Clinical Information

Sodium is the primary extracellular cation. Sodium is responsible for almost one-half the osmolality of the plasma and, therefore, plays a central role in maintaining the normal distribution of water and the osmotic pressure in the extracellular fluid compartment. The amount of sodium in the body is a reflection of the balance between sodium intake and output.

Hyponatremia (low sodium) is a predictable consequence of decreased intake of sodium, particularly that precipitated or complicated by unusual losses of sodium from the gastrointestinal tract (eg, vomiting and diarrhea), kidneys, or sweat glands. Renal loss may be caused by inappropriate choice, dose, or use of diuretics; by primary or secondary deficiency of aldosterone and other mineralocorticoids; or by severe polyuria. It is common in metabolic acidosis. Hyponatremia also occurs in nephrotic syndrome, hypoproteinemia, primary and secondary adrenocortical insufficiency, and congestive heart failure. Symptoms of hyponatremia are a result of brain swelling and range from weakness to seizures, coma, and death.

Hypernatremia (high sodium) is often attributable to excessive loss of sodium-poor body fluids. Hypernatremia is often associated with hypercalcemia and hypokalemia and is seen in liver disease, cardiac failure, pregnancy, burns, and osmotic diuresis. Other causes include decreased production of antidiuretic hormone (ADH; also known as vasopressin) or decreased tubular sensitivity to the hormone (ie, diabetes insipidus), inappropriate forms of parenteral therapy with saline solutions, or high salt intake without corresponding intake of water. Hypernatremia occurs in dehydration, increased renal sodium conservation in hyperaldosteronism, Cushing syndrome, and diabetic acidosis. Severe hypernatremia may be associated with volume contraction, lactic acidosis, and increased hematocrit. Symptoms of hypernatremia range from thirst to confusion, irritability, seizures, coma, and death.