Skip Navigation

British Journal of Anaesthesia 2007 99(1):4-9; doi:10.1093/bja/aem131
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow E-Letters: Submit a response to the article
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (26)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Werner, C.
Right arrow Articles by Engelhard, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Werner, C.
Right arrow Articles by Engelhard, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Board of Management and Trustees of the British Journal of Anaesthesia 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Pathophysiology of traumatic brain injury

C. Werner* and K. Engelhard

Klinik für Anästhesiologie, der Johannes Gutenberg-Universität Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany

* Corresponding author. E-mail: werner{at}anaesthesie.klinik.uni-mainz.de

The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options.

Keywords: brain, cerebral blood flow; complications, vasospasm; head, trauma; inflammation; pathophysiology


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 TraumaHome page
J. Hulme
Resuscitation of patients after traumatic brain injury
Trauma, January 1, 2008; 10(1): 55 - 63.
[Abstract] [PDF]

Home page
 Br J AnaesthHome page
O. L. Cremer, A. Lavinio, and (on behalf of the authors)
Hypothermia and cerebrovascular reactivity
Br. J. Anaesth., October 1, 2007; 99(4): 593 - 594.
[Full Text] [PDF]

Home page
 Br J AnaesthHome page
I. K. Moppett
Traumatic brain injury: assessment, resuscitation and early management
Br. J. Anaesth., July 1, 2007; 99(1): 18 - 31.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.