Katana VentraIP

Cerebral edema

Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain.[1] This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels.[1] Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, death.[1]

Not to be confused with Hydrocephalus.

Cerebral edema

Brain edema,[1] Cerebral oedema, [2] Brain swelling

Headache, nausea, vomiting, decreased consciousness, seizures

ischemic stroke, subdural hematoma, epidural hematoma, intracerebral hematoma, intraventricular hemorrhage, subarachnoid hemorrhage, hydrocephalus, traumatic brain injury, brain abscess, brain tumor, hyponatremia, hepatic encephalopathy

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.[1][3][4][5][6] Diagnosis is based on symptoms and physical examination findings and confirmed by serial neuroimaging (computed tomography scans and magnetic resonance imaging).[3]


The 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.[3][7][8] Extensive cerebral edema can also be treated surgically with a decompressive craniectomy.[7] Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries.[4][9]


As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.[1] The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage.[1] For example, malignant brain edema was present in roughly 31% of people with ischemic strokes within 30 days after onset.[10]

Signs and symptoms[edit]

The 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.[1] As the skull is a fixed and inelastic space, the accumulation of cerebral edema can displace and compress vital brain tissue, cerebral spinal fluid, and blood vessels, according to the Monro–Kellie doctrine.[8]


Increased intracranial pressure (ICP) is a life-threatening surgical emergency marked by symptoms of headache, nausea, vomiting, decreased consciousness.[1] Symptoms are frequently accompanied by visual disturbances such as gaze paresis, reduced vision, and dizziness.[1] Increased pressures within the skull can cause a compensatory elevation of blood pressure to maintain cerebral blood flow, which, when associated with irregular breathing and a decreased heart rate, is called the Cushing reflex.[1] The Cushing reflex often indicates compression of the brain on brain tissue and blood vessels, leading to decreased blood flow to the brain and eventually death.[1]

[8]

Traumatic brain injury

[1]

Stroke

[1]

Tumors

Infections (such as a brain abscess or )[3][11]

meningitis

[5]

Hepatic encephalopathy

[12]

Posterior reversible encephalopathy syndrome

Radiation-induced brain edema

[13]

Post-surgical changes[15]

[14]

(ARIA-E)[16]

Amyloid-related imaging abnormalities associated with edema

[17]

Hyponatremia

[6]

High-altitude cerebral edema

Commonly caused by , intracerebral hemorrhage, and the early phase of ischemic stroke.[1]

traumatic brain injuries

Also seen in where toxic waste, most notably ammonia, accumulates in the blood stream and crosses the blood–brain barrier.[5] Hyperammonemia in central nervous system (CNS) cells causes oxidative stress and mitochrondrial dysfunction, leading to astrocytic cell swelling.[1] Additionally, ammonia is converted to glutamine in CNS cells which acts as an osmolyte and draws further water into the cell through osmosis.[5] Cerebral edema occurs most commonly in conjunction with a rapid rise in ammonia levels.[5]

acute liver failure

Toxic exposures to , cuprizone, isoniazid, triethyltin, hexachlorophene, and hydrogen cyanide have been associated with cytotoxic edema and swelling of astrocytic cells.[21]

methionine sulfoximine

Hypoxia, anoxia can lead to cytotoxic edema through several mechanisms

[18]

is a highly concentrated solution of sodium chloride in water and is administered intravenously.[3] It has a rapid-onset, with reduction of pressures within 5 minutes of infusion, lasting up to 12 hours in some cases, and with negligible rebound pressure.[44] The exact volume and concentration of the hypertonic saline varies between clinical studies.[3][44][45] Bolus doses, particularly at higher concentrations, for example 23.4%, are effective at reducing ICP and improving cerebral perfusion pressure.[44][46] In traumatic brain injuries, a responsiveness to hypertonic saline lasting greater than 2 hours was associated with decreased chance of death and improved neurologic outcomes.[44] The effects of hypertonic saline can be prolonged with combination to agents such as dextran or hydroxyethyl starch, although their use is currently controversial.[44] When compared to mannitol, hypertonic saline has been shown to be as effective as mannitol in decreased ICP in neurocritical care and is more effective in many cases.[44] Hypertonic saline may be preferable to mannitol in persons with hypovolemia or hyponatremia.[44]

Hypertonic saline

is an alcohol derivative of simple sugar mannose, and is historically the most commonly used osmotic diuretic.[3] Mannitol acts as an inert solute in the blood, decreasing ICP through osmosis as discussed above.[44] Additionally, mannitol decreases ICP and increased cerebral perfusion pressure by increasing reabsorption of cerebrospinal fluid, dilutes and decreased the viscosity of the blood, and can cause cerebral vasoconstriction.[44] Furthermore, mannitol acts in a dose-dependent manner and will not lower ICP if it is not elevated.[44] However, the common limitation of the use of mannitol is its tendency to cause low blood pressure hypotension.[44] Compared to hypertonic saline, mannitol may be more effective at increasing cerebral perfusion pressures and may be preferable in those with hypoperfusion.[44]

Mannitol

commonly furosemide, act within kidney to increase excretion of water and solutes.[3] Combination with mannitol produces a profound diuresis and increases the risk of systemic dehydration and hypotension.[3] Their use remains controversial.[3]

Loop diuretics

a carbonic anhydrase inhibitor, acts as a weak diuretic and modulates CSF production but has not role in the management of cerebral edema from acute brain injuries.[3] It can be used in the outpatient management of cerebral edema caused by idiopathic intracranial hypertension (pseudotumor cerebri).[3]

Acetazolamide

Cerebral edema is the cause of death in 5% of all patients with cerebral infarction and mortality after large ischemic strokes with cerebral edema is roughly 20 to 30% despite medical and surgical interventions.[38] Cerebral edema usually occurs between the second and fifth day after onset of symptoms.[9] Large territory ischemic strokes can lead to the rapid development of malignant brain edema and increased intracranial pressure.[52] Cerebral edema in the context of a malignant middle cerebral artery (MCA) infarct has a mortality of 50 to 80% if treated conservatively.[9] Individuals with cerebral edema had a worse 3-month functional outcome than those without edema.[9] These effects were more pronounced with increasing extent of cerebral edema and were independent of the size of the infarct.[9]

[9]

Mild (TBI) represents 70–90% of all reported head injuries.[34] The presence of brain edema on the initial CT scan of those with traumatic brain injuries is an independent prognostic indicator of in-hospital death.[34] The association of brain edema with increased in hospital risk of death was observed in TBI across all level of severity.[34] Edema in the acute and chronic phases were associated with a worse neurologic and clinical outcome.[34] Children with TBI and cerebral edema have worse clinical outcomes as well.[34]

traumatic brain injury

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.[3][10][34]

In one study, cerebral edema was found in 28% of those individuals with thrombolysis-treated ischemic strokes, 10% of which occurred in severe forms. A further study detected cerebral edema in 22.7% of cerebral ischemic strokes.[9] A meta-analysis of current studies showed that 31% of those affected by ischemic strokes developed cerebral edema in 31% of cases.[10]

[9]

In traumatic brain injuries, cerebral edema occurred in greater than 60% of those with mass lesions, and in 15% of those with initial normal CT scans.

[53]

As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.[1] The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage.[1]

Research[edit]

The current understanding of the pathophysiology of cerebral edema after traumatic brain injury or intracerebral hemorrhage is incomplete.[8][54] Current treatment therapies aimed at cerebral edema and increased intracranial pressure are effective at reducing intracranial hypertension but have unclear impacts on functional outcomes.[53] Additionally, cerebral and ICP treatments have varied effects on individuals based on differing characteristics like age, gender, type of injury, and genetics.[53] There are innumerable molecular pathways that contribute to cerebral edema, many of which have yet to be discovered.[8][54] 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.[8][53] At the same time, improvement of radiographic markers, biomarkers, and analysis of clinical monitoring data is essential in treating cerebral edema.[53]


Many studies of the mechanical properties of brain edema were conducted in the 2010s, 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.[55] A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.[56]

Intracranial pressure

Edema

Amyloid-related imaging abnormalities

Vasogenic Edema

MedPix