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Systemic glucose and brain energy metabolism after subarachnoid hemorrhage.
Neurocrit Care. 2010 Jun; 12(3):317-23.NC

Abstract

BACKGROUND

Brain energy metabolic crisis (MC) and lactate-pyruvate ratio (LPR) elevations have been linked to poor outcome in comatose patients. We sought to determine if MC and LPR elevations after subarachnoid hemorrhage (SAH) are associated with acute reductions in serum glucose.

METHODS

Twenty-eight consecutive comatose SAH patients that underwent multimodality monitoring with intracranial pressure and microdialysis were studied. MC was defined as lactate/pyruvate ratio (LPR) > or = 40 and brain glucose < 0.7 mmol/l. Time-series data were analyzed using a multivariable general linear model with a logistic link function for dichotomized outcomes.

RESULTS

Multimodality monitoring included 3,178 h of observation (mean 114 +/- 65 h per patient). In exploratory analysis, serum glucose significantly decreased from 8.2 +/- 1.8 mmol/l (148 mg/dl) 2 h before to 6.9 +/- 1.9 mmol/l (124 mg/dl) at the onset of MC (P < 0.001). Reductions in serum glucose of 25% or more were significantly associated with new onset MC (adjusted odds ratio [OR] 3.6, 95% confidence interval [CI] 2.2-6.0). Acute reductions in serum glucose of 25% or more were also significantly associated with an LPR rise of 25% or more (adjusted OR 1.6, 95% CI 1.1-2.4). All analyses were adjusted for significant covariates including Glasgow Coma Scale and cerebral perfusion pressure.

CONCLUSIONS

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.

Authors+Show Affiliations

Division of Critical Care Neurology, Department of Neurology, Columbia University Medical Center, Milstein Hospital 8 Center, 177 Fort Washington Ave, New York, NY 10032, USA. raimund.helbok@uki.atNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20135362

Citation

Helbok, Raimund, et al. "Systemic Glucose and Brain Energy Metabolism After Subarachnoid Hemorrhage." Neurocritical Care, vol. 12, no. 3, 2010, pp. 317-23.
Helbok R, Schmidt JM, Kurtz P, et al. Systemic glucose and brain energy metabolism after subarachnoid hemorrhage. Neurocrit Care. 2010;12(3):317-23.
Helbok, R., Schmidt, J. M., Kurtz, P., Hanafy, K. A., Fernandez, L., Stuart, R. M., Presciutti, M., Ostapkovich, N. D., Connolly, E. S., Lee, K., Badjatia, N., Mayer, S. A., & Claassen, J. (2010). Systemic glucose and brain energy metabolism after subarachnoid hemorrhage. Neurocritical Care, 12(3), 317-23. https://doi.org/10.1007/s12028-009-9327-4
Helbok R, et al. Systemic Glucose and Brain Energy Metabolism After Subarachnoid Hemorrhage. Neurocrit Care. 2010;12(3):317-23. PubMed PMID: 20135362.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Systemic glucose and brain energy metabolism after subarachnoid hemorrhage. AU - Helbok,Raimund, AU - Schmidt,J Michael, AU - Kurtz,Pedro, AU - Hanafy,Khalid A, AU - Fernandez,Luis, AU - Stuart,R Morgan, AU - Presciutti,Mary, AU - Ostapkovich,Noeleen D, AU - Connolly,E Sander, AU - Lee,Kiwon, AU - Badjatia,Neeraj, AU - Mayer,Stephan A, AU - Claassen,Jan, PY - 2010/2/6/entrez PY - 2010/2/6/pubmed PY - 2010/8/4/medline SP - 317 EP - 23 JF - Neurocritical care JO - Neurocrit Care VL - 12 IS - 3 N2 - BACKGROUND: Brain energy metabolic crisis (MC) and lactate-pyruvate ratio (LPR) elevations have been linked to poor outcome in comatose patients. We sought to determine if MC and LPR elevations after subarachnoid hemorrhage (SAH) are associated with acute reductions in serum glucose. METHODS: Twenty-eight consecutive comatose SAH patients that underwent multimodality monitoring with intracranial pressure and microdialysis were studied. MC was defined as lactate/pyruvate ratio (LPR) > or = 40 and brain glucose < 0.7 mmol/l. Time-series data were analyzed using a multivariable general linear model with a logistic link function for dichotomized outcomes. RESULTS: Multimodality monitoring included 3,178 h of observation (mean 114 +/- 65 h per patient). In exploratory analysis, serum glucose significantly decreased from 8.2 +/- 1.8 mmol/l (148 mg/dl) 2 h before to 6.9 +/- 1.9 mmol/l (124 mg/dl) at the onset of MC (P < 0.001). Reductions in serum glucose of 25% or more were significantly associated with new onset MC (adjusted odds ratio [OR] 3.6, 95% confidence interval [CI] 2.2-6.0). Acute reductions in serum glucose of 25% or more were also significantly associated with an LPR rise of 25% or more (adjusted OR 1.6, 95% CI 1.1-2.4). All analyses were adjusted for significant covariates including Glasgow Coma Scale and cerebral perfusion pressure. CONCLUSIONS: 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. SN - 1556-0961 UR - https://www.unboundmedicine.com/medline/citation/20135362/Systemic_glucose_and_brain_energy_metabolism_after_subarachnoid_hemorrhage_ L2 - https://dx.doi.org/10.1007/s12028-009-9327-4 DB - PRIME DP - Unbound Medicine ER -