Preventing and managing dehydration

Preventing and managing dehydration

Rosemarie Suhayda

Optimal physiologic function depends on a balance of body water and electrolytes. In periods of health, the volume, concentration, and composition of body fluids are regulated by a combination of renal, metabolic, and neurologic functions. Changes in osmotic gradients, such as a gain or loss of sodium, affect water balance (Sansevero, 1997). Sodium imbalance occurs in response to alterations in water volume. Dehydration develops when water loss exceeds water intake, resulting in a negative balance. A water loss of 1% to 2% impairs cognitive and physical performance, and a loss of 7% can lead to body collapse (Armstrong & Epstein, 1999; Sansevero, 1997). Water and sodium imbalances can be classified as either isotonic, hypertonic, or hypotonic dehydration.

While all adults are at risk for developing dehydration, elders are more vulnerable. Metabolic changes that occur with aging impede homeostatic mechanisms. Further, symptoms of dehydration can be insidious and easily overlooked in postoperative patients or patients receiving enteral nutrition. Chronic physical or mental illness, medications that enhance fluid loss, or self-imposed fluid restriction to manage incontinence all can contribute to dehydration. The classic early signs and symptoms of dehydration may be missing in older adults until the problem is well advanced (Weinberg, Minaker, and Council on Scientific Affairs, 1995). When living in the community, older adults, and especially those who are frail, are at an even higher risk for dehydration because they may go unmonitored by family and professional caregivers for long periods of time.

Since dehydration is a preventable problem, promoting fluid balance, identifying patients at risk, and providing information are effective ways to reduce morbidity and mortality (Sansevero, 1997). Nurses play a key role in the prevention, early detection, and treatment of water and electrolyte imbalances. To improve patients’ health, nurses must understand the distribution, composition, and regulation of water and electrolytes; recognize the types of dehydration; use effective assessment and monitoring tools; and plan and implement strategies for adequate hydration.

Distribution and Composition of Body Fluids

Body fluids are distributed between two main compartments: intracellular (ICF) and extracellular (ECF) (see Table 1). The sum of fluids within all compartments constitutes the total body water (TBW), which in an average adult male is approximately 42 L or 55% to 60% of total body weight. Heitz and Horne (2001) categorize the severity of ECF deficit in terms of acute weight loss. Acute weight loss is categorized as follows: mild fluid deficit (2%-5%), moderate (10%), severe (15%), and fatal (20%) (Heitz & Horne, 2001).

Besides water, fluid compartments contain dissolved electrolytes. Sodium, the major ECF solute, is the primary determinant of ECF osmolality (number of osmotically active solutes per kg of water). Potassium, the major ICF solute, is the primary determinant of ICF osmolality. A pump system exists in the wall of body cells that pumps sodium out and potassium in. The concentrations of sodium and potassium in the ECF are summarized in Table 2.

Normally, ECF and ICF osmolality are equal. Sodium and potassium move freely in and out of cells to maintain equilibrium. Disruption of osmolality impairs the movement of sodium and potassium and causes cells to restore equilibrium through water shifts at the expense of cell volume. Decreased plasma osmolality causes cellular swelling. Increased plasma osmolality causes cellular shrinking.

Regulation of Water and Sodium

Because the ECF consists primarily of water and sodium, the regulation of these two entities is critical in maintaining the volume and concentration of the ECF.

Thirst and the secretion of antidiuretic hormone (ADH) are two important regulators of water balance (Huether, 1994; Iggulden, 1999). Dry mucous membranes, hyperosmolality, and reduced plasma volume activate hypothalamic osmoreceptors, which trigger thirst and stimulate the secretion of ADH from the posterior pituitary. Water losses equaling 2% of total body weight trigger the thirst sensation (Huether, 1994). Ingestion of water restores plasma volume and osmolality of the ECF. Individuals who do not have a normal thirst mechanism or have no access to water develop symptomatic hyperosmolality.

ADH acts on the collecting ducts of the kidneys to increase water reabsorption and urine concentration, thereby restoring plasma volume. The release of ADH is also stimulated by volume-sensitive receptors found in the cardiac atria and thoracic vessels and by baroreceptors found in the aortic arch. These receptors respond to changes in circulating blood volume and pressure. The release of ADH is increased by stress and pain, medications such as morphine and barbiturates, surgery and certain anesthetics, positive-pressure ventilators, decreased circulating volume, and increased plasma osmolality. ADH release is decreased by drugs such as phenytoin and ethyl alcohol, increased circulating volume and blood pressure, and decreased plasma osmolality. In addition, there are medications that suppress or enhance the action of ADH on the renal collecting system. Lithium, demeclocycline, and methoxyflurane suppress the action of ADH, permitting water loss. Chlorpropamide and indomethacin enhance the action of ADH, permitting water retention (Heitz & Home, 2001).

Sodium functions primarily to maintain osmotic pressures and acid-base balance, and, in conjunction with calcium and potassium, to transmit nerve impulses. In healthy states, the sodium content of the body remains fairly constant despite wide fluctuations in sodium intake. Sodium is ingested in fluid and food primarily in the form of salt (NaCl), which is 40% sodium by weight. It is lost primarily in the urine, although modest amounts are lost in perspiration. The minimal daily requirement of sodium needed to maintain ECF homeostasis has not been established (Whitmire, 2001). The National Academy of Science recommends the Estimated Safe and Adequate Daily Dietary Intake (ESADDI) for sodium is 500 mg to 3,000 mg. (Whitmire, 2001). Sodium balance is regulated by the kidney under the influence of aldosterone, ADH, and atrial natriuretic peptide (ANP). Low serum sodium levels inhibit ADH and ANP while stimulating the secretion of aldosterone. These actions increase renal sodium reabsorption and renal water loss, thereby increasing serum sodium levels. High serum sodium levels stimulate secretion of ADH and ANP and inhibit secretion of aldosterone, thereby increasing renal excretion of sodium and reabsorption of water. Low circulating volume and decreased renal perfusion activate the reninangiotensin system. The subsequent vasoconstriction and secretion of aldosterone restore vascular volume and renal perfusion by increasing water and sodium reabsorption and systemic pressure.

Sources of Water Gains and Losses

Fluids and food are the major sources of water gain. A small amount is produced by metabolic processes, primarily carbohydrate metabolism. Normal renal excretion is responsible for most water loss. In adults, the average daily urine output is 1,500 ml. A minimum of 400 ml of maximally concentrated urine must be produced to excrete the daily load of metabolic wastes. Individuals who cannot concentrate urine must produce a larger volume to excrete the daily metabolic load, subjecting them to greater obligatory water loss. Water eliminated through the skin, lungs, and stool is termed insensible water loss. Insensible losses can be significant in hypermetabolic states and in extremes of exercise and ambient temperature. Water losses from the GI tract, although minimal in healthy states, can be profound in disease and can exceed 3 to 6 liters per day. This is the amount that is secreted into and reabsorbed daily by the GI tract. The average daily water gains and losses in adults are summarized in Table 3.

Weight, Gender, and Age Effects

A person’s ratio of lean body mass to body fat, gender, and age influence the volume and distribution of body fluids. Individuals with a higher proportion of body fat are more susceptible to fluid imbalances that cause dehydration (Huether, 1994). Fat cells are hydrophobic and contain very little water. An obese male has approximately 20% less total body water than does a lean male of similar stature and age (Huether, 1994). Because women have a higher percentage of body fat than do men, a woman of any age has less total body water than does a man of similar stature and age.

With aging, there is a decline in the percentage of total body water by approximately 10% to 15%. This can be attributed to a net loss of muscle mass, a reduced ratio of lean body weight to total body weight, and reduced renal regulation of sodium and water balance (Heitz & Home, 2001; Huether, 1994). The normal reduction of total body water places the elderly at a greater risk for water-deficit states.

Types of Dehydration

Alterations in sodium and water balance are closely related and can be classified as changes in tonicity; for example, changes in concentration of solutes in relation to water. There are three types of dehydration: isotonic, hypertonic, and hypotonic.

Isotonic dehydration, or hypovolemia, is the most common type and occurs when changes in total body water are accompanied by proportional changes in electrolytes. There is a contraction of the ECF with normal plasma osmolality and serum sodium levels. As a result, fluid shifts between compartments do not occur. Isotonic dehydration is caused most commonly by hemorrhage, excessive GI losses, and capillary leak syndrome (third spacing of intravascular fluids). Conditions such as tissue ischemia, endotoxemia, and trauma, including surgical trauma, damage capillary membranes and permit the flow of water, solutes, and plasma proteins into the interstitial (third) space (McSweeney, 2000). The fluid loss can be severe enough to cause cardiovascular collapse and death. Isotonic dehydration is characterized by acute weight loss and indications of hypovolemia. Skin turgor may be an unreliable indicator in young adults unless volume loss is profound (Kokko, 2000). Similarly, mouth breathing may dry oral mucous membranes independent of other factors.

Hypertonic dehydration results in higher mortality than isotonic and occurs when water loss exceeds sodium loss (Marino, 1998). The majority of patients have a primary defect in urinary concentrating ability along with insufficient administration of free water (Kokko, 2000; Whitmire, 2001). Intracellular fluid moves into the plasma and extracellular fluid spaces resulting in the contraction of the intracellular compartments and restoration of plasma volume. As a result, signs and symptoms of hypovolemic shock may not be present; however, membrane excitability and cardiac contractility are affected by altered plasma calcium and potassium levels. The most serious consequence of hypertonic hypernatremia is a hypernatremic encephalopathy, which has an associated mortality rate of up to 50% (Kokko, 2000; Marino, 1998). Clinically important symptoms generally do not appear until the serum sodium level exceeds 160 mmol/L and ECF osmolality exceeds 320 to 330 mOsm (Kokko, 2000; McSweeney, 2000). Coma and respiratory arrest may occur when the ECF osmolality exceeds 360 to 380 mOsm (Kokko, 2000).

Clinical manifestations are the result of central nervous system (CNS) dehydration and brain shrinkage that result from the increased ECF osmolality. Clinical findings include somnolence and confusion which progress to coma, respiratory paralysis, and death (Marino, 1998; McSweeney, 2000). Perhaps the most common type of hypertonic dehydration is excessive insensible water loss combined with limited ability to increase oral fluid intake (Weinberg et al., 1995; Whitmire, 2001). Other common causes include diabetes insipidus, hyperglycemia, hyperosmolar tube feedings, parenteral nutrition, and severe diarrhea (Weinberg et al., 1995; Whitmire, 2001). With chronic hypertonicity there are generally fewer central nervous system manifestations. The brain generates compounds called ideogenic osmoles, which raise intracellular osmolality and minimize brain shrinkage (Kokko, 2000; Marino 1998).

Hypotonic dehydration occurs when either sodium loss exceeds water loss or when sodium concentrations are diluted by excessive TBW. Clinically important symptoms generally do not appear until the serum sodium is <120 mmol/L (McSweeney, 2000). True sodium depletion results from gastrointestinal losses, excessive diuretic therapy, adrenal insufficiency, or electrolyte-free replacements for perspiration losses (Kokko, 2000; McSweeney, 2000). Dilutional hyponatremia is associated with conditions such as congestive heart failure, cirrhosis with ascites, renal disease, administration of large volumes of IV fluids, syndrome of inappropriate ADH (SIADH), or psychogenic polydipsia (Kokko, 2000; Marino, 1998; McSweeney, 2000). The accumulation of osmotically active substances such as glucose and lipids may also dilute sodium levels by causing water to move from the interstitial to the intravascular space. Symptoms of hyponatremia are the result primarily of CNS water intoxication and brain swelling (Kokko, 2000; McSweeney, 2000). Untreated acute hyponatremia is generally fatal and presents as a medical emergency. CNS manifestations are less common in chronic hyponatremia (Kokko, 2000). The types of dehydration are summarized in Table 4.

Management of Dehydration

Management of dehydration begins with screening for dehydration risk (see Table 5). The patient’s age, medical history, cognitive and functional abilities, and psychosocial status provide data to determine dehydration risk. The record of intake and output, patient’s vital signs and physical presentation, and laboratory values provide data to determine fluid status. Since acute weight fluctuations usually indicate fluid change, daily weight monitoring is the most sensitive indice of fluid statistics (Heitz & Horne, 2001). An acute weight loss of one kilogram (2.2 pounds) suggests a fluid loss of one liter. Weights should be measured at the same time each day, preferably before breakfast, on a balanced scale.

Strategies for maintaining or restoring adequate hydration should be discussed with all members of the health care team, the patient, and caregivers in order to develop a collaborative overall plan. In addition to fluid and electrolyte replacement, the plan should emphasize promoting effective airway clearance, maintaining integrity of skin and oral mucous membranes, preventing fall injuries related to orthostatic and cognitive changes, and educating the patient and family. Education should not only include maintaining adequate hydration, but information regarding medications that affect hydration status and underlying disease.

The major goal of treating dehydration is to correct the underlying causes while restoring fluid compartment values to normal ranges. The amount of water and sodium needed to replace losses, maintain adequate tissue perfusion, and produce adequate urine output varies according to body size and type of dehydration. The 24-hour water maintenance needs of patients can be determined by the following calculation: 100 ml of water/kg for the first 10 kg of body weight; 50 mi of Water/kg for the next 10 kg of body weight; and 20 mi of water for each kg of body weight exceeding 20 kg (McSweeney, 2000). Ideal body weight is usually used to calculate water need for obese patients. For febrile patients, add an extra 10% of the calculated water need for each 1 degree C elevation in body temperature (McSweeney, 2000). Patients receiving ADH-suppressing medications such as lithium should increase their daily water intake, as well. Fluid replacements should always include sodium and potassium, since other electrolyte deficiencies develop more slowly. Twenty-four hour maintenance needs for sodium and potassium are 3 and 2 mEq/100 ml of water, respectively (McSweeney, 2000).

Fluids can be provided by dietary, oral, and intravenous routes. Mild-to-moderate dehydration can be treated with dietary fluid replacement, provided patients are able to swallow and tolerate oral fluids and foods (Ignatavicius, Workman, & Mishler, 1999). Dietary fluids are obtained from both oral liquids and solid foods. Fruits and vegetables are approximately 90% water by weight; meat is approximately 70% water (Heitz & Horne, 2001). Dietary fluids should include patient’s preferences and should be offered throughout the day and evening hours. Offering small amounts of fluids every hour to conscious patients can improve compliance (Ignatavicius et al., 1999).

Oral rehydration is the easiest, least expensive, and most effective method for treating dehydration caused by diarrhea (Iggulden, 1999; Ignatavicius et al., 1999). Carbohydrate-electrolyte solutions such as sports replacement drinks, cola, and ginger ale are more palatable than other rehydrating solutions and are easily absorbed by the stomach, even in the presence of diarrhea and vomiting (Heitz and Horne, 2001; Ignatavicius et al., 1999). Oral rehydrating solutions such as Pedialyte[R] and Rehydralyte[R] have lower carbohydrate and higher electrolyte concentrations than do sports drinks, making them more appropriate for prolonged vomiting and diarrhea (Campbell & Hall, 1997; Heitz & Horne, 2001). Fluids lost from diarrhea can exceed two liters per day and should be replaced on a liter for liter basis, particularly in the elderly (Ignatavicius et al., 1999). Patients and/or caregivers should be instructed that too rapid administration of oral rehydrating solutions can cause gastric distention and reflex vomiting (Heitz & Horne, 2001). Common types of commercially available oral rehydrating solutions are summarized in Table 6.

During exercise, water deficit and electrolyte losses can develop when sweat output exceeds water intake, particularly in situations of increased ambient temperatures (Sawka & Montain, 2000). To prevent dehydration from exceeding 2% of body weight, it is recommended that exercising individuals drink 400 to 600 mi of fluid 2 hours prior to exercising and 150 to 300 mi every 15 to 20 minutes during exercise, depending on the sweating rate (Latzka & Montain, 1999). Excessive water intake can inhibit thirst and promote diuresis which may lead to negative water balance (Maughan, Leiper, & Shirreffs, 1997). For exercise lasting less than 90 minutes, water alone is sufficient for fluid replacement. For exercise exceeding 90 minutes, carbohydrate-electrolyte solutions should be considered to replace carbohydrate sources (Latzka & Mountain, 1999). Since electrolytes typically are replaced by solid foods, electrolyte replacement during regular exercise is unnecessary unless caloric intake is inadequate (Latzka & Mountain, 1999; Maughan et al., 1997; Sawka & Montain, 2000).

For more severe fluid volume deficits or when patients are unable to ingest oral liquids, restoration of fluid volume and electrolyte balance is accomplished with intravenous fluid therapy. Typically, the replacement fluid is similar in composition to the fluid that is lost (Heitz & Home, 2001; McSweeney, 2000). Two categories of solutions commonly used are crystalloids and colloids. The most common crystalloid solutions are dextrose in water or saline, isotonic (normal) saline, and Ringer’s (Heitz & Home, 2001; McSweeney, 2000). The most common colloid solutions are blood and blood components such as plasma and albumin (Kokko, 2000; Heitz & Horne, 2001). A summary of common intravenous solutions is found in Table 7.

Normal (0.9%) saline and lactated Ringer’s (LR) are intravascular volume expanders used most commonly to replace loss of isotonic fluids (Heitz & Horne, 2001). Normal saline preferentially expands the ECF and does not enter the ICF (Heitz & Horne, 2001; Kokko, 2000). One liter of normal saline increases blood volume by about 300 ml or 6% (Kokko, 2000). The remainder is distributed in the interstitial compartment. Normal saline contains sodium and chloride in excess of plasma levels and does not provide free water, calories, or other electrolytes (Heitz & Horne, 2001). Prough and Svensen (2001) reported that 0.9% saline, a long mainstay of fluid therapy, produces a dose-dependent hyperchloremic acidosis in direct response to rapid intravascular volume expansion. Solutions such as LR, which contain bicarbonate substrates, resolve mild metabolic acidosis more quickly than do solutions with excess chloride (Prough & Svensen, 2001). Lactated Ringer’s is similar in composition to normal plasma but does not provide free water, calories, or magnesium. Since it contains lactate, it should not be used to treat lactic acidosis (Heitz & Horne, 2001).

The use of colloids for volume expansion remains controversial, particularly for the treatment of fluid losses associated with capillary leak syndrome or “third spacing” (McSweeney, 2000). Colloids temporarily decrease the movement of fluid into the third space but may exacerbate hypovolemia 24 to 36 hours later when the colloids migrate into the interstitial space, pulling fluids from the intravascular space (McSweeney, 2000). Albumin, one of the more commonly used colloids, is available in 5% and 25% solutions. Solutions are administered at a rate of 2 to 4 ml/minute depending on the severity of protein loss and volume deficit (Kuhn, 1998). Rapid infusion of albumin may precipitate circulatory overload. The 25% solution is commonly used in patients with hypoproteinemia and will expand vascular volume 3 to 4 ml for each ml administered (Heitz & Horne, 2000). Colloid-containing solutions are most helpful in burns when cutaneous protein losses are significant and in circulatory collapse when rapid intravascular expansion is critical (Kokko, 2000). Unless serum albumin levels fall below 20 to 25 g/L or aggressive crystalloid therapy is ineffective in restoring vascular volume, the routine use of colloid solutions is not justified (Heitz & Horne, 2000; Kokko, 2000; McSweeney, 2000).

Blood is the most potent intravascular volume expander because a unit of packed red cells will remain entirely in the vascular bed (Kokko, 2000). Hypovolemia caused by blood loss is treated with the administration of whole blood or packed red blood cells along with normal saline or LR. Blood, however, has no role in treating isotonic fluid losses associated with capillary leak syndrome, since formed blood elements are not lost into the third space (McSweeney, 2000).

During fluid resuscitation, the rate of fluid administration can exceed 1 L/hour in extreme cases and should be adjusted hourly to maintain a minimum urine output of 0.5 mL/kg/hour (McSweeney, 2000). Normalization of heart rate and CVP along with urine output indicate normal intravascular volume. It is important to note that some patients may develop edema during fluid resuscitation (McSweeney, 2000). This extra fluid is caused by capillary leakage and will return to the vascular space once healing begins. Treating the edema with diuretics can further deplete intravascular volume. Fluid resuscitation should be discontinued if the patient shows signs of respiratory distress or hemodynamic measures which exceed those specified by protocol.

Hypertonic dehydration is almost always the result of a free water deficit and indicates a loss of TBW, not just intravascular volume (Kokko, 2000; Marino, 1998; McSweeney, 2000). The deficit is replaced with electrolyte-free solutions such as dextrose in water (D5W) which provides free water only and is distributed evenly throughout the ECF and ICF (Heitz &Horne, 2001). Rapid correction of hypertonicity to normal serum osmolality is hazardous and can cause cerebral edema (Kokko, 2000; Marino, 1998). To limit the risk of cerebral edema, free water deficits should be replaced slowly, over 48 to 72 hours (Marino, 1998). For patients receiving enteral feedings, supplemental free water should be provided since commercial preparations do not provide daily free water needs (Weinberg et al., 1995). The free water requirement for patients receiving enteral feedings is generally 30 ml/kg of body weight (Campbell & Hall, 1997). If hypernatremia is caused by actual increases in sodium, treatment involves diuretics along with D5W to eliminate sodium while maintaining normal TBW (Marino, 1998; McSweeney, 2000).

The major goal of treating hypotonic dehydration is to correct water osmolality and restore cell volume (Kokko, 2000). Hypotonic dehydration can be caused by dilution of sodium with excess TBW or by actual sodium loss. Dilutional hyponatremia is treated by water restriction of 600 to 1,000 ml/day (Huether 1994; Kokko, 2000), bedrest to increase venous return, and correction of the primary disorder (McSweeney, 2000). Diuretics are not a treatment of choice since diuretics cause sodium excretion. Dilutional hyponatremia usually resolves within a few days (Huether, 1994).

True hyponatremia with a sodium concentration of less than 120 mEq/L and CNS manifestations requires immediate therapy (Kokko, 2000). The amount of sodium administered must be sufficient to raise the TBW osmolality to approximately 250 mmOsm/kg of water (Kokko, 2000; Marino, 1998). Appropriate solutions to replace the sodium deficit are 0.9% saline for asymptomatic patients or 3% saline for symptomatic patients (McSweeney, 2000; Marion, 1998; Wyngaarden, Smith, & Bennett, 1992). A 250 mL solution of either 3% or 5% saline infused over 4 to 6 hours will usually raise the serum sodium concentration and abate neurologic symptoms (Kokko, 2000). Rapid elevation of serum sodium to values greater than 125 mEq/L may be hazardous and can result in CNS damage (Kokko, 2000; Marino, 1998). Serum sodium levels should not be increased by more than 12 mEq/L in a 24-hour period (Heitz & Horne, 2001).

Dehydration in Older Adults

Dehydration poses a significant problem for older adults and is the most common fluid and electrolyte problem in both long-term and at-risk community-dwelling elderly (Burke & Laramie, 2000; Weinberg et al., 1995). It is one of the ten most common diagnoses reported for hospital admissions in patients 65 years of age and older (Sheehy, Perry, & Cromwell, 1999). “Annually, almost 200,000 Medicare patients are hospitalized with a primary diagnosis of dehydration” (Yoshikawa, Cobbs, & Brummel-Smith, 1998, p. 157). Medicare expenditures for treating dehydration in the elderly are substantial (Weinberg et al., 1995).

Dehydration increases mortality in older adults across all settings. It is estimated that mortality rates may exceed 50% in untreated patients hospitalized with dehydration (Weinberg et al., 1995). The consequences of even mild dehydration can range from increasing constipation to lowered cognitive and functional status (Sansevero, 1994). As serum osmolality increases without water replacement, the neurologic symptoms such as nausea and vomiting, headache, and/or lethargy can develop, and the patient can proceed from mild confusion and disorientation to coma and death (Sheehy et al., 1999). Because of the significance of dehydration in long-term care facilities, the Omnibus Budget Reconciliation Act (OBRA) of 1987 and 1990 established dehydration behavioral and symptom triggers to alert staff of the potential problem (see Table 8).

Normatively with aging, systems that regulate the volume and concentration of body fluids reduce the body’s reserve capacity and ability to respond rapidly. It is estimated that by age 80, the glomerular filtration rate is reduced to about 300 ml/min and creatinine clearance has declined by about 30% (Sheehy et al., 1999). In addition, there is a decrease in the sensitivity of the volume osmoreceptors responsible for stimulating thirst (Stachenfeld, Dipietro, Nadel, & Mack, 1997; Toto, 1994). In comparison to young adults, a number of studies have reported that there is a slower response to thirst and drinking behavior in older adults following exercise (Gottschlick, 2001; Sheehy et al., 1999). Because older adults have less intracellular reserve, they become dehydrated more quickly (Cacciamani & Schwab, 2000).

Superimposed on the aging body are the complications of chronic illness, and medication use that can affect overall kidney function and the motivation to rehydrate. Acute and chronic illnesses can reduce the older adult’s ability to maintain fluid regulation by causing febrile illness, excess mucous secretion, or changes in functional status. Fever results in insensible fluid loss via skin and lungs and, when coupled with the inability to replace lost fluid, represents the most common cause of hypernatremic dehydration (Sheehy et al., 1999; Weinberg et al., 1995). Either hyponatremic or hypernatremic dehydration may develop after hospitalization, particularly postoperatively. In older adults, where nutrition and fluid care are managed parenterally or via gastric tube, close fluid assessment is necessary to monitor for and prevent dehydration.

Decreased fluid intake and increased fluid losses cause risk for dehydration in older adults (Weinberg et al., 1995). Mental or physical impairment can affect functional ability and can contribute to an inability to recognize the need for fluids or to access needed fluid replacement. Problems with physical mobility, such as those caused by arthritis or stroke, can affect manual dexterity and the ability to grasp and hold a cup or glass. Limited self-care abilities may necessitate partial or full assistance with fluid and nutritional intake, thus limiting free access to fluid replacement. Dysphagia may impact swallowing. In some cases, the older adult may be fearful of drinking because of urinary frequency and risk of incontinence. In addition, low air loss beds for pressure ulcer prevention can contribute to insensible fluid loss in the elderly. Diseases, such as type 2 diabetes, can cause glycosuria and polyuria, and, when complicated with hyperosmolar hyperglycemic nonketotic coma (HHNKC), as much as 4.8 to 12.6 liters of water can be lost daily (Sansevero, 1997). Diuretics and laxatives directly influence fluid loss while pain medications, sedatives, and tranquilizers can impede the motivation or physical ability to rehydrate (Sansevero, 1997).

Careful assessment and history taking is a critical factor in determining hydration status in the older adult. Often the first indication of dehydration is an acute change in mental status, reasoning, problem-solving ability, memory, or attention (Sheehy et al., 1999; Walton & Miller, 1998). Other signs of dehydration include “tongue furrows, dry oral mucous membranes, and the absence of a saliva pool” (Sansevero, 1996, p. 63). However, symptoms of dehydration may be subtle, deceptive, or even nonexistent (Weinberg et al., 1995). Skin turgor is a less reliable indicator because of the skin’s decreased elasticity in older adults. In this patient population, skin turgor is best assessed on the inner aspect of the thigh or over the sternum (Heitz & Horne, 2001). Because cardiac disease and medications can increase orthostatic blood pressure and pulse changes, these signs are less reliable indicators of dehydration in the elderly.

Adequate hydration for elderly patients can prevent clinically significant problems. Supplemental fluids may be all that are necessary to promote well-being. Some research suggests that oral rehydrating solutions, often used with children, are effective when used to treat mild-to-moderate dehydration in nursing home patients (Iggulden, 1999). Since decreased thirst perception may be present, regular encouragement and monitoring of fluid intake are required (Weinberg et al., 1995). Patients who are agitated, confused, or demented will need additional support and observation. Unless contraindicated by medical condition, elderly patients weighing between 50 and 80 kg should have a minimum fluid intake of 1,500 to 2,500 ml/day (Weinberg et al., 1995). For adults older than 65 years, the daily fluid requirement is 30 ml/kg of body weight at baseline or approximately 2,000 ml/day (Hoffman 1991; Sansevero, 1997).

For patients requiring substantial fluid replacement, intravenous therapy or hypodermoclysis may be alternatives (Iggulden, 1999; Weinberg et al., 1995). Hypodermoclysis is the subcutaneous infusion of isotonic or hypotonic solutions. Solutions are infused through needles into the subcutaneous tissues of the abdomen or the anterior or lateral thighs at a rate of 1 ml/min (Weinberg et al., 1995). Infusions of up to 1,500 ml through a single site and 3,000 mi through two sites can be administered in a 24-hour period (Weinberg et al., 1995). Particularly in long-term care settings where intravenous therapy is not routinely performed, hypodermoclysis can be a very useful strategy (Iggulden, 1999; Weinberg et al., 1995).

For elderly with free water deficits, a general rule of thumb is: “30-50% of free water deficit may be repleted in the first 24 hours–no faster” (Cacciamani & Schwab, 2000, p. 270). Free water deficit (FWD) in the elderly can be calculated by the following formula: FWD [L] = weight [kg] X 0.45 – ([140/measured serum sodium] X weight [kg] X 0.45) (Weinberg et al., 1995). The patient’s baseline weight prior to becoming dehydrated must be known to use this calculation. Because many elderly suffer from cardiac problems, they are particularly prone to volume overload and need careful monitoring during fluid replacement.


The current complexity of hospital care, with staff resources often stretched, requires astute and effective nursing care. By recognizing early and subtle changes in patients’ physical and cognitive status, nurses play a critical role in preventing complications and reducing hospital stays. Monitoring for dehydration is an important area of clinical practice and one that can be easily overlooked in older adults. However, in all patients, dehydration superimposed on other health problems can increase complications in often already vulnerable patients. With the importance of this clinical role, nurses who understand the process of water regulation, the sources of water gains and losses, assessment, and the types and treatment of dehydration are better prepared to assess and intervene from a sound scientific and physiologic base.

Table 1.

Distribution of Total Body Water

% of Total Body % of Total Body Volume in

Water Weight Liters (L)

Intracellular 60% 40% 27 L

Extracellular 40% 20% 15 L

(interstitial) (15%) (11 L)

(intravascular) (5%) (3L)

Source: Huether (1994)

Table 2.

Concentration of Sodium and Potassium in the ECF



Electrolyte Normal Range Units (mmol/L)

Sodium 136-145 mEq/L 136-145 mmol/L

Critical value [less than or equal to]

110 mEq/L

60-90 years 136-145 mEq/L 136-145 mmol/L

>90 years 132-146 mEq/L 132-146 mmol/L

Potassium 3.5-5.3 mEq/L 3.5-5.3 mmol/L

Critical value 6.6 mEq/L

>60 years male 3.5-4.5 mEq/L 3.5-4.5 mmol/L

>60 years female 3.4-4.4 mEq/L 3.4-4.4 mmol/L

Source: Chernecky & Berger (2001)

Table 3.

Average Daily Water Gains and Losses

Water Gains Water Losses

Sensible Sensible

Fluids 1,100-1,800 mL Urine 1,200-1,800 mL

Food 700-1,000 mL Stool 100-200 mL

Perspiration 50 mL

Insensible Insensible

Oxidative metabolism 300-400 mL Lungs 400-600 mL

Skin 500-600 mL

Total 2,100-3,200 mL Total 2,250-3,200 mL

Source: Heitz & Horne (2001); Whitmire (2001)

Table 4.

Types of Dehydration

Hypotonic Dehy- Hypertonic Dehy-

Isotonic Dehydration dration (water dration (water

(water loss = sodium loss sodium

loss) loss) loss)

Signs and * Acute weight loss * Lethargy * Anorexia,

Symptoms > 2% * Somnolence nausea,

* 24-hour urine * Skeletal muscle vomiting

output < 500 mL weakness * Headache

* Rapid, thready * Muscle cramps * Apathy

pulse * Nausea, * Agitation,

* Decreased BP with anorexia delerium

orthostatic * Seizures * Seizures

changes (ortho- * Coma * Hyperactive

static systolic * Hypernatremia tendon reflexes

[greater than or and other * Coma and

equal to] 15-20 pertinent respiratory

mmHg; orthostatic laboratory arrest

diastolic of 10 tests * Hyponatremia

mmHg; pulse and other

[greater than or pertinent

equal to] 10 laboratory

beats/minute) tests

* Decreased body


* CVP < 2 mmHg or

< 5cm [H.sub.2]O

* Flattened neck and

hand veins

* Decreased skin

turgor with

tenting over fore-

arm, sternum, or

dorsum of hand

* Furrowed, dry


* Flush dry skin and

dry mucous


* Dry axilla

* Decreased GI


Laboratory * BUN/plasma * Serum sodium

Values creatinine > 20:1 120 mEq/L 150 mEq/L

F[E.sub.Na] < 1% * Serum * Serum osmola-

* Sodium – 147 mEq/L osmolality lity > 290 mOsm

* serum osmolality > < 290 mOsm * Normal or

290 mOsm/L * Increased Hg, decreased Hg,

* Increased Hg, Hct, Hct, protein, Hct, protein

protein in BUN, creatinine * Urine osmola-

proportion to * Urine specific lity > 400 mOsm

plasma deficit gravity < 1.010 * Urine-specific

* Urine-specific * Urine osmola- gravity > 1.03

gravity 1.016- lity > 500 mOsm * Urine sodium:

1.020 in absence * Urine sodium decreased with

of impaired renal < 10-15 mEq/L renal water

function loss; increased

* Urine osmolality > with sodium

500 mOsm gain

* Urine sodium < 10


Treatment * Normal (0.9%) * True hyponatre- * Electrolyte

saline mia: hypertonic free oral or

* Lactated Ringer’s saline infusion intravenous

* Lactated Ringer’s over 4-6 hours solutions such

* Dilutional as D5W infusion

hyponatremia: over 18-24

fluid hours

restrictions * Normal (0.9%)


Sources: Cacciamani & Schwab (2000); Cherncky & Berger (2001); Heitz

& Horne (2001); Ignatavicius, Workman, & Mishler (1999); Kokko (2000);

McSweeney (2001); Weinberg et al. (1995)

Table 5.

Screening for Dehydration Risk

* General survey (age, physical appearance)

* History of acute and chronic illness (prolonged fever,

hyperventilation, diaphoresis, diuresis, vomiting, diarrhea,

anorexia, dysphagia, burns, draining wounds, trauma, NPO status,

nasogastric suction, hypertonic enemas, enteral feedings, blood

loss, renal disease, cardiac disease, liver disease, bowel

obstruction, hip fracture, terminal illness, surgery)

* Medications (diuretics, laxatives, ADH suppressants, anesthetics,

narcotics, alcohol, other drugs)

* Cognitive ability (dementia, confusion, cognitive impairment)

* Functional ability (muscle weakness, dependency, limited mobility,

CNS depression)

* Psychosocial status (mental illness, living conditions, social


* Nutrition history (patterns of weight loss or gain, thirst response

and pattern, knowledge of daily fluid requirements)

* Incontinence history

* Bowel pattern

* Environmental factors (environmental and ambient temperature)

Sources: Iggulden (1999); Ignatavicius et al (1999)

Table 6.

Commercial Solutions for Oral Reydration Therapy

[Na.sup.+] [K.sup.+] [Cl.sup.-] Base Calories

Formula (mEq/L) (mEq/L) (mEq/L) (mEq/L) (kcal/L)

45 20 35 30 100




(Ross) 75 20 65 30 100



Johnson 50 25 45 34 126



Ayers) 50 20 50 34 84


(Rorer) 60 20 60 10 84

Source: Heitz & Horne (2001); Ignatavicius et al. (1999)

Table 7.

Characteristics of Common Intravenous Therapy Solutions


Solution (mOsm/L) pH Calories Tonicity Indications

Saline 308 5.0 0 Isotonic ** Replaces ECF

0.9% and expands



** Only solution


with blood


** Can cause


overload or



** Used as a


fluid and to

treat isoto-

nic and



0.45% 154 5.0 0 Hypotonic ** Provides free

water in

addition to




** Used as a


fluid and to

treat hypoto-

nic fluid


3.0% 1,026 5.0 0 Hypertonic ** Used to treat



** Administered

slowly to

avoid volume



in Water 272 3.5-6.5 170 Isotonic * ** Provides free

5% water only.

** Used to treat



10% 500 3.5-5.6 340 Hypertonic * ** Provides free

water only.

** Used as a


fluid during

sudden inter-

ruption of



Dextrose 355 4.0 170 Hypertonic * ** Same as 0.45%

in with added

Saline calories.

5% in


5% in 560 3.5-5.6 170 Hypertonic * ** Same as 0.9%

0.9% with added


Lactated 274 6.5 9 Isotonic ** Similar to

Ringer’s plasma but



** Used to treat

mild metabo-

lic acidosis.

** Replaces

heavy loss of

fluids (burns

and lower Gl


Table 8.

Minimum Data Set (MDS)

Tracking Form

(For nursing home resident

assessment and core screening)

MDS Triggers

* Diagnosis of dehydration

* Insufficient fluid intake (did not

consume all liquids provided)

* Weight fluctuation of 3+ lbs.

* Urinary tract infection

* Fever

* Bleeding

* Parenteral/or tube feeding

* Diarrhea

* Diuretic therapy

Source: Lorvorn (2000)


Armstrong, L.E., & Epstein, Y. (1999). Fluid electrolyte balance during labor and exercise: Concepts and misconcepts. International Journal of Sports Nurtrition, 9(1), 1-12.

Burke, M.M., & Laramie, J.A. (2000). Primary care of the older adult: A multidisciplinary approach. St. Louis: Mosby.

Cacciamani, J.D., & Schwab, E.P. (2000). Dehydration. In M.A. Forciea, R. Lavizzo-Mourey, & E.P. Schwab (Eds.) Geriatric secrets (2nd ed.) (pp. 268271). Philadelphia: Haney & Belfus.

Campbell, S., & Hall, J. (1997). Enteral nutrition handbook. Cleveland, OH: Abbott Laboratories, Ross Division.

Chernecky, C., & Berger, B. (2001). Laboratory tests and diagnostic procedures (3rd ed.). Philadelphia: W.B. Saunders Co.

Gottschlick, M.M. (Ed.) (2001). The science and practice of nutritional support: American Society for parenteral and enteral nutrition: A case-based core curriculum. Dubuque, IA: Kendall/Hunt Publishing Company.

Heitz, U.E., & Horne, M.M. (2001). Fluid, electrolyte, and acid-base balance (4th ed.). St. Louis, MO: Mosby.

Hoffman, N. (1991). Dehydration in the elderly: Insidious and manageable. Geriatrics, 46(6), 35-38.

Huether, S.E. (1994). The cellular environment: Fluids, and electrolytes, acids and bases. In K.L. McCance, & S.E. Huether (Eds.), Pathophysiology: The biological basis for disease in adults and children. St. Louis: Mosby.

Iggulden, H. (1999). Dehydration and electrolyte disturbance. Nursing Standard, 13(19), 48-56.

Ignatavicius, D.D., Workman, M.L., & Mishler, M.A. (1999). Medical-surgical nursing across the health continuum (3rd ed.) (pp. 229-242). Philadelphia: W.B. Saunders Co.

Kokko, J.P. (2000). Fluids and electrolytes. In L. Goldman & J. Bennett (Eds.), Cecil textbook of medicine (21st ed.). Philadelphia: W.B. Saunders.

Kuhn, M. (1998). Pharmaco-therapeutics: A nursing process approach (4th ed.). Philadelphia: F.A. Davis Co.

Latzka, W.A., & Montain, S.J. (1999). Fluid and electrolyte supplementation for exercise. Clinical Sports Medicine, 18(3), 513-524.

Lorvorn, B. (2000). Resident assessment instrument MDS 2.0: Comprehensive users guide. Albertville, AL: Heaton Publisher.

Marino, P. (1998). Hypertonic and hypotonic syndromes. In R Marino (Ed.), The ICU book (2nd ed.). Baltimore: Williams & Wilkins.

Maughan, R.J., Leiper, J.B., & Shirreffs, S.M. (1997). Factors influencing the restoration of fluid and electrolyte balance after exercise in heat. British Journal of Sports Medicine, 31(3), 175-182.

McSweeney, G. (2000). Fluid and electrolyte therapy and acid balance. E. Hefindale, & D. Gorlie (Eds), Textbook of therapeutics: Drug and disease measurements. Baltimore: Lippincott Williams & Wilkins.

Prough, D., & Svensen, C. (2001). Current concepts in perioperative fluid management. Anesthesia and Analgesia, 92(3S), 70-77.

Sansevero, A.C. (1997). Dehydration in the elderly: Strategies for prevention and management. The Nurse Practitioner, 24(4), 41-42, 51-57, 63-66.

Sawka, M.N., & Montain, S.J. (2000). Fluid and electrolyte supplementation for exercise heat stress. American Journal of Clinical Nutrition, 72(2), 564S-572S.

Sheehy, C.M., Perry, P.A., & Cromwell, S.L. (1999). Dehydration: Biological considerations, age-related changes, and risk factors in older adults. Biological Research in Nursing, 1(1), 30-37.

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Walton, J.C., & Miller, J.M. (1998). Evaluating physical and behavioral changes in older adults. MEDSURG Nursing, 7(20), 85-90.

Weinberg, D.A., Minaker, K.L., and the Council on Scientific Affairs, American Medical Association. (November 15, 1995). Dehydration: Evaluation and management in older adults. JAMA, 274(19), 1552-1556.

Whitmire, S.J. (2001). Fluid and electrolytes. In M. Gottschlich (Ed.), The science and practice of nutrition support: A case-based core curriculum. Dubuque, IA: Kendall/Hunt Publishing Company.

Wyngaarden, J.B., Smith, L.H., & Bennett, J.C. (1992). Texbook of medicine. (9th ed., vol. 1). Philadelphia: W.B. Saunders.

Yoshikawa, T.T., Cobbs, E.L., & Brummel-Smith, K. (1998). Practical ambulatory geriatrics (2nd ed.). St. Louis: Mosby.

Additional Readings

Hoffman, N. (1999). Health management for older adults II: Module 4: Dehydration and nutrition. Retrieved September 22, 2001 from cme/homa2/dehyd.html

Holben, D.H., Hassell, J.T., Williams, J.L., & Helle, B. (1999). Fluid intake compared with established standards and symptoms of dehydration among elderly residents of a long term care facility. Journal of American Dietetic Association, 909(11), 1447-1450.

Reese, J.L. (2001). Fluid volume deficit dehydration: Isotonic, hypotonic, and hypertonic. In M.L. Maas, K.C. Buckwalter, M.D. Hardy, T. Trippreemer, M.G. Titler, & J.P. Specht (Eds.), Nursing care of older adults: Diagnosis, outcomes, and interventions (pp. 183-200). St. Louis: Mosby.

Rosemarie Suhayda, PhD, RN, APN/ANP, is an Assistant Professor and Director of Evaluation, Adult Health Nursing, Rush University College of Nursing, Chicago, IL.

Jane C. Walton, PhD, RN, APN/CCS, is an Assistant Professor, Adult Health Nursing, Rush University College of Nursing, Chicago, IL.

Answer/Evaluation Form: Preventing and Managing Dehydration


This educational activity is designed for nurses and other health care professionals who care for and educate patients regarding dehydration. The evaluation that follows is designed to test your achievement of the following educational objectives. After reading this article, you will be able to:

1. Describe regulation of water and sodium and sources of water gains and losses.

2. List types of dehydration.

3. Discuss management strategies for dehydration.

Posttest Instructions

1. To receive continuing education credit for individual study after reading the article, complete the answer/evaluation form to the left.

2. Detach and send the answer/evaluation form along with a check or money order payable to Jannetti Publications/MEDSURG Nursing to MEDSURG Nursing, CE Series, East Holly Avenue Box 56, Pitman, NJ 08071-0056.

4. Test returns must be postmarked by December 31, 2004. Upon completion of the answer/evaluation form, a certificate for 3.2 contact hour(s) will be awarded and sent to you.

This independent study activity is provided by Anthony J. Jannetti, Inc., which is accredited as a provider and approver of continuing education in nursing by the American Nurses Credentialing Center’s Commission on Accreditation (ANCC-COA).

This article was reviewed and formatted for contact hour credit by Catherine Todd Magel, EdD, RN, C, Assistant Professor, College of Nursing, Villanova University, Villanova, PA; Sally S. Russell, MN, RN, C, AMSN Education Director, and Marilyn S. Fetter, PhD, RN, CS, Assistant Professor, College of Nursing, Villanova University, Villanova, PA.

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