A 70-year-old man developed rapid-onset pulmonary fibrosis following cardiopulmonary bypass, illustrating a rare complication likely triggered by CPB-induced inflammatory lung injury.
Case Report (n=1)
This case highlights the rare development of early post-cardiac-surgery pulmonary fibrosis likely triggered by CPB-induced inflammatory lung injury, emphasizing the need to differentiate it from early-onset amiodarone toxicity.
Abstract Pulmonary complications after cardiac surgery are common, yet the development of progressive fibrosis following cardiopulmonary bypass (CPB) remains exceptionally rare and poorly understood. CPB initiates a systemic inflammatory cascade through activation of complement, neutrophils, and cytokine release, which can precipitate diffuse alveolar damage and acute lung injury. Although postoperative hypoxia is often transient, persistent respiratory failure with subsequent fibrotic remodeling is highly unusual. Amiodarone-induced pulmonary toxicity (AIPT) is a recognized cause of interstitial lung disease, but it typically arises weeks to months after drug exposure. This case highlights a diagnostic challenge in differentiating CPB-related inflammatory lung injury from early-onset AIPT and shows the need for vigilance in managing postoperative hypoxia. A 70-year-old man with coronary artery disease, prior percutaneous coronary intervention, ischemic stroke, and chronic tobacco use underwent elective coronary artery bypass grafting for multivessel disease. He received perioperative amiodarone for atrial fibrillation prophylaxis. He was extubated on postoperative day two but developed worsening dyspnea and hypoxia with bilateral infiltrates on chest imaging consistent with acute respiratory distress syndrome (ARDS). He was reintubated for respiratory failure and required vasopressor support for hypotension. Broad-spectrum antibiotics were initiated for presumed pneumonia but discontinued after negative cultures and clinical improvement. CT chest revealed diffuse bilateral ground-glass and consolidative opacities without focal infection. Over the subsequent week, his oxygenation gradually improved, and he was extubated to low-flow oxygen. He was discharged to cardiac rehabilitation on 4 L/min supplemental oxygen. However, a follow-up CT chest two weeks later demonstrated extensive bilateral reticulation, traction bronchiectasis, and honeycombing consistent with newly developed pulmonary fibrosis. Pulmonary function testing confirmed a restrictive defect with reduced diffusing capacity. This case illustrates a rare trajectory of early post-cardiac-surgery fibrosis likely triggered by CPB-induced inflammatory lung injury. The rapid onset of fibrosis, absence of cumulative amiodarone exposure, and negative infectious workup support a cytokine-mediated process rather than drug toxicity. While amiodarone toxicity cannot be entirely excluded, its typical subacute presentation contrasts sharply with the accelerated course observed here. CPB-related lung injury is typically self-limited, and progression to fibrosis has been reported only in isolated cases. This case emphasizes the importance of early recognition, serial imaging, and consideration of corticosteroid or antifibrotic therapy in patients with persistent postoperative hypoxia. Awareness of this uncommon complication may guide clinicians in differentiating inflammatory injury from drug-induced interstitial disease and improve long-term pulmonary outcomes following cardiac surgery. This abstract is funded by: None
Chaney et al. (Fri,) conducted a case report in Pulmonary Fibrosis following Cardiopulmonary Bypass (n=1). Cardiopulmonary bypass and perioperative amiodarone was evaluated. A 70-year-old man developed rapid-onset pulmonary fibrosis following cardiopulmonary bypass, illustrating a rare complication likely triggered by CPB-induced inflammatory lung injury.
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