Dehydration

Last Updated: January 2, 2002

Background: Dehydration describes a state of negative fluid balance that may be caused by a number of disease entities. Diarrheal illnesses are the most common etiologies. Worldwide, dehydration secondary to diarrheal illness is the leading cause of infant and child mortality.

Pathophysiology: The negative fluid balance causing dehydration results from decreased intake, increased output (renal, gastrointestinal, or insensible losses), or fluid shift (ascites, effusions, and capillary leak states such as burns and sepsis). The decrease in total body water causes reductions in both the intracellular and extracellular fluid volumes. Clinical manifestations of dehydration are most closely related to intravascular volume depletion. As dehydration progresses, hypovolemic shock ultimately ensues resulting in end organ failure and death.

Dehydration is often categorized according to serum sodium concentration as isonatremic (130-150 mEq/L), hyponatremic (<130 mEq/L), or hypernatremic (>150 mEq/L). Isonatremic dehydration is the most common (80%). Hypernatremic and hyponatremic dehydration each comprise 5-10% of cases. Variations in serum sodium reflect the composition of the fluids lost and have different pathophysiologic effects.

Isonatremic (isotonic) dehydration occurs when the fluid that is lost is similar in sodium concentration to the blood. Sodium and water losses are of the same relative magnitude in both the intravascular and extravascular fluid compartments.

Hyponatremic (hypotonic) dehydration occurs when the fluid that is lost contains more sodium than the blood (loss of hypertonic fluid). Relatively more sodium than water is lost. Since the serum sodium is low, intravascular water will shift to the extravascular space, exaggerating intravascular volume depletion for a given amount of total body water loss.

Hypernatremic (hypertonic) dehydration occurs when the fluid that is lost contains less sodium than the blood (loss of hypotonic fluid). Relatively less sodium than water is lost. Since the serum sodium is high, extravascular water will shift to the intravascular space, minimizing intravascular volume depletion for a given amount of total body water loss.

Neurologic complications can occur in hyponatremic and hypernatremic states. Rapid correction of chronic hyponatremia (>2 mEq/L/hour) has been associated with central pontine myelinolysis. During hypernatremic dehydration water is osmotically pulled from cells into the extracellular space. To compensate, cells can generate osmotically active particles (idiogenic osmoles) that pull water back into the cell and maintain cellular fluid volume. During rapid rehydration of hypernatremia the increased osmotic activity of these cells can result in a large influx of water, causing cellular swelling and rupture, with cerebral edema being the most devastating consequence. Slow rehydration over 48 hours generally minimizes this risk.

Frequency:

  • Internationally: Diarrheal illnesses with subsequent dehydration account for nearly 4 million deaths per year in infants and children.

Mortality/Morbidity: Mortality and morbidity are generally dependent upon the severity of dehydration and the promptness of oral or intravenous rehydration. If treatment is rapidly and appropriately obtained, morbidity and mortality are low.

Age: Children younger than 5 years are at the highest risk.

History:

  • Urine output, including the frequency of voiding, presence of concentrated or dilute urine, hematuria
  • Stool output, frequency of stools, stool consistency, presence or blood or mucus in stools
  • Emesis, including frequency and volume, bilious or non-bilious, hematemesis
  • Contact with ill people, especially others with gastroenteritis
  • Underlying illnesses, especially cystic fibrosis, diabetes mellitus, hyperthyroidism, renal disease
  • Fever
  • Appetite patterns
  • Weight loss
  • Travel
  • Recent antibiotic use
  • Possible ingestions

Physical:

  • A complete physical exam is essential to determine the underlying cause of the patient’s dehydration and to define the severity of dehydration. The clinical assessment of severity of dehydration will determine the approach to management.
  • Table 1: Clinical Findings of Dehydration

    Symptom / Sign

    Mild Dehydration

    Moderate Dehydration

    Severe Dehydration

    Level of consciousness*

    alert

    lethargic

    obtunded

    Capillary refill*

    2 sec

    2-4 sec

    >4 sec, cool limbs

    Mucous membranes*

    normal

    dry

    parched, cracked

    Tears*

    normal

    decreased

    absent

    Heart rate

    slight increase

    increased

    very increased

    Respiratory rate

    normal

    increased

    increased and hyperpnea

    Blood pressure

    normal

    normal, but orthostasis

    decreased

    Pulse

    normal

    thready

    faint or impalpable

    Skin turgor

    normal

    slow

    tenting

    Fontanel

    normal

    depressed

    sunken

    Eyes

    normal

    sunken

    very sunken

    Urine output

    decreased

    oliguria

    oliguria / anuria

     * Best indicators of hydration status

  • Table 2: Estimated Fluid Deficit

    Severity

    Infants (weight < 10 kg)

    Children (weight > 10 kg)

    Mild Dehydration

    5% or 50 mL/kg

    3% or 30 mL/kg

    Moderate Dehydration

    10% or 100 mL/kg

    6% or 60 mL/kg

    Severe Dehydration

    15% or 150 mL/kg

    9% or 90 mL/kg

Causes: Determination of the cause of dehydration is essential. Poor fluid intake, excessive fluid output and increased insensible fluid losses all may cause intravascular volume depletion. Successful treatment requires identification of the underlying disease state.

  • Common causes
    • Gastroenteritis: This is the most common cause of dehydration. If both vomiting and diarrhea are present, dehydration may progress rapidly.
    • Stomatitis: Pain may severely limit oral intake.
    • Febrile illness: Fever causes increased insensible fluid losses and may affect appetite.

    • Pharyngitis: This may decrease oral intake.
  • Life-threatening causes
    • Gastroenteritis
    • Diabetic ketoacidosis
    • Burns: Fluid losses may be extreme. Very aggressive fluid management is required (see Burns, Thermal).
    • Congenital adrenal hyperplasia: This may have associated hypoglycemia, hypotension, hyperkalemia, and hyponatremia
    • Gastrointestinal obstruction: This often is associated with poor intake and emesis. Bowel ischemia can result in extensive capillary leak and shock.
    • Heat stroke: Hyperpyrexia, dry skin, and mental status changes may occur.
    • Cystic fibrosis: This results in excessive sodium and chloride losses in sweat, at risk for severe hyponatremic hypochloremic dehydration.
    • Diabetes insipidus: Excessive output of very dilute urine can result in large free water losses and severe hypernatremic dehydration.
    • Thyrotoxicosis: Weight loss is observed, despite increased appetite. Diarrhea occurs.
 

Lab Studies:

  • Laboratory data generally are not required if the etiology is apparent and mild to moderate dehydration is present.

  • With severe dehydration, the following laboratory studies are suggested:
    • Serum sodium should be determined, as hyponatremia (Na <130 mEq/L) and hypernatremia (Na >150 mEq/L) require specific treatment regimens.
    • Potassium may be elevated (congenital adrenal hyperplasia, renal failure) or low (pyloric stenosis, alkalosis).
    • Chloride may be low in pyloric stenosis (hypochloremic, hypokalemic, metabolic alkalosis).
    • Bicarbonate: poor tissue perfusion in dehydration results in production of lactic acid. Bicarbonate is consumed as lactic acid levels increase. In DKA, ketoacids will also consume bicarbonate. Bicarbonate levels also can be reduced due to loss of bicarbonate in diarrheal stools.
    • Glucose may be dangerously low because of poor intake or extremely elevated in diabetic ketoacidosis.
    • Blood urea nitrogen and creatinine may be elevated because of renal hypoperfusion.
    • Urine specific gravity may be elevated; diabetes insipidus causes the urine to be dilute.
    • Urinalysis may show findings of diabetic ketoacidosis (ketones, glucose).
    • Electrolyte analysis of any fluid that is lost (eg, urine, stool, gastric fluid) can be done to further refine the composition of replacement fluids.

Procedures:

  • Intravenous line
    • If severe dehydration is present peripheral intravenous line insertion may be difficult. The preferred sites for initial insertion attempts include the basilic and cephalic veins in the antecubital fossa and the saphenous veins near the ankle. Transillumination of the insertion site with a fiberoptic light source may be used to facilitate locating the desired vein.
    • If peripheral intravenous access cannot be rapidly achieved (<90 s) in a child with severe dehydration and shock, intraosseous cannulation should be attempted. If the child is not in extremis, more time may be taken to establish central venous access percutaneously (femoral, subclavian, internal or external jugular).
  • Intraosseous line
    • Intraosseous cannulation can easily and rapidly be achieved in children younger than 6 years. Specially designed intraosseous infusion needles or Jamshidi-type bone marrow aspiration needles may be used. Short, large bore spinal needles may also be used but often bend during placement. The ideal site of insertion is the anteromedial surface of the tibia, 1-3 cm below the anterior tibial tuberosity.

TREATMENT

Medical Care:

  • Medications, such as loperamide, opiates, anticholinergics, bismuth subsalicylate, and adsorbents, are not recommended because of questionable efficacy and potential adverse effects.

  • Oral rehydration solutions (ORS): During gastroenteritis the intestinal mucosa retains absorptive capacity. Sodium and glucose in the correct proportions can be passively cotransported with fluid from the gut lumen into the circulation. Rapid oral rehydration with the appropriate solution has been shown to be as effective as intravenous fluid therapy in restoring intravascular volume and correcting acidosis.

  • Table 3: Composition of Appropriate Oral Rehydration Solutions

    Solution

    CHO, g/dL

    Na, mEq/L

    K, mEq/L

    Base, mEq/L

    Osmolality

    Pedialyte

    2.5

    45

    20

    30

    250

    Infalyte

    3

    50

    25

    30

    200

    Rehydralyte

    2.5

    75

    20

    30

    310

    WHO/UNICEF ORS

    2

    90

    20

    30

    310

     

  • All of the commercially available rehydration fluids are acceptable for oral rehydration therapy (ORT). They contain 2-3 g/dL of glucose, 45-90 mEq/L of sodium, 30 mEq/L of base, and 20-25 mEq/L of potassium. Osmolality is 200-310 mOsm/L.

  • Table 4: Composition of Inappropriate Oral Rehydration Solutions

    Solution

    CHO, g/dL

    Na, mEq/L

    K, mEq/L

    Base, mEq/L

    Osmolality

    Apple juice

    12

    0.4

    26

    0

    700

    Ginger ale

    9

    3.5

    0.1

    3.6

    565

    Milk

    4.9

    22

    36

    30

    260

    Chicken broth

    0

    2

    3

    3

    330

     

  • Traditional clear fluids are not appropriate for ORT. Many contain excessive concentrations of carbohydrate (CHO) and low concentrations of sodium. The inappropriate glucose to sodium ratio impairs water absorption and the large osmotic load creates an osmotic diarrhea, further worsening the degree of dehydration.

  • Oral rehydration therapy for mild or moderate dehydration

    • Mild or moderate dehydration can usually be treated very effectively with ORT.

    • Vomiting is generally not a contraindication to ORT. If evidence of bowel obstruction, ileus, or acute abdomen exists, then intravenous rehydration is indicated.

    • Calculate fluid deficit. Physical findings consistent with mild dehydration suggest a fluid deficit of 5% of body weight in infants and 3% in children. Moderate dehydration occurs with a fluid deficit of 5 to 10% in infants and 3 to 6% in children (see Tables 1 and 2). The fluid deficit should be replaced over 4 hours.

    • The oral rehydration solution (ORS) should be given in small volumes very frequently to minimize gastric distention and reflex vomiting. Generally, 5 mL of ORS every minute is well tolerated. Hourly intake and output should be recorded by the caregiver. As the child becomes rehydrated, vomiting often decreases and larger fluid volumes may be used.

    • If vomiting persists, infusion of ORS via a nasogastric tube may used temporarily to achieve rehydration. Intravenous fluid administration (20-30 mL/kg of normal saline over 1-2 hours) may also be used until oral rehydration is tolerated.

    • Replace ongoing losses from stools and emesis (estimate volume and replace) in addition to replacing the calculated fluid deficit.

    • Once the child is rehydrated, start an age-appropriate diet (see below).
  • Severe dehydration

    • Laboratory evaluation and intravenous rehydration are required. The underlying cause of the dehydration must be determined and treated appropriately.

    • Phase 1 focuses on emergency management. Severe dehydration is characterized by a state of hypovolemic shock requiring rapid treatment. Initial management includes placement of an intravenous or intraosseous line and rapid administration of 20 mL/kg of lactated Ringer solution or normal saline. Additional fluid boluses may be required depending on the severity of the dehydration. The child should be frequently reassessed to determine the response to treatment. As intravascular volume is repleted, tachycardia, capillary refill, urine output, and mental status all should improve. If improvement is not seen after 60 mL/kg of fluid administration, other etiologies of shock (cardiac, anaphylaxis, sepsis) should be considered. Hemodynamic monitoring and inotropic support may be indicated.

    • Phase 2 focuses on deficit replacement, provision of maintenance fluids, and replacement of ongoing losses. Daily maintenance fluid requirements may calculated as follows:

        <10 kg = 100 mL/kg

        10-20 kg = 1000 + 50 mL/kg for each kg over 10 kg

        >20 kg = 1500 + 20 mL/kg for each kg over 20 kg

    • Severe dehydration by clinical examination suggests a fluid deficit of 10-15% of body weight in infants, and 6-9% of body weight in older children. The daily maintenance fluid is added to the fluid deficit. It generally is recommended that one half of this volume is given over 8 hours, the remainder is given over the following 16 hours. Continued losses (emesis, diarrhea) must be replaced promptly.

    • If the child is isonatremic (130-150 mEq/L) the sodium deficit incurred can generally be corrected by giving the fluid deficit plus maintenance as 5% dextrose in 0.45% NaCl. Potassium (20 mEq/L KCl) may be added once urine output is established.

    • An alternative approach to the deficit therapy approach is rapid replacement therapy. With this approach a child with severe isonatremic dehydration is given 20-40 ml/kg of normal saline or lactated Ringer solution over 15 to 60 minutes. As perfusion is restored the child improves and is able to tolerate an ORS for the remainder of his rehydration. This approach is not appropriate for hypernatremic or hyponatremic dehydration.
  • Hyponatremic dehydration

    • Phase 1 management of hyponatremic dehydration is identical to that of isonatremic dehydration. Rapid volume expansion with 20 mL/kg of normal saline or Lactated Ringer's solution should be given and repeated until perfusion is restored.

    • Severe hyponatremia (<130 mEq/L) indicates additional sodium loss. In phase 2 management rehydration is calculated as for isonatremic dehydration. The additional sodium deficit must be calculated and added to the rehydration fluids. The deficit may be calculated to restore the sodium to 130 mEq/L and administered over 24 hours:

        Sodium deficit = (Sodium desired-sodium actual) x volume of distribution x weight (kg)

        Example: Na = 123, weight = 10 kg, assumed volume of distribution of 0.6; Na deficit = (130-123) x 0.6 x 10 kg = 42 mEq Na

    • A simplified approach is to use 5% dextrose in 0.9% NaCl or 0.45% NaCl as the replacement fluid. The sodium is followed closely and the amount of sodium in the fluid is adjusted to maintain a slow correction(<0.5 mEq/L/hour).

    • It is imperative to frequently reassess the serum sodium level during correction. Rapid correction of chronic hyponatremia (>2 mEq/L/h) has been associated with central pontine myelinolysis. Rapid partial correction of symptomatic hyponatremia has not been associated with adverse effects. Therefore, if the child is symptomatic (seizures) a more rapid, partial correction is indicated. Hypertonic (3%) normal saline (0.5 mEq/mL) may be used for rapid partial correction of symptomatic hyponatremia. A dose of 4 mL/kg will raise the serum sodium by 3-4 mEq/L.

  • Hypernatremic dehydration

    • Phase 1 management of hypernatremic dehydration is identical to that of isonatremic dehydration. Rapid volume expansion with 20 mL/kg of normal saline or Lactated Ringer's solution should be given and repeated until perfusion is restored.

    • There are varied regimens that may be successfully followed to achieve correction of severe hypernatremia (>150 mEq/L). In phase 2 management the most important goal is to reestablish intravascular volume and return serum sodium levels toward normal by not more than 10 mEq/L/24 hr. Rapid correction of hypernatremic dehydration can have disastrous neurologic consequences, including cerebral edema and death.

    • The most cautious approach is to plan a slow correction of the fluid deficit over 48 hours. Following adequate intravascular volume expansion, rehydration fluids should be initiated with 5% dextrose in 0.9% NaCl. Serum sodium levels should be assessed every four hours. If the sodium has decreased by less than 0.5 mEq/L/hour, then the sodium content of the rehydration fluid is decreased. This allows for a slow, controlled correction of the hypernatremic state.

    • Hyperglycemia and hypocalcemia are sometimes associated with hypernatremic dehydration. Serum glucose and calcium levels should be followed closely.

Diet:

  • Once the child is rehydrated, an age-appropriate diet should be started. Children with dehydration from gastroenteritis have decreased duration of diarrhea when feedings are rapidly restarted.
  • Diluting milk or formula is not indicated. Breast-feeding should be resumed as soon as possible.
  • Foods containing complex carbohydrates (rice, wheat, potatoes, bread, cereals) lean meats, fruits, and vegetables are encouraged. Fatty foods and simple carbohydrates should be avoided.

Further Inpatient Care:

  • Severe dehydration warrants hospital admission for rehydration, as do hypernatremic or hyponatremic states.
  • Inability to tolerate oral rehydration therapy may necessitate hospital admission for nasogastric or intravenous fluid therapy.

Further Outpatient Care:

  • ORT may be continued at home if clear instructions are provided for the family, and if the family members can be relied upon to carry out the hydration regimen. Close follow-up by the primary physician is recommended.

Complications:

  • Complications may include irreversible shock, sagittal or other venous sinus thrombosis, intractable seizures and renal failure.

Prognosis:

  • Prognosis is excellent if the child is promptly and effectively treated. The child with severe dehydration and hypovolemic shock, however, can have significant morbidity and mortality if treatment is delayed.

Patient Education:

Medical/Legal Pitfalls:

  • Failure to recognize and appropriately treat diabetic ketoacidosis
  • Failure to recognize hypoglycemia
  • Failure to recognize severe hyponatremia or hypernatremia
  • Failure to recognize an acute abdomen
  • Inadequate volume administration (too slow, not enough) for the child with severe dehydration
  • Failure to recognize cardiogenic shock (gallop rhythm, hepatomegaly); rapid fluid resuscitation may further impair cardiac output

BIBLIOGRAPHY

  • American Academy of Pediatrics: Practice parameter: the management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics 1996 Mar; 97(3): 424-35
  • Avner ED: Clinical disorders of water metabolism: hyponatremia and hypernatremia. Pediatr Ann 1995 Jan; (1): 23-30
  • Cronan KM, Norman ME: Renal and electrolyte emergencies. Fleisher GR, ed. Textbook of Pediatric Emergency Medicine. Williams and Wilkins 1993; 3rd Edition: 670-717.
  • Duggan C, Refat M, Hashem M: How valid are clinical signs of dehydration in infants? J Pediatr Gastroenterol Nutr 1996 Jan; 22(1): 56-61
  • Duggan C, Santosham M, Glass RI: The management of acute diarrhea in children: oral rehydration, maintenance, and nutritional therapy. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep 1992 Oct 16; 41(RR-16): 1-20[Medline].
  • Goepp JG, Katz SA: Oral rehydration therapy. Am Fam Physician 1993 Mar; (4): 843-51
  • Gorelick MH, Shaw, KN, Murphy, KO: Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics. 1997; May;(5):99: E6[Medline].
  • Gregorio L, Sutton CL, Lee DA: Central pontine myelinolysis in a previously healthy 4-year-old child with acute rotavirus gastroenteritis. Pediatrics. 1997; May;99(5): 738-43
  • Holliday M: The evolution of therapy for dehydration: should deficit therapy still be taught? Pediatrics 1996 Aug; 98(2 Pt 1): 171-7
  • Holliday MA, Friedman AL, Wassner SJ: Extracellular fluid restoration in dehydration: a critique of rapid versus slow. Pediatr Nephrol 1999 May; (4): 292-7
  • Kallen RJ, Lonergan JM: Fluid resuscitation of acute hypovolemic hypoperfusion states in pediatrics. Pediatr Clin North Am 1990 Apr; (2): 287-94
  • Marks JF: Abnormalities of fluids, electrolytes, and calcium. Levin DL, ed. Essentials of Pediatric Intensive Care. Churchhill Livingstone 1997; 2nd Edition: 543-547.
  • Reid SR, Bonadio WA: Outpatient rapid intravenous rehydration to correct dehydration and resolve vomiting in children with acute gastroenteritis. Ann Emerg Med 1996 Sep; 28(3): 318-23
  • Sarnaik AP, Meert K, Hackbarth R: Management of hyponatremic seizures in children with hypertonic saline: a safe and effective strategy. Crit Care Med. 1991; Jun;19(6): 758-62

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