C52-17 When Benign Turns Fatal: Hemoptysis and Massive Hemothorax From a Stable Calcified Pleural Mass

Abstract Introduction Spontaneous hemothorax is the accumulation of blood within the pleural cavity in the absence of trauma. Common etiologies include rupture of pleural adhesions, neoplasms, pleural metastases, arteriovenous malformations, and complications from anticoagulant therapy. Rarely, spontaneous hemothorax manifests as a massive hemothorax, defined as blood loss exceeding 1,500 mL within 24 hours. Here, we describe an exceptionally rare case of a benign calcified pleural-based lung mass leading to spontaneous massive hemothorax, hemoptysis, and hemodynamic collapse secondary to cardiac tamponade physiology. Case Presentation A 71-year-old woman with a history of atrial fibrillation on chronic rivaroxaban and a known 5 cm calcified left pleural-based mass, stable for eight years, presented with acute hemoptysis and dyspnea. Initial chest radiography demonstrated alveolar infiltrates in the left mid and lower lung fields. Subsequent computed tomography (CT) angiography of the chest revealed a large left pleural effusion causing near-complete collapse of the left lung, without evidence of pulmonary embolism. She then developed acute hemodynamic collapse requiring intubation and circulatory shock refractory to fluids and transfusion. Bedside echocardiography revealed a large left pleural effusion with rightward cardiac displacement, consistent with extrinsic cardiac compression. Following emergent chest tube placement, rapid evacuation of large volumes of blood led to immediate hemodynamic stabilization, confirming tamponade physiology secondary to the pleural effusion. She received Kcentra for anticoagulation reversal and aggressive transfusion support. A thoracic aortogram found no active arterial extravasation, while bronchoscopy showed bleeding from the left upper lobe controlled with a temporary endobronchial blocker. Cardiothoracic surgery was consulted, but after discussing risks and benefits, patient declined thoracotomy. Anticoagulation was permanently discontinued. She was discharged in stable condition. Discussion This case demonstrates a life-threatening complication of a benign calcified pleural-based lung mass. The lesion’s pleural attachment likely predisposed it to rupture during episodes of vigorous coughing, with anticoagulation exacerbating hemorrhage and resulting in both intrapleural and endobronchial bleeding. This case highlights tamponade physiology caused by a massive hemothorax, an extremely uncommon but critical phenomenon. The rapid recognition of cardiac compression due to the expanding pleural effusion and timely chest tube decompression were pivotal in reversing circulatory collapse and preventing death. While surgical intervention remains the standard for unstable massive hemothorax, this case illustrates that prompt correction of anticoagulation, aggressive resuscitation, and immediate decompression can achieve hemostasis and restore stability without emergent thoracotomy. Early recognition of this reversible form of shock is therefore lifesaving and represents the distinctive feature of this presentation. This abstract is funded by: None