Cerebral glycerol during haemorrhagic shock in normal and raised intracranial pressure resuscitated with total REBOA: an experimental porcine study.

BACKGROUND

Haemorrhagic shock (HS) is frequently associated with secondary cerebral injury due to compromised cerebral perfusion. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an effective haemorrhage control strategy; however, concerns persist regarding its cerebral effects, particularly in the presence of elevated intracranial pressure (ICP). Cerebral microdialysis (CMD) derived glycerol (CGly) is a recognised marker of cellular membrane stress and injury.

OBJECTIVE

To investigate CGly dynamics during prolonged total REBOA (tREBOA) in HS and to compare cerebral cellular responses between animals with normal and elevated ICP.

METHODS

In this experimental porcine study, eighteen pigs were subjected to controlled HS and resuscitated with tREBOA for 90 min. Animals were allocated to either a normal ICP group (NICPG, n = 9) or an elevated ICP group (EICPG, n = 9). Continuous monitoring of proximal arterial pressure, ICP, and cerebral perfusion pressure was performed. CGly concentrations were measured using CMD throughout the experimental protocol.

RESULTS

tREBOA effectively restored proximal arterial pressure and cerebral perfusion pressure in both groups. CGly concentrations remained relatively stable during the haemorrhage phase and increased progressively during prolonged aortic occlusion. Importantly, CGly responses did not differ significantly between animals with normal and elevated ICP. The observed increases in CGly during prolonged occlusion were consistent with cellular membrane perturbation rather than irreversible neuronal injury.

CONCLUSIONS

In this experimental model of HS, prolonged total REBOA restored macrocirculatory parameters but was associated with time-dependent increases in CGly. Elevated ICP was not associated with exacerbation of cerebral cellular membrane stress during total aortic occlusion under the conditions studied. These findings suggest that intracranial hypertension alone does not worsen cerebral cellular responses during tREBOA, while highlighting the importance of occlusion duration and the need for further studies to optimise cerebral protection during prolonged aortic occlusion.