Health Articles

Metabolic alkalosis is a primary increase in blood HCO3 ; pH and carbon dioxide content are increased. Acid loss can result from vomiting, prolonged gastric suctioning, and diuretic-induced renal potassium loss. Alkalosis can also result from increased renal bicarbonate reab-sorption in the proximal tubule as a consequence of plasma volume contraction and primary or secondary aldosteronism. Potassium depletion further enhances the renal tubular reabsorption of bicarbonate stimulated by volume contraction. Metabolic alkalosis may also develop in patients who have respiratory failure and hypercapnia after mechanical ventilation therapy.
The goal of therapy is to eliminate the factors maintaining the alkalosis. Plasma volume expansion with 0.9% sodium chloride solution should be initiated, and potassium deficits should be corrected. Acetazolamide 500 to 1000 mg/day given orally in divided doses may help in chronic alkalosis.

Metabolic acidosis is a primary decrease in ECF HCO3 ; pH and carbon dioxide content are decreased. Metabolic acidosis with no increase in the anion gap (normal 8 to 15 mEq) can result from renal tubular acidosis or from a loss of bicarbonate or organic acid anions in patients with diarrhea; the condition is characterized by hyperchloremia. Acidosis with an increased anion gap (such as occurs with lactic acidosis, diabetic ketoacidosis, salicylate toxicity, and renal failure) is more common.
The history; physical examination findings such as hyperpnea; and laboratory measurements such as blood gas determinations, urine pH, and BUN, creatinine, blood glucose, and ketone levels usually establish the diagnosis and point to the underlying disease process. A urine pH > 5.5 with metabolic acidosis occurs in renal tubular acidosis.
Initial treatment is directed toward correcting the underlying disease process. When severe acidosis (pH < 7.2) is accompanied by symptoms such as anorexia, nausea, lethargy, and hyperventilation, treatment should be started with IV sodium bicarbonate. The sodium bicarbonate requirement can be estimated with this formula: mEq of sodium HCO3_ required = (HCO3~ desired - HCO3″” observed) x 40% body weight in kilograms. Acute complete correction of arterial pH is not a goal of therapy, and caution must be used to avoid volume and sodium overload.

The pH of the ECF (normal range 7.35 to 7.45) is unaffected by normal aging, although age-associated changes do occur in certain respiratory and renal regulatory processes involved in maintaining a normal pH. Thus, the ability to respond to a challenge may be limited. For example, the ability to hyperventilate in response to acute metabolic acidosis may be blunted, leading to a further decline in pH. The aging kidney is slower to respond to an acid load, so that the blood pH may recover more slowly. Many disorders common in the elderly can overwhelm the regulatory systems and contribute to acid-base disturbances. Such disorders include heart failure, anemia, sepsis, renal disease, pulmonary disease, and diabetes mellitus. Also, many common drugs—including salicylates, diuretics, and laxatives—may precipitate acid-base disturbances.
The combination of impaired homeostatic mechanisms and the high prevalence of drug use and disease in the elderly make disturbances of acid-base balance common. Metabolic and respiratory acidosis and alkalosis can occur as simple disorders or, frequently in the elderly, as mixed disorders. For example, metabolic acidosis with concomitant respiratory acidosis can occur with heart failure, pneumonia, and acute respiratory failure. Similarly, a patient with heart failure may have a metabolic acidosis from poor tissue perfusion and a metabolic alkalosis from diuretic therapy. In general, changes in serum bicarbonate (HCO3~) concentration reflect metabolic acidosis or alkalosis, and PaCO2 changes reflect respiratory acidosis and alkalosis. Characteriz inn the disturbance requires measurements of arterial pH, PaO2, and I’;Ko.’ aloiiK with serum electrolyte, BUN, and creatinine levels. Urinary electrolyte levels and pH may also be helpful.

A serum potassium level of>5 mEqIL. Total body potassium is normal, but distribution between intracellular and extracellular compartments is abnormal.
Etiology
An elevated serum potassium level may result from pseudohyper-kalemia caused by hemolysis or the release of potassium from platelets during sample storage. Platelets are rich in potassium, and with thrombocytosis, enough potassium may be released during the clotting process to raise serum levels above normal. However, plasma potassium levels remain normal.
Noi inally, potassium from excessive intake is excreted in the urine. Only m patients with renal disease or impaired tubular function does excessive intake lead to hyperkalemia. Patients with acute oliguric renal lailui e are at especially high risk. Chronic renal disease with hyperkalemia may result from hyporeninemic hyperaldosteronism, particularly in patients with diabetes mellitus. The possibility of primary or secondary adrenal insufficiency must also be considered. Active GI bleeding, especially in a patient with a reduced glomerular filtration rate, can also lead to hyperkalemia.
In the elderly, hyperkalemia can be caused by several common medications, including potassium-sparing diuretics (triamterene, amiloride, and spironolactone) and nonsteroidal anti-inflammatory drugs. Angiotensin converting enzyme inhibitors and β-adrenergic blockers, which interfere with potassium excretion, can also cause hyperkalemia. A relatively small shift of potassium from the intracellular compartment to the extracellular compartment can result in marked hyperkalemia. This may occur in metabolic acidosis, especially diabetic ketoacidosis. Rhabdomyolysis from trauma can also shift potassium into the ECF.
Symptoms and Signs
Hyperkalemia may be asymptomatic until evidence of cardiac toxicity develops. Initial ECG changes—shortened QTC interval and tall, narrow I waves—usually signify a serum potassium level of > 5.5 mKq/L. A further rise in the serum potassium level causes nodal and ventricular arrhythmias along with widened QRS complexes and prolonged PR intervals. Ultimately, ventricular fibrillation or asystole can develop.
Nonspecific neuromuscular symptoms, including vague weakness and paresthesias, may occur. With severe hyperkalemia, flaccid paralysis may occur.
Treatment
In patients with mild hyperkalemia (5.0 to 5.5 mEq/L), decreasing potassium intake to 40 to 60 mEq/day may correct the serum values. Potentially causative drugs and foods should be discontinued. If the patient has chronic renal disease or another clinical disorder in which hypoaldosteronism is a suspected cause, trial therapy with fludrocortisone acetate 0.05 to 0.2 mg/day may produce a normal serum potassium level in several days.
A patient with moderate hyperkalemia (5.5 to 6.0 mEq/L) and no significant ECG changes can be given the ion exchange resin sodium polystyrene sulfonate 15 to 20 gm orally. Administering 30 mL of a 50% solution of sorbitol orally enhances the effectiveness of the sodium polystyrene sulfonate and prevents constipation. If oral intake is not possible, sodium polystyrene sulfonate can be given as a retention enema of 50 to 60 gm in 200 mL of tap water at 4-h to 6-h intervals. Furosemide in doses of 40 to 100 mg IV may also help by rapidly in creasing potassium excretion in the urine. Intravascular volume repletion with 0.9% sodium chloride is essential in ensuring the maximum renal capacity for excreting potassium.
Severe hyperkalemia (> 6.0 mEqlL) or a rising serum potassium level in a patient with renal insufficiency warrants prompt, aggressive therapy and may constitute a medical emergency. The first priority is to reverse cardiac toxicity. Thus, if an atrioventricular block or changes in the QRS complex or P wave appear on the ECG, 10 to 20 mL of 10% calcium gluconate should be given IV along with 50 to 100 mL of 7.5% sodium bicarbonate solution. Calcium gluconate must be given cautiously to patients receiving digitalis preparations. An infusion of 100 to 300 mL of 50% glucose containing 1 u. of regular insulin per 3 gm of glucose given over 30 min will shift potassium to the intracellular space. Sodium polystyrene sulfonate and sorbitol in the doses described above will facilitate potassium excretion. If these emergency measures do not adequately control severe hyperkalemia, hemodialysis should be initiated promptly.

A serum potassium level of< 3.5 mEqlL. Total be normal or decreased.

Etiology
Common in the elderly, hypokalemia can result from decreased dietary intake of potassium, increased renal or GI losses caused by diseases of these organs, use of drugs that interfere with normal regulatory mechanisms, and excessive mineralocorticoid or glucocorticoid levels (see TABLE 3-4). Hypokalemia may also result when potassium shifts from the ECF into the cells, as may occur in response to alkalosis, insulin administration, or use of β-adrenergic agonists. In diabetic acidosis, potassium shifts from the intracellular compartment to the extracellular compartment and is subsequently excreted in the urine. The resulting potassium depletion is usually masked by the intercompartmental shift, so that when the acidosis is corrected by insulin administration and fluid deficits are corrected, marked hypokalemia may occur.
One of the most common causes of hypokalemia is treatment with thiazide or loop diuretics. About 20% of patients receiving thiazide diuretics develop hypokalemia, but serum potassium levels rarely fall below 3 mEq/L.
Symptoms and Signs
Common symptoms of hypokalemia in the elderly are fatigue, confusion, and muscle weakness and cramps from impaired skeletal muscle function. Severe hypokalemia (< 2.5 mEq/L) can result in frank paralysis, as occurs in periodic paralysis. Smooth muscle function of the GI tract can also be affected, leading to adynamic ileus.
Potassium deficiency can affect cardiac function, resulting in atrial and ventricular ectopic beats, atrial and ventricular tachycardia, ventricular fibrillation, and sudden death—particularly in patients who have preexisting heart disease or those taking digitalis preparations.
The ECG often shows ST segment depression, T wave flattening, and a prominent U wave. With severe potassium depletion, atrioventricular conduction disturbances can develop.
Polyuria and secondary polydipsia can result from hypokalemic nephropathy, which is characterized by a vasopressin-resistant impairment in urinary concentrating capacity that makes the isotonicity of urine about that of plasma. Potassium depletion increases renal ammonia synthesis and acid excretion, resulting in metabolic alkalosis and elevated serum bicarbonate levels. Hypokalemia can impair insulin secretion without altering peripheral glucose use. Thus, about 33% of patients receiving long-term thiazide therapy develop glucose intolerance, most likely from hypokalemia. However, overt diabetes mellitus is uncommon.
Treatment
Treatment consists of correcting the underlying cause if possible, correcting total body deficits, and restoring normal serum potassium levels. When no cause (ie, use of a diuretic or chronic diarrhea) is apparent, measuring urinary potassium excretion helps establish whether urinary loss is abnormal. In a patient with hypokalemia, urinary excretion of > 20 mEq/L suggests an excessive urinary loss.
When urgent treatment is not required, potassium chloride 10 to 15 mEq orally q 4 to 8 h should be given until the serum potassium level is normal. Using timed-release preparations decreases local exposure of the GI mucosa to high concentrations of potassium and thus reduces the risk of irritation and ulceration. If hypokalemia is caused by a thiazide diuretic, adding a potassium-sparing agent such as triamterene, amiloride, or spironolactone may maintain normal blood potassium levels once the deficit has been corrected. Magnesium depletion may need to be corrected before hypokalemia responds to treatment. In patients with severe diarrhea or ureteral diversions such as an ileal bladder, hypokalemia may be accompanied by a hyperchloremic metabolic acidosis. In such cases, potassium replacement should be accomplished with potassium bicarbonate.
When urgent treatment is needed (ie, when the patient has serious symptoms or an arrhythmia), potassium chloride should be given IV. The potassium concentration in the IV fluid usually should not exceed 40 mEq/L, and the administration rate should not exceed 10 to 20 mEq/h with a total dose of 100 to 300 mEq/24 h. In rare emergencies when a patient has a serious cardiac arrhythmia and the serum potassium level is < 2 mEq/L, the infusion can be given in a concentration of 60 mEq/L at a rate up to 40 mEq/h. Such therapy should be given for only a few hours and requires continuous ECG monitoring and frequent measurement of serum potassium levels.

sipidus or with acquired vasopressin resistance resulting from chronic renal disease, hypercalcemia, or hypokalemia. Excessive water depletion commonly results from potent loop diuretics.
Occasionally, hypernatremia occurs without accompanying dehydration because of a high sodium intake. This may occur after sodium bicarbonate administration for cardiac arrest or metabolic acidosis or after an infusion of 0.9% sodium chloride solution for fluid loss or shock.
Symptoms and Signs
The symptoms of moderate hypernatremia may be nonspecific; weakness and lethargy are common. More severe hypernatremia (serum sodium levels > 152 mEq/L) may be accompanied by obtundation, stupor, coma, and seizures. The clinical signs are those of volume depletion and dehydration—weight loss, decreased skin turgor, dry mucous membranes, and orthostatic hypotension. Besides an increased serum sodium level, the laboratory findings are those of hemoconcen-tration—increased hematocrit, serum osmolality, BUN, and creatinine values. Urine osmolality may not be greatly increased because of age-associated impairment in renal concentrating capacity.
Normal total body stores of potassium are about 3500 to 4000 mEq, most of which is within the cells, where levels range from 120 to 160 mEq/L. Only about 2% of total body potassium is in the ECF, where levels are 4 to 5 mEq/L. Thus, a serum potassium measurement is often inadequate for estimating total body potassium. However, small shifts of potassium between the extracellular and intracellular compartments can have profound effects on the serum potassium level with marked functional consequences.
Several homeostatic mechanisms help maintain serum potassium levels within a relatively narrow range. The usual dietary intake of potassium is 70 to 100 mEq/day, of which about 90% is taken up into the ECF7 and subsequently excreted by the kidney. The kidney can respond to variations in dietary potassium intake because most is filtered at the glomerulus, and about 90% of this potassium is passively reabsorbed at the level of the proximal tubule and loop of Henle. At the level of the distal tubule and collecting duct, potassium is secreted into the tubular lumen, partly through the action of aldosterone; the amount excreted daily is similar to the amount of oral intake. In response to severe potassium depletion, urinary potassium levels will fall but rarely to < 5 to 10 mHq/L. Besides the kidney, the distal colon also can increase potassium excretion in response to increased intake.
Transcellular flux is also important in regulating the serum potassium level. Cellular uptake is stimulated by insulin, aldosterone, epinephrine, and alkalosis and can modulate the impact of high oral potassium intake on serum levels. Thus, the intracellular mass of potassium serves as a buffer system to help maintain consistency in the ECF.
With normal aging, total body potassium decreases. This decrease reflects the decline in lean body muscle mass, which contains about 75% of intracellular potassium. Although cross-sectional data generally do not show that age influences serum potassium levels, several studies of healthy elderly people and longitudinal data suggest a slight increase, especially in men, but not to values above normal. The kidney’s ability to regulate potassium excretion is unaffected by aging, even though an age-associated decline in aldosterone secretion has been documented.

A .serum sodium level of > 146 mEq/L that results from decreased body water relative to total body sodium content.
Common in the elderly, hypernatremia has a prevalence of about 1% in hospitalized patients > 60 yr of age. A similar prevalence was noted among elderly residents of a long-term care facility, with the incidence increasing to 18% when the population was evaluated over 12 mo.
Hypernatremia in the elderly poses a high risk of morbidity and mortality; often, the more severe the predisposing factor, the higher the risk. The CNS manifestations are common, often leading to a depressed sensorium and chronic functional decline in those who survive the acute episode. In one study of elderly hospitalized patients who developed hypernatremia with serum sodium levels > 148 mEq/L, the mortality rate was about 40%. The mortality rate was highest in those with a rapid onset and those with a serum sodium level > 160 mEq/L.
Etiology
The most common mechanism underlying hypernatremia is an excessive loss of body water relative to the loss of sodium in association with inadequate fluid intake (see TABLE 3-3). The water deficit can reach 11 L or 30% of the total body water volume. Disorders leading to such severe water depletion include febrile illness with increased insensible losses, tachypnea with increased water loss from the lungs, fever-related obtundation or debilitating illness with decreased oral fluid intake, diarrhea from hyperosmolar tube feedings, and polyuria from uncontrolled diabetes mellitus with glycosuria. Rarely, dehydration and hypernatremia occur in elderly patients with central diabetes in sipidus or with acquired vasopressin resistance resulting from chronic renal disease, hypercalcemia, or hypokalemia. Excessive water depletion commonly results from potent loop diuretics.
Occasionally, hypernatremia occurs without accompanying dehydration because of a high sodium intake. This may occur after sodium bicarbonate administration for cardiac arrest or metabolic acidosis or after an infusion of 0.9% sodium chloride solution for fluid loss or shock.
Treatment
Early recognition and treatment of mild hypernatremia and maintenance of fluid balance are especially important in hospitalized elderly patients. Many cases of severe hypernatremia develop after admission and evolve rapidly as a result of therapeutic interventions or progression of the underlying disease.
Correcting hypernatremia requires replacing body water deficits with hypotonic fluid. The severity of the water deficit can be estimated as described under VOLUME DEPLETION AND DEHYDRATION, above. Either 0.45% sodium chloride solution or 5% dextrose in water should be administered at a rate that will correct the hypernatremia in about 48 h. The serum sodium level should be lowered no more rapidly than 2 mEq/L/h. Excessively rapid correction may lead to cerebral edema with either permanent brain damage or death. In the elderly patient with coexisting cardiac disease, caution must be used to avoid heart failure.
When the cause of hypernatremia is identified (eg, diabetes insipidus, diuretic therapy, increased sodium intake), specific treatment measures should be implemented.

The severity of the symptoms and signs depends on the severity of the hyponatremia and the rapidity with which the serum sodium level declined. Mild chronic hyponatremia may be asymptomatic. When serum levels fall to < 125 mEq/L, lethargy, fatigue, and muscle cramps may occur. Such GI symptoms as anorexia and nausea may also occur early.
The CNS manifestations of hyponatremia—ranging from disorientation to confusion, coma, and seizures—are often related to the severity of the hyponatremia. Severe hyponatremia may be accompanied by depressed sensorium, depressed deep tendon reflexes, hypothermia, Cheyne-Stokes respiration, and pathologic reflexes. Serum sodium values < 115 mEq/L may result in sudden death. The overall mortality rate in patients with symptomatic hyponatremia and a serum sodium level < 120 mEq/L is about 40%; with coexisting alcoholism or cachexia, the rate reaches about 70%.
When hyponatremia results from volume depletion, the physical examination may reveal signs of hypovolemia; when hyponatremia results from sodium retention and decreased effective plasma volume, the examination may reveal edema. Edema rarely occurs in patients with SIADH.
Measurements of serum BUN and creatinine levels also help determine the type of hyponatremia. These values are usually elevated in patients with combined sodium and ECF volume depletion and in those with decreased effective plasma volume. Serum BUN and creatinine values are usually normal or low in patients with dilutional hyponatremia or SIADH. The urinary sodium level is usually < 20 mEq/L in patients with volume depletion or edema; it is usually > 20 mEq/L in patients with expanded ECF volume, such as occurs in SIADH.
An oral water-loading test may help diagnose SIADH. However, this test should not be performed on patients who have serum sodium levels < 125 mEqlL or those who have symptomatic hyponatremia regardless of the serum sodium level. A patient undergoing the test receives an oral water load of 20 mL/kg of body weight over 15 to 30 min. The patient is then kept recumbent for 5 h, except when voiding. Urine is collected hourly for 5 h, and the volume and osmolality of each specimen are measured. A normal response is excretion of > 80% of the water load in 5 h and a decrease in urine osmolality to < 100 mOsm/kg in at least one specimen, usually that collected for the second hour. Patients with SIADH have an impaired ability to excrete the water load and dilute the urine. A normal response in a hyponatremic person whose clinical and laboratory findings indicate a normal or expanded ECF volume suggests that the hyponatremia may result from primary polydipsia or a low-set osmoreceptor mechanism.
Other possible causes of hyponatremia, such as hyperglycemia from diabetes mellitus, must be excluded. With hyperglycemia, the glucose-induced hyperosmolar state produces a shift of body water into the intravascular space, diluting serum sodium by about 1.6 mEq/L for each 100 mg/dL increase in blood glucose above normal. Correcting the hyperglycemia returns the serum sodium level to normal.
Pseudohyponatremia may occur in patients with marked hyperlipid-emia or hyperproteinemia. In these conditions, the increased lipid or protein replaces a portion of sodium-containing plasma so that the measured sodium concentration per liter of plasma is reduced. However, a plasma osmolality determination will reveal a normal value for solute concentration because this measurement reflects solute concentration of plasma water.
Treatment
In patients with hyponatremia from sodium and ECF volume depletion, treatment is based on correcting the volume deficit with 0.9% sodium chloride. If the serum sodium level is < 125 mEq/L, some of the IV fluid should be hypertonic sodium chloride solution. In hypona tremic patients who have decreased effective plasma volume and edema, treatment should be directed at the underlying cause—ie, heart failure, cirrhosis, or nephrotic syndrome. Although diuretics (eg, furosemide) can often reduce edema, they may cause a natriuresis that further decreases the serum sodium level. In such cases, moderate fluid restriction (eg, 1000 to 1500 mL/24 h) may be sufficient to correct the hyponatremia.
Symptomatic hyponatremia, particularly that resulting from a dilutional state, warrants prompt intervention. In the mildly symptomatic patient with a serum sodium level > 125 mEq/L, restricting fluid to 800 to 1000 mL/day is usually sufficient. In a patient with more severe symptoms, serum sodium should be increased more rapidly by infusing hypertonic sodium chloride solution until symptoms begin to clear and the serum sodium level reaches about 120 to 125 mEq/L. A goal is to elevate the serum sodium level at a rate of 1 to 2 mEq/L/h. This can usually be accomplished by administering 200 to 300 mL of 3% sodium chloride solution over 4 to 6 h. Patients with serum sodium levels < 105 mEq/L and symptoms of seizure or coma may benefit from simultaneous administration of IV furosemide to promote diuresis. These patients may require larger amounts of hypertonic sodium chloride solution to compensate for the enhanced natriuresis, and serum electrolyte levels must be monitored to avoid diuretic-induced hypokalemia and hypomagnesemia.
Overcorrection of hyponatremia must be avoided. Usually, restoring the serum sodium level to about 120 to 125 mEq/L corrects the major symptoms. In severely malnourished patients and especially in alcoholics, central pontine myelinolysis may result from rapidly increasing the level to > 140 mEq/L.
Chronic management of hyponatremia is based on identifying and correcting the underlying cause. Fluid intake may also be restricted (usually 1000 to 1500 mL/day) to maintain a serum sodium level > 130 mKq/1.. In patients who do not respond to or are unable to comply with fluid restriction, the tetracycline antibiotic demeclocycline 600 to 1200 mg/day can induce mild nephrogenic diabetes insipidus with polyuria of 2 to 4 I ,/24 h. Patients treated with this drug require careful monitoring of fluid balance to avoid excessive fluid loss. Also, some patients have markedly elevated serum BUN levels as a result of demeclocycline treatment.

Hyponatremia may occur in association with combined sodium and ECF volume depletion, as with vomiting, diarrhea, GI suction, renal disorders, and diuretic therapy. In such 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 being < 125 mEq/L.
Disorders producing edematous states, eg, heart failure, cirrhosis, nephrotic syndrome, or acute glomerulonephritis, are associated with an elevated total body sodium content and normal or increased ECF volume. However, effective plasma volume is reduced, restricting the delivery of sodium and water to the diluting segments of the nephron. Consequently, sodium-retaining mechanisms are activated as ADH release increases. Over time, a net gain of water relative to sodium leads to dilutional hyponatremia.
In a form of hyponatremia common among the elderly, total body sodium content is normal but water is retained because of increased ADH secretion, ie, the syndrome of inappropriate secretion of ADH (SIADH). This syndrome, which has many causes, is defined by inappropriate hypertonicity of the urine, often with hypotonicity of the plasma; increased excretion of sodium in the urine; plasma volume dilution, as suggested by normal or low BUN and creatinine levels; and no edema. Elderly patients with underlying disorders that may lead to SIADH often have normal serum sodium levels because fluid intake may not be sufficient to produce a dilutional hyponatremia. However, when fluid intake increases (eg, when IV fluids are administered or when oral intake is encouraged to treat febrile illness), the increase in body water may lead to rapid development of hyponatremia. This condition is especially likely to occur in institutionalized patients, whose fluid intake is not primarily determined by thirst or custom (see TABLE 3-1).
Another common cause of hyponatremia in elderly patients is the use of nutritional supplements such as Isocal, Ensure, or Osmolite. Such formulas are almost universally low in sodium content, containing about 20 to 30 mEq/1000 calories. These dietary sources should be supplemented with sodium to provide a total intake of about 100 mEq daily.

A serum sodium level of < 136 mEq/L that occurs with an excess of water relative to total sodium. Total ECF volume may be increased, normal, or decreased.
Older persons are at increased risk for developing hyponatremia. An analysis of 139 sets of plasma electrolyte values for healthy persons revealed an age-related decrease of 1 mEq/L/decade from a mean value of 141 ± 4 mEq/L in younger persons. In another study, 7% of ambulatory persons > 65 yr who were living at home and showed no evidence of acute illness had serum sodium levels < 137 mEq/L. An increased prevalence of hyponatremia has also been found in hospitalized patients. An analysis of 5000 consecutive sets of plasma electrolyte values from hospitalized patients with a mean age of 54 yr revealed a mean serum sodium level of 134 mEq/L, with values skewed toward the hy-ponatremic end of the frequency distribution curve. Among elderly patients in long-term care facilities, an 18% to 22% prevalence of serum sodium levels ≤ 135 mEq/L was noted. In a longitudinal study over 12 mo, the incidence of hyponatremia in this population was about 50%. While hyponatremia is common in the elderly, it often does not produce clinically apparent symptoms, especially when it is mild.