Hyponatremia is relatively common in hospitalized patients. It occurs when an imbalance between the intake and excretion of water results in excess water relative to sodium. This imbalance may be the consequence of impaired water excretion or fluid intake that exceeds the excretory capacity of the kidneys (as in primary polydipsia6 or iatrogenic administration7).
Water excretion may be deficient because of renal dysfunction, or it may be inhibited by the persistent release of ADH induced by volume depletion or the secretion of inappropriate ADH. The of inappropriate secretion of antidiuretic hormone (SIADH) has many possible causes:8,9
Hyponatremia may also be seen in cerebral or renal salt-wasting conditions. Sodium depletion from the kidneys is associated with adrenal insufficiency (Addison’s disease) and the use of thiazide diuretics. Extrarenal sodium loss occurs with vomiting, diarrhea, or third-spacing. Other causes of hyponatremia are hypothyroidism, hyperlipidemia and hyperproteinemia (in which serum osmolality is normal), and hyperglycemia (in which the serum is hyperosmolar).
Because acute hyponatremia causes plasma osmolality to fall, water moves into cells to maintain osmotic equilibrium between the extracellular and intracellular fluid. In the brain, water entry into neurons results in cerebral edema. Consequently, the symptoms of acute hyponatremia are predominantly neurological and parallel the severity of cerebral edema.10
In one retrospective series, hyponatremia was the cause of seizures in 70% of infants younger than 6 months who lacked other findings suggesting a cause.13
Coma and respiratory arrest may occur if the plasma sodium concentration rapidly falls below 115 to 120 meq/L.14 The associated mortality rate can be over 50%10 and survivors risk permanent neurological damage.
The diagnostic evaluation of hyponatremia requires a search for causes of water retention, sodium loss, or both. Besides serum sodium concentration, other key laboratory studies are the plasma osmolality, the urine osmolality, and the urine sodium concentration. If plasma osmolality is low, the urine osmolality can be used to distinguish between impaired water excretion (inappropriately high urine osmolality) and primary polydipsia (appropriately low urine osmolality). SIADH is confirmed by inappropriately elevated urine osmolality (often above 300 mOsm/kg) and urine sodium concentration (usually above 40 mEq/liter).
Other tests that may be indicated are plasma creatinine concentration to evaluate for renal dysfunction, and assays of adrenal and thyroid function to rule out an endocrinopathy.
The treatment of hyponatremia should be guided by the clinical setting. Patients with chronic hyponatremia require no specific therapy other than restricting water intake. Rapid sodium correction in patients with chronic asymptomatic hyponatremia may be hazardous.15 Water restriction to below the level of water output is the primary therapy for chronic hyponatremia associated with:
If fluid must be given to patients with SIADH, then the osmolality of the administered fluid must exceed the osmolality of the urine. Otherwise, the hyponatremia may worsen. Consequently, isotonic saline has a limited role in the correction of the hyponatremia, because the urine osmolality in SIADH is usually above 300 mOsm/kg.
Because of the high associated mortality, acute hyponatremia represents a medical emergency. Isotonic saline should be administered to patients with true volume depletion, diuretic therapy, or adrenal insufficiency, in which cortisol replacement is also indicated. Although sodium concentrations should generally not be increased faster than 1.5–2.0 mmol/liter per hour or 12 mmol/liter per day,16,17 higher correction rates have been well tolerated in children.18 The risks of fast correction are central pontine and extrapontine myelinolysis, characterized by spastic quadriparesis, pseudobulbar palsy, and an encephalopathy ranging from confusion to coma.15–17,19
Adapted from: Schachter SC and Lopez MR. Metabolic disorders. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;195–208.
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