ArticleEuropean journal of trauma and emergency surgery : official publication of the European Trauma Society2026
Resuscitative endovascular occlusion of the aorta restores cerebral metabolic markers of ischaemia induced by haemorrhagic shock.
Article in European journal of trauma and emergency surgery : official publication of the European Trauma Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundResuscitative endovascular balloon occlusion of the aorta (REBOA) is used as an adjunct in haemorrhagic shock (HS) to restore proximal perfusion. Its cerebral metabolic effects during haemorrhagic shock, particularly in the presence of elevated intracranial pressure (ICP), remain incompletely characterised.
methodsIn 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.
resultsHS 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.
conclusionsTotal REBOA restored cerebral metabolic markers of ischaemia during haemorrhagic shock, 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 tREBOA in the setting of elevated ICP is not contra indicated and can be a bridge to further treatment. Our findings do not demonstrate absence of tissue injury, or long-term neurological recovery. Further studies incorporating complementary physiological and structural outcome measures would be recommended.
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