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On Brain Oedema

Jungner, Mårten LU (2012) In Lund University, Faculty of Medicine Dissertation Series 2012:19.
Abstract
Traumatic brain injury and bacterial meningitis may at a glance appear as two different disease entities. The host reaction, however, to both trauma and infection involves a strong inflammatory response, with the classical symptomology of rubor, tumor, calor, dolor et functio laesa. Tumor, swelling, will increase the volume within the closed cranial vault, and may thereby raise the intracranial pressure to critical levels, affecting cerebral blood flow and oxygenation. In this thesis, brain oedema and its origins are investigated in experimental models of brain trauma and bacterial meningitis, and in patients suffering severe head injury. The studies are focused on fluid therapy, blood-brain barrier permeability changes, and their effects... (More)
Traumatic brain injury and bacterial meningitis may at a glance appear as two different disease entities. The host reaction, however, to both trauma and infection involves a strong inflammatory response, with the classical symptomology of rubor, tumor, calor, dolor et functio laesa. Tumor, swelling, will increase the volume within the closed cranial vault, and may thereby raise the intracranial pressure to critical levels, affecting cerebral blood flow and oxygenation. In this thesis, brain oedema and its origins are investigated in experimental models of brain trauma and bacterial meningitis, and in patients suffering severe head injury. The studies are focused on fluid therapy, blood-brain barrier permeability changes, and their effects on oedema formation.

In study I and II, it was shown that plasma volume expansion with crystalloid compared to colloid fluids resulted in increased cortical brain oedema after brain trauma in rats, and increased intracranial pressure in experimental meningitis in cats. Evidence is given that increased permeability of the blood-brain barrier is a key determinant of tissue water content after the insults.

In study III, it was shown that post treatment with prostacyclin in experimental meningitis reduces systemic plasma volume loss, and may diminish the rise in intracranial pressure.

In study IV, the effect of statin treatment after brain trauma in rats was investigated. No effect on brain oedema, cortical blood flow, or the transfer constant for a small molecule was detected, but capillary patency was better preserved in the statin group. Statin treatment was associated with increased plasma levels of nitric oxide, and decreased levels of prostacyclin.

In study V, post-traumatic permeability changes of the blood-brain barrier in 17 brain trauma patients were quantified using contrast enhanced computerized tomography with multiple scanning during 25 minutes. It was shown that blood to brain transfer for iohexol was increased up to 20-fold in traumatized tissue. The relevance of these results regarding our understanding of the pathophysiology of post-traumatic brain oedema, and the implications for the clinical management of brain trauma patients are discussed. (Less)
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author
supervisor
opponent
  • Professor Weitzberg, Eddie, Karolinska Institute, Department of Anaesthesiology and Intensive Care
organization
publishing date
type
Thesis
publication status
published
subject
keywords
traumatic brain injury, brain oedema, fluid therapy, blood-brain barrier
in
Lund University, Faculty of Medicine Dissertation Series
volume
2012:19
pages
127 pages
publisher
Lund University, Faculty of Medicine
defense location
Segerfalksalen, Wallenberg Neurocentrum
defense date
2012-03-09 09:00
ISSN
1652-8220
ISBN
978-91-86871-81-9
language
English
LU publication?
yes
id
887f5544-ee31-46f4-a840-9c17c5a6632d (old id 3131999)
date added to LUP
2012-10-25 09:27:11
date last changed
2016-09-19 08:44:46
@phdthesis{887f5544-ee31-46f4-a840-9c17c5a6632d,
  abstract     = {Traumatic brain injury and bacterial meningitis may at a glance appear as two different disease entities. The host reaction, however, to both trauma and infection involves a strong inflammatory response, with the classical symptomology of rubor, tumor, calor, dolor et functio laesa. Tumor, swelling, will increase the volume within the closed cranial vault, and may thereby raise the intracranial pressure to critical levels, affecting cerebral blood flow and oxygenation. In this thesis, brain oedema and its origins are investigated in experimental models of brain trauma and bacterial meningitis, and in patients suffering severe head injury. The studies are focused on fluid therapy, blood-brain barrier permeability changes, and their effects on oedema formation.<br/><br>
In study I and II, it was shown that plasma volume expansion with crystalloid compared to colloid fluids resulted in increased cortical brain oedema after brain trauma in rats, and increased intracranial pressure in experimental meningitis in cats. Evidence is given that increased permeability of the blood-brain barrier is a key determinant of tissue water content after the insults.<br/><br>
In study III, it was shown that post treatment with prostacyclin in experimental meningitis reduces systemic plasma volume loss, and may diminish the rise in intracranial pressure.<br/><br>
In study IV, the effect of statin treatment after brain trauma in rats was investigated. No effect on brain oedema, cortical blood flow, or the transfer constant for a small molecule was detected, but capillary patency was better preserved in the statin group. Statin treatment was associated with increased plasma levels of nitric oxide, and decreased levels of prostacyclin. <br/><br>
In study V, post-traumatic permeability changes of the blood-brain barrier in 17 brain trauma patients were quantified using contrast enhanced computerized tomography with multiple scanning during 25 minutes. It was shown that blood to brain transfer for iohexol was increased up to 20-fold in traumatized tissue. The relevance of these results regarding our understanding of the pathophysiology of post-traumatic brain oedema, and the implications for the clinical management of brain trauma patients are discussed.},
  author       = {Jungner, Mårten},
  isbn         = {978-91-86871-81-9},
  issn         = {1652-8220},
  keyword      = {traumatic brain injury,brain oedema,fluid therapy,blood-brain barrier},
  language     = {eng},
  pages        = {127},
  publisher    = {Lund University, Faculty of Medicine},
  school       = {Lund University},
  series       = {Lund University, Faculty of Medicine Dissertation Series},
  title        = {On Brain Oedema},
  volume       = {2012:19},
  year         = {2012},
}