As plasma sodium concentrations rise in healthy subjects, thirst is stimulated and eventually quenched, and ADH is released. Both actions lower the plasma sodium concentration back to normal. Hypernatremia, a relative deficit of water to sodium solute, may occur in patients who do not respond to thirst by drinking fluids. Infants, confused adults, and the elderly are at particularly high risk.20
Other causes of hypernatremia are:
Generalized tonic-clonic seizures, particularly those that result in lactic acidosis, may transiently elevate serum sodium. Intracellular glycogen is metabolized to lactate in muscles during seizures. Intracellular osmolality increases, because lactate is more osmotically active than glycogen. As a result, water moves into cells, causing hypernatremia. Sodium concentrations normalize within 5 to 15 minutes after the cessation of exertion.
The rise in plasma sodium concentration and therefore plasma osmolality causes acute water movement out of brain cells. Consequently, the symptoms of hypernatremia are primarily neurologic and are related to the severity of the hypernatremia and the rapidity with which it develops.21 As brain volume decreases, there may be rupture of cerebral veins, focal intracerebral and subarachnoid hemorrhages, and irreversible neuronal damage.21,22 If hypernatremia is untreated, lethargy, weakness, and irritability progress to twitching, seizures, coma, and death, especially with severe hypernatremia.23
The cause of hypernatremia is usually apparent from the history of the patient and can be confirmed by measuring urine osmolality.21 If urine osmolality exceeds 700–800 mOsm/kg, then both hypothalamic and renal function are intact, and the hypernatremia is likely due to incompletely replaced insensible or gastrointestinal fluid losses, sodium overload, or insufficient oral water intake.
These possible causes can be distinguished by measuring the urine sodium concentration:
Plasma osmolality that exceeds urine osmolality is consistent with diabetes insipidus, either central (i.e., ADH is deficient) or nephrogenic (i.e., the kidney resists the action of ADH). The site of the problem can be determined by administering exogenous ADH. If the disorder is central, the urine osmolality rises by 50% or more. If it is nephrogenic, there is no response.21 Nephrogenic diabetes insipidus in adults is associated with chronic lithium use and hypercalcemia.
Patients with chronic hypernatremia are generally asymptomatic. Lowering their plasma sodium concentrations too rapidly can be dangerous because of the possibility of inducing cerebral edema.25
In patients with hypernatremia caused by water loss or inadequate fluid intake, 120 mL of free water per hour should be administered orally or intravenously, while carefully monitoring the plasma and urine sodium concentrations, as well as central venous pressure when necessary.23
In patients with diabetes insipidus, the goals of therapy are to decrease the urine output and give specific therapy for the underlying cause.
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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