Rupture of an occult hepatic hemangioma after prolonged cardiopulmonary resuscitation in a patient receiving ECPR for pulmonary embolism: a case report

Abstract

High-risk pulmonary embolism (PE) may cause refractory cardiac arrest. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) can provide temporary circulatory and oxygenation support during extracorporeal cardiopulmonary resuscitation (ECPR) while definitive reperfusion is pursued. Liver injury is a recognized complication of prolonged chest compressions, but rupture of an occult hepatic hemangioma after CPR in a patient receiving ECPR, anticoagulation, and reperfusion therapy is rarely reported. A 50-year-old woman with dyspnea, hypoxemia, hypotension, and irregular vaginal bleeding developed cardiac arrest 12 min after emergency department arrival. Manual CPR was initiated immediately. Epinephrine (1 mg intravenously every 3 min) was administered, endotracheal intubation was completed 3 min after arrest, and no defibrillation was performed. After 20 min without return of spontaneous circulation (ROSC), the ECPR pathway was activated and compressions were transitioned to an MCC-E1 mechanical device. Peripheral VA-ECMO flow was established 32 min after arrest through a 22-Fr right femoral venous drainage cannula and a 16-Fr left femoral arterial return cannula; ROSC with sinus rhythm occurred 1 min later. Coronary angiography excluded obstructive disease, and pulmonary angiography confirmed PE. Pulmonary artery thrombectomy and catheter-directed thrombolytic infusion were performed. Three hours later, ECMO flow and blood pressure abruptly decreased, followed by abdominal distension, an intra-abdominal pressure of 20 mmHg, free intraperitoneal fluid, and a hemoglobin level of 35 g/L. Emergency laparotomy revealed 3,000 mL of hemoperitoneum and rupture of a segment VI hepatic hemangioma. Partial hepatectomy and cholecystectomy achieved hemostasis, and ECMO was subsequently discontinued after stabilization. The rupture was more plausibly a multifactorial hemorrhagic event after prolonged CPR in an ECPR-supported patient than a direct complication of ECPR cannulation. Compression-related mechanical stress may have contributed, while thrombolysis, anticoagulation, and ECMO-associated hemostatic changes may have aggravated bleeding. Abrupt ECMO flow reduction with hypotension should prompt immediate evaluation for occult hemorrhage.