Water and Sodium Metabolism

Aging is associated with impaired water conservation and sodium balance--factors that determine extracellular fluid (ECF) volume and tonicity. Thirst and the secretion of antidiuretic hormone (ADH or arginine vasopressin [AVP]) control water balance. The elderly have a delayed and less intense thirst response than do younger persons. The older body tends to secrete ADH despite decreased blood tonicity (the syndrome of inappropriate ADH secretion [SIADH]), especially in a person with chronic cardiac, hepatic, or renal disease. Increased ADH concentration and secretion increase the risk of hyponatremia most intensely when fluid intake increases--a situation common with IV hydration during hospitalization or surgery.

Renal filtration of sodium and water at the glomerulus, renal tubular conservation of sodium, and renal tubular natriuretic substances (eg, atrial natriuretic peptide, renal prostaglandins) control sodium balance. These are all altered with aging (all but atrial natriuretic peptide decrease). Other factors that affect sodium balance include cardiac output, blood pressure, renal blood flow, glomerular filtration rate, and renal sympathetic nerve activity. Again, many of these parameters are altered with age and tend to be severely altered in elderly persons with coexisting cardiovascular or renal disease.

With age, total body water decreases because of an increase in fat and a decrease in lean body mass (from about 60% of body weight in healthy young adults to about 45% of body weight in the elderly). Therefore, the margin of error is reduced for maintaining normal electrolyte balance when water losses occur during acute illness due to fever, because of increased transpiration with tachypnea, or as a result of renal and GI losses.

Serum sodium concentration is determined primarily by body water balance; thus, hyponatremia usually results from excessive water retention and hypernatremia from water loss. With total body sodium and water excess, edema may result. With pure water excess, edema is not present. With a sodium and water deficit, the presentation often includes orthostatic hypotension. With a pure water deficit, vital signs do not change.

The ability to concentrate urine decreases with age in part because of tubular senescence. Many elderly persons also have resistance to the renal action of ADH, ie, a form of acquired partial nephrogenic diabetes insipidus.

The ability to decrease renal sodium excretion is impaired with age and may result partly from an age-related nephron loss, a decrease in circulating renin and aldosterone, and partly from decreased responsiveness to acute stimuli. Elderly persons with an acute illness who are not ingesting sodium develop a negative sodium balance quicker than do younger persons. In the elderly, basal blood levels of atrial natriuretic peptide are increased; atrial natriuretic peptide inhibits aldosterone secretion and may decrease aldosterone blood levels.

Dehydration and Volume Depletion

Dehydration: A decrease in total body water without an equal reduction in total body sodium. Volume depletion: A loss of body water and sodium resulting in decreased ECF volume.

Dehydration is the most common fluid and electrolyte disturbance of the elderly. A history of decreased food or fluid intake, febrile illness, polyuria, vomiting, diarrhea, chronic renal disease, diabetes mellitus, use of diuretics, or nasogastric suction is common. Other factors include impaired renal concentrating ability, reduced thirst, and impaired access to water due to neurologic or orthopedic problems or to deconditioning from medical or surgical conditions. Hot weather is a common contributing factor. Nurses can help prevent dehydration by closely monitoring fluid balance in elderly patients.

Symptoms, Signs, and Diagnosis

The patient may present with altered mental status, lethargy, light-headedness, or syncope. In general, mild dehydration produces reduced skin turgor, dry mucous membranes, and orthostatic hypotension; moderate dehydration produces these symptoms as well as oliguria or anuria, confusion, and resting hypotension; and severe hypotension produces shock or near shock. However, decreased skin turgor, dry mucous membranes, tachycardia, and orthostatic hypotension may also occur in elderly persons with normal volume status.

Increased Hct, blood urea nitrogen (BUN), and serum creatinine levels may occur. The BUN/creatinine ratio is often elevated because slow urinary flow leads to reabsorption of urea but not of creatinine. The serum sodium concentration may be high, normal, or low, depending on the cause. Urinary sodium concentration is usually < 20 mEq/L when sodium intake has been chronically reduced or when vomiting or diarrhea causes losses. A urinary sodium concentration > 20 mEq/L can occur with volume depletion. In these cases, higher concentrations occur when chronic renal disease impairs the ability to conserve sodium or the patient has been taking diuretics.

Although adrenal insufficiency is less common, it must always be considered. Hypercalcemia, hypokalemia, and hyperglycemia with consequent glycosuria leading to osmotic diuresis must be excluded as causes of the impaired renal ability to conserve water.

Treatment

It is important to estimate the fluid deficit. Elderly persons who are mildly dehydrated have lost fluid equivalent to < 5% of body weight, those moderately dehydrated have lost about 10%, and those severely dehydrated have lost >= 15%.

Mild volume depletion can be treated initially with aggressive oral fluid intake (ie, 2 to 3 L of water or clear liquids) followed by continued oral hydration. However, oral hydration may be problematic if a GI disorder or impaired mental status is present. For larger deficits, IV fluid therapy is required, usually with 0.9% sodium chloride, even if the serum sodium concentration is elevated. Free water replacement is not appropriate until the intravascular deficit has been replaced. In general, at least 50% of the loss should be replaced within the first 12 hours (about 1 L/day in nonfebrile patients). For example, in a moderately dehydrated 75-kg woman who has lost 7.5 L of fluid, an appropriate replacement rate is nearly 350 mL/h. Although such rates of replacement are sometimes frightening to clinicians, they can be given safely with adequate monitoring. Inadequate rehydration that is not accomplished quickly can lead to serious complications, including renal failure, heart attack, stroke, and rhabdomyolysis.

Although the initial rate of administration should be high enough to resolve orthostatic hypotension and tachycardia and produce adequate urine output within 24 hours, the remaining deficit should be corrected more slowly. The rate may need to be reduced to replace the calculated deficit and ongoing fluid needs over 2 to 3 days, with monitoring to avoid precipitating heart failure.

Hyponatremia

A decrease in the plasma sodium concentration <136 mEq/L caused by an excess of water relative to solute.

An age-related decrease in serum sodium concentration of 1 mEq/L/decade occurs after age 40 (from a mean value of 141 6 4 mEq/L in younger persons); however, this decrease, especially when mild, often does not produce clinically apparent symptoms. Total ECF volume may be increased, normal, or decreased with hyponatremia.

Etiology and Pathophysiology

In most cases of hyponatremia in the elderly, the concentration of sodium or any other osmotic substance in the plasma is low relative to water content (ie, is hypo-osmolar).

Dilutional hyponatremia is probably the most common type of hyponatremia in the elderly; it is often the most severe hyponatremia, resulting in the greatest morbidity and mortality in the elderly. A common cause of dilutional hyponatremia in elderly patients is the use of nutritional supplements such as Isocal, Ensure, and Osmolite, which are low in sodium. IV fluid administration of hypotonic fluids may also cause dilutional hyponatremia, especially in patients with elevated ADH levels. Primary polydipsia (excessive fluid intake in association with a neuropsychiatric disorder) occurs rarely in the elderly.

Hyponatremia with sodium depletion may occur with vomiting, diarrhea, GI suction, renal disorders, and diuretic therapy. In these cases, volume depletion stimulates ADH release so that excess water is retained in excess of sodium. Hyponatremia resulting from these events is usually mild (rarely < 125 mEq/L).

Hyponatremia in the elderly is rarely caused by the presence of osmotically active solutes in plasma, which draw intracellular water into the extracellular space to dilute the plasma sodium by the shift of water. Although rare, this disorder can occur when plasma osmolality is increased due to ingestion of toxic alcohols (eg, methanol, ethylene glycol). It can also occur when mannitol is administered.

Hyponatremia with total body sodium excess may occur with cirrhosis, nephrosis, and heart failure. These disorders are said to have ineffective circulating volume because they lead to impaired renal ability to create a dilute urine. ADH may also be elevated in these conditions.

Elderly patients with any cause of total body sodium depletion often have normal baseline serum sodium concentrations. However, when fluid intake increases (eg, when IV fluids are given or when oral intake is increased), the increase in body water may lead rapidly to hyponatremia. This condition may occur in institutionalized patients, whose fluid intake is not determined primarily by thirst but by the availability of or access to fluids or by the iatrogenic administration of fluids (as in IV fluids or tube feedings).

Symptoms, Signs, and Diagnosis

The severity of symptoms and signs depends on the degree of hyponatremia and the rapidity with which serum sodium concentration decreases. Hyponatremia is one of the most common causes of delirium in elderly patients.

Severe hyponatremia may be accompanied by depressed sensorium, depressed deep tendon reflexes, hypothermia, Cheyne-Stokes respiration, and pathologic reflexes.

Plasma osmolality should be determined. If plasma osmolality is low, the next step is to assess volume status. If hypo-osmolar hyponatremia with edema is present, the diagnosis is cirrhosis, nephrosis, or heart failure. When orthostasis is present with hypo-osmolar hyponatremia, the diagnosis is renal, adrenal, or GI disorders that lead to salt and water loss from GI fluids or urine. When neither edema nor orthostasis is present with hypo-osmolar hyponatremia, the diagnosis is pure water retention due either to excessive oral intake, IV solute administration, or SIADH. A summary of test results is presented in Table 57-1.

If plasma osmolality is normal but hyponatremia is present, the diagnosis is pseudohyponatremia, which occurs in patients with marked hyperlipidemia or hyperproteinemia. No mental status changes occur because water does not shift into the brain or other tissues. Pseudohyponatremia may occur in a patient with multiple myeloma with very high protein -globulin levels.

Treatment

Usually, restoring the serum sodium concentration to about 120 to 125 mEq/L corrects most symptoms. Both overcorrection and too-rapid correction create worsening neurologic status, which is sometimes irreversible (osmotic demyelination syndrome).

In patients with severe symptomatic hyponatremia, particularly that resulting from a dilutional state, hypertonic sodium chloride solution is infused carefully until symptoms begin to resolve and the serum sodium concentration reaches 120 mEq/L. For symptomatic hyponatremia, especially when accompanied by seizure or coma, aggressive management consists of giving 100 to 200 mL of 3% sodium chloride solution over 4 to 6 hours, along with simultaneous administration of IV furosemide. For gentler correction of the hyponatremia, 0.9% sodium chloride is given with furosemide. In addition to close monitoring of serum sodium, serum electrolytes must be measured often to allow for potassium and magnesium replacement because of the concomitant diuretic administration.

In hypo-osmolar hyponatremic patients with orthostasis (ie, sodium and ECF volume depletion), the sodium and volume deficit is corrected with 0.9% sodium chloride. Further fluid losses can be prevented with antiemetic therapy and antidiarrheal agents and by stopping diuretics. In hypo-osmolar hyponatremic patients with edema, loop diuretics (eg, furosemide) are used. When hyponatremia is dilutional, it is refractory to treatment. In asymptomatic patients with hypo-osmolar hyponatremia with neither orthostasis nor edema, water restriction of 800 to 1000 mL/day is the treatment of choice.

In patients with hyponatremia due to consumption of nutritional supplements, sodium supplementation starting with 100 mEq/L should be given daily.

In patients with hyperosmolar hypernatremia, osmotically active molecules need to be reduced (eg, through insulin administration to lower hyperglycemia or through urinary elimination or dialysis to eliminate the toxic alcohol).

Management of chronic hyponatremia usually includes restriction of fluid intake (usually 1000 to 1500 mL/day) to maintain a serum sodium concentration > 130 mEq/L. In more refractory or severe cases of chronic dilutional hyponatremia, furosemide may be given along with sodium chloride tablets and restriction of free water. Demeclocycline 600 mg to 1200 mg/day po can induce mild nephrogenic diabetes insipidus with polyuria of 2 to 4 L/24 hours. Patients receiving demeclocycline require close monitoring of fluid balance to avoid excessive fluid loss, elevated serum BUN levels, and drug-induced tubular necrosis.

Patients with pseudohyponatremia require no treatment.

Hypernatremia

An elevation in the plasma sodium concentration > 146 mEq/L caused by a deficit of water relative to solute; total body sodium content is usually normal or nearly normal.

Excessive loss of body water relative to the loss of sodium underlies hypernatremia (see Table 57-2). The prevalence of hypernatremia is about 1% in elderly hospitalized patients and in residents of long-term care facilities. Lower body weight is a risk factor in the elderly. Mortality rate is about 40% in the elderly hospitalized patient and is highest in patients with a rapid onset and in those with serum sodium concentrations >160 mEq/L.

Symptoms and Signs

The symptoms of moderate hypernatremia may be nonspecific; weakness and lethargy are common. More severe hypernatremia (serum sodium concentrations > 152 mEq/L) may cause a focal neurologic deficit (eg, hemiparesis), severe obtundation, stupor, coma, and seizures. CNS manifestations are common and often lead to a depressed sensorium and chronic functional decline in patients who survive the acute episode. Because hypernatremia represents a pure water loss, the signs of volume depletion (eg, decreased skin turgor, dry mucous membranes, orthostatic hypotension) are absent.

In addition to an increased serum sodium concentration, laboratory findings include increased Hct, serum osmolality, BUN, and creatinine levels. Urine osmolality may not be greatly increased because renal ability to concentrate urine is impaired with age.

Treatment

Body water deficits are replaced with hypotonic fluid. A simple way of estimating the deficit is by using the rule of 7's: for every 10 mEq/L the serum sodium is elevated, a 7% deficit of total body water exists.

Either 0.45% sodium chloride solution or 5% dextrose in water should be given at a rate that corrects the water deficit in about 48 hours. The serum sodium concentration should be lowered by <= 2 mEq/L/h. Excessively rapid correction may lead to cerebral edema with permanent brain damage or death. In the elderly patient with coexisting cardiac disease, caution and close monitoring (checking every few hours for symptoms and signs of heart failure) are needed to avoid heart failure from too-rapid administration of hypotonic IV solutions. When the cause of hypernatremia (eg, diabetes insipidus, diuretic therapy, increased sodium intake) is identified, specific treatment should be implemented to correct the cause.