Monitoring the injured brain to predict outcome and indivualize patient care
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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.
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Read the online book
"Microdialysis in Neuro Intensive care"
by professor Urban Ungerstedt
(Click the book icon. The book appears on a new page. Use the tool bar at the top of
the page to move between pages. Click on a page to enlarge it for easier reading.)
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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.
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Lactate and Pyruvate-ratio is a sensitive marker of ischemia
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Elevated Lactate and Pyruvate-ratio is a sensitive marker of ischemia following acute brain Injury. The Lund group (Nordstrom et al.) 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.
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Early detection of ischemia
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Cerebral Microdialysis measures changes at the cellular level and it has the potential to detect ischemia 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.
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