The outcome prediction models that have evolved from these databases are undergoing further refinement and validation, and it is likely that these advances will prove valuable in training clinicians, counselling patients' families, auditing unit performance, designing better clinical trials, and rational allocation of resources.

No abstract

No abstract

No abstract

This commentary considers some of the factors that affect cerebral glucose metabolism in patients with traumatic brain injury. A study recently reported in Critical Care suggested a blood glucose range that may optimize cerebral glucose utilization; the findings of this study are evaluated and discussed. Some of the mechanisms of cerebral glucose control are explored, including the impact of intensive insulin therapy on cerebral metabolism.Although glycaemic control in intensive care patients has been fertile ground for research over many years, optimizing cerebral glucose in acute brain injury has more recently attracted the interest of physicians involved in neurocritical care. The key research themes that are emerging include determining the range of arterial blood glucose that optimizes brain glucose concentration; the threshold of extracellular glucose below which neuronal injury occurs; determining the pathophysiological changes in the brain caused by deranged glucose control; and elucidating the effects of insulin therapy on cerebral glucose metabolism.Holbein and coworkers [1] have begun to address some of these questions by using arterial and jugular venous measurements to determine a range of plasma glucose between which cerebral metabolism is optimized in patients with traumatic brain injury (TBI). Their findings, albeit from retrospective data, suggest an optimal arterial blood glucose level of 6 to 8 mmol/l. On the face of it, this would seem a very useful clinical parameter, particularly because cerebral glucose levels were thought to be dependent on plasma glucose concentrations in a near linear relationship [2]. However, evidence demonstrating increased glucose utilization after head injury, coupled with data showing that low brain glucose levels measured by cerebral microdialysis is related to poor outcome after TBI, suggest that plasma glucose concentration may not be a good reflection of extracellular cerebral glucose concentrations [3,4]. This is supported by Schlenk and coworkers [5], who found that cerebral glucose levels varied independently of plasma glucose in patients with subarachnoid haemorrhage. This clearly makes control of cerebral glucose based on plasma glucose much more difficult to achieve, particularly when significant metabolic heterogeneity exists after TBI, as reported by Abate and colleagues [6]. This heterogeneity implies that techniques to detect regional changes in glucose and oxygen metabolism such as microdialysis and positron emission tomography may be preferable to jugular bulb measurements -an issue eluded to in the discussion by Holbein and colleagues [1].Using arterial-jugular differences in oxygen and glucose, both Holbein [1] and Vespa [7] and their colleagues demonstrated that higher arterial blood glucose levels may be associated with a lower oxygen extraction ratio (OER). However, Abate and coworkers [6] -using positron emission tomographydemonstrated that in some cases a higher glucose metabolism is associated with a higher OER. The mechanisms under...

No abstract

No abstract