Acute eosinophilic pneumonia associated with COVID-19 infection

Knowledge of COVID-19 infection and sequelae is evolving. Acute eosinophilic pneumonia (AEP) is not a well-known complication of COVID-19 infection and is rarely reported in the literature. We report a case of a 60-year-old man with a history of chronic immunosuppressive sympathetic heart transplantation who developed AEP 3 weeks after COVID-19 infection. He presented with diarrhea without respiratory symptoms and acute kidney injury. After discharge, the patient experienced progressive fever, dyspnea, and cough, resulting in a second admission to the hospital with acute hypoxic respiratory failure requiring oxygen supplementation. Imaging showed frosted glassy opacity with hardened areas and bronchoalveolar lavage fluid showed AEP. The patient was treated with steroids and the symptoms and radiographic findings disappeared. This case highlights the potential for AEP to complicate COVID-19 infection.

Preface

Acute eosinophilic pneumonia (AEP) is a rare lung disease. Chest x-ray or chest computer tomography (CT) shows symptoms of acute fever, cough, and dyspnea with bilateral invasion. It is associated with inhalation exposure to smoking, drugs / toxins, infections (usually fungi or parasites). The modified Philit criteria are used to diagnose “clear” AEP. This includes pulmonary eosinophils indicated by 25% or more of eosinophils in acute respiratory disease up to 1 month, lung infiltrates on chest radiographs or CT, and bronchoalveolar lavage. (BAL) Lack of humoral or eosinophilic pneumonia and other specific pulmonary eosinophilic diseases in lung biopsy [1].. AEP is rarely reported in association with viral illness. We report a case of AEP associated with COVID-19 infection.

Case presentation

A 60-year-old man was hospitalized with acute fever, hypoxia, dyspnea, and cough three weeks after being diagnosed with COVID-19 in the fall of 2021. His medical history was important for the 2018 orthotopic heart transplant. For non-ischemic cardiomyopathy. He was taking 500 mg of mycophenolate mofetil twice daily, 1.5 mg in the morning and 1.0 mg of tacrolimus in the evening. Twenty days ago, he was hospitalized with gastrointestinal complaints and acute kidney injury. He was found to be COVID-19 positive by screening with a reverse transcriptase-polymerase chain reaction (RT-PCR) nasal swab. He had no respiratory symptoms, did not require oxygen, and had not received COVID-19-specific treatment. He was discharged in good condition three days later.

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On the third day of my second hospitalization, I consulted with the respiratory team. The patient had intermittent fever, tachycardia, tachypnea, and received 2 liters of oxygen supplemented by nasal cannula.His lab was noteworthy with a white blood cell count of 14.7×103/ µL, 86% neutrophils, zero absolute eosinophils, procalcitonin 0.47 ng / ml, C-reactive protein (CRP) 20.2 mg / dL, and COVID-19 PCR positive at 36 cycle threshold. Blood cultures and other infection tests were unobtrusive.Chest CT was notable for ground-glass opacity (GGO) in the upper left lobe, bibasal dense consolidation, and small left pleural effusion (figure). 1A). He started intravenous infusion, vancomycin, cefepime, and azithromycin on his admission.

Bronchoscopy using bronchoalveolar lavage (BAL) was performed on the lower left lobe. About 25 ml of BAL fluid was obtained with 170 leukocytes and no epithelial cells. There were 37% eosinophils, 38% macrophages, 17% neutrophils, and 8% lymphocytes. We investigated other causes of eosinophilia, such as infections (parasites / fungi) and asthma. Studies of fecal eggs and parasites, BAL galactomannan, Gram stain, acid-fast bacillus stain, and all cultures were negative. Serum immunoglobulin (Ig) E levels were normal and the patient lacked signs or symptoms of asthma. These findings were consistent with AEP and the patient started 60 mg prednisone (approximately 1 mg / kg). He felt better the next day and was deoxygenated by the sixth day of Prednisone. After receiving 60 mg of prednisone for 7 days, his dose was reduced to 40 mg. Overall, he was instructed to take 40 mg for 7 days, 30 mg for 7 days, and 20 mg for up to 6 weeks of follow-up. After six weeks of follow-up, he improved significantly and returned to work part-time.His CT scan at the time showed a solution to the integration process (figure). 1B), And he slowly taper prednisone over the next three weeks.

Discussion

This case highlights the unusual association between AEP and COVID-19 infection and the diagnostic challenges of abnormal pneumonia during a pandemic. [2]..As far as we know, this association between AEP and COVID-19 has only been reported in the other two case reports (Table). 1). [3,4]..

Age / gender Medical history presentation diagnose Potential confounding factors process result
case 1 [4] 77 year old man asthma Acute dyspnea and chest pain BAL Favipiravir and Ruskfloxacin Prednisolone 0.5 mg / kg, long-term taper Significant improvement in images and symptoms in 4 weeks
Case 2 [3] 61 year old man none Fever and dyspnea about 4 weeks after symptoms appear biopsy Hydroxychloroquine, azithromycin, and lopinavir / ritonavir Methylprednisolone 60 mg / day, followed by 30 mg prednisone / day at discharge Significant improvement in images and symptoms in 4 weeks
Case 3 (Vogel) 60 year old man Heart transplant Fever and dyspnea 3 weeks after positive test BAL Tacrolimus 1 mg / kg prednisone with extended taper Significant improvement in images and symptoms in 6 weeks

The first case was a 77-year-old man with a history of asthma with chest pain and dyspnea. He was COVID-19 positive and his chest CT showed bilateral pulmonary infiltrates. He was treated with favipiravir and ruskfloxacin. His peripheral eosinophils were 12.1% at his admission and worsened during admission. Favipiravir or ruskfloxacin may have caused a drug reaction, but the authors opposed it because it did not improve after discontinuation. Eosinophils were found in his BAL fluid, but there was no difference. The authors have clinically reached the diagnosis of AEP.He was treated with steroids and improved [4]..

The second case was a 61-year-old man with no medical history who showed fever, cough, and dyspnea for 2 weeks. He was COVID-19 positive with bilateral pulmonary infiltrates. He was treated with hydroxychloroquine, azithromycin, and lopinavir / ritonavir. He was discharged, but returned a week after his symptoms worsened. He was treated with methylprednisolone and ceftriaxone. He underwent a BAL on a transbronchial biopsy 5 days after admission. Although only 5% of white blood cells were eosinophils, his biopsy showed a mixture of eosinophils in the stromal tissue and alveoli. Hydroxychloroquine, azithromycin, or lopinavir / ritonavir may have caused AEP, but the author opposed this because he improved while still using them.They argued that steroids were likely contributing to the reduction in eosinophil counts in his BAL fluid. [3]..

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COVID-19 became a more convincing cause of AEP because our patients had not been exposed to new medications or exposures prior to his presentation. Viral diseases are rarely associated with AEP, but there are case reports associated with influenza and the human immunodeficiency virus (HIV). [5-7].. Since some treatments for COVID-19 are new or rare, it is difficult to conclude that they do not cause AEP. The website Pneumotox contains a link between tacrolimus and AEP, which is rare. [8].. It is unlikely that this caused his episode, as our patient has been taking tacrolimus for over 2 years and has improved.

Our patient’s presentation is the same as any other patient in COVID-19. A few weeks after diagnosis, he showed worsening respiratory symptoms and bilateral hardening. These findings suggest duplicate bacterial infections or organized pneumonia (OP). Given his lack of exposure and peripheral eosinophilia, AEP was unquestioned. If he did not develop immunodeficiency due to concerns about atypical infection, he was empirically treated with steroids for OP and clinically improved without us knowing the true cause. prize. The incidence of AEP after COVID-19 infection may be underestimated based on this case.

Conclusion

Overall, the reported incidence of virus-related AEP is low but increasing. At this time, it is unclear why acute viral diseases cause AEP, and more information is needed to elucidate. Anyway, AEP should be in the differential diagnosis of patients with recent COVID-19 infections who present with worsening respiratory symptoms and pulmonary infiltrates. Early recognition and treatment with steroids may improve the patient’s condition quickly and significantly.

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