Cerebral edema is a frequent and challenging problem in the clinical setting and is a major cause of morbidity and mortality in patients with acute brain injury. It is simply defined as an increase in brain water content (normal brain water content is approximately 80%) and is invariably a consequence of a primary brain insult. Etiologies of these neurologic injuries that cause cerebral edema are diverse and commonly include:

1. ▪ Traumatic brain injury (TBI)

2. ▪ Subarachnoid hemorrhage (SAH)

3. ▪ Ischemic stroke

4. ▪ Intracerebral hemorrhage (ICH)

5. ▪ Neoplasms (primary and metastatic)

6. ▪ Inflammatory diseases (meningitis, ventriculitis, cerebral abscess, encephalitis)

7. ▪ Toxic-metabolic derangements (hyponatremia, fulminant hepatic encephalopathy)

CEREBRAL EDEMA: CLASSIFICATION

Traditional classification of cerebral edema into cytotoxic, vasogenic, and interstitial (hydrocephalic) is overly simplistic in that it does not reflect the complexity of pathophysiologic and underlying molecular mechanisms. However, it serves as a simple therapeutic guide.

1. ▪ Cytotoxic edema results from swelling of the cellular elements (neurons, glia, and endothelial cells) because of substrate and energy (Na+, K+ pump) failure and affects both gray and white matter. This edema subtype is the initial accompaniment of any brain injury irrespective of etiology and conventionally is thought to be resistant to any known medical treatment.

2. ▪ Vasogenic edema that predominantly affects white matter, typically encountered in TBI, neoplasms, and inflammatory conditions, results from breakdown of the blood-brain barrier (BBB) due to increased vascular permeability and consequent leakage of plasma components. This edema subtype is responsive to both steroids (notably edema associated with neoplasms) and osmotherapy.

3. […]