Introduction Hyperglycaemia following aneurysmal subarachnoid hemorrhage (SAH) is associated with complications and impaired neurological recovery. The aim of this study was to determine the effect of insulin treatment for glucose control on cerebral metabolism in SAH patients. Methods This prospective, nonrandomized study was conducted in 31 SAH patients in an intensive care unit (age 52 ± 10 years, World Federation of Neurological Surgeons grade 2.9 ± 1.6). A microdialysis catheter was inserted into the vascular territory of the aneurysm after clipping. Blood glucose levels above 140 mg/dl were treated with intravenous insulin and the microdialysates were analyzed hourly for the first 12 hours of infusion. Results No hypoglycaemia occurred. Twenty-four patients were treated with insulin for glucose control. Higher age and World Federation of Neurological Surgeons score were risk factors for need for insulin treatment ( P < 0.05). Although blood glucose remained stable after initiation of insulin infusion, insulin induced a significant decrease in cerebral glucose at 3 hours after onset of the infusion until the end of the observation period ( P < 0.05), reflecting high glucose utilization. The lactate:pyruvate ratio and glutamate did not increase, excluding ischaemia as possible cause of the decrease in glucose. Glycerol tended toward higher values at the end of the observation period (9 to 12 hours), reflecting either tissue damage after SAH or the beginning of cellular distress after insulin infusion. Conclusion Higher SAH grade was among the risk factors for need for insulin. Intensive glycaemic control using insulin induced a decrease of cerebral glucose and a slight increase in glycerol, though blood glucose remained normal. Future studies might detect relevant metabolic derangements when insulin treatment starts at low cerebral glucose levels, and may allow us to design a strategy for avoidance of insulin-induced metabolic crisis in SAH patients.

Although hyperglycemia was more frequent in symptomatic patients and associated with high glycerol levels, hyperglycemia was not related to cerebral high glucose. It appears that the association of adverse outcome with acute-phase hyperglycemia is not mediated by cerebral glucose metabolism. Cerebral low glucose was associated with severe metabolic distress and may present a target for therapy to improve clinical outcome.

Though initial GCS was worse in pediatric TBI patients who underwent decompressive craniectomy compared to the conservatively treated patients, long-term outcome was comparable. In children, decompressive craniectomy might be favored early in the management of uncontrollable ICP.

Intracranial hypertension is associated with a strong activation of the inflammatory cascade in the brain and systemic circulation, and might be underestimated as proinflammmatory trigger in the pathogenesis of complications after SAH. Future therapies targeting anti-inflammatory response in plasma may help to reduce the inflammatory cascade responsible for development of intracranial hypertension.

The authors confirmed the relevance of intracranial hypertension as a severe complication in patients with aSAH. Because high ICP is associated with a severely deranged cerebral metabolism and poor outcome, future studies focusing on metabolism-guided, optimized ICP therapy could help minimize secondary brain damage and improve prognosis in patients with aSAH.

Outcome was poor in all SAH patients with intracranial hypertension. Although glucose utilization was improved after DC, no improvement in outcome could be shown for this small patient population. Future studies will have to demonstrate whether markers of cerebral crisis may support the decision for DC in aneurysmal SAH patients.

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