnosed as pulmonary infectious disease or ARDS. some scholars suggest that when acute respiratory failure with pulmonary infiltrative shadow and no other evidence of pulmonary infection, AEP should be considered and bronchoalveolar lavage or lung biopsy should be performed to clarify the diagnosis. ARDS mostly has clear causative factors, and neutrophils are predominant in BAL, which is less responsive to hormones, so it is not consistent with this case.