• Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
Updated: Dec 31, 2015


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.

For patient education materials, see Children's Health Center as well as Dehydration in Children.



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, as follows:

  • 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. [1, 2]
  • 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. [2, 3, 4]

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.



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 of dehydration include the following:

  • Gastroenteritis: This is the most common cause of dehydration. If both vomiting and diarrhea are present, dehydration may rapidly progress. [5, 6]  Rotaviruses are the most common global causes for dehydration and severe diarrheal disease in infants and young children. [7]
  • 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 of dehydration include the following:

  • Gastroenteritis
  • Diabetic ketoacidosis (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. [8]
  • 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.


United States statistics

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


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.





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

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.

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

Contributor Information and Disclosures

Lennox H Huang, MD, FAAP Associate Professor and Chair, Department of Pediatrics, McMaster University School of Medicine; Chief of Pediatrics, McMaster Children's Hospital

Lennox H Huang, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for Physician Leadership, Canadian Medical Association, Ontario Medical Association, Society of Critical Care Medicine

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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, Ontario Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

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Table 1. Clinical Findings of Dehydration
Symptom/Sign Mild Dehydration Moderate Dehydration Severe Dehydration
level of consciousness Alert Lethargic Obtunded
Capillary refill* 2 s 2-4 s >4 s, cool limbs
Mucous membranes Normal Dry Parched, cracked
Tears Normal Decreased Absent
Heart rate Slightly increased Increased Very increased
Respiratory rate/pattern* 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[10]
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
Table 3. Composition of Appropriate Oral Rehydration Solutions
Solution Carbohydrate (g/dL) Sodium (mEq/L) Potassium (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* 2 90 20 30 310
* World Health Organization/United Nations Children's Fund
Table 4. Composition of Inappropriate Oral Rehydration Solutions
Solution Carbohydrate (g/dL) Sodium (mEq/L) Potassium (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
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