- Microdialysis is a technique for sampling the brain extracellular space. An invasive probe is inserted into the brain substance and perfused with fluid (perfusate) at ultralow flow rates (typically 0.3 μl/minute). A semipermeable membrane at the tip of the catheter allows substances to diffuse into the catheter and are recovered in the exiting fluid (microdialysate).
- For clinical purposes, the commonest analytes are glucose, lactate, pyruvate, glutamate (an excitotoxic neurotransmitter) and glycerol (a measure of cellular membrane breakdown).
- The ratio between lactate and pyruvate (LPR, lactate-pyruvate ratio) provides a measure of the balance between anaerobic and aerobic respiration.
- An LPR more than 25 is regarded as pathological and correlates with poor clinical outcome in TBI.
- Allows bedside analysis of biochemical substances in brain tissue extracellular fluid.
- Location of catheter
- Placed in ‘at risk’ tissue so that biochemical changes in the area of brain most vulnerable to secondary insults can be monitored.
- It may identify cerebral compromise at the cellular level before it is detectable clinically or by other monitored variables.
- Compounds assayed include:
- Lactate/pyruvate ratio
- A marker of anaerobic metabolism
- >25 marker of poor clinical outcome
- Elevated lactate:pyruvate ratio (LPR) more than 40 combined with low brain glucose (<0.7– 1 mmol/ litre) suggests severe hypoxia/ischaemia and correlates with poor outcome after TBI (Timofeev et al., 2011).
- Marker of anaerobic and aerobic respiration
- Correlates with outcome after TBI.
- Increase in the lactate/pyruvate ratio can be due to
- Cerebral ischaemia or
- Mitochondrial dysfunction.
- In patients with elevated cerebral lactate/ pyruvate ratio (LPR), microdialysis demonstrates that exogenous lactate therapy significantly increases cerebral glucose levels.
- This correlates with previous evidence that lactate is directly oxidized to pyruvate in the mitochondria of neurons and astrocyte to contribute to cerebral aerobic metabolism (Lazaridis and Andrews, 2014).
- Is a good indicator of widespread mitochondrial dysfunction causing metabolic depression following TBI,
- Further impairing brain capacity to meet metabolic demands in coping with secondary insults.
- Low CMRO2 indicates irreversible cell injury,
- LPR a sensitive marker of reversible mitochondrial dysfunction in regions with no observable tissue damage.
- Glucose
- Glutamate
- Urea and electrolytes
- K+
- Calcium.
- Some observational data:
- Lactate levels increase during episodes of SjVO2 desaturation
- Decreased extracellular glucose was associated with increased mortality
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