Clinical meaning
Cerebral edema is abnormal accumulation of fluid in brain parenchyma, increasing intracranial volume and potentially causing herniation. Three distinct pathophysiological mechanisms exist: (1) Cytotoxic edema — cellular swelling from ATP depletion and Na+/K+ ATPase pump failure (ischemic stroke, hypoxia, metabolic encephalopathy). Water shifts from extracellular to intracellular space; the BBB is initially intact. On MRI, cytotoxic edema restricts on DWI (bright) with decreased ADC values. (2) Vasogenic edema — BBB disruption allows plasma proteins and fluid to extravasate into extracellular space (brain tumors, abscess, trauma, hypertensive encephalopathy). This edema follows white matter tracts and responds to corticosteroids. On MRI, vasogenic edema is bright on T2/FLAIR without DWI restriction. (3) Interstitial (hydrocephalic) edema — obstructive hydrocephalus causes CSF to transude through ependymal lining into periventricular white matter. Treatment is CSF diversion (ventriculostomy or shunt). The Monro-Kellie doctrine states that the rigid skull contains three components (brain ~80%, blood ~10%, CSF ~10%) in a fixed volume; increase in any component must be compensated by decrease in another, or ICP rises. Compensation mechanisms (CSF displacement to spinal canal, venous blood compression) are exhausted above ICP ~20 mmHg, after which small volume increases cause exponential ICP rises. Cerebral perfusion pressure (CPP = MAP - ICP) must be maintained >60 mmHg to prevent secondary ischemic injury.