Preventing and managing dehydration.
12/1/2002; Walton, Jane C.
Sufficient body water and electrolyte homeostasis are essential for
healthy physiologic functioning. Nurses are key to preventing, detecting
early, and treating fluid and electrolyte imbalances. Dehydration
significantly alters both physical and psychological functioning, and
older adults are at increased risk. Identifying fluid disorders early
can prevent complications and reduce hospital stays. Understanding the
mechanisms of fluid homeostasis enables nurses to assess, prevent, and
collaborate in managing isotonic, hypertonic, and hypotonic dehydration.
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
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
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
Distribution and Composition of Body Fluids
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).
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
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
the ECF consists primarily of water and sodium, the regulation of these
two entities is critical in maintaining the volume and concentration of
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.
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).
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.
of Water Gains and Losses
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.
Gender, and Age Effects
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
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.
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
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;
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
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
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
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).
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).
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.
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 &
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.
(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).
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).
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).
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).
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
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,
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
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).
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;
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).
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.
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
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)
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]
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 <2.5 or >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)
Average Daily Water Gains and Losses
Water Gains Water Losses
Fluids 1,100-1,800 mL Urine 1,200-1,800 mL
Food 700-1,000 mL Stool 100-200 mL
Perspiration 50 mL
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)
Types of Dehydration
Hypotonic Dehy- Hypertonic Dehy-
Isotonic Dehydration dration (water dration (water
(water loss = sodium 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
* Decreased body
* CVP < 2 mmHg or
< 5cm [H.sub.2]O
* Flattened neck and
* Decreased skin
tenting over fore-
arm, sternum, or
dorsum of hand
* Furrowed, dry
* Flush dry skin and
* Dry axilla
* Decreased GI
Laboratory * BUN/plasma * Serum sodium < * 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
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)
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,
* 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)
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)
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
** Can cause
** Used as a
fluid and to
0.45% 154 5.0 0 Hypotonic ** Provides free
** Used as a
fluid and to
3.0% 1,026 5.0 0 Hypertonic ** Used to treat
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
** Used as a
Dextrose 355 4.0 170 Hypertonic * ** Same as 0.45%
in with added
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
heavy loss of
and lower Gl
Minimum Data Set (MDS)
(For nursing home resident
assessment and core screening)
* Diagnosis of dehydration
* Insufficient fluid intake (did not
consume all liquids provided)
* Weight fluctuation of 3+ lbs.
* Urinary tract infection
* Parenteral/or tube feeding
* 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.
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
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.
J.P. (2000). Fluids and electrolytes. In L. Goldman & J. Bennett (Eds.),
Cecil textbook of medicine (21st ed.). Philadelphia: W.B. Saunders.
M. (1998). Pharmaco-therapeutics: A nursing process approach (4th ed.).
Philadelphia: F.A. Davis Co.
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.
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.
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,
M.N., & Montain, S.J. (2000). Fluid and electrolyte supplementation for
exercise heat stress. American Journal of Clinical Nutrition, 72(2),
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.
Stachenfeld, N.S., DiPietro, L., Nadel, E.R., & Mack, G.W. (1997).
Mechanism of attenuated thirst in aging: Role of central volume
receptors. American Physiological Society, 272(1 PT 2), R148-157.
K.H. (1994). Regulation of plasma osmolality: Thirst and vasopressin.
Critical Care Clinics of North America, 6(4), 661-673.
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.
Hoffman, N. (1999). Health management for older adults II: Module 4:
Dehydration and nutrition. Retrieved September 22, 2001 from
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.
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.
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
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:
Describe regulation of water and sodium and sources of water gains and
types of dehydration.
Discuss management strategies for dehydration.
receive continuing education credit for individual study after reading
the article, complete the answer/evaluation form to the left.
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.
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.
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
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.
COPYRIGHT 2002 Jannetti
The above article is from
Nursing, December 1, 2002.