(1128) Loss of Pneumocytes Leading to Acute Lung Injury: A Case Report

Introduction: The pulmonary alveolar epithelial lining, consisting of type I and type II pneumocytes and alveolar macrophages, is vital for gas exchange and creating the air-blood barrier. Acute inflammation or trauma can result in pneumocyte loss, leading to diffuse alveolar damage (DAD). Although DAD is commonly found in acute lung injury (ALI), complete loss of pneumocytes is a distinctive finding that has not been well reported. This case report demonstrates a total absence of pneumocytes, including type II pneumocytes, as a cause of ALI.

Description: A 56-year-old male with no medical history presented to a community hospital with acute shortness of breath and hypoxia. He had an 8-pack year smoking history. He smoked marijuana daily and described recently smoking a new strain. Computed tomography (CT) chest imaging showed ground glass infiltrates with peripheral consolidation, and he began antibiotic treatment. Initial work-up was negative for infection and autoimmune disorders. During his stay, he developed bilateral pneumothoraces and acutely decompensated. He was transferred to a tertiary care center and intubated upon arrival. Repeat CT chest showed pneumomediastinum and worsening ground glass opacifications consistent with acute respiratory distress syndrome (ARDS). He did not respond to standard ARDS therapy and veno-venous extracorporeal membrane oxygenation (VV ECMO) was initiated. Bronchoscopic alveolar lavage showed reactive bronchial and inflammatory cells and alveolar macrophages. Lung cryobiopsy pathology showed reactive alveolated parenchyma with initial epithelial loss, absence of type II pneumocytes without excessive eosinophils or neutrophils. He has since been extubated but remains on VV ECMO.

Discussion: Type II pneumocytes play a crucial role in alveolar epithelium repair. Pneumocyte regeneration can be seen within days of acute alveolar injury. Our patient’s lung biopsy was on hospital day 17, suggesting delayed reepithelialization. Similar case reports of delayed reepithelialization showed both slow and no recovery requiring transplant. This unique finding may be related to acute fibrinous organizing pneumonia, hypersensitivity pneumonitis, or inhalation toxic injury. Further research is needed to understand delayed alveolar epithelialization’s role in ALI and recovery.