Arterial hepatic perfusion is preserved during early resuscitation after hemorrhagic shock in a large animal polytrauma model.

Abstract

Hemorrhagic shock is a major contributor to morbidity and mortality after polytrauma and plays a central role in the development of multiple organ dysfunction syndrome (MODS). The liver is particularly vulnerable due to its high metabolic demand and dependence on adequate oxygen delivery, and hepatic dysfunction is associated with poor outcomes after trauma. This study aimed to assess hepatic perfusion and biochemical liver function following hemorrhagic shock without direct hepatic trauma in a standardized porcine polytrauma model. 32 landrace pigs were used in the current study and randomized into four groups (n = 8): Tissue trauma group received a blunt chest injury and bilateral femur fractures. In the shock group, hemorrhagic shock was induced and maintained at a mean arterial pressure of 35 mmHg for 1.5 h by controlled blood withdrawal. The polytrauma group underwent both tissue trauma and hemorrhagic shock. 8 sham animals served as control. At the beginning of resuscitation, hepatic perfusion was assessed using spectral CT-based iodine density imaging. Regions of interest were placed in homogeneous liver parenchyma (segments III, IV, and VII) by a blinded investigator. Serum transaminases (AST, ALT, GGT), bilirubin, and lactate were measured at defined time points. Arterial hepatic perfusion during resuscitation did not differ significantly between shock and non-shock animals. Mean iodine uptake was 2.00 ± 0.39 mg/ml in the shock group and 2.22 ± 0.42 mg/ml in the non-shock group (p = 0.159). AST levels increased significantly after hemorrhagic shock at 3, 8, and 24 h (p < 0.05), while ALT, GGT, and bilirubin remained unchanged. A strong positive correlation between AST and lactate was observed (r = 0.741, p < 0.001). Spectral CT-based iodine perfusion imaging enables real-time assessment of arterial hepatic perfusion in hemorrhagic shock. The observed elevation of AST suggests that trauma-induced liver-associated enzyme release is present despite no statistically significant reduction in arterial liver perfusion during resuscitation.