INTRODUCTION:Hyperglycaemia is detrimental, but maintaining low blood glucose levels within tight limits is controversial in patients with severe traumatic brain injury, because decreased blood glucose levels can induce and aggravate underlying brain injury.METHODS:In 228 propensity matched patients (age, sex and injury severity) treated in our intensive care unit (ICU) from 2000 to 2004, we retrospectively evaluated the influence of different predefined blood glucose targets (3.5 to 6.5 versus 5 to 8 mmol/l) on frequency of hypoglycaemic and hyperglycaemic episodes, insulin and norepinephrine requirement, changes in intracranial pressure and cerebral perfusion pressure, mortality and length of stay on the ICU.RESULTS:Mortality and length of ICU stay were similar in both blood glucose target groups. Blood glucose values below and above the predefined levels were significantly increased in the 3.5 to 6.5 mmol/l group, predominantly during the first week. Insulin and norepinephrine requirements were markedly increased in this group. During the second week, the incidences of intracranial pressure exceeding 20 mmHg and infectious complications were significantly decreased in the 3.5 to 6.5 mmol/l group.CONCLUSION:Maintaining blood glucose within 5 to 8 mmol/l appears to yield greater benefit during the first week. During the second week, 3.5 to 6.5 mmol/l is associated with beneficial effects in terms of reduced intracranial hypertension and decreased rate of pneumonia, bacteraemia and urinary tract infections. It remains to be determined whether patients might profit from temporally adapted blood glucose limits, inducing lower values during the second week, and whether concomitant glucose infusion to prevent hypoglycaemia is safe in patients with post-traumatic oedema.

Journal of Neurosurgical Anesthesiology 19(2):p 143-144, April 2007. | DOI: 10.1097/ANA.0b013e31802b41bd

Critical Care Medicine: May 2006 - Volume 34 - Issue 5 - p 1582-1583 doi: 10.1097/01.CCM.0000216697.37348.FC

Norepinephrine and corresponding intra- and interorgan pathways are of clinical pathophysiologic and pharmacologic importance as exaggerated activation needs to be reduced and insufficient activation must be supported to prevent further deterioration and therapy-induced organ damage. This is of high relevance in critically ill patients in whom various norepinephrine-influenced organ systems are simultaneousy affected with varying degrees of tolerability and resistance to norepinephrine-induced cell damage and finds its maximal challenge in patients suffering from severe traumatic brain injury (TBI). This comprehensive review describes complex pathophysiologic interactions, including hemodynamic, microcirculatory, hormonal, metabolic, inflammatory, and thrombocytic alterations overshadowed by differential consequences of commonly applied pharmacological interventions following TBI. Overall, investigations published to date suggest that receptor-dependent effects of norepinephrine might predispose to complex evolving deterioration especially during intensive care which is characterized by differentiated complication-driven changes and specific complication-dependent needs. In this context, thrombocytes and leukocytes with their adrenergic receptors and differential norepinephric functional regulation are ideal candidates to influence all organs at once. Despite its secure integration of norepinephrine in clinical routine, future emphasis must be directed at unmasking, monitoring, and controlling possible receptor-mediated detrimental influences which could offset anticipated organ protection.

Despite the envisioned breakthrough prophesied for the end of the past century in healing brain injured patients, both clinicians and basic scientists are still struggling with this burden. In the past decades, intensive research has brought forward a plethora of different targets which—in part—have already been integrated in clinical routine directed at detailed monitoring, therapeutic interventions, and prevention of secondary deterioration. While intracellular targets remain obscure alterations on a larger scale as e. g., measured intracranial pressure (ICP), calculated cerebral perfusion pressure (CPP), and various imaging techniques are fundamental components of our present clinical understanding. At bedside, comprehension of pathophysiological loops and circuits of a given value (e. g., ICP) depends on individual knowledge, interpretation, and availability of additional diagnostic steps. As stated in the guidelines brought forward by the American Association of Neurological Surgeons and evaluated in various reports by the Cochrane Library we are still lacking prospective, randomized trials for the majority of the proposed diagnostic and therapeutic interventions. In this context, a recent meta-analysis even questioned the importance of ICP monitoring as we are lacking data from randomized controlled trials clarifying the role of ICP monitoring. The present review is to give an overview of various diagnostic and therapeutic possibilities based on reports published in the past 5 years to strengthen current approaches and nourish future well-designed investigations how to avoid and treat intracranial hypertension.