Rapid-Onset Cystic Bronchiectasis in a Mechanically Ventilated Patient with COVID-19

Michael Gilmartin ,  Ahmad Basirat ,  Conor Barry , et al

Am J Respir Crit Care Med Vol 205, Iss 6, pp 721–722, Mar 15, 2022

A 40-year-old man presented to the ICU after intubation due to respiratory failure secondary to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonitis. Past medical history revealed a history of intravenous drug use (heroin). Early blood and sputum cultures also grew a Panton-Valentine leukocidin–positive Staphylococcus aureus. Dexamethasone and antibiotics were administered and lung-protective ventilation and proning were instituted. Imaging during the first and second week of illness revealed rapid progression from pneumonitis to severe cystic bronchiectasis (Figures 1–3). The patient developed persistent hypercapnic acidosis, despite high Ve. Bedside calculations revealed dead space ventilation ranging from 5.14 L/min to 5.92 L/min. The patient received a tracheostomy in his third week of stay to facilitate weaning of mechanical ventilation. After ICU discharge, he received rehabilitation for critical illness myopathy and developed a mild persistent productive cough. He was discharged to a step-down facility for ongoing rehabilitation 5 months after admission.

Bronchiectasis is characterized by abnormal bronchial wall thickening and luminal dilation due to a cycle of infection and inflammation (1). Its development is a known complication of severe respiratory infection and is a reported complication of SARS-CoV-2, found in up to 11% of cases (2–5). The long-term sequelae of SARS-CoV-2 pneumonitis have yet to be fully elucidated. However, a number of authors have highlighted the potential for postinfective bronchiectasis to be an important issue (6, 7). This case is unusual for its rapid progression and highlights the association between SARS-CoV-2 and the development of bronchiectasis, particularly in the setting of Panton-Valentine leukocidin–positive S. aureus coinfection.