A large part of an individual's body weight is made up of water and chemicals (e.g., sodium, potassium, and chloride), which are called electrolytes. Although the proportions of these electrolytes are tightly regulated throughout life, as people age the relative amount of body weight made up by water changes. In the normal young adult, the capacity of the kidney to regulate fluid and electrolyte balance far exceeds the ordinary demands for conservation and excretion. Even when this capacity is substantially reduced in old age, renal function allows adequate regulation of the volume and composition of the body's fluids under most normal conditions. Inability to maintain normal fluid volumes and electrolyte concentrations is generally due to causes (defects) outside the kidney necessary for their regulation (homeostasis) rather than to insufficient kidney function.
Dehydration, by definition, means a decrease in total body water. Sodium is the primary electrolyte outside the cell (extracellular). This electrolyte has a positive charge (cation) that must be matched to a negatively charged electrolyte (anion), for example, chloride or bicarbonate, and is responsible for maintaining the state of hydration outside the cell. Dehydration may develop from a primary loss of water (insufficient intake of water, excessive sweating, vomiting or diarrhea, or an inability to concentrate the urine), in which case the concentration of sodium in the blood (serum) increases (hypernatremia). Dehydration also may occur when one loses salt (sodium chloride) with its obligated water. This can occur with excessive intestinal and urinary losses containing salt, certain hormone (adrenal) insufficiencies, and with excessive use of diuretic medications. Individuals with this condition become volume depleted, but maintain normal serum sodium concentrations (136–144 mEq/L) until blood volume becomes sufficiently depleted that antidiuretic hormone (ADH) release from the pituitary gland is stimulated. ADH is the hormone primarily responsible for reducing urine volume to conserve water, and for turning a dilute urine into a concentrated urine. If fluid is then replaced, water is retained and the concentration of sodium in the blood falls (hyponatremia).
Older persons are more prone to the development of dehydration. This dehydration is due to a combination of three factors. First, there is an inability of the kidney to conserve sodium when challenged by inadequate intake or excessive losses elsewhere. Second, there is an inability to concentrate the urine as well when similarly challenged by fluid loss. Finally and most importantly, the older person loses normal thirst. Whereas a young person becomes acutely thirsty when dehydrated and drinks to correct for the water loss, an older person often is not similarly motivated. If this becomes severe enough, especially in those with cerebrovascular disease, ingestion of a prescribed amount of water (generally 1–2 quarts) each day may become necessary to prevent recurrent dehydration. Dehydration is most likely to occur after hospital admission for acute illness, for example, infection or emergency surgery, when fluid replacement is often insufficient. Overhydration occurs when an individual retains too much salt and water. This results in edema that can be identified by applying pressure over the shin and creating an indentation that does not quickly return to normal. Usually salt and water are retained in proportionate amounts so serum sodium concentration remains normal. Olderpersons lose the ability to excrete in the urine large amounts of salt.
Older persons also are more prone to the development of low levels of sodium. This can be seen with a decreased (contracted) volume outside the cells (extracellular fluid volume) due to salt depletion followed by stimulation of ADH release to retain water and dilute the blood as described above. Sometimes it is due to dilution, when extracellular fluid volume becomes increased due to an inability to excrete water normally. This is seen with congestive heart failure, and end-stage kidney or liver failure, and is characterized by swelling of the legs (edema) and abdomen (ascites). Most commonly, it is seen when ADH continues to be secreted when the normal stimuli are no longer present. This causes retention of water that, in turn, causes dilution of sodium in the blood. The normal stimuli to secretion of ADH are either a decrease in blood (extracellular fluid) volume, or an increase in the concentration of sodium or solute (osmolality) in the blood. When high levels of ADH persist in the presence of both an increased volume and low concentrations of sodium or solute (both of which should shut off ADH), this is referred to as the syndrome of inappropriate antidiuretic hormone (SIADH). This is often due to pain, but can be due to a tumor (most commonly lung) that independently makes the hormone or something that acts like the hormone; failure of the receptors in the left side of the heart to get the message that blood volume is sufficient, for example, poor blood flow through the lungs due to tuberculosis or pneumonia; or pathology in the brain that abnormally stimulates the release of the hormone. In some cases, generally very old and frail elders, the cause remains unknown (idiopathic). Older persons secrete more ADH in response to any given increase in serum osmolality than younger persons, perhaps helping to explain the greater propensity of older persons to develop hyponatremia. Symptoms consisting of confusion and lethargy progressing to coma and seizures are caused by brain swelling. One can treat this condition with water restriction, or with drugs that interfere with the ability to concentrate the urine (furosemide, lithium, declomycin).
Potassium is the primary cation inside the cell with only 2 percent of total body potassium found outside the cell. Because there is a steep concentration gradient for potassium between inside and outside the cell, the serum concentration (normally between 3.5 and 5.0 mEq/L) is not always an accurate measure of potassium in the body. However, the serum potassium concentration usually determines whether or not there are going to be problems with a deficit or excess of this electrolyte in the body. Low serum potassium concentrations (hypokalemia) can be due to inadequate intake, losses from the intestine (vomiting, diarrhea), or losses from the kidney (renal and adrenal causes). The most common cause is diuretic therapy, but also common in the elderly is excessive use of enemas and purgatives, often overlooked unless the individual is specifically questioned about this. Muscular weakness and pain (cramps) can be early symptoms. Potassium replacement is available in a variety of powder, liquid, and pill forms, but requires a physician's prescription to avoid potentially lethal complications from overdosage.
A high serum potassium concentration (hyperkalemia) can be caused by excessive intake, release of potassium from cells due to tissue breakdown (catabolism), inability of the kidney to excrete potassium, or often a combination of factors. Older persons are much more likely to develop hyperkalemia than younger persons for several reasons. First, they are more likely to have impaired kidney function limiting their ability to excrete potassium in the urine. Second, they secrete less of the adrenal hormone aldosterone into the circulation. This is the hormone that aids secretion of potassium into the urine. A number of medications commonly used by elders (potassium-sparing diuretics; beta-adrenergic blocking agents; nonsteroidal anti-inflammatory agents, or NSAIDs; and angiotensin converting enzyme (ACE) inhibitors) also impair the ability of the kidney to excrete potassium. The symptoms of hyperkalemia are very subtle (anxiety, restlessness, apprehension, weakness), and may precede potentially lethal cardiac arrythymias only briefly, making it important to check serum potassium concentrations periodically if risk is present, for example, during potassium replacement therapy.
Other important electrolytes in the blood and body include calcium and magnesium, both of which can cause symptoms when present in deficient or excessive amounts.
ROBERT D. LINDEMAN
LINDEMAN, R. D. "Renal and Electrolyte Disorders." In Practice of Geriatrics, 3d ed. Edited by E. H. Duthie, Jr. and P. R. Katz. Philadelphia: W. B. Saunders Co., 1998. Pages 546–561.
ZAWADA, E. T., JR. "Disorders of Water and Electrolyte Balance." In The Merck Manual of Geriatrics, 3d ed. Edited by M. H. Beersand and R. Berkow. Whitehouse Station, N.J.: Merck Research Laboratories, 2000. Pages 561–571.
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