pediatric dehydration case study test

AMY CANAVAN, MD, AND BILLY S. ARANT, JR., MD

Am Fam Physician. 2009;80(7):692-696

Author disclosure: Nothing to disclose.

The most useful individual signs for identifying dehydration in children are prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern. However, clinical dehydration scales based on a combination of physical examination findings are better predictors than individual signs. Oral rehydration therapy is the preferred treatment of mild to moderate dehydration caused by diarrhea in children. Appropriate oral rehydration therapy is as effective as intravenous fluid in managing fluid and electrolyte losses and has many advantages. Goals of oral rehydration therapy are restoration of circulating blood volume, restoration of interstitial fluid volume, and maintenance of rehydration. When rehydration is achieved, a normal age-appropriate diet should be initiated.

Clinical dehydration scales based on a combination of physical examination findings are the most specific and sensitive tools for accurately diagnosing dehydration in children and categorizing its severity. Overdiagnosis of dehydration may lead to unnecessary tests and treatment, whereas underdiagnosis may lead to increased morbidity (e.g., protracted vomiting, electrolyte disturbances, acute renal insufficiency).

Among children in the United States, fluid and electrolyte disturbances from acute gastroenteritis result in 1.5 million outpatient visits, 200,000 hospitalizations, and 300 deaths per year. 1 Additionally, children may become dehydrated because of a variety of other illnesses that cause vomiting, diarrhea, or poor fluid intake.

PARENTAL OBSERVATION

Parental report of vomiting, diarrhea, or decreased oral intake is sensitive, but not specific, for identifying dehydration in children. If parents report that the child does not have diarrhea, has normal oral intake, and has normal urine output, the chance of dehydration is low. Likewise, when parents are asked about physical signs of dehydration, a number of positive answers suggest dehydration. However, if the parents report normal tear production, the chance of dehydration is low. 2 , 3

PHYSICAL EXAMINATION

Comparing change in body weight from before and after rehydration is the standard method for diagnosing dehydration. 4 To identify dehydration in infants and children before treatment, a number of symptoms and clinical signs have been evaluated and compared with this standard method. Physical examination findings during dehydration represent desiccation of tissue, the body's compensatory reaction to maintain perfusion, or both. The most useful individual signs for identifying dehydration are prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern. 5 However, clinical dehydration scales based on a combination of physical examination findings are much better predictors than individual signs. 5

In one study, four factors predicted dehydration: capillary refill time of more than two seconds, absence of tears, dry mucous membranes, and ill general appearance; the presence of two or more of these signs indicated a fluid deficit of at least 5 percent. 6 In a similar validated scale, general appearance, degree of sunken eyes, dryness of mucous membranes, and tear production were associated with length of hospital stay and need for intravenous fluids in children with acute gastroenteritis. 7

Capillary refill time is performed in warm ambient temperature, and is measured on the sternum of infants and on a finger or arm held at the level of the heart in older children. The measurement is not affected by fever and should be less than two seconds. 8 Assessment of skin turgor is performed by pinching skin on the lateral abdominal wall at the level of the umbilicus. Turgor (i.e., time required for the skin to recoil) is normally instantaneous and increases linearly with degree of dehydration. 9 Respiratory pattern and heart rate should be compared with age-specific normal values.

LABORATORY ASSESSMENT

Unlike in adults, calculation of the blood urea nitrogen (BUN)/creatinine ratio is not useful in children. Although the normal BUN level is the same for children and adults, the normal serum creatinine level changes with age (0.2 mg per dL [17.68 μmol per L] in infants to 0.8 mg per dL [70.72 μmol per L] in adolescents). BUN alone and urine specific gravity also have poor sensitivity and specificity for predicting dehydration in children. 10

In combination with a clinical dehydration scale, a serum bicarbonate level of less than 17 mEq per L (17 mmol per L) may improve sensitivity of identifying children with moderate to severe hypovolemia. 11 Additionally, a serum bicarbonate level of less than 13 mEq per L (13 mmol per L) is associated with increased risk of failure of outpatient rehydration efforts. 12

PATHOPHYSIOLOGY

Most of the volume loss in dehydration is extracellular fluid. The extracellular fluid space has two components: plasma and lymph as a delivery system, and interstitial fluid for solute exchange. 13 The goal of rehydration therapy is first to restore the circulating blood volume, if necessary; then to restore the interstitial fluid volume; and finally to maintain hydration and replace continuing losses, such as diarrhea and increased insensible losses caused by fever.

ORAL REHYDRATION THERAPY

The American Academy of Pediatrics recommends oral rehydration therapy (ORT) as the preferred treatment of fluid and electrolyte losses caused by diarrhea in children with mild to moderate dehydration. 14 ORT is as effective as intravenous fluid in rehydration of children with mild to moderate dehydration—there is no difference in failure rate or hospital admission rate between the two treatments. 15 Additionally, ORT has many advantages compared with intravenous fluid therapy. It can be administered at home, reducing the need for outpatient and emergency department visits; requires less emergency department staff time; and leads to shorter emergency department stays. Parents are also more satisfied with the visit when ORT had been used. 16 With ORT, the same fluid can be used for rehydration, maintenance, and replacement of stool losses; and ORT can be initiated more quickly than intravenous fluid therapy. 17

The principles of ORT to treat dehydration from gastroenteritis apply to the treatment of dehydration from other causes. Altered mental status with risk of aspiration, abdominal ileus, and underlying intestinal malabsorption are contraindications. Cost to the family may be a deterrent to home ORT; therefore, ORT solution provided by the physician's office or emergency department increases the likelihood that parents will use ORT and reduces unscheduled follow-up visits. 16

Nasogastric rehydration therapy with ORT solution is an alternative to intravenous fluid therapy in patients with poor oral intake. Nasogastric hydration using oral rehydration solution is tolerated as well as ORT. Failure rate of nasogastric tube placement is significantly less than that of intravenous lines, and significant complications of nasogastric tube placement are rare. Nasogastric rehydration therapy is also less expensive than intravenous fluid therapy. 18

As soon as children with acute gastroenteritis are rehydrated, a regular age-appropriate diet should be initiated. This does not worsen the symptoms of mild diarrhea, and may decrease its duration. 14

Preparations . Use of an appropriate ORT solution, such as commercial electrolyte solutions for children (e.g., Pedialyte), corrects and helps prevent electrolyte disturbances caused by gastroenteritis. 17 – 19 The World Health Organization ORT solution contains 90 mEq per L of sodium, mimicking the sodium content of diarrhea caused by cholera. Commercial ORT preparations typically contain around 50 mEq per L of sodium, which is more consistent with the sodium content of diarrhea caused by rotavirus. 20 Commercial ORT solutions contain 25 g per L of dextrose, which helps prevent hypoglycemia without causing osmotic diuresis, 21 and 30 mEq per L of bicarbonate, which leads to less vomiting and more efficient correction of acidosis. 19 Commercial ORT solutions are recommended over homemade solutions because of the risk of preparation errors. 22 Clear sodas and juices should not be used for ORT because hyponatremia may occur. Table 1 compares the electrolyte composition of commercial electrolyte solutions with other clear liquids.

Administration . For mild dehydration, 50 mL per kg of ORT solution should be administered over four hours using a spoon, syringe, or medicine cup 14 ; this can be accomplished by giving 1 mL per kg of the solution to the child every five minutes. Patients may be treated at home. 14 If the child vomits, treatment should be resumed after 30 minutes. 15 After the four-hour treatment period, maintenance fluids should be given and ongoing losses assessed and replaced every two hours. Maintenance therapy includes providing anticipated water and electrolyte needs for the next 24 hours in the child who is now euvolemic with expected normal urine output. The Holliday-Segar method ( Table 2 23 ) is a simple, reliable formula for estimating water needs. 24 Based on average weights of infants and children, this method can be further simplified to provide maintenance ORT at home: 1 oz per hour for infants, 2 oz per hour for toddlers, and 3 oz per hour for older children. To replace ongoing losses, 10 mL per kg for every loose stool and 2 mL per kg for every episode of emesis should be administered.

For moderate dehydration, 100 mL per kg of ORT solution should be given over four hours in the physician's office or emergency department. 14 If treatment is successful and ongoing losses are not excessive, the child may be sent home. At home, caregivers should provide maintenance therapy and replace ongoing losses every two hours as described for mild dehydration. ORT is considered to be unsuccessful if vomiting is severe and persistent (i.e., at least 25 percent of the hourly oral requirement) or if ORT cannot keep up with the volume of stool losses. 17

Severe dehydration should be treated with intravenous fluids until the patient is stabilized (i.e., circulating blood volume is restored). Treatment should include 20 mL per kg of isotonic crystalloid (normal saline or lactated Ringer solution) over 10 to 15 minutes. 25 No other fluid type is currently recommended for volume resuscitation in children. 26 Treatment should be repeated as necessary, with monitoring of the patient's pulse strength, capillary refill time, mental status, and urine output. Stabilization often requires up to 60 mL per kg of fluid within an hour. 25 Electrolyte measurement should be performed in all children with severe dehydration and considered in those with moderate dehydration because it may be difficult to predict which children have significant electrolyte abnormalities. 27 After resuscitation is completed and normal electrolyte levels are achieved, the patient should receive 100 mL per kg of ORT solution over four hours, then maintenance fluid and replacement of ongoing losses. If ORT fails after initial resuscitation of a child with severe dehydration, intravenous fluid therapy should be initiated. First, 100 mL per kg of isotonic crystalloid should be administered over four hours, followed by a maintenance solution. This method also may be used when a child with moderate dehydration fails ORT.

The electrolyte content of intravenous maintenance fluid for infants and children with normal serum electrolyte levels should be 5 percent dextrose and 25 percent normal saline, plus 20 mEq per L of potassium. 23 , 28 , 29 Intake, output, and vital signs must be checked every four hours, and adjustments made to the therapy as necessary (e.g., in the setting of ongoing losses, such as excessive stool output, or persistent fever). If stool output exceeds 30 mL per kg per day, it should be replaced in an equal volume every four hours with an intravenous solution comparable in electrolytes with the stool (50 percent normal saline plus 20 to 30 mEq per L of potassium), in addition to the volume of maintenance fluid, until ORT can be tolerated. Children with persistent fever may require 1 mL per kg per degree centigrade every hour, in addition to the calculated maintenance therapy. Postoperatively and in children with central nervous system infection or injury, 20 to 50 percent less fluid and fluid with higher sodium content may be needed because of abnormal antidiuretic hormone secretion. 28 These adjustments in fluid rates are guided by regular measurement of urine output and vital signs.

MEDICATIONS

Pharmacologic agents are not recommended to decrease diarrhea because of limited evidence and concern for toxicity. Although Lactobacillus has no major toxic effects, its effectiveness in patients with diarrhea has not been demonstrated. 14 A single dose of ondansetron (Zofran) has been shown to facilitate ORT by reducing the incidents and frequency of vomiting and, therefore, reducing the failure of ORT and the need for intravenous fluid therapy. 30 Recurrent dosing of ondansetron has not been studied.

Complications

Hypernatremia, hyponatremia, and hypoglycemia occasionally complicate dehydration. Serum electrolyte levels should be measured in children with severe dehydration and in those with moderate dehydration that presents in atypical ways.

Hypernatremia (serum sodium level of greater than 145 mEq per L [145 mmol per L]) indicates water loss in excess of sodium loss. Because sodium is restricted to the extracellular fluid space, the typical signs of dehydration are less pronounced in the setting of hypernatremia, and significant circulatory disturbance is not likely to be noted until dehydration reaches 10 percent. Findings that may aid in the diagnosis of hypernatremia in children include a “doughy” feeling rather than tenting when testing for skin turgor, increased muscle tone, irritability, and a high-pitched cry. 31 Hyponatremia is often caused by inappropriate use of oral fluids that are low in sodium, such as water, juice, and soda. If severe dehydration is present, a child with hypernatremia or hyponatremia should receive isotonic crystalloid until stabilized. If after initial volume repletion, hyponatremia or hypernatremia remains moderate to severe (serum sodium level of less than 130 mEq per L [130 mmol per L] or greater than 150 mEq per L [150 mmol per L]), replacement of the remaining fluid deficit should be altered, with a principal goal of slow correction.

In one study, blood glucose levels of less then 60 mg per dL (3.33 mmol per L) were detected in 9 percent of children younger than nine years (mean age 18 months) admitted to the hospital with diarrhea. 27 History and physical examination findings did not indicate that these children were at risk; therefore, blood glucose screening may be indicated for toddlers with diarrhea.

King CK, Glass R, Bresee JS, Duggan C for the Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Porter SC, Fleisher GR, Kohane IS, Mandl KD. The value of parental report for diagnosis and management of dehydration in the emergency department. Ann Emerg Med. 2003;41(2):196-205.

Armon K, Stephenson T, MacFaul R, Eccleston P, Werneke U. An evidence and consensus based guideline for acute diarrhoea management. Arch Dis Child. 2001;85(2):132-142.

Friedman JN, Goldman RD, Srivastava R, Parkin PC. Development of a clinical dehydration scale for use in children between 1 and 36 months of age. J Pediatr. 2004;145(2):201-207.

Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated?. JAMA. 2004;291(22):2746-2754.

Gorelick MH, Shaw KN, Murphy KO. Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics. 1997;99(5):E6.

Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics. 2008;122(3):545-549.

Gorelick MH, Shaw KN, Murphy KO, Baker MD. Effect of fever on capillary refill time. Pediatr Emerg Care. 1997;13(5):305-307.

Laron Z. Skin turgor as a quantitative index of dehydration in children. Pediatrics. 1957;19(5):816-822.

Teach SJ, Yates EW, Feld LG. Laboratory predictors of fluid deficit in acutely dehydrated children. Clin Pediatr (Phila). 1997;36(7):395-400.

Vega RM, Avner JR. A prospective study of the usefulness of clinical and laboratory parameters for predicting percentage of dehydration in children. Pediatr Emerg Care. 1997;13(3):179-182.

Reid SR, Bonadio WA. Outpatient rapid intravenous rehydration to correct dehydration and resolve vomiting in children with acute gastroenteritis. Ann Emerg Med. 1996;28(3):318-323.

Holliday MA, Friedman AL, Wassner SJ. Extracellular fluid restoration in dehydration: a critique of rapid versus slow. Pediatr Nephrol. 1999;13(4):292-297.

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;97(3):424-435.

Atherly-John YC, Cunningham SJ, Crain EF. A randomized trial of oral vs intravenous rehydration in a pediatric emergency department. Arch Pediatr Adolesc Med. 2002;156(12):1240-1243.

Duggan C, Lasche J, McCarty M, et al. Oral rehydration solution for acute diarrhea prevents subsequent unscheduled follow-up visits. Pediatrics. 1999;104(3):e29.

Spandorfer PR, Alessandrini EA, Joffe MD, Localio R, Shaw KN. Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial. Pediatrics. 2005;115(2):295-301.

Nager AL, Wang VJ. Comparison of nasogastric and intravenous methods of rehydration in pediatric patients with acute dehydration. Pediatrics. 2002;109(4):566-572.

Islam MR, Ahmed SM. Oral rehydration solution without bicarbonate. Arch Dis Child. 1984;59(11):1072-1075.

Molla AM, Rahman M, Sarker SA, Sack DA, Molla A. Stool electrolyte content and purging rates in diarrhea caused by rotavirus, enterotoxigenic E. coli , and V. cholerae in children. J Pediatr. 1981;98(5):835-838.

Rahman O, Bennish ML, Alam AN, Salam MA. Rapid intravenous rehydration by means of a single polyelectrolyte solution with or without dextrose. J Pediatr. 1988;113(4):654-660.

Meyers A, Sampson A, Saladino R, Dixit S, Adams W, Mondolfi A. Safety and effectiveness of homemade and reconstituted packet cereal-based oral rehydration solutions: a randomized clinical trial. Pediatrics. 1997;100(5):E3.

Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics. 1957;19(5):823-832.

Holliday MA, Ray PE, Friedman AL. Fluid therapy for children: facts, fashions and questions. Arch Dis Child. 2007;92(6):546-550.

Boluyt N, Bollen CW, Bos AP, Kok JH, Offringa M. Fluid resuscitation in neonatal and pediatric hypovolemic shock: a Dutch Pediatric Society evidence-based clinical practice guideline. Intensive Care Med. 2006;32(7):995-1003.

Pediatric Advanced Life Support Provider Manual Dallas, Tex: American Heart Association; 2006: 232.

Wathen JE, MacKenzie T, Bothner JP. Usefulness of the serum electrolyte panel in the management of pediatric dehydration treated with intravenously administered fluids. Pediatrics. 2004;114(5):1227-1234.

Friedman AL, Ray PE. Maintenance fluid therapy: what it is and what it is not. Pediatr Nephrol. 2008;23(5):677-680.

Assadi F, Copelovitch L. Simplified treatment strategies to fluid therapy in diarrhea [published correction appears in Pediatr Nephrol . 2004;19(3):364]. Pediatr Nephrol. 2003;18(11):1152-1156.

Freedman SB, Adler M, Seshadri R, Powell EC. Oral ondansetron for gastroenteritis in a pediatric emergency department. N Engl J Med. 2006;354(16):1698-1705.

Conley SB. Hypernatremia. Pediatr Clin North Am. 1990;37(2):365-372.

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Dehydration in Children

Pathophysiology |
Symptoms and Signs |
Diagnosis |
Treatment |
Practical Rehydration Example |
Procedure |
More Information |

Dehydration is significant depletion of body water and, to varying degrees, electrolytes. Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree of dehydration progresses, tachycardia, hypotension, and shock. Diagnosis is based on history and physical examination. Treatment is with oral or IV replacement of fluid and electrolytes.

Dehydration remains a major cause of morbidity and mortality in infants and young children worldwide. Dehydration is a symptom or sign of another disorder, most commonly diarrhea . Infants are particularly susceptible to the ill effects of dehydration because of their greater baseline fluid requirements (due to a higher metabolic rate), higher evaporative losses (due to a higher ratio of surface area to volume), and inability to communicate thirst or seek fluid.

Etiology of Dehydration in Children

Dehydration results from

Increased fluid loss

Decreased fluid intake

The most common source of increased fluid loss is the gastrointestinal tract—from vomiting , diarrhea , or both (eg, gastroenteritis ). Other sources are renal (eg, diabetic ketoacidosis ), cutaneous (eg, excessive sweating , burns ), and 3rd-space losses (eg, into the intestinal lumen in bowel obstruction or ileus).

Decreased fluid intake is common during mild illnesses such as pharyngitis or during serious illnesses of any kind. Decreased fluid intake is particularly problematic when the child is vomiting or when fever, tachypnea, or both increase insensible losses. It may also be a sign of neglect .

Pathophysiology of Dehydration in Children

All types of lost fluid contain electrolytes in varying concentrations, so fluid loss is always accompanied by some degree of electrolyte loss. The exact amount and type of electrolyte loss varies depending on the cause. For example, significant amounts of bicarbonate may be lost with diarrhea, predisposing to metabolic acidosis ; however, with vomiting, hydrogen ions are lost, predisposing to metabolic alkalosis . However, fluid lost always contains a lower concentration of sodium than the plasma. Thus, in the absence of any fluid replacement, the serum sodium usually rises (hypernatremia).

Hypernatremia causes water to shift from the intracellular and interstitial space into the intravascular space, helping, at least temporarily, to maintain vascular volume. With hypotonic fluid replacement (eg, with plain water), serum sodium may normalize but can also decrease below normal (hyponatremia). Hyponatremia results in some fluid shifting out of the intravascular space into the interstitium at the expense of vascular volume.

Symptoms and Signs of Dehydration in Children

Symptoms and signs of dehydration vary according to degree of deficit (see table Clinical Correlates of Dehydration ) and by the serum sodium level.

Because of the fluid shift out of the interstitium into the vascular space, children with hypernatremia appear more ill (eg, with very dry mucous membranes, a doughy appearance to the skin) for a given degree of water loss than do children with hyponatremia. However, children with hypernatremia have better hemodynamics (eg, less tachycardia and better urine output) than do children with hyponatremia, in whom fluid has shifted out of the vascular space.

Dehydrated children with hyponatremia may appear only mildly dehydrated but are actually closer to hypotension and cardiovascular collapse than are equally dehydrated children with elevated or normal sodium levels.

Diagnosis of Dehydration in Children

Clinical evaluation

In general, dehydration is defined as follows:

Mild: No hemodynamic changes (about 5% body weight in infants and 3% in adolescents)

Moderate: Tachycardia (about 10% body weight in infants and 5 to 6% in adolescents)

Severe: Hypotension with impaired perfusion (about 15% body weight in infants and 7 to 9% in adolescents)

However, using a combination of symptoms and signs to assess dehydration is a more accurate method than using only one sign.

Another way to assess the degree of dehydration in children with acute dehydration is change in body weight; all short-term weight loss > 1%/day is presumed to represent fluid deficit. However, this method depends on knowing a precise, recent preillness weight. Parental estimates are usually inadequate; a 1-kg error in a 10-kg child causes a 10% error in the calculated percentage of dehydration—the difference between mild and severe dehydration.

Laboratory testing is usually reserved for moderately or severely ill children, in whom electrolyte disturbances (eg, hypernatremia , hypokalemia , metabolic acidosis or metabolic alkalosis

Treatment of Dehydration in Children

Fluid replacement (oral if possible)

Treatment of dehydration is best approached by considering the following separately:

Fluid resuscitation requirements

Current deficit

Ongoing losses

Maintenance requirements.

The volume (eg, amount of fluid), composition, and rate of replacement differ for each. Formulas and estimates used to determine treatment parameters provide a starting place, but treatment requires ongoing monitoring of vital signs, clinical appearance, urine output, weight, and sometimes serum electrolyte levels.

The American Academy of Pediatrics and the World Health Organization (WHO) both recommend oral replacement therapy for mild and moderate dehydration. Children with severe dehydration (eg, evidence of circulatory compromise) should receive fluids IV. Children who are unable or unwilling to drink or who have repetitive vomiting can receive fluid replacement orally through frequently repeated small amounts, through an IV, or through a nasogastric tube (see Solutions ).

Resuscitation

Patients with signs of hypoperfusion should receive fluid resuscitation with boluses of isotonic fluid (eg, 0.9% saline or Ringer's lactate). The goal is to restore adequate circulating volume to restore blood pressure and perfusion.

The resuscitation phase should reduce moderate or severe dehydration to a deficit of about 6 to 8% body weight. If dehydration is moderate, 20 mL/kg (2% body weight) is given IV over 20 to 30 minutes, reducing a 10% deficit to 8%. If dehydration is severe, 3 boluses of 20 mL/kg (6% body weight) may be required.

The end point of the fluid resuscitation phase is reached when peripheral perfusion and blood pressure are restored and the heart rate is returned to normal (in an afebrile child).

Deficit replacement

Total deficit volume is estimated clinically as described previously. Sodium deficits are usually about 60 mEq/L (60 mmol/L) of fluid deficit, and potassium deficits are usually about 30 mEq/L (30 mmol/L) of fluid deficit. The resuscitation phase should have reduced moderate or severe dehydration to a deficit of about 6 to 8% body weight; this remaining deficit is typically replaced over the next 24 hours.

Because 0.45% saline has 77 mEq sodium per liter (77 mmol/L), it is usually an appropriate fluid choice, particularly in children with diarrhea, because the electrolyte content of diarrhea is typically 50 to 100 mEq/L (50 to 100 mmol/L) (see table Estimated Electrolyte Deficits by Cause ); 0.9% saline may be used as well.

Potassium replacement (usually by adding 20 to 40 mEq potassium per liter [20 to 40 mmol/L] of replacement fluid) should not begin until adequate urine output is established.

Dehydration in neonates, particularly with significant hypernatremia (eg, serum sodium > 160 mEq/L [> 160 mmol/L]) or hyponatremia (eg, serum sodium < 120 mEq/L [

Volume of ongoing losses should be measured directly (eg, nasogastric tube, catheter, stool measurements) or estimated (eg, 10 mL/kg per diarrheal stool). Replacement should be milliliter for milliliter in time intervals appropriate for the rapidity and extent of the loss.

Ongoing electrolyte losses can be estimated by source or cause (see table Estimated Electrolyte Deficits by Cause ).

Urinary electrolyte losses vary with intake and disease process but can be measured if electrolyte abnormalities fail to respond to replacement therapy.

(See also the American Academy of Pediatrics' clinical practice guideline (2018) for maintenance IV fluids in children.)

Fluid and electrolyte needs from basal metabolism must also be accounted for. Maintenance requirements are related to metabolic rate and affected by body temperature. Insensible losses (evaporative free water losses from the skin and respiratory tract) account for about one third of total maintenance water (slightly more in infants and less in adolescents and adults).

Volume rarely must be exactly determined but generally should aim to provide an amount of water that does not require the kidney to significantly concentrate or dilute the urine. The most common estimate is the Holliday-Segar formula, which uses patient weight to calculate metabolic expenditure in kcal/24 hours, which approximates fluid needs in mL/24 hours (see table Holliday-Segar Formula for Maintenance Fluid Requirements by Weight ). More complex calculations (eg, those using body surface area) are rarely required.

Maintenance fluid volumes can be given as a separate simultaneous infusion, so that the infusion rate for replacing deficits and ongoing losses can be set and adjusted independently of the maintenance infusion rate.

Baseline estimates are affected by fever (increasing by 12% for each degree > 37.8 ° C), hypothermia, and activity (eg, increased for hyperthyroidism or status epilepticus, decreased for coma).

The traditional approach to calculating the composition of maintenance fluids was also based on the Holliday-Segar formula. According to that formula, patients require

Sodium: 3 mEq/100 kcal/24 hours (3 mEq/100 mL/24 hours)

Potassium: 2 mEq/100 kcal/24 hours (2 mEq/100 mL/24 hours)

(NOTE: 2 to 3 mEq/100 mL is equivalent to 20 to 30 mEq/L [20 to 30 mmol/L].)

hyponatremia . This development is likely due to volume-related ADH release as well as to significant amounts of stimuli-related ADH release (eg, from stress, vomiting, dehydration, or hypoglycemia). The ADH causes increased free water retention. Iatrogenic hyponatremia may be a greater problem for more seriously ill children and those who are hospitalized after surgery where stress plays a bigger role.

Because of this possibility of iatrogenic hyponatremia, many centers are now using a more isotonic fluid such as 0.45% or 0.9% saline for maintenance in dehydrated children. The American Academy of Pediatrics' clinical practice guideline (2018)

Practical Rehydration Example

A 7-month-old infant has diarrhea for 3 days with weight loss from 10 kg to 9 kg. The infant is currently producing 1 diarrheal stool every 3 hours and refusing to drink. Clinical findings of dry mucous membranes, poor skin turgor, markedly decreased urine output, and tachycardia with normal blood pressure and capillary refill suggest 10% fluid deficit. Rectal temperature is 37 ° C. Serum measurements are sodium, 136 mEq/L (136 mmol/L); potassium, 4 mEq/L (4 mmol/L); chloride, 104 mEq/L (104 mmol/L); and bicarbonate, 20 mEq/L (20 mmol/L).

Fluid volume is estimated by deficits, ongoing losses, and maintenance requirements.

The total fluid deficit given 1 kg weight loss = 1 L.

Ongoing diarrheal losses are measured as they occur by weighing the infant’s diaper before application and after the diarrheal stool.

Baseline maintenance requirements by the weight-based Holliday-Segar method are 100 mL/kg × 10 kg = 1000 mL/day = 1000 mL/24 hours or 40 mL/hour.

Electrolyte losses resulting from diarrhea in a eunatremic patient (see table Estimated Electrolyte Deficits by Cause ) are an estimated 80 mEq of sodium and 80 mEq of potassium.

Fluid selection

The patient is given an initial bolus of Ringer's lactate 200 mL (20 mL/kg × 10 kg) over 30 minutes. This amount replaces 26 mEq of the estimated 80 mEq sodium deficit.

Residual fluid deficit is 800 mL (1000 initial − 200 mL resuscitation). This residual amount is given over the next 24 hours. Typically, half (400 mL) is given over the first 8 hours (400 ÷ 8 = 50 mL/hour) and the other half is given over the next 16 hours (25 mL/hour).

The estimated residual sodium deficit is 54 mEq (80 − × 77 mEq sodium/L [77 mmol/L] = 62 mEq sodium); the additional 62 mEq of sodium given by using 0.9% saline is not clinically significant as long as renal function is intact.

When urine output is established, potassium is added at a concentration of 20 mEq/L (20 mmol/L; for safety reasons, no attempt is made to replace complete potassium deficit acutely).

Maintenance fluid

More information.

The following English-language resource may be useful. Please note that THE MANUAL is not responsible for the content of this resource.

American Academy of Pediatrics: Clinical practice guideline for maintenance intravenous fluids in children (2018)

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Dehydration in Children

by Michelle Bischoff
Aug 29, 2010

This podcast gives medical students an approach to identifying and correcting dehydration, plus calculating fluid requirements, in pediatric patients. It was written by Michelle Bischoff and Dr. Melanie Lewis. Michelle is a medical student at the University of Alberta and Dr. Lewis is a General Pediatrician and Associate Professor of Pediatrics at the Stollery Children’s Hospital and University of Alberta.

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Epidemiology

Maintenance fluid and electrolyte requirements, alterations in fluid needs in illness, pathophysiology, illustration of the steps in managing hypertonic dehydration showing the effects on brain volume of rapid versus slow development of hypernatremia and the results of rapid versus slow correction of hypernatremia, physical examination, laboratory tests, imaging studies, parenteral fluid therapy, management of electrolyte disturbances, case resolution, selected references, 80: management of dehydration in children: fluid and electrolyte therapy.

Published: April 2021
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Gangadarshni Chandramohan, MD, MSc, FASN, FAAP, "Management of Dehydration in Children: Fluid and Electrolyte Therapy", Berkowitz’s Pediatrics : A Primary Care Approach , Carol D. Berkowitz, MD, FAAP

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Reference Manager

A 2-year-old boy presents to your office after 2 days of vomiting and diarrhea. His siblings were both ill a few days previously with similar symptoms. At a well-child visit 2 weeks previously, his weight was 12 kg (26.5 lb). Today his weight is 10.8 kg (23.8 lb). He has a pulse of 130 beats per minute, respiratory rate of 28 breaths per minute, and blood pressure of 85/55 mm Hg. He is alert and responsive but appears tired. He has dry mucous membranes, no tears with crying, and slightly sunken-appearing eyeballs. His capillary refill is 2 seconds. He urinated a small amount approximately 6 hours before this office visit. Despite his mother’s best efforts in your office, the patient has vomited all the oral rehydration therapy given to him. You draw blood for analyzing electrolyte, blood urea nitrogen, and creatinine levels and initiate intravenous rehydration by administering 2 boluses each of 240 mL normal saline (0.9% sodium chloride solution).

How is the magnitude of dehydration in a child assessed?

What are the different types of dehydration?

How is the type and amount of fluid required by the dehydrated child determined?

How is renal status assessed in the dehydrated child?

What is the role of electrolyte and acid-base laboratory tests in the evaluation of the dehydrated child?

Dehydration resulting from gastrointestinal (GI) and other disorders, especially diarrhea, is among the most common medical problems encountered in children younger than 5 years. During the past 50 years or more, the usual therapy for children who are hospitalized with dehydration has been to administer intravenous (IV) fluids starting with 1 or 2 boluses of normal saline (NS; 0.9% sodium chloride [NaCl] solution at 20 mL/kg). This is followed by the administration of a sodium (Na + ) solution of variable concentration (usually 0.45% NaCl) mixed with 5% dextrose over the next 24 to 48 hours until the child is able to take oral fluids. The exact amount of fluid and electrolytes is calculated using complicated formulas to provide maintenance fluids and correction of remaining deficit (ie, deficit therapy). The calculation of maintenance therapy was first recommended in the 1950s, but more recently it has been suggested that dehydration management should focus on rapid restoration of extracellular fluid (ECF deficit) followed by oral rehydration therapy (ORT), and traditional calculations of fluid deficits should be abandoned. Alternatively, pediatric nephrologists and intensivists have recommended that physicians forgo sodium calculations in hospitalized children and rely solely on isotonic NS (0.9% NaCl solution) for management. Although this chapter incorporates these suggestions where appropriate, it describes the traditional approach to maintenance and deficit therapy because an understanding of the pathophysiology of dehydration helps in the treatment not only of the dehydrated child but also of children with other types of fluid and electrolyte disorders.

Over the past 30 years, hospital admissions and mortality resulting from diarrhea and dehydration have decreased worldwide; nevertheless, diarrhea remains 1 of the leading medical problems in children younger than 5 years. According to the Centers for Disease Control and Prevention, more than 200,000 hospitalizations and 300 deaths of children occur each year in the United States resulting from diarrhea. Additionally, diarrhea is responsible for 2 to 3 million outpatient visits each year and contributes to 10% of all hospital admissions.

The body has a maintenance fluid requirement to replace daily normal losses that occur through the kidney, intestines, skin, and respiratory tract. Of the various methods used to determine fluid needs, the most common is the caloric method, also called the Holliday-Segar method, which is based on the linear relationship between metabolic rate and fluid needs. For every calorie expended in metabolism, a child requires approximately 1 mL of water. Metabolic rate in children is a function of body surface area. Infants, with their higher relative surface areas per unit of body weight, have higher metabolic rates and, therefore, higher fluid requirements per unit weight compared with older children and adults. As the child grows, the relative surface area decreases, as do the metabolic rate and fluid requirement per unit weight. Using this relationship, maintenance fluid needs can be calculated for the healthy child using the method outlined in Table 80.1 . These calculations of fluid needs are often used to determine the amount of IV fluids provided to a hospitalized child or to calculate the approximate amount of fluid a healthy child requires orally to maintain hydration. These calculations may not be appropriate for children who are critically ill, however, some of whom require fluid restriction and others of whom may have increased fluid needs. Moreover, the caloric method makes no allowance for extra fluid needed for weight gain, growth, activity, or pathophysiological states that increase fluid needs (eg, fever). The fluid requirement derived from this method is valid to determine the daily fluid need for an essentially healthy child. Thriving infants normally drink more fluid than indicated by this method. On average, a growing infant may take 150 to 200 mL/kg per day of milk (human milk or infant formula) as desired to support the average weight gain of 30 g (1.1 oz) per day usually observed in the first few months after birth.

Caloric (ie, Holliday-Segar) Method of Determining Maintenance Fluid Requirements in Healthy Children

Excluding neonates and preterm infants.

Replacement of normal daily losses of electrolytes is considered when a child is not able to take adequate nutritional intake orally (as in the example in Box 80.1 , in which the child receives nothing orally in preparation for surgery). Electrolyte quantities usually are expressed as milliequivalent (mEq) or millimole (mmol) amount per 100 mL of fluid required. Traditionally, the recommended sodium requirement for a healthy child is 3 mEq/100 mL fluid required (approximately 0.2% NaCl or 0.25 NS), and the potassium (K + ) requirement is 2 to 2.5 mEq/100 mL of fluid (see Box 80.1 , part B, for sample calculation and IV order). Potassium should be administered only after ensuring adequate renal function. These estimations of sodium and potassium requirements are meant to replace normal daily losses and would not be adequate in the setting of increased electrolyte losses that can occur in a number of pathologic conditions (eg, diarrhea). Additionally, increased attention has recently been given to the risk of hyponatremia and related complications in hospitalized ill children.

Example of Fluid Calculations a

Case: A boy weighing 22 kg is given nothing orally in preparation for an elective abdominal surgery. The following calculation is used to determine the appropriate amount of IV fluid per hour to administer as he awaits surgery.

For first 10 kg: 100 mL/kg/day × 10 kg = 1,000 mL

For next 10 kg (to get to 20 kg): 50 mL/kg/day × 10 kg = 500 mL

For next 2 kg (to get to 22 kg): 20 mL/kg/day × 2 kg = 40 mL

1,000 mL + 500 mL + 40 mL = 1,540 mL/24 hour

IV rate per hour = 64.2 mL/hour (with a healthy child, round off to 65 mL/hour for ease of administration)

Question: How much Na + and K + should this patient receive in his IV fluids?

Based on physiologic losses: 3 mEq Na + /100 mL (1 dL) of fluid = 3 mEq × 15.4 dL = 46.2 mEq Na + /day in 1,540 mL of water or 30 mEq NaCl/L

2.0 mEq K + /100 mL (1 dL) of fluid = 2.0 × 15.4 = 30.8 mEq K + /day in 1,540 mL of water or 20 mEq KCl/L

Therefore, IV order for this patient is as follows:

D5 0.2% NaCl (or 0.25 NS) with 20 mEq KCl/L to run at 65 mL/hour

Abbreviation: D5 = 5% dextrose water; IV, intravenous; K + , potassium; KCl = potassium chloride; Na + , sodium; NaCl, sodium chloride; NS, normal saline.

Even though in this example the calculations for sodium concentration in the IV fluid is physiologic, recent American Academy of Pediatrics guidelines recommend use of NS with 5% dextrose preoperatively to prevent potential postoperative hyponatremia.

Relatively healthy, well-nourished children receiving IV fluids for a brief period (ie, 1–2 days) during hospitalization do not routinely require supplementation with other electrolytes, such as calcium and magnesium. However, it is important to realize that standard IV fluids containing 5% dextrose, sodium chloride, and potassium chloride provide only minimal caloric needs and do not adequately support weight gain or provide other necessary nutrients. The child who requires prolonged IV therapy because of inadequate GI tract function should receive total parenteral nutrition to better meet the child’s caloric and nutritional needs.

Several conditions can influence fluid requirements. Conditions that increase a patient’s metabolic rate (eg, fever) will also increase a patient’s fluid requirement. A child’s metabolic rate is increased 12% for every 1°C temperature elevation above normal. Most otherwise healthy children with free access to fluids will increase their own intake to account for increased needs when febrile. Other less common hypermetabolic states, such as thyrotoxicosis or salicylate poisoning, may have an even more dramatic effect, perhaps increasing metabolic rate by 25% to 50% over maintenance. In these cases and for children who are dependent on others to provide their fluids, the physician must be aware of the magnitude of increased need and provide supplemental fluids to avoid dehydration.

Other conditions may decrease a child’s fluid requirement. In hypometabolic states, such as hypothyroidism, metabolic rate and fluid needs are decreased by 10% to 25%. Fluid requirements are decreased by 10% to 25% in high environmental humidity unless the ambient temperature is also high and results in visible sweating. In these situations, a healthy child with normal renal function given extra fluid beyond what is needed can, within limits, effectively excrete any excessive intake. The child with renal failure, however, poses a special challenge for the physician in the management of fluid and electrolytes. When a child cannot adequately excrete excessive fluid intake, this fluid can accumulate and result in complications such as congestive heart failure and pulmonary edema. Without functioning kidneys, only insensible fluid losses need replacing. Insensible losses occur primarily through the skin and respiratory tract; they account for approximately 40% of maintenance fluid needs. However, fluid needs for patients with renal failure usually are estimated to be 30% of the maintenance requirement, with additional fluids provided if necessary. Limiting fluids avoids the accumulation of excessive fluids that may require dialysis for removal.

Fluid requirements may also be decreased under circumstances in which arginine vasopressin (AVP; also called antidiuretic hormone) is increased. In addition to hypovolemia or hypertonicity (ie, hyperosmolality), AVP release is also stimulated by pain, nausea, surgery (ie, in the postoperative period), central nervous system (CNS) infections (eg, meningitis, encephalitis), severe pneumonia or respirator use, and certain medications, including thiazide diuretics, chemotherapeutic agents, and selective serotonin reuptake inhibitors. Arginine vasopressin release in the absence of hypovolemia or hypertonicity results in hyponatremia and is referred to as syndrome of inappropriate antidiuretic hormone secretion . In patients with this syndrome, fluid restriction as well as administration of fluids with a higher sodium concentration may be indicated.

The most appropriate sodium concentration of IV fluids for the hospitalized child admitted to a pediatric intensive care unit or in the postoperative patient is controversial. Over the past 25 years, most such children have been maintained on a solution containing 5% dextrose water in half NS (D5 0.5 NS) or lower sodium concentrations (D5 0.25 NS). Studies suggest that because the kidney retains free water in response to excessive AVP in these children, they are at risk for hyponatremia, hyponatremic encephalopathy, brain stem herniation, permanent brain damage, or death. Recently, some pediatric nephrologists and intensivists have recommended forgoing sodium calculations in hospitalized very sick children and instead relying solely on isotonic fluids. Others have cautioned that physicians must make certain that the new recommendations to use isotonic fluids do not result in excessive congestive heart failure or hypernatremia before abandoning previous practices. Regardless of the approach used, close attention to the type and quantity of fluids provided, quantity of body fluid output, weight change, and serial electrolyte assessments are important in the management of all sick children, and fluid and electrolytes must be individualized to each patient to prevent serious complications.

Dehydration is among the most common pathophysiological alterations in fluid balance encountered in pediatrics. Although strictly speaking, dehydration means deficit of water only, most children with dehydration have lost water and electrolytes. Dehydration can result from diminished intake, excessive losses through the GI tract (eg, diarrhea, vomiting), excessive losses from the kidney or skin (eg, polyuria resulting from osmotic diuresis in uncontrolled diabetes), or a combination of these factors.

Children are at increased risk for episodes of dehydration for many reasons. Infants and young children have 2 to 4 times the body surface area per unit body weight compared with adults and as a result have relatively higher fluid needs. It is therefore much easier for children to become dehydrated in the setting of decreased intake or increased losses that often accompany common childhood illnesses. For example, acute gastroenteritis, which is common in young children, often results in anorexia, recurrent vomiting, and frequent or large-volume stools, with proportionately more severe fluid loss than in older children and adults. Additionally, infants and young children are dependent beings who are unable to increase their own fluid intake in response to thirst and must rely on others to provide their fluid needs. If these fluid needs are not met or are underestimated, a child can easily become dehydrated.

Dehydration is classified as isotonic, hypotonic, or hypertonic. These terms often are used interchangeably with isonatremic, hyponatremic, and hypernatremic, respectively. The latter terms reflect the sodium content of the ECF that largely determines serum osmolality in the otherwise healthy dehydrated child. Acute isotonic or isonatremic dehydration (serum Na + 135–145 mEq/L), which is the most common type of dehydration, involves net loss of isotonic fluid containing sodium and potassium ( Figure 80.1 , top). In diarrhea-related dehydration, sodium, the primary ECF cation, is not only lost from the body but also shifts into the intracellular fluid (ICF) compartment to balance the loss of potassium, because potassium losses from cells generally are not accompanied by intracellular anionic losses in acute dehydration. The sodium that has shifted into the ICF compartment will return to the ECF compartment during rehydration as potassium is being replenished, by the action of sodium/potassium adenosinetriphosphatase (ATPase). No net loss of fluid from the ICF occurs in this process; the total water deficit in dehydration comes primarily from the ECF, although some investigators have suggested, in the absence of valid data, that two-thirds of the losses come from ECF and one-third from ICF.

Pathophysiology of various types of dehydration. Top, Isotonic/ isonatremic dehydration. Middle, Hypotonic dehydration. Bottom, Hypertonic dehydration. Abbreviations: ECF, extracellular fluid; H 2 O, water; ICF, intracellular fluid; K + , potassium; Na + , sodium.

A variety of mechanisms exist by which hyponatremia (serum Na + <135 mEq/L) occurs in association with dehydration. In hypotonic or hyponatremic dehydration, the ECF volume is compromised to a greater degree than in isotonic dehydration because of osmotic shifts of ECF into the cells, resulting in more severe signs of dehydration ( Figure 80.1 , middle). Hypotonic dehydration typically occurs in children with gastroenteritis in the setting of excessive sodium losses in stool and oral fluids replacement with a reduced amount of sodium (ie, water, low-sodium beverages [eg, juice, tea]). Furthermore, the kidneys often retain free water (ie, excrete a concentrated urine) despite hyponatremia, because AVP is stimulated by the decreased effective circulating volume in such settings. Intravascular volume depletion seems to be a potent stimulus for AVP release, overriding the AVP suppressive effect of hypotonicity/hyponatremia. The result is that serum sodium levels are further decreased because of dilution. Hypotonic dehydration also may occur as the result of excessive loss of sodium (relative to body water) in stool (eg, cholera) or in the urine (eg, adrenogenital syndrome, cerebral salt wasting, pseudohypoaldosteronism, other salt-wasting renal disorders). This is the most dangerous form of dehydration because it can result in cerebral edema and eventually, brain herniation.

Hypertonic or hypernatremic dehydration (serum Na + >145 mEq/L) occurs when net loss of water exceeds that of solute loss ( Figure 80.1 , bottom). It usually is seen in clinical conditions in which rapid loss of hypotonic fluid in stool, vomit, or urine occurs, accompanied by failure of adequate water intake because of anorexia or vomiting. Fever or hyperventilation, if present, may intensify the disproportionate loss of water. Occasionally, hypertonic dehydration may be caused by excessive solute intake. Urinary excretion of excess solute obligates loss of large volumes of water, resulting in dehydration. The history may reveal that the child was accidentally fed a high sodium solution because of incorrect mixing of oral rehydration packets or concentrated formula. In hypertonic dehydration, shift of fluid from the ICF to the ECF occurs to attain osmotic balance. As such, the ECF volume is somewhat spared at the expense of the ICF, and signs of dehydration may be delayed. However, fluid loss from the ICF results in intracellular dehydration, the most serious effect of which can occur in the brain. If hypernatremia occurs rapidly, not only does a decrease in brain size occur, but a fall in cerebrospinal fluid pressure occurs as well resulting from diffusion of water from cerebrospinal fluid to the blood. As the brain shrinks, the bridging veins within the skull may stretch and even tear, resulting in intracranial hemorrhage or other complications. If the hypertonic state manifests more slowly, brain cell size may initially shrink minimally but will gradually return to normal size even with continued hypernatremia. Preservation of the brain cell volume despite hypernatremia is thought to be caused by the generation of idiogenic osmoles (eg, myoinositol, trimethylamines, taurine, and other amino acids) that prevent water loss and attract water back into the cell and thus maintain cell volume. Rehydration of the patient with hypernatremia must occur slowly and cautiously to avoid brain cell swelling ( Figure 80.2 ). In the child with hypertonic dehydration, on clinical examination the skin may sometimes feel “doughy” because of intracellular dehydration. This finding, however, is inconsistent even when evaluation is done by an experienced pediatrician; thus, clinical examination of the skin should not substitute for serum sodium measurements in the diagnosis of hypernatremia.

In addition to signs and symptoms of the current illness, the history should focus on the cause of dehydration. The parent or guardian should be questioned about the type and amount of oral intake; the duration, quality, and frequency of vomiting or diarrhea; whether blood is present in the stool; the presence or absence of fever; frequency of urination; and whether a recent pre-illness weight is known for the child ( Box 80.2 ). Changes of mental status reported by a parent or guardian is of particular concern because this can occur as the result of significant electrolyte (eg, sodium) disturbance, marked dehydration, or other serious infection or illness. The most accurate means of assessing the degree of dehydration is to compare current weight with a recent pre-illness weight. In acute dehydration, weight loss is primarily the result of fluid loss. The difference between pre-illness and current weight can be used to determine the degree of the fluid deficit.

What to Ask

Dehydration

Has the child been vomiting and/or having diarrhea?

How many stools has the child had, and how large was each stool?

How many times did the child vomit, and how much vomitus occurred each time?

Does the child have fever?

What type fluid has the child been drinking?

Has the child been urinating? How many wet diapers did the child have in a day?

How much did the child weigh at the last visit to the physician?

Has your child’s behavior or level of alertness changed from normal?

An important goal of the physical examination of the dehydrated child is to assess the degree of dehydration. In the process, vital signs, including blood pressure and a current weight, should be obtained. Specific attention should be paid to the general appearance of the child and, in particular, whether the child is ill-appearing, listless, or less reactive. In addition to the usual components of the physical examination, it is important to assess for the following factors: whether the oral mucosal membranes appear tacky or dry, whether tears are present or absent, if tenting of the skin is present (ie, tenting remains after the skin is pinched between 2 fingers), and perfusion status of the extremities. In the process, it is important that the physician recognize whether shock is present, because this is a life-threatening condition requiring emergent treatment (see Chapter 74 ).

If comparison to an accurate recent pre-illness weight is not possible, the physician must rely on vital signs as well as clinical signs and symptoms to assess the degree of dehydration ( Table 80.2 ). In infants and young children (ie, younger than 5 years), the estimated fluid loss for mild dehydration is less than or equal to 5% deficit of body water; moderate dehydration, 6% to 9%; and severe dehydration, 10% to 15%. The corresponding numbers for estimated fluid loss in children 5 years and older are 3%, 6%, and 9%, respectively. A variety of clinical signs have been proposed to evaluate the degree of dehydration—some more valid and reliable than others. A systematic review found that assessment of capillary refill was the most useful single sign in detecting dehydration of 5% or more. Capillary refill is assessed by placing brief pressure on the distal palmar aspect of a fingertip and assessing the amount of time for the blanched area to refill; normal is considered less than or equal to 2 seconds. Two other single signs found to be important in predicting dehydration of 3% to 5% or more were abnormal skin turgor (ie, tenting) and respiratory disturbance, in particular hyperpnea (ie, deep, rapid breathing without other signs of respiratory distress) suggestive of acidosis. Generally, the more signs that are present, the greater the severity of dehydration; however, a combination of prolonged capillary refill, absent tears dry mucosal membranes, and general ill appearance may be more diagnostic than tenting and hyperpnea combined in identifying the child with more than mild to moderate dehydration.

Clinical Assessment of Magnitude of Dehydration

Abbreviations: ++, certain to occur; +, likely to occur; ±, may occur.

In mild dehydration, may be only a history of fluid loss in the form of diarrhea or vomiting without any of the signs of dehydration listed in this table.

Often, such patients present with hypovolemic shock, need more intense treatment, and may require additional volume expanders (eg, colloids, blood products).

Usually corrects with restoration of intravascular volume.

Laboratory tests typically are not indicated in the child who presents with mild dehydration. The dehydrated child who is treated with IV fluids after a failed attempt at oral rehydration either at home or in the emergency department should undergo initial assessment of serum electrolyte, blood urea nitrogen, and creatinine levels. Initial and serial measurements of these values also should be performed during rehydration in the child with shock, severe dehydration, or decreased urine output who does not improve after initial restoration of intravascular volume; with a history and clinical findings inconsistent with straightforward isotonic dehydration; or who is found to have dysnatremia (ie, serum sodium outside the normal range of 135–145 mEq/L, whether too low or too high). Dehydration in association with dysnatremia can have serious complications, and treatment requires special considerations. Hemolytic uremic syndrome, although uncommon, should be considered in any child with gastroenteritis, particularly with a history of grossly bloody stool, who also has decreased urine output.

Very ill children may require an arterial blood gas measurement to more accurately assess their acid-base status; in others, assessing serum electrolyte levels is sufficient. The usual acid-base derangement in the moderately dehydrated child is a non-anion gap acidosis with decreased serum bicarbonate and hyperchloremia resulting from bicarbonate losses in the stool. Additionally, the severely dehydrated child also may exhibit anion gap acidosis resulting from lactic acid or ketone accumulation in the peripheral tissues secondary to the decreased perfusion that accompanies hypovolemia. The exception is in infants with pyloric stenosis, who typically develop a hypokalemic, hypochloremic metabolic alkalosis.

Imaging studies, such as chest radiography, abdominal ultrasonography, and computed tomography, are indicated based on the suspected etiology of the dehydration.

Fluid management of the dehydrated child involves consideration of 3 components: normal maintenance, deficit replacement, and the ongoing losses of fluid and electrolytes incurred during the present illness. Most commonly, ongoing losses result from continued vomiting and diarrhea. Losses from diarrhea can be estimated at 10 mL/ kg per stool and for vomiting at 5 mL/kg per episode. Other forms of ongoing losses that occasionally must be considered and replaced include those associated with burns, gastric secretion suctioned via nasogastric tube, hyperventilation, or prolonged fever. The estimation of the child’s fluid and electrolyte needs and losses are almost always an approximation and require close follow-up, reassessment, and readjustment throughout treatment. At the very least, monitoring during treatment for dehydration requires regular assessment of vital signs, body weight, intake, and output.

Fluid given to the dehydrated child may be provided enterally or parenterally. Whenever possible, oral replacement therapy using oral rehydration solution (ORS) is preferred for the child with mild dehydration and for most children with moderate dehydration. Parenteral fluid therapy should be used in the child with more severe dehydration, in the setting of failure of oral therapy (eg, resulting from intractable vomiting or lethargy) despite an adequate trial, in the child in shock or impending shock, or in the child with a suspected anatomic defect, such as pyloric stenosis or ileus.

The parenteral management of moderate or severe dehydration can be divided into 2 phases: an initial phase (first 1–2 hours) and the main phase of rehydration. The aim of the initial phase is to restore intravascular volume, thus improving perfusion and renal function and reversing tissue hypoxia, metabolic acidosis, and increased AVP. Regardless of the type of dehydration (ie, isotonic, hypertonic, hypotonic), NS (0.9% NaCl) at 20 mL/kg per hour generally provides the most rapid and effective means of expanding the intravascular volume at acute presentation. If shock is present or imminent, treatment is more aggressive (see Chapter 74 ). The child should in rapid succession receive 2 to 4 boluses of 20 mL/kg of NS given over 20 to 30 minutes each. After each bolus, the child should be reassessed, and if signs and symptoms of intravascular depletion persist, the next IV bolus of 20 mL/kg of NS should be given over 20 to 30 minutes and the child admitted to the hospital for further careful evaluation, including assessment for other causes of shock (eg, sepsis). Rapid restoration of ECF volume with up to 4 boluses of NS, if necessary, in the first 4 hours is currently recommended. The physician must take care not to give excessive fluids to a child with cardiac compromise, because doing so could precipitate congestive heart failure. Administration of excess fluids also results in decreased AVP/antidiuretic hormone levels and the chances of hyponatremia in subsequent therapy even if 0.45% NaCl (0.5 NS) solutions are used rather than NS to correct the remaining deficit and maintenance therapy. The validity of rapid restoration of ECF volume with up to 4 boluses of NS, however, has not been substantiated compared with the past standard rehydration therapy in which typically only 1 or 2 boluses were used. All ORT fluids generally use hypotonic containing sodium concentrations of 45 to 75 mEq/L.

During the second phase of rehydration, the remaining fluid and electrolyte deficits are replaced based on the magnitude of these losses. These replacements are in addition to the daily maintenance requirements as well as any ongoing losses, as discussed previously, but must take into consideration the NS boluses administered during the initial phase, which may have already restored a substantial portion of the total fluid deficit. Each 20 mL/kg fluid bolus corrects 2% dehydration. Thus, in the child with moderate dehydration use of 3 boluses of 20 mL/kg of NS would correct 6% dehydration, with the result that the child may no longer have any remaining fluid deficit. Various protocols exist to restore fluid and electrolyte deficits, and approaches to treatment of dehydration vary by institution. Many of the differences in rehydration strategies lie in the composition of treatment fluid and the rate at which it is administered. Some physicians prefer to administer one-half of the total fluid needs over the first 8 hours and the remainder over the next 16 hours, whereas other physicians prefer to replace the fluid at the same rate over the entire rehydration period. The latter method is presented in the case resolution at the end of the chapter. Usually the fluid deficit is replaced within 24 hours, although noteworthy exceptions exist. The management of dehydration associated with dysnatremia (ie, abnormally low or high serum Na + ) should entail slower return (12 mEq serum Na + change per 24 hours or 0.5 mEq change per hour) to a normal range and may require 48 to 72 hours for correction.

Sodium replacement in the child with dehydration depends on the type of dehydration. In the management of isotonic dehydration, some physicians elect to replace the entire fluid deficit with NS, whereas others use a saline solution containing 110 mEq Na + /L, and still others use 0.5 NS (77 mEq Na + /L). We recommend NS (154 mEq Na + /L) to replace the fluid deficit (see Case Resolution for example). This amount of sodium is somewhat more than the actual loss of sodium to the environment, which is closer to 110 mEq Na + /L, because during isotonic dehydration some sodium lost from the ECF is shifted intracellularly to balance potassium losses and thus returns to the ECF during rehydration. To calculate the ongoing losses, although the content of excreted body fluids can be analyzed for electrolyte content for more exact replacement, the diarrheal stools are commonly replaced with 0.5 NS at 10 mL/kg per stool. (This amount should be adequate in sodium content for most patients because diarrhea secondary to rotavirus contains approximately 30–40 mEq Na + /L and enterotoxigenic Escherichia coli , 50–60 mEq/L; however, sodium stool losses in cholera are 90–120 mEq/L.)

Hypernatremia and Hyponatremia

In hypernatremic/hypertonic dehydration, the patient is considered to have a relative free water deficit but usually has lost not only body water but also some sodium. The amount of free water required to restore serum sodium to normal (eg, 145 mEq/L is desired serum Na + ) is calculated as follows:

For serum sodium greater than 170 mEq/L, 3 mL/kg of free water is estimated to decrease the sodium to the desired level, in which case the 4 mL/kg shown in the equation is changed to 3 mL/kg. The quantity of free water provided by this equation is only part of the patient’s total needs. The remainder of the patient’s fluid needs include isotonic losses that occurred during the dehydration process, ongoing losses, and maintenance fluids as well. Hypertonic dehydration is corrected slowly to avoid cerebral edema, which can result in brain stem herniation and death. In hypernatremia, the various equations used for phase 2 of therapy often calculate the sodium concentration of the final solution considering the amount of free water to achieve isotonicity. We recommend initially providing 0.9% NaCl in 5% dextrose (a higher content of sodium than calculated by various equations) to ensure a slow rate of serum sodium decline and later decreasing the sodium concentration to 0.45% NaCl if the serum Na level remains high 24 to 48 hours after this treatment is begun. Serial monitoring of electrolytes at least every 6 hours and as necessary is important to ensure that the sodium level is decreasing at the expected slow rate and is not decreasing so quickly as to result in life-threatening CNS complications.

Management of hyponatremia/hypotonic dehydration also poses challenges. In addition to isotonic losses, additional sodium loss may have occurred. The amount of additional sodium (in mEq) to correct the serum sodium into a normal range (desired Na + level [eg, 135 mEq/L]) historically has been calculated using the following equation (where 0.6 represents the body space affected by Na + changes):

This amount of sodium represents an additional need beyond a patient’s isotonic losses, ongoing losses, and maintenance requirements. Although precise calculations of sodium requirement to manage hypotonic dehydration may be desirable, in most patients with hyponatremia treatment with NS (0.9% NaCl) in 5% dextrose is adequate for gradual correction of the hyponatremia. The use of hypertonic saline (3% containing 513 mEq Na + /L) is generally reserved for the child with symptomatic hyponatremia (eg, a child who is seizing) or in the setting of serum Na level of less than 120 mEq/L. Hypertonic saline is administered as 3.0 mL/kg of 3% saline given by IV over 15 to 30 minutes or until seizures stop. This volume of 3% saline raises the serum sodium approximately 2.5 mEq/L. Based on a volume of 3.0 mL/kg of 3% saline, the child should receive volume sufficient to bring up the serum Na level to above 120 mEq/L, which is considered to be the safe level, at which improvement in serious signs and symptoms are anticipated. Recalculation is done 4 hours after the initial 3% NaCl infusion to determine the need for another infusion, if the level is still low or if there is no improvement in CNS-related symptoms. After a level of greater than 120 mEq/L is achieved or the patient is asymptomatic, any remaining deficit is corrected more slowly to avoid exceeding an increase of 12 mEq/L per 24 hours. A too rapid correction of serum sodium, particularly in the setting of long-standing hyponatremia, can potentially cause central pontine demyelination, manifested by disorientation and eventual coma.

As stated previously, hyponatremia in the hospitalized child can result from factors other than sodium loss. Arginine vasopressin release in response to hypovolemia, hypertonicity, or other stimuli followed by free water retention can result in dilutional hyponatremia (ie, water intoxication). Hyponatremia in infants given excessively diluted baby formula results from inadequate sodium intake and free water retention. Encephalopathy, brain stem herniation, and death occurring in hospitalized children with hyponatremia have been reported. The adverse effects of hyponatremia on the CNS are accentuated in the setting of hypoxemia. With rehydration and sodium administration, kidneys excrete relatively more dilute urine that can sometimes result in rapid and unpredictable increases in serum sodium levels, necessitating close monitoring of serum electrolyte levels. Consultation with a pediatric nephrologist or pediatric intensivist experienced in managing alterations in fluid and electrolyte balance is helpful.

Potassium Replacement

Potassium deficits are more difficult to determine, and no specific method exists for calculating the exact amount of potassium required by a dehydrated child. Additionally, as the acidosis that commonly accompanies moderate and severe dehydration corrects, potassium shifts intracellularly. What initially seems to be a normal serum potassium may fall into the hypokalemic zone, potentially resulting in adverse effects on neuromuscular and cardiac function. Frequent reassessment of serum potassium and adjustment of potassium content of the IV fluids may be necessary. Generally, after adequate urine output has been established, potassium may be added to the IV fluids to provide 3 to 4 mEq/kg per 24 hours. Usually, this need can be met by adding potassium chloride 20 mEq/L to the IV fluids. The child with decreased urine output or another indicator of renal impairment should not receive potassium until normal urine output has been restored. Hyperkalemia, which is a serious and life-threatening condition, may occur if a child is unable to excrete excess potassium via the kidney because of renal impairment.

Oral Rehydration

Oral rehydration therapy refers to specially prepared, balanced preparations of carbohydrates and electrolytes meant for oral consumption. Clinical trials have repeatedly shown ORT to be as efficacious as IV therapy in the treatment of the child with mild or moderate dehydration. Additional advantages of ORT over IV therapy are that it costs less, is noninvasive, and requires little technology. Oral rehydration therapy has been credited with the dramatic reduction in death associated with diarrhea in the developing world. In 2002, the World Health Organization and United Nations Children’s Fund announced a new ORS with reduced osmolarity (proportionally lower Na + and glucose concentration) based on several clinical studies demonstrating less vomiting, lower stool output, and reduced need for IV fluids relative to the prior formulation.

In the United States, Pedialyte and generic equivalents are the most widely commercially available products. Flavored solutions and freezer pop preparations of these solutions are available and often are preferred by older children over the unflavored variety. Rice-based oral electrolyte solutions contain rice syrup solids as their source of carbohydrates. Electrolyte solutions with rice syrup solids may reduce stool output as well as replete fluid volume. It is not necessary to change to ORT in a breastfed child who is tolerating human milk; these children can continue to receive human milk for rehydration, although they may require shorter, more frequent feedings.

The composition of various ORSs is presented in Table 80.3 . The cost of commercially available ORS may be prohibitive for some families. Given the simplicity of the ORS packet in the developing world and commercially available ORS in the developed world, these remain the first choice. Some solutions, such as fruit juices, ORSs, or chicken broth, do not contain the proper balance of sodium and carbohydrate to effectively rehydrate a dehydrated patient; however, these can be used at home for mild cases of diarrhea if the patient still tolerates oral fluids.

Composition of Various Oral Rehydration Solutions

Abbreviation: UNICEF, United Nations Children’s Fund.

These fluids should be avoided because they have very high osmolality that can worsen diarrhea.

The amount of ORT fluid necessary for rehydration can be calculated in much the same fashion as for determining the parenteral fluid requirement for a dehydrated child ( Table 80.4 ). However, most children with mild dehydration can be rehydrated relatively quickly and, in response to thirst, are likely to request the amount of fluid they need. Therefore, a simplified method of determining ORT fluid requirements has been developed ( Table 80.5 ). This quantity of fluid is given over a period of 3 to 4 hours. In the child with ongoing losses, these losses should be replaced as well. Typically, it is not necessary to calculate the quantity of electrolytes that should be provided because these solutions are designed to adequately replace electrolytes in the otherwise healthy child who is dehydrated.

Guidelines for Administration of Oral Solutions to Replace Deficit Over 4 Hours

Reprinted with permission from Powers KS. Dehydration: isonatremic, hyponatremic, and hypernatremic recognition and management. Pediatr Rev . 2015;36(7):274–285.

Treatment With Oral Rehydration Therapy

Abbreviations: ORS, oral rehydration solution; ORT, oral rehydration therapy.

The parent or guardian should receive guidance about the volume (converted into common household measures [eg, 5 mL = 1 teaspoon and 15 mL = 1 tablespoon of water or ORS]) as well as the frequency and duration of ORT to be given at home. Small volumes of 5 to 15 mL administered with a syringe or teaspoon every 2 to 5 minutes are much more likely to be retained by the child who vomits larger volumes. Although this technique is labor intensive, it can be done by the parent or guardian and can deliver 150 to 300 mL/hour. As dehydration is corrected, vomiting often decreases and the child subsequently can tolerate larger volumes. With ORT, the frequency and amount of passing stool often increases during the initial period of treatment. The parent or guardian should be made aware that the primary purpose of ORT is to rehydrate the child, not to stop diarrhea, and that diarrhea will gradually decrease spontaneously. “Gut rest” (limiting oral intake) is not appropriate in most cases, and early refeeding with a return to the usual formula or milk and solids, if appropriate, should be prioritized.

The child with mild or moderate dehydration resulting from a self-limited childhood illness is likely to recover completely when given timely and appropriate rehydration therapy. It is more difficult to predict the prognosis of the child with severe dehydration or significant aberration in electrolyte balance. If managed appropriately, most such children also completely recover; however, despite closely monitored care, some children may experience permanent sequelae or poor outcomes.

The child has moderate dehydration. Based on clinical assessment and weight change since the boy’s last clinic visit, he is approximately 10% dehydrated. He does not show evidence of shock. His laboratory studies show a sodium level of 140 mEq/L, potassium of 3.7 mEq/L, chloride of 112 mEq/L, bicarbonate of 13 mEq/L, blood urea nitrogen of 13 mg/dL, and creatinine of 0.4 mg/dL. His renal status is likely to be adequate because he is urinating, and blood urea nitrogen and creatinine are normal for the patient’s age. The child’s serum sodium is 140 mEq/L, which is in the isotonic range. The serum potassium is 3.7 mEq/L, which is within normal range; however, this level may not accurately reflect this patient’s total body potassium status. The level may decrease substantially as he is rehydrated and acidosis is corrected, indicating total body potassium depletion. His serum bicarbonate is 13 mEq/L, and his anion gap is 15 [140 − (112 + 13)], which is mildly increased and likely related to ketosis or mild lactic acidosis.

The calculation of this child’s fluid and electrolyte needs is as follows, keeping in mind that his pre-illness weight was 12 kg:

Maintenance

Fluid requirement: 1,000 mL for first 10 kg + 100 mL for next 2 kg = 1,100 mL.

Fluid replacement: 10% of the child’s weight has been lost during this episode of dehydration = 1,200 mL deficit.

Ongoing Losses

Additional Fluid: Estimate this child’s ongoing losses at 10 mL/kg for each stool. He had 1 loose stool while in the office, so 120 mL of additional fluid is added.

Sodium: The sodium content of diarrhea is variable; however, it is usually replaced with 0.9% NS.

Total fluid needs: 1,100 mL (maintenance) + 1,200 mL (deficit) + 120 mL (ongoing losses) = 2,420 mL/24 hours.

Electrolyte Needs

Sodium: 0.9% NS is used based on current recommendation.

Potassium: Estimate the child’s maintenance and replacement needs to be 20 mEq K + /1,000 mL fluid provided; this estimate can be modified based on follow-up laboratory values, if necessary.

In the initial phase of therapy, provide NS 40 mL/kg per hour for approximately 2 hours. During this period, the patient’s heart rate normalizes and he urinates. The initial parenteral phase provides 480 mL fluid as NS (0.9% NaCl). This amount of fluid is subtracted from the patient’s total fluid needs. The remaining amount to be provided is 1,940 mL fluid. It is not necessary to prepare a special IV solution; 5% dextrose in 0.9% NS with 20 mEq/L KCl to run at 80 mL per hour is appropriate. As his GI symptoms improve, IV therapy is discontinued and ORT is instituted. The patient tolerates the ORT well and is discharged home.

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Acute Gastroenteritis: Evidence-Based Management of Pediatric Patients

*new* quick search this issue.

For a pediatric patient who presents with acute gastroenteritis, the degree of dehydration can help guide the management and necessary interventions. In this issue, you will learn:

What signs and symptoms indicate a case of acute gastroenteritis and which suggest a more serious illness, how to use various dehydration scales to approximate a patient’s degree of dehydration, when laboratory testing is indicated, and which tests are essential in cases of severe dehydration, how to use antiemetics to increase the chance that oral rehydration will be successful, which solutions are best for oral rehydration of mild-to-moderately dehydrated patients and which are recommended for severely dehydrated patients, alternate methods for rehydration when intravenous access may be difficult, which strains of probiotics should be recommended for reduction of the duration of diarrhea, evidence-based recommendations for diet and fluid intake for patients who are discharged home, case presentations, selected abbreviations, introduction, critical appraisal of the literature.

Viral Pathogens
Bacterial Pathogens
Antibiotics
Pathophysiology
Inflammatory Bowel Disease
Allergic Colitis
Other Diagnoses
Prehospital Care
Physical Examination
Determining the Degree of Dehydration
Laboratory Studies
Stool Studies
Imaging Studies
Dosages and Administration Routes for Ondansetron
Side Effects of Ondansetron
Oral Rehydration
Intravenous Fluid Resuscitation
Dextrose-Containing Fluids
Rapid Versus Standard Rehydration
Bismuth Subsalicylate
Special Populations
Racecadotril
Gelatin Tannate
N-acetylcysteine
Disposition

Risk Management Pitfalls in Management of Pediatric Patients With Gastroenteritis

Time- and Cost-Effective Strategies
Case Conclusions
Clinical Pathway for Management of Pediatric Patients With Suspected Acute Gastroenteritis
Table 1. Differential Diagnosis of Conditions That Cause Vomiting and-or Diarrhea
Table 2. The 4- and 10-Point Gorelick Scale for Dehydration for Children Aged 1 Month to 5 Years
Table 3. Antibiotic Therapy for Bacterial Gastroenteritis

Although most cases of acute gastroenteritis require minimal medical intervention, severe dehydration and hypoglycemia may develop in cases of prolonged vomiting and diarrhea. The mainstay of treatment for mild-to-moderately dehydrated patients with acute gastroenteritis should be oral rehydration solution. Antiemetics allow for improved tolerance of oral rehydration solution, and, when used appropriately, can decrease the need for intravenous fluids and hospitalization. This issue reviews the common etiologies of acute gastroenteritis, discusses more-severe conditions that should be considered in the differential diagnosis, and provides evidence-based recommendations for management of acute gastroenteritis in patients with mild-to-moderate dehydration, severe dehydration, and hypoglycemia.

An 18-month-old girl who is up-to-date on her immunizations and has no prior medical history presents with vomiting and diarrhea for the last 3 days. She initially had multiple episodes of nonbloody, nonbilious emesis that stopped yesterday. On the second day, watery, voluminous diarrhea started. Her parents estimate she has had approximately 20 episodes of diarrhea since yesterday; they cannot quantify urine output because she has had so many episodes of diarrhea. The girl does not have a fever or other symptoms. On examination, she is lying on the stretcher with her eyes closed. The girl weighs 12 kg, and her vital signs are: rectal temperature, 37.6°C (99.7°F); heart rate, 165 beats/min; blood pressure, 90/65 mm Hg; respiratory rate, 22 breaths/min; oxygen saturation, 100% on room air. Although she is crying during the examination, the girl produces no tears. Her lips are dry and her eyes appear sunken. Her abdomen is soft, with no tenderness elicited on palpation. Her capillary refill is 2 seconds. She has watery, yellow-colored stool in her diaper. Should you give this child a dose of ondansetron and attempt oral hydration or does she need intravenous hydration? Do you need to send the stool for culture? Do any laboratory studies need to be performed?

A 2-year-old boy with no past medical history is brought to the ED by his parents. His mother states that his illness started with vomiting, approximately 4 episodes, that has now resolved. He has had 10 episodes of watery, nonbloody stools in the last 2 days. He is drinking well and has appropriate urine output. The boy attends daycare, and several other children at the daycare center have the same symptoms. On examination, he is playing with his toy cars while sitting on the stretcher. His vital signs are within normal limits. He has moist oral mucosa and normal cardiac and lung examinations. His abdomen is soft, with no tenderness elicited. You diagnose him with acute gastroenteritis and inform his parents that they should continue with aggressive oral hydration. The parents ask you whether there is any medication you could prescribe that might stop his diarrhea. They also want to know if there are specific foods he should avoid. As you consider the parents' questions, you think about whether you should prescribe an antidiarrheal agent for this child? Should you recommend that the parents prescribe the traditional BRAT (bananas, rice, applesauce, toast) diet for the next few days? Are probiotics appropriate in this clinical scenario?

Nausea, vomiting, and diarrhea are some of the most common presenting complaints of pediatric patients presenting to the emergency department (ED); and these symptoms may be associated with abdominal pain. The most common discharge diagnosis for children who present with these symptoms is acute gastroenteritis (AGE). AGE is defined as inflammation of the stomach and intestines, typically resulting from viral infection or bacterial toxins. Both vomiting AND diarrhea must be present for the diagnosis of AGE. Most cases of AGE are due to viral pathogens and are usually mild and self-limited, with no need for major medical intervention. Bacterial and parasitic infections are less common, but should be considered in the appropriate clinical context. Antibiotic-associated diarrhea and Clostridium difficile colitis are also possible etiologies of AGE symptoms.

This issue of Pediatric Emergency Medicine Practice discusses various etiologies of AGE, details how to determine the level of a patient's dehydration, and reviews practice guidelines and high-quality studies that can inform the emergency clinician of the most recent and proven treatments for AGE.

A literature search was performed in PubMed using the search terms gastroenteritis, colitis, cows' milk protein allergy, and allergic colitis. Filters included the English language and ages birth to 18 years. No date limits were imposed. Several thousand articles were found, which were screened by title and then abstract. The Cochrane Database of Systematic Reviews and policy statements by the American Academy of Pediatrics (AAP) were also searched. One hundred-seventy articles were reviewed in full, and 119 were ultimately selected for inclusion.

There are many randomized controlled trials related to pediatric AGE. The most common topics include the use of antiemetics, the ideal intravenous (IV) fluid for resuscitation, and the utility of probiotics. While many of these studies come to similar conclusions about the utility of various treatments, several involve relatively few subjects. The most recent practice guidelines published by the AAP are over 20 years old, 1 but more recent studies exist. The studies by Roslund et al and Ramsook et al are robust randomized trials of oral ondansetron use in AGE. 2,3 Articles evaluating probiotic use were also reviewed, such as Dinleyici et al 4 and Van Niel et al, 5 that evaluate Saccharomyces and Lactobacillus therapy for diarrhea, respectively. There is also a recent guideline for the treatment of AGE in children that was developed and published in 2014 by the European Society for Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) and the European Society for Pediatric Infectious Diseases. 6 These recommendations were also endorsed by the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition.

3. “I didn’t find out that the patient had hypoglycemia until the electrolyte panel came back.”

If you are starting IV hydration in a child that you suspect has severe dehydration, point-of-care glucose testing should be performed rather than waiting for the formal metabolic panel. Young children have low glucose reserves and can easily develop hypoglycemia when they are dehydrated. Hypoglycemia should be treated promptly.

5. “The child was slightly tachycardic but had no other signs of dehydration on examination and had only been sick for a few hours. It was late at night and the child was sleeping, so we gave IV fluids immediately.”

Almost all children with mild-to-moderate dehydration due to AGE can rehydrate via the enteral route. IV placement is painful, IV fluids are more expensive, and the complication rate is higher than from enteral rehydration.

9. “She had been vomiting for the last 3 days. I just assumed that she had the AGE that everyone else was coming in with lately. It turns out she had acute pancreatitis.”

Most cases of vomiting alone will be early AGE; however, there are many other serious entities that will also cause vomiting. Prolonged vomiting without diarrhea is concerning. Look carefully for signs and symptoms that might suggest other diagnoses, such as severe abdominal pain, jaundice, polyuria/polydipsia, bilious emesis, abdominal distension, etc.

gastroenteritis - Acute Gastroenteritis - dehydration - inflammatory bowel disease - pediatric - Table 1. Differential Diagnosis of Conditions That Cause Vomiting and-or Diarrhea

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study is included in bold type following the references, where available. The most informative references cited in this paper, as determined by the author, are noted by an asterisk (*) next to the number of the reference.

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KeriAnne Brady, MD, FAAP

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Landon A. Jones, MD; Alexander Toledo, DO, PharmD, FAAEM, FAAP

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February 2, 2018

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World J Clin Cases
v.8(20); 2020 Oct 26

Dehydrated patient without clinically evident cause: A case report

Federica palladino.

Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy

Maria Cristina Fedele

Marianna casertano, laura liguori, tiziana esposito, stefano guarino, emanuele miraglia del giudice, pierluigi marzuillo.

Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy. [email protected]

Corresponding author: Pierluigi Marzuillo, MD, PhD, Assistant Professor, Doctor, Postdoc, Postdoctoral Fellow, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Via Luigi De Crecchio 2, Naples 80138, Italy. [email protected]

Patients affected by cystic fibrosis can present with metabolic alkalosis such as Bartter’s syndrome. In this case report we want to underline this differential diagnosis and we aimed focusing on the suspect of cystic fibrosis, also in case of a negative newborn screening.

CASE SUMMARY

In a hot August –with a mean environmental temperature of 36 °C– an 8-mo-old female patient presented with severe dehydration complicated by hypokalemic metabolic alkalosis, in absence of fever, diarrhea and vomiting. Differential diagnosis between cystic fibrosis and tubulopathies causing metabolic alkalosis (Bartter’s Syndrome) was considered. We started intravenous rehydration with subsequent improvement of clinical conditions and serum electrolytes normalization. We diagnosed a mild form of cystic fibrosis (heterozygous mutations: G126D and F508del in the cystic fibrosis transmembrane conductance regulator gene). The trigger factor of this condition had been heat exposure.

When facing a patient with hypokalemic metabolic alkalosis, cystic fibrosis presenting with Pseudo-Bartter’s syndrome should be considered in the differential diagnosis, even if the newborn screening was negative.

Core Tip: We report a case of cystic fibrosis presenting with hypokalemic metabolic alkalosis caused by dehydration after heat exposure. We diagnosed a mild form of cystic fibrosis. In particular we wanted focusing on differential diagnosis between cystic fibrosis and Bartter’s Syndrome. We want to highlight that atypical forms of cystic fibrosis could escape to neonatal screening and prompt diagnosis is important for prognosis.

INTRODUCTION

Cystic fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator ( CFTR ) gene on chromosome 7. CF is complex and greatly variable in clinical expression[ 1 ]. Airways, pancreas, male genital system, intestine, liver, bone, and kidney are involved. CFTR -related disorders are conditions determined by mutations in the CFTR gene but not giving the usual CF clinical picture. They are often mild form of CF and their clinical manifestations are limited to a single district and include episodes of recurrent pancreatitis or isolated bilateral bronchiectasis. Males can manifest bilateral agenesis of the vas deferens with no digestive or respiratory involvement[ 2 ]. Both CF and CFTR -related disorders can present metabolic alkalosis, such Bartter’s syndrome (BS).

In this case report we want to underline differential diagnosis between cystic fibrosis and tubulopathies causing metabolic alkalosis (such as BS). Moreover, we aimed focusing on the possibility of suspect diagnosis of cystic fibrosis, nevertheless a negative newborn screening.

CASE PRESENTATION

Chief complaints.

In a hot August –with a mean environmental temperature of 36 °C– an 8-mo-old female patient come to our observation because of somnolence and reduced response to stimuli.

History of present illness

Weight loss in the last 7 d and low-quantity micturition in the last 24 h were reported.

History of past illness

In the first months of life the patient presented three episodes of upper respiratory tract infections.

Personal and family history

Neonatal screening for cystic fibrosis, hypothyroidism, and phenylketonuria were normal. She was assuming about 400 mL/d of milk. With the exception of 400 IU/d of Vitamin D, no other medications were administered.

Physical examination

She showed slightly dry mucous membranes, tachycardia (140 beats/min) and refill time of about 2 s. Fever was absent as such as vomiting or diarrhea.

Laboratory examinations

Urinalysis did not reveal any abnormality. Serum chemistry was as follows: Venous pH 7.5, bicarbonate 35.1 mmol/L, sodium 135 mEq/L, potassium 2.6 mEq/L, chloride 86 mEq/L, creatinine 0.31 mg/dL, calcium 10.7 mg/dL, phosphorous 4.3 mg/dL, magnesium 2.2 mEq/L. Aspartate and alanine aminotransferase, γ-Glutamyl-transferase, glycaemia, bilirubin, erythrocyte sedimentation rate, C-reactive protein, procalcitonin, alkaline phosphatase and complete blood count were within normal limits. Urinary calcium/creatinine ratio was 0.02 mg/mg, fractional excretion of sodium (FeNa) 0.7%. Electrocardiography was normal.

After 36 h of treatment, clinical conditions of the patient and serum electrolytes improved. Venous pH was 7.44, HCO3- 25.5 mmol/L, Na 142 mEq/L, K 4.5 mEq/L, CL 105 mEq/L.

We submitted our patient to sweat test when she became well hydrated with normal acid-base and electrolyte balance. The sweat test showed NaCl in the sweat of 100 mmol/L (normal value < 60 mmol/L). High sweat NaCl values were confirmed at the following sweat test after 2 d (sweat NaCl 87 mmol/L). So, we performed genetics analysis for cystic fibrosis. Molecular diagnosis showed the following heterozygous mutations: G126D and F508del in the gene CFTR (Figure (Figure1). 1 ). This genotype has been described as cause of mild cases of cystic fibrosis or of atypical forms (better known as CFTR -related disorders)[ 3 ].

An external file that holds a picture, illustration, etc.
Object name is WJCC-8-4838-g001.jpg

Molecular diagnosis showed the following heterozygous mutations: G126D and F508del in the gene CFTR . A: Locus of cystic fibrosis transmembrane conductance regulator gene on Chromosome 7q31.2. The figure was created and modified by DECIPHER: Database of Chromosomal Imbalance and Phenotype in Humans using Ensembi Resources; B: Graphic view of cystic fibrosis transmembrane conductance regulator with pathogenic variants of our patient.

Imaging examinations

Abdomen ultrasonography was normal.

FINAL DIAGNOSIS

Hypokalemic metabolic alkalosis due to cystic fibrosis presenting with Pseudo-Bartter syndrome.

When patient was admitted intravenous rehydration with a solution containing NaCl 0.9% and glucose 2.5% with the addition of KCL 40 mEq/m 2 per day was started. When dehydration status and hypokalemic metabolic alkalosis was resolved this infusion was stopped.

OUTCOME AND FOLLOW-UP

Gene mutation analysis identified two heterozygous mutations of the CFTR gene: G126D and F508del. This genotype has been described as cause of mild cases of cystic fibrosis or of atypical forms (better known as CFTR -related disorders)[ 3 ].

The variable phenotype of patient affected by CFTR- Related disorders makes very complicated the genetic counseling. A regular clinical evaluation is necessary because CF symptoms may appear later[ 1 ]. She will undergo follow up visits at 3, 6, 12 mo after the diagnosis and yearly thereafter, because the atypical form (or CFTR -related disorders) could get worse over time. Proper immunization and influenza vaccination were recommended[ 4 ].

The main causes of metabolic alkalosis are shown in the Table Table1 1 [ 5 - 8 ]. Our patient had no signs of gastro-intestinal losses neither assumed any drug or too much calcium and absorbable alkali. Therefore, possible causes were or skin (due to cystic fibrosis) or renal (due mainly to BS) losses. However, our patient recovered too promptly compared with a dehydrated patient with BS[ 9 , 10 ]. Moreover, FeNa was < 1% demonstrating extra-renal losses of sodium (Table (Table2 2 )[ 11 ] and increasing the suspect of cystic fibrosis. In the cystic fibrosis, just chloride depletion (in our case through sweating) is the main cause of electrolyte abnormalities. Physical activity, fever, and heat exposure can determinate an excessive sweat production that causes an extracellular fluid volume and chloride depletion.

Main causes of metabolic alkalosis (modified from references[ 5 - 8 ])

11β-HSDH: 11β-hydroxysteroid-dehydrogenase.

Bartter’s syndrome and cystic fibrosis: Differential diagnosis (modified from references[ 9 - 18 ])

ABE: Acid-Basic Equilibria; FeNa + u : Urinary Fractional excretion of sodium; Na + pl : Plasmatic Sodium; Cl - pl : Plasmatic Chloride; Cl - u : Urinary Chloride.

The extracellular fluid volume depletion leads to a release of antidiuretic hormone with subsequent sodium reduction, and activation of renin-aldosterone system with potassium reduction. Moreover, chloride depletion causes increased renal bicarbonate reabsorption. This mechanism is regulated by a chloride–bicarbonate exchanger (pendrin) located on the intercalated cells, sited in cortical collected duct. When chloride depletion occurs, HCO 3 - secretion is inhibited by insufficient Cl - for anion exchange. In addition, pendrin is reduced in case of potassium depletion. All these mechanisms determine hypokalemic metabolic alkalosis. According to these pathophysiological mechanisms, chloride supplementation, more than sodium and potassium supplementation, is needed to correct the metabolic alkalosis state. The presence of chloride, in fact, increases pendrin activity, with bicarbonate secretion in the lumen of collected duct[ 12 , 13 ].

This kind of clinical and laboratory presentation of CF (known as Pseudo-BS)[ 14 - 18 ], usually, involves children < 2.5 years and is the presenting clinical picture of CF. Episode of vomiting, excessive sweating, heat exposure, fever or respiratory infection could cause a Pseudo-BS, in case of an underlining CF[ 15 , 18 ]. In our case, with the exception of heat exposure, there were no other reasons justifying the dehydration (gastrointestinal fluid losses with diarrhea and/or vomiting, reduction of salt and fluid intake and/or absorption, excessive sweat production for physical activity or fever).

For this reason, we performed sweat test in the suspect of cystic fibrosis. Sweat test is the gold standard to diagnose classical or atypical forms of CF[ 19 ]. In fact, even with over 1000 mutations in the CFTR gene on chromosome 7 are known and it is possible to find children with cystic fibrosis which do not present identifiable gene mutations[ 20 ]. Nevertheless, some mutations could show atypical and very mild clinical manifestations[ 1 ]. In these cases, sweat test results can be intermediate or negative (2%) and so other diagnostic tests are indicated, if clinical manifestations persist ( i.e ., genetic CFTR tests, CFTR functional tests, such as nasal potential difference, intestinal current measurement)[ 21 , 22 ]. Moreover, it is possible that these patients passed the new-born screening because their sufficient pancreatic status[ 21 - 24 ]. So, clinicians must not exclude, a priori, the suspicious of CF in patients with 1 or more clinical manifestations of CF, despite of negative newborn screening results[ 25 - 27 ].

In conclusion, with this case presentation we would highlight that the Pseudo-Bartter’s syndrome could be an initial clinical presentation of cystic fibrosis, and that the heat exposure might be a trigger of this condition. When facing a Pseudo-Bartter’s syndrome, cystic fibrosis should not be excluded from differential diagnosis, even if the new-born screening was negative.

Informed consent statement: Informed written consent was obtained from the patient for publication of this reporting.

Conflict-of-interest statement: The authors declare that they have no conflict of interest.

CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).

Manuscript source: Invited manuscript

Peer-review started: April 10, 2020

First decision: September 14, 2020

Article in press: September 26, 2020

Specialty type: Medicine, research and experimental

Country/Territory of origin: Italy

Peer-review report’s scientific quality classification

Grade A (Excellent): 0

Grade B (Very good): B

Grade C (Good): C, C

Grade D (Fair): 0

Grade E (Poor): 0

P-Reviewer: Pandey A, Yang L S-Editor: Zhang L L-Editor: A P-Editor: Li JH

Contributor Information

Federica Palladino, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Maria Cristina Fedele, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Marianna Casertano, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Laura Liguori, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Tiziana Esposito, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Stefano Guarino, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Emanuele Miraglia del Giudice, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy.

Pierluigi Marzuillo, Department of Woman, Child and of General and Specialized Surgery, Università degli Studi della Campania “Luigi Vanvitelli”, Naples 80138, Italy. [email protected] .

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