Case report: refractory atelectasis after infection of adenovirus and Mycoplasma Pneumoniae in an immunocompetent patient.

backgroundAtelectasis is defined as collapse of alveolar spaces due to a variety of reasons. Most atelectasis could improve after removing the cause by chest physiotherapy, medical treatment, therapeutic bronchoscopy and so on. However, some atelectasis cannot be cleared with above treatments, resulting in long-term atelectasis, also called as refractory atelectasis. It easily leads to recurrent infection, bronchiectasis, bronchiolitis obliterans, and lung necrosis. So, it is important to identify causal mechanism of refractory atelectasis, which may contribute to explore effective approach and reducing complications. CASE PRESENTATION: We present the case of a 4-years-old girl admitted to hospital with fever and cough for 6 days, who had pulmonary consolidation in left lower lobe due to human adenovirus-7 and Mycoplasma pneumoniae. Although the patient did not have inborn errors of immunity, neuromuscular disease or inherited metabolic diseases through medical history and laboratory examination, the consolidation of the left lower lung still existed after a series of treatments, including mechanical ventilation, intravenous immunoglobulin, systemic corticosteroid, azithromycin and bronchoalveolar lavage. Even, chest HRCT showed left lung atelectasis one month after discharge. In the follow-up 1 years, she was hospitalized for respiratory infections and wheezing 4 times. In consideration of refractory atelectasis and recurrent infections, left lung was resected by thoracoscopy and postoperative pathology confirmed bronchiolitis obliterans. Specific antibodies was utilized to identify type I and II alveolar epithelial cells, club cells, ionocytes and ciliated cells respectively, which show a selective reduction in type I alveolar epithelial cells.

conclusionIt is rare that a previously healthy child developed to refractory atelectasis after an infection which ultimately resulted in a lobectomy. The cellular analysis of the atrophic lung tissue showed a selective reduction in type I alveolar epithelial cells.