Abstract Introduction Septic pulmonary embolism (SPE) can cause cavitary infarcts that predispose to pneumothorax (PTX). Positive-pressure ventilation may precipitate rupture of these fragile subpleural cavities, yet this mechanism is rarely documented in mechanically ventilated SPE patients. Case Presentation A 59-year-old man with history of untreated hepatitis C acquired from IV drug use s/p TIPS presented with confusion, dyspnea, and diffuse wheezing. CT chest revealed scattered nodular opacities throughout bilateral lungs with cavitation and moderate size right sided pleural effusion. Findings were concerning for infective endocarditis with associated septic emboli. Blood cultures grew methicillin-resistant Staphylococcus aureus (MRSA). Transthoracic echocardiography did not reveal vegetations, but transesophageal ultrasound was not performed due to history of esophageal varices. Despite targeted antibiotics, he developed hypoxemic respiratory failure requiring intubation. A right pigtail catheter was placed for a parapneumonic effusion. After three days, worsening oxygenation was noted and chest radiograph revealed bilateral, right-predominant pneumothoraces. Additional pigtail catheters were inserted, but persistent air leaks suggested bilateral bronchopleural fistulas. The patient ultimately developed multiorgan failure with disseminated MRSA, VRE, and Candida glabrata infections and died. Discussion This case highlights the under-recognized risk of barotrauma in SPE during mechanical ventilation. Cavitary, subpleural septic infarcts create structurally fragile lung tissue that may rupture even under lung-protective settings. In this patient, bilateral pneumothoraces developed despite a low, stable PEEP of 5 cm H2O, demonstrating that even modest positive pressure can cause alveolar disruption when infection has weakened parenchyma. Worsening gas exchange or abrupt desaturation in mechanically ventilated SPE should prompt immediate evaluation for PTX rather than assuming ARDS progression. Preventive strategies include anticipating subpleural cavitary disease and applying ultra-protective ventilation with low driving pressure and careful plateau-pressure monitoring. Persistent or bilateral air leaks should raise suspicion for diffuse necrotizing infection or bronchial disruption rather than isolated barotrauma. This case reinforces that SPE with cavitary disease represents a distinct ‘fragile-lung’ phenotype in which even standard protective pressures may exceed tissue tolerance. Recognizing this vulnerability early can guide safer ventilatory management and prevent catastrophic air leaks in critically ill patients with septic emboli. This abstract is funded by: None
Derevenskikh et al. (Fri,) studied this question.