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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 2  |  Page : 215-216

Cerebral dialysis for intracerebral glucose in traumatic brain injury

Department of Neurosurgery, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Date of Web Publication3-Mar-2016

Correspondence Address:
Altaf Umar Ramzan
Department of Neurosurgery, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.177602

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How to cite this article:
Ramzan AU. Cerebral dialysis for intracerebral glucose in traumatic brain injury. Neurol India 2016;64:215-6

How to cite this URL:
Ramzan AU. Cerebral dialysis for intracerebral glucose in traumatic brain injury. Neurol India [serial online] 2016 [cited 2020 Nov 28];64:215-6. Available from:

Traumatic brain injury (TBI) remains a major cause of mortality, morbidity and long-term disability, with profound and often long-lasting social and economic consequences. It is recognized that the outcome following TBI is related to the initial characteristics of injury, reflecting its severity, such as the Glasgow Coma Scale score, pupillary reactivity and radiological appearance, as well as the patient's age and presence or absence of early physiological insults such as hypoxia and hypotension.[1] This relationship of early and largely non-modifiable factors to mortality and neurological outcome has been confirmed by the analysis of demographic data from several, recent, large randomized controlled trials [2] and has led to the development of prognostic scoring systems, which can be used to predict outcome at a group level. Nevertheless, ongoing pathophysiological processes and secondary insults also influence outcomes.[3] These continue to take place after the initial injury and resuscitation. Detection of these secondary events remains a major target for neuromonitoring and an area of ongoing research. Intracranial pressure and cerebral perfusion pressure are the most widely accepted neuromonitoring parameters and have been shown in many studies to be related to mortality after TBI.[4] Cerebral microdialysis recently has gained popularity as a method for the clinical monitoring of brain metabolism and neurochemistry after TBI.[5] Preliminary studies have outlined several neurochemical markers of acute brain injury and disturbed metabolism, including elevated glutamate, glycerol, and lactate/pyruvate ratio (LPR) as well as low glucose concentrations. These markers are useful in prediction of neurologic outcome.[6] However, the relationship between commonly used microdialysis markers and ratios, and neurological outcome following TBI has not been clearly established. Lack of such information makes it difficult to interpret the significance of both spontaneous and treatment associated changes in tissue chemistry and may limit the clinical utility of cerebral microdialysis. It is well known that hyperglycemia and hypoglycemia need to be avoided to prevent aggravation of underlying brain damage. Hyperglycemia exacerbates tissue acidosis and oxidative stress aggravating the underlying brain damage, which in turn, promote the development of multiorgan failure. Hypoglycemia impairs energy supply, causing metabolic perturbations and inducing spreading cortical depolarization. In the present study, the authors analyzed the relationship of intracerebral glucose measured by intraparenchymal cerebral microdialysis and its relationship to blood glucose and the relation of these values to the outcome.[7] It was a prospective study where the authors studied 25 patients with traumatic brain injury who underwent decompressive craniectomy. Twenty cases had a unilateral intraparenchymal catheter placement 20 mm inside the brain parenchyma to accommodate 10 mm of the semipermeable catheter tip and another 10 mm of extra catheter length. Bilateral cerebral microdialysis (CMD) catheters were placed in five patients, two patients had placement of pericontusional catheters in bilateral frontal contusions during the bifrontal decompressive craniectomies, while the remaining three cases had contralateral catheters in the normal brain parenchyma. The position of the catheters was confirmed on postoperative CT scans. Due to cost constraints, they could not place bilateral CMD catheters to compare the differences in the cerebral biochemical values of glucose in the penumbric zone and the normal brain. The relation between plasma glucose and CMD measured interstitial brain glucose concentrations as well as the temporal pattern of CMD glucose was studied for 3–5 days following the decompressive craniectomy using bedside CMD analyzer at 1 hourly intervals. Fifteen patients had a good outcome in terms of Glasgow outcome scale (GOS) score at 3 months while 10 patients had a poor GOS score at 3 months. There was a significant difference in the incidence of hyperglycemia (>10 mmol/L) between the two groups. The difference between the two groups while comparing episodes of hypoglycemia was also significant. However, the CMD glucose values during the episodes of systemic hypoglycemia or hyperglycemia did not show a significant difference between the two groups. They observed that the good outcome group had fewer episodes of brain hypoglycemia during systemic hypoglycemia. Neither the mean blood glucose values nor the mean cerebral glucose values predicted the outcome at 3 months. A multivariate analysis suggested that higher, rather than lower, cerebral glucose was associated with increased mortality.[1] Meierhans et al., in their study, observed that blood glucose levels within the range 6–9 mM and CMD glucose levels of 1–5 mM were associated with minimal levels of the corresponding microdialysate lactate/pyruvate ratio and glutamate concentration, while microdialysate glucose levels <1 mM and >5 mM were associated with a high lactate/pyruvate ratio and a high glutamate concentration, respectively. The study, however, had a small number of subjects. They concluded that arterial blood glucose levels appear to be optimal at 6–9 mM. While low brain glucose levels below 1 mM are detrimental and need to be addressed, elevated brain glucose should also be targeted (with insulin). The latter should be done despite the presence of increased brain glutamate at brain glucose levels >5 Mm.[8]

  References Top

Timofeev I, Carpenter KL, Nortje J, Al-Rawi PG, O'Connell MT, Czosnyka M, et al. Cerebral extracellular chemistry and outcome following traumatic brain injury: A microdialysis study of 223 patients. Brain 2011;134(Pt 2):484-94.  Back to cited text no. 1
Murray GD, Butcher I, McHugh GS, Lu J, Mushkudiani NA, Maas AI, et al. Multivariable prognostic analysis in traumatic brain injury: Results from the IMPACT study. J Neurotrauma 2007;24:329-37.  Back to cited text no. 2
Chesnut RM, Marshall LF, Klauber MR, Blunt BA, Baldwin N, Eisenberg HM, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216-22.  Back to cited text no. 3
Balestreri M, Czosnyka M, Hutchinson P, Steiner LA, Hiler M, Smielewski P, et al. Impact of intracranial pressure and cerebral perfusion pressure on severe disability and mortality after head injury. Neurocrit Care 2006;4:8-13.  Back to cited text no. 4
Bullock R, Zauner A, Woodward JJ, Myseros J, Choi SC, Ward JD, et al. Factors affecting excitatory amino acid release following severe human head injury. J Neurosurg 1998;89:507-18.  Back to cited text no. 5
Vespa P, Bergsneider M, Hattori N, Wu HM, Huang SC, Martin NA, et al. Metabolic crisis without brain ischemia is common after traumatic brain injury: A combined microdialysis and positron emission tomography study. J Cereb Blood Flow Metab 2005;25:763-74.  Back to cited text no. 6
Gupta DK, Singla R, Kale SS, Sharma BS. Intracerebral hypoglycemia and its clinical relevance as prognostic indicator in severe traumatic brain injury: A cerebral microdialysis study from India. Neurol India 2016;64:259-64.  Back to cited text no. 7
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Meierhans R, Béchir M, Ludwig S, Sommerfeld J, Brandi G, Haberthür C, et al. Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 Mm in patients with severe traumatic brain injury. Crit Care 2010;14:R13.  Back to cited text no. 8


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