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Background <p>Resuscitative 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.</p> Methods <p>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&#xa0;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.</p> Results <p>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&#xa0;min following occlusion. Overall metabolic trajectories were similar thereafter.</p> Conclusions <p>Total 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.</p>

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Resuscitative endovascular occlusion of the aorta restores cerebral metabolic markers of ischaemia induced by haemorrhagic shock

  • 期刊论文

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  • 发表日期：

    2026年6月24日

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  • Sam Er Bader,
  • A. Magnuson,
  • C. Brorsson,
  • G. Wallin,
  • N. Löfgren,
  • F. Löfgren,
  • P-J Blind,
  • M. Öman,
  • M. Olivecrona

摘要

Background

Resuscitative 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.

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.

Conclusions

Total 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.