RESUMO
OBJECTIVE: Hyperglycemia after aneurysmal subarachnoid hemorrhage (SAH) is associated with serious complications. Blood glucose may indicate a target for therapy to prevent delayed ischemic neurological deficits (DIND) and improve outcome. The objective of this study was to investigate energy metabolism in the extracellular/cerebrospinal fluid and blood in relation to outcome. METHODS: Prospective non-randomized study was carried out in the intensive care unit (ICU) of university hospital (n = 170 aneurysmal SAH patients, age: 51.0 +/- 12.6 years old). Following approval by the ethics committee, a microdialysis catheter was inserted into the vascular territory of the aneurysm after clipping. Patients were studied for 165 +/- 84 hours and classified according to the presence of neurological symptoms as asymptomatic (n = 66) and symptomatic (n = 104): acute focal neurological deficits (AFND, n = 61) and delayed ischemic neurological deficits (DIND, n = 43). The microdialysates were analysed hourly for energy metabolites. Daily morning blood glucose and cerebrospinal fluid (CSF) levels (glucose and lactate) were determined. Six-month Glasgow outcome scale (GOS) was assessed. RESULTS: Hyperglycemia on admission and high blood glucose levels on the following days were significantly related to the presence of symptoms, most pronounced in patients with poor outcome (p<0.05). In symptomatic patients (high blood glucose), the lowest extracellular fluid (ECF) glucose concentrations were found, most pronounced in the AFND group (1.0 +/- 1.2 mmol/l). The anaerobic metabolites lactate, lactate/pyruvate ratio (LPR) and lactate/glucose ratio (LGR) were higher in symptomatic patients (p<0.001) indicating cerebral metabolic distress. CSF concentrations of glucose and lactate were of no specific value. CONCLUSION: This study confirms the relevance of hyperglycemia to neurological outcome in SAH patients. Cerebral glucose was significantly lower in AFND patients despite hyperglycemic blood levels. More detailed works are necessary to select risk patients for optimized targeted therapy to avoid insulin-induced cerebral metabolic crisis.
