Acute hypernatremia often results in significant brain shrinkage, thus causing mechanical traction of cerebral vasculature.
Stretching of bridging veins can result in subdural hemorrhages.
Venous congestion can lead to thrombosis of the intracranial venous sinuses.
Arterial stretching can result in subcortical hemorrhages and cerebral infarctions.
Seizures are possible.
Hypernatremia of more than 2 days' duration is considered chronic hypernatremia and is associated with an increased mortality rate.
Patients whose serum sodium level exceeds 180 mEq/L often have residual CNS damage.
If hypernatremia is corrected too rapidly, brain edema and associated neurologic sequelae can occur. Patients with chronic hypernatremia are especially prone to this complication.
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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
