Cerebral edema is a life-threatening condition where there is an increase in fluid in the brain tissue.
Swelling or edema is part of inflammation. It is a natural response of the body to injury and can happen anywhere. But when it happens in the brain, it poses a unique situation. Being enclosed in the skull, brain edema can lead to a rise in intracranial pressure with morbid or fatal consequences.
Cerebral edema can lead to irreversible damage and, in some cases, be fatal.
Pathophysiology of Cerebral Edema
An injury of any kind leads to activation of an injury cascade which results in cellular damage and leakage from vessels forcing the fluid to enter brain tissues.
Injury cascade at cellular level involves many mediators and substrates and is a complex process that is discussed separately.
The sequence of events leads to water moving from the extracellular to the intracellular compartment and is followed by an inflammatory response. Free radicals and proteases are released which further contribute to leakage from cell membranes and capillaries.
Normal skull volume is occupied by
- Brain- 1400 ml
- Cerebral spinal fluid- 150 ml
- Blood 150 ml
Since the skull is rigid, increase in the volume of one component is at the cost of reduction of volume of other components. When this cannot be compensated it gives rise to an increase in intracranial pressure.
A substantial rise in intracranial pressure eventually causes a reduction in cerebral blood flow which might cause cerebral infarction on lesser scale or widespread ischemia when severe.
The continuous rise of intracranial pressure further leads to brain herniation which is a life-threatening condition.
Types of Cerebral Edema
There are two main categories of cerebral edema though specific separation is almost impossible as there is an overlap of types in a given case.
Cytotoxic Edema
Edema results from the swelling of brain cells due to the release of toxic agents. It is seen in head injury, hypoxia, and infection, etc. This type of cerebral edema begins within minutes of insult and is caused by the swelling of glia, neurons and endothelial cells. Cytotoxic edema affects predominantly the gray matter.
Vasogenic Cerebral Edema
It refers to the inflow of the fluid and solutes into the brain following a deficient blood-brain-barrier. It is the most common type of brain edema. As it results from increased permeability of the capillary endothelial cells, it mainly affects the white matter.
Interstitial Edema
It is seen when the outflow of cerebrospinal fluid is obstructed leading to an increase in intraventricular pressure as in hydrocephalus. The result is the movement of sodium and water across the ventricular wall into space around.
Osmotic Cerebral Edema
It results when there is decrease in osmotic pressure of the blood [for example in blood dilution].
Causes of Cerebral Edema
Both neurological and non-neurological conditions can lead to cerebral edema.
- Ischemic stroke
- Intracerebral hemorrhage
- Brain tumors by causing pressure and preventing fluid drainage.
- Meningitis
- Encephalitis
- Cysticercosis
- Tuberculosis
- Toxoplasma infection
- Diabetic ketoacidosis
- Coma due to lactic acidosis
- Malignant hypertension
- Hypertensive encephalopathy
- Fulminant hepatitis
- Hepatic encephalopathy
- Reye’s syndrome
- Carbon monoxide poisoning
- Lead poisoning
- Hyponatremia [low sodium levels in blood]
- Syndrome of inappropriate antidiuretic hormone secretion
- Opioid drug abuse
- Bites of certain animals
- High altitude cerebral edema [generally above 4000 meters]
- Brain hemorrhage
Clinical Presentation-Symptoms
Depending upon the clinical cause, the findings of cerebral edema may be subtle or masked due to the primary underlying condition.
The symptoms vary depending on the severity and underlying cause of the swelling.
Initially, the symptoms and signs of cerebral edema are subtle and nonspecific like headaches, nausea, and dizziness. The rise in intracranial pressure ultimately may lead to neural symptoms due to ischemia and these could be loss of memory, difficulty in speaking, vision loss, weakness of part of body and loss of consciousness.
Following signs point towards a rise in intracranial pressure
- Alteration in the level of consciousness
- Decrease in heart rate [bradycardia] in the presence of raised blood pressure [hypertension]
- Abnormal breathing patterns
- Extraocular movement abnormalities [adduction, abduction of the eye, etc]
- Unequal pupil size
In addition, there could be an extensor plantar response on the side of the lesion (may occur in cases of localized lesions).
Investigations
CT scan
It excellently shows the presence of brain water content. Edema areas appear as low density and there is a dilution of all the constituents of the white matter.
CT is also able to recognize the type of edema and underlying local lesions like infarction or tumor.
CT is an excellent method for following the resolution of brain edema following therapeutic intervention.
MRI
MRI can detect localized causes of cerebral edema [for example- tumor] in addition to identifying the edema; as it is a good imaging technique to identify the structural changes in the parenchyma.
Intracranial Pressure Monitoring (ICP)
The routine use of ICP monitoring remains controversial as clinical signs and imaging are more reliable.
EEG
EEG is not very helpful in the management of cerebral edema.
Treatment
The treatment of cerebral edema is complex, and a positive outcome is expected only if the diagnosis and intervention occur in time.
General Measures
The patient is monitored in ICU when the signs of raised intracranial pressure are evident. The patient should lie on the bed with head-end elevated by 15-30 degrees. [The bed is not raised in acute carotid or basilar artery occlusion as it would cause a decrease in blood supply]
The head is kept in the midline to avoid venous compression at the neck
Correction of Contributory Factors
Following factors are known to increase intracranial pressure and need to be corrected
- Increase in CO2 levels [hypercarbia]
- Decrease in blood oxygen levels [hypoxia]
- Increase in body temperature [hyperthermia]
- Acidosis
- Decrease in blood pressure
For correction, following measures are done
- Control of hypotension
- Normal saline or diluted saline
- Control low blood volume but prevent overcorrection
- Endotracheal intubation and mechanical ventilation to hyperventilate
- PaCO2 of 25 mm Hg is desirable
- Monitor by blood gas analysis and chest radiograph.
Osmotic Therapy
This treatment aims to draw water out of the brain by osmotic gradient by decreasing blood viscosity. This helps to decrease intracranial pressure and increase cerebral blood flow.
Mannitol is the most popular osmotic agent. It is supposed to act by the following mechanisms though exact mechanisms are not known.
- Decreasing overall water content
- Vasoconstriction leading to reduction in blood volume
- Decrease in cerebrospinal fluid volume by decreasing water content
- Improving cerebral perfusion by decreasing viscosity of blood
- May protect against biochemical insult
Mannitol is given intravenously in the dosage of 1.0 g/kg, then 50 g every 2-3 hours. It should be cautioned that prolonged administration of mannitol may result in an electrolyte imbalance and requires monitoring.
Another agent is glycerol. It is given in doses of 30 ml every 4-6 hour orally [via a nasogastric tube in an unconscious patient] or IV 50g in 500 ml of 2.5% in the whole day. However, the effectiveness of glycerol decreases after few days.
Diuretics
Duretics like furosemide help to prolong the effect along with the osmotic agents.
Corticosteroids
They are beneficial primarily in vasogenic edema but less effective in cytotoxic edema. Steroids are also used in chronic meningitis and in acute bacterial meningitis under cover of antibiotics. They are thought to reduce tumor-associated vasogenic edema, probably by decreasing the increased capillary permeability and are used in brain tumor management. The role of corticosteroids in head trauma is uncertain.
Surgery
It is recommended occasionally for large hemispherical infarcts with edema and life-threatening brain-shifts.
Decompression procedures like temporary ventriculostomy or decompressive craniectomy [opening of skull to decompress] may prevent deterioration and may be lifesaving.
Decompressive craniectomy should be considered in younger patients who are deteriorating neurologically.
Decompression is also life-saving in large cerebellar infarcts with cerebral edema.
In cases of severe hydrocephalus, ventriculoperitoneal shunt is very helpful
Prognosis
Cerebral edema can have severe and irreversible consequences. The outlook can vary considerably and depends on location and severity of the edema, and prompt initiation of the treatment.
References
- Rosenberg GA. Ischemic brain edema. Prog cardiovasc Dis. 1999;42(3):209–216.
- North B, Reilly P. Raised intracranial pressure – a clinical guide. 1st ed. Heinemann Medical Books; Oxford: 1990. pp. 71–85.
- de los Reyes RA, Ausman JI, Dias FG. Agents for cerebral edema. Clin Neurosurg. 1981;28:98–107.
- Richling B. Current status of treatment of cerebral edema. Anaesthesist. 1987;36(5):191–196.