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Chapter 13 - Therapeutic Options in Neurocritical Care

Optimising Brain Physiology

Published online by Cambridge University Press:  28 April 2020

Peter C. Whitfield
Affiliation:
Derriford Hospital, Plymouth
Jessie Welbourne
Affiliation:
University Hospitals, Plymouth
Elfyn Thomas
Affiliation:
Derriford Hospital, Plymouth
Fiona Summers
Affiliation:
Aberdeen Royal Infirmary
Maggie Whyte
Affiliation:
Aberdeen Royal Infirmary
Peter J. Hutchinson
Affiliation:
Addenbrooke’s Hospital, Cambridge
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Summary

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.

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