Microdialysis is a well established technique for chemical monitoring of brain tissue during neurointensive care. By introducing Microdialysis catheters into the brain after severe trauma or subarachnoid hemorrhage, it is possible to monitor brain tissue metabolism in the tissue at risk, i.e. the penumbra of a lesion or a region affected by vasospasm.
by professor Urban Ungerstedt
A large number of studies have clarified the chemistry of metabolic crises and ischemia during SAH and TBI and identified markers that make it possible to assess the extent of tissue pathology, its change over time and its relationship to other variables monitored bedside such as ICP and CPP.
Microdialysis has also shown to predict outcome in SAH, TBI and MCA patients and is rapidly finding its way into routine multimodal monitoring in the neuro ICU setting.
It can also be used to monitor hour by hour the level of and changes in amyloid beta protein plaque tangles in Alzheimer’s disease and other progressive neurodegenerative diseases.
Increased Lactate and Pyruvate-ratio indicate ischemia or mitochondrial dysfunction
Elevated Lactate and Pyruvate-ratio is a sensitive marker of ischemia following acute brain Injury. The Lund group (Nordstrom et al. Anesthesiology 2003,(4), 98:809-14) have concluded that cerebral Microdialysis can be used to assess the safe lower limit of CPP, suggesting that CPP management might be individualized rather than delivered to a generic target value.
If the patients has an elevated Lactate and Pyruvate-ratio the single value of Pyruvate can distinguish if the increase is due to ischemia or mithocondrial dysfunction.
“During mitochondrial dysfunction, the increase in LP-ratio is characterized by a very high lactate level and a pyruvate concentration within or above normal limits, in contrast during cerebral ischemia, the increase in LP-ratio is associated with a very low pyruvate concentration”(Nielsen et al Neuro Critical care 2013).
Early detection of metabolic crisis
Cerebral Microdialysis measures changes at the cellular level and it has the potential to detect ischemia or mithocondrial dysfunction before changes can be detected in the patient’s neurological status or by more conventional monitoring techniques such as ICP measurement. In patients with SAH, Microdialysis markers has shown to predict the occurrence of a delayed ischemic deficit related to cerebral vasospasm 11–23 h before its clinical appearance.
Microdialysis should not be used as sole basis for diagnosis.
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