Cerebral edema

Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Diagnosis is based on symptoms and physical examination findings and confirmed by serial neuroimaging (computed tomography scans and magnetic resonance imaging). Extensive cerebral edema can also be treated surgically with a decompressive craniectomy.

As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined.

Signs and symptoms

thumb|Cerebral oedema, [[glioma right cerebral cortex]]

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.

Hepatic encephalopathy
Radiation-induced brain edema
Post-surgical changes
Amyloid-related imaging abnormalities associated with edema (ARIA-E)
Hyponatremia
High-altitude cerebral edema

The following individual sub-types have been identified:

Cytotoxic

In general, cytotoxic edema is linked to cell death in the brain through excessive cellular swelling. The ultimate consequence of cytotoxic edema is the oncotic death of neurons. Researchers have proposed that "cellular edema" may be more preferable to the term "cytotoxic edema" given the distinct swelling and lack of consistent "toxic" substance involved.

Hypoxia, anoxia can lead to cytotoxic edema through several mechanisms
Brain hemorrhage

Ionic (Osmotic)

In ionic edema, the solute concentration (osmolality) of the brain exceeds that of the plasma and the abnormal pressure gradient leads to accumulation of water intake into the brain parenchyma through the process of osmosis.

Subtypes

High-altitude cerebral edema

If not properly acclimatized to high altitude, a person may be negatively affected by the lower oxygen concentration available. The edema can be characterized by vasogenic cerebral edema with symptoms of impaired consciousness and truncal ataxia. Human monoclonal antibodies such as aducanumab, solanezumab, and bapineuzumab have been associated with these neuroimaging changes and additionally, cerebral edema. Familiarity with ARIA can aid radiologists and clinicians in determining optimal management for those affected. PRES in general has a benign course, but PRES-related intracranial hemorrhage has been associated with a poor prognosis.

Idiopathic delayed-onset edema

Deep brain stimulation (DBS) is effective treatment for several neurological and psychiatric disorders, most notably Parkinson's disease. DBS is not without risks and although rare, idiopathic delayed-onset edema (IDE) surrounding the DBS leads have been reported. Data suggests that pathologic changes are triggered immediately following the procedure, especially an acute increase in intracranial pressure. The exact mechanism is unclear but hypothesized that cancerous glial cells (glioma) of the brain can increase secretion of vascular endothelial growth factor (VEGF), which weakens the tight junctions of the blood–brain barrier. Historically, corticosteroids such as dexamethasone were used to reduce brain tumor-associated vascular permeability through poorly understood mechanisms and was associated with systemic side effects. Therefore, diagnosis of cerebral edema earlier with rapid intervention can improve clinical outcomes and can mortality, or risk of death. The Brain Trauma Foundation guidelines recommend ICP monitoring in individuals with TBI that have decreased Glasgow Coma Scale (GCS) scores, abnormal CT scans, or additional risk factors such as older age and elevated blood pressure. Pretreatment with a sedative agent and neuromuscular blocking agent to induce unconsciousness and motor paralysis has been recommended as part of standard Rapid Sequence Intubation (RSI). Blood serum ion concentration, or osmolality, should be maintained in the normo to hyperosmolar range.

Seizure prophylaxis

Seizures, including subclinical seizure activity, can complicate clinical courses and increase progression of brain herniation in persons with cerebral edema and increased intracranial pressure. Anticonvulsants can be used to treat seizures caused by acute brain injuries from a variety of origins. Therefore, maintaining a stable body temperature within the normal range is strongly recommended. Depolarizing neuromuscular blocking agents, most notably succinylcholine, can worsen increased ICP due to induction of muscle contraction within the body. The management of individual diseases are discussed separately.

The following interventions are more specific treatments for managing cerebral edema and increased ICP:

Osmotic therapy

The goal of osmotic therapy is to create a higher concentration of ions within the vasculature at the blood–brain barrier.

Hypertonic saline is a highly concentrated solution of sodium chloride in water and is administered intravenously. The exact volume and concentration of the hypertonic saline varies between clinical studies. Bolus doses, particularly at higher concentrations, for example 23.4%, are effective at reducing ICP and improving cerebral perfusion pressure. 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. In traumatic brain injury, induced hypothermia may reduce the risks of mortality, poor neurologic outcome in adults. However, outcomes varied greatly with depth and duration of hypothermia as well as rewarming procedures. The adverse effects of hypothermia are serious and require clinical monitoring including increased chance of infection, coagulopathy, and electrolyte derangement. However, no individual study has shown an improvement in the percentage of survivors with good functional outcomes. Cerebral edema in the context of a malignant middle cerebral artery (MCA) infarct has a mortality of 50 to 80% if treated conservatively.

Research

The current understanding of the pathophysiology of cerebral edema after traumatic brain injury or intracerebral hemorrhage is incomplete. Current treatment therapies aimed at cerebral edema and increased intracranial pressure are effective at reducing intracranial hypertension but have unclear impacts on functional outcomes. A second line of research on the condition looks at thermal conductivity, which is related to tissue water content.

References

External links

MedPix Vasogenic Edema