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Chapter 12 - Multimodality Monitoring in Head Injury

Published online by Cambridge University Press:  28 April 2020

By
Tamara Tajsic ,
Andrew Gvozdanovic ,
Ivan Timofeev  and
Peter J. Hutchinson
Edited by
Peter C. Whitfield ,
Jessie Welbourne ,
Elfyn Thomas ,
Fiona Summers ,
Maggie Whyte  and
Peter J. Hutchinson
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

The major determinant of outcome from TBI is the severity of the primary injury; however, not all brain damage happens at that time point. Invariably, primary injury activates cellular and molecular cascades which mediate potentially reversible, secondary injury in the ensuing hours and days. These events can lead to progressive brain swelling and increased intracranial pressure (ICP) thus compromising cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) resulting in tissue ischaemia, hypoxia and cellular energy failure. Further cell damage exacerbates the brain swelling, forming part of a vicious circle that can lead to life-threatening brain herniation. A large body of evidence links post-traumatic intracranial hypertension at levels above 20 to 25 mmHg with excess mortality and worse functional outcomes.

Type
Chapter
Information
Traumatic Brain Injury
A Multidisciplinary Approach
 , pp. 132 - 145
Publisher: Cambridge University Press
Print publication year: 2020

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