Hypernatremia in the Elderly
Hypernatremia is common in elderly persons, who may present with signs that are easily overlooked. Prompt diagosis and appropriate therapy can sometimes lead to a remarkable recovery. To avoid cerebral edema, rehydration must be accomplished gradually over 48 to 72 hours. The recommended replacement for the first 24 hours is approximately 30 percent of the estimated water loss.
Hypernatremia, defined as a serum sodium level above 145 mEq per L (145 mmol per L), is a common problem in elderly persons, especially those who are institutionalized.1 The reported mortality rates range from 46 to 70 percent, depending on the degree of the hypernatremia and the underlying disease process.2 In the elderly, the leading cause of hypernatremia is dehydration.
An 85-year-old woman was transferred to the hospital from an extended-care facility because of a gradual loss of consciousness. The patient had a long history of Alzheimer's disease.
Physical examination on admission revealed a blood pressure of 110/65 mm Hg; temperature, 37 degree C (98.6 degree F); respiratory rate, 24, and pulse, 88. The patient was unresponsive to deep stimuli. The skin was warm and dry, and the mucous membranes were dry. Pupils were fixed at 2 mm in diameter.
Laboratory data revealed the following: venous pH, 7.37; serum sodium, 199 mEq per L (199 mmol per L); serum chloride, 150 mEq per L (150 mmol per L); serum potassium, 2.9 mEq per L (2.9 mmol per L); blood urea nitrogen, 91 mg per dL (32.5 mmol per L); serum creatinine, 2.7 mg per dL (240 mol per L); venous CO2, 27 mEq per L (27 mmol per L); serum osmolality, 420 mOsm per kg (420 mmol per kg), and urine osmolality, 720 mOsm per kg (720 mmol per kg). Urinalysis revealed more than 50 white blood cells per high-power field, and urine culture demonstrated 100,000 Escherichia coli organisms per mL. The urinary tract infection was treated with urinary tract infection was treated with appropriate intravenous antibiotics.
The patient was slowly rehydrated, with 30 percent of the calculated body water deficit replaced during the first 24 hours. The remainder of the water deficit was replaced over the next 48 hours. The patient's laboratory values gradually returned to normal, as shown in Table 1. The patient's sensorium gradually improved and had returned to baseline by the sixth day of hospitalization. The dehydration was thought to be due to the patient's loss of thirst sensation in combination with the urinary tract infection.
Signs and Symptoms
The various causes of hypernatremia are summarized in Table. The prognosis of hypernatremia in elderly patients depends on the severity of underlying disease, prompt recognition of hypernatremia and rapid initiation of proper therapy.
A serum osmolality greater than 290 mOsm per kg (290 mmol per kg) or a serum sodium level greater than 145 mEq per L (145 mmol per L) may be due to increased body sodium, decreased body water or a combination of these factors.3 In elderly patients, dehydration accounts for over 90 percent of the cases of hypernatremia.4
Symptoms of moderate hypernatremia are often nonspecific in elderly patients, who may present with vague symptoms such as weakness and lethargy. The diagnosis of hypernatremia can be easily overlooked. Signs of dehydration can be difficult to detect in elderly persons, because of the changes associated with normal aging. For example, the changes in aging skin mimic loss of skin turgor. In addition, oral mucous membranes may be dry because of mouth breathing, which is common in some elderly patients.
The skin over the sternum is a more reliable guide to hydration status than the skin of other areas. More useful clues to dehydration include reduced eye pressure or the failure of jugular veins to fill when the patient is in a supine position.4 Severe hypernatremia may be manifested by neurologic abnormalities, such as obtundation, stupor and coma.5 Sensorium tends to be more severely impaired in patients with higher serum sodium values. 2,6
Mechanisms of Hypernatremia
Table 3 outlines the features of urine osmolality and volume in three of the major causes of hypernatremia in the elderly. Febrile illness is the most common cause of dehydration. Fever increases insensible water loss and is frequently associated with tachypnea, causing further insensible water loss. The obtundation associated with fever and hypernatremia may make it difficult for elderly patients to maintain oral hydration and may also interfere with the thirst mechanism. 7
Nutritional supplementation is another cause of hypernatremia. Enteral tube feeding in particular may result in hypernatremia because of osmotic-induced diarrhea, hyperglycemia and associated glucosuria or free water intake inadequate for the osmotic load of the nutritional supplement. Hypernatremia may also develop in situations that mandate infusion of a sodium-containing solution, such as in cardiac arrest, drug overdose and acidosis. 8,9
Patients with hypernatremia related to infirmity include those who are unable to obtain water for themselves, such as stroke victims and patients with dementia or delirium. Patients with gastrointestinal bleeding may become hypernatremic because of inadequate fluid intake to counteract the hypovolemia. Gastrointestinal bleeding causes an increased blood urea nitrogen level, which also can lead to osmotic diuresis. Loop diuretics, such as furosemide (Lasix) and ethacrynic acid (Edecrin), can cause hypernatremia by increasing the free water loss over solute loss.
Diabetes insipidus, a disorder characterized by impaired renal conservation of water, has a myriad of causes and should be considered in the differential diagnosis of hypernatremia in the elderly. Loss of renal concentrating ability, such as from interstitial disease or sickle cell trait, may also facilitate dehydration.10 Adrenal hyperfunction (Cushing's disease or primary hyperaldosteronism) is a less common cause of hypernatremia in elderly patients.
The major therapeutic objectives in patients with hypernatremia due to water loss are to treat the underlying medical problems, minimize ongoing water loss and replace the water deficit. The approximate water deficit may be calculated by following the steps outlined in Table 4.
Replacement of the total water deficit should be accomplished gradually. Replacing the deficit too quickly can lead to rapid fluid shifts and fatal cerebral edema.2 The cause of the cerebral edema is unclear but is probably related to generation of osmotically active solute in brain cells in response to the hypernatremic state.11,12
Hypernatremia should be corrected over a period of 48 to 72 hours. To avoid cerebral edema, the water deficit should be calculated, and no more than 30 percent of the deficit plus ongoing water losses should be replaced over the first 12 to 24 hours. A study of severely dehydrated elderly patients showed that replacement of 31 to 71 percent of the water deficit during the first 24 hours of therapy was associated with an increased mortality rate as compared with the mortality rate when 31 percent or less of the deficit was replaced in the same period.2
The route of administration of water replacement is guided by the patient's clinical condition. If the patient is conscious and alert, water should be replaced orally. For intravenous replacement, 5 percent dextrose and water is a reasonable solution. When hypernatremia is caused by losses of both sodium and water (with the water loss in excess of sodium loss) and circulatory collapse is present, volume expanders and even isotonic saline may be necessary initially.
Hypernatremia in the elderly has numerous etiologies and can sometimes be difficult to diagnose. Proper treatment and slow replacement of the water deficit can sometimes produce remarkable results. The patient in our illustrative case, with a serum sodium of 199 mEq per L (199 mmol per L), was initially thought to have a condition incompatible with life. Gradual replacement of her total body water over a period of 72 hours led to a return of the patient's mental function to the baseline level. 1. Himmelstein DU, Jones AA, Woolhandler S. Hypernatremic dehydration in nursing home patients: an indicator of neglect. J Am Geriatr Soc 1983;31:466-71. 2. Snyder NA, Feigal DW, Arieff AI. Hypernatremia in elderly patients. A heterogenous, morbid, and iatrogenic entity. Ann Intern Med 1987;107:309-19. 3. Cadnapaphorncha P. Disordered sodium metabolism: sodium retention states. Crit Care Clin 1987;3:779-95. 4. Lye M. Electrolyte disorders in the elderly. Clin Endocrinol Metab 1984;13:377-98. 5. Simon RP, Freedman DD. Neurologic manifestations of osmolar disorders. Geriatrics 1980;35(6):71-83. 6. Arieff AI. Central nervous system manifestations of disordered sodium metabolism. Clin Endocrinol Metab 1984;13:269-94. 7. Lindeman RD. Mineral metabolism in the aging and the aged. J Am Coll Nutr 1982;1:49-73. 8. Barratt LJ. Common clinical electrolyte disorders. Med J Aust 1983;2:84-6. 9. Bastron RD. Sodium balance. Contemp Anesth Pract 1983;6:33-56. 10. Marsden PA, Halperin ML. Pathophysiological approach to patients presenting with hypernatremia. Am J Nephrol 1985;5:229-35. 11. Lindeman RD, Klingler EL Jr. Combating sodium and potassium imbalance in older patients. Geriatrics 1981;36(8):97-106. 12. Mahowald JM, Himmelstein DU. Hypernatremia in the elderly: relation to infection and mortality. J Am Geriatr Soc 1981;29:177-80.
Table : Serial Laboratory Data for the Patient in the Illustrative Case
Table : Urine Osmolality and Volume in Common Causes of Hypernatremia in the Elderly
Table : Calculation of Water Deficit
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