Cerebral edema: Difference between revisions
No edit summary |
m Added 2 dois to journal cites using AWB (10081) |
||
| Line 26: | Line 26: | ||
==Research== |
==Research== |
||
Many studies on the mechanical properties of brain edema were conducted in the 2000s, most of them based on [[Finite Element Analysis]] (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used FEA method to study changes in intracranial pressure during craniotomy operations.<ref>{{cite journal | author=Gao CP, Ang BT | title=Biomechanical modeling of decompressive craniectomy in traumatic brain injury | journal=Acta Neurochirurgica | volume=102 | issue=supplement | year=2008 | pages=279–282 }}</ref> A second line of research on the condition looks at [[thermal conductivity]], which is related to tissue water content.<ref>S.-B. Ko, H. Alex Choi, G. Parikh, J. Michael Schmidt, K. Lee, N. Badjatia, J. Claassen, E. Sander Connolly, and S. a. Mayer, "Real time estimation of brain water content in comatose patients)," Ann. Neurol., 2012.</ref> |
Many studies on the mechanical properties of brain edema were conducted in the 2000s, most of them based on [[Finite Element Analysis]] (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used FEA method to study changes in intracranial pressure during craniotomy operations.<ref>{{cite journal | author=Gao CP, Ang BT | title=Biomechanical modeling of decompressive craniectomy in traumatic brain injury | journal=Acta Neurochirurgica | volume=102 | issue=supplement | year=2008 | pages=279–282 | doi=10.1007/978-3-211-85578-2_52}}</ref> A second line of research on the condition looks at [[thermal conductivity]], which is related to tissue water content.<ref>S.-B. Ko, H. Alex Choi, G. Parikh, J. Michael Schmidt, K. Lee, N. Badjatia, J. Claassen, E. Sander Connolly, and S. a. Mayer, "Real time estimation of brain water content in comatose patients)," Ann. Neurol., 2012.</ref> |
||
==Types== |
==Types== |
||
| Line 56: | Line 56: | ||
It occurs due to a disruption in cellular [[metabolism]] that impairs functioning of the sodium and potassium pump in the [[glial cell]] membrane, leading to cellular retention of [[sodium]] and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including [[dinitrophenol]], triethyltin, [[hexachlorophene]], and [[isoniazid]]. It can occur in [[Reye's syndrome]], severe [[hypothermia]], early [[ischemia]], [[encephalopathy]], early [[stroke]] or [[Hypoxia (medical)|hypoxia]], cardiac arrest, and pseudotumor cerebri. |
It occurs due to a disruption in cellular [[metabolism]] that impairs functioning of the sodium and potassium pump in the [[glial cell]] membrane, leading to cellular retention of [[sodium]] and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including [[dinitrophenol]], triethyltin, [[hexachlorophene]], and [[isoniazid]]. It can occur in [[Reye's syndrome]], severe [[hypothermia]], early [[ischemia]], [[encephalopathy]], early [[stroke]] or [[Hypoxia (medical)|hypoxia]], cardiac arrest, and pseudotumor cerebri. |
||
During an [[ischemic stroke]], a lack of [[oxygen]] and [[glucose]] leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive build up of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells.<ref name="Rosenberg 1999 209–16">{{cite journal|last=Rosenberg|first=Gary|title=Ischemic Brain Edema|journal=Progress in cardiovascular diseases|year=1999|volume=42|issue=3|pages=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|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> |
During an [[ischemic stroke]], a lack of [[oxygen]] and [[glucose]] leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive build up of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells.<ref name="Rosenberg 1999 209–16">{{cite journal|last=Rosenberg|first=Gary|title=Ischemic Brain Edema|journal=Progress in cardiovascular diseases|year=1999|volume=42|issue=3|pages=209–16|pmid=10598921|doi=10.1016/s0033-0620(99)70003-4}}</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|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> |
||
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 name="Rosenberg 1999 209–16"/> 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=December 1997|volume=87|issue=6|pages=900–7|pmid=9384402|doi=10.3171/jns.1997.87.6.0900}}</ref> |
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 name="Rosenberg 1999 209–16"/> 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=December 1997|volume=87|issue=6|pages=900–7|pmid=9384402|doi=10.3171/jns.1997.87.6.0900}}</ref> |
||
Revision as of 07:58, 29 April 2014
 | This article may require copy editing for grammar, style, cohesion, tone, or spelling. (March 2013) |
| Cerebral edema |
|---|
Cerebral edema or cerebral œdema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.
Causes
Cerebral edema is caused by physical trauma or other injuries to the brain. Non-traumatic causes include ischemic stroke, cancer, and brain inflammation (including meningitis and encephalitis).[1] The blood–brain barrier or the blood–cerebrospinal fluid (CSF) barrier may break down, allowing fluid to accumulate in the brain's extracellular space; altered metabolism may cause brain cells to retain water; and dilution of the blood plasma may cause excess water to move into brain cells. Fast travel to high altitude without proper acclimatization can cause High-altitude cerebral edema (HACE).
Symptoms
Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.
Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory center.
Research
Many studies on the mechanical properties of brain edema were conducted in the 2000s, most of them based on Finite Element Analysis (FEA), a widely used numerical method in solid mechanics. For example, Gao and Ang used FEA method to study changes in intracranial pressure during craniotomy operations.[2] A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.[3]
Types
Four types of cerebral edema have been identified:[4]
Vasogenic
Vasogenic edema occurs due to a breakdown of the tight endothelial junctions which make up the blood–brain barrier (BBB). This allows intravascular proteins and fluid to penetrate into the parenchymal extracellular space. Once plasma constituents cross the BBB, the edema spreads; this may be quite rapid and extensive. As water enters white matter it moves extracellularly along fiber tracts and can also affect the gray matter. This type of edema may result from trauma, tumors, focal inflammation, late stages of cerebral ischemia and hypertensive encephalopathy.
Mechanisms contributing to BBB dysfunction include physical disruption by arterial hypertension or trauma, and tumor-facilitated release of vasoactive and endothelial destructive compounds (e.g. arachidonic acid, excitatory neurotransmitters, eicosanoids, bradykinin, histamine, and free radicals). Subtypes 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 capillaries with transudation of fluid from the capillaries into the extravascular compartment.
- 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.[5]
- High altitude cerebral edema
- High altitude cerebral edema (or HACE) is a severe and sometimes fatal form of altitude sickness.Results from capillary fluid leakage due to the effects of hypoxia on the mitochondria-rich endothelial cells of the blood–brain barrier.[6]
- Symptoms can include headache, loss of coordination (ataxia), weakness, disorientation, memory loss, psychotic symptoms (hallucinations and delusions), and coma. HACE generally occurs after a week or more at high altitude. If not treated quickly, severe cases can result in death. Immediate descent by 2,000 - 4,000 feet is a crucial life-saving measure. Medications such as dexamethasone can be prescribed for treatment in the field, but proper training in their use is required. Anyone suffering from HACE should 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 cytotoxic edema, the BBB remains intact. It occurs due to a disruption in cellular metabolism that impairs functioning of the sodium and potassium pump in the glial cell membrane, leading to cellular retention of sodium and water. Swollen astrocytes occur in gray and white matter. Cytotoxic edema is seen with various toxins, including dinitrophenol, triethyltin, hexachlorophene, and isoniazid. It can occur in Reye's syndrome, severe hypothermia, early ischemia, encephalopathy, early stroke or hypoxia, cardiac arrest, and pseudotumor cerebri.
During an ischemic stroke, a lack of oxygen and glucose leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive build up of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells.[7] 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.[8] While not all patients who have experienced a stroke will develop a severe edema, those who do have a very poor prognosis.[9]
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 [10]
Osmotic
Normally, the osmolality of cerebral-spinal fluid (CSF) and extracellular fluid (ECF) in the brain is slightly lower than that of plasma. Plasma can be diluted by several mechanisms, including 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). Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. This creates an abnormal pressure gradient and movement of water into the brain, which can cause progressive cerebral edema, resulting in a spectrum of signs and symptoms from headache and ataxia to seizures and coma.
Interstitial
Interstitial edema occurs in obstructive hydrocephalus due to a rupture of the CSF-brain barrier. This results in trans-ependymal flow of CSF, causing CSF to penetrate the brain and spread to the extracellular spaces and the white matter. Interstitial cerebral edema differs from vasogenic edema as CSF contains almost no protein.
Treatments
Treatment approaches can include osmotherapy using mannitol, diuretics to decrease fluid volume, corticosteroids to suppress the immune system, and surgical decompression to allow the brain tissue room to swell without compressive injury.[11]
References
- ^ Raslan A, Bhardwaj A (2007). "Medical management of cerebral edema". Neurosurgical Focus. 22 (5): E12.
- ^ Gao CP, Ang BT (2008). "Biomechanical modeling of decompressive craniectomy in traumatic brain injury". Acta Neurochirurgica. 102 (supplement): 279–282. doi:10.1007/978-3-211-85578-2_52.
- ^ S.-B. Ko, H. Alex Choi, G. Parikh, J. Michael Schmidt, K. Lee, N. Badjatia, J. Claassen, E. Sander Connolly, and S. a. Mayer, "Real time estimation of brain water content in comatose patients)," Ann. Neurol., 2012.
- ^ 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) - ^ a b Rosenberg, Gary (1999). "Ischemic Brain Edema". Progress in cardiovascular diseases. 42 (3): 209–16. doi:10.1016/s0033-0620(99)70003-4. 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) - ^ 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) - ^ Barzó, P (December 1997). "Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging". Journal of neurosurgery. 87 (6): 900–7. doi:10.3171/jns.1997.87.6.0900. PMID 9384402.
{{cite journal}}: 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