The Association of Pediatric Gastroenterology and Nutrition Nurses
Help & Hope for Children with Digestive Disorders GIKids
Journal of Pediatric Gastroenterology and Nutrition Journal of Pediatric Gastroenterology and Nutrition

Acute and Chronic Diarrhea

Chapter quoted in part from: 
Bentley D, Lifschitz C, Lawson M. Pediatric Gastroenterology and Clinical Nutrition. 2001. 
ReMedica Publishing, London U.K. with permission.

"Too much stress can be put on poverty as a prime cause of diseases and malnutrition, but poverty of knowledge and initiative is, in nearly very case, as important as poverty of material possessions."    Williams and Jelliffe, 1972

Acute diarrhea

At the end of the 19th century, the mortality caused by dehydration from diarrhea among hospitalized infants worldwide was in the order of 80%. Now, in the USA, within the population under the age of 3 years, the overall incidence of acute diarrhea is about 1.3 episodes per child per year, but among children who attend day care the rate is almost double. Diarrhea accounts for approximately 9% of all hospitalizations of children under the age of 5 years, and almost 300 children die each year as a consequence of dehydration from diarrhea. Principally affected are premature infants; children of adolescent mothers; children of mothers who have received inadequate prenatal care; and children of mothers who are poor and/or belong to minority groups. The combined cost of inpatient and outpatient care for pediatric diarrhea is greater than US$2 billion per year.

Most of the acute diarrheal episodes in children are caused by rotavirus and are malabsorptive (impaired dietary carbohydrate absorption) and characterized by the following:

  • Diarrhea stops when enteral nutrition is discontinued 

  • Stools may demonstrate presence of carbohydrate (positive response to reducing substances or presence of glucose)

  • Fecal pH is £5.5 

  • Stool sodium concentration is <60mmol/l

  • Stool volume is <20 ml/kg.day.

In cases of severe carbohydrate malabsorption, continuation of feedings with high amounts of carbohydrate can lead to hypertonic diarrhea.

Management

Historical perspective

In 1935, Darrow and Yannet [1] demonstrated that hypotonicity and cell swelling are the result of a deficit in sodium chloride, which creates a relative excess of water, while the converse produces hypertonicity and a loss of cell water. In the following years, determination of serum sodium levels became more readily available and hyponatremia and hypernatremia were noted as frequent complications of diarrheal dehydration. One factor in clinical practice that contributed to the occurrence of hyponatremia was the low concentration of the sodium solutions used in the replacement therapy for dehydration from diarrhea. To correct hyponatremia, oral solutions containing an excess of salt and/or sugar were developed, but the use of these resulted in an increase in the incidence of hypernatremia, which is associated with brain injury. Excessively rapid correction of hypernatremia causes convulsions. The recommended treatment, using the deficit therapy model, was to infuse a hypotonic solution calculated to correct the hypernatremia over 48-72 hours. These calculations for correction of hyponatremia and hypernatremia added complexity to the deficit therapy regimen.

The first report of success using oral rehydration therapy (ORT) to treat dehydration in infants with diarrhea came from Hirschhorn and colleagues in 1973 [2]. By 1980, the experience was that 90% of infants with dehydration successfully recovered with ORT without the need for intravenous therapy [3]. In 1996, a meta-analysis of data from published randomized, controlled trials in which the safety and efficacy of glucose-based ORT were compared with those of intravenous therapy and/or oral rehydration solutions of varying sodium content, found that the combined overall rate of ORT failure was less than 4% [4]. It has been demonstrated in ambulatory children in the USA that oral rehydration solutions containing 90, 50, or 30 mmol/l of sodium can be used safely for the treatment of mild acute diarrhea [5]

The success of ORT suggests that calculating rehydration volumes based on estimated fluid deficit may not be necessary. Today, the recommendation is the aggressive use of ORT, only preceded by intravenous saline when needed.

Current recommendations

The treatment of choice to replace fluid and electrolyte losses is ORT, as it can successfully rehydrate most infants and children at a lower cost and with fewer complications than intravenous therapy. A certain amount of emesis is not a contraindication for attempting to use ORT.

Administration of small volumes (5 ml) on a frequent basis (every 1-2 min) may be successful. The use of a nasogastric tube, including the possibility of a continuous infusion, is another option. The stool number and total volume, duration of diarrhea, and rate of weight gain are similar with both oral and intravenous therapies. Children who are dehydrated rarely refuse ORT, despite its salty flavor (sodium concentration ranges from 45 to 50 mmol/l in the solutions used in developed countries). 

Recommended treatment guidelines for dehydrated children who are between 1 month and 5 years of age, live in developed areas, are well nourished, and have no serious underlying illnesses, are listed in Table 3.1.

All kind of beverages with a high carbohydrate content and electrolytes at non-physiologic concentrations have been used inappropriately to treat children with diarrhea. The use of such drinks can exacerbate the problem, as they have very low electrolyte concentrations and are hypertonic due to their high carbohydrate content.

Laboratory analysis

There is no need to perform quantification of serum electrolytes as a routine, as most diarrheal episodes in well-nourished infants lead to isotonic dehydration. These laboratory tests, however, may be helpful in moderately dehydrated children, particularly those whose histories or physical findings are inconsistent with a pure diarrheal episode, and in all severely dehydrated children [6]

Feeding the child who has diarrhea

The old concept of bowel rest has been completely abandoned for children with uncomplicated acute diarrhea . Many studies have now demonstrated that, once rehydrated, children with diarrhea should receive their usual diet. It has been shown that unrestricted, age-appropriate diets not only do not worsen mild diarrhea but also can result in a lower stool output compared with ORT or intravenous therapy alone [7]. A multicenter study has demonstrated that when treating well-nourished infants, there is no need to delay the reintroduction of nutrients [8]. Early refeeding during diarrhea has been found to shorten the duration of symptoms by 0.43 days, which, although small, is relevant when one considers the benefit of improved nutrition [9]. At present, in well- nourished infants in the developed world, carbohydrate malabsorption rarely follows rotavirus illness [10]

        Brown et al. [11] performed a meta-analysis to compare the effects of continued feeding of lactose-containing versus lactose-free regimens to young children during acute diarrhea. The results suggested that children with mild or no dehydration and those who are managed according to appropriate treatment protocols, such as that promoted by the WHO, can be treated as successfully with lactose-containing diets as with those lacking lactose. The conclusion of this and many other published studies is that the majority of young children with acute diarrhea can be successfully managed with continued feeding of undiluted non-human milks. Routine dilution of milk and use of a lactose-free milk formula are therefore not necessary, especially when ORT and early feeding (in addition to milk) form the basic approach to the clinical management of diarrhea in infants and children. Early introduction of age- appropriate foods is also recommended [12,13]

Vaccine and medications 

After exhaustive international trials, RotaShield, an oral tetravalent rotavirus vaccine, was introduced in 1998. The Advisory Committee on Immunization Practices (ACIP) recommended infants in the USA routinely receive three doses, at 2, 4, and 6 months, respectively. However, almost 1 year after the vaccine was licensed and 1.5 million doses had been administered, the CDC postponed the program because of an association with intussusception, and the product was withdrawn. Notwithstanding, it is estimated that in Africa, Asia, South America, three million children die annually because of diarrhea, 600,000 to 800,000 of which cases are caused by rotavirus. The vaccine would have prevented 80% of these deaths. Hence, if a new vaccine takes 3-5 years to develop, the wait will have caused 1.4 to 3.2 million preventable deaths in these territories [14,15]. Although some studies have demonstrated beneficial effects of certain medications for the management of acute diarrhea in children, the American Academy of Pediatrics - in common with other academic bodies - does not recommend the routine use of antiemetics, antiperistaltics, or antisecretories. One of the drugs found to be beneficial in the treatment of acute diarrhea, when used in conjunction with ORT, is loperamide [16]. However, many studies have reported a high incidence of side effects associated with this agent, such as ileus, lethargy, respiratory depression, coma, and even death, especially in infants [17]. Use of bismuth subsalicylate in children, every 4 hr for 5 days, has been associated with a (modest) decrease in the duration of diarrhea and frequency of loose stools [18]. It should be remembered, however, that salicylate can be absorbed and result in toxicity. The supplementation of infant formula with Bifidobacterium bifidum and Streptococcus thermophilus has been shown to reduce the incidence of acute diarrhea and rotavirus shedding, a factor of relevance in hospitalized infants. Several studies in young children have demonstrated that administration of lactobacillus GG can reduce the duration of diarrhea caused by rotavirus [19,20]

Chronic diarrhea

Diarrhea lasting more than 14 days it is considered to be chronic. Awareness of the causes for chronic diarrhea has resulted in earlier diagnosis and a lower number of consultations. In developed countries, severe, protracted diarrhea has become far less common. Another frequent cause for consultation used to be chronic, non-specific (or toddler) diarrhea, but physicians who treat children have become more familiar with its benign course. Most chronic diarrheas are due to nutrient malabsorption and/or excessive fluid intake rather than secretory (Table 3.2). Most common causes need to be ruled out before performing any complicated investigations. Malabsorptive diarrheas improve dramatically when the child is fasted or given oral rehydration solution alone. Secretory diarrheas persist even when the patient is fasted. In children, the majority of the secretory diarrheas are infectious and are rarely caused by a neuroendocrine tumor.

The etiology of chronic diarrhea varies according to age. Table 3.3 lists the causes of chronic diarrhea seen in various age groups.

Diagnostic tests

Feces

Stools should be examined for the following:

  • pH and presence of reducing substances to characterize carbohydrate malabsorption (normally stool pH is >5.5 and carbohydrate is negative, but the latter may be minimally present in the neonate)

  • Presence of fat globules (seen under the microscope); prolonged (72 hr) fecal collection for quantitation of fat is rarely necessary

  • Occult blood - this may be present in protein-hypersensitive colitis, but a severe diaper rash with skin excoriation can also result in a positive test

  • Parasites - the yield is increased if samples from three bowel movements are collected; however, assay of Giardia antigen is much more sensitive than observation under the microscope and one sample is sufficient

  • Macroscopic evidence of non-digested food - this is not necessarily indicative of malabsorption but is frequently seen in toddler diarrhea.

  • Electrolytes, for the diagnosis of secretory diarrhea - make sure that urine does not contaminate the sample.

Blood 

Blood tests are not very useful in the work-up of chronic diarrhea except as an aid to determine electrolyte balance and specific nutrient deficiencies.

Peripheral eosinophilia is rarely seen in cases of protein-hypersensitive enteritis or colitis.

Urine

Urinary tract infection can be associated with diarrhea in young infants.

Radiologic

Flocculation of barium in the small bowel may be indicative of malabsorption (flocculation caused by excessive amounts of luminal fluid). This phenomenon, however, may be a normal finding in the first year of life.

Contrast studies for the investigation of chronic diarrhea are rarely helpful in infants and children, unless a stricture or inflammatory bowel disease is suspected.

Breath hydrogen test

This is difficult to interpret in infants for the following reasons:

  • Carbohydrate (lactose) malabsorption is normal in the first 6 months of life 

  • Mouth-to-cecum transit time is shorter than in adults, making it difficult to reach conclusions regarding small-bowel bacterial overgrowth

  • Crying children hyperventilate and dilute the hydrogen in the sample, which can result in a falsely negative test.

Use 1 g/kg of the carbohydrate to be tested in a 20% solution.

Carbohydrate malabsorption

Acquired

Up to 10% of well-nourished infants may suffer transient lactose intolerance which can last 10 to 15 days following an episode of acute gastroenteritis [21]. Malnourished infants, those who have experienced an episode of diarrhea in the recent past, and those with a history of severe gastroenteritis are more likely to suffer from lactose malabsorption [22]. Lactose malabsorption can also be seen when the intestinal mucosa is damaged by protein hypersensitivity [23]. Prolonged lactose intolerance can complicate acute gastroenteritis in malnourished infants [24]. In cases of lactose malabsorption, other carbohydrates need to be used. Glucose polymers are digested by glucoamylase and maltase, enzymes that are quite resistant to damage of the intestinal mucosa [25] However, in cases of severe damage to the integrity of the intestinal villi, malabsorption of glucose polymers can also occur.

Diagnosis

Characteristically, diarrhea occurs after feeding formula, mainly if it contains lactose, and improves when the child is kept hydrated with oral rehydrating solution or intravenous fluids. Stools are watery, with an acid pH (< 5.0) and there is presence of reducing substances or glucose.
The breath hydrogen test is difficult to interpret in infants and may have false negatives in acute diarrhea [26]. However, it may help in confirming carbohydrate malabsorption after recovery from diarrhea.

Treatment

As a general rule, "NO bowel rest" is necessary. A formula containing glucose polymers should be used in place of lactose. If the infant has intolerance to glucose polymers consider:

(a) protein hypersensitivity - try a formula with hydrolyzed protein;
(b) administering the formula as a constant intragastric infusion.

If an infant is unable to tolerate formula by constant infusion, initiate parenteral nutrition. Do not administer an insufficient amount of calories (100 kcal/kg body weight in the first 6 to 9 months of life) for more than 2 or 3 days.

The duration of lactose intolerance in chronic diarrhea is difficult to predict, and can extend from 10 days to several months [27,28]. Gradual reintroduction of lactose and monitoring of stools is the best way to determine tolerance. Feeding lactose to a lactose-intolerant child with chronic diarrhea can have adverse effects in his or her nutritional recovery [22]. 

Congenital

Sucrase-isomaltase deficiency

This congenital disaccharidase deficiency, inherited as an autosomal recessive trait, is caused by a complete or almost total lack of sucrase activity, a decrease of maltase to about one-third of normal, and a very marked reduction of isomaltase. Molecular studies have revealed at least three phenotypes:

  • One in which sucrase-isomaltase protein accumulates intracellularly, probably in the endoplasmic reticulum, as a membrane-associated high-mannose precursor

  • One in which the intracellular transport of the enzyme may be blocked in the Golgi apparatus

  • One where catalytically altered enzyme is transported to the cell surface [29]

Probably small mutations in the sucrase-isomaltase gene lead to the synthesis of transport-incompetent or functionally altered enzyme, which results in congenital sucrose intolerance. Symptoms develop following the introduction of cereals or table sugar to the diet.

Diagnosis

Diagnosis can be made by a breath hydrogen test following the ingestion of a sucrose solution. Confirmation requires a small-bowel biopsy and assay for disaccharidases. Histologic features will be normal.

Treatment

Exclude complex starches and sucrose from the diet until the child is older: colonic fermentation of malabsorbed carbohydrate may result in gas and short-chain fatty acid formation but less diarrhea than in an infant. Recently, an enzyme preparation (sacrosidase) has been marketed to produce sucrose hydrolysis in vivo for patients with sucrase-isomaltase deficiency [30] 

Glucose-galactose malabsorption

This rare autosomal recessive disease results from a specific defect in the intestinal Na+/glucose co-transporter (SGLT1). The SGLT1 gene - located on chromosome 22q13.1 - encodes the primary carrier protein responsible for the uptake of dietary glucose and galactose from the intestinal lumen. The 75--kDa glycoprotein is localized in the brush border of the intestinal epithelium and is predicted to comprise 12 membrane spans. In two patients with glucose-galactose malabsorption, the underlying cause was found to be a missense mutation in SGLT1, and the Asp28®  Asn change was demonstrated in vitro to eliminate SGLT1 transport activity [31]. Following the first feeding, infants have profuse diarrhea with evidence of carbohydrate malabsorption (carbohydrate in stools). Initially, fecal pH is not below 5.0 because the fecal flora has not yet developed; thus, there is no colonic fermentation of malabsorbed carbohydrate. Diarrhea rapidly resolves when the infant is fasted and receives intravenous fluids, but recurs after feeding. Fructose is well tolerated.

Treatment

Substitution of fructose for glucose-yielding carbohydrates is the only effective treatment [32]. This can be added to an infant formula that does not contain any carbohydrate (RCF, Ross Carbohydrate-Free, Ross Laboratories, Columbus, OH). In the second or third year of life, as the colonic capacity to ferment carbohydrates is better developed, children can ingest limited amounts of a greater variety of carbohydrates, resulting in formation of gas, but generally not diarrhea.

Congenital lactase deficiency

The existence of this is questioned by some authors. If real, it is an extremely rare condition, characterized by watery acidic stools and the presence of carbohydrate following the ingestion of lactose-containing milk. Symptoms resolve if the infant is fed a lactose-free milk.

Protein hypersensitivity

Diarrhea caused by hypersensitivity to dietary protein may occur primarily in the first month of life, and secondarily in the first 6 months of life, or at any time after an episode of severe gastroenteritis. As a consequence of mucosal damage, there can be blood in the stools and/or carbohydrate malabsorption.

Excessive formula, water, or fruit juice intake 

The capacity of the small bowel to digest carbohydrate, as well as that of both the small and large bowel to absorb water, can be overwhelmed by excessive formula intake and this can result in diarrhea. Excessive fluid intake can also cause diarrhea [33]. Unfortunately, it is not unusual to see children with all-day access to a bottle or a ‘'sippy-cup'’ of juice and achieving daily fluid intakes as high as 2 l. Infants and children have difficulty absorbing volumes larger than 200 ml/kg per day; an excess results in diarrhea. In fact, diarrhea can occur at much lower volumes with certain fruit juices, particularly those which contain a mixture of carbohydrates in a proportion that impairs absorption, such as apple juice [34]

Diagnosis

Detailed questions about dietary intake should be part of the routine history-taking in patients with diarrhea. Stools may have the presence of carbohydrate and an acidic pH, but these may also be normal. Sometimes parents continue to offer the child (excess) fluids to prevent dehydration after an episode of acute diarrhea.

Treatment

Reduce fluids, allowing a milk intake of up to 1 l a day in those aged 18-24 months and 500 ml in older children. Total fluid intake should be no more than 200 ml/kg per day during the first 2 years of life. Juice intake should also be limited [35]
Parents of infants who have diarrhea due to an excessive intake of formula need advice on appropriate feeding practices.

Post-enteritis syndrome and intractable diarrhea

Post-enteritis syndrome is the persistence of diarrhea following an episode of acute gastroenteritis. This is characterized by carbohydrate malabsorption, and there may be a component of protein hypersensitivity [36]. The typical history is that of a previously healthy infant, formula-fed or (less commonly) breastfed, who develops an episode of acute gastroenteritis and, instead of improving over the following 3-7 days, continues with loose, watery, explosive stools, with evidence of carbohydrate malabsorption. Although oral hydration and small amounts of diluted formula may be tolerated, the infant is unable to ingest an appropriate amount of calories and therefore loses weight.
Intractable diarrhea or idiopathic prolonged diarrhea, also known as acquired monosaccharide intolerance [37] is a syndrome whereby the patient has persistent malabsorptive diarrhea with severe villus atrophy and acquired disaccharidase deficiency with complete intolerance to oral or enteral nutrition. It is possible that this is the extreme of post-enteritis syndrome [38,39]. In the developing world, this syndrome is still seen in large numbers, and affects infants after weaning (6-18 months of age). In developed countries, intractable diarrhea was more common among formula-fed than breastfed infants, and occurred predominantly in the first 3 months of life. Nowadays, intractable diarrhea is rarely seen in developed countries, probably as a consequence of one or more of the following therapeutic modalities for acute gastroenteritis: 

  • Oral rehydration

  • Elimination of the "bowel rest" policy (prolonged fasting) recommended in former times for treatment of acute diarrhea

  • Elimination of lactose in cases of persistent diarrhea

  • Use of protein hydrolysates when there is suspicion of protein intolerance. 

The two major groups of intractable diarrhea are due to (1) primary epithelial abnormalities (which usually present within the first few days of life) and (2) immunologically mediated (which generally present after the first few weeks of life.

Diagnosis

There are no specific tests for the diagnosis of post-enteritis syndrome or intractable diarrhea. Suggestive features include:

  • History of acute diarrhea with partial recovery and relapse

  • Diarrhea with evidence of carbohydrate intolerance and inability to feed the infant a sufficient amount of calories to gain weight.

In intractable diarrhea, a flat intestinal mucosa can be seen in the biopsy.

Treatment

Early identification of the problem and change to a formula that can be tolerated, is the only effective approach in the treatment of post-enteritis syndrome. In cases where diarrhea becomes chronic and does not respond to replacement of carbohydrate by a more digestible preparation, or temporary formula dilution, or small, frequent volumes, then protein hypersensitivity should be suspected. Elimination of sensitizing dietary proteins (casein and soy) will be necessary to prevent further inflammation of the small-bowel mucosa and consequent villus damage. For more details, see information above regarding the treatment of carbohydrate malabsorption and protein hypersensitivity. Total intravenous nutrition and complete bowel rest may be necessary in cases of intractable diarrhea.

Infections 

A urinary tract infection can cause chronic diarrhea in young infants.

Viruses

Although viruses do not produce chronic diarrhea, they may be the cause of the initial illness which may subsequently lead to post-enteritis syndrome, or predispose to protein-hypersensitive enteropathy or even intractable diarrhea. Rotavirus is the most common pathogen associated with gastroenteritis [40]. Enteric adenovirus and Norwalk agent may also lead to chronic diarrhea.

Bacteria

The most common organisms that produce diarrhea are [41]:

  • Campylobacter jejuni 

  • Escherichia coli

  • Salmonella enteritidis 

  • Shigella

  • Clostridium difficile.

  • E. coli

In addition to the enterotoxigenic, enteroinvasive, and enterohemorrhagic E. coli, there is an enteroadhesive or pathogenic organism that does not invade the mucosa, but adheres to the brush border and affects its integrity. Children may present with an acute episode of secretory diarrhea from which they do not completely recover, followed by diarrhea with malabsorptive characteristics, and then possibly present with another episode of secretory diarrhea. Progressive malnutrition occurs until an appropriate diagnosis is made and suitable antibiotic treatment instituted.

Salmonella

This causes a colitis with bloody, mucusy stools. Antibiotic treatment of diarrhea caused by S. typhi is only indicated for immunocompromised hosts, including the neonate and those in a toxic state.

Shigella

The diarrhea is bloody and mucusy. Infections by Shigella may lower the tone of the anal sphincter, and rectal prolapse can occur. Shigellosis involves the colon and is a self-limiting disease.

Clostridium difficile

This may be present in the bowel of normal neonates, and between 10% and 50% of asymptomatic infants and young children have C. difficile toxin. By the end of the first year of life, fewer than 5% of these infants excrete the organism and an even smaller number the toxin. The absence of toxin receptors may explain why infants can be asymptomatic.

Parasites

Giardia lamblia (a protozoon) and Cryptosporidium species are among the most common parasites affecting children. In a study performed in Canada [42], it was found that the prevalence of enteric parasites in hospitalized children was 4% (35 of 829) compared with rates of 10% and 13% for children attending the emergency room or other outpatient clinics and the gastroenterology clinic, respectively. G. lamblia was found most often (31%), followed by Dientamoeba fragilis (23%), Entamoeba coli (16%), Blastocystis hominis (13%), Cryptosporidium (8%), Endolimax nana (4%), Enterobius vermicularis (2%), Hymenolepis nana (2%), and Iodamoeba buetschlii (1%). Most children (85%) were colonized/infected with a single parasite. Both Giardia and Cryptosporidium parasites can be found in asymptomatic children, particularly those attending day-care centers. Chronic diarrhea is the commonest symptom caused by these parasites. Excessive burping and/or intestinal gas can be produced by small-bowel bacterial overgrowth associated with the parasite.

Diagnosis

A number of stool samples need to be cultured and analyzed for parasites as well as Giardia antigen before any invasive tests are performed in children with chronic diarrhea, unless the history or other symptoms indicate another problem such as inflammatory bowel disease.

Treatment options

These include:

  • C. jejuni - erythromycin 

  • E. coli - trimethoprim-sulfamethoxazole

  • Salmonella - trimethoprim-sulfamethoxazole, ampicillin, chloramphenicol

  • Shigella - trimethoprim-sulfamethoxazole

  • Giardia - metronidazole, 30 mg/kg/day for 3 days; tinidizole, 30 mg/kg as a single dose; mepacrine, 2 mg/kg three times a day for 7 days; furazolidone, 1.25 mg/kg four times a day for 7 days 

  • Cryptosporidium - parasite numbers and stool volume can be lowered with antibiotics such as erythromycin, spiramycin, and clindamycin.

Cystic fibrosis and other causes of fat malabsorption

Stools are pale-white, malodorous, and shiny. When fat malabsorption is significant, infants have failure to thrive and diarrhea, and may present with clinical evidence of fat-soluble vitamin and essential fatty acid deficiency. Fat malabsorption may be associated with any of the following:

  • Post-enteritis syndrome

  • Cystic fibrosis (see Chapter 8)

  • Celiac disease (put link to celiac disease here) see Chapter 7)

  • Giardiasis in a patient with immunodeficiency (e.g. selective IgA)

  • Intrahepatic or extrahepatic cholestasis

  • Shwachman syndrome (neutropenia, metaphyseal chondrodysplasia, and other features - see Chapter 8)

  • Impaired bile acid synthesis

  • Congenital malabsorption of bile acids

  • Congenital enterokinase deficiency

  • Congenital trypsinogen deficiency.

Cystic fibrosis (see Chapter 8) must be considered as a cause of chronic diarrhea, particularly in the presence of any of the following:

  • History of meconium ileus, peritonitis, or plug

  • Poor weight gain

  • Hyperinflation of lungs, pneumonia

  • Recurrent pulmonary infections.

Diagnosis 

Fat malabsorption can be documented by the presence of fat globules in stools. Confirmation of diagnosis is by sweat test. Sodium values above 70 mmol/l (or mEq/l) are abnormal.

Treatment

Use a formula with medium-chain triglycerides. Protein absorption may be enhanced by use of a formula with hydrolyzed protein. Breastfed infants and those fed a soy-based formula may develop hypoproteinemia.
Pancreatic enzymes are frequently required to optimize lipolysis of dietary fats. The usual dosage of pH-sensitive microspheres is as follows:

  • Infants - 8000 U lipase per 120 ml formula

  • Children - 24,000 U lipase per meal.

Immunodeficiency states

Acquired immunodeficiency (AIDS)

Perinatal transmission of HIV infection can present as failure to thrive with or without diarrhea. The long-term effects are demonstrated in results from a study which showed that a decline in weight occurred in the first 4 months of life, followed by decreased linear growth [43]. In older children, weight and height seem to fall in parallel, but loss of lean body mass may occur prior to a decline in weight [44]. Adequate caloric intake can improve weight gain, but has little effect on height velocity and lean body mass [45]. Long-term survivors with HIV infection are shorter than anticipated, and these changes cannot be explained solely by inadequate nutrition or by endocrine abnormalities [46]. Diffuse lymphoadenopathy, oral candidiasis resistant to therapy, and hepatosplenomegaly are frequently present. Recurrent or intractable diarrhea with malabsorption is common and difficult to manage. Organisms known to produce disease of the gastrointestinal tract are similar to those affecting adult patients with AIDS [47]. Children diagnosed in the first few months of life have worse outcome than those who present with symptoms later.

Treatment 

Children with AIDS suffering from chronic diarrhea may benefit from nutritional supplements delivered by nasogastric tube as a constant infusion. The use of formulas that are lactose- free and contain hydrolyzed protein and medium-chain triglycerides may result in better dietary tolerance.

Congenital immunodeficiency

Congenital immunodeficiency usually becomes symptomatic in infants older than 6 months of age, particularly if they are breastfed, because maternal immunoglobulins will protect them during the first few months of life [43]. The most common immunodeficiencies associated with chronic diarrhea are listed below.

X-linked agammaglobulinemia

Typically, the patient is a male, 6 to 9 months of age, with severe respiratory infection or meningitis, and diarrhea that may or may not be associated with pathogens or bacterial overgrowth.

Selective IgA deficiency

IgA deficiency is the commonest form of primary immune deficiency. Diarrhea and malabsorption due to giardiasis may be present. A number of disorders are associated with reduced or absent IgA, including celiac disease and inflammatory bowel disease.

Severe combined immunodeficiency

The infant presents with major infections, chronic persistent diarrhea, malabsorption, and failure to thrive. The diarrhea may become bloody or mucopurulent.

Lymphangiectasia

Intestinal lymphangiectasia is a rare disorder of the small bowel that impairs lymphatic flow from the intestine. It can be due to a congenital malformation or secondary to cardiovascular anomalies such as constrictive pericarditis or operations (e.g. the Fontan procedure for hypoplastic left heart syndrome), infection, inflammatory bowel disease, or drugs. Primary intestinal lymphangiectasia is associated with hypoalbuminemia, hypogammaglobulinemia (particularly IgG), hypolipidemia, and lymphopenia, with an increased vulnerability to infections. Diarrhea and edema are found frequently. Many of the clinical features are similar to those seen in celiac disease. Lymphangiectasia has been associated with other syndromes. In a study of eight patients, the presenting features were diarrhea (n=6), vomiting (n=4), and growth deficit (n=7) [48]. Additional conditions in these patients included asthma, urinary tract infection, esophageal atresia, hydrops fetalis, inflammatory bowel disease, malabsorption syndrome, and thymic hypoplasia. Hypoalbuminemia and edema (n=4) were more prominent in those patients under 5 years of age. The patients responded variably to hyperalimentation and dietary supplements, depending on the extent of their lymphangiectasia and the age at onset of symptoms. Dilated lymphatics were seen in the small-intestinal mucosa under the surface epithelium. Lesions were often focal, requiring several biopsies or serial sections for detection (see Fig. 9.1). Other common findings were lymphoplasmocytic inflammation and mild-to-moderate villous injury with blunting and edema. Mild inflammation without lymphangiectasia was also present in esophageal, gastric, or colonic biopsies. Thus, diagnosis should be made on the basis of endoscopic findings or in small-intestinal inflammatory conditions even in the absence of a classic clinical picture. Histologic confirmation may require more than one serially sectioned biopsy.

Neuroblastoma

Rarely, neuroblastoma is associated with diarrhea, which is of secretory nature as a result of the vasoactive intestinal peptide produced by tumour cells. Approximately 77% of neuroblastomas occur in children under 5 years of age and 90% under the age of 7. Peak age is between 1 and 3 years. Increased amounts of urinary homovanillic acid and vanillylmandelic acid derived from catecholamine metabolism are found in 75% of patients.

Congenital chloridorrhea

This is a rare autosomal recessive disorder of the chloride transport mechanism which results in secretory diarrhea and alkalosis [49] The condition begins in utero and is lifelong. Treatment has not been successful. Fluid replacement is the mainstay approach. Proton-pump inhibitors have been used [50]

Intestinal villi inclusion disease

This congenital abnormality of the structure of the intestinal mucosa results in chronic secretory and malabsorptive diarrhea [51]

Congenital defective jejunal Na+/H+ exchange

This rare disorder results in secretory diarrhea. It is seen in those between 7 and 23 months of age.

Chronic non-specific diarrhea ("toddler diarrhea") 

The exact cause of this diarrhea is not known, but may be the result of an inability of the colon to handle the fluid load [52]. Typically, the patient is a healthy 11- to 24-month-old whose only problem is the presence of watery and runny stools [48]. By definition, if no dietary restrictions are imposed in an attempt to control the diarrhea, the child continues to gain weight normally. Unfortunately, parents or physicians often discontinue milk, dairy products, and other foods; so, eventually, the child might experience failure to thrive or actual weight loss. In many cases, excessive fluid intake can be identified as a possible cause (see below). In an attempt to prevent dehydration, carers provide even more fluids, creating overhydration-diarrhea, which perpetuates the problem. The child's sleep is not interrupted by the diarrhea, and dehydration does not arise.

Diagnosis

The diagnosis is suspected by a combination of the following:

  • Age between 11 and 24 months

  • Healthy-looking, well-hydrated child (unless dietary restrictions have been imposed)

  • Up to10 loose bowel movements a day, containing undigested and recognizable items of food (e.g. corn, peas and carrots, etc)

  • Feces contain no blood but often mucus.

The common dietary transgressions observed are:

  • Low-fat milk

  • Excess milk, water, juices, and/or fruit.

Tests

The feces should be tested for:

  • Electrolytes - sodium should be less than 40 mmol/l (mEq/l)

  • Evidence of carbohydrate - negative test for reducing substances

  • pH - >5.5

  • Parasites - screen for G. lamblia antigen (a test which is not as yet universally available) and C. difficile toxin.

Treatment

If dietary transgressions are identified, correction can improve or resolve the problem completely. Fiber supplementation can give bulk to the stools. Parental advice is very important.

Small-bowel bacterial overgrowth

The causes of small-bowel bacterial overgrowth in children are the same as in adults. It may occur after infection with Giardia or prolonged diarrhea, and could be a component of post-enteritis syndrome. Bacterial overgrowth can also be associated with cystic fibrosis, previous abdominal surgery (e.g. for intestinal atresia), intestinal pseudo-obstruction, short-bowel syndrome, Crohn's disease, and tropical enteropathy [49]. The main symptoms are excessive burping and passage of gas, abdominal distension, abdominal pain, and diarrhea, which can be malabsorptive and/or secretory.

Diagnosis

The diagnosis is mainly clinical. The breath hydrogen test can be helpful if the baseline is elevated or if a peak is obtained at 10 or 20 min after ingestion of lactulose (0.5 g/kg). Peaks appearing later than this could correspond to colonic fermentation, because transit time, particularly in young children, might be short compared with that in adults [53, 49].

Treatment

Patients may respond to metronidazole (30 mg/kg/day divided into three doses a day, for 7 to 10 days). Co-trimoxazole (trimethoprim-sulfamethoxazole; 8 mg/kg/day divided into two doses a day, for 7 to 10 days) can also be used.

Celiac disease

Celiac disease has a prevalence of 1:2000-1:6000 in parts of Europe, but is less common in the USA and Canada. There is a peak estimated prevalence of 1:300 in the west of Ireland. Therefore, if both of the child's parents have Irish ancestry, that should increase the index of suspicion. Onset of diarrhea can be identified by history: it develops some weeks to months after the introduction of wheat to the diet and, depending on weaning practices, can occur from age 6 to 18 months (or in adulthood). Children may have abdominal distension and foul-smelling, pale and frothy stools, appear moody, and experience weight loss or inadequate weight gain.

Diagnosis

Diagnosis is based on the following:

  • Fat globules in stool

  • Presence of serum IgA antiendomysial and/or antigliadin antibodies (less specific and sensitive) and tissue glutaminidase IgA antibodies, the latest and most reliable screening test.

  • Small-bowel biopsy.

Munchausen syndrome by proxy

This syndrome involves falsification of the child's medical history, usually by the mother. Pediatricians as well as neonatologists are becoming increasingly aware of its existence. Gastrointestinal bleeding, diarrhea, and vomiting are common complaints, resulting in extensive and unnecessary investigation and treatment of fabricated illnesses. Symptoms can at times be confused with intestinal pseudo-obstruction [54]. Symptoms are generally absent when the involved carer is not in attendance. He or she presents as concerned, usually refusing to leave the hospital. Intravenous lines may be tampered with or become contaminated; medications reportedly are vomited. Frequently, the carrier has had some medical or nursing training.

Diagnosis

Suspect Munchausen syndrome by proxy whenever there are inconsistent symptoms, signs, and/or features that only the main carer reports, and there is an absence of associated symptoms, etc. The carer may be noted to eavesdrop when doctors and nurses are privately discussing the child. Filming the carer with infant using a hidden camera, or entering the room without warning, and observation when urine samples are collected, as well as searching the room for laxatives or other drugs, may be helpful in making the diagnosis. Phenolphthalein is a commonly used laxative in these cases. Its presence can be identified by the development of a pink color when stools are alkalinized to pH 8.5. Fecal sulfate and magnesium can also be determined to establish the illicit use of laxatives. Screen urine from both the patient (for poisons) and the carer (for evidence of drug abuse). In a long-term follow up of 54 victims of this syndrome in Leeds, England, 13 had been exposed to repetitive poisoning [55].

Graft-versus-host enteropathy

Following bone marrow transplantation, graft-versus-host disease can affect the intestine, causing protein-losing enteropathy. Weisdorf et al. [56] measured fecal protein losses before and after transplantation in 25 consecutive patients. The mean a1-antitrypsin concentration and serum clearance before transplantation were below 2.6 mg/g stool and 13.0 ml/day, respectively (upper limits for normals). Values for all patients increased moderately after pre-transplant conditioning. Levels for patients who did not develop graft-versus-host disease of the intestine returned to baseline; however, those for patients with graft-versus-host disease of the intestine became markedly and persistently elevated (concentration ranged from 16.6 to 51.1 mg/g, clearance from 66.6 to 384.5 ml/day). Usually this problem improves with corticosteroid therapy.

Autoimmune enteropathy

This is a rare small-bowel disorder characterized by damaged intestinal mucosa secondary to an autoimmune mechanism. Infants have chronic diarrhea and, characteristically, crypt hyperplasia, villous atrophy with enterocyte autoantibodies in the blood, activation of mucosal lymphocytes, and increased epithelial HLA-DR. There is no cure and the prognosis is poor. Treatment includes high doses of corticosteroids and immunosuppressants [57]

Irritable bowel syndrome 

In children, episodes of diarrhea alternate with those of constipation and/or abdominal pain, particularly under stressful conditions [58]. Many pre-adolescent and adolescent patients use this as a pretext to miss school or to pay frequent visits to the nurse's station when they ought to be in the classroom. Characteristically, constipation and pain is during daytime, and improves on weekends and vacation time. Some parents who are separated or divorced report diarrhea when the child returns from visiting the former partner and may use this against the other party for the manipulation of their preferred visitation rights.

Adult-type hypolactasia

Genetically determined hypolactasia can become symptomatic at 10 or 11 years of age, and cause chronic diarrhea and/or abdominal pain. The incidence is higher in non-whites. Diagnosis can be made by elimination of lactose from the diet and confirmed by a lactose breath hydrogen test.

Encopresis

Encopresis is defined as the act of defecation in socially non-acceptable places, and the initial complaint may be that of chronic diarrhea. The liquid stool is by overflow.

Inflammatory bowel disease

Crohn's disease and ulcerative colitis can occur at almost any age, but primarily affect pre-adolescents and adolescents. One of the common forms of presentation is chronic diarrhea.

Excessive intake of laxatives

In children, excessive use of laxatives can be seen in Munchausen syndrome by proxy and in anorexia nervosa and bulimia nervosa.

Purgatives to consider include:

  • Diphenolic laxatives (phenolphthalein)

  • Anthraquinones (senna, cascara, rhubarb aloe, frangula, and dantheron)

  • Osmotic laxatives such as lactulose, sodium sulfate, sodium phosphate, magnesium sulfate, and magnesium citrate.

Include ricinoleic acid when screening the stool for laxatives and electrolytes.

References

1. Darrow DC, Yannet H. The changes in the distribution of body water accompanying increase and decrease in extracellular electrolyte. J Clin Invest 1935;14:266-75.

2. Hirschhorn N, McCarthy BJ, Ranney B, et al. Ad libitum oral glucose-electrolyte therapy for acute diarrhea in Apache children. J Pediatr 1973;83:562-71.

3. Hirschhorn N. The treatment of acute diarrhea in children: an historical and physiological perspective. Am J Clin Nutr 1980;33:637-63.

4. Gavin N, Merrick N, Davidson B. Efficacy of glucose-based oral rehydration therapy. Pediatrics 1996;98:45-51.

5. Santosham M, Burns B, Nadkarni V, et al. Oral rehydration therapy for acute diarrhea in ambulatory children in the United States: a double-blind comparison of four different solutions. Pediatrics 1985;76:159-66.

6. Holliday M. The evolution of therapy for dehydration: should deficit therapy still be taught? Pediatrics 1996;98(2 Pt 1):171-7.

7. Ulshen MH. Refeeding during recovery from acute diarrhea. J Pediatr 1988;112:239-40.

8. Sandhu BK, Isolauri E, Walker-Smith JA, et al. A multicentre study on behalf of the European Society of Paediatric Gastroenterology and Nutrition Working Group on Acute Diarrhoea. Early feeding in childhood gastroenteritis. J Pediatr Gastroenterol Nutr 1997;24:522-7.

9. Brown KH, Gastanaduy AS, Saavedra JM, et al. Effect of continued oral feeding on clinical and nutritional outcomes of acute diarrhea in children. J Pediatr 1988;112:191-200.

10. Beattie RM, Vieira MC, Phillips AD, Meadows N, Walker-Smith JA. Carbohydrate intolerance after rotavirus gastroenteritis: a rare problem in the 1990s. Arch Dis Child 1995;72:466 (letter).

11. Brown KH, Peerson JM, Fontaine O. Use of nonhuman milks in the dietary management of young children with acute diarrhea: a meta-analysis of clinical trials. Pediatrics 1994;93:17-27.

12. Brown KH. Dietary management of acute childhood diarrhea: optimal timing of feeding and appropriate use of milks and mixed diets. J Pediatr 1991;118(4 Pt 2):S92-8.

13. Lifschitz CH, Torun B, Chew F, Boutton TW, Garza C, Klein PD. Absorption of carbon 13 C-rice in milk by infants during acute gastroenteritis. J Pediatr 1991;118:526-30.

14. Melton L. Lifesaving vaccine caught in an ethical minefield. Lancet 2000;356:318.

15. Weijer C. The future of research into rotavirus vaccine. Br Med J 2000;321:525-6.

16. Diarrhoeal Diseases Study Group (UK). Loperamide in acute diarrhoea in childhood: results of a double-blind, placebo controlled multicentre clinical trial. Br Med J (Clin Res Ed) 1984;289:1263-7.

17. Bowie MD, Hill ID, Mann MD. Loperamide for treatment of acute diarrhoea in infants and young children. A double-blind placebo-controlled trial. S Afr Med J 1995;85:885-7.

18. Soriano-Brucher H, Avendano P, O'Ryan M, et al. Bismuth subsalicylate in the treatment of acute diarrhea in children: a clinical study. Pediatrics 1991;87:18-27.

19. Isolauri E, Juntunen M, Rautanen T, Sillanaukee P, Koivula T. A human Lactobacillus strain (Lactobacillus casei sp strain GG) promotes recovery from acute diarrhea in children. Pediatrics 1991;88:90-7.

20. Pant AR, Graham SM, Allen SJ, et al. Lactobacillus GG and acute diarrhoea in young children in the tropics. J Trop Pediatr 1996;42:162-5.

21. Hyams JS, Krause PJ, Gleason PA. Lactose malabsorption following rotavirus infection in young children. J Pediatr 1981;99:916-8.

22. Penny ME, Paredes P, Brown KH. Clinical and nutritional consequences of lactose feeding during persistent post-enteritis diarrhea. Pediatrics 1989;84:835-44.

23. Walker-Smith JA. Cow's milk intolerance as a cause of post-enteritis diarrhoea. J Pediatr Gastroenterol Nutr 1982;1:163-73.

24. Penny ME, Brown KH. Lactose feeding during persistent diarrhoea. Acta Paediatr Suppl 1992;381:133-8.

25. Lebenthal E, Lee PC. Glucoamylase and disaccharidase activities in normal subjects and in patients with mucosal injury of the small intestine. J Pediatr 1980;97:389-93.

26. Solomons NW, Garcia R, Schneider R, Viteri F, Argueta von Kaenel V. H2 breath test during diarrhea. Acta Paediatr Scand 1979;68:171-2.

27. Davidson GP, Goodwin D, Robb TA. Incidence and duration of lactose malabsorption in children hospitalized with acute enteritis: study in a well-nourished urban population. J Pediatr 1984;105:587-90.

28. Lifschitz CH, Bautista A, Gopalakrishna GS, Stuff J, Garza C. Absorption and tolerance of lactose in infants recovering from severe diarrhea. J Pediatr Gastroenterol Nutr 1985;4:942-8.

29. Naim HY, Roth J, Sterchi EE, et al. Sucrase-isomaltase deficiency in humans. Different mutations disrupt intracellular transport, processing, and function of an intestinal brush border enzyme. J Clin Invest 1988;82:667-79.

30. Treem WR, McAdams L, Stanford L, Kastoff G, Justinich C, Hyams J. Sacrosidase therapy for congenital sucrase-isomaltase deficiency. J Pediatr Gastroenterol Nutr 1999;28:137-42.

31. Turk E, Klisak I, Bacallao R, Sparkes RS, Wright EM. Assignment of the human Na+/glucose cotransporter gene SGLT1 to chromosome 22q13.1. Genomics 1993;17:752-4.

32. Abad-Sinden A, Borowitz S, Meyers R, Sutphen J. Nutrition management of congenital glucose-galactose malabsorption: a case study. J Am Diet Assoc 1997;97:1417-21.

33. Greene HL, Ghishan FK. Excessive fluid intake as a cause for chronic diarrhea in young children. J Pediatr 1983;102:836-40.

34. Kneepkens CM, Hoekstra JH. Fruit juice and chronic nonspecific diarrhea. J Pediatr 1993;122:499.

35. Lifschitz CH. Carbohydrate absorption from fruit juices in infants. Pediatrics 2000;105:e4.

36. Sullivan PB, Marsh MN, Mirakian R, Hill SM, Milla PJ, Neale G. Chronic diarrhea and malnutrition - histology of the small intestinal lesion. J Pediatr Gastroenterol Nutr 1991;12:195-203.

37. Gryboski JD. The role of allergy in diarrhea: cow's milk protein allergy. Pediatr Ann 1985;14:31-2, 33-4, 36.

38. Nichols VN, Fraley JK, Evans KD, Nichols BL. Acquired monosaccharide intolerance in infants. J Pediatr Gastroenterol Nutr 1989;8:51-7.

39. Murch SH. The molecular basis of intractable diarrhoea of infancy. Baillieres Clin Gastroenterol 1997;11:413-40.

40. Greenberg HB, Clark HF, Offit PA. Rotavirus pathology and pathophysiology. Curr Top Microbiol Immunol 1994;185:255-83.

41. Kotloff KL. Bacterial diarrheal pathogens. Adv Pediatr Infect Dis 1999;14:19-67.

42. Kabani A, Cadrain G, Trevenen C, Jadavji T, Church DL. Practice guidelines for ordering stool ova and parasite testing in a pediatric population. Am J Clin Pathol 1995;104:272-8.

43. McKinney RE Jr, Robertson JW. Effect of human immunodeficiency virus infection on the growth of young children. Duke Pediatric AIDS Clinical Trials Unit. J Pediatr 1993;123:579-82.

44. Miller TL, Evans SJ, Orav EJ, Morris V, McIntosh K, Winter HS. Growth and body composition in children infected with the human immunodeficiency virus-1. Am J Clin Nutr 1993;57:588-92.

45. Henderson RA, Saavedra JM, Perman JA, Hutton N, Livingston RA, Yolken RH. Effect of enteral tube feeding on growth of children with symptomatic human immunodeficiency virus infection. J Pediatr Gastroenterol Nutr 1994;18:429-34.

46. Winter H. Gastrointestinal tract function and malnutrition in HIV-infected children. J Nutr 1996;126(10 Suppl.):2620S-2622S.

47. Benkov KJ. Gastrointestinal aspects of acquired immunodeficiency syndrome in children. In: Wyllie R, Hyams JS, editors. Pediatric Gastrointestinal Disease. Pathophysiology, Diagnosis, Management. Philadelphia: WB Saunders,1993:712-23.

48. Abramowsky C, Hupertz V, Kilbridge P, Czinn S. Intestinal lymphangiectasia in children: a study of upper gastrointestinal endoscopic biopsies. Pediatr Pathol 1989;9:289-97.

49. McReynolds EW, Roy S 3rd, Etteldorf JN. Congenital chloride diarrhea. Am J Dis Child 1974;127:566-70.

50. Aichbichler BW, Zerr CH, Santa Ana CA, Porter JL, Fordtran JS. Proton-pump inhibition of gastric chloride secretion in congenital chloridorrhea. N Engl J Med 1997;336:106-9.

51. Desjeux J-F. Congenital transport defects. In: Walker WA, Durie PR, Hamilton JR, Walker-Smith JA, Watkins JB, editors. Pediatric Gastrointestinal Disease, Volume 1. Philadelphia: BC Decker, 1991:668-88.

52. Treem WR. Chronic nonspecific diarrhea of childhood. Clin Pediatr 1992;31:413-20.

53. Perman JA, Modler S, Barr RG, Rosenthal P. Fasting breath hydrogen concentration: normal values and clinical applications. Gastroenterology 1984;87:1358-63.

54. Baron HI, Beck DC, Vargas JH, Ament ME. Overinterpretation of gastroduodenal motility studies: two cases involving Munchausen syndrome by proxy. J Pediatr 1995;126:397-400.

55. Bools CN, Neale BA, Meadow SR. Follow up of victims of fabricated illness (Munchausen syndrome by proxy). Arch Dis Child 1993;69:625-30.

56. Weisdorf SA, Salati LM, Longsdorf JA, Ramsay NK, Sharp HL. Graft-versus-host disease of the intestine: a protein losing enteropathy characterized by fecal alpha 1-antitrypsin. Gastroenterology 1983;85:1076-81.

57. Bousvaros A, Leichtner AM, Book L, et al. Treatment of pediatric autoimmune enteropathy with tacrolimus (FK506). Gastroenterology 1996;111:237-43.

58. Schuster MM. Irritable bowel syndrome. In: Sleisenger MH, Fordtran JS, editors. Gastrointestinal Diseases: Pathophysiology, Diagnosis, Management, 4th ed. Philadelphia: WB Saunders, 1989:21-52.

TABLES

Table 3.1  

Guidelines for rehydration therapy for children 1 month to 5 years of age. 

These guidelines apply to children who are well nourished and have no serious underlying illnesses. 

Mild dehydration (3-5%)
50 ml/kg oral rehydration solution + ongoing losses replaced at 10 ml/kg

Moderate dehydration (6-9%)
100 ml/kg oral rehydration solution + ongoing losses replaced over a 40 hr period.

Severe dehydration (>10%)
20-60 ml/kg Ringer's lactate solution (or normal saline) intravenously over a 15- to 60-min period until circulation, extracellular fluid volume, and renal perfusion are restored, followed by oral rehyration therapy and early refeeding.

Table 3.2  

Causes of chronic diarrhea.

Common causes

  • Excessive intake of formula or other fluid (water, fruit juice, high-carbohydrate beverages) 

  • Chronic non-specific diarrhea of the toddler 

  • Irritable bowel syndrome

  • Encopresis (overflow diarrhea)

Less common causes

  • Parasitosis (Giardia lamblia, Cryptosporidium)

  • Celiac disease

  • Post-enteritis syndrome

Table 3.3  

Causes of chronic diarrhea in various age groups.

0-6 months
Carbohydrate malabsorption: 
acquired
congenital 
Protein hypersensitivity
Excessive intake of formula, water, or fruit juice 
Post-enteritis syndrome and intractable diarrhea
Infections
Cystic fibrosis and other causes of fat malabsorption
Immunodeficiency 
Lymphangiectasia
Neuroblastoma
Congenital chloridorrhea
Intestinal villi inclusion disease
Congenital defective jejunal Na+/H+ exchange

7-23 months
Chronic non-specific diarrhea ("toddler diarrhea") (usually 11 months or older)
Small-bowel bacterial overgrowth 
Celiac disease
Immunodeficiency
Munchausen syndrome by proxy
Graft-versus-host enteropathy
Autoimmune enteropathy

as well as the following from the first age group described:
Carbohydrate malabsorption
Protein hypersensitivity
Excessive intake of fruit juice/ high-carbohydrate drinks
Post-enteritis syndrome
Cystic fibrosis
Infections
Fat malabsorption
Neuroblastoma

24 months and older
Irritable bowel syndrome
Adult-type hypolactasia
Encopresis
Inflammatory bowel disease
Excessive intake of laxatives

as well as the following from the previous two age groups described:
Excessive intake of fruit juice/high-carbohydrate drinks
Infections
Small-bowel bacterial overgrowth 
Celiac disease
Munchausen syndrome by proxy
Graft-versus-host enteropathy
Carbohydrate malabsorption