Traumatic brain edema [Neurosurgery Wiki]

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=====Traumatic brain edema=====
Cerebral [[edema]] can result from a combination of several pathological mechanisms associated with primary and secondary injury patterns in [[traumatic brain injury]] (TBI)
((Xi G, Keep RF, Hoff JT. Pathophysiology of brain edema formation. Neurosurg Clin N Am. Jul 2002;13(3):371-383. PMID: 12486926.)).

For many years, [[vasogenic edema]] was accepted as the prevalent edema type following [[traumatic brain injury]] TBI. 

Traumatic [[brain edema]] is predominantly cytotoxic and that water entry is modulated in part by [[aquaporins]]. 

[[Cytotoxic edema]] is of decisive pathophysiological importance following traumatic brain injury TBI as it develops early and persists while [[blood brain barrier]] (BBB) integrity is gradually restored. These findings suggest that cytotoxic and vasogenic brain edema are two entities which can be targeted simultaneously or according to their temporal prevalence
((Unterberg AW, Stover J, Kress B, Kiening KL. Edema and brain trauma. Neuroscience. 2004;129(4):1021-9. Review. PubMed PMID: 15561417.)).
====Treatment====
Currently, there are no pharmacological treatments available for traumatically induced brain edema and the subsequent rise of [[intracranial pressure]] ICP.

see [[decompressive craniectomy]].
====Diagnosis====
Non-invasive diffusion-weighted MRI (DWI) quantifies the diffusion of water in the brain associated with edema  and contributes essentially to the understanding of stroke and stroke-related cerebral edema formation. The use of DWI offers the opportunity to identify the predominant edema type after TBI and, in this way, to distinguish between vasogenic and cytotoxic edema.

====Outcome====
As pressure within the skull increases, brain tissue displacement can lead to cerebral herniation, resulting in disability or death
((Dunn LT. Raised intracranial pressure. J Neurol Neurosurg Psychiatry. Sep 2002;73 Suppl 1:i23-27. PMID: 12185258.))
((Farahvar A, Gerber LM, Chiu YL, et al. Response to intracranial hypertension treatment as a predictor of death in patients with severe traumatic brain injury.[Erratum appears in J Neurosurg. 2011 Jul;115(1):191 added Froelich, Matteus]. J Neurosurg. May 2011;114(5):1471-1478. PMID: 21214327.))
((Vik A, Nag T, Fredriksli OA, et al. Relationship of "dose" of intracranial hypertension to outcome in severe traumatic brain injury. J Neurosurg. Oct 2008;109(4):678-684. PMID: 18826355.))

The predominant cause of death and long-term disability after [[traumatic brain injury]] TBI is brain edema 
((Marmarou A, Fatouros PP, Barzo P, et al. Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients. J Neurosurg 2000; 93: 183–193.))
((Unterberg AW, Stover J, Kress B, et al. Edema and brain trauma. Neurosci 2004; 129: 1021–1029.))