Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and positron emission tomography study

被引:436
作者
Vespa, P [1 ]
Bergsneider, M [1 ]
Hattori, N [1 ]
Wu, HM [1 ]
Huang, SC [1 ]
Martin, NA [1 ]
Glenn, TC [1 ]
McArthur, DL [1 ]
Hovda, DA [1 ]
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, UCLA Med Ctr, Los Angeles, CA 90095 USA
关键词
brain injury; ischemia; lactate; lactate/pyruvate ratio; microdialysis; positron emission tomography; pyruvate;
D O I
10.1038/sj.jcbfm.9600073
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Brain trauma is accompanied by regional alterations of brain metabolism, reduction in metabolic rates and possible energy crisis. We hypothesize that microdialysis markers of energy crisis are present during the critical period of intensive care despite the absence of brain ischemia. In all, 19 brain injury patients (mean GCS 6) underwent combined positron emission tomography (PET) for metabolism of glucose (CMRglu) and oxygen (CMRO2) and cerebral microdialysis (MD) at a mean time of 36h after injury. Microdialysis values were compared with the regional mean PET values adjacent to the probe. Longitudinal MD data revealed a 25% incidence rate of metabolic crisis (elevated lactate/pyruvate ratio (LPR)> 40) but only a 2.4% incidence rate of ischemia. Positron emission tomography imaging revealed a 1% incidence of ischemia across all voxels as measured by oxygen extraction fraction (OEF) and cerebral venous oxygen content (CvO(2)). In the region of the MD probe, PET imaging revealed ischemia in a single patient despite increased LPR in other patients. Lactate/pyruvate ratio correlated negatively with CMRO2 (P < 0.001), but not with OEF or CvO(2). Traumatic brain injury leads to a state of persistent metabolic crisis as reflected by abnormal cerebral microdialysis LPR that is not related to ischemia.
引用
收藏
页码:763 / 774
页数:12
相关论文
共 48 条
[1]  
ANDERSEN BJ, 1989, INTRACRANIAL PRESSUR, V7, P575
[2]  
[Anonymous], CHILDRENS ENV Q
[3]  
[Anonymous], J CEREB BLOOD FLOW M
[4]   INJURY SEVERITY SCORE - METHOD FOR DESCRIBING PATIENTS WITH MULTIPLE INJURIES AND EVALUATING EMERGENCY CARE [J].
BAKER, SP ;
ONEILL, B ;
HADDON, W ;
LONG, WB .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1974, 14 (03) :187-196
[5]   Cerebral hyperglycolysis following severe traumatic brain injury in humans: A positron emission tomography study [J].
Bergsneider, M ;
Hovda, DA ;
Shalmon, E ;
Kelly, DF ;
Vespa, PM ;
Martin, NA ;
Phelps, ME ;
McArthur, DL ;
Caron, MJ ;
Kraus, JF ;
Becker, DP .
JOURNAL OF NEUROSURGERY, 1997, 86 (02) :241-251
[6]   Metabolic recovery following human traumatic brain injury based on FDG-PET: Time course and relationship to neurological disability [J].
Bergsneider, M ;
Hovda, DA ;
McArthur, DL ;
Etchepare, M ;
Huang, SC ;
Sehati, N ;
Satz, P ;
Phelps, ME ;
Becker, DP .
JOURNAL OF HEAD TRAUMA REHABILITATION, 2001, 16 (02) :135-148
[7]   Dissociation of cerebral glucose metabolism and level of consciousness during the period of metabolic depression following human traumatic brain injury [J].
Bergsneider, M ;
Hovda, DA ;
Lee, SM ;
Kelly, DF ;
McArthur, DL ;
Vespa, PM ;
Lee, JH ;
Huang, SC ;
Martin, NA ;
Phelps, ME ;
Becker, DP .
JOURNAL OF NEUROTRAUMA, 2000, 17 (05) :389-401
[8]   CEREBRAL-CIRCULATION AND METABOLISM AFTER SEVERE TRAUMATIC BRAIN INJURY - THE ELUSIVE ROLE OF ISCHEMIA [J].
BOUMA, GJ ;
MUIZELAAR, JP ;
CHOI, SC ;
NEWLON, PG ;
YOUNG, HF .
JOURNAL OF NEUROSURGERY, 1991, 75 (05) :685-693
[9]   Induced mitochondrial failure in the feline brain: implications for understanding acute post-traumatic metabolic events [J].
Clausen, T ;
Zauner, A ;
Levasseur, JE ;
Rice, AC ;
Bullock, R .
BRAIN RESEARCH, 2001, 908 (01) :35-48
[10]   Defining ischemic burden after traumatic brain injury using 15O PET imaging if cerebral physiology [J].
Coles, JP ;
Fryer, TD ;
Smielewski, P ;
Rice, K ;
Clark, JC ;
Pickard, JD ;
Menon, DK .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2004, 24 (02) :191-201