Cerebral edema: Difference between revisions
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In this type of edema the BBB remains intact. |
In this type of edema the BBB remains intact. |
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This edema is due to the derangement in cellular [[metabolism]] resulting in inadequate functioning of the sodium and potassium pump in the [[glial cell]] membrane. As a result there is cellular retention of sodium and water. There are swollen astrocytes in gray and white matter. Cytotoxic edema is seen with various intoxications ([[dinitrophenol]], triethyltin, [[hexachlorophene]], [[isoniazid]]), in [[Reye's syndrome]], severe [[hypothermia]], early [[ischemia]], [[encephalopathy]], early [[stroke]] or [[Hypoxia (medical)|hypoxia]], cardiac arrest, pseudotumor cerebri, and cerebral toxins. |
This edema is due to the derangement in cellular [[metabolism]] resulting in inadequate functioning of the sodium and potassium pump in the [[glial cell]] membrane. As a result there is cellular retention of sodium and water. There are swollen astrocytes in gray and white matter. Cytotoxic edema is seen with various intoxications ([[dinitrophenol]], triethyltin, [[hexachlorophene]], [[isoniazid]]), in [[Reye's syndrome]], severe [[hypothermia]], early [[ischemia]], [[encephalopathy]], early [[stroke]] or [[Hypoxia (medical)|hypoxia]], cardiac arrest, pseudotumor cerebri, and cerebral toxins. |
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During an ischemic stroke a lack of oxygen and glucose results in a breakdown of the sodium-calcium pumps normally responsible for maintaining appropriate ion levels in brain cells. The result is a massive build up of sodium and calcium levels within these cells. This in turn leads to a rapid uptake of water and subsequent swelling of the cells.<ref>{{cite journal|last=Rosenberg|first=Gary|title=Ischemic Brain Edema|journal=Progress in cardiovascular diseases|year=1999|volume=42|issue=3|page=209-16|pmid=10598921}}</ref> . It is this swelling of the individual cells of the brain that is seen as the main distinguishing characteristic of cytotoxic edema (as opposed to vasogenic wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves <ref>{{cite journal|last=Klatzo|first=Igor|title=Pathophysiological aspects of brain edema|journal=Acta Neuropathologica|date=1 January 1987|year=1987|month=09|volume=72|issue=3|pages=236–239|doi=10.1007/BF00691095}}</ref>. While not all patients who have experienced a stroke will develop a severe edema, those who do have a very poor prognosis <ref>{{cite journal|last=Hacke|first=W.|coauthors=Schwab, S.; Horn, M.; Spranger, M.; De Georgia, M.; von Kummer, R.|title='Malignant' Middle Cerebral Artery Territory Infarction: Clinical Course and Prognostic Signs|journal=Archives of Neurology|date=1 April 1996|volume=53|issue=4|pages=309–315|doi=10.1001/archneur.1996.00550040037012}}</ref> . |
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In most instances cytotoxic and vasogenic edema occur together. It is generally accepted that cytotoxic edema is dominant immediately following an injury or infarct, but gives way to a vasogenic edema that can persist for several days or longer <ref>{{cite journal|last=Rosenberg|first=Gary|title=Ischemic Brain Edema|journal=Progress in cardiovascular diseases|year=1999|volume=42|issue=3|page=209-16|pmid=10598921}}</ref>. The use of specific MRI techniques has allowed for some differentiation between the two mechanisms and suggests that in the case of trauma, the cytotoxic response dominates <ref>{{cite journal|last=Barzó|first=P|coauthors=Marmarou, A; Fatouros, P; Hayasaki, K; Corwin, F|title=Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging.|journal=Journal of neurosurgery|date=1997 Dec|volume=87|issue=6|pages=900-7|pmid=9384402}}</ref> |
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===Osmotic=== |
===Osmotic=== |
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Revision as of 10:25, 28 February 2013
| Cerebral edema |
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Cerebral edema or cerebral œdema is an excess accumulation of water in the intracellular or extracellular spaces of the brain.
Causes
After trauma or injury, some brain vessels will be broken and causing the water content, sodium content and potassium content change inside the brain. Water and sodium content would keep increasing in the first several days, and the regional cerebral ischemia would occur. The cerebral edema always appear in these regions.[1] [2]
Research
Recently, many studies on mechanical property of the brain edema are conducted. Most of them are based on the technique of Finite Element Analysis (FEA), which is a widely-used numerical method in solid mechanics. For example, Gao and Ang used the FEA to study the change of intracranial pressure during the creanietomy operation. [3] The model can match the clinical data very well. The advantages of using FEA are obvious. First, the cost of the numerical procedure is much less than that of experiment on the cadaver. Second, people can modify any parameters easily using the computer model. Third, the numerical results can provide a more clear insight and help for better understanding of such disease. However, due to the complicated theories of the nonlinear mechanics, some details of the FEA, such as the constitutive equations and meshing process, still need to be improved for such research topic.
[1] O. Gotoh, T. Asano, T. Koide, and K. Takakura, “Ischemic brain edema following occlusion of the middle cerebral artery in the rat. I: The time courses of the brain water, sodium and potassium contents and blood-brain barrier permeability to 125I-albumin,” Stroke, vol. 16, no. 1, pp. 101–109, Jan. 1985.
[2] C. M. Shaw, E. C. Alvord, and R. G. Berry, “Swelling of the brain following ischemic infarction with arterial occlusion.,” Archives of neurology, vol. 1, pp. 161–77, Aug. 1959.
[3] C. P. Gao and B. T. Ang, “Biomechanical modeling of decompressive craniectomy in traumatic brain injury.,” Acta neurochirurgica. Supplement, vol. 102, pp. 279–82, Jan. 2008.
Types
Four types of cerebral edema have been distinguished:[1]
Vasogenic
Due to a breakdown of tight endothelial junctions which make up the blood–brain barrier (BBB). This allows normally excluded intravascular proteins and fluid to penetrate into cerebral parenchymal extracellular space. Once plasma constituents cross the BBB, the edema spreads; this may be quite fast and widespread. As water enters white matter it moves extracellularly along fiber tracts and can also affect the gray matter. This type of edema is seen in response to trauma, tumors, focal inflammation, late stages of cerebral ischemia and hypertensive encephalopathy.
Some of the mechanisms contributing to BBB dysfunction are: physical disruption by arterial hypertension or trauma, tumor-facilitated release of vasoactive and endothelial destructive compounds (e.g. arachidonic acid, excitatory neurotransmitters, eicosanoids, bradykinin, histamine, and free radicals). Some of the special subcategories of vasogenic edema include:
- Hydrostatic cerebral edema
- This form of cerebral edema is seen in acute, malignant hypertension. It is thought to result from direct transmission of pressure to cerebral capillary with transudation of fluid into the extravascular compartment from the capillaries.
- Cerebral edema from brain cancer
- Cancerous glial cells (glioma) of the brain can increase secretion of vascular endothelial growth factor (VEGF) which weakens the junctions of the blood–brain barrier. Dexamethasone can be of benefit in reducing VEGF secretion.[2]
- High altitude cerebral edema
- High altitude cerebral edema (or HACE) is a severe form of (sometimes fatal) altitude sickness. HACE is the result of swelling of brain tissue from leakage of fluids from the capillaries due to the effects of hypoxia on the mitochondria-rich endothelial cells of the blood–brain barrier.[3]
- Symptoms can include headache, loss of coordination (ataxia), weakness, and decreasing levels of consciousness including disorientation, loss of memory, hallucinations, psychotic behavior, and coma. It generally occurs after a week or more at high altitude. Severe instances can lead to death if not treated quickly. Immediate descent is a necessary life-saving measure (2,000 - 4,000 feet). There are some medications (e.g. dexamethasone) that may be prescribed for treatment in the field, but these require proper medical training in their use. Anyone suffering from HACE must be evacuated to a medical facility for proper follow-up treatment. A Gamow bag can sometimes be used to stabilize the sufferer before transport or descending.
- Climbers may also suffer high altitude pulmonary edema (HAPE), which affects the lungs. While not as life threatening as HACE in the initial stages, failure to descend to lower altitudes or receive medical treatment can also lead to death.
Cytotoxic
In this type of edema the BBB remains intact. This edema is due to the derangement in cellular metabolism resulting in inadequate functioning of the sodium and potassium pump in the glial cell membrane. As a result there is cellular retention of sodium and water. There are swollen astrocytes in gray and white matter. Cytotoxic edema is seen with various intoxications (dinitrophenol, triethyltin, hexachlorophene, isoniazid), in Reye's syndrome, severe hypothermia, early ischemia, encephalopathy, early stroke or hypoxia, cardiac arrest, pseudotumor cerebri, and cerebral toxins.
During an ischemic stroke a lack of oxygen and glucose results in a breakdown of the sodium-calcium pumps normally responsible for maintaining appropriate ion levels in brain cells. The result is a massive build up of sodium and calcium levels within these cells. This in turn leads to a rapid uptake of water and subsequent swelling of the cells.[4] . It is this swelling of the individual cells of the brain that is seen as the main distinguishing characteristic of cytotoxic edema (as opposed to vasogenic wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves [5]. While not all patients who have experienced a stroke will develop a severe edema, those who do have a very poor prognosis [6] .
In most instances cytotoxic and vasogenic edema occur together. It is generally accepted that cytotoxic edema is dominant immediately following an injury or infarct, but gives way to a vasogenic edema that can persist for several days or longer [7]. The use of specific MRI techniques has allowed for some differentiation between the two mechanisms and suggests that in the case of trauma, the cytotoxic response dominates [8]
Osmotic
Normally cerebral-spinal fluid (CSF) and extracellular fluid (ECF) osmolality of the brain is slightly lower than that of plasma. When plasma is diluted by excessive water intake (or hyponatremia), syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic state (HHS), formerly hyperosmolar non-ketotic acidosis (HONK), the brain osmolality will then exceed the serum osmolality creating an abnormal pressure gradient down which water will flow into the brain causing edema.
Interstitial
Occurs in obstructive hydrocephalus. This form of edema is due to rupture of the CSF-brain barrier resulting in trans-ependymal flow of CSF which causes CSF to penetrate the brain and spread to the extracellular spaces and the white matter. This is differentiated from vasogenic edema in that interstitial cerebral edema CSF contains almost no protein.
Treatment
Treatment approaches can include osmotherapy using mannitol, diuretics and surgical decompression.[9]
References
- ^ Qureshi AI, Suarez JI (2000). "Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension". Critical Care Medicine. 28 (9): 3301–3313. doi:10.1097/00003246-200009000-00032. PMID 11008996.
- ^ Heiss JD, Papavassiliou E, Merrill MJ, Nieman L, Knightly JJ, Walbridge S, Edwards NA, Oldfield EH (1996). "Mechanism of dexamethasone suppression of brain tumor-associated vascular permeability in rats. Involvement of the glucocorticoid receptor and vascular permeability factor". Journal of Clinical Investigation. 98 (6): 1400–1408. doi:10.1172/JCI118927. PMC 507566. PMID 8823305.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Van Osta A, Moraine JJ, Mélot C, Mairbäurl H, Maggiorini M, Naeije R (2005). "Effects of high altitude exposure on cerebral hemodynamics in normal subjects". STROKE. 36 (3): 557–560. doi:10.1161/01.STR.0000155735.85888.13. PMID 15692117.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Rosenberg, Gary (1999). "Ischemic Brain Edema". Progress in cardiovascular diseases. 42 (3): 209-16. PMID 10598921.
- ^ Klatzo, Igor (1 January 1987). "Pathophysiological aspects of brain edema". Acta Neuropathologica. 72 (3): 236–239. doi:10.1007/BF00691095.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: date and year (link) - ^ Hacke, W. (1 April 1996). "'Malignant' Middle Cerebral Artery Territory Infarction: Clinical Course and Prognostic Signs". Archives of Neurology. 53 (4): 309–315. doi:10.1001/archneur.1996.00550040037012.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Rosenberg, Gary (1999). "Ischemic Brain Edema". Progress in cardiovascular diseases. 42 (3): 209-16. PMID 10598921.
- ^ Barzó, P (1997 Dec). "Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging". Journal of neurosurgery. 87 (6): 900–7. PMID 9384402.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Raslan A, Bhardwaj A (2007). "Medical management of cerebral edema". Neurosurgical focus. 22 (5): E12. doi:10.3171/foc.2007.22.5.13. PMID 17613230.
External links
- MedPix Vasogenic Edema