Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.
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Cerebral edema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain.
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Cerebral edema is commonly seen in a variety of brain injuries including ischemic stroke, subarachnoid hemorrhage, traumatic brain injury, subdural, epidural, or intracerebral hematoma, hydrocephalus, brain cancer, brain infections, low blood sodium levels, high altitude, and acute liver failure.
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Treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids.
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Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries.
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Extent and severity of the symptoms of cerebral edema depend on the exact etiology but are generally related to an acute increase of the pressure within the skull.
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Cerebral edema is frequently encountered in acute brain injuries from a variety of origins, including but not limited to:.
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Cerebral edema is present with many common cerebral pathologies and risk factors for development of cerebral edema will depend on the cause.
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Cerebral edema has been traditional classified into two major sub-types: cytotoxic and vasogenic cerebral edema.
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In general, cytotoxic Cerebral edema is linked to cell death in the brain through excessive cellular swelling.
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The swelling of the individual cells of the brain is the main distinguishing characteristic of cytotoxic Cerebral edema, as opposed to vasogenic Cerebral edema, wherein the influx of fluid is typically seen in the interstitial space rather than within the cells themselves.
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Ionic brain Cerebral edema can occur around the sites of brain hemorrhages, infarcts, or contusions due to a local plasma osmolality pressure gradient when compared to the high osmolality in the affected tissue.
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Interstitial Cerebral edema can be best characterized by in noncomunnicating hydrocephalus where there is an obstruction to the outflow of cerebrospinal fluid within the ventricular system.
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Hydrostatic extracellular brain Cerebral edema is typically caused by severe arterial hypertension.
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For example, when cytotoxic Cerebral edema occurs in the endothelial cells of the blood–brain barrier, oncotic cell death contributes to loss of integrity of the blood–brain barrier and promotes the progression to vasogenic Cerebral edema.
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When brain Cerebral edema types are combined, there is typically a primary form and the Cerebral edema type and context of the cause must be determined in order to start appropriate medical or surgical therapy.
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The edema can be characterized by vasogenic cerebral edema with symptoms of impaired consciousness and truncal ataxia.
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The syndrome features acute neurological symptoms and reversible subcortical vasogenic Cerebral edema predominantly involving the parieto-occipital areas on MR imaging.
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Radiation-induced brain Cerebral edema is a potentially life threatening complication of brain tissue radiation and is characterized radiation necrosis, endothelial cell dysfunction, increased capillary permeability, and breakdown of the blood–brain barrier.
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Cerebral edema is commonly present in a variety of neurological injuries.
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Cerebral edema with sustained increased intracranial hypertension and brain herniation can signify impending catastrophic neurological events which require immediate recognition and treatment to prevent injury and even death.
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Primary goal in cerebral edema is to optimize and regulate cerebral perfusion, oxygenation, and venous drainage, decrease cerebral metabolic demands, and to stabilize the osmolality pressure gradient between the brain and the surrounding vasculature.
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Cerebral edema is a severe complication of acute brain injuries, most notably ischemic stroke and traumatic brain injuries, and a significant cause of morbidity and mortality.
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Current treatment therapies aimed at cerebral edema and increased intracranial pressure are effective at reducing intracranial hypertension but have unclear impacts on functional outcomes.
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Researchers argue that the future treatment of cerebral edema will be based on advances in identifying the underlying pathophysiology and molecular characteristics of cerebral edema in a variety of cases.
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Many studies of the mechanical properties of brain Cerebral edema were conducted in the 2010s, most of them based on finite element analysis, a widely used numerical method in solid mechanics.
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