Electrolyte, acid-base balance; water balance; water intoxication; diagnose dehydration.
Hypernatremia occurs in dehydration. For instance, nasogastric protein feeding with insufficient fluids may cause hypernatremia. Hypernatremia without obvious cause may relate to Cushing syndrome, central or nephrogenic diabetes insipidus with insufficient fluids, primary aldosteronism, and other diseases. Severe hypernatremia may be associated with volume contraction, lactic acidosis, azotemia, weight loss, and increased hematocrit as evidence of dehydration. The corrected serum sodium is often high in nonketotic hyperosmolar coma. (A corrected Na+ is calculated by increasing Na+ by 1.3−1.6 mmol/L for each 100 mg/dL increment in serum or plasma glucose). 100 mg equals 5.56 mmol/L. The corrected serum sodium level calculated in nonketotic hyperosmolar coma: apparent mild hyponatremia with very high glucose may actually mean (corrected) hypernatremia.1
Hyponatremia occurs with nephrotic syndrome, cachexia, hypoproteinemia, intravenous glucose infusion, in congestive heart failure, and other clinical entities. Serum sodium is a predictor of cardiovascular mortality in patients in severe congestive heart failure.2
Hyponatremia without congestive failure or dehydration may occur with hypothyroidism, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), renal failure, or renal sodium loss.
The differential diagnosis of hyponatremia includes Addison disease, hypopituitarism, liver disease including cirrhosis, hypertriglyceridemia, and psychogenic polydipsia. Diuretics and other drugs may cause hyponatremia. Sodium decreasing to levels <115 mmol/L can lead to significant neurological dysfunction with cerebral edema and increased intracranial pressure.
The differential diagnosis of hyponatremia includes determination of urine sodium and osmolality and serum urea nitrogen (BUN). BUN is often decreased in SIADH.