Cerebral Edema

CT brain tumor[1]

Cerebral edema is not an uncommon disorder in medicine and can occur from a variety of conditions. By definition, cerebral edema is the excess accumulation of water in the extra or intracellular space of the brain.


There are no specific features on a clinical exam about cerebral edema. A very high index of suspicion is required to make the diagnosis. The clinical features may be “on” and “off” and hence some signs may be missed. The intracranial pressure has to reach a critical point in the brain before symptoms start to develop. In general, the features of elevated intracranial pressure may include the following:

  • Varying state of alertness or consciousness. Often the patient or family will complain of increased drowsiness and difficulty with arousal.
  • Lethargy is also a common presentation. The patient may appear moribund, disinterested and have diminished motor activity.
  • Headache maybe the initial presenting feature. But headache can present with any number of disorders and is usually not diagnostic for cerebral edema
  • Bradycardia and elevated blood pressure. The cushing reflex may appear in patients who are continuously monitored. Unfortunately, many healthcare workers rarely make a correlation between bradycardia and hypertension in relation to elevated intracranial pressure. The cushing reflex may also appear with irregular breathing (see below).
  • Abnormal breathing pattern which may vary from shallow to deep breathing with numerous sigh. When appearing with the cushing reflex, it is a negative prognostic factor and a sign of herniation.
  • Abnormal eye movements and/or pupillary dilatation. The pupils may become dilated and unresponsive to light. Associated with the sluggish movement of the pupil, one may also see deviation of the pupil if there is unilateral compression or herniation.
  • Extensor plantar responses may be positive and brisk.


The test of choice to investigate a patient with cerebral edema is a CT scan. The areas of edema appear as low density on an enhanced CT scan. The low density is due to dilution of all the constituents of white matter. The CT scan may appear blurry and it may be hard to decipher any specific anatomy due to the increased water accumulation. CT scan can also help demonstrate presence of any underlying lesion like a tumor, infection or an infarct that may be causing the cerebral edema. CT scan can also be used to follow patients following intervention to determine if the condition is resolving. MRI appears to be more sensitive than CT scan at detecting brain abscess and lymphomas. Unfortunately, unlike CT scan, MRI is not readily available and is also much more expensive.

Intracranial pressure monitoring is also an important tool to monitor patients with cerebral edema. It is now often routine in neurosurgery wards to have an ICP monitor in patients with suspected elevated intracranial pressure. EEG may be done if the patient develops seizures. If meningitis is suspected, a lumbar puncture is required. However, it is important to be cognizant that there is always the risk of herniation during lumbar puncture in the presence of elevated intracranial pressure. A CT scan of the head should be done first prior to a lumbar puncture.

Other tests to work up a patient with cerebral edema include the following:

  • Complete blood count
  • Coagulation profile
  • Electrolytes
  • Liver and renal function tests
  • Blood sugar levels
  • Arterial blood gas
  • Urine for illicit drugs
  • Carbon monoxide levels


Cerebral edema is a medical emergency and needs prompt treatment. The brain swelling needs to be lowered by decreasing tissue water and brain volume using osmotherapy. The aim of osmotic therapy is to draw water out of brain tissues by an osmotic gradient and lower the blood viscosity.[6][7] These changes can rapidly decrease intracranial pressure and increase cerebral blood flow.

  • Serial bedside monitoring of the patient’s levels of consciousness, and observing for any new neurological deficit is mandatory. Glasgow coma scale must be recorded every 30-60 mins and if any new changes occur, a CT scan is recommended.[8]
  • Mannitol is the most popular osmotic agent used to treat cerebral edema. How this agent lowers elevated intracranial pressure is still not known, but it is thought to lower brain volume by decreasing overall water content and promoting vasoconstriction, which further reduces CSF volume. Mannitol may also improve cerebral perfusion by decreasing blood viscosity and have a protective effect by preventing oxidative injury. The dose of mannitol is 1g/kg given IV. Prolonged administration of mannitol can lead to hypokalemia and hence, electrolyte levels needs to be monitored too. There is also accumulating evidence that mannitol may worsen cardiovascular function, and thus hemodynamic monitoring is necessary.
  • Glycerol is another osmotic agent that may be given orally or IV. Unlike mannitol, its effects decrease in a few days due to tachyphylaxis. In unconscious patients or those with poor IV access, it may be give via the nasogastric tube.
  • Diuretics also have an osmotic effect. Loop diuretics like furosemide can be administered IV. Furosemide is often administered at high doses for 12-24 hours. Urine output must be monitored to ensure that the patient does not become dehydrated.
  • Corticosteroids are known to lower intracranial pressure in vasogenic and cytotoxic edema. However, the role of steroids in decreasing cerebral edema is fraught with controversy. These medications have not proven to be effective in ischemic stroke unless there is documented evidence of cerebral vasculitis. Steroids have been used to treat edema caused by brain tumors and following CNS surgery. The role of steroids in people with cerebral edema from head trauma is uncertain.

Other drugs

Many other agents have empirically been used to treat cerebral edema. The list includes propofol, local anesthetics like procaine and lidocaine, THAM and indomethacin. Most of these agents have been used in the past and only anecdotal reports exist regarding their benefits. Barbiturates are known to decrease the metabolic rate, lower cerebral blood flow and ICP. However, these drugs also cause profound sedation, hypotension and may even induce pulmonary edema. Thus, ICU monitoring of the patient is required.

Surgical intervention may be required when the cerebral edema is life threatening and associated with herniation. A temporary ventriculostomy or a craniotomy maybe required to reduce the intracranial pressure and prevent deterioration of the patient. Patients with hydrocephalus may benefit from a ventriculo-peritoneal shunt. If an intracranial monitoring device is inserted the pressure must be serially monitored.[9]

Hypothermia has been shown to protect the brain by lowering metabolic rate and avoiding energy depletion. Many studies exist to show that hypothermia may slow down the hypoxic ischemic injury in people with cerebral edema. Hypothermia may be required for several days and reversed when organ dysfunction starts to improve.
Blood pressure control is vital in patients with cerebral edema as hypertension is detrimental.
Lumbar puncture has also been advocated in some patients to reduce cerebral edema. Again, clinical judgement is required prior to perform this procedure in order to avoid brain herniation.

Other measures

  • The patient should have the head of bed elevated to 15-30 degrees to promote venous drainage, and the head should be kept in the midline to prevent venous compression near the neck.[10]
  • All other contributory facts like hypoxia, hyperthermia, acidosis, hypotension or hypovolemia should be corrected. For hyperventilation, the patient needs to be intubated and mechanically ventilated.
  • Fluid restriction has minimal effects on cerebral edema and excess fluid restriction can lead to hypotension which may worsen brain perfusion.
  • Glucose containing fluids should be avoided as there is data which indicate poor neurological outcomes with hyperglycemia. The euvolemia should be maintained with normal saline, and excess urinary loses that occur after use of mannitol should be replaced with normal saline.
  • Hyperventilation can help lower elevated ICP. The cerebral vasculature is very sensitive to changes in arterial PCO2. ICP usually falls very rapidly with hyperventilation, but the effects are not sustained as the body’s buffering mechanism quickly restores the pH to normal. During hyperventilation, the PCO2 should not be decreased to levels below 25 mmHg, because at this point the vasoconstriction caused by low PCO2 can cause hypoxemia and potentiate ischemic cell injury.


The prognosis of patients with cerebral edema depends on the cause, presence of comorbidity (eg. malignant hypertension, vasculitis, cancer), age, time to make the diagnosis and treatment. When patients are comatose and treatment is delayed, the prognosis is usually poor. Persistent vegetative state from ischemic injury to the brain is not uncommon. When the intracranial pressure is not relieved, herniation has also been reported. Because in most cases the diagnosis is not made early, some degree of residual brain injury is common. In patients with reversible causes of cerebral edema like diabetic ketoacidosis or encephalitis, the prognosis is slightly better.


There are many causes of cerebral edema which include the following:

CNS causes

  • Brain malignancies, both primary and secondary cancers can incite an inflammatory reaction resulting in cerebral edema, plus a mass effect. The majority of these patients are symptomatic.
  • Encephalitis from a viral infection can also lead to mild to moderate cerebral edema. Once encephalitis resolves, the cerebral edema lessens.
  • Infections like toxoplasmosis, cysticercosis and tuberculosis can all cause an inflammatory reaction with resulting cerebral edema.
  • Intracerebral hemorrhage from a subarachnoid hemorrhage is the most serious cause of cerebral edema.
  • Ischemic stroke is one of the most common causes of cerebral edema.
  • Meningitis from almost any bacterial infection.

Non CNS causes


The frequency of cerebral edema is not known but the disorder is not rare. Because cerebral edema is often a secondary feature of many disorders, it is often not cited in the literature. Cerebral edema often has a sinister presentation and without specific signs and symptoms, the diagnosis is often missed. There is no test that is specific for cerebral edema. Often the diagnosis is made at post mortem. There are many anecdotal reports about cerebral edema presenting in many different disorders, suggesting that the complication is not rare at all.

Sex distribution
Age distribution


The pathophysiology of cerebral edema is complex. In general, the increased fluid in the brain may be due to systemic disorder or a localized pathology in the brain. Cerebral edema may be cytotoxic or vasogenic. Cytotoxic edema is seen after head injury or hypoxia and assorted with swelling of brain cells. This type of edema predominantly affects the gray mater. Vasogenic cerebral edema is due to influx of solutes and fluid into the brain. There is usually increase permeability of the capillary endothelial cells and the white matter is chiefly affected in this pathology.

With cerebral edema there is an increased amount of fluid in the brain, either the nerve cells swell and increase volume or there may be excess fluid in the brain tissues. When damage occurs to neuronal cells from any cause, this results in swelling. The resultant swelling leads to blockade of absorption pathways, forcing fluid to enter brain tissues. Brain injury is generally associated with an injury cascade which results in release of various cytotoxins, neurotransmitters and ions like calcium and sodium in the extracellular space. The accumulation of sodium within the cell leads to an osmotic gradient with resulting entry of water. The swelling of the cell is associated with a compressive effect, which leads to hypoxia, that results in depletion of energy stores and disabling of critical enzymes.

In the brain, there is normally about 150 ml of cerebrospinal fluid (CSF) which remains constant. Thus, when this volume of fluid increases it can compress the brain. The continuing intracranial pressure can reduce cerebral blood flow and lead to severe ischemic injury. If the brain cerebral edema is allowed to progress, it can lead to brain herniation and death.


There are many causes of cerebral edema and prevention can be a difficult task. However, all patients should be educated on keeping the blood pressure under control, remaining complaint with anti-hypertensive medications, monitor blood sugars closely, get regular follow up with their healthcare provider if they have any type of chronic illness, eat healthy and obtain regular exercise.


Cerebral edema is defined as an increase in the water content in the brain, primarily in response to some type of injury. The injury may include an ischemic stroke, traumatic brain injury, subarachnoid hemorrhage, primary and secondary malignancies, metabolic derangements, infectious disorders and a variety of inflammatory disorders. Cerebral edema is an insidious disorder that can present suddenly and is a common cause of morbidity and mortality in patients with brain injury. Because the skull is unable to expand, any increase in brain volume due to increased fluid can quickly lead to compression of critical structures in the central nervous system. If the condition is missed, death can quickly ensue because of herniation. Almost every organ system can be affected by elevated intracranial pressure due to cerebral edema [1].

Patient Information

Cerebral edema is a disorder where there is increased fluid in the brain. Because the skull Is not able to expand, the increased fluid exerts pressure on brain tissues. The resulting effect of increased pressure can lead to dysfunction of many organ systems in the body. Cerebral edema is a life threatening disorder that needs to be treated immediately. There are many causes of cerebral edema and often the presentation is subtle. CT scan is frequently used to make the diagnosis. The treatments basically involving decreasing the fluid volume in the brain. Despite prompt therapy, residual neurological deficits are not uncommon.


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Media References

  1. CT brain tumor, GFDL