Continuous monitoring of cerebral metabolism in traumatic brain injury: a focus on cerebral microdialysis

2006 ◽  
Vol 12 (2) ◽  
pp. 112-118 ◽  
Author(s):  
Lars Hillered ◽  
Lennart Persson ◽  
Pelle Nilsson ◽  
Elisabeth Ronne-Engstrom ◽  
Per Enblad
2005 ◽  
Vol 25 (6) ◽  
pp. 763-774 ◽  
Author(s):  
Paul Vespa ◽  
Marvin Bergsneider ◽  
Nayoa Hattori ◽  
Hsiao-Ming Wu ◽  
Sung-Cheng Huang ◽  
...  

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 36 h 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 (CvO2). 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 CvO2. Traumatic brain injury leads to a state of persistent metabolic crisis as reflected by abnormal cerebral microdialysis LPR that is not related to ischemia.


2012 ◽  
Vol 29 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
Michèle Tanguy ◽  
Philippe Seguin ◽  
Bruno Laviolle ◽  
Jean-Paul Bleichner ◽  
Xavier Morandi ◽  
...  

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity


Author(s):  
Geoffrey T. Manley ◽  
John K. Yue ◽  
Hansen Deng ◽  
Ethan A. Winkler ◽  
John F. Burke ◽  
...  

This chapter provides summative information on the biomechanics, classification, and metabolism of traumatic brain injury (TBI). Impact, impulse, static/quasistatic loading, and related biomechanical sequelae following rotational shear and strain are discussed. Morphological classifications across extradural, acute/chronic subdural, subarachnoid, and intraventricular haemorrhages, as well as cerebral contusions and axonal injuries, are characterized and correlated with injury severity. Management options and implications for penetrating TBI and mild TBI/concussion are described. Cerebral metabolism including pressure/viscosity, CO2 reactivity, and autoregulation are explained in detail to provide for in-depth exploration of a spectrum of secondary injury cascades, encompassing glutamatergic excitotoxicity, autoregulatory loss, and the pressure reactivity index, flow disturbances, elevated intracranial pressure, cortical spreading depression and seizures/epilepsy. Beta-amyloid deposition in response to TBI, and genetic susceptibilities to poor recovery are covered. Current developments to standardize TBI classification systems, establish evidentiary benchmarks for quality of care, and accelerate advances in diagnosis and prognosis are highlighted.


EBioMedicine ◽  
2019 ◽  
Vol 44 ◽  
pp. 607-617 ◽  
Author(s):  
Michael Eiden ◽  
Nicolas Christinat ◽  
Anirikh Chakrabarti ◽  
Sarah Sonnay ◽  
John-Paul Miroz ◽  
...  

2008 ◽  
Vol 25 (6) ◽  
pp. 603-614 ◽  
Author(s):  
Paula A. Casey ◽  
Mary C. McKenna ◽  
Gary Fiskum ◽  
Manda Saraswati ◽  
Courtney L. Robertson

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