Cerebral glycerol during haemorrhagic shock in normal and raised intracranial pressure resuscitated with total REBOA: an experimental porcine study
Sam Er Bader, Anders Magnusson, Camilla Brorsson, Göran Wallin, Niklas Löfgren, Filip Löfgren, Per-Jonas Blind, Mikael Öman, Magnus OlivecronaAbstract
Introduction
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 ICP. Cerebral microdialysis (CMD) derived glycerol (CGly) is a recognised marker of cellular membrane stress and injury.
The objective if this study is 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
18 pigs were subjected to controlled HS and resuscitated with tREBOA for 90 min. Animals were allocated to either a normal ICP group or an elevated ICP group . Monitoring of proximal arterial pressure (pMAP), ICP. CGly concentrations were measured using CMD.
Results
tREBOA effectively restored pMAP 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.
Discussion
tREBOA 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. 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.