To Örebro University

Introduction: Cerebral glucose (CGlu) is essential for maintaining neuronal function. Haemorrhagic shock (HS) impaires cerebral substrate delivery. Resuscitative endovascular balloon occlusion of the aorta (REBOA) effectively restores arterial pressure; however, its effects on cerebral glucose dynamics, particularly in the presence of elevated ICP, remain incompletely understood. The aim of this study is to investigate CGlu dynamics during HS and subsequent resuscitation with total REBOA (tREBOA), and to assess the influence of intracranial pressure (ICP) on cerebral metabolic responses.

Methods: 18 pigs were assigned to either a normal ICP group (NICPG) or an elevated ICP group (EICPG) and were subjected to controlled HS followed by resuscitation with tREBOA. CGlu concentrations were measured using cerebral microdialysis throughout baseline, HS, and aortic occlusion (AO). Proximal mean arterial pressure (pMAP) and ICP were continuously monitored. Data were analysed using linear mixed-effects models.

Results: HS was associated with a reduction in CGlu in both groups, indicating early cerebral metabolic stress. Following initiation of tREBOA, CPP increased markedly; however, CGlu concentrations did not immediately normalise, particularly in EICPG. Instead, CGlu availability demonstrated time-dependent changes during prolonged AO. No consistent differences in CGlu concentrations between groups were observed once perfusion pressure was restored.

Discussion: tREBOA restored CPP and supported recovery of CGlu availability, even in the presence of elevated ICP. However, haemodynamic restoration was not accompanied by immediate metabolic normalization, demonstrating a dissociation between perfusion and CGlu regulation. These findings provide important physiological insights into the cerebral effects of tREBOA and support its cautious, time-limited use in complex trauma scenarios.