Pediatric Dehydration

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Practice Essentials

Dehydration is a common complication of illness observed in pediatric patients presenting to the emergency department (ED). Early recognition and early intervention are important to reduce risk of progression to hypovolemic shock and end-organ failure.

In most cases, volume depletion in children is caused by fluid losses from vomiting or diarrhea. On physical examination, combinations of findings can be used to determine the degree of dehydration. Laboratory studies are of limited utility in cases of mild dehydration, but they may be considered under certain conditions and are recommended in patients with more severe dehydration.

Mild or moderate volume depletion should be treated with oral rehydration when possible. Intravenous fluid therapy is necessary when oral therapy fails or volume depletion is severe.

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

Pathophysiology

Dehydration versus volume depletion

The terms dehydration and volume depletion are commonly used interchangeably but they refer to different physiologic conditions resulting from different types of fluid loss.[1] Volume depletion denotes reduction of effective circulating volume in the intravascular space, whereas dehydration denotes loss of free water in greater proportion than the loss of sodium. The distinction is important because volume depletion and dehydration can exist independently or concurrently and the treatment for each is different. However, much of clinical literature does not differentiate between the 2 conditions; this article will therefore follow this convention and use the terms dehydration, hypovolemia, and volume depletion interchangeably to refer to intravascular fluid deficits here. 

Body fluid distribution

The body contains 2 major fluid compartments: the intracellular fluid (ICF) and the extracellular fluid (ECF). The ICF comprises of two thirds of the total body water (TBW), while the ECF accounts for the remaining third. The ECF is further divided into the interstitial fluid (75%) and plasma (25%). The TBW comprises approximately 70% of body weight in infants, 65% in children, and 60% in adults.

Infants' and children’s higher body water content, along with their higher metabolic rates and increased body surface area to mass index, contribute to their higher turnover of fluids and solute. Therefore, infants and children require proportionally greater volumes of water than adults to maintain their fluid equilibrium and are more susceptible to volume depletion. Significant fluid losses may occur rapidly, leading to depletion of the intravascular volume.

Sodium

Volume depletion can be concurrent with hyponatremia. This is characterized by plasma volume contraction with free water excess. An example is a child with diarrhea who has been given water to replace diarrheal losses. Free water is replenished relative to the lack of sodium and other solutes.

In hyponatremic volume depletion, the patient may appear more ill clinically than actual fluid losses would otherwise indicate. The degree of volume depletion may be clinically overestimated. Serum sodium levels less than 120 mEq/L may result in seizures—the risk of seizure is much higher in the setting of acute onset of hyponatremia, as opposed to gradual onset. If intravascular free water excess is not corrected during volume replenishment, the shift of free water to the intracellular fluid compartment may cause cerebral edema, especially in children. 

In hypernatremic volume depletion, plasma volume contracts with a disproportionately larger loss of free water. An example is the child with diarrhea whose fluid losses have been replenished with hypertonic soup, boiled milk, water and baking soda, or improperly diluted infant formula. Volume has been restored, but free water has not. The degree of volume depletion may be underestimated and the patient may appear less ill clinically than fluid losses indicate. Usually, at least a 10% volume deficit exists with hypernatremic volume depletion.

As in hyponatremia, hypernatremic volume depletion may result in serious central nervous system (CNS) effects as a result of structural changes in central neurons. However, cerebral shrinkage occurs instead of cerebral edema. This may result in intracerebral hemorrhage, seizures, coma, and death. Overly rapid correction of hypernatremia, however, may result in cerebral edema. For this reason, volume restoration should be performed gradually over 48 hours, not to exceed a rate of 8 mEq/L per 24 hours.[2] Gradual restoration prevents a rapid shift of fluid across the blood-brain barrier and into the intracellular fluid compartment.

Potassium

Potassium shifts between intracellular and extracellular fluid compartments occur more slowly than free water shifts. Serum potassium levels may not reflect intracellular potassium levels. Although a potassium deficit is present in all patients with volume depletion, it is not usually clinically significant. However, failure to correct for a potassium deficit during volume replacement may result in clinically significant hypokalemia. Potassium should not be added to replacement fluids until adequate urine output is obtained. 

Acid and base problems

The most common acid-base derangement that occurs with volume depletion, especially in infants, is metabolic acidosis. Mechanisms include bicarbonate loss in stool, ketone production from starvation, and lactic acid production from decreased tissue perfusion. Decreased renal perfusion also causes decreased glomerular filtration rate, which, in turn, leads to decreased hydrogen (H+) ion excretion. These factors can combine to produce a metabolic acidosis.

In most patients, acidosis is mild and easily corrected with volume restoration; increased renal perfusion permits excretion of excess H+ ions in the urine. Administration of glucose-containing fluids after initial resuscitation further decreases ketone production.

Etiology

The mechanisms of dehydration may be broadly divided into 3 categories: (1) decreased intake e.g. due to diseases such as stomatitis, (2) increased fluid output e.g. from diarrhea or osmotic diuresis from uncontrolled diabetes mellitus, and (3)increased insensible losses e.g. such as with fever.

Pediatric dehydration is frequently the result of increased output from gastroenteritis, characterized by vomiting and diarrhea.[3] However, vomiting and diarrhea may be caused by other processes as summarized below.

CNS causes of vomiting include the following:

GI causes of vomiting include the following:

Endocrine causes of vomiting include the following:

Renal causes of vomiting include the following:

GI causes of diarrhea include the following:

Endocrine causes of diarrhea include the following:

Volume depletion from increased output not caused by vomiting or diarrhea may be divided into renal or extrarenal causes. Renal causes of volume depletion include the following examples:

Hormonal pathology impacting renal physiology

Extrarenal causes of volume depletion include the following examples:

Other causes of volume depletion as mentioned above include poor oral intake and insensible losses from fever, sweating, burns, or pulmonary processes.

Epidemiology

Dehydration, particularly from gastroenteritis, is a common pediatric complaint in the ED. Approximately 30 million children are affected annually, with 1.5 million presenting to outpatient care, 200,000 requiring hospitalizations, and 300 dying in the United States.[5]

Worldwide, according to the Centers for Disease Control and Prevention (CDC), for children younger than 5 years, the annual incidence of diarrheal illness is approximately 1.5 billion, while deaths are estimated between 1.5 and 2.5 million per year. Though these numbers are staggering, they actually represent an improvement from the early 1980s, when the death rate was approximately 5 million per year.[5]

Infants and younger children are more susceptible to volume depletion than older children. In general, however, pediatric patients with volume depletion have an excellent prognosis if they are appropriately treated.

Morbidity varies with the degree of volume depletion and the underlying cause. The severely volume-depleted infant or child is at risk for death from cardiovascular collapse. Hyponatremia resulting from replacement of free water alone may cause seizures. Improper management of volume repletion may cause iatrogenic morbidity or mortality.

History

The goal of the history and physical examination is to determine the severity and etiology of the child's condition. Accurate classification of the degree of dehydration as mild, moderate, or severe allows for appropriate therapy and disposition of the patient in a timely fashion.

Obtaining a complete history from the parent or caregiver is important because it provides clues to the type of dehydration present. The emergency physician should be diligent in obtaining the following information:

Physical Examination

The severity of dehydration is typically measured as the acute weight loss (presumably fluid) as a percentage of preillness weight. However, the pre-illness weight is often not available in the ED setting and clinicians have to rely on the patient’s history and physical examination findings to assess the severity of dehydration.

On the basis of a systematic review, Steiner et al found that the most useful signs (ie, highest likelihood ratios) for recognizing 5% dehydration are the following[6] :

The Table highlights the physical findings seen with different levels of pediatric dehydration.

Table. Physical Examination Findings in Pediatric Dehydration



View Table

See Table

Approach Considerations

Laboratory studies are of limited use in cases of mild dehydration. However, they should be considered under certain conditions, such as the following:

For children who are in hypovolemic shock, the following studies are recommended:

Serum electrolyte levels are important to determine sodium concentration, which can guide resuscitation. Bicarbonate and potassium levels also are important to assess the degree of metabolic acidosis from volume depletion and tissue hypoperfusion as well a screen for coexisting hypokalemia. Blood urea nitrogen and creatinine levels measure renal function and intravascular volume. The glucose measurement may reveal hyperglycemia or hypoglycemia.

Serum lactate elevation is indicative of tissue perfusion and oxygenation resulting in anaerobic metabolism. It may be helpful in cases of severe dehydration or sepsis. The CBC may be helpful in cases in which volume depletion is due to sepsis or hemorrhage. On urinalysis, the urine specific gravity indicates the degree of volume depletion. Urinalysis may also reveal an underlying infectious etiology.

Bedside ultrasound has also been used to measure the inferior vena cava and the aorta diameter ratio and has been found to be a marginally accurate measurement of acute weight loss in children with dehydration due to gastroenteritis.[8, 9] A study also reported that ultrasound measured inspiratory inferior vena cava collapse and physician gestalt were poor predictors of the actual level of dehydration.[9]

Jauregui et al designed a study to validate if the ratio of the ultrasound-measured diameter of the inferior vena cava (IVC) to the aorta (Ao) correlates with the level of dehydration in children as previous studies have reported. The study also tested the accuracy of the ultrasound measured inspiratory IVC collapse and physician gestalt to predict significant dehydration in children in the emergency department. The authors concluded that the ultrasound-measured IVC/Ao ratio is a modest predictor of significant dehydration in children. The inspiratory IVC collapse and physician gestalt were poor predictors of the actual level of dehydration in this study.[10]

Obtaining Vascular Access

Prior to vascular access attempts, consider oral rehydration in mild and moderate dehydration. A significant body of evidence indicates that an initial trial of oral rehydration with small, frequent volumes of electrolyte-containing solution (5-10 mL every 5-10 min) for pediatric patients with mild to moderate volume depletion is simple and effective, avoiding the more resource-intensive methods that are noxious to infants and children.[11]

Typical sites for intravenous access include superficial veins in the dorsum of the hand, the antecubital fossa (median cephalic or basilic veins), dorsum of the foot, and scalp veins.

Use intraosseous access if attempts to start percutaneous intravenous lines are unsuccessful. Typical sites are the proximal anterior tibia and the distal femur.[12]

For central venous access, typical sites are as follows:

Bedside ultrasound guidance should be used whenever possible to facilitate direct visualization when placing these lines. In infants and young children, access to the internal jugular vein may be difficult because of the short necks. Umbilical vein catheterization may be difficult and usually is not recommended for neonates who have been discharged from the hospital and are returning to the ED.

Use venous cutdown for emergent access and resuscitation only when intraosseous access is not available or fails. Safe performance depends on the skill of the provider. The typical site is the distal saphenous vein, which is anterior and superior to the medial malleolus.

Approach Considerations

Address emergent airway, breathing, and circulatory problems first. Obtain intravenous access, and give a 20 mL/kg isotonic fluid bolus (Ringer lactate or normal saline) to children with severe volume depletion. This should not delay transport to the appropriate facility. Reassessment of perfusion, cardiac function, mentation should take place after each intervention. At times, cardiac failure can mimic volume depletion leading to further deterioration of clinical findings after fluid administration.

Failure to diagnose appendicitis, intussusception, or small bowel obstruction places patients at risk of serious complications (including death).

Antidiarrheal medications have adverse effects and are generally not recommended without medical supervision.

Mild Volume Depletion

Patients with minimal to mild volume depletion should be encouraged to continue an age-appropriate diet and adequate intake of oral fluids. Oral rehydration solution (ORS) should be used. Children should be given sips of ORS (5 mL or 1 teaspoon) every 2 minutes.[11] As an estimate for the amount of fluid to replace, the goal should be to drink 10 mL/kg body weight for each watery stool and estimate volume of emesis for each episode of vomiting.[5, 11, 21]

If commercially prepared ORS is not available, the following recipe may be used:

Inpatient therapy generally is not indicated for mild volume depletion. However, it is prudent to arrange outpatient follow-up evaluation within 48 hours, with instructions to return sooner if symptoms worsen.

Guidelines from the American Academy of Pediatrics on fruit juice in infants, children and adolescents recommend against the use of fruit juice in the treatment of dehydration or the management of diarrhea.[13]

A study by Freedman et al indicated that in children with mild gastroenteritis and minimal dehydration, better oral rehydration results can be achieved by substituting dilute apple juice (initially) and a preferred fluid (later) for electrolyte maintenance solution.[14]

Moderate Volume Depletion

The literature supports use of oral rehydration for the moderately dehydrated child. Similar outcomes have been achieved in randomized studies comparing ORS with intravenous fluid therapy with fewer complications and higher parent satisfaction in the ORS groups. Moreover, ORS can typically be initiated sooner than IV fluid therapy. However, children must be cooperative and have caregivers available to instruct and administer the oral fluids.[11]

With ORS, patients should receive approximately 50-100 mL/kg body weight over 2-4 hours, again starting with 5 mL every 5 minutes.[5] If the child can tolerate this amount and asks for more fluids, the amount given can gradually be increased. Once the fluid deficit has been corrected, parents should be instructed on how to replace volume losses at home if the child continues to have vomiting or diarrhea.

Children in whom ORS fails should be given a bolus (20 mL/kg) of isotonic fluid intravenously. This may be followed by 1.5-2 times maintenance therapy. Over the next few hours, the patient may be transitioned to oral rehydration as tolerated, at which point the intravenous therapy may be discontinued.

Children with moderate volume depletion may require inpatient treatment if they are unable to tolerate oral fluids despite rehydration. Hospitalization may also be required for treatment of the underlying cause of the fluid deficit.

Severe Volume Depletion

Patients with severe volume depletion should receive intravenous isotonic fluid boluses (20-60 mL/kg).[5] In children with difficult peripheral access, perform intraosseous or central access promptly. Fluid boluses should be repeated until vital signs, perfusion, and capillary refill have normalized.

If a patient reaches 60-80 mL/kg in isotonic crystalloid boluses and is not significantly improved, consider other causes of shock (eg, sepsis, hemorrhage, cardiac disease). In addition, consider administering vasopressors and instituting advanced monitoring, such as a bladder catheter, central venous pressure, and measuring mixed venous oxygen saturation.

Although physicians typically give normal saline for these initial boluses, it is important to remember to check a bedside glucose level for patients who appear lethargic or altered. Treat hypoglycemia promptly. The appropriate dose is 0.25 g/kg IV (2.5 mL/kg of 10% dextrose or 1 mL/kg of 25% dextrose) with reassessment of glucose level after administration of dextrose.

Once vital sign abnormalities are corrected, initiate maintenance fluid therapy plus additional fluid to make up for any continued losses. Daily requirements for maintenance fluids can be approximated as follows:

Daily fluid requirements may be met using dextrose 5% in half-normal saline solution. For patients with significant hyponatremia or hypernatremia, it is preferable to use dextrose 5% in normal saline. Dextrose is important to include because these patients generally have a notable ketosis.

The emergency physician also should consider daily sodium and potassium requirements as follows:

Isonatremic and hyponatremic volume depletion states may be treated with normal saline or other isotonic solutions. The goal for correction rates for either hyponatremic or hypernatremic patients should be no more than 0.5 mEq/L/h or no more than 8mEq/L per 24 hour period to prevent the devastating CNS complications of over-rapid correction (central pontine myelinolysis and cerebral edema). Full correction of severe sodium abnormalities usually should be staged over 24-48 hours or longer.[2]

Although a potassium deficit is present in all cases of volume depletion, it is not usually clinically significant; few patients with moderate dehydration require supplemental potassium. However, failure to correct for hypokalemia during volume repletion may result in clinically significant hypokalemia.

Add potassium to fluids when the patient has documented hypokalemia. For all other patients, avoid adding potassium to fluids until the patient has received resuscitation and has demonstrated adequate urine output.

Children with severe volume depletion, especially those with hypernatremia or hyponatremia, require inpatient therapy. Children with severe hyperosmolar states, severe electrolyte derangements, or associated renal failure may require admission to a critical care unit.

Pharmacologic Therapy

The emergency medicine literature now supports the use of a single dose of oral ondansetron in combination with oral rehydration for patients with dehydration, nausea, and vomiting.[12, 15, 16] However, the use of an antiemetic should not shift the focus away from adequate fluid resuscitation.

Acute gastroenteritis is typically a self-limited condition that does not require antibiotics.[17] Chronic infectious cases of diarrhea may require antimicrobial agents after appropriate stool studies have indicated the etiology.[18] Antidiarrheal agents are not recommended. When dehydration is caused by other disease processes, such as diabetic ketoacidosis or sepsis, appropriate pharmacologic therapy should be initiated as soon as possible.

Consultations

Infants and children who present to the ED with mild to moderate dehydration may respond to fluid boluses and may be discharged home with close follow-up with their primary care provider. Patients who are severely volume depleted or who are unable to tolerate oral fluids must be admitted, with a pediatric consultation.

If the child is in shock, is unable to drink fluids, or does not respond to intravenous bolus therapy, significant abnormalities requiring correction may exist. In such patients, obtain pediatric consultation for admission and further therapy. If renal tubular acidosis or other primary renal or endocrine disorder is suspected, specialty consultation may be indicated.

Ondansetron (Zofran, Zuplenz)

Clinical Context:  Odansetron is a selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. It prevents nausea and vomiting.

Class Summary

Use a single dose of oral ondansetron in combination with oral rehydration for patients with dehydration, nausea, and vomiting.[12, 15, 16] However, the use of an antiemetic should not shift the focus away from adequate fluid resuscitation.

As dopamine antagonists, these agents are effective in treating nausea and vomiting. They also may act as prokinetics to increase gastric motility and enhance absorption.

In a double-blind, randomized, placebo-controlled trial of children under age 5 years with acute diarrhea with vomiting and some dehydration, Danewa et al found that oral rehydration was improved by administration of a single oral dose of ondansetron prior to the start of oral rehydration therapy.[19]

What causes dehydration in children?What is the difference between dehydration and volume depletion?Why are children more susceptible to dehydration than adults?How does hyponatremia occur in pediatric dehydration?What is hyponatremic volume depletion in pediatric dehydration?What is the role of hypernatremic volume depletion in the pathophysiology of pediatric dehydration?What is the role of potassium in the pathophysiology of pediatric dehydration?What is the role of metabolic acidosis in the pathophysiology of pediatric dehydration?What are the mechanisms of pediatric dehydration?What are the causes of vomiting leading to pediatric dehydration?What are causes of diarrhea leading to pediatric dehydration?What are renal causes of volume depletion leading to pediatric dehydration?What are hormonal causes of volume depletion leading to pediatric dehydration?What are extrarenal causes of volume depletion leading to pediatric dehydration?What is the prevalence of pediatric dehydration?What is the prognosis of pediatric dehydration?What is the goal of the history and physical exam in the evaluation of pediatric dehydration?What should be the focus of history in suspected pediatric dehydration?How is the severity of dehydration measured in children?Which physical findings are characteristic of dehydration in children?What are the differential diagnoses for Pediatric Dehydration?What is the role of lab studies in the evaluation of pediatric dehydration?Which studies are performed in the evaluation of pediatric dehydration with hypovolemic shock?What is the role of serum electrolyte levels in the evaluation of pediatric dehydration?Which lab studies may be helpful in the evaluation of pediatric dehydration?What is the role of bedside ultrasound in the evaluation of pediatric dehydration?When is a trial of oral rehydration indicated in the evaluation of pediatric dehydration?What are typical sites for central venous access?When is ultrasound-guided vascular access indicated in the management of pediatric dehydration?When is venous cutdown indicated in the management of pediatric dehydration?What is the initial approach to the treatment of pediatric dehydration?What are the treatment options for mild volume depletion in pediatric dehydration?What is the alternative to commercially-prepared oral rehydration solution (ORS) for the treatment of pediatric dehydration?What is the role of apple juice in the treatment of pediatric dehydration?What are the treatment options for moderate volume depletion in pediatric dehydration?What are the treatment options for severe volume depletion in pediatric dehydration?Once vital sign abnormalities are corrected, fluid requirements for the treatment of severe dehydration?What is the role of dextrose in the treatment of severe pediatric dehydration?What are the daily sodium and potassium requirements for children with severe dehydration?What is the role of normal saline in the treatment of severe pediatric dehydration?How is hypokalemia managed in children with severe dehydration?What are the indications for inpatient therapy of pediatric dehydration?What is the role of pharmacologic therapy in the treatment of pediatric dehydration?Which consultations are needed for the treatment of pediatric dehydration?Which medications in the drug class Antiemetics are used in the treatment of Pediatric Dehydration?

Author

Alex Koyfman, MD, Assistant Professor, Department of Emergency Medicine, University of Texas Southwestern Medical Center, Parkland Memorial Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

Carrie Ng, MD, Resident Physician, Department of Pediatrics, Bellevue Hospital Center, New York University School of Medicine

Disclosure: Nothing to disclose.

Mark P Foran, MD, MPH, Assistant Professor of Emergency Medicine, New York University School of Medicine; Attending Emergency Physician, Bellevue Hospital Center and NYU Langone Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Kirsten A Bechtel, MD, Associate Professor of Pediatrics, Section of Pediatric Emergency Medicine, Yale University School of Medicine; Co-Director, Injury Free Coalition for Kids, Yale-New Haven Children's Hospital

Disclosure: Nothing to disclose.

Chief Editor

Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA, Professor of Emergency Medicine in Clinical Pediatrics, Weill Cornell Medical College; Attending Physician, Departments of Emergency Medicine and Pediatrics, Lincoln Medical and Mental Health Center; Adjunct Professor of Emergency Medicine, Adjunct Professor of Pediatrics, St George's University School of Medicine, Grenada

Disclosure: Nothing to disclose.

Additional Contributors

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

Disclosure: Nothing to disclose.

Acknowledgements

Richard G Bachur, MD Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston

Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Ann G Egland, MD Consulting Staff, Department of Operational and Emergency Medicine, Walter Reed Army Medical Center

Ann G Egland, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Association of Military Surgeons of the US, Medical Society of Virginia, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Terrance K Egland, MD Director, Business Planning and Development, Bureau of Medicine and Surgery

Terrance K Egland, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Alison Wiley Lozner, MD Resident Physician, Harvard Affiliated Emergency Medicine Residency, Brigham and Women's Hospital; Clinical Fellow in Emergency Medicine, Harvard Medical School

Alison Wiley Lozner, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

James Kimo Takayesu, MD, MSc Assistant Professor in Surgery, Director of Undergraduate Medical Education, Consulting Staff, Massachusetts General Hospital; Associate Residency Director, Harvard Affiliated Emergency Medicine Residency Partners

James Kimo Takayesu, MD, MSc is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Sigma Xi, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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.

Wayne Wolfram, MD, MPH Associate Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References

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  5. King CK, Glass R, Bresee JS, Duggan C. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003 Nov 21. 52:1-16. [View Abstract]
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  10. Jauregui J, Nelson D, Choo E, Stearns B, Levine AC, Liebmann O, et al. The BUDDY (Bedside Ultrasound to Detect Dehydration in Youth) study. Crit Ultrasound J. 2014. 6(1):15. [View Abstract]
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  16. Alhashimi D, Alhashimi H, Fedorowicz Z. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database Syst Rev. 2006 Oct 18. CD005506. [View Abstract]
  17. 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. [View Abstract]
  18. Barkin RM, Ward DG. Infectious diarrheal disease and dehydration. Marx JA. Rosen's Emergency Medicine: Concepts and Clinical Practice. 6th ed. Philadelphia, Pa: Mosby/Elsevier; 2006. Vol 3: 2623-34.
  19. Danewa AS, Shah D, Batra P, Bhattacharya SK, Gupta P. Oral Ondansetron in Management of Dehydrating Diarrhea with Vomiting in Children Aged 3 Months to 5 Years: A Randomized Controlled Trial. J Pediatr. 2016 Feb. 169:105-9.e3. [View Abstract]
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Symptom Degree of Dehydration
Mild (< 3% body weight lost) Moderate (3-9% body weight lost) Severe (>9% body weight lost)
Mental statusNormal, alertRestless or fatigued, irritableApathetic, lethargic, unconscious
Heart rateNormalNormal to increasedTachycardia or bradycardia
Quality of pulseNormalNormal to decreasedWeak, thready, impalpable
BreathingNormalNormal to increasedTachypnea and hyperpnea
EyesNormalSlightly sunkenDeeply sunken
FontanellesNormalSlightly sunkenDeeply sunken
TearsNormalNormal to decreasedAbsent
Mucous membranesMoistDryParched
Skin turgorInstant recoilRecoil < 2 secondsRecoil >2 seconds
Capillary refill< 2 secondsProlongedMinimal
ExtremitiesWarmCoolMottled, cyanotic
Adapted from King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. Nov 21 2003;52(RR-16):1-16.[5]