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Traumatic Brain Injury (TBI) is a major cause of mortality and morbidity. The severity of primary injury is the major determinant of outcome and occurs during the initial insult, as result of displacement of the physical structures of the brain. However, several factors can occur in the post-injury phase and have also been independently demonstrated to contribute to ‘secondary brain injury’ and to worsen patients’ outcome. These include intracranial hypertension, systemic hypotension, hypoxemia, hyperpyrexia, hypocapnoea and hyper- and hypoglycaemia; many of these factors are amenable to clinical manipulation. It is not well understood how much primary and secondary injuries respectively contribute towards the clinical manifestations of TBI. The exact mechanisms leading to secondary brain injury are not fully elucidated, but exacerbation of cerebral ischaemia and cerebral hypoperfusion are thought to be crucial factors. The integrated management of these factors forms the basis for specialist neurocritical care.
Cerebral microdialysis is now widely used as a bedside monitor of brain tissue biochemistry to identify cerebral hypoxia/ischaemia and assess cellular bioenergetics after brain injury. This chapter reviews the principles of cerebral microdialysis and identifies its role in detecting derangements of cerebral metabolism after brain injury. Microdialysis is used for a variety of clinical indications, including tissue monitoring in myocutaneous flap surgery, transplant surgery and bowel anastamoses. The concentration of substances in the dialysate will depend on the balance between substrate delivery to, and uptake from, the brain extracellular fluid (ECF) but also on several other factors. The pathophysiology of acute brain injury is complex, but two factors are of crucial importance: reduction of substrate delivery below critical thresholds, and the inability of brain cells to utilize delivered oxygen and glucose because of failing cellular metabolism.