Acute gastroenteritis in children

What is the epidemiology and impact of gastroenteritis?

Acute gastroenteritis—diarrhoea or vomiting (or both) of more than seven days duration—may be accompanied by fever, abdominal pain, and anorexia. Diarrhoea is the passage of excessively liquid or frequent stools with increased water content. Patterns of stooling vary widely in young children, and diarrhoea represents a change from the norm.1 Worldwide, 3-5 billion cases of acute gastroenteritis and nearly 2 million deaths occur each year in children under 5 years.2 In the United States, gastroenteritis accounts for about ∼10% (220 000) of admissions to hospital, more than 1.5 million outpatient visits, and around 300 deaths in children under 5 annually, with a cost of around $1bn (£0.5bn; €0.8bn).2 In the same age group in Australia, about 10 000 hospital admissions, 22 000 visits to emergency departments, and 115 000 general practice consultations occur annually for rotavirus alone, with an estimated cost of $A30m (£12m; €18m; $23m).3 In the United Kingdom, 204 of 1000 consultations with general practitioners in children under 5 are for gastroenteritis, and the annual hospital admission rate in this group is about seven per 1000 children.4 Children in childcare settings are often infected but asymptomatic and may unwittingly transmit infection.

Children with poor nutrition are at increased risk of complications. In the north end of Australia, Aboriginal and Torres Strait Islander children have increased rates of admission for gastroenteritis, malnutrition, comorbidity, and electrolyte disturbance (especially hypokalaemia) and a longer hospital stay than their non-indigenous counterparts.5 The cost of gastroenteritis to the community is huge but often underestimated if costs to the family, including lost time at work, are not considered.

What are the causes and clinical characteristics?

Box 1 lists some causes of acute gastroenteritis in children. Worldwide, most cases are due to viral infection (fig 1⇓; box 2), with rotaviruses and noroviruses being most common. Viral infections damage small bowel enterocytes and cause low grade fever and watery diarrhoea without blood. Rotavirus infection is seasonal in temperate climates, peaking in late winter, but occurs throughout the year in the tropics. Rotavirus strains vary by season and geographically within countries.6 The peak age for infection is between 6 months and 2 years, and the mode of spread is by the faecal-oral or respiratory route.

Fig 1 Rotavirus particles seen under the electron microscope. Courtesy of Alan Philips

• Download figure
• Open in new tab
• Download powerpoint

Bacterial pathogens such as Campylobacter jejuni and Salmonella spp invade the lining of the small and large intestine and trigger inflammation.7 Children with bacterial gastroenteritis are more likely to have high fever and may have blood and white blood cells in the stool. Bacterial pathogens occasionally spread systemically, especially in young children. Infection with Shiga toxin producing Escherichia coli or Shigella dysenteriae may cause haemorrhagic colitis (with severe bloody diarrhoea), which may be complicated by haemolytic uraemic syndrome. This syndrome is endemic worldwide and characterised by acute onset of microangiopathic haemolytic anaemia (fig 2⇓), thrombocytopenia, acute renal impairment, and multisystem involvement (see appendix on bmj.com).8

Fig 2 Typical peripheral blood film in a patient with haemolytic uraemic syndrome, microangiopathic haemolytic anaemia, and thrombocytopenia. It shows irregular, fragmented, and helmet shaped red blood cells (schistocytes) and an immature platelet

• Download figure
• Open in new tab
• Download powerpoint

The enteric fevers (due to Salmonella typhi and S paratyphi) cause severe illness in young children, characterised by high swinging fever, diarrhoea or constipation, leucopenia, and sometimes central nervous system involvement, including encephalopathy.7 Encephalopathy is a rare complication of non-typhoid Salmonella infection. Vibrio cholera toxin causes chloride and water secretion from the small bowel but does not damage the intestinal mucosa; it results in “rice water” stools that have a high sodium content but do not contain blood or white blood cells.7

Gastroenteritis is acquired by person to person spread or ingestion of contaminated food and drink (“food poisoning”).7 Undercooked, or inappropriately stored cooked or processed meats (chicken, beef, pork) and seafood are common sources of bacterial pathogens. Ingestion of food containing toxins produced by bacterial contaminants (for example, Staphylococcus aureus in ice cream or Bacillus cerus in reheated rice) causes rapid onset of vomiting or diarrhoea (or both). Water may be contaminated with bacteria, viruses, or protozoa including Giardia lamblia, cryptosporidium, V cholera, and Entamoeba histolytica, which causes amoebic dysentery. With increasing rates of overseas travel and immigration, clinicians in developed countries increasingly see children with “traveller's diarrhoea” caused by a range of organisms not normally seen in that environment.

How is it diagnosed?

Diagnosis can be made clinically. Information should be sought about recent contact with people with gastroenteritis, nature and frequency of stool and vomitus, fluid intake and urine output, travel, and use of antibiotics and other drugs that may cause diarrhoea. Chronic constipation is common in children, and faecal overflow incontinence may present as spurious diarrhoea. Diarrhoea and vomiting are non-specific symptoms in young children, and the diagnosis of gastroenteritis should be questioned in children with high fever, prolonged symptoms, or signs suggesting a surgical cause (such as severe abdominal pain, bilious vomiting, abdominal mass). Children with diabetes mellitus and inborn errors of metabolism may present with vomiting. Children with underlying diseases may be at increased risk of complications and referral to a paediatric service should be considered.

It is not necessary or practical to take stool specimens from all children with gastroenteritis. Samples should be taken during outbreaks—especially in childcare, school, hospital, or residential settings—where there is a public health imperative to identify the pathogen and establish its source. Samples should be cultured for bacteria and tested for viral pathogens. Testing for rotavirus, norovirus, and sometimes other viruses is available in most children's hospitals using methods for rapid antigen detection (such as enzyme linked immunosorbent assay). Rapid diagnosis allows for isolation of the child to prevent nosocomial infection, which is common and is often used as a marker of the effectiveness of precautions to control contact infection. Stool samples should also be taken from children with bloody diarrhoea, a history of recent foreign travel, and from young or immunocompromised children with high fever. In many countries legislation requires clinicians to notify public health authorities about a range of viral and bacterial infections.

How is dehydration assessed?

It is important to assess hydration in gastroenteritis as hydration status determines the immediate management of this condition. The infant or child with profuse watery diarrhoea and frequent vomiting is most at risk. Clinicians often overestimate the extent of dehydration. Clinical signs are usually not present until a child has lost at least 5% of his or her body weight. Documented recent weight lost is a good indicator of the degree of dehydration, but this information is rarely available. The best clinical indicators of more than 5% dehydration are prolonged capillary refill, abnormal skin turgor, and absent tears.9 The recommendations for assessing and managing dehydration shown in table 1⇓ are adapted from the World Health Organization classification and are supported by the literature.9 10 11 Serum electrolytes are not routinely required but should be measured before and after starting intravenous fluids.

How is gastroenteritis treated?

Table 1⇑ summarises the management of dehydration2 4 10 11 12 13 14 15 16 17 18 19 20 21 22 23 and table 2⇓ lists the type of evidence supporting management decisions in gastroenteritis (a longer version of table 2 (table A) is available on bmj.com). Management aims to prevent and treat dehydration, maintain nutrition, and minimise harm.

Which fluid therapy?

Children with no dehydration or mild dehydration can usually be managed at home, although children with high risk for complications or who cannot be adequately cared for at home should be considered for admission.2 11 13 Children with mild-moderate dehydration who do not tolerate oral fluids should be admitted for observation. Oral rehydration solutions are preferable to other clear fluids for preventing and treating dehydration.2 4 11 Fluids high in sugar (such as cola, apple juice, and sports drinks, which contain ≤20 mmol/l sodium and have a high osmolality of 350-750 mOsm/l) may exacerbate diarrhoea and should be avoided.11 Breast feeding should be continued during acute gastroenteritis and supplemented with an oral rehydration solution if needed.11 12

Although most children with dehydration drink readily, some refuse rehydration solutions because they dislike the taste, feel nauseated, or have profuse vomiting. Older children may be afraid of vomiting and parents may perceive fluids are the cause of vomiting. If small sips cannot be tolerated, use of a syringe can help in infants. If oral intake is inadequate, a fine bore nasogastric tube is usually well tolerated.14 15 Alternatively, fluids may be given intravenously.11 Enteral (oral or nasogastric) and intravenous fluids are equally safe and effective for mild-moderate dehydration,14 15 and rehydration can usually be achieved in four to six hours.

In developed communities children with severe dehydration are routinely admitted for intravenous therapy,2 11 although enteral rehydration has been used safely in severe dehydration with fewer adverse effects than intravenous therapy (table 2⇑).14 15 Children with shock require intravenous resuscitation before rehydration.2 10 11

The most common adverse effect of intravenous cannulation is infiltration at the cannula site, but infection, pain, bleeding, and physical and emotional trauma may also occur. Intravenous therapy is more expensive than oral rehydration therapy and requires hospital admission. Iatrogenic complications—especially electrolyte disturbance due to inappropriate composition, rate of administration, or volume of intravenous fluids—may lead to complications, including hyponatraemia with brain injury or death (box 3). If rapid intravenous rehydration is used, careful supervision is needed to avoid fluid overload (dehydration is often overestimated) and electrolyte imbalance.

Which oral rehydration solution?

Solutions with low osmolality (200-250 mOsm/l) and sodium (60-70 mmol/l) that contain glucose, potassium, and a base (such as citrate) are recommended for developed and developing communities (table 2⇑; table B on bmj.com).16 17 18 Although cereal based oral dehydration solutions are beneficial in cholera-like diarrhoea,19 evidence of benefit in non-cholera diarrhoea is scant and further trials are needed to evaluate efficacy and cost effectiveness.

What about diet?

In a systematic review, probiotics—used as an adjunct to oral rehydration therapy—decreased the duration of diarrhoea, especially in rotavirus gastroenteritis (table 2⇑).20 Further research is needed to determine the optimal type, dosage, and regimen of probiotics before they are recommended for routine use.

Children should resume their normal diet once their appetite returns.2 10 11 Published guidelines recommend early reintroduction of milk and solids including complex carbohydrates, lean meats, yogurt, and vegetables, but foods high in fat and sugars should be avoided.3 Early refeeding reduces the duration of diarrhoea. In formula fed infants feeds do not need to be diluted when reintroduced.21

What is the role of drugs?

Drugs are rarely needed.3 10 11 They deal with the symptoms rather than causes of disease and may distract from the use of appropriate fluid therapy. Antibiotics are not indicated in viral or uncomplicated bacterial gastroenteritis and may cause harm. For example, in non-typhoid Salmonella infections antibiotics increase the risk of prolonged carriage and disease relapse. Treating gastroenteritis due to Shiga toxin producing E coli with antibiotics may increase the risk of haemolytic uraemic syndrome. Antibiotics are required, however, for bacterial gastroenteritis complicated by septicaemia and in cholera, shigellosis, amoebiasis, giardiasis, and enteric fever.

Antidiarrhoeal and antiemetic agents are not recommended for routine use because of the risk of adverse effects (table 2⇑; table A on bmj.com).3 10 11 Although new generation antiemetics (such as the serotonin antagonist ondansetron) do not have extrapyramidal effects and reduce the duration and frequency of vomiting, they also increase diarrhoea. Antimotility agents (such as loperamide) decrease the duration of diarrhoea, but they have potential severe adverse effects and evidence that benefits outweigh potential harms is lacking.6

In developing countries, oral zinc given at the onset of symptoms decreases the duration and severity of acute diarrhoea and is recommended by the WHO.10 Vitamin A does not influence the course of acute gastroenteritis.

Is a lactose-free diet necessary?

Carbohydrate (particularly lactose) intolerance is a common complication of viral gastroenteritis as a result of damage to and loss of mature enterocytes containing lactase. Lactose intolerance is usually mild and self limiting and does not require treatment.3 21 If lactose intolerance persists, a lactose-free formula is recommended for four to six weeks.3 21 The damaged gut is more permeable to foreign antigens and intolerance to food proteins (β lactoglobulin in cow's milk and other proteins) is occasionally seen after gastroenteritis; it can be managed by a period of dietary exclusion.3 10 11

Can gastroenteritis be prevented?

Although rotavirus may be spread in aerosols, gastroenteritis is usually spread by the faecal-oral route. Bacterial gastroenteritis can occur in young children served uncooked fermented meats, undercooked hamburgers, unwashed fruits and salads, and water contaminated by animal faeces. Gastroenteritis may also be acquired from environmental sources, such as children's animal farms, swimming pools, and beaches. Good hygiene is important to prevent spread of infection. This includes careful hand washing, nappy disposal, and preparation and storage of food and drinking water, as outlined in the WHO's five step guide to safe food (table C on bmj.com). Hygiene is particularly important in institutions, including hospitals where nosocomial infection is common.

A major recent advance in prevention has been the development and licensing of two oral rotavirus vaccines, whose safety and efficacy have been confirmed in recent large scale trials, each involving more than 60 000 children.24 25 Rotateq (Merck) is a three dose live human-bovine pentavalent reassortant vaccine. Rotarix (GSK) is two dose attenuated human (strain G1P) monovalent vaccine. Both vaccines are highly immunogenic. They provide cross protection against common serotypes and decrease rates of severe gastroenteritis, the need for intravenous fluids, and hospital admission. Importantly, neither is associated with appreciable adverse effects or increased risk of intussusception, which was seen with the first licensed vaccine, RotaShield. Free access to rotavirus vaccine in all communities is imperative and will have an enormous impact on childhood morbidity and mortality.