eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Dehydration

Author: Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Coauthor(s): Krishnapriya R Anchala, MD, MS, FAAP, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, McMaster University; Dan L Ellsbury, MD, Consulting Staff, Pediatrix Medical Group of Iowa; Consulting Staff, Department of Pediatrics, Neonatology Intensive Care Unit, Mercy Medical Center of Des Moines; Caroline S George, MD, Associate Professor, Consulting Staff, Department of Pediatrics, Division of Critical Care Medicine, University of Minnesota Medical School
Contributor Information and Disclosures

Updated: Jul 21, 2008

Introduction

Background

Dehydration describes a state of negative fluid balance that may be caused by numerous 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 that causes dehydration results from decreased intake, increased output (renal, GI, 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.

Young children are more susceptible to dehydration due to larger body water content, renal immaturity and inability to meet their own needs independently. Older children show signs of dehydration sooner than infants due to lower levels of extracellular fluid (ECF).

Dehydration can be categorized according to osmolarity and severity. Serum sodium is a good surrogate marker of osmolarity assuming the patient has a normal serum glucose. Dehydration may be 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 lost fluid 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 lost fluid contains more sodium than the blood (loss of hypertonic fluid). Relatively more sodium than water is lost. Because the serum sodium is low, intravascular water shifts to the extravascular space, exaggerating intravascular volume depletion for a given amount of total body water loss.
  • Hypernatremic (hypertonic) dehydration occurs when the lost fluid contains less sodium than the blood (loss of hypotonic fluid). Relatively less sodium than water is lost. Because the serum sodium is high, extravascular water shifts 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. Severe hyponatremia may lead to intractable seizures, whereas rapid correction of chronic hyponatremia (>2 mEq/L/h) 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; cerebral edema is the most devastating consequence. Slow rehydration over 48 hours generally minimizes this risk.

Frequency

United States

Diarrheal illnesses in children causes 3 million physician visits, 220,000 hospitalizations (10% of all children who require hospitalization), and 400 deaths per year. On average, North American children younger than 5 years have 2 episodes of gastroenteritis per year.

International

Diarrheal illnesses with subsequent dehydration account for nearly 4 million deaths per year in infants and children. The overwhelming majority of these deaths occur in developing nations.

Mortality/Morbidity

Mortality and morbidity generally depend on the severity of dehydration and the promptness of oral or intravenous rehydration. If treatment is rapidly and appropriately obtained, morbidity and mortality are low.

Routine use of hypotonic parenteral fluids in hospitalized children has been associated with hyponatremia and subsequent neurologic complications and death. Monitoring the efficacy and complications of parenteral rehydration with accurate fluid balances and serum electrolytes is crucial.

Age

Children younger than 5 years are at the highest risk.

Clinical

History

  • Intake of fluids, including the volume, type (hypertonic or hypotonic), and frequency
  • Urine output, including the frequency of voiding (last wet diaper), presence of concentrated or dilute urine, hematuria
  • Stool output, frequency of stools, stool consistency, presence of blood or mucus in stools
  • Emesis, including frequency and volume and whether bilious or nonbilious, hematemesis
  • Contact with ill people, especially others with gastroenteritis, use of daycare
  • 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 examination may assist in determining the underlying cause of the patient's dehydration and in defining the severity of dehydration. The clinical assessment of severity of dehydration determines the approach to management. In general, physical signs of dehydration have poor precision and accuracy. Rather than attempting to assign an exact percentage of dehydration, one should attempt to place the child in one of 3 broad categories. 

Determination dehydration severity should be based on the overall constellation of symptoms. Patients in a given category need not exhibit all the signs and symptoms listed below. Literature reviews have suggested that delayed capillary refill, delayed skin turgor, and abnormal respiratory pattern are the most reliable clinical signs of dehydration in children.

Table 1. Clinical Findings of Dehydration

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Table
Symptom/SignMild DehydrationModerate DehydrationSevere Dehydration
Level of consciousnessAlertLethargicObtunded
Capillary refill*2 Seconds2-4 SecondsGreater than 4 seconds, cool limbs
Mucous membranesNormalDryParched, cracked
TearsNormalDecreasedAbsent
Heart rateSlightly increasedIncreasedVery increased
Respiratory rate/pattern*NormalIncreasedIncreased and hyperpnea
Blood pressureNormalNormal, but orthostasisDecreased
PulseNormalThreadyFaint or impalpable
Skin turgor*NormalSlowTenting
FontanelNormalDepressedSunken
EyesNormalSunkenVery sunken
Urine outputDecreasedOliguriaOliguria/anuria
Symptom/SignMild DehydrationModerate DehydrationSevere Dehydration
Level of consciousnessAlertLethargicObtunded
Capillary refill*2 Seconds2-4 SecondsGreater than 4 seconds, cool limbs
Mucous membranesNormalDryParched, cracked
TearsNormalDecreasedAbsent
Heart rateSlightly increasedIncreasedVery increased
Respiratory rate/pattern*NormalIncreasedIncreased and hyperpnea
Blood pressureNormalNormal, but orthostasisDecreased
PulseNormalThreadyFaint or impalpable
Skin turgor*NormalSlowTenting
FontanelNormalDepressedSunken
EyesNormalSunkenVery sunken
Urine outputDecreasedOliguriaOliguria/anuria

* Best indicators of hydration status1  

Table 2. Estimated Fluid Deficit

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Table
SeverityInfants (weight <10 kg)Children (weight >10 kg)
Mild dehydration5% or 50 mL/kg3% or 30 mL/kg
Moderate dehydration10% or 100 mL/kg6% or 60 mL/kg
Severe dehydration15% or 150 mL/kg9% or 90 mL/kg
SeverityInfants (weight <10 kg)Children (weight >10 kg)
Mild dehydration5% or 50 mL/kg3% or 30 mL/kg
Moderate dehydration10% or 100 mL/kg6% or 60 mL/kg
Severe dehydration15% or 150 mL/kg9% or 90 mL/kg

Causes

Determination of the cause of dehydration is essential. Poor fluid intake, excessive fluid output, increased insensible fluid losses, or a combination of the above 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 rapidly progress.
    • Stomatitis: Pain may severely limit oral intake.
    • Diabetic ketoacidosis (DKA): Dehydration is caused by osmotic diuresis. Weight loss is caused by both excessive fluid losses and tissue catabolism. Rapid rehydration, especially rapid initial volume resuscitation, may be associated with a poor neurologic outcome. DKA requires very specific and controlled treatment (see Diabetic Ketoacidosis).
    • Febrile illness: Fever causes increased insensible fluid losses and may affect appetite.
    • Pharyngitis: This may decrease oral intake.
  • Life-threatening causes
    • Gastroenteritis
    • DKA
    • 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.
    • GI obstruction: This is often 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, placing patients 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.

More on Dehydration

Overview: Dehydration
Differential Diagnoses & Workup: Dehydration
Treatment & Medication: Dehydration
Follow-up: Dehydration
References

References

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  26. Nalin DR, Hirschhorn N, Greenough W, et al. Clinical concerns about reduced-osmolarity oral rehydration solution. JAMA. Jun 2 2004;291(21):2632-5. [Medline].

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  28. Phin SJ, McCaskill ME, Browne GJ, Lam LT. Clinical pathway using rapid rehydration for children with gastroenteritis. J Paediatr Child Health. Jul 2003;39(5):343-8. [Medline].

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Further Reading

Keywords

dehydration, negative fluid balance, diarrheal illness, diarrhea, isonatremic dehydration, hypernatremic dehydration, hyponatremic dehydration, end organ failure, cerebral edema, gastroenteritis, cystic fibrosis, diabetes mellitus, hyperthyroidism, gastroenteritis, stomatitis, diabetic ketoacidosis, DKA, pharyngitis, burns, congenital adrenal hyperplasia, hypotension, hyperkalemia, GI obstruction, hyperkalemia, hypoglycemia, hypotension, bowel ischemia, diabetes insipidus, pyloric stenosis, alkalosis

Contributor Information and Disclosures

Author

Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, Canadian Medical Association, Ontario Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Krishnapriya R Anchala, MD, MS, FAAP, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, McMaster University
Krishnapriya R Anchala, MD, MS, FAAP is a member of the following medical societies: American Academy of Pediatrics, Canadian Medical Association, and Ontario Medical Association
Disclosure: Nothing to disclose.

Dan L Ellsbury, MD, Consulting Staff, Pediatrix Medical Group of Iowa; Consulting Staff, Department of Pediatrics, Neonatology Intensive Care Unit, Mercy Medical Center of Des Moines
Dan L Ellsbury, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Caroline S George, MD, Associate Professor, Consulting Staff, Department of Pediatrics, Division of Critical Care Medicine, University of Minnesota Medical School
Caroline S George, MD is a member of the following medical societies: American Academy of Pediatrics and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Barry J Evans, MD, Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center
Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Associate Professor, Department of Clinical Pediatrics, State University of New York at Stony Brook
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
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