Hyponatremia: Symptoms, Causes, Treatments

Overview

What is hyponatremia?

Hyponatremia is usually discovered on laboratory tests as a lower than normal sodium level in the blood. It will appear as sodium or Na+ in your lab results. Actually, the main problem in the vast number of situations is too much water that dilutes the Na+ value rather than too much sodium. As a result, water moves into body cells, causing them to swell. This swelling causes the major problem, which is a change in mental status that can progress to seizures or coma.

Hyponatremia can result from multiple diseases that often are affecting the lungs, liver or brain, heart problems like congestive heart failure, or medications. Most people recover fully with their doctor’s help.

Who is most at risk for hyponatremia?

Anyone can develop hyponatremia. Hyponatremia is more likely in people living with certain diseases, like kidney failure, congestive heart failure, and diseases affecting the lungs, liver or brain. It often occurs with pain after surgery. Also, people taking medications like diuretics and some antidepressants are more at risk for this condition.

How common is hyponatremia?

Hyponatremia is very common. Hyponatremia is the most common chemical abnormality seen among patients in the hospital. Rates of hyponatremia are higher among people admitted to inpatient hospital care units or with the medical conditions mentioned above.

Symptoms and Causes

What causes hyponatremia?

In general, too much water in your body is usually the main problem and this dilutes the sodium levels. Much less frequently, hyponatremia is due to significant sodium loss from your body.

Too much water in your body causes your blood to become “watered down.” A good example is people who run in long races or run on hot days. They lose both salt and water in their sweat and often replace these losses with mostly water. This combination can be deadly because it dilutes the remaining sodium in the body.

It’s also possible to lose too much sodium from your body. Medications, like diuretics, can cause your kidneys to increase the amount of sodium excreted in urine. Medical problems like diarrhea may cause excessive sodium loss if left untreated. Chronic or binge alcohol consumption can cause people to lose too much sodium through increased urination and vomiting. You can have hyponatremia without feeling dehydrated or volume depleted. This is most often the case in hospitalized patients.

What are the symptoms of hyponatremia?

Hyponatremia causes neurologic symptoms ranging from confusion to seizures to coma. The severity of the symptoms depends on how low the sodium levels are in the bloodstream and how quickly they fall. In many cases, blood sodium levels fall gradually, producing only mild symptoms as the body has time to make adjustments. Symptoms are more serious when blood sodium levels fall quickly.

Other symptoms of moderate to severe hyponatremia include:

Diagnosis and Tests

How is hyponatremia diagnosed?

The only way your doctor can know that hyponatremia is present is with blood tests that measure the amount of sodium (Na+) in the bloodstream. Your doctor will also perform a physical examination to detect the severity and cause(s) of hyponatremia.

Management and Treatment

How is hyponatremia treated?

Treatment for hyponatremia depends on the underlying cause and the severity of your symptoms. If you have mild symptoms, your doctor makes small adjustments to your therapy to correct the problem. This usually involves restricting water intake, adjusting medications and removing or treating the causes. Therapy may be short-term or long-term. For the short-term, we may restrict water intake, adjust or stop medications, and treat any underlying problems. For the long-term, we may continue the short-term treatments and add salt to your diet or try some newer medications.

People with moderate to severe hyponatremia require thorough medical evaluation and treatment, usually in the hospital. For the sickest patients, we may replace sodium intravenously (straight into a vein) and really limit water consumption. Certain newer medications, like tolvaptan (Samsca®), may be used to correct blood sodium levels.

Treatment to correct any underlying medical problems – like congestive heart failure (when poor heart function causes fluid to build up in the body) – is also used to improve hyponatremia.

What complications are associated with hyponatremia?

In many cases, hyponatremia causes extra water to move out of the bloodstream and into body cells, including brain cells. Severe hyponatremia causes this to occur quickly, resulting in swollen brain tissue. If left untreated, complications can include:

• Mental status changes
• Seizures
• Coma
• Death

Prevention

Can hyponatremia be prevented?

If you have certain underlying medical conditions, particularly involving the kidneys, heart, lung, liver or brain, hyponatremia is more likely. You can lower your risk for hyponatremia by following your treatment plan and restricting your water intake to levels recommended by your doctor. Also, notify your doctor of any new symptoms immediately. Monitoring must include blood tests.

Outlook / Prognosis

What are the outcomes after treatment for hyponatremia?

With treatment, many people recover fully from hyponatremia. Even long-term hyponatremia can be managed and problems prevented.

Living With

When should I call my doctor?

If you develop any symptoms of hyponatremia, contact your doctor immediately. Hyponatremia can become an emergency if your sodium level falls too much or too quickly.

Hyponatremia and Hypernatremia in the Elderly

JOHN P. KUGLER, COL, MC, USA, and THOMAS HUSTEAD, CPT, MC, USA, Dewitt Army Community Hospital, Fort Belvoir, Virginia

Am Fam Physician. 2000 Jun 15;61(12):3623-3630.

Management of abnormalities in water homeostasis is frequently challenging. Because age-related changes and chronic diseases are often associated with impairment of water metabolism in elderly patients, it is absolutely essential for clinicians to be aware of the pathophysiology of hyponatremia and hypernatremia in the elderly. The sensation of thirst, renal function, concentrating abilities and hormonal modulators of salt and water balance are often impaired in the elderly, which makes such patients highly susceptible to morbid and iatrogenic events involving salt and water. Clinicians should use a systematic approach in evaluating water and sodium problems, utilizing a comprehensive history and physical examination, and a few directed laboratory tests to make the clinical diagnosis. Furthermore, clinicians should have a clear appreciation of the roles that iatrogenic interventions and lapses in nutrition and nursing care frequently play in upsetting the homeostatic balance in elderly patients, particularly those who are in long-term institutional and inpatient settings.

The aging process is frequently accompanied by various maladaptations to stress in different organ systems and physiologic functions. The complex mechanisms associated with water metabolism are particularly vulnerable to age-related maladaptations and to the various disease processes and medical interventions that frequently occur in the elderly.

Hyponatremia and hypernatremia are common in the elderly, particularly among those who are hospitalized or living in long-term care facilities. Hyponatremia is defined as a serum sodium concentration of less than 137 mEq per L (137 mmol per L). It is estimated that nearly 7 percent of healthy elderly persons have serum sodium concentrations of 137 mEq per L or less.1 Cross-sectional studies suggest that hyponatremia may be present in 15 to 18 percent of patients in chronic care facilities.2 A 12-month longitudinal study showed that more than 50 percent of nursing home residents had at least one episode of hyponatremia.3 Similarly, cross-sectional studies suggest a 1 percent prevalence of hypernatremia in nursing home residents.4 Among nursing home patients who require acute hospitalization, the prevalence of hypernatremia has been reported to be more than 30 percent.5 Thus, it would be an unusual day in many family physicians’ practices that at least one diagnostic or therapeutic issue related to water metabolism did not arise.

Normal Water Metabolism

The status of water homeostasis in the body is efficiently reflected by the serum sodium concentration. Sodium is the dominant cation in extracellular fluid and the primary determinant of serum osmolality. If a change in the total-body water concentration occurs without an accompanying change in total-body solute, osmolality changes along with the serum sodium concentration. Simply put, hypernatremia and hyponatremia are primary disturbances of free water and reflect pathologic alterations in water homeostasis.

At steady state, water intake and water losses are matched. If losses exceed intake, thirst is stimulated, and fluid intake increases. Thirst is stimulated when the serum osmolality rises above 290 to 295 mOsm per kg (290 to 295 mmol per kg). Thirst is also stimulated by hypotension and hypovolemia. Renal water conservation is the first-line defense against water depletion, but this mechanism is insufficient in settings of significant dehydration and hypertonicity. Moreover, the stimulation of thirst is required to ultimately maintain homeostasis. In conditions of volume depletion or hypertonicity, secretion of antidiuretic hormone (ADH) is stimulated, water is reabsorbed, and a concentrated urine is excreted. In conditions of hypotonicity, ADH is normally suppressed, and a dilute urine is excreted.

Impact of Aging on Water Metabolism

The age-related decrease in total-body water (relative and absolute) makes elderly persons markedly susceptible to stresses on water balance.6 Average healthy 30- to 40-year-old persons have a total-body water content of 55 to 60 percent. By age 75 to 80 years, the total-body water content has declined to 50 percent, with even more of a decline in elderly women.7

Clearly, the thirst mechanism diminishes with age, which significantly impairs the ability to maintain homeostasis and increases the risk for dehydration.8 There is also a clear age-related decrease in maximal urinary concentrating ability, which also increases the risk for dehydration. 9 ADH release is not impaired with aging, but ADH levels are increased for any given plasma osmolality level, indicating a failure of the normal responsiveness of the kidney to ADH.2

The ability to excrete a water load is delayed in the elderly.10 This propensity may contribute to the frequently observed episodes of hyponatremia in hospitalized elderly patients who are receiving hypotonic intravenous fluids or whose fluid intake is not properly monitored.2

Other changes in renal physiology and anatomy that increase the elderly patient’s susceptibility to alterations of water imbalance include decreased renal mass,11 cortical blood flow2 and glomerular filtration rate,12 as well as impaired responsiveness to sodium balance.2

The impact of a lifetime of accumulated disease and comorbidities must also be duly considered in every clinical situation with an elderly patient, in addition to age-related physiologic changes. The elderly patient has a diminished reserve of water balance and an impaired regulatory mechanism. Thirst sensation, concentrating abilities and hormonal modulators of salt and water balance are sluggish and highly susceptible to being overtaken by morbid or iatrogenic events.

Hyponatremia

ETIOLOGY

Hyponatremia is most commonly associated with states of hypotonicity; however, it can also occur in states of normal or high osmolarity. Hyponatremia in association with normal tonicity is a laboratory phenomenon. It is caused by extreme hyperlipidemia or hyperproteinemia13,14 and now rarely occurs as a result of improved laboratory techniques for measuring serum sodium. Hypertonic hyponatremia is caused by the accumulation of osmotically active nonelectrolyte solutes, which causes the movement of water from the intracellular compartment to the extracellular fluid.14 This action dilutes the sodium concentration and is usually the result of hyperglycemia.

Hypotonicity is most commonly associated with hyponatremia. Hypotonic hyponatremia can be divided into two categories based on the extracellular fluid volume: hypovolemic and euvolemic hypotonic hyponatremia. Hypovolemic hyponatremia is caused by true volume depletion or by volume depletion of the effective arterial volume.

Euvolemic hyponatremia is usually the result of an increase in free water with little change in body sodium. This condition is most commonly associated with nonosmotic vasopressin secretion. Causes of euvolemic hyponatremia include certain drugs (such as hydrochlorothiazides), glucocorticoid deficiency, hypothyroidism, the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat syndrome.13

SIADH is characterized by the continued release of ADH in the face of dilution of body fluids and increased extracellular volume. The urine is “inappropriately” concentrated when the body is trying to correct a state of hypotonicity. SIADH is a diagnosis of exclusion. The diagnostic criteria for SIADH are listed in Table 1,13  and the etiologies of this disorder are summarized in Table 2.15  SIADH can also be precipitated by certain drugs (Table 3). 15

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TABLE 1.

Criteria for SIADH

TABLE 1.

Criteria for SIADH

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TABLE 2.

Causes of SIADH

TABLE 2.

Causes of SIADH

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TABLE 3.

Drugs That Can Cause SIADH

TABLE 3.

Drugs That Can Cause SIADH

EVALUATION

Patients with hyponatremia usually are asymptomatic. Symptoms often do not occur until the serum sodium concentration drops below 125 mEq per L (125 mmol per L). The most common manifestations of hyponatremia are neurologic, the result of swelling of brain cells secondary to intracellular movement of water. Patients with severe hyponatremia may present with nausea, headache, lethargy, confusion, coma or respiratory arrest. If hyponatremia develops rapidly, muscular twitches, irritability and convulsions can occur. The only manifestations of chronic hyponatremia may be lethargy, confusion and malaise.

Figure 1 shows an algorithm for the evaluation of patients with hyponatremia.13,16 The first step is to determine the plasma and urine osmolality and to perform a clinical assessment of volume status. If the urine osmolality is less than 100 mOsm per kg (100 mmol per kg), evaluation for psychogenic polydipsia should be conducted. If the urine osmolality is 100 mOsm per kg or greater, renal function should be evaluated. Evidence of renal failure (elevated blood urea nitrogen [BUN] and creatinine levels) points to primary renal disease as the likely cause of hyponatremia. If BUN and creatinine levels are normal, assessment of the extracellular fluid volume should be conducted. The urine sodium determination should be used as a guide in noneuvolemic states to determine whether further evaluation for renal failure or pathophysiologic renal sodium loss is required. It should be kept in mind, however, that diuretics can alter the urine sodium concentration and confuse the clinical picture.

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Assessment of Hypotonic Hyponatremia

FIGURE 1.

Algorithm for the assessment of hyponatremia. (BUN = blood urea nitrogen; HCTZ = hydrochlorothiazide; SIADH = syndrome of inappropriate antidiuretic syndrome secretion; CHF = congestive heart failure)

Information from Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am 1997;81:585–609, and Kaji DM. Hyponatremia and hypernatremia. In: Taylor RB, ed. Difficult diagnosis. Philadelphia: Saunders, 1985:290–9.

Assessment of Hypotonic Hyponatremia

FIGURE 1.

Algorithm for the assessment of hyponatremia. (BUN = blood urea nitrogen; HCTZ = hydrochlorothiazide; SIADH = syndrome of inappropriate antidiuretic syndrome secretion; CHF = congestive heart failure)

Information from Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am 1997;81:585–609, and Kaji DM. Hyponatremia and hypernatremia. In: Taylor RB, ed. Difficult diagnosis. Philadelphia: Saunders, 1985:290–9.

TREATMENT

If the patient is symptomatic because of severe hyponatremia, it is generally considered safe to raise the serum sodium concentration at a rate of 0.6 to 2.0 mEq per L (0.6 to 2.0 mmol per L) per hour or no more than 12 mEq per L (12 mmol per L) in the first 24 hours. A too-rapid increase in the serum sodium concentration, with the rapid transfer of free water out of the brain cells, can cause diffuse cerebral demyelination, specifically in the pons (central pontine myelinolysis). In the setting of acute hyponatremia, when rapid correction of the serum sodium concentration may be needed, hypertonic solutions such as 3 percent saline may be administered at a rate of approximately 1 to 2 mL per kg per hour. 13,17 Loop diuretics are often used in conjunction with normal saline or 3 percent saline to prevent volume overload and the potentiation of congestive heart failure.

Because hyponatremia is usually only mildly symptomatic or asymptomatic, treatment should be tailored to the clinical situation. Hyponatremia in a euvolemic patient can be managed with fluid restriction and discontinuation of any medications that affect free-water excretion, along with initiation of treatment of the underlying cause. Fluid restriction must be less than free-water losses, and total fluid intake should typically be less than 500 to 800 mL per day in the elderly patient with euvolemic hyponatremia.2

If hyponatremia is secondary to a low extra-cellular volume (volume contraction), the fluid deficit should be corrected by administration of normal saline solution. Once the patient is clinically euvolemic, the drive for the body to produce ADH is gone, and the patient is able to excrete the excess free water. 6 If the clinical picture is one of an “effective” low extracellular volume, but the patient appears to have fluid overload, the underlying cause of the low sodium level, such as congestive heart failure, nephrotic syndrome, cirrhosis or hypoalbuminemia, should be treated. For example, hyponatremia related to heart failure should resolve if treatment to decrease the afterload, increase the preload or increase the contractility of the heart corrects the clinical situation.

SIADH is treated with free-water restriction until the underlying cause of the disorder is corrected. Administration of normal saline is not an appropriate therapy because the sodium may be rapidly excreted while the water is retained, exacerbating hyponatremia.13 An adjunct to free-water restriction, in some circumstances, is the addition of therapy with demeclocycline (Declomycin) in a dosage of 600 to 1,200 mg per day. Demeclocycline induces nephrogenic diabetes insipidus and helps to correct hyponatremia, especially in a patient in whom free-water restriction is highly difficult. 18 Demeclocycline, however, is contraindicated in patients with renal or hepatic disease.

Hypernatremia

ETIOLOGY

Hypernatremia is primarily a defect in water intake and usually implies an impairment in the thirst mechanism or a lack of access to adequate fluid intake. Hypernatremia may be broadly viewed in four major etiologic categories, as follows13:

Primary Hypodipsia. Primarily a defect of thirst, hypodipsia is usually associated with destruction of the hypothalamic thirst center secondary to primary or metastatic tumors, granulomatous disease, vascular disease or trauma.

Diabetes Insipidus. Diabetes insipidus is primarily a defect in the secretion or action of ADH, which may be hypothalamic (central) or nephrogenic (Tables 4 and 5). Severe diabetes insipidus is manifested by severe polyuria and polydipsia in the setting of markedly dilute urine.

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TABLE 4.

Etiologies of Hypothalamic Diabetes Insipidus

TABLE 4.

Etiologies of Hypothalamic Diabetes Insipidus

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TABLE 5.

Etiologies of Nephrogenic Diabetes Insipidus

TABLE 5.

Etiologies of Nephrogenic Diabetes Insipidus

Pure Hypertonic Saline Gain. This is a relatively unusual cause of hypernatremia. It is the consequence of accidental or intentional ingestion of hypertonic solutions, such as hypertonic saline or bicarbonate-containing solutions.

Inadequate Fluid Intake in the Setting of Increased Free-Water Loss. Hypernatremia in the elderly is most commonly due to the combination of inadequate fluid intake and increased fluid losses. Age-related impairment in the thirst mechanism and barriers to accessible fluids are often contributing factors. Renal concentrating ability is impaired, and adaptability to losses is compromised. Pure water loss is frequently associated with fever, hyperventilation or diabetes insipidus. More commonly, hypotonic loss is seen related to gastrointestinal sources, burns, diuretic therapy or osmotic diuresis. Recognition of free-water loss in elderly patients is frequently delayed, and the frail elderly patient can quickly slip into a clinically significant hypernatremic state.

EVALUATION

The clinical manifestations of hypernatremia are nonspecific and often subtle in the elderly. They are primarily central nervous system (CNS) manifestations, such as irritability, restlessness, lethargy, muscular twitching, spasticity and hyperreflexia, all of which are secondary to decreased water content in the brain cells.13 Water exits the intra-cellular compartment, and cells shrink. In the brain, this action can lead to traction on vessels, which may result in hemorrhage.

The first step in the clinical assessment of the patient with hypernatremia is a detailed analysis of the clinical circumstance. This includes a careful review of the patient’s weight, intake and output, and a critical analysis of fluid nutrition and nursing care. The urgency of the clinical state should be evaluated by carefully assessing the volume status and by performing a neurologic examination. Such an analysis provides the answer in most hospitalized patients who acquire hypernatremia during their hospital stay. Measurements of spot urine/plasma osmolality and urine sodium levels may yield valuable clues in more difficult cases. 13

The algorithm in Figure 2 summarizes the work-up of hypernatremia.19 High urine osmolality (greater than 700 mOsm per kg [700 mmol per kg]) in a setting of a low urine sodium level usually indicates an extrarenal hypotonic loss of free water. Urine osmolality that is “inappropriately” low in the setting of hypernatremia suggests renal free-water loss. Finally, a urine osmolality that is quite low (less than 150 mOsm per kg [150 mmol per kg]) is diagnostic of diabetes insipidus in the setting of hypernatremia and polyuria. Sophisticated and more dangerous dehydration testing is rarely necessary in the evaluation of hypernatremia and is reserved for more difficult cases of diabetes insipidus.

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Assessment of Hypernatremia (serum sodium >145 mEq/L [>145 mmol/L])

FIGURE 2.

Algorithm for the assessment of hypernatremia. (U/P = urine/plasma; ADH = antidiuretic hormone; CNS = central nervous system)

Figure 2 adapted with permission from Healey PM, Jacobson EJ. Common medical diagnosis: an algorithmic approach. 2d ed. Philadelphia: Saunders, 1994:84–5.

Assessment of Hypernatremia (serum sodium >145 mEq/L [>145 mmol/L])

FIGURE 2.

Algorithm for the assessment of hypernatremia. (U/P = urine/plasma; ADH = antidiuretic hormone; CNS = central nervous system)

Figure 2 adapted with permission from Healey PM, Jacobson EJ. Common medical diagnosis: an algorithmic approach. 2d ed. Philadelphia: Saunders, 1994:84–5.

TREATMENT

Because of the adaptation of the CNS to cell shrinkage and because too-rapid correction can lead to dangerous cerebral edema, chronic hypernatremia should be treated slowly and carefully. A general guideline is to correct 50 percent of the calculated water deficit in the first 12 to 24 hours, with the remainder corrected over the next one to two days.2 Initially, ongoing water losses should be identified and quantified, and continuing water losses should be replaced continually. Extracellular volume should be restored in hypovolemic patients.20

With chronic hypernatremia, water deficits should be calculated and replaced slowly; with acute hypernatremia, water deficits should be replaced more rapidly.13 The net water deficit is calculated by first estimating the total-body water (TBW) in liters and then applying the following formula20:

A worsening in neurologic status during free-water replacement may indicate the development of cerebral edema and requires prompt reevaluation and temporary discontinuation of water replacement. Volume depletion should be corrected before initiating replacement therapy to correct the deficit. If the hypernatremia is secondary to solute excess, a diuretic along with water replacement may be needed. In some circumstances of volume overload, dialysis may be indicated.

A standing prescription for free-water intake that matches losses should be written in the medical record of patients with primary hypodipsia. Hypothalamic diabetes insipidus is treated with ADH replacement. Nephrogenic diabetes insipidus is often treated with a low-salt diet and thiazide diuretics. When possible, precipitating medications should be discontinued and underlying conditions treated to minimize the clinical manifestations.

Prevention

One of the most important points with regard to hyponatremia and hypernatremia is to recognize the role that the medical care system sometimes plays in precipitating these conditions in frail elderly patients. Meticulous attention to fluid intake and fluid losses is required in all medical settings. The more impaired the patient, the greater the likelihood that water homeostasis will be overcome by medical events. Anticipation that a “sodium/free-water” problem will occur in a patient during hospitalization or in a long-term care facility is perhaps the safest assumption. It is essential for physicians to work with other members of the health care team, including nursing staff, dietary staff and family members, to prevent or at least minimize the degree of disruption to water balance in susceptible patients.

Exercise-Associated Hyponatremia | American Society of Nephrology

Abstract

Exercise-associated hyponatremia has been described after sustained physical exertion during marathons, triathlons, and other endurance athletic events. As these events have become more popular, the incidence of serious hyponatremia has increased and associated fatalities have occurred. The pathogenesis of this condition remains incompletely understood but largely depends on excessive water intake. Furthermore, hormonal (especially abnormalities in arginine vasopressin secretion) and renal abnormalities in water handling that predispose individuals to the development of severe, life-threatening hyponatremia may be present. This review focuses on the epidemiology, pathogenesis, and therapy of exercise-associated hyponatremia.

Severe and potentially life-threatening hyponatremia can occur during exercise, particularly in athletes who participate in endurance events such as marathons (42. 2 km), triathlons (3.8 km of swim, 180 km of cycling, and 42.2 km of running), and ultradistance (100 km) races. In fact, hyponatremia has been stated to be one of the most common medical complications of long-distance racing and is an important cause of race-related fatalities (1). On the basis of recent studies of the incidence and risk factors of hyponatremia in endurance athletes, along with well-publicized reports of fatalities as a result of hyponatremia, medical directors and marathon organizations have begun to warn participants of the dangers of hyponatremia and excessive fluid intake (2).

Exercise-associated hyponatremia (EAH) first was described in Durban, South Africa, in 1981; subsequently, Noakes et al. (3) in 1985 described the occurrence of severe hyponatremia in four athletes who participated in endurance events that were longer than 7 h. This report was followed by a similar paper by Frizzel et al. (4) that described the development of EAH in two of the authors. Importantly, before 1981, athletes were advised to avoid drinking during exercise, leading to the development of hypernatremia and dehydration in some athletes (5). Since that time, it generally has been advised that athletes consume as much fluid as possible during exercise, and rates of fluid intake during running races vary widely from 400 to 1500 ml/h or greater (6–8). In fact, most race organizers currently provide copious supplies of water and “sports beverages” throughout the race course to fend off dehydration. Concomitant with these recommendations, the incidence of hyponatremia in athletes seems to be increasing, especially in the United States (1,9–13). As the popularity of marathon races and other endurance events increase, more athletes are likely to be at risk for the development of EAH.

EAH can take two forms, depending on whether specific symptoms that are attributable to hyponatremia are present (14). Athletes may present with symptoms such as confusion, seizures, and altered mental status in association with serum sodium levels <135 mmol/L and are considered to have exercise-associated hyponatremic encephalopathy (EAHE). Alternatively, athletes may present with isolated serum sodium levels <135 mmol/L without easily discernible symptoms and have EAH.

This review focuses on important historic, epidemiologic, and pathophysiologic aspects of this condition, highlighting recent articles that show the importance of excessive water intake in the genesis of EAH. Important treatment-related issues also are discussed.

Incidence

Until recently, the incidence of hyponatremia during endurance exercise was unknown and thought to be relatively uncommon. However, recent studies have shown that endurance athletes not uncommonly develop hyponatremia at the end of the race, usually in the absence of clear central nervous system symptoms (9,10,12,15–25). For example, in the 2002 Boston Marathon, Almond et al. (15) found that 13% of 488 runners studied had hyponatremia (defined as a serum sodium concentration of 135 mmol/L or less) and 0.6% had critical hyponatremia (serum sodium concentration of 120 mmol/L or less). Speedy et al. (21) investigated 330 athletes who finished an ultramarathon race. In this study, 58 (18%) were hyponatremic (defined as a serum sodium <135 mmol/L) and 11 had severe hyponatremia (serum sodium <130 mmol/L). Studies of other endurance events have reported the incidence of hyponatremia to be up to 29% (9,10,12,15–25). These incidence rates may be overestimations as a result of sampling biases. For example, in the 2002 Boston Marathon study, of 766 runners enrolled in the study, only 488 runners had serum sodium values assayed (15). Some of these runners did not finish the race, and others had time constraints that did not allow them to have blood samples obtained. As is discussed later, the majority of these athletes are asymptomatic or mildly symptomatic (nausea, lethargy). However, severe manifestations such as cerebral edema, noncardiogenic pulmonary edema, and death can occur (11–14).

There have been at least 8 reported deaths from EAH (5,10,11,26–29). Many of these reports relate to a series of fatalities in the military between 1989 and 1996 (27–29). During this period, military recruits were encouraged to ingest 1.8 L of fluid for every hour they were exposed to temperatures above 30°C (30). At least four other deaths have been attributed to EAH in the United States (5,10,11,26,31). It is interesting that two of these deaths occurred in doctors (31). The exact incidence of mortality related to EAH is not known but is likely to be low.

Risk Factors

Several risk factors have been linked with the development of EAH (Table 1). The major risk factor seems to be overhydration or excessive fluid consumption during activity (reviewed in reference [31]). This first was suggested by Noakes et al. in their original publication in 1985 and confirmed in this group’s later studies (3,5,21). The chronological history of the incidence of EAH also points to the primary role of overhydration in the pathogenesis. Before 1981, athletes were encouraged to drink heavily during exertion to avoid dehydration (7,31). With the description of EAH in South Africa and New Zealand in 1985, new fluid consumption guidelines that restricted overzealous fluid intake for endurance events in these countries were promoted (32,33). Concomitant with these recommendations, the incidence of EAH fell in both of these regions (19,20). Similar observations were made after the US military revised its guidelines for fluid consumption during training activities after the incidence of EAH increased (31). With an upper limit of fluid consumption set at 1.0 to 1.5 L/h, the incidence of EAH in the US military fell (31).

Table 1.

Risk factors for the development of EAH^a

In a study of runners in the Boston Marathon, Almond et al. (15) found significant correlations between fluid intake and the incidence of hyponatremia. Specifically, a fluid intake of >3 L, a postrace weight greater than prerace weight, self-reported water loading (increased fluid consumption above baseline in preparation for the marathon), and self-reported fluid intake during the race all were found to be significant predictors for the development of hyponatremia (P < 0. 05) (15). Substantial weight gain during the duration of the activity seemed to be the most important predictor of hyponatremia and correlated well with increased fluid intake. Speedy et al. (21) also found correlations between intrarace weight gain and hyponatremia; 73% of patients who were found to be severely hyponatremic had either gained or maintained weight during the race. Noakes et al. (34) in the largest study to date investigated the changes in serum sodium concentration associated with changes in body weight in 2135 endurance athletes. The mean ± SD serum sodium was 136.1 ± 6.4 mmol/L for athletes who gained weight during the race, 140.5 ± 3/7 mmol/L for those with minimal weight gain, and 141.1 ± 3.7 mmol/L for those who lost weight during the race. The authors estimated that athletes who gained >4% body weight during exercise had a 45% probability of developing hyponatremia. Importantly, 70% of individuals who gained weight during exercise did not develop hyponatremia, pointing to other important factors in the pathogenesis, as discussed next (34).

Almond et al. (15) were not able to find a correlation in the type of fluids consumed (water versus electrolyte-containing solutions) and the subsequent development of hyponatremia. Other studies also have shown that the consumption of a carbohydrate/electrolyte-containing sports drink does not protect against the development of hyponatremia (35–38). This likely reflects the relative hypotonicity of most of the commercial sports drinks in which the sodium concentration typically is 18 mmol/L (39).

Gender likely plays a role in the risk for development of EAH, with female athletes more likely than male athletes to develop hyponatremia during endurance events (10–12,15,21,40). Of 26 cases of EAH reported after the San Diego Marathon, 23 occurred in women (12). Hyponatremia was three times more common in women than in men in the 1997 New Zealand Ironman triathlon (21). Almond et al. (15) also found that hyponatremia developed more commonly in women in the Boston Marathon. However, in this study, when these results were corrected for body mass index, racing time, and weight change, the difference did not reach statistical significance, suggesting that body size and duration of exercise may explain the gender differences. Furthermore, the incidence of hyponatremia in US military recruits reflects the gender distribution of this cohort and is not skewed to women (41). Some investigators also have suggested that women adhere more stringently to hydration recommendations during exercise and therefore consume more fluids (42). The finding of a gender association for the risk for symptomatic hyponatremia also has been seen in the postoperative state. Ayus et al. (43) noted that despite equal incidences of postoperative hyponatremia in men and women, 97% of those with permanent brain damage were women and 75% of them were menstruant. This predisposition likely is explained by the effects of sex hormones on the Na⁺-K⁺-ATPase (44). Both estrogen and progesterone inhibit the function of the Na⁺-K⁺-ATPase, which normally has an important function in the extrusion of sodium from cells during the development of hyponatremia. Ultimately, this inhibition may result in a higher risk for cerebral edema and increased intracranial pressure in women who are exposed to acute hyponatremia.

The development of hyponatremia also has been correlated with the number of marathons run, the training pace, and the race duration (10,12,15,45). Those who have run fewer marathons (less experienced runners), have slower training paces, and have longer race times (especially >4 h) each were shown independently to have a significantly higher risk for developing hyponatremia (10,12,15,45). Longer race times likely correlate with increased water consumption and increased sodium losses (10,12,46). For example, participants who developed hyponatremia in the 1998 and 1999 San Diego Marathons had an average finishing time of 5 h and 38 min, and many of these individuals admitted to drinking as much fluid as possible during and after the event (12). A low body mass index also was shown to be a significant risk factor, perhaps as a result of the ingestion of larger amounts of fluid in proportion to size and total body water (TBW) (15).

Medications also may play a significant role in the hyponatremia that is found in endurance athletes, but this largely is unproved. Nonsteroidal anti-inflammatory drug (NSAID) use is common among marathon runners, being used in 50 to 60% of men and women, respectively (10,22,47). NSAID are known to potentiate the effects of arginine vasopressin (AVP) by inhibiting renal prostaglandin synthesis via the COX-2 isoform of cyclo-oxygenase (48–50). Furthermore, NSAID decrease the GFR when given to those with effective volume depletion, such as exercising endurance athletes (51). These effects may impair the urine-diluting capacity of the kidney (51). Despite these theoretical considerations, Almond et al. (15) were unable to associate the use of NSAID with the development of hyponatremia in the runners who were studied in the 2002 Boston Marathon. Other studies also have not been able to ascribe conclusively to NSAID use the development of hyponatremia, although several of these studies were underpowered to do so (10,22). However, a recent study in 330 triathletes demonstrated a significant association of NSAID use and the development of hyponatremia (23). In this study, the incidence of NSAID use in athletes was 30%, and NSAID use was highly associated with the development of hyponatremia (P = 0.0002), as well as higher plasma potassium and creatinine levels. Several other, smaller studies and case reports also have suggested a potentiating role for NSAID use (11,12,52). Therefore, the role of NSAID in the development of EAH remains controversial but in some runners likely is a potentiating factor. Whether other medications, such as selective serotonin reuptake inhibitors or thiazide diuretics, that are associated with hyponatremia in nonathletes can potentiate the development of EAH is not known. It is important to recognize that these risk factors do not suggest causation or even an independent association with the development of hyponatremia. However, they do offer important clues to the pathogenesis of the condition.

Pathophysiology

Normally, renal and hormonal systems maintain the plasma osmolality within tight limits with variability of no more than 1 to 2% (reviewed in reference [53]). These tight limits reflect the physiologic importance of osmolality regulation on cell volume and function (54). The development of hyponatremia (usually, in the setting of hypo-osmolality) reflects either defects in these hormonal and renal control mechanisms or water ingestion that overwhelms them. In the specific instance of EAH, defects in renal diluting mechanisms, hormonal control of water excretion, excessive sodium losses, and excessive water intake all contribute to the development of hypo-osmolality (summarized in Figure 1).

Figure 1.

Pathophysiologic factors in the development of exercise-associated hyponatremia (EAH). AVP, arginine vasopressin.

Current evidence strongly supports that EAH is, in large part, dilutional in nature. In the majority of athletes who develop hyponatremia, there is an increase in TBW relative to that of total body exchangeable sodium (34). As described previously, this seems to occur by the ingestion of hypotonic fluids (water or sports drinks) in excess of sweat, urine, and insensible (mainly respiratory and gastrointestinal) losses. In a seminal study, Noakes et al. (34) described a linear relationship with a negative slope between the serum sodium after racing and the degree of weight change in 2135 athletes (Figure 2). The primary cause of this weight gain during exercise must be the consumption of fluids during exercise. This consumption of fluids during exercise can be driven by thirst or through conditioned behavior. Some have hypothesized that in some athletes, the thirst drive may be excessive, but, more likely, the excessive fluid intake during exercise reflects conditioned behavior that is based on recommendations to drink fluid during exercise to avoid dehydration as well as the wide availability of fluids along the race course (31,55). This hypothesis is supported by data, previously described, that the incidence of EAH was rare or nonexistent before 1981, when recommendations for fluid intake during exercise were conservative. EAH was seen only after recommendations for more aggressive hydration were promulgated (31). Occasionally, some athletes may drink up to 3 L/h in an attempt to produce dilute urine to escape detection of banned drugs in the urine (56). Finally, some athletes may drink large volumes of fluid in the days leading up to a marathon in an attempt to ward off dehydration. This was the case for one female runner who drank 10 L of fluid on the evening before a marathon and then experienced postrace hyponatremia (57).

Figure 2.

Relationship between serum sodium after racing and the weight change (in %) during exercise in 2135 athletes who competed in endurance events. •, asymptomatic athletes; ○, athletes with symptoms compatible with EAH encephalopathy (EAHE). The majority of athletes who develop clinically significant hyponatremia have positive weight changes. Reprinted from reference (34), with permission. Copyright 2005 National Academy of Sciences.

However, excessive fluid consumption is not the sole explanation for the development of EAH. In the study of Noakes et al. (34), hyponatremia did not develop in 70% of the athletes who overconsumed fluids and had an increase in TBW. This indicates that other important factors must be operational in the pathogenesis of EAH. The importance of other factors also is highlighted by the fact that the maximum water excretory capacity of the kidneys is between 750 and 1500 ml/h (53). In combination with fluid losses from sweating and insensible losses (which may be in excess of 500 ml/h), most athletes should be able to consume fluids in excess of 1500 ml/h before retaining weight and increasing TBW. This amount of fluid consumption is at the upper limit of what most athletes would consume during an activity (31). Therefore, either defects in renal water excretion and/or significant sodium losses or failure to mobilize exchangeable sodium stores may occur in athletes who develop EAH. Furthermore, some athletes develop hyponatremia without appreciable gains in total body weight (34). As discussed next, these athletes may have significant sodium losses or also may have gained net body free water as a result of the metabolism of glycogen and triglycerides and not as a result of ingestion. However, the contribution of fuel metabolism or metabolic water production to TBW likely is small. During treadmill running at 74% of maximal oxygen consumption, metabolic water production averages 144 g/h (in contrast, sweat loss during this time was 1200 g/h) (58). There is a possibility that water that is stored with glycogen can be released with glycogen breakdown. This may be an important component in the cause of hyponatremia that occurs without weight gain because each kilogram of glycogen can contain upwards of 3 kg of associated water (59,60).

Data on the levels of AVP during exercise are conflicting. Unfortunately, systematic measurement of AVP levels or free water clearances in athletes who present with hyponatremia has not been done except in isolated cases. There are several potential pathways for stimulation of AVP release in exercising athletes. Controlled laboratory studies have demonstrated that as exercise intensity increases above 60% of maximal oxygen consumption, there are concomitant increases in AVP levels (61). Nonspecific stresses that are experienced by athletes and caused by factors such as pain, emotion, or physical exercise have been thought to cause nonosmotic release of AVP (62). However, it is difficult to determine whether this effect is mediated by a specific pathway or is due to a secondary stimulus, such as hypotension or nausea, that may occur in exercising athletes. AVP production also may be stimulated appropriately in athletes who develop volume depletion. However, the level of volume depletion that is required to stimulate AVP production in the absence of hyperosmolality is in excess of 7 to 8% of body volume. These levels of volume depletion typically are not seen in athletes (e.g., in the 2001 South African Ironman Triathlon, only 7% of finishers had a net body weight loss >5% [20]). Furthermore, the majority of athletes with EAH finish events with an increase in body weight and possibly an expanded plasma volume (34). Exposure to heat also can lead to the secretion of AVP (63). However, this effect of temperature may be influenced secondarily by changes in effective arterial volume that occur with heat-induced vasodilation. Despite these considerations, in some athletes during prolonged exercise, plasma AVP levels may not be suppressed maximally despite maintenance or even excess of plasma volume. This has been described in studies of hikers who developed hyponatremia in the Grand Canyon and in an army recruit during a prolonged field march (40,64). Speedy et al. (46) also described median AVP levels that were significantly higher in athletes who developed hyponatremia in the 1997 New Zealand Ironman Triathlon.

An intriguing link between exercise and the nonosmotic stimulation of AVP release may be related to the release of inflammatory cytokines by the exercising and injured skeletal muscle as postulated by Siegel (65). As glycogen stores are depleted, rhabdomyolysis or lesser degrees of muscle injury can occur with the release of inflammatory cytokines such as IL-6. Independent of rhabdomyolysis, studies have shown that exercise primes an array of pro- and anti-inflammatory and growth factor expressions within circulating leukocytes (66,67). Mastorakos et al. (68) demonstrated that IL-6 can act as an AVP secretagogue. This effect of IL-6 on hypothalamic AVP secretion also was seen in children after head trauma (69). It is interesting that women respond to exercise-induced stress with the production of higher levels of IL-6, perhaps explaining, in part, the increased risk for EAH in women (66). Along these lines, single-nucleotide polymorphisms in the promoter region of inflammatory cytokines are important in determining the levels of cytokine production (70). A particular athlete may be predisposed to EAH on the basis of the single-nucleotide polymorphism profile and specific inflammatory response to exercise. Conversely, IL-6 in a rat sepsis model has been shown to reduce the expression of aquaporin-2, the downstream target of AVP and ultimate regulator of water diuresis (71). How these factors interact to cause EAH is not known but should be an avenue of research.

Consistent with the probable role of AVP in EAH, athletes who have finished races with hyponatremia have also been demonstrated, in some cases, to have inappropriately elevated urine osmolality (72). In this setting, even small increases in plasma AVP levels can cause significant water retention and hyponatremia, especially in combination with excessive water intake. Furthermore, gastrointestinal blood flow and water absorption from the stomach and intestine may be impaired during exercise (73). When the athlete stops activity, water absorption may increase rapidly and significantly (73). In the setting of elevated AVP levels, this rapid absorption of large quantities of water or hypotonic fluids can lead to significant falls in serum sodium.

Whether AVP levels are increased inappropriately in all athletes who develop EAH is not known. Speedy et al. (74) measured normal (suppressed) AVP levels in two triathletes who developed hyponatremia during an Ironman event and demonstrated that other causes for renal impairment of free water excess must be present in some athletes. A possible cause of EAH is that during exercise, the diluting capability of the kidney is likely to be diminished (75). In both the thick ascending limb of Henle and the distal tubule, reabsorption of sodium chloride in the absence of water (and thus dilution of the urine) depends on the delivery of filtrate to these segments and is affected by the renin-angiotensin-aldosterone system, the sympathetic nervous system, renal blood flow, and proximal tubular reabsorption of sodium. During exercise, there is a release of catecholamines and angiotensin II that leads to an increase in sodium and water reabsorption in the proximal tubule, thereby decreasing the amount of filtrate that is delivered to the distal diluting segments of the kidney (75). Furthermore, renal blood flow and GFR are decreased in the setting of endurance exercise and further limit the delivery of filtrate to the diluting segments of the kidney (75). These effects on the diluting capacity of the kidney may be significant in leading to impairments of free water excretion.

Although overdrinking clearly is the most important causative factor in the development of EAH, there is a variable and important contribution of sodium loss from sweating (38). The concentration of sodium in sweat varies widely but is usually 15 to 65 mEq/L, with highly fit athletes generally excreting sweat with sodium concentrations <40 mEq/L (38,76). The volume of sweat during exercise also varies widely, from approximately 250 ml/h to >2 L/h, again being less in more fit athletes (77,78). This loss of a substantial amount of hypotonic fluid may seem to protect against the development of hyponatremia. However, these losses are replaced by the ingestion of more hypotonic fluids (water or sports drinks), and the extracellular volume loss in sweat may serve as a stimulus for antidiuretic hormone (ADH) secretion. In fact, mathematical models demonstrate that the magnitude of sweat sodium loss is insufficient to produce EAH (38,79). For example (as discussed in reference [38]), in a 90-km ultramarathon race, an athlete may lose approximately 8.6 L of sweat. Assuming sweat sodium concentrations of either 25 or 50 mmol/L and that all fluid losses were replaced by water, the resulting sodium deficits would be 215 and 430 mmol, respectively. For a 70-kg athlete, the resulting serum sodium concentration would be either 135 or 130 mmol/L, respectively. However, for longer duration events and for those with high sweat sodium concentrations (>75 mmol/L), a sufficient sweat sodium deficit can occur for athletes to finish the race both dehydrated and hyponatremic. This is supported by the finding that some athletes finish races with net weight loss and hyponatremia (34). Furthermore, one case report of a patient who had cystic fibrosis (patients with cystic fibrosis excrete large amounts of sodium in their sweat) and developed EAH points to the possibility that some people may be genetically predisposed to EAH as a result of high sweat sodium losses (80).

As mentioned previously, in the study by Noakes et al. (34) 70% of athletes who were overhydrated did not develop EAH. Why is it that only a percentage of athletes develop EAH? What are the factors that protect these athletes from developing EAH? An intriguing possibility discussed by Noakes et al. (34) is that some athletes are able to mobilize sodium from internal stores that otherwise are osmotically inactive. This exchangeable sodium store has been described by Edelman and colleagues, Titze and colleagues, and Heer and colleagues (81–86). For example, in the study by Heer et al. (86) participants were fed a diet of varying sodium amounts with a fixed amount of water ingestion. Despite these conditions, serum sodium levels remained constant without a concomitant increase in TBW. These studies indicated that up to one fourth of the total body sodium may exist in bone and cartilage stores that are not osmotically active (i.e., in an insoluble crystal compound) but potentially recruitable into an osmotically active form (81–83). In rats, this nonosmotically active sodium may reside bound to skin proteoglycans (87,88). This dynamic pool of exchangeable sodium also can lead to the osmotic inactivation of sodium if sodium moves into this compartment. This concept was explored indirectly in early studies of syndrome of inappropriate ADH secretion (SIADH) (89,90). In these studies, the balance of sodium loss and water gain could not explain adequately the extent to which serum sodium was reduced. Therefore, it was hypothesized that hyponatremia was related to the osmotic inactivation (sequestration) of previously osmotically active sodium. It should be pointed out that the presence of this exchangeable sodium store is not supported by all investigators. Seelinger et al. (91) showed in sodium balance studies in dogs that the changes in TBW and electrolyte levels can be accounted for without invoking an osmotically inactive sodium pool. Furthermore, most of the experimental data supporting an exchangeable osmotically inactive sodium pool are derived from studies on sodium loading that occurs over a more extended period and may not be applicable to the situation that is encountered by athletes. However, the data presented by Noakes et al. (34) do support that an exchangeable sodium pool may serve as a buffer for losses of sodium that occur through sweat or urine and also can buffer changes in serum sodium levels that occur with changes in TBW. Therefore, athletes who gain TBW and maintain a normal serum sodium concentration are able to mobilize this store of exchangeable sodium, whereas athletes who develop EAH either cannot mobilize the exchangeable pool or sodium or may osmotically inactivate sodium (34). The factors that govern the exchange of sodium between these compartments is unknown but may involve hormonal factors such as angiotensin II or aldosterone (81–86). The magnitude of this effect in athletes is large with up to 700 mmol of sodium being mobilized from the osmotically inactive pool in the calculations by Noakes et al. (34).

Another possibility that may explain the discrepancy between weight gain and the development of hyponatremia is the contribution of water that remains in the lumen of the gastrointestinal tract. This is especially important in athletes who may have consumed a large amount of fluid toward the end of a race and in those with elevated AVP levels. In this setting, rapid absorption of this hypotonic fluid coupled with impaired free water excretion would lead to a rapid fall in serum (especially arterial) sodium levels.

Clinical Features

The clinical manifestations of EAH range from no or minimal symptoms to severe encephalopathy, seizures, respiratory distress, and death. In general, the degree of clinical symptoms is related not to the absolute measured level of serum sodium but to both the rate and the extent of the drop in extracellular tonicity. However, individual variability in the clinical manifestations of hyponatremia is great. It seems that the majority of runners with EAH have mild (weakness, dizziness, headache, nausea/vomiting) or no symptoms (usually associated with serum sodium values ranging from 134 to 128 mmol/L) (1,9–13,15). In athletes with serum sodium values <126 mmol/L, there is a higher likelihood of severe clinical manifestations such as cerebral edema, altered mental status, seizures, pulmonary edema, coma, and death (11,17,19,20,24). However, a systematic survey of symptoms that are associated with hyponatremia in athletes has not been performed.

Hew et al. (10) examined the clinical manifestations of 21 hyponatremic runners who finished the Houston Marathon in 2000. These clinical manifestations were compared with those of runners who did not have hyponatremia and presented to the medical tent at the conclusion of the race. The only symptom that was more common (P = 0.03) in the hyponatremic group was vomiting. Other symptoms such as headache, nausea, dizziness, and lightheadedness could not distinguish hyponatremia from other causes, attesting to the nonspecific nature of signs and symptoms that are associated with hyponatremia.

A common scenario for medical personnel who staff endurance athletic events is the care of the “collapsed athlete.” Several studies have examined the incidence of hyponatremia in this cohort, and a range of 6 to 30% of these athletes had serum sodium values below normal (9,10,12,15–25). The wide range of incidence likely reflects differences in fluid replacement guidelines that were prevalent at the time and place of the study.

Given the difficulty in using clinical symptoms to identify athletes with hyponatremia and the potential for life-threatening consequences, recommendations have been made that medical facilities at endurance events have the capability for onsite analysis of serum or plasma sodium (14). Any athlete who presents with signs or symptoms that are compatible with hyponatremia should be screened for EAH by direct measurement of serum or plasma sodium.

It is critically important to realize that a postrace venous serum sodium measurement may underestimate significantly the severity of hyponatremia (92). This occurs for three reasons: (1) Water may be retained in the gastrointestinal tract during the athletic event only to be absorbed rapidly in the postrace period. If AVP levels are elevated, this retained water can lower rapidly the serum sodium when reabsorbed into the circulation. (2) Shafiee et al. (93) demonstrated that the arterial sodium concentration can be significantly lower than the venous sodium concentration, with this difference being accentuated with more rapid absorption of water (there may be as much as a 4-mM difference between arterial and venous sodium concentrations when water is ingested rapidly). Because it is the arterial sodium concentration that determines the risks for acute central nervous system symptoms, runners with a large amount of retained water in the gastrointestinal tract may be at higher risk for cerebral edema than their venous serum sodium concentration would indicate. Therefore, in athletes with low body mass, mildly depressed venous sodium concentrations, and recent large water intakes, the risk for deterioration secondary to worsening hyponatremia may go unrecognized. (3) There may be transient rises in venous sodium concentration at the end of a race (especially if sprinting) as muscle lactic acid accumulates and leads to a shift of water intracellularly (94). This transient rise in serum sodium can be as high as 10 mM and may mask significant hyponatremia.

Prevention of EAH

Because EAH primarily develops by consumption of fluid in excess of urinary and sweat losses, most efforts at prevention have been focused on education about the risks of the overconsumption of fluids (14,95). In many respects, EAH can be viewed as an iatrogenic condition because of the prevailing view that exercising athletes should drink as much fluid as tolerable during a race. Given that there is a wide variation of sweat production and renal water excretory capacity both between individual athletes and in the same individual depending on ambient conditions during the race, universal guidelines for prevention are not feasible. However, several general recommendations for the prevention of EAH have been made (14,95–98). The first is to drink only according to thirst and no more than 400 to 800 ml/h (95). The higher rates of fluid intake would be recommended for runners with higher rates of exertion (e.g., heavier runners, warmer conditions, longer times of exertion). This rate of fluid intake is well below the levels of intake that are seen in athletes who develop EAH (up to 1.5 L/h water) but above the level that would be associated with dehydration. The second recommendation is to use the USA Track and Field guidelines or other methods to estimate hourly sweat losses during exercise and avoid consuming amounts that are greater than this amount during endurance events (96,97). This is facilitated by serial measurements of weights during and after exercise with the goal to maintain weight or even finish exercise with a slighter lower weight. However, this is difficult, time-consuming, and less likely to be followed by casual athletes. That these recommendations can be effective was demonstrated by Speedy et al. (99), who were able to show that prerace education and limiting fluid availability at a race were able to reduce the incidence of hyponatremia without deleterious effects.

Currently, there is insufficient evidence to support the suggestion that ingestion of sodium prevents or decreases the risk for EAH; neither is there any evidence that consumption of sports drinks (electrolyte-containing hypotonic fluids) can prevent the development of EAH (1,35–38,42,100,101). Again, most commercial sports drinks are hypotonic with a sodium content of 10 to 20 mmol/L (230 to 460 mg/L). Overconsumption of such fluids may decrease the rate of serum sodium decline but is unlikely to prevent EAH (35–38,42,100–102). Currently, the American College of Sports Medicine recommends an intake of 0.5 to 0.7 g sodium/L of water as the appropriate level of sodium intake to replace the sodium that is lost in sweat during endurance events (6).

Therapy of EAH

Ideally, medical facilities at endurance events should be able to measure serum or plasma sodium concentrations in any athlete who manifests symptoms that are compatible with EAH or EAHE. However, this may not be universally feasible, and caregivers may have to act empirically on the suspicion of EAH or EAHE as the cause of symptoms. It is crucial for on-site caregivers to be vigilant for the possibility of EAH and not diagnose incorrectly volume depletion and implement a reflex therapy of normal saline infusion.

In 2005, a consensus panel made specific recommendations for the treatment of EAH and EAHE (14). The specific treatment recommended depends on the level of symptoms that the athlete is exhibiting at the time of presentation. Most forms of mild hyponatremia (serum [Na] 130 to 135 mmol/L) will be asymptomatic and found only by laboratory testing. Most athletes with mild, asymptomatic hyponatremia will require only fluid restriction and observation until spontaneous diuresis occurs. It is important that hydration with intravenous 0.9% sodium chloride (NS) be used with utmost caution because this therapy runs the potential risk for further decreasing the serum sodium if AVP levels remain elevated in some athletes (103). Furthermore, the absorption of large amounts of retained hypotonic fluids in the gastrointestinal tract may continue to lower the serum sodium for some time after the event is finished. Therefore, intravenous hydration with NS should be reserved for athletes who manifest clear clinical signs of volume depletion and used cautiously with mandatory monitoring of serum sodium levels (20). Furthermore, cases of pulmonary edema have been described in individuals who received aggressive hydration with 0.9% NS (21). Monitoring of urinary sodium and potassium concentrations and calculation of the urinary free water excretion rate can be helpful in this situation. Athletes who are excreting free water can be monitored safely without need for intravenous fluids, whereas athletes with a negative free water clearance should not receive 0.9% NS because this may worsen the hyponatremia.

The treatment of severe (serum [Na] <120 mmol/L) or symptomatic EAH requires the administration of hypertonic saline (11,104–106). There are some important considerations when deciding to treat EAH with hypertonic saline. First is the assumption that all EAH is acute (<48 h). This allows the correction of the hyponatremia to be done rapidly and safely (107,108). The second consideration is that no cases of osmotic demyelination syndrome have been reported with the treatment of EAH (14). In the case series by Ayus et al. (11), six of seven marathon runners were treated with hypertonic saline for hyponatremia, cerebral edema, and noncardiogenic pulmonary edema. All six of the athletes who received hypertonic saline made a full recovery. Of the five athletes who had follow-up magnetic resonance imaging scans obtained 1 yr after treatment, all were normal. The one athlete who was not treated with hypertonic saline died.

There is no general consensus on the amount of hypertonic saline to be given in athletes with EAH. In the field, it has been suggested that experienced medical staff may give 100 ml of 3% saline over 10 min (14,106). This has been suggested to be safe, raising the serum sodium concentration 2 to 3 mmol/L in a short period of time, and should be used in athletes who exhibit symptoms of severe hyponatremia (confusion, vomiting, respiratory insufficiency) (11,106). The use of hypertonic saline has been shown to induce a greater-than-expected increase in the serum sodium, likely as a result of a decrease in AVP, and the restoration of a dilute urine; therefore, it is imperative that all athletes who receive therapy for EAH or EAHE be transported to a medical center where the serum sodium can be monitored closely (11,14,106,107). Use of hypertonic saline should be continued in the hospital to correct the hyponatremia using standard protocols. In general, 3% hypertonic saline can be given at 1 to 2 ml/kg per h with close monitoring of both serum electrolytes and urinary sodium and potassium excretion. In cases of severe antidiuresis, the rate of infusion may need to be increased to 3 to 4 ml/kg per h. Once significant water diuresis begins, the rate of infusion can be decreased or stopped. Special mention should be made of the patient who presents with severe EAHE and pulmonary edema. It is imperative that these patients receive emergent therapy with 3% hypertonic saline despite evidence of volume overload. As described by Ayus et al. (21), patients who do not receive hypertonic saline have poor outcomes. The addition of a loop diuretic can be considered in two circumstances: (1) Significant volume overload and (2) significant antidiuresis with a very elevated urinary osmolality, sodium, and/or potassium level.

Recently, selective vasopressin receptor antagonists (VRA) have been developed for the therapy of hyponatremia that is associated with SIADH, cirrhosis, and congestive heart failure (109). These agents include two oral preparations (lixivaptan and tolvaptan) and an intravenous agent (conivaptan). In the phase 2 trial with lixivaptan, patients with SIADH had an increase in serum sodium from 126 ± 5 to 133 ± 5.6 mmol/L after 48 h with concomitant increases in urine flow rate and falls in urine osmolality (110). Conivaptan has the advantage that correction of serum sodium is faster than with the oral agents, likely owing to enhanced bioavailability. In one study with conivaptan, the median time to a 4-mmol/L increase in serum sodium was 23.7 h (111). However, in the treatment of EAH and other forms of acute hyponatremia, the role of these agents is unclear. It is not known whether VRA alone will achieve sufficiently rapid correction of acute, severe hyponatremia without the use of hypertonic saline. As detailed by Greenberg and Verbalis (111), both VRA and hypertonic saline could be used initially. Once there is a small correction in the serum sodium, the hypertonic saline could be stopped and the VRA continued to facilitate water diuresis. One fear of the use of VRA in the treatment of EAH is that athletes could have an extremely rapid water diuresis with the risk for resultant hypernatremia; therefore, these agents are not likely to be useful for the therapy of EAH. Overall, in the therapy of EAH, hypertonic saline remains the therapy of choice.

Hypokalemia can develop during athletic events especially after the event is completed (112). It is important that the potential for hypokalemia be appreciated because it can have important implications for treatment. First, hypokalemia is a risk factor for the development of osmotic demyelination that is associated with correction of chronic hyponatremia (113). Whether hypokalemia is a risk factor for poor neurologic outcomes that are associated with therapy for acute hyponatremia is not known. Second, replacement of potassium deficits will increase the serum sodium as sodium shifts out of cells. With concomitant potassium repletion, the serum sodium may rise faster than anticipated, and correction of hyponatremia should be less aggressive (108).

Conclusion

EAH and EAHE are potentially devastating complications of endurance events that occur in otherwise healthy, active, and young individuals. The pathophysiology of this condition includes multiple intersecting pathways that include both environmental (overabundance of fluids and recommendations for overdrinking) and innate physiologic control systems. When appropriately recognized, EAH and EAHE can be treated effectively with a low rate of morbidity and mortality. However, when not recognized, this condition can be fatal. Fortunately, preventive measures that stress judicious use of fluid replacement during exercise are effective and should be widely publicized and implemented.

• Copyright © 2007 by the American Society of Nephrology

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Every Year, More Athletes Are Injured By Hyponatremia than By Dehydration

The Myths of Dehydration and Heat Illnesses

• The primary cause of hyponatremia in athletes is drinking too much water.
• The incidence of hyponatremia appears to be between 13% and 15% among endurance athletes.
• Gender and the duration of athletic activity appear to be predictors of the incidence of hyponatremia.
• Sodium supplementation has no effect on the occurrence of hyponatremia.
• There seems to not be a single case of death resulting from sports-related dehydration in the medical literature.

The data continue to accumulate showing that hyponatremia is a greater risk to athletes than is dehydration. Every summer in the United States, athletes die and suffer neurologic complications from drinking too much. (SeeFigure.) The U.S. Army has seen the same result in a percentage of soldiers. The culprit is hyponatremia and the data suggest that the primary cause is simply drinking too much water.

A review and editorial published recently in The New England Journal of Medicine (NEJM) adds new data to the overwhelming body of evidence showing that physicians must counsel athletic patients about the dangers of overhydration when exercising in hot weather. Generally hyponatremia does not occur in athletes who undertake relatively brief (<1 hour) workouts. However, it can occur in any athlete who is overly focused on the illusory risks of dehydration and simply drinks too much water.

The most practical advice that physicians can offer is the following: Do not drink so much water that you weigh more after your workout than you did before it. Any athlete who is exercising in hot weather should lose body weight during exercise simply in the mass of sweat that is lost during exercise.

Recent Data

The data published recently in the NEJM as as follows:

“Among the 1089 triathletes who participated in the study, 932 were men and 157 were women. The mean (±SD) time in which participants completed the race was 12:39±1:59 hours (range, 7:59 to 16:20). The mean race time for female participants was 13:15±1:57 hours and that for male participants was 12:33±1:58 hours. The mean plasma sodium level at the finish line was 140.5±4.2 mmol per liter (range, 111 to 152). Among all 1089 athletes, 115 (10.6%) had documented hyponatremia: 95 had mild hyponatremia (8.7%), 17 severe hyponatremia (1.6%), and 3 critical hyponatremia (0.3%). Among the latter 3 athletes, the plasma sodium levels were 120, 119, and 111 mmol per liter, respectively. A multivariate analysis showed a significant association between hyponatremia and participants who were female or who took longer times to complete a race. The first cases of hyponatremia appeared in the cluster of participants who finished in the 9th hour of the race; cases of critical hyponatremia occurred in the clusters of participants who finished in the 12th and 14th hours of the race.

“A previous study involving marathon runners showed that 12 to 13% of participants had hyponatremia and that the incidence of critical hyponatremia was 0.5 to 1%. In contrast, the observed incidence of hyponatremia in long-distance triathlons was 10.6%. The incidence of critical hyponatremia was 0.3% (approximately half the incidence seen among marathoners). Our data show that exercise-associated hyponatremia occurs in a considerable percentage of long-distance triathletes. Female triathletes with a racing time of 9 hours or more appear to be the most susceptible to hyponatremia.”

Drinking Too Much Water

The rate of exercise-associated hyponatremia (EAH) has been reported at 15.1% among 887 finishers of a 100-mile (161-km) running race in Northern California. A study of runners in the 2002 Boston Marathon (27.2mi/43.8km) found 13% of 488 runners studied had hyponatremia (defined as a serum sodium concentration of ≤135mmol/L) and 0.6% had critical hyponatremia (serum sodium concentration of ≤120mmol/L) after finishing the race.

Currently, there is scientific agreement that overhydration resulting from drinking too much water is the primary cause of hyponatremia in athletes. Sodium supplementation appears to have no relationship with the occurrence of hyponatremia.

See a summary of the literature on this complex topic here.

Overweight and Obesity

The second most common causes of these deaths appear to be cardiac complications related to overweight and obesity. Heat deaths in the U.S. are more common in males and, according to Centers for Disease Control data from 2005-2009, the most recent data available, nearly 68% of those boys were overweight or obese.

The Myth of Dehydration

In the popular press, these heat-related deaths are often attributed to “heatstroke,” but no medical evidence is given. In other cases, if the death occurred under hot conditions, it is attributed to dehydration, but again, no medical evidence is given in these press reports. While dehydration can certainly be lethal, it is not clear how many of the deaths reported in the media are caused by dehydration. These cases were simply properly studied.

The rate of death due to dehydration in marathon and ultramarathon athletes appears to be unknown. This may be due to its exceedingly low rate. A PubMed search for “dehydration, athletes, death” returns 11 results. The strongest of these appears to be the Mortality and Morbidity Report referenced above. A search for “dehydration, runners, death,” returns 4 results. A review of these 15 studies reveals no case of death. There seems to not be a single case of death resulting from sports-related dehydration in the medical literature.

This report does not refer to death by dehydration at all. In each case it refers to heat-related injury. We have no way of knowing whether these injuries were due to dehydration, hyponatremia, heatstroke, elevated overall body temperature, cardiac, or other events.

Talk to Your Patients

While we still do not fully understand the effects of dehydration on athletes, it is much clearer that too much water kills and injures athletes. If hyponatremia is the most common cause of heat-related injury in athletes, suggestions to hydrate without limit can be injurious.

Caution endurance athletes to drink only when they are thirsty and to monitor their body weight before and after an event. Remind them that it is better to be thirsty than it is to be hyponatremic.

While the advice for patients is simple, the evidence is complicated, as you can see in our literature review on the topic.

Figure: CT brain scan signs of hydrocephalus, high intracranial pressure and brain stem herniation. Brain CT (axial slices) in a male patient in his 30’s who died of brain stem herniation after completing a marathon. The CT shows (A) loss of the rostral cerebral sulci suggesting increase in ICP, (B) and (C) a large hydrocephalus with widening of both temporal horns. The grey matter can still be differentiated from the white matter, but all sulci are lost. This suggests that the brain edema is of relative recent onset and massive tissue ischemia has not yet occurred. (D) Compression of the fourth ventricle with dilatation of the third ventricle and the caudal aspect of both temporal horns. This is observed with considerable brain edema and obstructive hydrocephalus. (E) Herniation of the medulla and pons into the foramen magnum. (F) The tonsils are located at the level of the dens which is a good indicator for foramen magnum herniation. (All images are from the case presented here.)
(Source: Copyright © 2007 Petzold et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.)

Coding for Electrolyte Disorders

May 26, 2008

Coding for Electrolyte Disorders
For The Record
Vol. 20 No. 11 P. 32

Electrolyte disorders are classified to ICD-9-CM category 276, Disorders of fluid, electrolyte, and acid-base balance. This column focuses on abnormal potassium and sodium levels in the blood.

Hypernatremia
Hypernatremia (hyperosmolality; 276.0) is defined as an elevated sodium level in the blood that is more than 145 milliequivalents per liter. Hypernatremia results from a decrease of free water in the body rather than excess sodium. Therefore, physicians may document the term dehydration instead of hypernatremia. Dehydration is classified to code 276.51. If, however, dehydration is documented with hypernatremia, assign only code 276.0 per coding directives in ICD-9-CM.

Common causes of hypernatremia include inadequate water intake, inappropriate water excretion, and the intake of a hypertonic fluid. Symptoms include lethargy, weakness, irritability, and edema, and seizures and coma may occur in more severe cases. The treatment for hypernatremia is the infusion of a water solution containing 0.9% sodium chloride.

Hyponatremia
Hyponatremia (hyposmolality; 276.1) is a sodium concentration in the blood of less than 135 milliequivalents per liter and occurs when the sodium in the blood is diluted by excess water. Signs and symptoms of hyponatremia include nausea/vomiting; headache; confusion; lethargy; fatigue; appetite loss; restlessness; irritability; muscle weakness, spasms, or cramps; seizures; and decreased consciousness or coma.

Common causes of hyponatremia include the consumption of excessive water during exercise, diuretics, syndrome of inappropriate antidiuretic hormone (SIADH; 253.6), dehydration, diet, and congestive heart failure. Per coding directives, if dehydration is documented with hyponatremia, assign only a code for the hyponatremia (276.1). In addition, if the patient has SIADH and hyponatremia, only code 253.6 is assigned. Hyponatremia is an integral part of the SIADH and would not be coded separately (AHA Coding Clinic for ICD-9-CM, 1993, fifth issue, page 8).

Hyperkalemia
Hyperkalemia (hyperpotassemia; 276.7) is an elevated level of potassium in the blood above 5 milliequivalents per liter. Hyperkalemia may be caused from a consumption of too much potassium salt, the failure of the kidneys to normally excrete potassium ions into the urine, or the leakage of potassium from cells into the bloodstream. Symptoms of hyperkalemia include heart abnormalities such as arrhythmia or cardiac arrest. Hyperkalemia can be treated with a low potassium diet or Kayexalate.

Hypokalemia
Hypokalemia (hypopotassemia; 276.8) is a below-normal level of potassium in the blood of less than 3.5 milliequivalents per liter. Hypokalemia may be caused from an overall depletion in the body’s potassium or an excessive uptake of potassium by muscle from surrounding fluids. Hypokalemia is most commonly caused by the use of diuretics. Because of this, a physician may order an infusion of potassium chloride when the patient is receiving diuretics such as Lasix. This is done for preventative measures and does not mean that the patient has hypokalemia.

Although a patient with mild hypokalemia does not have any symptoms, moderate hypokalemia results in confusion, disorientation, weakness, and discomfort/cramps of muscles. Hypokalemia is treated with potassium supplements, potassium chloride, potassium bicarbonate, and potassium acetate.

Coding Notes
An abnormal lab value—either too high or too low—alone does not constitute a diagnosis. The physician has to document the condition. In addition, the documentation must also reflect one of the following before the diagnosis can be coded: clinical evaluation, therapeutic treatment, diagnostic procedure, extended length of hospital stay, or increased nursing care and/or monitoring.

It is the physician’s responsibility to document the patient’s diagnosis. In the inpatient setting, a diagnosis based on an abnormal lab result or diagnostic test should not be determined by someone other than a physician. The physician must document the diagnosis in the medical record before it can be coded. In addition, it is not adequate for a physician only to use arrows (Ý or ß) to indicate a diagnosis, even if treatment was given for that condition. For example, the physician documents “Na ß 129. Decrease fluid intake. Change IV fluids.” In this example, hyponatremia (276.1) could not be coded without the physician documenting it. Query the physician regarding the patient’s specific diagnosis.

Coding and sequencing for electrolyte disorders are dependent on the physician documentation in the medical record and application of the Official Coding Guidelines for inpatient care. Also, use specific AHA Coding Clinic for ICD-9-CM and American Medical Association CPT Assistant references to ensure complete and accurate coding.

— This information was prepared by Audrey Howard, RHIA, of 3M Consulting Services. 3M Consulting Services is a business of 3M Health Information Systems, a supplier of coding and classification systems to nearly 5,000 healthcare providers. The company and its representatives do not assume any responsibility for reimbursement decisions or claims denials made by providers or payers as the result of the misuse of this coding information. More information about 3M Health Information Systems is available at www.3mhis.com or by calling 800-367-2447.

Too Much Water? It’s Possible, and a Problem

Aug 27, 2015 1:00 AM

Author:
Libby Mitchell

It’s something you hear at every sports practice, from peewee soccer to the high school football field: drink lots of water. While it’s good advice, it may be a bit misguided. A new report about over hydration shows that by encouraging kids to drink, drink, drink, we may be putting them at risk for serious health complications – and in some cases even death.

“What we need to be telling athletes is to drink enough,” says Jeffery Cline, MD, a pediatrician and sports medicine specialist with University of Utah Health. “Use thirst as a guide and have adequate and appropriate fluids available to maintain hydration.”

Drinking too much fluid can lead to a condition known as hyponatremia. “This is where sodium in the body is too low from excessive sodium loss in sweat or urine,” says Cline. “Or it is diluted by taking in too much free water without any electrolytes.” 

Hyponatremia can cause headaches, nausea, dizziness, confusion, muscle cramps, and in severe cases coma, seizures, and death. “These are difficult as they can also mimic signs of dehydration,” says Cline. “That’s why you need to monitor fluid intake to determine if the symptoms are being caused by excessive fluid intake or very limited intake.”

Hyponatremia is seen most commonly in sports like marathon running, or other endurance contests where athletes would take in more water than they would lose during the event. The prevalence actually led to a change on many courses. “Marathons have started to decrease the number of water stations to help avoid runners who think that forcing water down will help improve their performance by minimizing dehydration,” says Cline.

To walk the line between dehydration and over hydration, it’s best to listen to your body. “Don’t force yourself to drink excessively but don’t be afraid to drink if you feel thirsty,” says Cline. “I usually recommend taking water breaks every 15 minutes in the heat. One sports drink per hour of exercise is also recommended to replace electrolyte losses.”

Libby Mitchell is the Social Media Coordinator for University of Utah Health Care. Follow her on Twitter @UUHCLibby.

Hydration Issues in the Athlete and Exercise Associated Hyponatremia – PM&R KnowledgeNow

Disease/ Disorder

Definition

Hydration issues in the endurance athlete are centered on the two components of the extracellular fluid compartments: total body sodium balance and water balance. Exercise-associated hyponatremia (EAH) is defined by serum sodium ([Na⁺]) concentration <135 millimoles per liter (mmol/L) occurring during or up to 24 hours after physical activity and is severe if <125 mmol/L.¹ It is clinically divided into asymptomatic or symptomatic, whereby the latter is often seen with [Na⁺] <128 mmol/L.² Dehydration is defined as a deficit in total body water (TBW) with accompanying disruption of metabolic processes and typically results in hypernatremia. Changes in TBW can be best measured in a lab using deuterium oxide; however changes in body weight have been used as a practical surrogate measure with dehydration being defined as body weight loss >3%.³ This is estimated to be about 5% TBW.¹ Dehydration must be distinguished from hypovolemia, which pertains to a reduction in plasma volume. Less common electrolyte abnormalities include hypernatremia and hypomagnesmia.¹

Etiology

The etiology of EAH has been described through two generalized models: dilutional and depletional.^1,2 The dilutional model proposes that sustained overhydration with hypotonic fluids in the setting of impaired water clearance though inappropriate arginine vasopressin (AVP) secretion results in euvolemic or hypervolemic hyponatremia and is associated with weight gain. The depletional model proposes that excessive loss of under-replaced solute (sodium and potassium) occurs through sweat or impaired renal retention resulting in hypovolemic hyponatremia and is associated with weight loss. It is widely accepted that EAH is multifactorial and is predominately caused by dilutional mechanisms. Thus, when weight is gained during an endurance event, there is greater likelihood that an athlete will be hyponatremic.³ Excessive water loss through hypotonic sweat is the primary cause of dehydration in endurance athletes.

Epidemiology including risk factors and primary prevention

Guidelines in the past for ad libitum fluid intake were aimed at preventing rapid and severe dehydration in extreme conditions. It is now known that the single most important risk factor for EAH is sustained, excessive fluid (water, sports drinks, or other hypotonic fluid) intake in excess of water loss through sweat, respiratory and renal excretion resulting in a positive fluid balance.¹ Prevention is primarily aimed at organized educational programs advising athletes to drink to thirst, monitor their body weight, and be cognizant of symptoms of EAH. Pre-event sodium supplementation has proven to have little to no role in prevention.²

Other risk factors include weight gain during exercise, exercise duration >4 hours (i.e., slow pace), event inexperience or inadequate training, high or low body mass index (BMI), and readily available fluids.¹ The use of non-steroid anti-inflammatory drugs (NSAIDs) has also been a proposed risk factor presumably due to potentiation of renal water retention.^4,5,6 Incidence is greater in females compared to males; however, when adjusting for BMI and racing time, the apparent sex difference is not significant.¹ When organizing or supervising an endurance event, reducing the availability of fluids along the routes of exercises could be consider as a strategy to minimize the incidence of hyponatremia. ⁸

Symptomatic EAH is rare, with severe complications representing <1% of all EAH cases. There have been 14 reported deaths since 1981.¹ Over the past decade, EAH deaths have been confirmed in the lay press in high school football players following practice, a soldier on the first day of Ranger training, a policeman participating in a 19 km bike ride, a college student performing calisthenics for a fraternity, a bushwalker, an ironman triathlete, and a canoeist during an ultradistance race. The literature also reports symptomatic cases of EAH after long distance swimming, mountain cycling, yoga, 2h of weightlifting plus tennis, and in an individual with cystic fibrosis after low-intensity lawn bowling.¹⁴ More recently, there have been 3 deaths in American football players encouraged to drink copious volumes of hypotonic fluids to relieve exercises-associated muscle cramps (EAMC). It is now recognized that EAMC reflects neurological fatigue rather than dehydration and electrolyte imbalances.¹

Cases of asymptomatic EAH (diagnosed through routine screenings for research purposes) have recently been documented in 33% of 10 rugby players following an 80-min match, 70% of 30 elite junior rowers during an extended training period, 11% of 1,089 Ironman triathletes tested post-race, 6% of 33 endurance cyclists tested pre- and post-race, 67% of 15 ultramarathon runners testing during the race, 5% of 161 marathon and half-marathon runners tested pre-race, and 8% of 192 marathon and half-marathon runners tested post-race. Thus, despite increased awareness of the hazards of overdrinking; EAH fatalities, case reports, and incidence rates have spread into a wider variety of sporting activities.¹⁴

Patho-anatomy/physiology

Dilutional hyponatremia results from total body water expansion relative to total body exchangeable sodium.¹ Osmotic gradients result in water shifting into the intracellular compartment leading to cellular edema. Symptoms result from pathologic central nervous system (CNS) tissue expansion and become life threatening with elevated intracranial pressures.

The excretory rate of the kidneys is between 800-1000 milliliters/hour (mL/h) in the normal resting adult and the athlete loses about 500 ml/h during exercise. Thus, fluid consumption at a rate of 1.5 liters/hour (L/h) theoretically should prevent overhydration.²

Osmoreceptors within the circumventricular organ of the brain lack a blood-brain barrier and are in communication with blood and baroreceptors (carotid and aortic arch), thus act as physiological sensors to regulate plasma osmolality and volume by coordinating thirst and AVP secretion.¹

AVP is synthesized in the hypothalamus, stored in the posterior pituitary gland, and acts at the V2 receptor in the collecting ducts of the kidney to open aquaporin channels thus reabsorbing water. Under normal circumstances, AVP is suppressed in the presence of hypoosmolality. In some athletes, AVP is not appropriately suppressed (as typified by the finding of inappropriately elevated urine osmolality). This release of AVP leads to water retention in the distal tubule of the kidney and impaired water excretion. Coupled with excessive water intake, inappropriate water retention will lead to hyponatremia.¹⁴

Non-osmotic AVP secretion or Syndrome of Inappropriate Antidiuretic Hormone (SIADH) may occur during exercise due to stimuli including elevated body temperature, volume contraction, hypoglycemia, interleukin-6 (IL-6) release, and nausea or vomiting, and medication use (such as NSAIDs and selective serotonin reuptake inhibitors (SSRIs)).^1,2,14

Osmotic inactivation and/or impaired mobilization of osmotically inactive sodium stores has also been theorized to play a role in the development of hyponatremia during endurance events.³ It has been hypothesized that athletes who develop EAH either cannot activate the exchangeable pool of sodium in response to sodium losses or alternatively sodium may move into non-osmotically active forms. The mechanisms that control the exchange of sodium between these compartments remain unknown.^3,14

In addition, glycogen metabolism may be an important component in the cause of hyponatremia that occurs without weight gain because each kilogram of glycogen can contain upwards of 3 kg of associated metabolic water. ¹⁵ As glycogen is metabolized, water is released and if not excreted could lead to depression of the serum sodium.

Moreover, absorption of water retained in the gastrointestinal system at the end of a race or exercise has been suggested to cause acute drop in serum sodium concentration. This may explain a “transient lucid period” followed by an acute presentation of EAHE about 30 minutes after stopping physical activity.¹⁶

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Serum [Na⁺] is not always a good predictor of symptoms. Asymptomatic EAH is a biochemical finding and athletes may only experience mild transient complaints that are typical of any endurance event. Mild symptomatic EAH may present with non-specific signs and symptoms such as light headedness, headaches, dizziness, nausea, bloating, puffiness, and/or increase in body weight.^1,2,15 These athletes usually do not improve in the Trendelenburg position, and they do not have signs of encephalopathy. Serum [Na⁺] levels should be measured as they may acutely progress to severe EAH or life-threatening exercise-associated hyponatremic encephalopathy (EAHE). EAHE is characterized by headache, vomiting, altered sensorium, seizures, dyspnea or frothy sputum (non-cardiogenic pulmonary edema), decorticate posturing or mydriasis (signs of brainstem herniation), and/or coma as sequelae of cerebral edema and brainstem herniation.¹

Dehydration levels greater than 8% may cause athletes to experience severe thirst and dry mouth. If the level of dehydration reaches 15-20%, serious health consequences such as tachycardia, hypotension, and even death may result.⁷

Specific secondary or associated conditions and complications

Athletes with asymptomatic EAH are at risk for developing delayed-onset symptomatic EAH up to 24 hours after the event.

A secondary complication of symptomatic EAH is CNS-triggered non-cardiogenic pulmonary edema, which may require supplemental oxygen or intubation if adequate oxygen saturation is not maintained.

Performance decrements and cardiovascular strain have been documented when baseline body fluid volume decreases are >2%.

Essentials of Assessment

History

Signs and symptoms can overlap between EAH, dehydration, heat illness, or acute altitude illnesses. Correct diagnosis of EAH versus dehydration guides appropriate management and athlete outcome, therefore EAH should be considered in differential diagnosis of an individual that has been or is currently participating in strenuous activity or prolonged exercise.¹⁶

Evaluation should include history of present illness, past medical history (with attention to hypertension, diabetes, hyperlipidemia, heart failure, chronic liver or kidney disease, and/or neurologic insults), supplements or medications (with attention to diuretics, antihistamines, anti-hypertensives, lithium, SSRIs and NSAIDs), pre- and post-race weight, amount of fluid and food ingested during the event and what type, urine production (clear or dark and amount), vomiting or diarrhea, shortness of breath, history of problems in past races, and amount of training prior to current event.

Physical examination

Physical exam focuses on the central nervous system, pulmonary system, and cardiovascular system. Assessment of vital signs is essential. Tachycardia and hypotension are associated with dehydration, whereas vital signs (including body temperature) are usually not grossly abnormal in hyponatremia. A rectal temperature should be obtained to most accurately measure core body temperature in cases of suspected concomitant exertional heat-related illness as this may impact initial treatment protocol.⁸ Basic cardiopulmonary exams may provide important information. Unconscious patients should be assessed for abnormal posturing and pupillary responses. In the conscious athlete, a brief mental status exam can be performed if there is question for altered sensorium. Evaluate for peripheral and pulmonary edema. Weight gain or loss can be used to assess water balance and may provide indication of serum [Na⁺]. Physical signs of dehydration include dry mucous membranes, poor skin turgor, sunken eyes, and delayed capillary refill.

Increased vulnerability to orthostatism is a common phenomenon after ultra-endurance races that does not necessarily correlate with dehydration status, although the mechanism is not completely understood. ¹⁷

Functional assessment

Presentation of EAH varies depending on severity, ranging from asymptomatic to seizures to coma, and death. Dehydration also has a wide range in presentation including mental status changes (confusion, behavioral changes including increased aggression).⁹

It is still controversial whether dehydration causes impairment in executive function and “mental readiness”, reason why different tests have been used for research, with controversial results. Differences have been noted in endurance versus track-and-field events, with no changes in endurance athletes after the race¹⁷, and reported perceived tiredness, alertness, confusion, fatigue, anger, or depression in track-and field¹⁸.

Laboratory studies

The Second International Exercise Associated Hyponatremia Consensus Development Conference was that “medical directors should ensure the availability of on-site serum [Na⁺]  analysis”.¹⁹ On-site serum [Na⁺] can be rapidly obtained within minutes using the i-STAT^® handheld blood analysis system. Medical teams at most endurance events are equipped with i-STAT^® analyzers and accompanying testing cartridges. Depending on which cartridges are available, renal function labs may also be obtained which can provide information on hydration status. There may be, however, instances where patients are suspected of having EAH and serum [Na⁺] cannot be obtained (see treatment section for management in this circumstance), especially in wilderness activities.¹⁶

Pseudohyponatremia should be considered. Glucometers can rapidly determine blood glucose levels providing important information considering serum [Na+] is artificially lowered (i.e., pseudohyponatremia) by hyperglycemic states and must be corrected using correction factors.¹⁰ Other causes of pseudohyponatremia include hyperlipidemia and hyperproteinemia, both of which need to be determined through laboratory blood panels.¹⁰

In the hospital setting, serum and urine osmolality should be obtained. As stated earlier, deuterium oxide is used to measure changes in TBW but is not practical for on-site testing. Further laboratory work-up can include Copeptin, AVP, aldosterone levels for electrolyte regulation, and urine lactate levels for hydration correlation. These laboratory tests require more studies to determine their diagnostic and treatment value (refer to the “Cutting Edge/emerging and Unique Concepts and Practice” section for further information).

Imaging

Neuroimaging such as computerized tomography (CT) of the brain may be obtained once an athlete with EAHE is at an advanced medical care facility, however this must not interrupt acute treatment.¹

Supplemental assessment tools

Having scales available for monitoring body weight should be considered when organizing an endurance event. Athletes should obtain their baseline event-day weight as it acts as a surrogate measurement of body fluid balance. If pre-race weight is not obtained, the history of the athlete’s normal weight is a good substitute. Lack of weight loss or weight gain during an endurance event is a positive indicator of fluid overload and possible hyponatremia, and fluid intake should be reduced.¹ Some weight loss (1.5-2.5 kilograms) is expected during an endurance race, but should not exceed 2% of body weight as this increases the risk for dehydration.¹¹ However, some athletes have shown to have better results despite more than 2% body weight loss in endurance races.^17,20,21,22 Recent studies suggest tailoring recommendations to individual performance, but more studies need to be done for better understanding of safety and performance guidelines.

Early predictions of outcomes

Severity of initial presenting symptoms and not absolute serum [Na⁺] can predict outcome and should guide therapy.¹ Any athlete suspected for EAH should have rapid determination of serum [Na⁺]. With appropriate recognition and management, the vast majority of asymptomatic or mildly symptomatic EAH or dehydration cases resolve without long-term sequelae. For both EAH and dehydration, loss of consciousness or disorientation suggests more severe abnormalities and should be acted upon emergently.

Social role and social support system

Athletes with asymptomatic EAH or those treated for mild symptomatic EAH should be discharged from the event’s medical assessment area with a companion to monitor for the development of neurological symptoms that would prompt immediate medical attention.¹

Environmental

Extreme environmental temperatures can affect the likelihood of developing either dehydration or EAH. Cold may elevate the osmotic set-point for secretion of AVP, especially when age >65 years.¹² Non-acclimatized athletes may require hydration beyond thirst drive in temperatures >38ºC (100.4ºF) to improve performance and prevent dehydration.¹² Prolonged exercise in warmer climates has suggested excessive-sodium losses as the primary mechanism for EAH, however evidence to date is limited.²

When organizing or supervising an endurance event, reducing the availability of fluids along the routes of exercises could be consider as a strategy to minimize the incidence of hyponatremia.²³

Professional Issues

Medical personnel at the sports events should be aware of proper treatment of EAH and differential diagnoses, as incorrect treatment can further compromise serum [Na⁺] and further deteriorate the athlete condition. Medical directors should consider education via pre-race briefings/webinars and by suggesting reading material or educational podcasts/videos.¹⁶

Good Samaritan laws vary among states, however, generally only cover doctors who are also bystander fans. Physicians might be participating and can help out in an emergency on the course if Good Samaritan laws are in place. If a doctor is an official race event volunteer, then additional malpractice insurance should be obtained. Recently insurance policies have been developed specifically for volunteer medical teams.

Rehabilitation Management and Treatments

Available or current treatment guidelines at different disease stages

Treatment should be determined by the degree of neurological impairment and not simply by serum [Na+], because both the magnitude and rate of development of hyponatremia influence brain edema.¹ On-site treatment guidelines for hyponatremia are now organized by whether serum [Na⁺] has or has not been confirmed by measurement and whether the athlete is asymptomatic, symptomatic, or in severe EAHE.^1,2

If EAH is confirmed by [Na⁺] measurement, and there are no neurological symptoms beyond headache, limiting fluid intake until onset of urination is typically sufficient. A salty snack or anoral hypertonic fluid such salty soup or bouillon, especially in those with [Na⁺] <130 mmol/L, may also be used to resolve hyponatremia. Observe for 60 minutes until symptoms resolve and educate on neurologic signs and symptoms of EAH.  Discharge athletes from the medical area with a companion and advise to seek immediate medical attention, should neurologic signs and symptoms develop. In the case of severe EAH or EAHE, emergent treatment with IV hypertonic saline (100 mL 3% bolus) to decrease intracranial pressure. is needed. Up to three 100-mL of 3% hypertonic saline boluses at 10-minute intervals may be given.

On-site treatment of suspected EAH but not confirmed by serum [Na⁺] measurement is challenging as symptoms are similar to that of volume depletion and heat illness. Consider the differential diagnosis and weigh risk versus benefit of fluid restriction. Hypotonic fluids should be restricted in suspected EAH with consideration of the potential harm that could result from fluid restriction if the diagnosis is incorrect. If there are symptoms of severe EAH or EAHE, and the clinical suspicion is high, empiric treatment with rapid infusion of IV hypertonic saline should be initiated emergently to prevent further neurological deterioration. As EAH is an acute and not chronic process, there is no risk of osmotic demyelination. If EAHE is wrongly assumed, a bolus of hypertonic saline has minimal negative consequences, even in the case of hypovolemia or hypernatremia, and may provide benefit as a volume expander. When serum [Na⁺] cannot be determined and field treatment has not been successful, emergency transport to a definitive care facility should be expedited.

Coordination of care

It is critical that medical personnel in emergency transport services are aware of the athlete’s diagnosis, prior treatments, and the importance of avoiding isotonic or hypotonic fluid resuscitation which would worsen hyponatremia. The patient may need management in an intensive care unit (ICU) if they do not improve.

Measurement of treatment outcomes

There are no current guidelines necessitating ongoing serum  [Na⁺] measurement during management for EAH as treatment is dictated primarily by symptoms, however this may be practiced in asymptomatic or mild symptomatic EAH athletes before discharge to ensure that the serum [Na⁺] is at least >130 mmol/L.

Patient & family education

Prevention through education is the main goal and requires broad programs targeted to athletes, coaches, trainers, and parents emphasizing the importance of appropriate hydration practices, recognition of EAH signs and symptoms, and urgency of therapy.¹ They must understand that excessive fluid intake will not prevent muscle cramps and exertional heat stroke. This education, along with management protocols, must also reach onsite, emergency, and hospital medical personnel.

Some practical recommendations from the International Marathon Director’s Association include:¹²

1. Drink to thirst. Obey the body’s natural physiological cues.
2. Water, sodium, and glucose should be available at fluid replacement stations spaced 1.6 km (minimum) to 5 km (maximum) apart.
3. Calibrated scales along a marathon course should be at the discretion of the medical team and weight loss of >4% or any weight gain constitutes justification for medical consultation.
4. Sports drinks contain less sodium than body fluids and can worsen EAH.¹³

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

It is important to be aware of factors that contribute to over hydration, as the most common cause of EAH is sustained excessive fluid intake greater than volume lost. These risk factors include exercise duration >4 hours (i.e., slow pace), event inexperience or inadequate training, and readily available fluids.¹ Athletes should be counseled to “drink to thirst” in order to avoid overhydration. Finely tuned osmoreceptors and baroreceptors regulate both plasma osmolality and circulating volume through thirst and AVP secretion. Hence using thirst as guide is most likely to avoid overhydration. During exercise, the recommendation is to drink no more than 500-1200 mL/h, depending on training level and environmental factors, but thirst is the best gauge for hydration. Sports drinks should not be used to maintain serum [Na⁺], and can worsen EAH,¹³ as all sports drinks are hypotonic to plasma.¹

Cutting Edge/ Emerging and Unique Concepts and Practice

The increasing usage of i-STAT^® handheld blood analysis systems has advanced on-site care of EAH by improving its early recognition. Recent evidence suggests that some athletes mobilize sodium stores more than others, yet this is not well understood.³ A small prospective observational study by Whatmough et al. ²⁴ demonstrated that marathon runners who used an NSAID before or during the marathon had decrease in serum [Na⁺] while the serum [Na⁺] increased in those who did not use an NSAID.

Gaps in the Evidence- Based Knowledge

Current controversy exists over the hypovolemic variant of EAH, particularly the contribution of sodium loss through hypotonic sweat and role of brain natriuretic peptide in urinary sodium losses. Current guidelines are to treat these individuals with IV hypertonic saline bolus, followed by IV normal saline to replete volume.¹ Other areas of future investigation include the role of diet and sodium supplementation, success of the “drink to thirst” strategy, recurrence rates of EAH, long-term health implications, possible genetic markers, the role of NSAIDs, investigating alternative treatments for mild EAH, and the variability in serum [Na⁺] and body weight in the days leading up to an event and at event start.¹

References

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14. Hew-Butler T, Loi V, Pani A, Rosner MH. Exercise-Associated Hyponatremia: 2017 Update. Front Med (Lausanne). 2017;4:21. Published 2017 Mar 3. doi:10.3389/fmed.2017.00021
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17. Martínez-Navarro I, Chiva-Bartoll O, Hernando B, Collado E, Porcar V, Hernando C. Hydration Status, Executive Function, and Response to Orthostatism After a 118-km Mountain Race: Are They Interrelated? J Strength Cond Res. 2018 Feb;32(2):441-449. doi: 10.1519/JSC.0000000000001614. PMID: 27548786.
18. Casa DJ, Cheuvront SN, Galloway SD, Shirreffs SM. Fluid Needs for Training, Competition, and Recovery in Track-and-Field Athletes. Int J Sport Nutr Exerc Metab. 2019 Mar 1;29(2):175-180. doi: 10.1123/ijsnem.2018-0374. Epub 2019 Apr 4. PMID: 30943836
19. Hew-Butler T, Ayus JC, Kipps C, Maughan RJ, Mettler S, Meeuwisse WH, Page AJ, Reid SA, Rehrer NJ, Roberts WO, Rogers IR, Rosner MH, Siegel AJ, Speedy DB, Stuempfle KJ, Verbalis JG, Weschler LB, Wharam P. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med. 2008 Mar;18(2):111-21. doi: 10.1097/JSM.0b013e318168ff31. PMID: 18332684.
20. Au-Yeung KL, Wu WC, Yau WH, Ho HF. A study of serum sodium level among Hong Kong runners. Clin J Sport Med. 2010 Nov;20(6):482-7. doi: 10.1097/JSM.0b013e3181f469f0. PMID: 21079446
21. Krabak BJ, Waite B, Lipman G. Evaluation and treatment of injury and illness in the ultramarathon athlete. Phys Med Rehabil Clin N Am. 2014 Nov;25(4):845-63. doi: 10.1016/j.pmr.2014.06.006. Epub 2014 Jul 19. PMID: 25442162.
22. Grozenski A, Kiel J. Basic Nutrition for Sports Participation, Part 1: Diet Composition, Macronutrients, and Hydration. Curr Sports Med Rep. 2020 Oct;19(10):389-391. doi: 10.1249/JSR.0000000000000753. PMID: 33031200.
23. Speedy DB, Rogers IR, Noakes TD, Thompson JM, Guirey J, Safih S, Boswell DR. Diagnosis and prevention of hyponatremia at an ultradistance triathlon. Clin J Sport Med. 2000 Jan;10(1):52-8. doi: 10.1097/00042752-200001000-00010. PMID: 10695851.
24. Whatmough S, Mears S, Kipps C. Serum sodium changes in marathon participants who use NSAIDs. BMJ Open Sport Exerc Med. 2018 Dec 5;4(1):e000364. doi: 10.1136/bmjsem-2018-000364. PMID: 30588325; PMCID: PMC6280910.

Bibliography

Danz M, Pöttgen K, Tönjes PM, et al. Hyponatremia among triathletes in the ironman European championship. New Engl J Med. 2016;374:997-998.

Godek SF, Bartolozzi AR, Peduzzi C, et al. Fluid consumption and sweating in National Football League and collegiate football players with different access to fluids during practice. J Athl Train. 2010;45(2):128-135.

Thomas DT, Erdman KA, Burke LM. Position of the Academy of Nutrition and Dietetics, Dieticians of Canada, and the American College of Sports Medicine: nutrition and athletic performance. J Acad Nutr Diet. 2016;116(3):501-528.

Zambraski EJ. The renal system. In: Tipton CM, ed. ACSM’s Advanced Exercise Physiology. Philadelphia, Baltimore: Lippincot Williams & Wilkins; 2006.

Original Version of the Topic

Robert Irwin, MD, Michelle D. Francavilla, MD. Hydration Issues in the Athlete and Exercise Associated Hyponatremia. 12/28/2012.

Previous Revision(s) of the Topic

Richard G. Chang, MD, Jameel J Khan, MD. Hydration Issues in the Athlete and Exercise Associated Hyponatremia. 8/25/2016.

Author Disclosures

Julio Vazquez-Galliano, MD
Nothing to Disclose

Daniela Mehech, MD
Nothing to Disclose

Cecilia Cordova Vallejos, MD
Nothing to Disclose

Jasal Patel, MD
Nothing to Disclose

90,000 What are the symptoms of hyponatremia?

Hyponatremia results from a lack of sodium in the body fluid that surrounds cells. Adequate sodium levels are important for maintaining blood pressure and maintaining normal nerve and muscle function. There are several symptoms of hyponatremia, and although it occurs in only a small percentage of people, it is the most common electrolyte disorder treated in the United States.

Common symptoms of this condition include fatigue, irritability, headache and water retention, loss of appetite, nausea or vomiting.Other symptoms of hyponatremia are mental in nature and include abnormal or confused mental status, hallucinations, and possibly loss of consciousness. Often, confusion and changes in a person’s mental state are the first serious signs, as brain cells cannot cope with the swelling caused by water retention that accompanies hyponatremia.

Hyponatremia is diagnosed by serum and urine tests. There is almost always an underlying cause of hyponatremia that also needs to be diagnosed and treated.Insufficient sodium levels can be treated with intravenous fluids, a restricted diet, and supplemental oxygen. Medications that compensate for some of the symptoms of hyponatremia can also be used to restore comfort and prevent seizures.

Causes of hyponatremia include burns, dehydration from excessive vomiting or diarrhea, congestive heart failure as a side effect of diuretics, kidney disease, and several other conditions. Acute hyponatremia, which is a sudden decrease in sodium levels within 24 to 48 hours, often due to excessive exercise or dehydration, is considered more dangerous than chronic hyponatremia, which can occur with certain diseases or disorders.

Hyponatremia can be life-threatening, especially if the brain cells cannot cope with the swelling that can occur. This condition can also affect the heart. Although some of the signs of hyponatremia can be confused with other conditions, if a person suspects that he or she has an electrolyte imbalance or other symptoms of hyponatremia or dehydration, he or she should see a doctor immediately.

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90,000 causes, symptoms and treatment.Articles of the company “FRESH⭐-natural preparations and cosmetics”

12 Apr. 2019

Hyponatremia is a condition that occurs when the sodium level in the blood is extremely low. Sodium is part of the electrolyte category that helps regulate the amount of water in and around cells.

In patients with hyponatremia, the sodium level in the body is diluted, which leads to an increase in the level of water in the body, which leads to inflammation of the cells.Treatment for hyponatremia is recommended depending on the underlying cause.

Causes of hyponatremia

Sodium maintains normal blood pressure, maintains muscle and nerve function, and regulates fluid levels in the body. A decrease in sodium levels in the body below normal limits can be caused by various diseases or other lifestyle factors. The most common causes of hyponatremia are:

Treatment with certain drugs – diuretics, antidepressants and pain relievers causes frequent urination and increased sweating, which can cause hyponatremia.

Diseases of the heart, kidneys or liver – Some of these organ damage can cause fluid build-up in the body, causing sodium dilatation and hyponatremia.

Chronic diarrhea or severe vomiting – These problems cause a large loss of fluids and electrolytes, including sodium.

Excessive water consumption – In case of high-priority activities such as running a marathon, it may be necessary to consume large amounts of water.Excessive water intake dissolves sodium from the body, causing hyponatremia.

Dehydration – and low fluid intake can have the same effect. This is because dehydration entails a loss of electrolytes.

Hormonal disorders. Hormonal disturbances 90,022 caused by diseases such as Addison’s disease can affect the body’s ability to maintain perfect balance of sodium, potassium and water levels in the body. And small amounts of hormones secreted by the thyroid gland can cause hyponatremia.

Drug use such as ecstasy – amphetamine increases the risk of hyponatremia and can even lead to death.

Syndrome of inadequate secretion of antidiuretic hormone (SIADH) – this lesion causes too much secretion of the diuretic hormone, causing water retention in the body. Therefore, the risk of hyponatremia is high.

Symptoms of hyponatremia

• Nausea and vomiting
• Headaches
• confusion
• Loss of energy and extreme fatigue
• Irritability, anxiety
• Muscle weakness, cramps and muscle spasms
• Apoplexy
• coma

Diagnosis of hyponatremia

The doctor will take a history and then a physical examination.To confirm a suspicion of hyponatremia, your doctor will run a blood or urine test to determine the exact sodium levels in your body.

Treatment of hyponatremia

Hyponatremia is treated depending on the underlying cause.

If hyponatremia is caused by a lifestyle, diuretic, or excessive water intake, your doctor will advise you to refrain from drinking fluids for a period of time.

Severe acute hyponatremia requires more aggressive treatment, such as intravenous fluids or symptoms that relieve medication.Drugs used to treat symptoms of hyponatremia include headache, antiemetics, and apoplexy.

SODIUM CHLORIDE | JSC “Avexima”

Indications for use

Plasma isotonic fluid replacement, hypochloremic alkalosis, hyponatremia with dehydration, intoxication, dissolution and dilution of parenterally administered drugs (as a base solution).

Contraindications

Hypernatremia, hyperchloremia, hypokalemia; extracellular hyperhydration; intracellular dehydration; circulatory disorders associated with the risk of developing edema of the brain and lungs; swelling of the brain; pulmonary edema; decompensated heart failure; chronic renal failure; conditions that can cause sodium retention, hypervolemia and edema (central and peripheral), such as: primary aldosteronism, secondary aldosteronism due, for example, arterial hypertension, congestive heart failure, liver disease (including cirrhosis), kidney disease (including renal stenosis arteries and nephrosclerosis), preeclampsia; concomitant administration of high-dose glucocorticosteroids; contraindications to the drugs added to the solution.

Storage conditions

Store at temperatures from 0 to 25 ° C.

Keep out of the reach of children.

Freezing the drug during transportation (provided that the container is tight) is not a contraindication to use.

After freezing, keep the containers or vials in the shipping container at room temperature until completely thawed, before using the solution in the container or vial, stir by shaking.

Expiry date:

2 years.

Do not use after the expiration date.

Name of the holder (owner) of the registration certificate / Organization accepting claims

LLC “Avexima Siberia”

652473, Russia, Kemerovo region, Anzhero-Sudzhensk, st. Herzen, 7.

Tel./ fax: (38453) 5-23-51

Manufacturer

LLC “Avexima Siberia”, Russia

Kemerovo region, Anzhero-Sudzhensk, st. Herzen, 7

90,000 symptoms, causes, treatment, prevention, complications

Reasons

The main reason for the development of hyponatremia in newborns is severe dehydration (dehydration) of the body.Dehydration can occur due to diarrhea, severe vomiting (or both), when fluid losses in the body are replaced by fluids with much less sodium than the infant needs.

A rarer, but nevertheless likely cause of hyponatremia in an infant is a disruption in the production of the hypothalamic hormone vasopressin (also known as ADH). This hormone is responsible for the regulation of water balance in the body. Problems with the secretion of ADH, in turn, can be caused by tumors or infectious diseases of the child’s central nervous system.

For infants who are bottle-fed since birth, hyponatremia is more typical due to too much dilution of the milk formula, which leads to water intoxication of the body, and the concentration of the substance in the blood plasma is greatly reduced.

Congenital renal or heart failure can also lead to metabolic disorders in the body, which causes water retention and the development of hyponatremia.

Symptoms

A baby who has a low sodium content in the blood plasma will show this with rather general symptoms, which include:

• profuse vomiting (regurgitation), regardless of the amount and time of feeding;
• cramps of the upper and lower extremities, twitching of the tongue, impaired movement of the eyeballs;
• weakness and lethargy.

The general serious condition of a newborn with hyponatremia is explained by a water imbalance in the cells of the body, due to which the natural metabolic processes in the body are disrupted.

The degree of manifestation of symptoms depends on the duration and severity of hyponatremia. With a significant sodium deficiency, they will be more pronounced, and more time will be required for treatment.

Diagnosis of hyponatremia in a newborn

The primary diagnosis of the disease is reduced to asking the baby’s mother about the symptoms that caused her anxiety.It is necessary to collect information about the frequency, strength of the manifestation of symptoms, their relationship with the baby’s day regimen (for example, weakness before feeding, profuse regurgitation after, etc.).

When primary signs of hyponatremia appear, it is necessary to first of all pass a clinical blood test. According to its results, one can judge the level of sodium in the blood plasma. An indirect sign is also an increase in the level of urea nitrogen in the blood, which indicates dehydration.

Due to the specific manifestation of the disease, additional examinations and tests, especially for a newborn baby, are not required.

Complications

Prolonged hyponatremia can lead to impaired renal function (due to increased urine concentration), problems with the central nervous system. In addition, to a severe degree, it causes seizures or even coma.

Treatment

What can you do

If you find suspicious symptoms in a baby, first of all, you need to consult a doctor who will be able to assess his condition and make the correct diagnosis.Self-administration of any medication to infants is strictly prohibited. Nevertheless, if there are clear signs of hyponatremia, you should pay attention to the diet and adjust the feeding of the baby. If he is breastfed, then with profuse diarrhea and regurgitation, frequent application is necessary so that the baby can restore fluid in the body.

If the child is on artificial or mixed feeding, then the first thing to do is to check the correct preparation of the mixture (strict adherence to the instructions is necessary), it is possible to add water to the baby to restore the water balance.

What the doctor does

Hyponatremia in newborns requires the most prompt treatment, since it can lead to serious consequences and disruptions in the work of several body systems at once. The essence of the treatment is to restore the water-salt balance, for which a solution of glucose and sodium chloride of certain concentrations is injected intravenously. The volume and period of drug administration depends on the quantitative sodium deficiency in the blood plasma. To monitor the effectiveness in dynamics, a constant blood test is required at regular intervals.

With intravenous administration of solutions, it is very important not to exceed the maximum volume of fluid administration (10-12 meq / l * day), as this can lead to a rapid entry of fluid into the brain.

In case of severe manifestations of hyponatremia (loss of consciousness, sluggish reactions), urgent treatment is used, which consists in the introduction of a 3% sodium chloride solution. This avoids seizures and coma.

Prevention

Depending on the type of feeding (breastfeeding or formula feeding), there are various ways to constantly maintain the correct water balance.

For infants, this is primarily on-demand feeding, which allows the baby to satisfy not only hunger, but also thirst. If the baby spits up profusely, he has diarrhea or it is very hot outside (which is important in the summer period in almost all latitudes), then more frequent applications may be needed. You need to understand that in this case, the frequent requirement of a breast for a baby is not a whim, but a necessity, on which his state of health depends.

For babies who, for one reason or another, are artificially fed with milk formulas from birth, the quality and quantity of food intake should also be monitored.The instructions for preparing the mixture should be followed exactly, and also, if necessary, give the baby an additional drink.

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Arm yourself with the knowledge and read a useful informative article about the disease hyponatremia in newborn children.After all, to be parents means to study everything that will help maintain the level of health in the family at the level of “36.6”.

Find out what can cause the disease hyponatremia in newborns, how to recognize it in a timely manner. Find information about what are the signs that can identify ailment. And what tests will help identify the disease and make the correct diagnosis.

In this article, you will read all about the methods of treating such a disease as hyponatremia in newborns.Clarify what effective first aid should be. How to treat: choose medicines or alternative methods?

You will also learn what the danger of untimely treatment of the disease hyponatremia in newborn children can be, and why it is so important to avoid the consequences. Everything about how to prevent hyponatremia in newborns and prevent complications. Be healthy!

90,000 Hyponatremia – causes, diagnosis and treatment

Hyponatremia is a decrease in plasma sodium (Na) levels below 135 mmol / L (meq / L).This condition has a wide range of causes – from excessive water consumption with a salt-free diet, uncontrolled use of drugs to severe kidney disease and malignant tumors. Clinical symptoms are represented mainly by neuropsychiatric disorders. The diagnosis is made on the basis of determining the level of sodium and osmolarity of blood serum and urine. Treatment should include controlling the cause, administering isotonic or hypertonic saline solutions, and maintaining euvolemia.

Hyponatremia is the most common electrolyte disorder encountered in clinical practice. Sodium is a vital macronutrient that performs many functions in the human body (providing rest and action potential, maintaining plasma osmotic pressure, acid-base balance). A decrease in Na concentration primarily adversely affects the functioning of neurons. The majority of cases of this condition occur in patients in intensive care units (about 15-20%).More accurate statistics on the incidence of hyponatremia are not available.

Causes of hyponatremia

Sometimes hyponatremia develops for conditionally physiological reasons. For example, blood sodium levels decrease in people on a salt-free diet. Hyponatremia can occur with prolonged increased sweating (this is often observed in professional athletes, in people working outdoors in hot countries). The pathological causes of the condition are as follows:

• Excessive sodium losses .Increased excretion of sodium from the body occurs in chronic diarrhea, profuse vomiting. The characteristic cause of hyponatremia is the so-called salt-wasting nephropathy, i.e. kidney diseases in which Na reabsorption in the nephron tubules is impaired (tubulointerstitial nephritis, polycystic kidney disease, congenital tubular dysfunction).
• Body fluid retention . A common cause of hyponatremia are pathologies characterized by impaired excretion of fluid from the body (acute or chronic renal failure, CHF, cirrhosis of the liver with ascites.Electrolyte imbalance can occur with the syndrome of inadequate secretion of antidiuretic hormone (SNSADH), which develops against the background of various diseases (endocrine, pulmonary, oncological).
• Pathological hemodilution (dilution) . An increase in the water content in the vascular bed can also cause hyponatremia. This occurs when drinking excess water (non-mineral) with diabetes mellitus or diabetes insipidus, psychogenic polydipsia.Parenteral administration of large quantities of low- or salt-free solutions as detoxification therapy causes iatrogenic hyponatremia.
• Endocrine Disorders . Deficiency of mineralocorticoid hormones, which is observed in primary and secondary adrenal insufficiency, a salt-wasting form of congenital adrenal cortex dysfunction, disrupts the absorption of sodium ions in the renal tubules. Hyponatremia can be caused by hypothyroidism, severe hyperglycemia in decompensated diabetes mellitus.
• Taking medications . The use of diuretics (especially thiazide and osmotic ones), such as hydrochlorothiazide, mannitol, to relieve emergency conditions in patients in the intensive care unit often causes a drop in sodium concentration. The condition can develop while taking medications such as hypoglycemic, psychotropic drugs.
• Other reasons . Hyponatremia occurs in pancreatitis, peritonitis, massive burns.This condition is observed with some surgical operations, especially transurethral resection of the prostate gland (TUR syndrome).

Pathogenesis

Sodium is one of the most important cations for the normal functioning of many cells, especially nerve and muscle cells. With a decrease in its content, the excitability of neurons and myocytes decreases as a result of changes in their membrane potential. Due to this, the formation and conduction of an excitation wave in the nervous system is inhibited, the tone of skeletal muscles, blood vessels and myocardium decreases, which causes clinical symptoms.

Hyponatremia leads to plasma hypoosmolarity, water rushes along the concentration gradient from the intercellular space into the cells. The result is swelling and swelling of cells, which disrupts their normal functioning. The volume of circulating blood (volemia) can vary. This is determined by the cause of the hyponatremia. With hypovolemia, the BCC decreases, the secretion of ADH increases compensatory, which further aggravates the pathology.

Classification

There are several types of hyponatremia:

1. Pseudohyponatremia .It is caused by a decrease in the proportion of the water part of the blood due to the large amount of proteins and lipids.
2. Hypertensive hyponatremia . It develops as a result of the movement of water from cells into the interstitial space due to the presence of highly osmotic substances (glucose, mannitol) in the blood.
3. Hyponatremia . Depending on the BCC, it is subdivided into:

• Hypovolemic. It is characterized by a deficiency of Na, water, and a decrease in BCC.It is observed with salt-wasting nephropathies, mineralocorticoid deficiency, vomiting and diarrhea.
• Isovolemic. This form occurs in SNSADH, in which water retention and increased natriuresis occur.
• Hypervolemic. With this type, the intravascular volume decreases due to the diffusion of fluid into various body cavities (abdominal, chest), which leads to an increase in ADH secretion and “dilution” of sodium. This is typical for CHF and liver cirrhosis.

According to the severity, hyponatremia is divided into:

• Light – from 130 to 134 mmol / L.
• Moderate – from 125 to 129 mmol / L.
• Severe – less than 125 mmol / L.

According to the rate of development, hyponatremia is:

• Acute – up to 48 hours.
• Chronic – lasting more than 48 hours.

Symptoms of hyponatremia

Clinical symptoms depend on the rate and severity of hyponatremia.With a slight and slowly developing decrease in the level of Na, serious symptoms of CNS damage are absent. There may be slight drowsiness, imbalance. With a severe degree, a pronounced somnolence, soporous state appears. The person begins to react poorly to external stimuli. Epileptiform seizures are characteristic.

Due to a decrease in the excitability of myocytes, vascular tone and contractile function of the myocardium, muscle weakness, symptoms of arterial hypotension (increased heart rate, dizziness, loss of consciousness) appear.Skin, mucous membranes become dry, skin turgor and elasticity decrease. Sometimes there is a decrease in urine output, symptoms from the gastrointestinal tract – decreased appetite, nausea.

Complications

A large number of complications are typical for this syndrome. The overwhelming majority of adverse effects are associated with damage to the central nervous system. These include coma, edema and wedging of the brain. Sometimes pulmonary edema, hypothalamic and posterior pituitary gland infarctions are observed.The lethal outcome at a Na level of 125 meq / l occurs in 25%, with values ​​below 115 meq / l – in 50% of cases.

A dangerous complication of inappropriate treatment of hyponatremia is osmotic demyelinating syndrome (pontine and extrapontine myelinolysis), which develops as a result of dehydration and shrinkage of brain cells due to a sharp increase in plasma osmolarity when saline solutions are administered too quickly. Symptoms include dysphagia, bulbar disorders, tetraplegia.The mortality rate in this syndrome reaches more than 50%.

Diagnostics

Almost all patients with hyponatremia, especially severe, should be under the joint supervision of a resuscitation physician and a specialized specialist (endocrinologist, nephrologist). To find out the cause of this syndrome, anamnestic data are important – previous diarrhea, vomiting, medication. To establish a specific type of pathology, it helps to identify signs that indicate dehydration – dry skin, hypotension, decreased urine output.

Information is also needed on the patient’s comorbid conditions. On examination, attention is paid to symptoms such as swelling of the face, lower extremities, enlargement and tension of the abdomen, expansion of the saphenous veins on the anterior abdominal wall. An additional examination is prescribed, aimed at establishing the type of hyponatremia and determining its cause:

• Laboratory research . Serum osmolarity and levels of other electrolytes (potassium, calcium, magnesium) are determined.A biochemical blood test measures the content of glucose, liver enzymes (ALT, AST), indicators of renal function (urea, creatinine). Studied the level of thyroid hormones, adrenal glands (TSH, St. T4, cortisol). The amount, osmolarity, specific gravity of urine, concentration of Na, glucose in it, and the presence of ketone bodies are checked.
• Instrumental studies . Measurement of central venous pressure (CVP) is of most clinical importance.This is the most accurate way to determine the BCC, which allows you to clarify the type of hyponatremia (hypovolemic, hypervolemic or euvolemic). If pulmonary edema is suspected, a chest x-ray is taken, if there are symptoms of cerebral edema, a CT scan of the brain.

This condition must be differentiated from hypernatremia, since both of these pathologies have almost completely identical clinical symptoms. Cerebral edema during hyponatremia should be distinguished from cerebral edema of another etiology (hypertensive crisis, stroke, traumatic brain injury).It is much more important to differentiate the varieties of this syndrome (hyper-, hypo-, euvolemic, hyper- and hypotonic).

Treatment of hyponatremia

Most often, patients with hyponatremia are admitted to the intensive care unit. First, you need to stop taking medications that can cause hyponatremia, and stop the administration of hypotonic solutions. You can additionally prescribe the intake of ordinary table salt inside.This is sometimes sufficient for mild hyponatremia. For moderate to severe degrees, the following treatment is performed:

• Liquid restriction . This is the main condition for the treatment of hypervolemic form, as well as SIADH. Fluid consumption, both orally and in the form of solutions, should not exceed 1000 ml / day.
• Saline injection . Infusion therapy with 0.9% NaCl solution is necessary both to eliminate sodium deficiency and to maintain the BCC in hypovolemic form.In parallel, it is necessary to compensate for the deficiency of other electrolytes. If vivid neurological symptoms occur, hypertronic (3%) NaCl is administered. For the prevention of osmotic demyelinating syndrome, it is necessary to monitor the rate of increase in serum sodium levels, it should be less than 0.8 mmol / day.
• Diuretics . They are used to remove excess fluid in hypervolemic form. For this purpose, loop diuretics (furosemide) are used. Thiazide diuretics are strictly contraindicated as they aggravate hyponatremia.
• Blockade ADH . Since hyponatremia often causes increased secretion of ADH (vasopressin), measures to suppress its effect are important. Demeclocycline, antagonists of ADH receptors (conivaptan, tolvaptan) have an inhibitory effect on ADH. However, the use of these drugs should be avoided in patients with kidney disease.

Since hyponatremia is itself a very dangerous condition that can be fatal in a short time, the sodium level is corrected first.Therefore, only after eliminating the symptoms of threatening cerebral edema, they begin to treat the disease that caused the hyponatremia:

• CHF : ACE inhibitors, beta-blockers, loop diuretics.
• Cirrhosis of the liver : administration of albumin, transfusion of fresh frozen plasma, refusal of alcohol.
• Endocrine disorders : hormone replacement therapy with fludrocortisone, hydrocortisone (for adrenal insufficiency), levothyroxine (for hypothyroidism).
• CPI : hemodialysis.

Forecast and prevention

Hyponatremia is a dangerous life-threatening condition with a fairly high mortality rate (with various forms of this pathology, from 25 to 50% of patients die). According to some authors, the death rate reaches 65%. The cause of death is mainly cerebral edema, coma. However, with promptly started competent treatment, serious complications do not occur.

Neurological disorders such as dysphagia, dysarthria, and tetraplegia due to generalized demyelination of nerve fibers due to inadequately rapid correction of serum Na may become unfavorable outcomes. Prevention of this condition comes down to timely treatment of those diseases that can potentially cause hyponatremia, regular monitoring of plasma sodium levels.

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Drinking regime

Compliance with the drinking regime during Nordic walking is very important.If this issue is not properly addressed, two problems may arise: dehydration or waterlogging (hyponatremia) of the body. To prevent them, you need to understand what, how and how much to drink before, during and after walking.

During exercise, the temperature is regulated by the evaporation of sweat from the surface of our body. Thus, if the body is dehydrated, then heat cannot be removed and this can lead to a rapid onset of heatstroke. In addition, dehydration leads to an increase in the concentration of salts in the blood and tissues, which can lead to the deposition of salts in the joints, kidneys, gall bladder, etc.

Excess water in the body leads to a detrimental effect on the central nervous system, brain, muscles.

Before training, 2 hours before the start, drink 500 ml of water (with lemon).

Drink water while walking, depending on your thirst. If you sweat more than usual, drink more than usual.

Big rises. When climbing to a high altitude, in warm and low humidity, you need to drink more than usual, as in these cases you lose more fluid.Again, take your thirst level as a basis and drink when you feel thirsty.

After training, after 15-20 minutes you can drink salted mineral water.

The basic rule of hydration is to rely more on your thirst level and do not force yourself to drink. However, it should also be remembered that many people have unfortunately lost their natural feeling of thirst. So until you feel thirsty again, try to drink one glass of water for about every hour you walk.
Signs of dehydration: Thirsty, dry and sticky mouth, dry eyes, nausea, dark yellow urine or no urine.

DO NOT…

Do not drink carbonated drinks or juices while walking. Gas, belching, and stomach cramps can lead to discomfort while walking.

Do not drink milk or drinks containing milk. Many people with lactose intolerance may experience effects such as

nausea, bloating, and diarrhea. They may not realize they are lactose intolerant until they start exercising, which

amplifies the effects.

Do not drink cold water during class – you can catch a cold.

Do not drink alcoholic beverages before, after and during exercise.

Get tested: Sodium | MedLab

Description of the analysis:

Sodium is a microelement vital for the human body, regulating the volume of extracellular fluid, the acid-base state, participating in the transmission of nerve impulses and regulating the water-salt balance of the body.96% of sodium in the body is found in the extracellular space.

Sodium enters our body with table salt, is absorbed in the intestines, after which part of it is taken by the body to maintain electrolyte levels, and the rest is filtered by the kidneys and excreted in the urine.

Indications for prescribing an analysis for the level of sodium in the blood

Most often, the analysis is prescribed by nephrologists, gastroenterologists, endocrinologists, cardiologists and traumatologists.

Indications for the appointment of examination in nephrology are:

• acute jade;
• chronic pyelonephritis;
• acute renal failure;
• osmotic diuresis.

An indication for analysis in gastroenterology may be:

90,074 90,075 diarrhea;

Indications for sodium measurement in endocrinology are:

• diabetes mellitus;
• diabetes insipidus;
• hypothyroidism;
• adrenal insufficiency;
• hyperaldosteronism;
• Itsenko-Cushing’s syndrome.

In therapy, the sodium level is controlled at:

90,074 90,075 edema;

90,075 febrile conditions.

In cardiology, , the blood sodium test serves as a marker of congestive heart failure. In traumatology sodium levels are monitored for burns.

Norm of sodium in blood

The normal concentration of sodium in the blood is 130-157 mmol / l, and its level is practically independent of age or gender. Sodium is the main electrolyte of the human body, therefore, when the sodium concentration goes beyond the indicated limits, it immediately affects the state of health.High sodium levels are called hypernatremia, and low sodium levels are called hyponatremia.

Causes of hyper- and hyponatremia

An increase in sodium levels is possible with dehydration caused by insufficient intake of fluid in the body or its strong loss in case of gastrointestinal disorders or febrile conditions. Taking anabolic steroids, calcium, androgens, fluorides, corticosteroids, estrogens, combined oral contraceptives or ACTH also provokes an increase in sodium in the blood.

Recent trauma, surgery, or a person in a state of shock also lead to an increase in sodium concentration.

Elevated sodium levels are possible in formula-fed infants due to the high sodium concentration in formula.

Sodium deficiency in the body appears when a large amount of fluid entered the body, heart failure, impaired absorption of nutrients, diabetes mellitus, hypothyroidism, burn disease or adrenal insufficiency.

Taking furosemide, non-steroidal anti-inflammatory drugs, haloperidol, heparin, sulfates, diuretics, carbamazepine and antidepressants also leads to a decrease in blood sodium levels.

Preparation for examination

Standard for analysis of biochemical parameters of blood:

• the analysis is taken in the morning and strictly on an empty stomach;
• half an hour before the examination, it is necessary to exclude smoking, physical activity and stress;
• when taking drugs that can affect the indicator – notify the doctor prescribing the analysis.