Abstract Introduction The pathophysiology of post-COVID interstitial lung disease (ILD) involves persistent inflammation and upregulated profibrotic signaling. The dysregulation of cellular repair pathways may contribute to elevated risk of rapidly progressive ILD (RP-ILD). We describe a case of a young male with mild post-COVID-19 ILD who developed severe RP-ILD without a clear underlying autoimmune cause. Description of Case A 35-year-old male with a history of heart failure, obesity, and ARDS from severe COVID-19 pneumonia in 2021 with post-COVID-19 ILD on room air presented to the hospital for dyspnea and cough. While admitted, he developed hypoxemic respiratory failure requiring 3L of oxygen. Initial CXR showed extensive bilateral ground glass and consolidative opacities concerning for pulmonary edema or multifocal pneumonia. Despite diuresis and empiric vancomycin and piperacillin-tazobactam, his respiratory function rapidly deteriorated and he was transferred to the ICU, requiring emergent intubation on hospital day three and subsequent paralysis and proning. Bronchoscopy with lavage was performed, notably with negative infectious studies. Serial lavage was bloody but not diagnostic for diffuse alveolar hemorrhage. Rheumatological workup was unrevealing, notable only for an isolated weakly positive anti-SS-A 52kD Ab IgG and mildly elevated serum aldolase (10.6) with normal creatine kinase. Broad infectious workup returned negative. Following multidisciplinary discussions with Pulmonology, Rheumatology, and Infectious Disease, the patient was started on 1g of methylprednisolone for three days with taper, intravenous immunoglobulin (IVIG), and tacrolimus. He subsequently began to improve and wean from the ventilator. Discussion RP-ILD is characterized by swift respiratory decompensation and carries high mortality rates despite advances in diagnosis and treatment. It remains unclear the extent to which cases of severe COVID-19 increase risk of future development of RP-ILD and whether there are differences in response to standard treatment. Risk factors include systemic inflammatory dysregulation, often in the setting of autoimmune rheumatic diseases, inflammatory myopathies, and post-COVID-19 ILD. More research is needed to understand the pathophysiology and optimal treatment for post-COVID-19 RP-ILD. This abstract is funded by: None
Liu et al. (Fri,) studied this question.