Traumatic Pulmonary Valve Insufficiency 25 Years After Blunt Chest Trauma: A Case Report and Literature Review

Background: Traumatic pulmonary valve insufficiency is an extremely rare sequela of blunt chest trauma due to the pulmonary valve’s low-pressure physiology and posterior anatomical location. Its subtle presentation often delays diagnosis until progressive right ventricular dilation leads to symptomatic right heart failure years or even decades later. We report a case of severe pulmonic insufficiency presenting 25 years after a motor vehicle collision, requiring surgical intervention, and review the existing literature. Case Presentation: A 47-year-old man with a remote history of major blunt chest trauma presented with progressive dyspnea, fatigue, and palpitations. His prior injuries included left hemopneumothorax, diaphragmatic hernia, multiple rib and pelvic fractures, splenic and renal contusions, empyema, and pericardial effusion. He had undergone left thoracotomy, pericardial drainage, and hernia repair during his initial hospitalization. Workup for his current symptoms revealed a severely dilated right ventricle with moderate to severe pulmonary regurgitation and dysfunction. Cardiac MRI demonstrated an RV end-diastolic volume of 477 mL (indexed 186 mL/m²), ejection fraction of 38%, and regurgitant fraction of 65%. Intraoperatively, he was found to have a 50% avulsion of the right pulmonary cusp from the annulus. A reverse-orientated 33-mm Mitral Mosaic bioprosthetic valve was implanted. Postoperative recovery was uneventful. At three months, echocardiogram showed significantly improved RV function and no residual pulmonary insufficiency. The patient experienced resolution of symptoms and improved functional capacity. Conclusions: Traumatic pulmonary valve insufficiency is an exceedingly rare complication of blunt chest trauma. This diagnosis should be considered in patients with a history of major thoracic trauma who present with unexplained right heart dysfunction. Advanced imaging, including echocardiography and cardiac MRI, facilitates diagnosis and guides surgical planning. This case demonstrates the potential for substantial RV functional recovery following timely pulmonary valve replacement. As seen in congenital and carcinoid valve disease, relief of chronic regurgitant volume load can promote RV reverse remodeling, particularly when surgery occurs before irreversible myocardial fibrosis. Our patient’s rapid symptomatic improvement and early imaging evidence of RV recovery suggest that even longstanding pulmonic regurgitation may be reversible if treated before end-stage dysfunction. Early recognition and intervention are essential to achieving favorable outcomes.