A case of blunt liver injury with rare hemodynamics: traumatic outflow block.

Abstract

Background: Non-operative management (NOM) has become the standard of care for blunt solid organ injury, with angioembolization (AE) playing a key role in achieving hemostasis, particularly in liver trauma. Although the dual blood supply to the liver provides relative protection against ischemia, AE can disrupt this balance and lead to major hepatic necrosis (MHN), a life- threatening complication associated with significant morbidity and mortality. Early identification of patients at risk of developing MHN is critical but remains challenging. While treatment strategies for MHN have been explored, early predictive markers, especially angiographic findings, remain underreported and are not yet established in the literature. We report a rare intrahepatic hemodynamic phenomenon observed on angiography that may serve as an early predictor of MHN.

Case presentation: A 32-year-old man sustained a Grade III liver injury predominantly involving the left hepatic lobe following a motor vehicle collision. Contrast-enhanced CT showed hepatic parenchymal injury with hemoperitoneum. Although no active extravasation was observed, contrast enhancement was noted in the left portal vein branch during the arterial phase. Selective angiography via the left hepatic artery revealed parenchymal enhancement of the left hepatic lobe, followed by retrograde opacification of the left portal vein branch. Notably, contrast did not proceed into the left hepatic vein, suggesting impaired hepatic venous outflow. This hemodynamic pattern, characterized by trans-sinusoidal arterial-to-portal flow without venous drainage, can be termed traumatic outflow block (TOFB), a phenomenon not previously reported in trauma. Despite this atypical flow pattern, AE was performed using gelatin sponge particles. The patient subsequently developed abdominal pain and fever, and CT showed non-perfusion of the lateral liver segment. Emergency surgery confirmed massive hepatic necrosis and lateral segmentectomy was performed. Intraoperatively, there were no observable lacerations or disruptions of the portal vein or hepatic veins. However, the liver parenchyma near the root of the left hepatic vein exhibited substantial contusion and hematoma, suggesting possible venous compression. The patient made an uneventful recovery and was discharged on postoperative day nine.

Conclusions: TOFB is a novel angiographic finding suggestive of hepatic venous congestion and may serve as an early predictor of MHN after embolization. While therapeutic strategies for TOFB remain undefined, early recognition of this hemodynamic pattern could guide selective embolization, prompt monitoring and potentially improve outcomes in patients with severe liver trauma.