Cerebrospinal Fluid Glucose and Lactate Levels After Subarachnoid Hemorrhage: A Multicenter Retrospective Study.
Journal
Journal of neurosurgical anesthesiology
ISSN: 1537-1921
Titre abrégé: J Neurosurg Anesthesiol
Pays: United States
ID NLM: 8910749
Informations de publication
Date de publication:
Apr 2020
Apr 2020
Historique:
pubmed:
23
5
2019
medline:
15
12
2020
entrez:
23
5
2019
Statut:
ppublish
Résumé
In patients with subarachnoid hemorrhage (SAH), abnormalities in glucose and lactate metabolism have been described using cerebral microdialysis. Glucose and lactate concentrations in cerebrospinal fluid (CSF) are more easily accessible, but scarce data are available in this setting. The aim of this study is to assess the relationship of CSF glucose and lactate with blood concentrations and with unfavorable neurological outcome after SAH. A retrospective cohort study was conducted in 5 European University intensive care units. Patients aged 18 years and above who were admitted after a nontraumatic SAH over a 4-year period (2011 to 2014) were included if they had an external ventricular drain placed, daily analysis of CSF including glucose (±lactate) concentrations for 1 to 4 consecutive days, and concomitant analysis of glucose and lactate concentrations in the arterial blood. A total of 144 patients were included in the final analysis (median age: 58 [49 to 66] y; male sex: 77/144). Median time from admission to external ventricular drain placement was 1 (0 to 3) day; median Glasgow Coma Scale on admission was 10 (7 to 13), and CT-scan Fisher scale was 4. A total of 81 (56%) patients had unfavorable neurological outcome at 3 months (Glasgow Outcome Scale ≤3). There was a weak correlation between blood and CSF glucose (r=0.07, P=0.007), and between blood and CSF lactate levels (r=0.58, P<0.001) on day 1, which were not influenced by insulin therapy. The presence of shock and low CSF glucose/lactate ratio were the only independent predictors of unfavorable outcome. CSF glucose and lactate levels poorly correlated with blood concentrations. Low CSF glucose/lactate ratio was associated with poor neurological outcome.
Sections du résumé
BACKGROUND
BACKGROUND
In patients with subarachnoid hemorrhage (SAH), abnormalities in glucose and lactate metabolism have been described using cerebral microdialysis. Glucose and lactate concentrations in cerebrospinal fluid (CSF) are more easily accessible, but scarce data are available in this setting. The aim of this study is to assess the relationship of CSF glucose and lactate with blood concentrations and with unfavorable neurological outcome after SAH.
METHODS
METHODS
A retrospective cohort study was conducted in 5 European University intensive care units. Patients aged 18 years and above who were admitted after a nontraumatic SAH over a 4-year period (2011 to 2014) were included if they had an external ventricular drain placed, daily analysis of CSF including glucose (±lactate) concentrations for 1 to 4 consecutive days, and concomitant analysis of glucose and lactate concentrations in the arterial blood.
RESULTS
RESULTS
A total of 144 patients were included in the final analysis (median age: 58 [49 to 66] y; male sex: 77/144). Median time from admission to external ventricular drain placement was 1 (0 to 3) day; median Glasgow Coma Scale on admission was 10 (7 to 13), and CT-scan Fisher scale was 4. A total of 81 (56%) patients had unfavorable neurological outcome at 3 months (Glasgow Outcome Scale ≤3). There was a weak correlation between blood and CSF glucose (r=0.07, P=0.007), and between blood and CSF lactate levels (r=0.58, P<0.001) on day 1, which were not influenced by insulin therapy. The presence of shock and low CSF glucose/lactate ratio were the only independent predictors of unfavorable outcome.
CONCLUSIONS
CONCLUSIONS
CSF glucose and lactate levels poorly correlated with blood concentrations. Low CSF glucose/lactate ratio was associated with poor neurological outcome.
Identifiants
pubmed: 31116707
doi: 10.1097/ANA.0000000000000584
pii: 00008506-202004000-00011
doi:
Substances chimiques
Blood Glucose
0
Lactic Acid
33X04XA5AT
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
170-176Références
Diringer MN, Bleck TP, Claude Hemphill J III, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15:211–240.
Wartenberg KE, Schmidt JM, Claassen J, et al. Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med. 2006;34:617–623.
Frontera JA, Fernandez A, Claassen J, et al. Hyperglycemia after SAH: predictors, associated complications, and impact on outcome. Stroke. 2006;37:199–203.
Dorhout Mees SM, van Dijk GW, Algra A, et al. Glucose levels and outcome after subarachnoid hemorrhage. Neurology. 2003;61:1132–1133.
Lanzino G, Kassell NF, Germanson T, et al. Plasma glucose levels and outcome after aneurysmal subarachnoid hemorrhage. J Neurosurg. 1993;79:885–891.
Naidech AM, Levasseur K, Liebling S, et al. Moderate hypoglycemia is associated with vasospasm, cerebral infarction, and 3-month disability after subarachnoid hemorrhage. Neurocrit Care. 2010;12:181–187.
Zygun DA, Steiner LA, Johnston AJ, et al. Hyperglycemia and brain tissue pH after traumatic brain injury. Neurosurgery. 2004;55:877–881.
Oddo M, Schmidt JM, Carrera E, et al. Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: a microdialysis study. Crit Care Med. 2008;36:3233–3238.
Bilotta F, Spinelli A, Giovannini F, et al. The effect of intensive insulin therapy on infection rate, vasospasm, neurologic outcome, and mortality in neurointensive care unit after intracranial aneurysm clipping in patients with acute subarachnoid hemorrhage: a randomized prospective pilot trial. J Neurosurg Anesthesiol. 2007;19:156–160.
Sarrafzadeh A, Haux D, Küchler I, et al. Poor-grade aneurysmal subarachnoid hemorrhage: relationship of cerebral metabolism to outcome. J Neurosurg. 2004;100:400–406.
Carteron L, Patet C, Solari D, et al. Non-Ischemic Cerebral Energy Dysfunction at the Early Brain Injury Phase following Aneurysmal Subarachnoid Hemorrhage. Front Neurol. 2017;8:325.
Samuelsson C, Hillered L, Zetterling M, et al. Cerebral glutamine and glutamate levels in relation to compromised energy metabolism: a microdialysis study in subarachnoid haemorrhage patients. J Cereb Blood Flow Metab. 2007;27:1309–1317.
Jacobsen A, Nielsen TH, Nilsson O, et al. Bedside diagnosis of mitochondrial dysfunction in aneurysmal subarachnoid hemorrhage. Acta Neurol Scand. 2014;130:156–163.
Robertson CS, Goodman JC, Narayan RK, et al. The effect of glucose administration on carbohydrate metabolism after head injury. J Neurosurg. 1991;74:43–50.
Nemoto EM, Hoff JT, Severinghaus JW. Lactate uptake and metabolism by brain during hyperlactatemia and hypoglycemia. Stroke. 1974;5:48–53.
Fujishima M, Sugi T, Choki J, et al. Cerebrospinal fluid and arterial lactate, pyruvate and acid-base balance in patients with intracranial hemorrhages. Stroke. 1975;6:707–714.
Drake CG. Report of World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale. J Neurosurg. 1988;68:985–986.
Fisher C, Kistler J, Davis J. Relation of cerebral vasospasm to subarachnoid hemorrhage visualised by computerised tomographic scanning. Neurosurgery. 1980;6:1–9.
Schlenk F, Nagel A, Graetz D, et al. Hyperglycemia and cerebral glucose in aneurysmal subarachnoid hemorrhage. Intensive Care Med. 2008;34:1200–1207.
Cranston I, Marsden P, Matyka K, et al. Regional differences in cerebral blood flow and glucose utilization in diabetic man: the effect of insulin. J Cereb Blood Flow Metab. 1998;18:130–140.
Hladky SB, Barrand MA. Mechanisms of fluid movement into, through and out of the brain: evaluation of the evidence. Fluids Barriers CNS. 2014;11:26.
King LR, McLaurin RL, Knowles HC Jr. Acid-base balance and arterial and CSF lactate levels following human head injury. J Neurosurg. 1974;40:617–625.
DeSalles AA, Kontos HA, Becker DP, et al. Prognostic significance of ventricular CSF lactic acidosis in severe head injury. J Neurosurg. 1986;65:615–624.
Lewelt W, Jenkins LW, Miller JD. Effects of experimental fluid-percussion injury of the brain on cerebrovascular reactivity of hypoxia and to hypercapnia. J Neurosurg. 1982;56:332–338.
Yang MS, DeWitt DS, Becker DP, et al. Regional brain metabolite levels following mild experimental head injury in the cat. J Neurosurg. 1985;63:617–621.
Froman C, Smith AC. Metabolic acidosis of the cerebrospinal fluid associated with subarachnoid haemorrhage. Lancet. 1967;1:965–967.
Oddo M, Levine JM, Frangos S, et al. Brain lactate metabolism in humans with subarachnoid hemorrhage. Stroke. 2012;43:1418–1421.
Persson L, Valtysson J, Enblad P, et al. Neurochemical monitoring using intracerebral microdialysis in patients with subarachnoid hemorrhage. J Neurosurg. 1996;84:606–616.
Goodman JC, Valadka AB, Gopinath SP, et al. Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis. Crit Care Med. 1999;27:1965–1973.
McMillan T, Wilson L, Ponsford J, et al. The Glasgow Outcome Scale-40 years of application and refinement. Nat Rev Neurol. 2016;12:477–485.