To Örebro University

Introduction: Cerebral glucose (CGlu) is essential for maintaining neuronal function. Haemorrhagic shock (HS) impaires cerebral substrate delivery. Resuscitative endovascular balloon occlusion of the aorta (REBOA) effectively restores arterial pressure; however, its effects on cerebral glucose dynamics, particularly in the presence of elevated ICP, remain incompletely understood. The aim of this study is to investigate CGlu dynamics during HS and subsequent resuscitation with total REBOA (tREBOA), and to assess the influence of intracranial pressure (ICP) on cerebral metabolic responses.

Methods: 18 pigs were assigned to either a normal ICP group (NICPG) or an elevated ICP group (EICPG) and were subjected to controlled HS followed by resuscitation with tREBOA. CGlu concentrations were measured using cerebral microdialysis throughout baseline, HS, and aortic occlusion (AO). Proximal mean arterial pressure (pMAP) and ICP were continuously monitored. Data were analysed using linear mixed-effects models.

Results: HS was associated with a reduction in CGlu in both groups, indicating early cerebral metabolic stress. Following initiation of tREBOA, CPP increased markedly; however, CGlu concentrations did not immediately normalise, particularly in EICPG. Instead, CGlu availability demonstrated time-dependent changes during prolonged AO. No consistent differences in CGlu concentrations between groups were observed once perfusion pressure was restored.

Discussion: tREBOA restored CPP and supported recovery of CGlu availability, even in the presence of elevated ICP. However, haemodynamic restoration was not accompanied by immediate metabolic normalization, demonstrating a dissociation between perfusion and CGlu regulation. These findings provide important physiological insights into the cerebral effects of tREBOA and support its cautious, time-limited use in complex trauma scenarios.

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.

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 neuronalinjury.

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 no tworsen cerebral cellular responses during tREBOA, while high-lighting the importance of occlusion duration and the need for further studies to optimise cerebral protection during prolonged aortic occlusion.

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.

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.

PURPOSE: To assess changes of cerebral haemodynamic and intracranial pressure (ICP) in animals, with or without elevated ICP, during controlled haemorrhagic shock and resuscitation with Total REBOA (tREBOA).

METHOD: In 22 anaesthetized and normoventilated pigs, after placement of catheters for monitoring invasive proximal blood pressure (pMAP), ICP, and vital parameters, and 60 min stabilisation phase, a controlled haemorrhagic shock (HS), was conducted. In 11 pigs (EICPG), an elevated ICP of 25-30 mmHg at the end HS was achieved by simulating an epidural mass. In 11 pigs (NICPG), the ICP was normal. tREBOA was then applied for 120 min. The changes of pMAP and ICP were followed, and cerebral perfusion pressure (CPP) calculated. The integrity of the autoregulation was estimated using a calculated Modified-Long Pressure Reactivity Index (mL-PRx).

RESULTS: After stabilisation, hemodynamics and physiological parameters were similar and normal in both groups. At the end of the HS, ICP was 16 mmHg in NICPG vs. 32 in EICPG (p = 0.0010). CPP was 30 mmHg in NICPG vs. 6 mmHg in EICPG (p = 0.0254). After aorta occlusion CPP increased immediately in both groups reaching after 15 min up to104 mmHg in NICPG vs. 126 mmHg in EICPG. Cerebrovascular reactivity seems to be altered during bleeding and occlusion phases in both groups with positive mL-PRx. The alteration was more pronounced in EICPG, but reversible in both groups.

CONCLUSION: tREBOA is lifesaving by restoration the cerebral circulation defined as CPP in animals with HS with normal or elevated ICP. Despite the observation of short episodes of cerebral autoregulation impairment during the occlusion, mainly in EICPG, tREBOA seems to be an effective tool for improving cerebral perfusion in HS that extends the crucial early window sometimes known as the "golden hour" for resuscitation even after a traumatic brain injury.

OBJECTIVE: Surgery for chronic subdural haematoma (CSDH) is one of the most frequent operations in neurosurgical practice. CSDH afflicts the elderly population most. In 2018, Kwon and co-workers published the Kwon Scoring System (KSS), whereby six clinical and radiological factors are used to facilitate, and promote quality in, surgical decision-making and counselling of relatives. The aim of this study is to validate the KSS.

METHOD: Patients operated on for unilateral CSDH at Orebro University Hospital, Sweden, between 2013 and 2019 constituted the study population. General data and the six outcome predictors according to the KSS were extracted from the electronic patient records. The pre-operative mRS score and the post-operative six-month mRS score were assessed.

RESULTS: We identified 133 patients (69.2% male) with a median age of 80.2 years (IQR 72.6-85.9). The median GCS at admission was 15; 57.1% had motor deficits and 36.81% were disoriented. For 39.1% of the patients, the prognosis was a favourable outcome (mRS 0-1) at six months. The median KSS score was 9; 63.9% of the patients scored ≥ 9, and 36 (42.4%) of these patients actually achieved a favourable outcome. This corresponds to a prediction model sensitivity of 0.667 and specificity of 0.424. A ROC curve analysis of the model yielded an AUC of 0.62441.

CONCLUSION: In our material, the KSS did not predict outcome precisely enough to base treatment decisions or counselling of relatives on the scores obtained.