Background and Purpose To identify a minimally-acceptable CPP threshold above which the risk of brain tissue hypoxia (BTH) and oxidative metabolic crisis is reduced for patients with SAH. Methods We studied thirty poor-grade SAH patients who underwent brain multimodality monitoring (3042 hours). Physiological measures were averaged over 60 minutes for each collected microdialysis sample. Metabolic crisis was defined as a lactate/pyruvate ratio (LPR) >40 with a brain glucose concentration ≤0.7 mmol/L. BTH was defined as PbtO2 <20 mm Hg. Outcome was assessed at 3 months with the modified Rankin Scale. Results Multivariable analyses adjusting for admission Hunt-Hess grade, intraventricular hemorrhage, systemic glucose, and end-tidal CO2 revealed that CPP ≤70 mm Hg was significantly associated with an increased risk of BTH (OR=2.0; 95%-CI: 1.2–3.3, P=0.007) and metabolic crisis (OR=2.1; 95%-CI 1.2–3.7, P=0.007). Death-or-severe-disability at 3 months was significantly associated with metabolic crisis (OR 5.4; 95%-CI: 1.8–16, P=0.002) and BTH (OR 5.1; 95%-CI: 1.2–23, P=0.03) after adjusting for admission Hunt-Hess grade. Conclusions Metabolic crisis and BTH are associated with mortality and poor functional recovery after SAH. CPP levels below 70 mm Hg was associated with metabolic crisis and BTH and may increase the risk of secondary brain injury in poor-grade SAH patients.

ICE can provide high-fidelity intracranial EEG in an intensive care unit setting, can detect ictal discharges not readily apparent on scalp EEG, and can identify early changes in brain activity caused by secondary neurological complications. We predict that ICE will facilitate the development of EEG-based alarm systems and lead to prevention of secondary neuronal injury.

IntroductionCerebral glucose metabolism and energy production are affected by serum glucose levels. Systemic glucose variability has been shown to be associated with poor outcome in critically ill patients. The objective of this study was to assess whether glucose variability is associated with cerebral metabolic distress and outcome after subarachnoid hemorrhage.MethodsA total of 28 consecutive comatose patients with subarachnoid hemorrhage, who underwent cerebral microdialysis and intracranial pressure monitoring, were studied. Metabolic distress was defined as lactate/pyruvate ratio (LPR) >40. The relationship between daily glucose variability, the development of cerebral metabolic distress and hospital outcome was analyzed using a multivariable general linear model with a logistic link function for dichotomized outcomes.ResultsDaily serum glucose variability was expressed as the standard deviation (SD) of all serum glucose measurements. General linear models were used to relate this predictor variable to cerebral metabolic distress and mortality at hospital discharge. A total of 3,139 neuromonitoring hours and 181 days were analyzed. After adjustment for Glasgow Coma Scale (GCS) scores and brain glucose, SD was independently associated with higher risk of cerebral metabolic distress (adjusted odds ratio = 1.5 (1.1 to 2.1), P = 0.02). Increased variability was also independently associated with in hospital mortality after adjusting for age, Hunt Hess, daily GCS and symptomatic vasospasm (P = 0.03).ConclusionsIncreased systemic glucose variability is associated with cerebral metabolic distress and increased hospital mortality. Therapeutic approaches that reduce glucose variability may impact on brain metabolism and outcome after subarachnoid hemorrhage.

Acute reductions in serum glucose, even to levels within the normal range, may be associated with brain energy metabolic crisis and LPR elevation in poor-grade SAH patients.

Anemia is associated with a progressively increased risk of cerebral metabolic distress and brain tissue hypoxia after subarachnoid hemorrhage.

Mannitol effectively reduces ICP and appeared to benefit brain metabolism as measured by the lactate-pyruvate ratio.

PRBC transfusion resulted in PbtO2 improvement without a clear effect on cerebral metabolism prior to SAH.

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