MECHANISMS AND SITUATIONS	MANIFESTATIONS	MANAGEMENT AND NURSING CARE
Water Depletion
Failure to absorb or reabsorb water Complete or sudden cessation of intake or prolonged diminished intake: • Neglect of intake by self or caregiver—confused, psychotic, unconscious, or helpless • Loss from gastrointestinal tract—vomiting, diarrhea, nasogastric suction, fistula Disturbed body fluid chemistry: inappropriate ADH secretion Excessive renal excretion: glycosuria (diabetes) Loss through skin or lungs: • Excessive perspiration or evaporation—febrile states, hyperventilation, increased ambient temperature, increased metabolic activity (BMR) • Impaired skin integrity—transudate from injuries • Hemorrhage Iatrogenic: • Overzealous use of diuretics • Improper perioperative IV fluid replacement • Use of radiant warmer or phototherapy	General symptoms depend to some extent on proportion of electrolytes lost with water Thirst Variable temperature—increased (infection) Dry skin and mucous membranes Poor skin turgor Poor perfusion (decreased pulse, prolonged capillary refill time) Weight loss Fatigue Diminished urinary output Irritability and lethargy Tachycardia Tachypnea Altered level of consciousness, disorientation Laboratory findings: • Increased hematocrit • Variable serum electrolytes • Low serum bicarbonate (CO₂) • Variable urine volume • Increased BUN • Increased serum osmolality	Provide replacement of fluid losses commensurate with volume depletion. Provide maintenance fluids and electrolytes. Determine and correct cause of water depletion. Measure fluid intake and output. Monitor vital signs. Monitor urine specific gravity. Monitor body weight. Monitor serum electrolytes.
Water Excess
Water intake in excess of output: • Excessive oral intake of solute-free water • Hypotonic fluid overload • Plain water enemas Failure to excrete water in presence of normal intake: • Kidney disease • Syndrome of Inappropriate Secretion of Antidiuretic Hormone • Heart failure • Malnutrition	Edema: • Generalized • Pulmonary (moist rales or crackles) • Intracutaneous (noted especially in loose areolar tissue) Elevated venous pressure Hepatomegaly Slow, bounding pulse Weight gain Lethargy Increased spinal fluid pressure CNS manifestations (seizures, coma) Laboratory findings: • Low urine specific gravity • Decreased serum electrolytes • Decreased hematocrit • Variable urine volume	Limit fluid intake. Administer diuretics. Monitor vital signs. Monitor neurologic signs as necessary. Determine and treat cause of water excess. Analyze laboratory electrolyte measurements. Implement seizure precautions.
Sodium Depletion (Hyponatremia)
Prolonged low-sodium diet Decreased sodium intake Fever Excess sweating Increased water intake without electrolytes Tachypnea; prolonged (infants) Cystic fibrosis Burns and wounds Vomiting, diarrhea, nasogastric suction, fistulas Adrenal insufficiency Renal disease DKA Malnutrition	Associated with water loss: • Same as with water loss—dehydration, weakness, dizziness, nausea, abdominal cramps, apprehension • Mild—apathy, weakness, nausea, weak pulse • Moderate—decreased blood pressure, lethargy Laboratory findings: • Sodium concentration <130 mEq/L (may be normal if volume loss) • Urine specific gravity depends on water deficit or excess	Determine and treat cause of sodium deficit. Administer IV fluids with appropriate saline concentration. Monitor fluid intake and output.
Sodium Excess (Hypernatremia)
High salt intake—enteral or IV Renal disease Fever Insufficient breast milk intake in neonate (dehydration hypernatremia) High insensible water loss: • Increased temperature • Increased humidity • Hyperventilation • Diabetes insipidus • Hyperglycemia	Intense thirst Dry, sticky mucous membranes Flushed skin Temperature possibly increased Hoarseness Oliguria Nausea and vomiting Possible progression to disorientation, seizures, muscle twitching, nuchal rigidity, lethargy at rest, hyperirritability when aroused Laboratory findings: • Serum sodium concentration ≥150 mEq/L • High plasma volume • Alkalosis	Determine and treat cause of sodium excess. Administer IV fluids as prescribed. Measure fluid intake and output. Monitor laboratory data. Monitor neurologic status. Ensure adequate intake of breast milk and provide lactation assistance with new mother–baby pair before hospital discharge.
Potassium Depletion (Hypokalemia)
Starvation Clinical conditions associated with poor food intake Malabsorption IV fluid without added potassium Gastrointestinal losses—diarrhea, vomiting, fistulas, nasogastric suction Diuresis Administration of diuretics Administration of corticosteroids Diuretic phase of nephrotic syndrome Healing stage of burns Potassium-losing nephritis Hyperglycemic diuresis (e.g., diabetic ketoacidosis) Familial periodic paralysis IV administration of insulin in DKA Alkalosis	Muscle weakness, cramping, stiffness, paralysis, hyporeflexia Hypotension Cardiac arrhythmias, gallop rhythm Tachycardia or bradycardia Ileus Apathy, drowsiness Irritability Fatigue Laboratory findings: • Decreased serum potassium concentration ≤3.5 mEq/L • Abnormal ECG—notched or flattened T waves, decreased ST segment, premature ventricular contractions	Determine and treat cause of potassium deficit. Monitor vital signs, and ECG. Administer supplemental potassium. Assess for adequate renal output before administration. For IV replacement, administer potassium slowly. Always monitor ECG for IV bolus potassium replacement. For oral intake, offer high-potassium fluids and foods. Evaluate acid–base status.
Potassium Excess (Hyperkalemia)
Renal disease Renal failure Adrenal insufficiency (Addison disease) Associated with metabolic acidosis Too rapid administration of IV potassium chloride Transfusion with old donor blood Severe dehydration Crushing injuries Burns Hemolysis Dehydration Potassium-sparing diuretics Increased intake of potassium (e.g., salt substitutes)	Muscle weakness, flaccid paralysis Twitching Hyperreflexia Bradycardia Ventricular fibrillation and cardiac arrest Oliguria Apnea—respiratory arrest Laboratory findings: • High serum potassium concentration ≥5.5 mEq/L • Variable urine volume • Flat P wave on ECG, peaked T waves, widened QRS complex, increased PR interval	Determine and treat cause of potassium excess. Monitor vital signs, including ECG. Administer exchange resin, if prescribed. Administer IV fluids as prescribed. Administer IV insulin (if ordered) to facilitate movement of potassium into cells. Monitor potassium levels. Evaluate acid–base status.

ADH, Antidiuretic hormone; BMR, basal metabolic rate; BUN, blood urea nitrogen; CNS, central nervous system; DKA, diabetic ketoacidosis; ECG, electrocardiogram; IV, intravenous.

Water Intoxication

Water intoxication, or fluid volume excess, is observed less often than dehydration. However, it is important that nurses and others who care for children be alert to this possibility in certain situations. Children who ingest excessive amounts of electrolyte-free water develop a concurrent decrease in serum sodium accompanied by central nervous system (CNS) symptoms. There is a large urinary output, and because water moves into the brain more rapidly than sodium moves out, the child may also exhibit irritability, somnolence, headache, vomiting, diarrhea, or generalized seizures. The affected child usually appears well hydrated but may be edematous or even dehydrated.

Fluid intoxication can occur during acute intravenous (IV) fluid replacement, too rapid dialysis, tap water enemas, feeding of incorrectly mixed formula, or excess water ingestion or with too rapid reduction of glucose levels in diabetic ketoacidosis. Patients with CNS infections occasionally retain excessive amounts of water. Administration of inappropriate hypotonic solutions (e.g., 0.45% sodium chloride) may cause a rapid reduction in sodium and result in symptoms of water excess or overload.

Infants are especially vulnerable to fluid volume excess. Their thirst mechanism is not well developed; therefore, they are unable to “turn off” fluid intake appropriately. A decreased glomerular filtration rate does not allow for repeated excretion of a water excess, and antidiuretic hormone (ADH) levels may not be maximally reduced. Consequently, infants are unable to excrete a water excess effectively.

Administration of inappropriately prepared formula is one of the more common causes of water intoxication in infants. Families who cannot afford to buy enough formula may dilute the formula to increase the volume or even substitute water for the formula. A family may run out of formula and dilute the remaining amount to make it last until they are able to purchase more. In addition, water is sometimes used for pacification when the infant is crying or fussy. Water intoxication can also occur in infants who receive overly vigorous hydration during a febrile illness.

A number of clinicians have reported water intoxication in children after swimming lessons. Although they hold their breath, some children apparently swallow a large amount of water during repeated submersion. Anticipatory guidance to parents should include a discussion of swimming instruction and advice to stop a lesson if the child swallows unusual amounts of water or exhibits any symptoms of hyponatremia (see Table 24-2).

Dehydration

Dehydration is a common body fluid disturbance in infants and children and occurs whenever the total output of fluid exceeds the total intake, regardless of the cause. Dehydration may result from a number of diseases that cause insensible fluid losses through the skin and respiratory tract, through increased renal excretion, and through the GI tract. Although dehydration can result from impaired oral intake, it is often a result of abnormal losses, such as those that occur in vomiting or diarrhea, when oral intake only partially compensates for the abnormal losses. Other significant causes of dehydration include diabetic ketoacidosis and burns.

Types of Dehydration

The pathophysiology of dehydration is understood by recognizing that the distribution of water between the ECF and ICF spaces depends on active transport of potassium into and sodium out of cells by energy-requiring processes. Sodium is the chief solute in ECF and is the primary determinant of ECF volume. Sodium is considered a unique electrolyte in that water balance determines sodium concentration; when water is lost and sodium concentration becomes elevated compensatory mechanisms in the kidney stop ADH secretion so water is retained. The thirst mechanism (not fully functional in infants) is also stimulated so water is replaced, thus increasing the total body water content and returning sodium to a normal level (Greenbaum, 2011). Potassium is primarily found inside the cell (intracellular) but small amounts are also found in extracellular fluid. Sodium depletion in diarrhea occurs in two ways: out of the body in stool and into the ICF compartment to replace potassium to maintain electrical equilibrium.

Case Study—Dehydration and Diarrhea

Dehydration is classified into three categories on the basis of osmolality and depends primarily on the serum sodium concentration: (1) isotonic, (2) hypotonic, and (3) hypertonic.

Isotonic (isosmotic or isonatremic) dehydration, the primary form of dehydration in children, occurs in conditions in which electrolyte and water deficits are present in approximately balanced proportions. Water and sodium are lost in approximately equal amounts. The observable fluid losses are not necessarily isotonic because losses from other avenues make adjustments so that the sum of all losses, or the net loss, is isotonic. There is no osmotic force between the ICF and the ECF, so the major loss is sustained from the ECF compartment. This significantly reduces the plasma volume and the circulating blood volume, which affects the skin, muscles, and kidneys. Shock is the greatest threat to life, and children with isotonic dehydration display symptoms characteristic of hypovolemic shock. Plasma sodium remains within normal limits, between 130 and 150 mEq/L.

Hypotonic (hyposmotic or hyponatremic) dehydration occurs when the electrolyte deficit exceeds the water deficit, leaving the serum hypotonic. Because ICF is more concentrated than ECF in hypotonic dehydration, water moves from the ECF to the ICF to establish osmotic equilibrium. This movement further increases the ECF volume loss, and shock is a frequent finding. Because there is a greater proportional loss of ECF in hypotonic dehydration, the physical signs tend to be more severe with smaller fluid losses than with isotonic or hypertonic dehydration. Serum sodium concentration is less than 130 mEq/L.

Hypertonic (hyperosmotic or hypernatremic) dehydration results from water loss in excess of electrolyte loss and is usually caused by a proportionately larger loss of water or a larger intake of electrolytes. This type of dehydration is the most dangerous and requires more specific fluid therapy. Hypertonic diarrhea may occur in infants who are given fluids by mouth that contain large amounts of solute, or in children who receive high-protein nasogastric (NG) tube feedings that place an excessive solute load on the kidneys. In hypertonic dehydration, fluid shifts from the lesser concentration of the ICF to the ECF. Plasma sodium concentration is greater than 150 mEq/L.

Because the ECF volume is proportionately larger, hypertonic dehydration consists of a greater degree of water loss for the same intensity of physical signs. Shock is less apparent. However, CNS disturbances, including alterations in consciousness, poor ability to focus attention, lethargy, increased muscle tone with hyperreflexia, and hyperirritability to stimuli, are more likely to occur. CNS changes are serious and may result in permanent damage.

Diagnosis of the type and degree of dehydration is necessary to develop an effective plan of therapy. The degree of dehydration has been described as a percentage of body weight dehydrated: mild—less than 3% in older children or less than 5% in infants; moderate—5% to 10% in infants and 3% to 6% in older children; and severe—more than 10% in infants and more than 6% in older children (Greenbaum, 2011). Water constitutes only 60% to 70% of an infant’s weight. However, adipose tissue contains little water and is highly variable in individual infants and children. A more accurate means of describing dehydration is to reflect acute loss (time frame of ≤48 hours) in milliliters per kilogram of body weight. For example, a loss of 50 ml/kg is considered to be a mild fluid loss, but a loss of 100 ml/kg produces severe dehydration. Weight is the most important determinant of the percent of total body fluid loss in infants and younger children. However, often the pre-illness weight is unknown. Other predictors of fluid loss include a changing level of consciousness (irritability to lethargy), altered response to stimuli, decreased skin elasticity and turgor, prolonged capillary refill (>2 sec), increased heart rate, and sunken eyes and fontanels.

Clinical signs provide clues to the extent of dehydration (Table 24-3). The earliest detectable sign is usually tachycardia followed by dry skin and mucous membranes, sunken fontanels, signs of circulatory failure (coolness and mottling of extremities), loss of skin elasticity, and prolonged capillary filling time (Table 24-4).

TABLE 24-3

EVALUATING EXTENT OF DEHYDRATION

	LEVEL OF DEHYDRATION
CLINICAL SIGNS	MILD	MODERATE	SEVERE
Weight loss—infants	3%–5%	6%–9%	≥10%
Weight loss—children	3%–4%	6%–8%	10%
Pulse	Normal	Slightly increased	Very increased
Respiratory rate	Normal	Slight tachypnea (rapid)	Hyperpnea (deep and rapid)
Blood pressure	Normal	Normal to orthostatic (>10 mm Hg change)	Orthostatic to shock
Behavior	Normal	Irritable, more thirsty	Hyperirritable to lethargic
Thirst	Slight	Moderate	Intense
Mucous membranes*	Normal	Dry	Parched
Tears	Present	Decreased	Absent, sunken eyes
Anterior fontanel	Normal	Normal to sunken	Sunken
External jugular vein	Visible when supine	Not visible except with supraclavicular pressure	Not visible even with supraclavicular pressure
Skin*	Capillary refill >2 sec	Slowed capillary refill (2–4 sec [decreased turgor])	Very delayed capillary refill (>4 sec) and tenting; skin cool, acrocyanotic or mottled
Urine	Decreased	Oliguria	Oliguria or anuria

^*These signs are less prominent in patients who have hypernatremia.

Data from Jospe N, Forbes G: Fluids and electrolytes—clinical aspects, Pediatr Rev 17(11):395–403, 1996 and Steiner MJ, DeWalt DA, Byerly JS: Is this child dehydrated? JAMA 291(22):2746–2754, 2004.

TABLE 24-4

CLINICAL MANIFESTATIONS OF DEHYDRATION

MANIFESTATION	ISOTONIC (LOSS OF WATER AND SODIUM)	HYPOTONIC (LOSS OF SODIUM IN EXCESS OF WATER)	HYPERTONIC (LOSS OF WATER IN EXCESS OF SODIUM)
Skin
Color	Gray	Gray	Gray
Temperature	Cold	Cold	Cold or hot
Turgor	Poor	Very poor	Fair
Feel	Dry	Clammy	Thickened, doughy
Mucous membranes	Dry	Slightly moist	Parched
Tearing and salivation	Absent	Absent	Absent
Eyeball	Sunken	Sunken	Sunken
Fontanel	Sunken	Sunken	Sunken
Body temperature	Subnormal or elevated	Subnormal or elevated	Subnormal or elevated
Pulse	Rapid	Very rapid	Moderately rapid
Respirations	Rapid	Rapid	Rapid
Behavior	Irritable to lethargic	Lethargic or comatose; seizures	Marked lethargy with extreme hyperirritability on stimulation

Compensatory mechanisms attempt to maintain fluid volume by adjusting to these losses. Interstitial fluid moves into the vascular compartment to maintain the blood volume in response to hemoconcentration and hypovolemia, and vasoconstriction of peripheral arterioles helps maintain pumping pressure. When fluid losses exceed the body’s ability to sustain blood volume and blood pressure, circulation is seriously compromised, and the blood pressure falls. This results in tissue hypoxia with accumulation of lactic acid, pyruvate, and other acid metabolites, which contribute to the development of metabolic acidosis.

Renal compensation is impaired by reduced blood flow through the kidneys, and little urine is formed. Increased serum osmolality stimulates the secretion of ADH to conserve fluid and initiates the renin–angiotensin mechanisms in the kidney, causing further vasoconstriction. Aldosterone is released to promote sodium retention and conserve water in the kidneys. If dehydration increases in severity, urine formation is greatly diminished, and metabolites and hydrogen ions that are normally excreted by this route are retained.

Shock, a common manifestation of severe depletion of ECF volume, is preceded by tachycardia and signs of poor perfusion and tissue oxygenation (by pulse oximeter readings). Peripheral circulation is poor as a result of reduced blood volume; therefore, the skin is cool and mottled, with decreased capillary filling after blanching. Impaired kidney circulation often leads to oliguria and azotemia. Although low blood pressure may accompany other symptoms of shock, in infants and young children, it is usually a late sign and may herald the onset of cardiovascular collapse.

Diagnostic Evaluation

To initiate a therapeutic plan, several factors must be determined:

• The degree of dehydration based on physical assessment

• The type of dehydration based on the pathophysiology of the specific illness responsible for the dehydrated state

• Specific physical signs other than general signs

• Initial plasma sodium concentrations

• Serum bicarbonate concentration (CO₂)

• Any associated electrolyte (especially serum potassium) and acid–base imbalances (as indicated)

Case Study—Dehydration

Initial and regular ongoing evaluations assess the patient’s progress toward equilibrium and the effectiveness of therapy.

In the examination of an infant or younger child, one of the most important determinants of the extent of dehydration is body weight because this can assist in determining the percentage of total body fluid lost; however, because the pre-illness weight is often unknown, clinical manifestations must be evaluated. Important clinical manifestations include changing sensorium (irritability to lethargy); decreased response to stimuli; integumentary changes (decreased elasticity and turgor); prolonged capillary refill; increased heart rate; sunken eyes; and, in infants, sunken fontanels. Using multiple predictors increases the sensitivity of assessing the fluid deficit, and early studies have shown a reasonably high degree of agreement between experienced observers in assessment of the level of dehydration. Objective signs of dehydration are present at a fluid deficit of less than 5%.

Laboratory data are said to be useful only when results are significantly abnormal (Emond, 2009). Urine specific gravity, urine ketones, and urinary output during rehydration are reportedly unreliable assessments for determining dehydration in children (Steiner, Nager, and Wang, 2007). Shock, tachycardia, and very low blood pressure are common features of severe depletion of ECF volume (see Shock, Chapter 25).

Therapeutic Management

Medical management is directed at correcting the fluid loss or deficit and treating the underlying cause. When the child is alert, awake, and not in danger, correction of dehydration may be attempted with oral fluid administration. Mild cases of dehydration can be managed at home by this method. Several commercial rehydration fluids are available for use (Table 24-5). Oral rehydration management consists of replacement of fluid loss over 4 to 6 hours, replacement of continuing losses, and provision for maintenance fluid requirements. In general, a mildly dehydrated child may be given 50 ml/kg of oral rehydration solution (ORS), and a child with moderate dehydration may be given 100 ml/kg of ORS. A child with fluid losses from diarrhea may be given 10 ml/kg for each stool. Amounts and rates are determined from body weight and the severity of dehydration and are increased if rehydration is incomplete or if excess losses continue until the child is well hydrated and the basic problem is under control.

TABLE 24-5

COMPOSITION OF SOME ORAL REHYDRATION SOLUTIONS

FORMULA	Na (mEq/L)	K (mEq/L)	Cl (mEq/L)	BASE (mEq/L)	GLUCOSE (g/L)
Pedialyte (Abbott)*	45	20	35	30 (citrate)	25
Rehydralyte (Abbott)	75	20	65	30 (citrate)	25
Infalyte (Mead Johnson)	50	25	45	34 (citrate)	30
World Health Organization^†	90	20	80	30 (bicarbonate)	20

Cl, Chloride; K, potassium; Na, sodium.

^*Note that many generic products are available with compositions identical to Pedialyte.

^†Must be reconstituted with 1 L water.

The child may not be thirsty even though dehydrated and may refuse oral fluids initially for fear of continued emesis (if occurring) or because of decreased strength, oral stomatitis, or thrush. In such children, rehydration may proceed by administering 2 to 5 ml of ORS by a syringe or small medication cup every 2 to 3 minutes until the child is able to tolerate larger amounts; if the child has emesis, administering small amounts (5–10 ml) of ORS every 5 minutes or so may help overcome fluid deficit, and the emesis will often lessen over time. Oral administration of ondansetron (Zofran) to children with acute gastroenteritis and vomiting may reduce emesis and increase time to oral rehydration, thus preventing IV therapy. Oral rehydration therapy (ORT) is effective for treating mild or moderate dehydration in children, is less expensive, and involves fewer complications than parenteral therapy (American Academy of Pediatrics [AAP], Committee on Infectious Diseases and Pickering, 2009).

Nursing Tip

Enhance the flavor of an ORS such as Pedialyte (unflavored) by adding 1 tsp of unsweetened powder Kool-Aid to each 60 to 90 ml of ORS. Older children may take a small Popsicle orally instead of fluids that require drinking. Many commercially available Popsicles are relatively inexpensive, contain small amounts of sucrose, and contain approximately 40 to 50 ml of fluid. Frozen oral hydration may be accepted by some children when conventional ORS is rejected.

Parenteral Fluid Therapy.

Parenteral fluid therapy is initiated whenever the child is unable to ingest sufficient amounts of fluid and electrolytes to (1) meet ongoing daily physiologic losses, (2) replace previous deficits, and (3) replace ongoing abnormal losses. Patients who usually require IV fluids are those with severe dehydration, those with uncontrollable vomiting, those who are unable to drink for any reason (e.g., extreme fatigue, coma), and those with severe gastric distention.

Because dehydration constitutes a great threat to life, the first priority is the restoration of circulation by rapid expansion of the ECF volume to treat or prevent shock. IV administration of fluid begins immediately, although the exact nature of the dehydration and the serum electrolyte values may not initially be known. The solution selected is based on what is known regarding the probable type and cause of the dehydration. This usually involves an isotonic solution such as 0.9% sodium chloride or lactated Ringer solution, both of which are close to the body’s serum osmolality of 285 to 300 mOsm/kg and do not contain dextrose (which is contraindicated in the early treatment stages of diabetic ketoacidosis).

Parenteral rehydration therapy has three phases. The initial therapy is used to expand ECF volume quickly and to improve circulatory and renal function. During initial therapy, an isotonic solution is used at a rate of 20 ml/kg, given as an IV bolus over 20 minutes, and repeated as necessary after assessment of the child’s response to therapy (Ford, 2009; Friedman, 2010). Subsequent therapy is used to replace deficits, meet maintenance water and electrolyte requirements, and catch up with ongoing losses. Water and sodium requirements for the deficit, maintenance, and ongoing losses are calculated at 8-hour intervals, taking into consideration the amount of fluids given with the initial boluses and the amount administered during the first 24-hour period. With improved circulation during this phase, water and electrolyte deficits can be evaluated, and acid–base status can be corrected either directly through the administration of fluids or indirectly through improved renal function. Potassium is withheld until kidney function is restored and assessed and circulation has improved (see Evidence-Based Practice box).

Evidence-Based Practice

Normal Saline or Heparinized Saline Flush Solution in Pediatric Intravenous Lines