Cerebral edema

Cerebral edema
Cerebral edema
Classification and external resources

Edema (darker areas) surrounding a secondary brain tumor.
ICD-10 G93.6
ICD-9 348.5
DiseasesDB 2227
MeSH D001929

Cerebral edema or cerebral œdema is an excess accumulation of water in the intracellular and/or extracellular spaces of the brain.



Four types of cerebral edema have been distinguished[1]:


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 ECF (extracellular fluid) 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.


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.


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.


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 approaches can include osmotherapy using mannitol, diuretics and surgical decompression.[4]


  1. ^ 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. 
  2. ^ 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. http://www.jci.org/articles/view/118927. 
  3. ^ 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. http://stroke.ahajournals.org/cgi/content/full/36/3/557. 
  4. ^ 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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