Cerebral Edema

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Cerebral edema is a challenging problem in the neurocritical
care setting. Different etiologies may cause increased
intracranial pressure. Secondary brain injury may ensue as a
result of cerebral edema, and may result in different herniation
syndromes.
Brain monitoring for increased intracranial pressure may by
employed in certain patient populations. Serial neuroimaging
may be useful in monitoring exacerbations of brain edema.
Osmotherapy has been recommended for management of
cerebral edema. Mannitol and hypertonic saline are the two
agents widely used for this purpose. Knowledge of possible side
effects of osmotherapeutic agents is necessary. Common
concerns of such therapies include renal insufficiency,
pulmonary edema, and exacerbation of congestive heart failure,
hypernatremia, hemolysis, and hypotension. Specific measures
as controlled ventilation, sedation and analgesia, pharmacologic
coma, hypothermia and surgical decompression may be required
in patient subpopulations. Important questions still need to be
answered regarding the timing of the decompressive surgery
and patient selection criteria.
Surgical decompression may be applicable in certain patients.
Recent studies indicate that surgical decompression may

significantly reduce mortality in young patients with malignant
cerebral infarcts.
General medical management is focused toward limiting
secondary brain damage. General measures include head and
neck position, optimization of cerebral perfusion and
oxygenation, management of fever, nutritional support and
glycemic control.
Abnormalities of intracranial pressure may result in pathology
requiring urgent evaluation and intervention to prevent lifethreatening
consequences. This pathology may represent
intracranial hyper- or hypotension, or it may manifest as an
abnormality of cerebrospinal fluid (CSF) dynamics, such as
hydrocephalus. Elevated intracerebral pressure is the final
common pathway for almost all pathology leading to brain
death, and interventions to treat ICP may preserve life and
improve neurologic function after head trauma, stroke, or other
neurologic emergencies.
Common causes of raised intracranial pressure are shown in
Table 7.1, symptoms and signs in Table 7.2.

Table 7.1 – Some common causes of increased intracranial pressure
(Czosnyka 1999)
Head injury Intracranial hematoma (extradural, subdural, and
intracerebral)
Diffuse brain swelling
Contusion
Cerebrovascular Subarachnoid hemorrhage
Intracerebral hematoma
Cerebral venous thrombosis
Major cerebral infarct
Hypertensive encephalopathy (malignant hypertension,
eclampsia)
Hydrocephalus Congenital or acquired
Obstructive or communicating
Craniocerebral
disproportion
Brain “tumour” (cysts; benign or malignant tumours)
Secondary hydrocephalus
Mass effect
Oedema
“Benign” intracranial hypertension (pseudotumor cerebri;
idiopathic intracranial hypertension)
CNS infection Meningitis
Encephalitis
Abscess
Cerebral malaria
Metabolic
encephalopathy
Hypoxic-ischemic
Reye’s syndrome, etc.
Lead encephalopathy
Hepatic coma
Renal failure
Diabetic ketoacidosis
Burns
Near drowning
Hyponatremia
Status epilepticus
Types of Cerebral Edema
Cerebral swelling or edema can complicate many intracranial
pathologic processes including neoplasms, hemorrhage, trauma,
autoimmune diseases, hyperemia, or ischemia. There are
essentially three types of cerebral edema:
1. Cytotoxic edema is associated with cell death and failure of
ion homeostasis. Cytotoxic edema results from energy
failure of a cell as a result of hypoxic or ischemic stress,

which leads to cell death. Intracellular swelling occurs and
results in the CT and MR appearance of both gray and
white matter edema, usually in the distribution of a
vascular or borderzone territory after hypoxia or stroke.
2. Vasogenic edema is associated with breakdown of the
blood-brain barrier. Vasogenic edema represents
breakdown of the blood-brain barrier, appears mostly in
the white matter, and is more likely to be associated with
neoplasms or cerebral abscesses. In reality, cerebral edema
in many situations, usually exhibit a combination of
vasogenic and cytotoxic edema.
3. Interstitial (hydrostatic or hydrocephalic) edema is
associated with hydrocephalus, in which there is increased
tension of CSF across the ependyma. Interstitial edema, or
transependymal flow, is radiographically seen with
hypodense areas surrounding the ventricular system and is
associated with increased CSF volume or pressure.
Table 7.2 – Signs and symptoms of increased intracranial pressure and
edema
Symptoms Physical Signs
Headache, worsened with Valsalva
Decreased visual acuity
Diplopia
Nausea
Vomiting
Progressive decline in level of
consciousness
Decreased upward gaze
Cranial nerve VI palsy
Papilledema
Loss of normal venous pulsations in the
fundus
Field cut or enlarged physiologic blind
spot
Alterations in vital signs
Management of Cerebral Edema
The treatment of cerebral edema depends mainly on treating the
underlying cause. In cytotoxic edema, osmotic therapy with
mannitol and hypertonic saline may not reduce edema in the

lesion itself, but may reduce the volume of normal brain
allowing for some increased margin of safety by decreasing
intracranial pressure (Raslan 2007). Steroids are of no value in
cytotoxic edema due to stroke, and may be harmful in the
settings of brain trauma. Surgical decompression of cytotoxic
edema with decompressive craniectomy may be therapeutic, and
life-saving (Hofmeijer 2009). Vasogenic edema responds to
steroids and surgical resection of the lesion, and may also
benefit from osmotic therapy with mannitol or hypertonic saline
(Oddo 2009). Hydrostatic edema is treated surgically with CSF
removal or shunting, and it is treated medically with agents to
decrease production of CSF, such as acetazolamide and
furosemide.