High Arterial Glucose is Associated with Poor Pressure Autoregulation, High Cerebral Lactate/Pyruvate Ratio and Poor Outcome Following Traumatic Brain Injury.
Adult
Arterial Pressure
/ physiology
Blood Glucose
/ metabolism
Blood Pressure
/ physiology
Brain
/ blood supply
Brain Injuries, Traumatic
/ metabolism
Cerebrovascular Circulation
/ physiology
Female
Glasgow Outcome Scale
Glucose
/ metabolism
Homeostasis
/ physiology
Humans
Hyperglycemia
/ metabolism
Intracranial Pressure
/ physiology
Lactic Acid
/ metabolism
Male
Microdialysis
Middle Aged
Prognosis
Pyruvic Acid
/ metabolism
Radial Artery
Retrospective Studies
Sweden
Young Adult
Autoregulation
Cerebral energy metabolism
Glucose
Traumatic brain injury
Journal
Neurocritical care
ISSN: 1556-0961
Titre abrégé: Neurocrit Care
Pays: United States
ID NLM: 101156086
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
pubmed:
28
5
2019
medline:
19
5
2020
entrez:
25
5
2019
Statut:
ppublish
Résumé
Arterial hyperglycemia is associated with poor outcome in traumatic brain injury (TBI), but the pathophysiology is not completely understood. Previous preclinical and clinical studies have indicated that arterial glucose worsens pressure autoregulation. The aim of this study was to evaluate the relationship of arterial glucose to both pressure reactivity and cerebral energy metabolism. This retrospective study was based on 120 patients with severe TBI treated at the Uppsala University hospital, Sweden, 2008-2018. Data from cerebral microdialysis (glucose, pyruvate, and lactate), arterial glucose, and pressure reactivity index (PRx55-15) were analyzed the first 3 days post-injury. High arterial glucose was associated with poor outcome/Glasgow Outcome Scale-Extended at 6-month follow-up (r = - 0.201, p value = 0.004) and showed a positive correlation with both PRx55-15 (r = 0.308, p = 0.001) and cerebral lactate/pyruvate ratio (LPR) days 1-3 (r = 0. 244, p = 0.014). Cerebral lactate-to-pyruvate ratio and PRx55-15 had a positive association day 2 (r = 0.219, p = 0.048). Multivariate linear regression analysis showed that high arterial glucose predicted poor pressure autoregulation on days 1 and 2. High arterial glucose was associated with poor outcome, poor pressure autoregulation, and cerebral energy metabolic disturbances. The latter two suggest a pathophysiological mechanism for the negative effect of arterial hyperglycemia, although further studies are needed to elucidate if the correlations are causal or confounded by other factors.
Sections du résumé
BACKGROUND
Arterial hyperglycemia is associated with poor outcome in traumatic brain injury (TBI), but the pathophysiology is not completely understood. Previous preclinical and clinical studies have indicated that arterial glucose worsens pressure autoregulation. The aim of this study was to evaluate the relationship of arterial glucose to both pressure reactivity and cerebral energy metabolism.
METHOD
This retrospective study was based on 120 patients with severe TBI treated at the Uppsala University hospital, Sweden, 2008-2018. Data from cerebral microdialysis (glucose, pyruvate, and lactate), arterial glucose, and pressure reactivity index (PRx55-15) were analyzed the first 3 days post-injury.
RESULTS
High arterial glucose was associated with poor outcome/Glasgow Outcome Scale-Extended at 6-month follow-up (r = - 0.201, p value = 0.004) and showed a positive correlation with both PRx55-15 (r = 0.308, p = 0.001) and cerebral lactate/pyruvate ratio (LPR) days 1-3 (r = 0. 244, p = 0.014). Cerebral lactate-to-pyruvate ratio and PRx55-15 had a positive association day 2 (r = 0.219, p = 0.048). Multivariate linear regression analysis showed that high arterial glucose predicted poor pressure autoregulation on days 1 and 2.
CONCLUSIONS
High arterial glucose was associated with poor outcome, poor pressure autoregulation, and cerebral energy metabolic disturbances. The latter two suggest a pathophysiological mechanism for the negative effect of arterial hyperglycemia, although further studies are needed to elucidate if the correlations are causal or confounded by other factors.
Identifiants
pubmed: 31123993
doi: 10.1007/s12028-019-00743-2
pii: 10.1007/s12028-019-00743-2
pmc: PMC6872512
doi:
Substances chimiques
Blood Glucose
0
Lactic Acid
33X04XA5AT
Pyruvic Acid
8558G7RUTR
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
526-533Références
Peeters W, van den Brande R, Polinder S, et al. Epidemiology of traumatic brain injury in Europe. Acta Neurochir (Wien). 2015;157(10):1683–96.
doi: 10.1007/s00701-015-2512-7
Jeremitsky E, Omert LA, Dunham CM, Wilberger J, Rodriguez A. The impact of hyperglycemia on patients with severe brain injury. J Trauma. 2005;58(1):47–50.
doi: 10.1097/01.TA.0000135158.42242.B1
Young B, Ott L, Dempsey R, Haack D, Tibbs P. Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients. Ann Surg. 1989;210(4):466.
doi: 10.1097/00000658-198910000-00007
Cummings PM, Giddens K, Nassar BA. Oral glucose loading acutely attenuates endothelium-dependent vasodilation in healthy adults without diabetes: an effect prevented by vitamins C and E. J Am Coll Cardiol. 2000;36(7):2185–91.
doi: 10.1016/S0735-1097(00)00980-3
Duckrow RB, Beard DC, Brennan RW. Regional cerebral blood flow decreases during hyperglycemia. Ann Neurol. 1985;17(3):267–72.
doi: 10.1002/ana.410170308
Lott ME, Hogeman C, Herr M, Gabbay R, Sinoway LI. Effects of an oral glucose tolerance test on the myogenic response in healthy individuals. Am J Physiol Heart Circ Physiol. 2007;292(1):H304–10.
doi: 10.1152/ajpheart.00940.2005
Ward ME, Yan L, Angle MR. Modulation of rat pial arteriolar responses to flow by glucose. Anesthesiology. 2002;97(2):471–7.
doi: 10.1097/00000542-200208000-00026
Czosnyka M, Smielewski P, Kirkpatrick P, et al. Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery. 1997;41(1):11–9.
doi: 10.1097/00006123-199707000-00005
Howells T, Johnson U, McKelvey T, Enblad P. An optimal frequency range for assessing the pressure reactivity index in patients with traumatic brain injury. J Clin Monit Comput. 2015;29(1):97–105.
doi: 10.1007/s10877-014-9573-7
Sorrentino E, Diedler J, Kasprowicz M, et al. Critical thresholds for cerebrovascular reactivity after traumatic brain injury. Neurocrit Care. 2012;16(2):258–66.
doi: 10.1007/s12028-011-9630-8
Peterson EC, Wang Z, Britz G. Regulation of cerebral blood flow. Int J Vasc Med. 2011;2011:823525
pubmed: 21808738
pmcid: 3144666
Donnelly J, Czosnyka M, Sudhan N, et al. Increased blood glucose is related to disturbed cerebrovascular pressure reactivity after traumatic brain injury. Neurocrit Care. 2015;22(1):20–5.
doi: 10.1007/s12028-014-0042-4
Young AM, Adams H, Donnelly J, et al. Glycemia is related to impaired cerebrovascular autoregulation after severe pediatric traumatic brain injury: a retrospective observational study. Front Pediatr. 2017;5:205.
doi: 10.3389/fped.2017.00205
Elf K, Nilsson P, Ronne-Engström E, Howells T, Enblad P. Cerebral perfusion pressure between 50 and 60 mm Hg may be beneficial in head-injured patients: a computerized secondary insult monitoring study. Neurosurgery. 2005;56(5):962–71.
pubmed: 15854244
Ronne-Engström E, Cesarini KG, Enblad P, et al. Intracerebral microdialysis in neurointensive care: the use of urea as an endogenous reference compound. J Neurosurg. 2001;94(3):397–402.
doi: 10.3171/jns.2001.94.3.0397
Teasdale GM, Pettigrew LE, Wilson JL, Murray G, Jennet B. Analyzing outcome of treatment of severe head injury: a review and update on advancing the use of the Glasgow Outcome Scale. J Neurotrauma. 1998;15(8):587–97.
doi: 10.1089/neu.1998.15.587
Wilson JL, Pettigrew LE, Teasdale GM. Structured interviews for the Glasgow Outcome Scale and the extended Glasgow Outcome Scale: guidelines for their use. J Neurotrauma. 1998;15(8):573–85.
doi: 10.1089/neu.1998.15.573
Nyholm L, Howells T, Enblad P, Lewén A. Introduction of the Uppsala traumatic brain injury register for regular surveillance of patient characteristics and neurointensive care management including secondary insult quantification and clinical outcome. Ups J Med Sci. 2013;118(3):169–80.
doi: 10.3109/03009734.2013.806616
Howells T, Elf K, Jones PA, et al. Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma. J Neurosurg. 2005;102(2):311–7.
doi: 10.3171/jns.2005.102.2.0311
Reinstrup P, Ståhl N, Mellergård P, et al. Intracerebral microdialysis in clinical practice: baseline values for chemical markers during wakefulness, anesthesia, and neurosurgery. Neurosurgery. 2000;47(3):701–10.
pubmed: 10981758
Schulz MK, Wang LP, Tange M, Bjerre P. Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg. 2000;93(5):808–14.
doi: 10.3171/jns.2000.93.5.0808
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(12):3233–8.
doi: 10.1097/CCM.0b013e31818f4026
Rostami E. Glucose and the injured brain-monitored in the neurointensive care unit. Front Neurol. 2014;5:91.
pubmed: 24936196
pmcid: 4047514
Marcoux J, McArthur DA, Miller C, et al. Persistent metabolic crisis as measured by elevated cerebral microdialysis lactate-pyruvate ratio predicts chronic frontal lobe brain atrophy after traumatic brain injury. Crit Care Med. 2008;36(10):2871–7.
doi: 10.1097/CCM.0b013e318186a4a0
Timofeev I, Carpenter KL, Nortje J, et al. Cerebral extracellular chemistry and outcome following traumatic brain injury: a microdialysis study of 223 patients. Brain. 2011;134(2):484–94.
doi: 10.1093/brain/awq353
Martin NA, Patwardhan RV, Alexander MJ, et al. Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm. J Neurosurg. 1997;87(1):9–19.
doi: 10.3171/jns.1997.87.1.0009
Adams H, Donnelly J, Czosnyka M, et al. Temporal profile of intracranial pressure and cerebrovascular reactivity in severe traumatic brain injury and association with fatal outcome: an observational study. PLoS Med. 2017;14(7):e1002353.
doi: 10.1371/journal.pmed.1002353
Russell JW, Golovoy D, Vincent AM, et al. High glucose-induced oxidative stress and mitochondrial dysfunction in neurons. FASEB J. 2002;16(13):1738–48.
doi: 10.1096/fj.01-1027com
Woolf PD, Hamill RW, Lee LA, Cox C, McDonald JV. The predictive value of catecholamines in assessing outcome in traumatic brain injury. J Neurosurg. 1987;66(6):875–82.
doi: 10.3171/jns.1987.66.6.0875
Rosner MJ, Newsome HH, Becker DP. Mechanical brain injury: the sympathoadrenal response. J Neurosurg. 1984;61(1):76–86.
doi: 10.3171/jns.1984.61.1.0076
Bosarge PL, Shoultz TH, Griffin RL, Kerby JD. Stress-induced hyperglycemia is associated with higher mortality in severe traumatic brain injury. J Trauma Acute Care Surg. 2015;79(2):289–94.
doi: 10.1097/TA.0000000000000716
Vespa PM, McArthur D, O’Phelan K, et al. Persistently low extracellular glucose correlates with poor outcome 6 months after human traumatic brain injury despite a lack of increased lactate: a microdialysis study. J Cereb Blood Flow Metab. 2003;23(7):865–77.
doi: 10.1097/01.WCB.0000076701.45782.EF
Magnoni S, Tedesco C, Carbonara M, et al. Relationship between systemic glucose and cerebral glucose is preserved in patients with severe traumatic brain injury, but glucose delivery to the brain may become limited when oxidative metabolism is impaired: implications for glycemic control. Crit Care Med. 2012;40(6):1785–91.
doi: 10.1097/CCM.0b013e318246bd45
Rostami E, Bellander BM. Monitoring of glucose in brain, adipose tissue, and peripheral blood in patients with traumatic brain injury: a microdialysis study. J Diabetes Sci Technol. 2011;5(3):596–604.
doi: 10.1177/193229681100500314
Diaz-Parejo P, Ståhl N, Xu W, et al. Cerebral energy metabolism during transient hyperglycemia in patients with severe brain trauma. Intensive Care Med. 2003;29(4):544–50.
doi: 10.1007/s00134-003-1669-3
Bilotta F, Caramia R, Cernak I, et al. Intensive insulin therapy after severe traumatic brain injury: a randomized clinical trial. Neurocrit Care. 2008;9(2):159–66.
doi: 10.1007/s12028-008-9084-9
Coester A, Neumann CR, Schmidt MI. Intensive insulin therapy in severe traumatic brain injury: a randomized trial. J Trauma Acute Care Surg. 2010;68(4):904–11.
Meier R, Béchir M, Ludwig S, et al. Differential temporal profile of lowered blood glucose levels (3.5 to 6.5 mmol/l versus 5 to 8 mmol/l) in patients with severe traumatic brain injury. Crit Care. 2008;12(4):R98.
doi: 10.1186/cc6974
Vespa P, Boonyaputthikul R, McArthur DL, et al. Intensive insulin therapy reduces microdialysis glucose values without altering glucose utilization or improving the lactate/pyruvate ratio after traumatic brain injury. Crit Care Med. 2006;34(3):850–6.
doi: 10.1097/01.CCM.0000201875.12245.6F
Hutchinson PJ, Jalloh I, Helmy A, et al. Consensus statement from the 2014 international microdialysis forum. Intensive Care Med. 2015;41(9):1517–28.
doi: 10.1007/s00134-015-3930-y