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

Dehydration

Lennox H Huang, MD, Associate Chair (Clinical), Assistant Professor, Department of Pediatrics, McMaster University School of Medicine; Interim Chief of Pediatrics, McMaster Children's Hospital
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

Updated: Nov 3, 2009

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

The following should be considered in patients with dehydration:

• 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. 

The determination of 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. Validated clinical dehydration scales may be a useful adjunct to predict need for intravenous fluid and longer stays in the emergency department.^{[1 ]}
[#table1]

Table 1. Clinical Findings of Dehydration

* Best indicators of hydration status^{[2 ]}

Table 2. Estimated Fluid Deficit

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.^{[3,4 ]}
  • 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.

Differential Diagnoses

Workup

Laboratory Studies

No definitive laboratory test for dehydration is available. Laboratory data are generally 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 because hyponatremia (<130 mEq/L) and hypernatremia (>150 mEq/L) require specific treatment regimens.
• Potassium may be elevated (eg, congenital adrenal hyperplasia, renal failure) or low (eg, pyloric stenosis, alkalosis).
• Chloride may be low in pyloric stenosis (eg, hypochloremic, hypokalemic, or metabolic alkalosis).
• Poor tissue perfusion in dehydration results in production of lactic acid. Bicarbonate is consumed as lactic acid levels increase. In diabetic ketoacidosis (DKA), ketoacids also consume bicarbonate. Bicarbonate levels can also be reduced because of loss of bicarbonate in diarrheal stools. Low bicarbonate levels have been correlated with increased severity of dehydration in some studies. 
• Glucose may be dangerously low because of poor intake or extremely elevated in DKA.
• BUN and creatinine levels may be elevated because of renal hypoperfusion.
• Urine specific gravity may be elevated in patients with dehydration but should not be relied on because it is not an accurate diagnostic test for dehydration.^{[5 ]}Further caution should be used in the setting of diabetes insipidus, in which the urine is dilute with low specific gravity, even in patients who are dehydrated.
• Urinalysis may show findings of DKA (eg, ketones, glucose).
• Electrolyte analysis of any fluid that is lost (eg, urine, stool, gastric fluid) can be performed to further refine the composition of replacement fluids after providing acute fluid resuscitation.

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 (eg, femoral, subclavian, internal, external jugular).
• Intraosseous line: Intraosseous cannulation can be easily and rapidly 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. Care must be taken to avoid injury to the physeal growth plate.
• Orogastric/nasogastric tube: An orogastric/nasogastric tube may be inserted to facilitate enteral rehydration in children with mild-to-moderate dehydration. These tubes should be considered to assist in the nutritional recovery of children who are critically ill or severely dehydrated.

Treatment

Medical Care

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

Oral rehydration solutions

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

* World Health Organization/United Nations Children's Fund

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

Traditional clear fluids are not appropriate for ORT. Many contain excessive concentrations of 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.

• ORT for mild or moderate dehydration
  • Mild or moderate dehydration can usually be treated very effectively with ORT.^{[6 ]}
  • Vomiting is generally not a contraindication to ORT. If evidence of bowel obstruction, ileus, or acute abdomen is noted, 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 5-10% in infants and 3-6% in children (see Table 1 and Table 2). The fluid deficit should be replaced over 4 hours.
  • The oral rehydration solution should be administered in small volumes very frequently to minimize gastric distention and reflex vomiting. Generally, 5 mL of oral rehydration solution 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 oral rehydration solution via a nasogastric tube may be temporarily used to achieve rehydration. Intravenous fluid administration (20-30 mL/kg of isotonic sodium chloride 0.9% solution over 1-2 h) may also be used until oral rehydration is tolerated. According to a Cochrane systematic review, for every 25 children treated with ORT for dehydration, one fails and requires intravenous therapy.^{[7 ]}
  • Replace ongoing losses from stools and emesis (estimate volume and replace) in addition to replacing the calculated fluid deficit.
  • An age appropriate diet may be started as soon as the child is able to tolerate oral intake.
• Severe dehydration
  • Laboratory evaluation and intravenous rehydration are required. The underlying cause of the dehydration must be determined and appropriately treated.
  • 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 an isotonic crystalloid (eg, lactated Ringer solution, 0.9% sodium chloride). 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 replenished, tachycardia, capillary refill, urine output, and mental status all should improve. If improvement is not observed after 60 mL/kg of fluid administration, other etiologies of shock (eg, cardiac, anaphylactic, septic) 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. Maintenance fluid requirements are equal to measured fluid losses (urine, stool) plus insensible fluid losses. Normal insensible fluid loss is approximately 400-500 mL/m² body surface area and may be increased by factors such as fever and tachypnea. Alternatively, daily fluid requirements may be roughly estimated as follows:
    • Less than 10 kg = 100 mL/kg
    • 10-20 kg = 1000 + 50 mL/kg for each kg over 10 kg
    • Greater than 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. In general, the recommended administration is one half of this volume administered over 8 hours and administration of the remainder over the following 16 hours. Continued losses (eg, emesis, diarrhea) must be promptly replaced.
  • If the child is isonatremic (130-150 mEq/L), the sodium deficit incurred can generally be corrected by administering the fluid deficit plus maintenance as 5% dextrose in 0.45-0.9% sodium chloride. Potassium (20 mEq/L potassium chloride) may be added to maintenance fluid once urine output is established and serum potassium levels are within a safe range.
  • An alternative approach to the deficit therapy approach is rapid replacement therapy. With this approach, a child with severe isonatremic dehydration is administered 20-40 mL/kg of isotonic sodium chloride solution or lactated Ringer solution over 15-60 minutes. As perfusion is restored, the child improves and is able to tolerate an oral rehydration solution 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 isotonic (0.9%) sodium chloride solution or lactated Ringer solution should be administered 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: Sodium = 123, weight = 10 kg, assumed volume of distribution of 0.6; Sodium deficit = (130-123) X 0.6 X 10 kg = 42 mEq sodium
  • A simplified approach is to use 5% dextrose in 0.9% sodium chloride as the replacement fluid. The sodium is closely monitored, and the amount of sodium in the fluid is adjusted to maintain a slow correction (<0.5 mEq/L/h).
  • Frequently reassessing the serum sodium level during correction is imperative. 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%) sodium chloride solution (0.5 mEq/mL) may be used for rapid partial correction of symptomatic hyponatremia. A bolus dose of 4 mL/kg raises 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 isotonic sodium chloride solution or lactated Ringer solution should be administered and repeated until perfusion is restored.
  • Varied regimens 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 the reference range by not more than 10 mEq/L/24h. 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% sodium chloride. Serum sodium levels should be assessed every 4 hours. If the sodium has decreased by less than 0.5 mEq/L/h, 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 closely monitored.
• Pharmacologic management
  • Antidiarrheal agents are not recommended because of a high incidence of side effects including lethargy, respiratory depression, and coma.
  • Routine empiric antibiotics should be avoided and may worsen some specific diarrheal disease states (eg, hemolytic-uremic syndrome, Clostridium difficile).
  • Over-the-counter antiemetics are not recommended due to side effects including drowsiness and impaired oral rehydration.
  • In an emergency department study, ondansetron has been shown to decrease likelihood of vomiting, increase oral intake, and decrease emergency department length of stay but has not shown significant effects on hospitalization rates or long-term outcomes.^{[8 ]}
  • Dimenhydrinate, although used in Europe and Canada, has not been found to improve oral rehydration.^{[9 ]}

Diet

• Children with dehydration from gastroenteritis have decreased duration of diarrhea when feedings are started as soon as the patient is able to tolerate oral intake.
• Diluting milk or formula is not indicated. Breast-feeding should be resumed as soon as possible.
• Foods that contain complex carbohydrates (eg, rice, wheat, potatoes, bread, cereals), lean meats, fruits, and vegetables are encouraged. Fatty foods and simple carbohydrates should be avoided.

Medication

Antiemetic, Serotonin Antagonist

In a recent emergency department study, ondansetron was shown to decrease likelihood of vomiting, increase oral intake, and decrease emergency department length of stay.^{[8 ]}

Ondansetron (Zofran)

Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. Prevents nausea and vomiting associated with emetogenic cancer chemotherapy (eg, high-dose cisplatin), and complete body radiotherapy.

Dosing

Adult

8 mg PO q1-2h for 3 doses
Alternatively, 0.15 mg/kg IV q8h for 3 doses or 32 mg IV once

Pediatric

Orally dissolving tablets:
8-15 kg: 2 mg as a single dose
15-30 kg: 4 mg as a single dose
>30 kg: 8 mg as a single dose

Interactions

Although there is potential for cytochrome P-450 inducers (eg, barbiturates, rifampin, carbamazepine, phenytoin) to change half-life and clearance of ondansetron, dosage adjustment is not usually required

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause headache

Follow-up

Further Inpatient Care

• Severe dehydration warrants hospital admission for rehydration, as do hypernatremic or hyponatremic states.
• Inability to tolerate oral rehydration therapy (ORT) 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. However, the child with severe dehydration and hypovolemic shock can have significant morbidity and mortality if treatment is delayed.

Patient Education

• An excellent Web site containing patient education materials regarding dehydration, gastroenteritis, and oral rehydration therapy can be found at AAFP Family Health Facts. Additional patient education resources can be found by visiting eMedicine's Children's Health Center. Also, see eMedicine's patient education article Dehydration in Children.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize and appropriately treat underlying cause for dehydration (eg, diabetic ketoacidosis [DKA], diabetes insipidus, pyloric stenosis)
• 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.
• Failure to identify and treat other causes of shock (eg, septic, anaphylactic)

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Keywords

dehydration, negative fluid balance, diarrheal illness, diarrhea, isonatremic dehydration, hypernatremic dehydration, hyponatremic dehydration, end organ failure, cerebral edema, gastroenteritis, cystic fibrosis, diabetes mellitus, treatment, diagnosis

Contributor Information and Disclosures

Author

Lennox H Huang, MD, Associate Chair (Clinical), Assistant Professor, Department of Pediatrics, McMaster University School of Medicine; Interim Chief of Pediatrics, McMaster Children's Hospital
Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Physician Executives, 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
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

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; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
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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