Resuscitative endovascular occlusion of the aorta (REBOA) restores cerebral metabolic markers of ischaemia induced by haemorrhagic shock
Sam Er Bader, Anders Magnusson, Camilla Brorsson, Göran Wallin, Niklas Löfgren, Filip Löfgren, Mikael Öman, Magnus OlivecronaAbstract
Introduction
REBOA is used as an adjunct in haemorrhagic shock (HS) to restore proximal arterial pressure. Its cerebral metabolic effects particularly in the presence of elevated ICP, remain incompletely characterised. The aim of this study is to describe the changes in cerebral metabolism during total AO during HS in animals with normal and elevated ICP.
Methods
In a controlled porcine model, HS was induced by controlled bleeding to a mean arterial pressure of approximately 40 mmHg. Animals were allocated to a normal ICP group or an experimentally elevated ICP group. Total REBOA (zone 1) was applied for 90 min. Cerebral metabolism was assessed using intracerebral microdialysis with measurements of lactate, pyruvate, and lactate–pyruvate ratio (LPR). Cerebral haemodynamics and ICP were continuously monitored.
Results
HS was associated with a statistically significant increase in LPR in both groups, indicating cerebral metabolic disturbance. Following aortic occlusion, LPR gradually decreased toward baseline in both groups. Animals with elevated ICP demonstrated a transient delay in metabolic normalisation during the early post-occlusion phase. Statistically significant differences between groups were limited to the first 10 min following occlusion. Overall metabolic trajectories were similar thereafter.
Discussion
REBOA restored cerebral metabolic markers of ischaemia in HS, as reflected by normalisation of LPR, even in the presence of experimentally elevated ICP. These findings indicate acute metabolic recovery and so suggest that the use of REBOA in the setting of elevated ICP is not contra indicated and can be a bridge to further treatment.