Cerebral edema

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Cerebral edema
Classification and external resources
CT brain tumor.jpg
Edema (darker areas) surrounding a secondary brain tumor.
ICD-10 G93.6
ICD-9 348.5
DiseasesDB 2227
MeSH D001929



Cerebral edema can result from brain trauma or from nontraumatic causes such as ischemic stroke, cancer, or brain inflammation due to meningitis or encephalitis.[1] The blood–brain barrier (BBB) 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 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.


Many studies of 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 the finite element 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]


Four types of cerebral edema have been identified:[4]




Hydrostatic cerebral edema
Cerebral edema from brain cancer
High altitude cerebral edema



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 buildup 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 edema, 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]






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]


  1. ^ Raslan A, Bhardwaj A (2007). "Medical management of cerebral edema". Neurosurgical Focus 22 (5): E12. doi:10.3171/foc.2007.22.5.13. 
  2. ^ 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. 
  3. ^ 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.
  4. ^ 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. 
  5. ^ 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. 
  6. ^ 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. 
  7. ^ 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. 
  8. ^ Klatzo, Igor (1 January 1987). "Pathophysiological aspects of brain edema". Acta Neuropathologica 72 (3): 236–239. doi:10.1007/BF00691095. 
  9. ^ Hacke, W.; Schwab, S.; Horn, M.; Spranger, M.; De Georgia, M.; von Kummer, R. (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. 
  10. ^ Barzó, P; Marmarou, A; Fatouros, P; Hayasaki, K; Corwin, F (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. 
  11. ^ 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. 

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