Hypernatremia

Definition

The normal concentration of sodium in the blood plasma is 136-145 mM. Hypernatremia is defined as a serum sodium level over 145 mM. Severe hypernatremia, with serum sodium above 152 mM, can result in seizures and death.

Description

Sodium is an atom, or ion, that carries a single positive charge. The sodium ion may be abbreviated as Na⁺ or as simply Na. Sodium can occur as a salt in a crystalline solid. Sodium chloride (NaCl), sodium phosphate (Na₂HPO₄) and sodium bicarbonate (NaHCO₃) are commonly occurring salts. These salts can be dissolved in water or in juices of various foods. Dissolving involves the complete separation of ions, such as sodium and chloride in common table salt (NaCl).

About 40% of the body's sodium is contained in bone. Approximately 2-5% occurs within organs and cells and the remaining 55% is in blood plasma and other extracellular fluids. The amount of sodium in blood plasma is typically 140 mM, a much higher amount than is found in intracellular sodium (about 5 mM). This asymmetric distribution of sodium ions is essential for human life. It makes possible proper nerve conduction, the passage of various nutrients into cells, and the maintenance of blood pressure.

The body continually regulates its handling of sodium. When dietary sodium is too high or low, the intestines and kidneys respond to adjust concentrations to normal. During the course of a day, the intestines absorb dietary sodium while the kidneys excrete a nearly equal amount of sodium into the urine. If a low sodium diet is consumed, the intestines increase their efficiency of sodium absorption, and the kidneys reduce its release into urine.

The concentration of sodium in the blood plasma depends on two things: the total amount of sodium and water in arteries, veins, and capillaries (the circulatory system). The body uses separate mechanisms to regulate sodium and water, but they work together to correct blood pressure when it is too high or too low. Too high a concentration of sodium, or hypernatremia, can be corrected either by decreasing sodium or by increasing body water. The existence of separate mechanisms that regulate sodium concentration account for the fact that there are numerous diseases that can cause hypernatremia, including diseases of the kidney, pituitary gland, and hypothalamus.

Causes and symptoms

Vasopressin, also called anti-diuretic hormone, is made by the hypothalamus and released by the pituitary gland into the bloodstream. There it travels to the kidney where it reduces the release of water into the urine. With less vasopressin production, the body fails to conserve water, and the result is a trend toward higher plasma sodium concentrations. Hypernatremia may occur in diabetes insipidus, a disease that causes excessive urine production. (It is not the same disease as diabetes mellitus, a disease resulting from impaired insulin production.) The defect involves either the failure of the hypothalamus to make vasopressin or the failure of the kidney to respond to vasopressin. In either case, the kidney is able to conserve and regulate the body's sodium levels, but is unable to conserve and retain the body's water. Hypernatremia does not occur in diabetes insipidus if the patient is able to drink enough water to keep up with urinary loss, which may be as high as 10 liters per day.

Hypernatremia may occur in unconscious (or comatose) patients due to the inability to drink water. Water is continually lost by evaporation from the lungs and in the urine. If the patient is not given water via infusion, the sodium concentration in the blood may increase and hypernatremia could develop. Hypernatremia can also occur in rare diseases in which the thirst impulse is impaired.

Hypernatremia can also occur accidentally in the hospital when patients are infused with solutions containing sodium, such as sodium bicarbonate for the treatment of acidosis (acidic blood). It can also be accidentally induced with sodium chloride infusions, especially in elderly patients with impaired kidney function.

Hypernatremia can cause neurological damage due to shrinkage of brain cells. Neurological symptoms include confusion, coma, paralysis of the lung muscles, and death. The severity of the symptoms is related to how rapidly the hypernatremia developed. Hypernatremia that comes on rapidly does not allow the cells of the brain time to adapt to their new high-sodium environment. Hypernatremia is especially dangerous for children and the elderly.

Diagnosis

Hypernatremia is diagnosed by acquiring a blood sample, preparing plasma, and using a sodium-sensitive electrode for measuring the concentration of sodium ions.

Treatment

Hypernatremia is treated with infusions of a solution of water containing 0.9% sodium chloride (0.9 grams NaCl/100 ml water), which is the normal concentration of sodium chloride in the blood plasma. The infusion is performed over many hours or days to prevent abrupt and dangerous changes in brain cell volume. In emergencies, such as when hypernatremia is causing neurological symptoms, infusions may be conducted with salt solutions containing 0.45% sodium chloride, which is half the normal physiologic level.

Prognosis

The prognosis for treating hypernatremia is excellent, except if neurological symptoms are severe or if overly rapid attempts are made to treat and reverse the condition.

Prevention

Hypernatremia occurs only in unusual circumstances that are not normally under a person's control.

Key Terms

Blood plasma and serum

Blood plasma, or plasma, is prepared by obtaining a sample of blood and removing the blood cells. The red blood cells and white blood cells are removed by spinning with a centrifuge. Chemicals are added to prevent the blood's natural tendency clot. If these chemicals include sodium, then a false measurement of plasma sodium content will result. Serum is prepared by obtaining a blood sample, allowing formation of the blood clot, and removing the clot using a centrifuge. Both plasma and serum are light yellow in color.

For Your Information

Books

• Harrison's Principles of Internal Medicine. Ed. Anthony S. Fauci, et al. New York: McGraw-Hill, 1997.

Periodicals

• Fried, L. F., and P. M. Palevsky. "Hyponatremia and hypernatremia." Medical Clinics of North America 81 (1997): 585-609.

• Frizzell, R. T., et al. "Hyponatremia and ultramarathon running." Journal of the American Medical Association 255 (1986): 772-774.

Source: Gale Encyclopedia of Medicine, Published December, 2002 by the Gale Group

The Essay Author is Tom Brody PhD.

Return to the previous page

Search