Previously well, 20 month old Joshua Ebbeck, presents with a 2-day history of temperature to 38°C and vomiting; the vomiting has settled but in the last 12 hours he has started passing frequent, loose bowel motions. On immediate assessment he is alert and well perfused. BP: 90/60 mmHg; HR: 110 bpm; RR 25 bpm; weight 14 kg
Diarrhoea is defined as a measured stool volume greater than 10ml/kg/day. Both the consistency of the stool (loose or watery) and frequency (usually at least three stools in 24-hour period) are important defining features of diarrhoea. Acute diarrhoea lasts less than 10 days and has a major impact on fluid and electrolyte status, while chronic diarrhoea suggests that the symptom is present for more than 2-3 weeks and can have a significant effect on the nutritional state of a child.
A history of contact with gastroenteritis can often be established in young children with diarrhoea and vomiting. However, diarrhoea and vomiting are non-specific symptoms in children and may also be associated with a range of infections outside the gastrointestinal tract (e.g., otitis media, urinary tract infection), structural gut abnormalities (malrotation), metabolic diseases (diabetes mellitus), and surgical problems (acute appendicitis).
Children with viral gastroenteritis (usually due to rotavirus) generally present in autumn or winter with watery diarrhoea without blood, with or without vomiting, low-grade fever and anorexia. Most of these children are under the age of 5 years.
Children with bacterial gastroenteritis are more likely to have a high fever and blood and mucus in the stool.
A travel history should be sought in children with bloody diarrhoea. Haemolytic–uraemic syndrome (characterised by acute renal impairment, thrombocytopenia and microangiopathic haemolytic anaemia) should be considered in any child with bloody diarrhoea, pallor and poor urine output.
Organisms frequently implicated in food- or water-borne infections include species of Salmonella, Campylobacter, Listeria and Clostridia; Norwalk-like viruses (noroviruses); Shiga-toxin-producing Escherichia coli; and cryptosporidium. These infections are most commonly acquired from imported and takeaway foods, including seafood, red meat or poultry, and unpasteurised milk and contaminated water.
It is not feasible or necessary to take a stool specimen in all children with diarrhoea in the community. However, stool cultures may help guide treatment in very young, immunocompromised children or children with high fever who look particularly unwell; in children with gross bloody diarrhoea or a history of recent foreign travel; and in children who are part of an outbreak of diarrhoea in a child-care, school, community or hospital setting.
Exclude surgical (acute) abdomen and other emergencies such as meningitis/sepsis.
Main focus is then on assessment of hydration. See grades of dehydration below (Question 6).
| Category | Conditions |
|---|---|
| Enteric infection |
Rotavirus Other viruses Bacterial: - Salmonella - Shigella spp. - Escherichia coli - Campylobacter jejuni Protozoa: - Cryptosporidium - Giardia lamblia - Entamoeba histolytica Food poisoning: - Staphylococcal toxin |
| Systemic infection |
Urinary tract infection Pneumonia Septicaemia |
| Surgical condition |
Appendicitis Intussusception Partial bowel obstruction Hirschsprung disease |
| Other |
Diabetes mellitus Antibiotic diarrhoea Haemolytic-uraemic syndrome |
| Osmotic | Secretory | Inflammatory | |
|---|---|---|---|
| Clinical features | Ceases when enteral feeding is ceased | Continues when enteral feeding is ceased | Presence of blood and mucus in the faeces |
| Stool volume | <200ml/day | >200ml/day | Variable, usually <200ml/day |
| Faecal sodium | <60mosmol/l | 90 osmol/l | Variable |
Rotavirus is the most common cause of gastroenteritis worldwide. It is noteworthy that it was first identified in 1973 by an Australian researcher, Professor Ruth Bishop, working at the Sydney Children's Hospital. Other viral pathogens include enteropathogenic adenoviruses (serotypes 40 and 41) and, occasionally, astroviruses. More recently, attention has been focused on norovirus, which was previously known as 'Norwalk agent', and on 'small round structured viruses' (SRSVs) as significant causes of gastroenteritis outbreaks, particularly in older children and the adult population.
About 15-20% of cases are a result of bacterial infections with pathogens such as campylobacter species, salmonella species, shigella, enteropathogenic Escherichia coli and Yersinia enterocolitica. Occasionally, infections due to shiga-toxin-producing E coli and vibrio species occur.
E coli that causes gastroenteritis can be further sub-classified into strains according to the mechanism by which they cause diarrhoea. Enteropathogenic E coli often occurs in infants and produces diarrhoea via the direct adherence of the bacteria to intestinal epithelial cells. Shiga-toxin- (or Vero toxin-) producing E coli produce the cytotoxins causing bloody diarrhoea and haemolytic uraemic syndrome.
Food poisoning arises from the ingestion of pre-formed bacterial toxins in food that is inadequately cooked or prepared. The effects are a result of toxins rather than direct infection of the GI tract by pathogenic organisms. Classically the organisms and the toxins implicated are those from Staphylococcus aureus and Bacillus cereus. Episodes often occur in clusters, with the pre-formed toxin resulting in a rapid onset of symptoms, typically less than 24 hours after ingestion. The illness is usually short-lived and comprises vomiting and diarrhoea without fever of less than 48 hours' duration. Foods typically contaminated with staphylococcal toxins are those that contain contaminated dairy products, such as cream. B cereus food poisoning is associated with rice dishes.
The remaining small percentages of cases of infective gastroenteritis in children are caused by protozoal parasite infections. The usual agents are Giardia intestinalis or cryptosporidium species.
Common childhood helminth infestations such as Ascaris lumbricoides and Enterobius vermicularis do not usually cause diarrhoea. Generally helminth parasitic infections cause few GI symptoms unless the worm load is heavy. Often patients are unaware of ascaris infections until a worm is passed in the stool or accidentally vomited or coughed up. E vermicularis (pinworm) infections in childhood are common and typically produce pruritus ani, especially at night when the female worm leaves the rectum to lay eggs on the perianal skin.
| Level | Clinical Features |
|---|---|
| Mild (≤5% body weight loss) |
Dry mucous membranes Decreased peripheral perfusion* Thirsty, alert, restless |
| Moderate (6-9% body weight loss) |
Exaggeration of the above Lethargic but irritable Rapid pulse, normal blood pressure Sunken eyes, sunken fontanelle Oliguria is usually obvious Pinched skin retracts slowly (1-2 s)* |
| Severe (≥10% body weight loss) |
General appearance: - Infants: drowsy, limp, cold, sweaty, cyanotic limbs, comatose - Older children: apprehensive, cold, sweaty, cyanotic limbs Rapid feeble pulse, low blood pressure Sunken eyes and fontanelle Pinched skin retracts slowly (>2s)* Deep acidotic breathing* |
* These are the only signs proven to discriminate between hydration and dehydration.
Assuming other emergencies are excluded, a trial of fluid would be instituted. If Joshua was tolerating fluids well, and attentive and supportive parents/guardians are assured, then he could be allowed home with education and advice about fluid & nutritional management, as well as a thorough discussion of the circumstances that should prompt a return to hospital. Joshua should otherwise be reviewed by a GP within 24 hours, with a letter outlining the details of his casualty visit. Handwashing and careful hygiene are also emphasised for those caring for the infant.
Oral rehydration solution (ORS) is the cornerstone of successful rehydration and is recommended globally for the management of acute diarrhoea. The success of ORS is based on the basic observation that intestinal sodium transport is enhanced by glucose transport in the small intestine and that this sodium-coupled mechanism for glucose transport remains intact during acute gastroenteritis.
To facilitate optimal reabsorption of sodium, glucose and water, the sodium and glucose must be in the range recommended [around 90 mmol/L for both Na and glucose]
Rehydration should take place over 4-6 hours and can be given orally or, if either vomiting or fluid refusal is a problem, a nasogastric tube may be used to achieve a steady infusion of fluid.
Volume required for rehydration = estimated deficit and maintenance.
Maintenance:
1-3 months of age = 120ml/kg/24h
3-12 months of age = 100ml/kg/24h
12 months onwards = 80 ml/kg/24h
Therefore in this case:
Deficit = 5% of 14kg = 0.7kg = approx. 700ml
Maintenance = 80ml x 14kg = 1120ml (in 24 hrs)
Therefore total is 700ml + 1120ml = 1820ml over 24 hrs.
If replaced orally, deficit can be replaced over hrs.
Therefore, in the first six hours we aim for 700ml + 6/24 x 1120ml = 980ml
Then maintenance at 1120/24 ml/hr = approx. 47ml/hr
Breastfeeding should continue through rehydration and maintenance phases of treatment, and formula feeds need to be restarted after rehydration. Use of special formulas or diluted formulas is unjustified.
Anti-diarrhoeal pharmacotherapy should NOT be used.
Pro-biotics are not currently recommended, though trials underway.
Antibiotics are of use in a limited number of situations for certain pathogens.
Deficit = 8% x 14kg = 1120ml
Maintenance = 80ml x 14kg = 1120ml (47ml/hr)
Requires: 2240ml over 24hrs.
Can replace deficit over 6 hrs = 1120/6 = 187ml/hr.
Therefore in first 6 hours give 187ml/hr + 47ml/hr = 234 ml/hr.
Thereafter, just maintenance @ 47ml/hr
An increase in stool frequency or fluid content is often of concern to parents, but does not necessarily imply significant organic disease, although this needs to be excluded. In every child who presents with chronic diarrhoea, the decision must be made as to whether further investigation is required. The algorithm outlines an approach to the child with chronic diarrhoea.
Key assessment steps for chronic diarrhoea:
Seen in children between the ages of 12 months and 4 years and current scientific evidence suggests that disturbed intestinal motility is pivotal in the pathogenesis of this condition.
The history is one of frequent, poorly formed and slightly offensive stools. Food material is often recognised in the stool, suggesting rapid gastrointestinal transit. The condition often resolves spontaneously at about 3-4 years of age.
The child is usually active, with unimpaired growth, appetite is normal, and there is a history of increased fluid intake. Further questioning about diet often reveals a high intake of fruit juices and cordial.
The cornerstone of successful treatment includes restriction of fruit juice in the diet, normalising fluid intake and (re-) introduction of wholemeal and other dietary fibres, which add bulk to the stool.
It has also been suggested that many of these children are on a relatively low fat diet, and normalising fat content acts to slow proximal gastrointestinal transit and improve symptoms.
This is defined as the persistence of diarrhoea and failure to gain weight for more than 7 days after hospital admission for gastroenteritis.
It is generally due to a sugar intolerance, which can be confirmed on the basis of stool analysis for reducing sugars and will resolve with elimination of the sugar from the diet.
Other causes include cow's milk protein hypersensitivity or a persistent gastrointestinal infection.
This is an uncommon inherited disorder (autosomal recessive), with symptoms beginning after sucrose is introduced into the diet.
Symptoms consist of watery diarrhoea and abdominal distension.
Growth is usually normal. Diagnosis is dependent on a positive breath hydrogen test using sucrose as the test sugar.
Alternatively a small bowel biopsy containing very low isomaltase and sucrase levels will establish the diagnosis.
Management is based on dietary restriction of sucrose.
The incidence of Crohn's disease (CD) has increased annually; that of ulcerative colitis (UC) has shown an annual fluctuation without an upward trend. Current opinion regarding the cause of IBD favours the hypothesis that these two conditions result from an interaction between immunological, genetic and environmental factors.
Crohn's disease can present in several ways:
Children with UC will usually present with lower abdominal pain, urgency, diarrhoea and rectal bleeding; additionally:
Children may experience the same symptoms, clinical presentations, complications and response to treatment as adults with IBD.
Investigation: Several laboratory tests will point to a diagnosis of IBD; however, endoscopy is the gold standard. Gastroscopy and colonoscopy (with ileoscopy) is essential, taking biopsies at all levels of the gut, whether or not there is macroscopic disease. Biopsies from a normal appearing stomach or duodenum may contain granulomas, making the diagnosis clear. Pathological alterations above the ileum exclude the diagnosis of UC. A barium meal and follow-through or a labelled white cell scan can be helpful in assessing the area of the gut that is involved in Crohn's disease. Capsule endoscopy is a new and evolving technique that is being used to image the small bowel mucosa.