Characterising the dynamics of cerebral metabolic dysfunction following traumatic brain injury: A microdialysis study in 619 patients.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2021
2021
Historique:
received:
27
04
2021
accepted:
05
11
2021
entrez:
16
12
2021
pubmed:
17
12
2021
medline:
20
1
2022
Statut:
epublish
Résumé
Traumatic brain injury (TBI) is a major cause of death and disability, particularly amongst young people. Current intensive care management of TBI patients is targeted at maintaining normal brain physiology and preventing secondary injury. Microdialysis is an invasive monitor that permits real-time assessment of derangements in cerebral metabolism and responses to treatment. We examined the prognostic value of microdialysis parameters, and the inter-relationships with other neuromonitoring modalities to identify interventions that improve metabolism. This was an analysis of prospective data in 619 adult TBI patients requiring intensive care treatment and invasive neuromonitoring at a tertiary UK neurosciences unit. Patients had continuous measurement of intracranial pressure (ICP), arterial blood pressure (ABP), brain tissue oxygenation (PbtO2), and cerebral metabolism and were managed according to a standardized therapeutic protocol. Microdialysate was assayed hourly for metabolites including glucose, pyruvate, and lactate. Cerebral perfusion pressure (CPP) and cerebral autoregulation (PRx) were derived from the ICP and ABP. Outcome was assessed with the Glasgow Outcome Score (GOS) at 6 months. Relationships between monitoring variables was examined with generalized additive mixed models (GAMM). Lactate/Pyruvate Ratio (LPR) over the first 3 to 7 days following injury was elevated amongst patients with poor outcome and was an independent predictor of ordinal GOS (p<0.05). Significant non-linear associations were observed between LPR and cerebral glucose, CPP, and PRx (p<0.001 to p<0.05). GAMM models suggested improved cerebral metabolism (i.e. reduced LPR with CPP >70mmHg, PRx <0.1, PbtO2 >18mmHg, and brain glucose >1mM. Deranged cerebral metabolism is an important determinant of patient outcome following TBI. Variations in cerebral perfusion, oxygenation and glucose supply are associated with changes in cerebral LPR and suggest therapeutic interventions to improve cerebral metabolism. Future prospective studies are required to determine the efficacy of these strategies.
Identifiants
pubmed: 34914701
doi: 10.1371/journal.pone.0260291
pii: PONE-D-21-13992
pmc: PMC8675704
doi:
Substances chimiques
Lactic Acid
33X04XA5AT
Pyruvic Acid
8558G7RUTR
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0260291Subventions
Organisme : Medical Research Council
ID : G1002277
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0600986
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0802251
Pays : United Kingdom
Organisme : Medical Research Council
ID : G9439390
Pays : United Kingdom
Déclaration de conflit d'intérêts
I have read the journal’s policy and the authors of this manuscript have the following competing interests: PJAH is a director of Technicam (Newton Abbot, UK), the manufacturer of the cranial access device used in this study. MC and PS have financial interest in a part of licensing fee for ICM+ software (Cambridge Enterprise Ltd., UK). This does not alter our adherence to PLOS ONE policies on sharing data and materials.
Références
Brain. 2011 Feb;134(Pt 2):484-94
pubmed: 21247930
Curr Opin Crit Care. 2017 Apr;23(2):103-109
pubmed: 28207601
Front Neurosci. 2015 Apr 08;9:112
pubmed: 25904838
Brain Res. 2013 Oct 16;1535:124-36
pubmed: 23994447
J Cereb Blood Flow Metab. 2012 Jul;32(7):1152-66
pubmed: 22027938
Acta Anaesthesiol Scand. 2013 Feb;57(2):229-35
pubmed: 23017022
J Neurochem. 2000 Aug;75(2):480-6
pubmed: 10899922
Cell Metab. 2011 Dec 7;14(6):724-38
pubmed: 22152301
Metab Brain Dis. 2015 Jun;30(3):615-32
pubmed: 25413449
Cell Metab. 2016 Jan 12;23(1):94-102
pubmed: 26698914
Nat Rev Neurol. 2013 Apr;9(4):231-6
pubmed: 23443846
J Neurol Neurosurg Psychiatry. 2004 Mar;75(3):353-61
pubmed: 14966145
Intensive Care Med. 2015 Sep;41(9):1517-28
pubmed: 26194024
Acta Neurochir (Wien). 2009 Jan;151(1):51-61; discussion 61
pubmed: 19099177
Front Hum Neurosci. 2017 Aug 25;11:422
pubmed: 28890692
J Neurotrauma. 2018 Sep 1;35(17):2025-2035
pubmed: 29690859
J Neurosci. 2011 May 18;31(20):7477-85
pubmed: 21593331
Acta Neurochir (Wien). 2017 Nov;159(11):2063-2065
pubmed: 28849287
Crit Care Med. 2008 Dec;36(12):3233-8
pubmed: 18936695
Crit Care Med. 2006 Mar;34(3):850-6
pubmed: 16505665
J Neurosurg. 1997 Feb;86(2):241-51
pubmed: 9010426
J Cereb Blood Flow Metab. 2021 Sep 8;:271678X211042112
pubmed: 34494481
J Neurotrauma. 2013 Dec 15;30(24):2031-7
pubmed: 23968221
J Cereb Blood Flow Metab. 2015 Jan;35(1):111-20
pubmed: 25335801
Br J Anaesth. 2007 Jul;99(1):32-42
pubmed: 17556349
Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10625-9
pubmed: 7938003
PLoS Med. 2017 Jul 25;14(7):e1002353
pubmed: 28742817
Crit Care. 2018 Jan 25;22(1):16
pubmed: 29368635
J Cereb Blood Flow Metab. 2017 Jun;37(6):2112-2124
pubmed: 27481936
J Neurotrauma. 1998 Dec;15(12):1059-66
pubmed: 9872462
J Neurosurg. 1991 Oct;75(4):545-51
pubmed: 1885972