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Table of Contents    
THE EDITORIAL DEBATE: PROS AND CONS
Year : 2016  |  Volume : 64  |  Issue : 2  |  Page : 217-218

Cerebral microdialysis for assessing intracerebral hypoglycemia: Can it act as a prognostic marker in severe traumatic brain injury?


1 Department of Neurosurgery, SMS Medical College, Jaipur, Rajasthan, India
2 Department of Neurosurgery, Eternal Hospital, Jaipur, Rajasthan, India

Date of Web Publication3-Mar-2016

Correspondence Address:
Virendra Deo Sinha
Department of Neurosurgery, SMS Medical College, Jaipur, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.177596

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How to cite this article:
Sinha VD, Chakrabarty A. Cerebral microdialysis for assessing intracerebral hypoglycemia: Can it act as a prognostic marker in severe traumatic brain injury?. Neurol India 2016;64:217-8

How to cite this URL:
Sinha VD, Chakrabarty A. Cerebral microdialysis for assessing intracerebral hypoglycemia: Can it act as a prognostic marker in severe traumatic brain injury?. Neurol India [serial online] 2016 [cited 2021 Mar 3];64:217-8. Available from: https://www.neurologyindia.com/text.asp?2016/64/2/217/177596


Traumatic brain injury (TBI) is often exacerbated by additional events that may lead to secondary brain damage. These are potentially modifiable causes of mortality and morbidity and may be assesed by newer diagnostic techniques.

Cerebral microdialysis is a novel addition to the armamentarium of diagnostic techniques in neuro-intensive care and is proving to be a useful bedside monitoring test to provide near real-time analysis of brain tissue biochemistry. It involves a continuous sampling of the brain interstial fluid chemistry.[1] The levels of glucose and the lactate/pyruvate ratio are among the most sensitive and specific indicators of deterioration in the cerebral metabolism during transient cerebral perfusion pressure (CPP) decrease.[2] Glucose, being the primary source of energy to the brain, is a key marker of variations that develop in the brain metabolism.

In the immediate post-injury period, there is a profound increase in glucose utilization that has been termed as 'hyperglycolysis.' This increase can persist for up to 1 week after injury and can be elicited by seizures or other forms of brain depolarization. Glycolysis serves as an important source of energy after brain injury but the ideal or optimal glycolytic rate is presently unknown. Using microdialysis, it is possible to assess the reduction in extracellular glucose levels after TBI, which correlates with increased glycolysis on positron emission tomography (PET). This evaluation indicates the potential for detection of a deficiency in the availability of extracellular glucose after TBI.[3]

Insufficient capillary blood flow (ischaemia), increased capillary blood flow (hyperaemia), hyperglycemia and hyper/hypo metabolism can lead to an abnormal brain glucose dialysate. As a thumb rule, if the brain and blood glucose are not changing correspondingly then the changes in brain glucose are due to an abnormality in the brain capillary perfusion or cellular metabolism. The normal brain glucose concentration in the dialysate with a 10mm dialysis membrane and a perfusion flow of 0.3micro l/min. is approximately 2mM. During its evaluation, it is important to ensure that the catheter is placed in the peri-contusional area in the case of diffuse axonal injury. A second catheter may be placed in the normal brain.

The authors have conducted a prospective non-randomised study to analyse the clinical relevance of intracerebral hypoglycaemia as a prognostic indicator in severe TBI by cerebral microdialysis.[4] A total of twenty five patients with severe TBI who underwent decompressive craniectomy were monitored by intracerebral microdialysis. Twenty patients has unilateral catheters and five had bilateral ones. Three of the patients with bilateral catheters had one in the normal brain tissue. The catheter position was confirmed by a check computed tomographic scan postoperatively. Bilateral catheters, including one in the normal brain tissue, could not be placed in all the patients due to the added financial burden. The catheter was placed in the peri contusional area and at a depth of 20mm intraparenchymally. The catheters were continued for three to five days following the decompressive craniectomy and cerebral microdialysis was done at bedside at hourly intervals.

Out of the twenty five patients, fifteen (60%) had a good outcome at three months. The good outcome group had fewer episodes of hypoglycaemia during the presence of systemic hypoglycaemia (P = 0.0026). This group also had fewer episodes of both hyper- and hypoglycaemia. Patients who were pregnant or with Glagow Coma Scale (GCS)=3 with fixed dilated pupils, or those who were hemodynamically unstable, were not considered for the study. Glucose, lactate, pyruvate, glutamate and glycerol concentrations in the microdialysate were measured. The plasma glucose levels were also measured hourly using the arterial blood gas study. The blood glucose levels were maintained between 70-140 mgs%.

There was a poor correlation between the plasma and cerebral glucose for the entire cohort suggesting that glucose values obtained using brain microdialysis are not reflective of the changes in the systemic glucose levels. Interestingly, microdialysis glucose values showed a rising trend in the good outcome group. The authors have hypothesised that this points to a recovering metabolic state in the brain tissue and may be considered a real-time, early bedside sign of a good neurological outcome.

While the investigation is promising, there are still potential problems associated with microdialysis. Apart from the small risk of infection and the complications associated with any invasive procedure, it is a technique limited to a focal area of the brain. Important biochemical changes occurring elsewhere or away from the catheter may, therefore, be different from those occurring adjacent to the catheter.[5]

Cerebral microdialysis enables an early initiation of appropriate therapeutic strategies to overcome cerebral ischemia and secondary brain damage, eventually leading to a better patient outcome.

 
  References Top

1.
Tisdall MM, Smith M. Cerebral microdialysis: Research technique or clinical tool. Br J Anaesth 2006; 97:18-25.  Back to cited text no. 1
    
2.
Omerhodžić I, Dizdarević K, Rotim K, Hajdarpašić E, Nikšić M, Enisa Bejtić-Čustović E, et al. Cerebral microdialysis: Perioperative monitoring and treatment of severe neurological patient. Acta Clin Croat 2011;50:13-20.  Back to cited text no. 2
    
3.
Vespa P, Boonyaputthikul R, McArthur DL, Miller C, Etchepare M, Bergsneider M, et al. Intensive insulin therapy reduces microdialysis glucose values without altering glucose utilization or improving the lactate/pyruvate ratio after traumatic brain injury. Critic Care Med 2006; 34:850-6.  Back to cited text no. 3
    
4.
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. 4
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5.
Dhawan V, DeGeorgia M. Neurointensive Care Biophysiological Monitoring. J NeuroIntervent Surg. 2012;4:407-413.  Back to cited text no. 5
    




 

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