How the two disorders are defined
Hyponatremia is a plasma sodium concentration below 135 mmol/L, and hypernatremia is a concentration above 145 mmol/L. The number defines the disorder, but it does not by itself say how ill the patient is, because the brain responds to the change in tonicity, the effective osmolality of the body fluids, and to how fast that change occurred.
Why the symptoms come from the brain
Plasma sodium is the main determinant of plasma osmolality, the concentration of dissolved solute in the plasma. Because cell membranes are permeable to water, a fall in plasma osmolality draws water into cells and a rise draws it out. Brain cells are the ones that suffer from this. When sodium falls, water enters them and they swell; because the brain sits inside a rigid skull that cannot expand, the swelling compresses the brain and produces the neurological features. When sodium rises, water leaves the brain cells and they shrink, and the neurological features follow from that shrinkage and from the damage it can do to the cerebral vessels. Other tissues tolerate the same shift of water far better, so it is the fixed volume of the skull that singles out the brain.
Clinical features of hyponatremia
The symptoms depend on how low the sodium falls and, more importantly, on how quickly it does so. A slow fall can be tolerated with few symptoms even at a low value, because over one to two days the brain cells adapt, unloading intracellular solutes and restoring their volume. A fast fall leaves no time for that adaptation, so the same sodium value causes far more. This is why a fall that develops within 24 to 48 hours is counted as acute.
The features run from mild to life-threatening:
- headache, fatigue, nausea, dizziness, forgetfulness, and an unsteady gait;
- confusion, lethargy, and a reduced level of consciousness;
- seizures and coma, and in the worst cases respiratory arrest and death from brain herniation.
Seizures are unusual when the sodium is above 115 mmol/L. Chronic hyponatremia is not harmless even when it looks quiet: it is associated with attention deficit and with falls, particularly in older patients, and these can improve when the sodium is corrected.
Clinical features of hypernatremia
Thirst is the main symptom, and the absence of thirst in a conscious patient with hypernatremia points either to a defective thirst mechanism or to no access to water. The remaining features are neurological and follow from brain-cell shrinkage: lethargy, weakness, irritability, confusion, neuromuscular excitability, hyperreflexia, seizures, and coma. Severe features are more likely when the sodium has risen quickly, and in adults they usually appear only above 160 mmol/L. Infants may instead show tachypnea, muscle weakness, restlessness, a high-pitched cry, and lethargy.
Hypernatremia of slow onset is tolerated better than a rapid rise of the same size, because over days the brain cells generate osmotically active solutes that raise their internal osmolality and limit the shrinkage. The same adaptation is why a high sodium that has been present for some time must not be lowered quickly.
The clinical picture therefore shows that the sodium is abnormal and how urgent it may be, but not why it is abnormal.