Specialist referral is indicated for serum sodium levels of less than 125 mEq/L or more than 155 mEq/L.
Hypernatremia affects people of all ages but is one of the more common electrolyte disorders seen in children and older adults.1 Defined as a serum sodium level of more than 145 mEq/L, hypernatremia can be caused by a fluid volume deficit, excessive sodium intake, chronic renal disease, or other disorders.2
Normally, water intake and water loss are balanced, but a disruption in water homeostasis can result in hypernatremia. When water loss exceeds water intake, serum osmolality rises, and thirst is stimulated. Water balance is achieved as water intake increases. Thirst receptors are stimulated when serum osmolality rises above the normal range of 290 to 295 mOsm/kg. Destruction of the thirst centers in the hypothalamus as a result of neoplasm, trauma, or vascular abnormalities leads to an inadequate thirst response and hypernatremia. In older adults, physiologic aging changes may increase susceptibility to electrolyte changes, but anyone unable to adequately express thirst, such as infants and those with a decreased sensorium, are also at risk for development of hypernatremia.
An excess of water loss in relation to intake leads to increased serum osmolality. In response to this rise in serum osmolality, antidiuretic hormone (ADH), or vasopressin, is secreted from the posterior pituitary gland. ADH increases the permeability of the renal collecting ducts to water. As a result, water is reabsorbed in the collecting ducts, and the urine becomes more concentrated. Patients with a deficit in the production of ADH or a diminished renal response to ADH will develop hypernatremia if water losses are not corrected. Older adults are especially at risk because of the diminished renal concentrating ability that occurs with aging.
Patients with diabetes insipidus develop hypernatremia when water intake is not enough to compensate for fluid loss. Also at risk for the development of hypernatremia as a result of losing large amounts of free water are patients who have osmotic diuresis because of hyperglycemia or the administration of osmotic diuretics such as mannitol.1,2
Hypernatremia also develops with an increase in insensible water losses. Normally, small amounts of fluids are lost from the skin, respiratory tract, and gastrointestinal tract. Conditions such as fever, tachypnea, diarrhea, vomiting, and burns increase the volume of insensible water loss. Hypernatremia results if these losses are not replaced. Patients who exercise vigorously and drink an insufficient amount of liquid and those with insufficient fluid intake in the setting of fever, vomiting, or diarrhea are at great risk for development of hypernatremia.1,2
Increased serum sodium is less often the result of excess sodium intake, including rapid intravenous administration of normal saline or high-solute tube feedings. However, the resultant sodium excess can cause an increase in serum osmolality and expansion of extracellular volume.1,2
Clinical Presentation and Physical Examination
The major clinical feature of hypernatremia is a central nervous system disturbance that results from dehydration and shrinkage of brain cells. The purpose of the history and physical examination is to determine the underlying cause of the increased serum sodium and guide diagnostics as well as treatment.3 A recent history of fever, vomiting, diarrhea, polyuria, heat exposure, or surgery is significant. A careful review of medications (particularly a history of lithium or diuretic therapy), fluid intake and output during the previous 24 hours, and any intravenous therapy or tube feedings should be reviewed along with the past medical history.
Patients may report weakness, thirst, or lightheadedness or, if the hypernatremia is related to a hypothalamic lesion, be asymptomatic. Signs and symptoms of hypernatremia can be nonspecific and not develop until the serum sodium level becomes higher than 150 mEq/L. Agitation, irritability, confusion, and personality changes are early signs. Muscle twitching, tremor, spasticity, hyperreflexia, and lethargy may also be seen. Coma, seizures, and muscle weakness are later signs. Thirst is usually present unless the thirst receptors are nonfunctioning. Indications of volume depletion include hypotension, tachycardia, and abnormal postural changes in vital signs. Weight loss, flat neck veins, dry mucous membranes, and diminished skin turgor may also be seen, depending on the severity of the volume loss.1,2
Diminished urinary output is also a possible finding, except in patients with diabetes insipidus or osmotic diuresis as the underlying cause of the hypernatremia. Fever, flushing, and dry mucous membranes may also be present.1,2
Classification of the patient’s fluid volume status is facilitated by evaluation of the patient’s appearance, weight, postural vital signs, passive leg raising, and careful examination of the pulmonary, cardiac, and gastrointestinal systems.4,5 Neurologic screening, including motor tone, strength, coordination, and cognitive and functional ability, is necessary to determine subtle neurologic changes.
• Determine if the serum sodium elevation is a result of water loss, sodium gain, or a combination of both.4 Initial diagnostic testing includes serum glucose, serum electrolytes, urea, calcium, blood urea nitrogen (BUN) concentration, creatinine level urinalysis, urine sodium, and urine osmolality.
• Urine specific gravity is not as precise as urine osmolality but is a quick test to determine urine concentration. The urine specific gravity of patients with hypernatremia is elevated, except in the cases noted previously.
It is important to determine the underlying cause of the sodium imbalance because treatment options vary with the cause. The patient with hypernatremia resulting from diabetes insipidus is treated differently from the patient whose imbalance is a result of excessive diarrhea caused by the use of lactulose.
The primary goal of treatment is the replacement of water loss and restoration of extracellular fluid volume.
• If the hypernatremia is caused by fluid loss, fluid volume must be replaced with a hypotonic intravenous fluid (0.45% NaCl) or 5% dextrose in water at 0.5 mEq/L/hr but not greater than 1 mmol/L/hr.1,4
• Acute hypernatremia (less than 48 hours) should be differentiated from chronic hypernatremia (greater than 48 hours), because correction of acute hypernatremia is more rapid (8 to 12 mmol/L/day, 2 to 3 mmol/L/hr) than the correction of chronic hypernatremia (no more than 8 to 10 mmol/L per day, 0.5 mmol/L/hr).4 Patients diagnosed with acute-on-chronic hypernatremia also require a rapid decrease (8 to 12 mmol/L/day) in serum sodium.4 The infusion rate is critical for patients with hypernatremia because a rate that is too slow or too rapid increases the risk for death.3,4
• Serum sodium, urine chemistry, and fluid volume status are monitored frequently (i.e., vital signs, intake and output, daily weight plus serum glucose, electrolytes, BUN, and creatinine; calculation of serum osmolality initially 2 hours after therapy is started, then periodically throughout the day in acute hypernatremia) while the patient is receiving intravenous therapy.4
• Nephrogenic diabetes insipidus is treated by discontinuing the offending agent and correcting electrolyte abnormalities.6 Serum electrolyte levels and fluid status must be monitored closely.
Life Span Considerations
Aging is associated with a decreased ability to cope with environmental, disease-related, and drug-related stressors in sodium and water balance. Hypernatremia is commonly associated with fever, dehydration, warm environments, high-solute tube feedings, and diuretic or laxative therapy.
If hypernatremia is not corrected, cerebrovascular damage occurs from brain dehydration and shrinkage. Hypovolemic shock results when severe volume depletion is not corrected. If hypernatremia is not corrected carefully, patients may experience significant cognitive dysfunction.4 Patients with cardiac disease should be monitored closely for signs and symptoms of congestive heart failure, which may occur if fluid is replaced too rapidly.1,3
Indications for Referral or Hospitalization
Hypernatremia may be managed on an outpatient basis if the degree of sodium imbalance is moderate and the patient is alert and able to drink sufficient amounts of fluids.
Older adults living alone or those at risk for development of congestive heart failure may best be managed in an inpatient setting.
Patient and Family Education
Patients and families should understand that 1500 to 2000 mL of fluid should normally be consumed each day. Patients at risk for hypernatremia should understand the importance of maintaining proper fluid balance.
Older patients in particular need to be aware of the dangers of dehydration, especially in hot weather or if fever is present.
Patients who are taking diuretics or medications such as lithium and carbamazepine (Tegretol), which cause hypernatremia, need to be aware of this side effect. Patients who exercise regularly should be educated about the need for appropriate fluid intake when exercising. Patients with underlying conditions that put them at risk for hypernatremia need to be educated accordingly.1,4
Hyponatremia is a common electrolyte disorder and a significant cause of morbidity and mortality, particularly in older adults.1,7 The costs associated with hyponatremia can approach 3.6 billion dollars each year and are largely related to hospitalization.8 Potential causes of hyponatremia include infections, traumatic brain injuries, malignant disease, endurance exercise, untoward medication effects, endocrine disorders, psychogenic polydipsia, syndrome of inappropriate antidiuretic hormone (SIADH), cerebral or renal salt wasting, acquired immunodeficiency syndrome (AIDS), and other illnesses.9,10 Hyponatremia may be related to a dysfunction in the release of ADH (i.e., vasopressin) or renal insensitivity to the hormone, but is also associated with hyperglycemia, hypokalemia, adrenal insufficiency (primary or secondary to pituitary dysfunction), hypothalamic disorders, pregnancy, or other conditions that lead to excess water in relation to body sodium or cause salt loss in excess of water loss.10
Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L and can be an acute or a chronic condition. Acute hyponatremia sometimes develops in hospitalized patients after surgery and is often associated with fluid overload, but thiazide therapy and other medications can also cause hyponatremia. Chronic hyponatremia usually occurs outside the hospital, often is acquired over a longer period, and can cause falls, gait problems, cognitive changes, and osteoporosis.10 This electrolyte disorder can affect more than 10% of outpatients and is associated with increased hospital length of stay and mortality.8 Hyponatremia is one of the more common electrolyte disorders in older adults, but premenopausal women and children are also at risk.
Exercise-associated hyponatremia (EAH) is usually associated with female gender, environment (extreme heat or cold), smaller body weight, and prolonged exercise, but EAH also affects males and occurs even in shorter exercise events.9 The incidence of EAH is variable, and those affected may often seem more asymptomatic than symptomatic.9 The causes of EAH are associated with increased water intake, inappropriate vasopressin secretion, increased brain natriuretic peptide (BNP), sudden water absorption from the gastrointestinal tract, sodium loss associated with sweating, impairment of sodium store mobilization, and/or possibly medications such as nonsteroidals and selective serotonin reuptake inhibitors.9,11 The Wilderness Medical Society practice guidelines were developed to assist in the prevention and management of EAH in the wilderness.9
Treatment of hyponatremia has always been challenging, and there has been increasing concern about how to treat patients appropriately.8 It is a complex disorder, the causes are myriad, and treatments vary depending on the underlying pathology and patient age.8 For example, treatment recommendations for children with hyponatremia differ significantly from treatment recommendations for adults and elders.10 In recent years, the U.S. Expert Panel recommendations for diagnosis, evaluation, and treatment of hyponatremia and the European clinical practice guidelines on diagnosis and treatment of hyponatremia were released to assist health care providers in identifying and treating hyponatremia appropriately.8,10 The European guidelines use a grading system to support the recommendations, but the U.S. panel determined that further research would be necessary to support a quality-of-evidence grading system.8,10 Both sets of guidelines emphasize the difference between hypotonic hyponatremia and nonhypotonic hyponatremia and emphasize the importance of recognizing this disorder and treating it appropriately to avoid significant morbidity and mortality.8,10
Sodium and other anions regulate body water and are determinants of serum osmolality. If serum sodium levels fall below normal limits, serum osmolality is decreased and extracellular water is permitted to seep into cells. This results in a hypotonic hyponatremia and the cerebral brain cell swelling that causes the neurologic features associated with hyponatremia. Normally, the body responds to an excess amount of water by diuresis. Renal mechanisms and vasopressin control body fluid volume and the composition of body fluids. An increase in serum osmolality above the normal 275 to 295 mOsm/kg stimulates the posterior pituitary to release vasopressin, which influences the distal tubules and collecting ducts in the kidneys to conserve water. As body fluid accumulates and serum osmolality becomes hypotonic, vasopressin is inhibited. In most circumstances, vasopressin release is affected by serum osmolality and blood pressure (i.e., baroregulation), but others factors can also affect vasopressin release and cause SIADH.10 Medications and a person’s genetic predisposition can also affect water output in the collecting ducts of the kidneys and thus decrease serum sodium.10
EAH is influenced by varied mechanisms. Primary causes include an overabundance of water intake or diminished vasopressin suppression, but increased levels of BNP during exercise may also affect some athletes.9 Others may experience increased sodium losses associated with certain medications, sweat during exercise, increased water absorption from the gastrointestinal tract after exercise, or decreased mobilization of sodium stores.9
Psychogenic polydipsia, beer potomania (the association of severe hyponatremia with ingestion of large quantities of beer), and a reset osmostat have also been identified as precipitants of hypotonic hyponatremia with euvolemia. Psychogenic polydipsia can be related to angiotensin-converting enzyme (ACE) inhibitor or lithium therapy or to a biologic or psychiatric disorder; it may also be a compensatory mechanism for medications that cause dry mouth. Individuals with beer potomania derive most of their calorie intake from large quantities of beer, which contains relatively few solutes. The reduced solute delivery to the distal tubule restricts urine production and results in hyponatremia. The reset osmostat phenomenon, a type of SIADH, is found in patients with malignancy, malnutrition, debilitating conditions, and even pregnancy. Changes in cellular metabolism cause hypothalamic osmoreceptors to reset to maintain a lowered serum osmolality. The diagnosis of reset osmostat is complex. BUN and creatinine concentrations are usually normal, but urine sodium and osmolality are variable.8
Hyponatremia is also associated with other causes. The high glucose levels associated with hyperglycemia can cause intracellular fluid to shift into the extracellular compartment, causing a lower serum sodium because of the increase in extracellular fluid.8 The solute changes that occur with hyperglycemia result in an isotonic or hypertonic hyponatremia.8 Mannitol, surgical irrigants (e.g., glycine), and radiographic contrast agents act similarly and cause a hypertonic hyponatremia.8 Significantly increased amounts of plasma proteins and lipids cause a factitious decrease in serum sodium and result in an isotonic pseudohyponatremia.8