Vomiting and Diarrhea

What is the difference between posseting, regurgitation, and vomiting in infants, and what causes gastro-oesophageal reflux in infancy?

Posseting refers to small amounts of milk returning with swallowed air (wind).

Regurgitation describes larger and more frequent losses of milk.

Vomiting is the forceful ejection of gastric contents.

Gastro-oesophageal reflux in infants is caused by functional immaturity of the lower oesophageal sphincter, which relaxes inappropriately. Contributing factors include a predominantly fluid diet, mainly horizontal posture, and the short intra-abdominal length of the oesophagus.

Nearly all symptomatic reflux resolves spontaneously by 12 months of age.

What are the red flag (alarm) clinical features that should be recognized in a vomiting child?

The following are red flag features in a vomiting child:

(1) Bile-stained vomit — suggests intestinal obstruction;

(2) Haematemesis — suggests oesophagitis, peptic ulceration, or oesophageal varices;

(3) Projectile vomiting in the first few weeks of life — suggests pyloric stenosis;

(4) Vomiting at the end of paroxysmal coughing — suggests whooping cough (pertussis);

(5) Abdominal tenderness or pain on movement — suggests surgical abdomen;

(6) Abdominal distension — suggests intestinal obstruction;

(7) Hepatosplenomegaly — suggests chronic liver disease or inborn error of metabolism;

(8) Blood in stool — suggests intussusception, bacterial gastroenteritis, or IBD;

(9) Severe dehydration/shock — suggests severe gastroenteritis, sepsis, or DKA;

(10) Bulging fontanelle or seizures — suggests raised intracranial pressure or meningitis;

(11) Faltering growth — suggests gastro-oesophageal reflux disease or coeliac disease.

What are the complications that define Gastro-oesophageal reflux disease (GORD), and who is at increased risk?

Gastro-oesophageal reflux disease (GORD) is defined when complications are present.

These complications include:

faltering growth from severe vomiting; oesophagitis causing haematemesis, discomfort on feeding, heartburn, or iron-deficiency anaemia; recurrent pulmonary aspiration causing recurrent pneumonia, cough, wheeze, or apnoea; dystonic neck posturing (Sandifer syndrome); and brief resolved unexplained events (apparent life-threatening events).

Children at increased risk include those with cerebral palsy or neurodevelopmental disorders, preterm infants, those who had surgery for oesophageal atresia or diaphragmatic hernia, obese children, and those with a hiatus hernia.

How is Gastro-oesophageal reflux disease (GORD) managed, including both medical and surgical options?

For uncomplicated gastro-oesophageal reflux, management involves parental reassurance, feeding assessment, smaller and more frequent feeds, and adding inert thickening agents (e.g., Carobel). A 1–2-week trial of alginate therapy (forms a protective gel above stomach contents) can be considered if other measures fail.

For GORD, stomach acid suppression with hydrogen receptor antagonists or proton-pump inhibitors (e.g., omeprazole) is used.

Drugs that enhance gastric emptying (e.g., domperidone) have poor evidence and significant side-effects and should be discouraged. Cow's milk protein allergy should be considered if the child fails to respond.

Surgical management (Nissen fundoplication — wrapping the fundus of the stomach around the intra-abdominal oesophagus) is reserved for complications unresponsive to intensive medical treatment or oesophageal stricture.

What is pyloric stenosis? Describe its clinical features, associated metabolic abnormality, diagnosis, and treatment.

Pyloric stenosis is hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at 2–8 weeks of age, is more common in boys (4:1 ratio), particularly first-born, and has a maternal family history tendency.

Clinical features include non-bilious vomiting that increases in frequency and forcefulness, ultimately becoming projectile; the infant feeds normally after vomiting until dehydration occurs; and weight loss if presentation is delayed. A hypochloraemic, hypokalaemic metabolic alkalosis develops due to loss of stomach contents; hyponatraemia may also be present.

Visible gastric peristalsis (wave from left to right) may be seen. The pyloric mass (feels like an olive) can be palpated during a test feed.

Diagnosis is confirmed by ultrasound (hypertrophied pylorus).

Treatment is surgical pyloromyotomy, but only after correction of fluid and electrolyte imbalances with IV fluids (which may take >24 hours).

What is eosinophilic oesophagitis? Describe its presentation, associations, diagnosis, and treatment.

Eosinophilic oesophagitis is an inflammatory condition of the oesophagus caused by activation of eosinophils within the mucosa and submucosa. It is probably an allergic phenomenon and is more common in children with atopy (asthma, eczema, hay fever). It can present with vomiting, discomfort on swallowing, or bolus dysphagia (food sticking in the upper chest). Diagnosis is made by endoscopy: macroscopically, linear furrows and trachealization are seen; microscopically, eosinophilic infiltration is identified. Treatment is with swallowed corticosteroids (fluticasone or viscous budesonide). Exclusion diets may be of benefit in young children.

What is the global importance of gastroenteritis in children, and what are its most common causative agents?

Gastroenteritis remains a major cause of child mortality in low- and middle-income countries, killing hundreds of thousands of children each year. In high-income countries, children under 3 experience 0.5–2 episodes per year. The most frequent causes in high-income countries are viruses: previously rotavirus was most common, but following vaccination its incidence has fallen markedly, and norovirus is now the most common (though causing less severe disease). Other viruses include sapovirus, enteric adenovirus, and astrovirus. In developing countries, the most important causes are rotavirus, enterotoxigenic E. coli, Shigella, Campylobacter jejuni, and Cryptosporidium. Bacterial causes (Campylobacter, Shigella, Salmonella) may produce dysentery with blood and pus in the stool. Protozoa (Giardia, Cryptosporidium) rarely cause acute gastroenteritis.

Why are infants particularly susceptible to dehydration from gastroenteritis compared to older children?

Infants are particularly susceptible to dehydration because they have a high turnover of fluids (100–120 ml/kg per day, i.e., 10–12% of body weight). Contributing factors include: high body water content; high metabolic rate; greater surface area-to-weight ratio leading to greater insensible water losses (15–17 ml/kg per day); immature renal tubular reabsorption; and inability to communicate their need for extra fluids. Infants under 6 months of age or those with low birthweight are at especially increased risk, as are those who have passed five or more diarrhoeal stools in 24 hours, vomited more than twice in 24 hours, have malnutrition or immune deficiency, or are unable to tolerate supplementary fluids.

How is dehydration classified clinically in a child with gastroenteritis, and what clinical signs are used for assessment?

Dehydration is classified as: (1) No clinically detectable dehydration — usually

What are the three types of dehydration in gastroenteritis, and how do they differ in pathophysiology and clinical features?

The three types are: (1) Isonatraemic dehydration (most common, >75%): losses of sodium and water are proportional, plasma sodium remains normal; presents with moderate signs. (2) Hyponatraemic dehydration (5–10%): greater net loss of sodium than water (e.g., child drinks large volumes of hypotonic fluid); plasma sodium falls; water shifts from extracellular to intracellular compartments, increasing brain volume causing seizures; extracellular depletion is exaggerated causing early, pronounced peripheral signs and increased susceptibility to shock. (3) Hypernatraemic dehydration (10–15%): water loss exceeds sodium loss (e.g., high insensible losses or low-sodium diarrhoea); plasma sodium rises; water shifts from intracellular to extracellular compartments, reducing brain volume causing cerebral shrinkage, irritability, and abnormal neurological signs; peripheral signs of dehydration are paradoxically reduced, making it harder to diagnose clinically, especially in obese infants. It is dangerous and has become less common since formula sodium content was adjusted.

Describe the stepwise management of dehydration in gastroenteritis (Plan A, Plan B, Plan C).

Plan A (No dehydration — prevention): Continue breastfeeding and other milk feeds; encourage fluid intake; discourage fruit juices and carbonated drinks; offer ORS as a supplemental fluid if at increased risk. Plan B (Clinical/some dehydration): Give ORS at 50–100 ml/kg (approximately 75 ml/kg) slowly over 4–6 hours by cup and spoon, dropper, syringe, or nasogastric tube; continue breastfeeding; reassess after 4 hours — if improving, move to Plan A; if worsening, move to Plan C. Plan C (Severe dehydration/shock): IV fluids (Ringer's lactate, Pansol, or Polyelectrolyte); total 100 ml/kg: give 30 ml/kg rapidly in 30–60 minutes, then 70 ml/kg slowly in 2.5–5 hours; assess hourly for return of radial pulse, level of consciousness, skin turgor, and urine output; once improved, step down to Plan B or A.

What is oral rehydration solution (ORS), how does it work, and why are drinks like Coca-Cola unsuitable alternatives?

ORS is a solution containing sodium chloride, trisodium citrate, potassium chloride, and glucose. It works by utilising the sodium-glucose co-transport mechanism in the intestinal epithelium: glucose actively transports sodium across the enterocyte, and water follows passively. This mechanism works effectively even in the presence of gut inflammation, making ORS effective even during active diarrhoea. ORS does not stop diarrhoea but ensures absorption of water and solutes exceeds secretion, keeping the child hydrated until the infection is cleared. It should be offered in small amounts frequently; a nasogastric tube can be used if necessary. Coca-Cola and apple juice are unsuitable because they have a much lower sodium content and much higher osmolarity than ORS, which can worsen fluid shifts and dehydration.

What are the indications for antibiotics in gastroenteritis, and what organisms specifically require antibiotic treatment?

Antibiotics are NOT routinely indicated for gastroenteritis, even if bacterial in origin. Indications for antibiotic use include: suspected or confirmed sepsis; extra-intestinal spread of bacterial infection; Salmonella gastroenteritis in children under 6 months of age; malnourished or immunocompromised children; and specific bacterial infections such as Clostridium difficile (pseudomembranous colitis), cholera, and shigellosis. For dysentery (5–10% of acute gastroenteritis cases): causes include Shigella (60%), Campylobacter, Salmonella, and E. histolytica. Treatment of dysentery involves fluids, feeding, and zinc as for acute watery diarrhoea, plus antibiotics: start with TMP/SMX; if no improvement after 2 days, modify to IV ceftriaxone for Shigella or metronidazole for amoebiasis. Antiparasitic therapy is used for Entamoeba histolytica trophozoites.

What is the role of zinc supplementation in the management of diarrhoea?

Zinc supplementation is recommended in all types of diarrhoea and in all degrees of dehydration. The dosage is: children under 6 months: 10 mg daily for 10–14 days; children over 6 months: 20 mg daily for 10–14 days. In low- and middle-income countries, zinc supplementation is specifically recommended by the WHO because zinc deficiency is common, delays mucosal repair, and impairs immune function. Zinc helps reduce the duration and severity of diarrhoeal episodes and decreases the risk of subsequent episodes.

What are the guidelines for feeding during and after acute gastroenteritis?

For breastfed infants: continue breastfeeding as usual throughout illness and after rehydration therapy. For formula-fed infants: continue the same normal formula at the same normal concentration after rehydration; low-lactose or lactose-free formula should only be used in cases of secondary lactose intolerance. For children on a mixed diet: continue normal feeding; give repeated small frequent feeds every 3–4 hours; avoid overly sweetened foods, high-fibre foods, foods with laxative effects, and fatty foods. After diarrhoea has improved, reintroduce solid food and milk, avoid fruit juices and carbonated drinks, and advise parents about hand hygiene. In low- and middle-income countries, nutritional intake should be increased following diarrhoea to combat malnutrition.

What is post-gastroenteritis syndrome and what is post-infective lactose intolerance?

Post-gastroenteritis syndrome occurs infrequently following an episode of gastroenteritis, when reintroduction of a normal diet leads to a return of watery diarrhoea. In such cases, oral rehydration therapy should be restarted. Post-infective lactose intolerance occurs because gut inflammation can damage the microvilli, reducing the expression of lactase enzymes. Without lactase, lactose is not broken down, resulting in foul-smelling loose stools when a normal dairy-containing diet is resumed. This is a cause of persistent diarrhoea after the acute infection has resolved. It typically resolves after a period of dairy-free exclusion diet.

What is persistent diarrhoea? Define it, describe its epidemiology, risk factors, and pathogenesis.

Persistent diarrhoea is a post-infectious diarrhoea that begins acutely (as watery diarrhoea or dysentery) and lasts 14 days or more. It accounts for about 10% of acute diarrhoeal episodes; peak age is around 18 months. It is responsible for 35% of all diarrhoea-associated deaths in developing countries, with its main sequelae being marked weight loss, malnutrition, and secondary immune deficiency with repeated infections. Risk factors include: low birth weight; malnutrition (delays mucosal repair); absence of breastfeeding; recent introduction of animal milk; recent or recurrent acute diarrhoea in very young infants; immunological impairment; and mismanagement of acute diarrhoea (antibiotic overuse, antidiarrheal drugs, prolonged starvation). Pathogenesis: intestinal pathogens in the presence of risk factors cause mucosal injury with villous flattening and atrophy, reducing nutrient absorption. The associated reduction in digestive enzymes from malnutrition causes osmotic diarrhoea that persists even after the infective agent is eliminated.

What is the pathogenesis of secretory diarrhoea versus osmotic diarrhoea in gastroenteritis?

In secretory diarrhoea (most important mechanism): pathogens or their toxins bind to specific enterocyte receptors and cause the release of chloride ions into the intestinal lumen. This creates an osmotic gradient that draws water and sodium into the lumen, producing large-volume watery diarrhoea. This occurs even when fasting, distinguishing it from osmotic diarrhoea. In osmotic diarrhoea: damage to the villous brush border of the intestine (e.g., by rotavirus) causes malabsorption of intestinal contents. Unabsorbed solutes remain in the lumen and draw in water osmotically. This type of diarrhoea stops when the patient fasts, as there are no ingested solutes to be malabsorbed.

What are the causes of acute abdominal pain in children, categorised by surgical, intra-abdominal medical, and extra-abdominal causes?

Surgical intra-abdominal causes include: acute appendicitis (most common surgical cause), intussusception, malrotation and volvulus, peritonitis, inflamed Meckel diverticulum, inguinal hernia, and trauma. Medical intra-abdominal causes include: non-specific abdominal pain, mesenteric adenitis, constipation, gastroenteritis, urinary tract infection, Henoch-Schönlein purpura, diabetic ketoacidosis, sickle cell disease, hepatitis, inflammatory bowel disease, pancreatitis, functional abdominal pain disorders, and gynaecological causes in pubertal females. Extra-abdominal causes include: upper and lower respiratory tract infection (lower lobe pneumonia causing referred pain), torsion of the testis, and hip and spine pathology. The differential diagnosis is extremely wide and requires careful evaluation; appendicitis must not be missed as it is the most common cause requiring surgical intervention.

What are the clinical features of acute appendicitis in older children versus preschool children, and how is it diagnosed and managed?

In older children, classic features include: anorexia, vomiting, abdominal pain (initially central and colicky, then localising to the right iliac fossa), fever, pain aggravated by movement (walking, coughing, jumping, bumps in the car), and persistent tenderness with guarding at McBurney's point. In preschool children: appendicitis is uncommon but more dangerous; presents as irritability, unexplained crying, refusal of feeding, vomiting, and high fever; diagnostic confusion and delay are common; perforation is rapid because the omentum is less developed. Diagnosis: no single investigation is consistently helpful; raised neutrophil count is not always present; white cells in urine do not exclude appendicitis; ultrasound (thickened, non-compressible appendix with increased blood flow) can support the diagnosis; laparoscopy is available in some centres. Management: uncomplicated — appendicectomy; complicated (abscess, perforation) — IV fluids and antibiotics then laparotomy or conservative management with delayed appendicectomy. Repeated clinical review every few hours is essential.

What is intussusception? Describe its pathophysiology, typical presentation, investigation, and treatment.

Intussusception is the invagination of proximal bowel into a distal segment, most commonly involving the ileum passing through the ileocaecal valve. It is the most common cause of intestinal obstruction in infants after the neonatal period, with a peak age of 3 months to 2 years. The most serious complication is stretching and constriction of the mesentery causing venous obstruction, bowel engorgement, bleeding, fluid loss, and ultimately perforation, peritonitis, and gut necrosis. Presentation includes: paroxysmal severe colicky pain with pallor (child draws up legs), possible bile-stained vomiting, a palpable sausage-shaped abdominal mass, redcurrant jelly stool (blood-stained mucus — a late but characteristic sign), abdominal distension, and shock. Most cases have no identifiable cause (though viral infection may enlarge Peyer's patches as a lead point); a Meckel diverticulum or polyp is more likely as a lead point in children over 2 years. Investigation: abdominal ultrasound shows the target/doughnut sign. Management: prompt IV fluid resuscitation; reduction by rectal air insufflation (success rate ~75%); surgery (operative reduction) for the remaining 25% or if peritonitis is present. Recurrence occurs in <5%.

What is a Meckel diverticulum? Describe its prevalence, contents, clinical presentations, investigation, and treatment.

A Meckel diverticulum is an ileal remnant of the vitello-intestinal duct occurring in approximately 2% of individuals. It contains ectopic gastric mucosa or pancreatic tissue. The majority are asymptomatic. Clinical presentations include: severe rectal bleeding (classically neither bright red nor true melaena, with an acute reduction in haemoglobin), intussusception, volvulus (twisting of the bowel), or diverticulitis (inflammation that mimics appendicitis). Investigation: a technetium scan demonstrates increased uptake by ectopic gastric mucosa in 70% of cases; a negative scan does not exclude the diagnosis. Laparoscopic examination can confirm the diagnosis if the scan is negative. Treatment is surgical resection.

What is malrotation and volvulus? Describe the anatomy, presentations, and management.

Malrotation is a congenital abnormality where the small intestine lies predominantly on the right side of the abdomen (failure to rotate and fix correctly during fetal life). Fibrous bands (Ladd bands) tether the caecum to the right upper quadrant, compressing the duodenum and causing intestinal obstruction. The poorly tethered gut can twist (volvulus), compromising the superior mesenteric arterial blood supply to the small and proximal large intestine, potentially causing infarction. Two presentations: (1) Obstruction with bilious vomiting — usually in the first few days of life; (2) Obstruction with compromised blood supply (vascular emergency). Any child with dark green (bilious) vomiting requires an urgent upper gastrointestinal contrast study unless signs of vascular compromise are present, in which case urgent laparotomy is required. Management: the volvulus is untwisted at operation, duodenum mobilised, bowel placed in the non-rotated position with the appendix removed to prevent future diagnostic confusion.

What are the red flags (alarming signals) that suggest organic disease rather than functional abdominal pain in a child with chronic or recurrent abdominal pain?

History-based alarming signals include: age under 5 years; nocturnal symptoms; persistent right upper or right lower quadrant pain (pain away from the umbilicus); referred pain; weight loss or growth retardation; vomiting (chronic, bile- or blood-stained); dysphagia; diarrhoea (prolonged, mucoid, or bloody); dysuria, haematuria, or flank pain; constitutional symptoms or extra-intestinal manifestations; and family history of organic GI disorders (IBD, coeliac disease, peptic ulcer disease). Abnormal physical exam findings include: growth deceleration or delayed puberty; jaundice; significant anaemia; rebound tenderness, guarding, or organomegaly; and perianal disease (tags, fissures, fistulas). These red flags guide further investigations to exclude serious causes before diagnosing functional pain.

What are functional abdominal pain disorders (FAPDs) in children? Describe the subtypes, pathogenesis, and management.

FAPDs are a group of conditions in which abdominal pain has no identifiable organic cause. Subtypes include: irritable bowel syndrome (most common — pain related to defecation, stool frequency, or stool appearance); abdominal migraine (paroxysms of intense periumbilical/midline pain lasting ≥1 hour with nausea, vomiting, pallor, and headache; often with personal/family history of migraine); functional dyspepsia (postprandial fullness, early satiety, upper abdominal bloating, nausea, or epigastric pain/burning); and functional abdominal pain not otherwise specified. Pathogenesis involves visceral hypersensitivity, neurological hypervigilance, and psychosocial stressors — a disorder of the gut-brain-microbiota axis. Management is based on a bio-psychosocial model: reassure family that pain is real; explain sensitisation of intestines; avoid unnecessary investigations; address psychosocial triggers. Medications: low-FODMAP diets and antispasmodics for IBS; anti-migraine medication for abdominal migraine; acid blockade (PPIs/H2 blockers) for functional dyspepsia. Behavioural modification (relaxation, distraction, hypnotherapy — the most effective) improves coping. Prognosis: ~50% become rapidly symptom-free; ~25% resolve over months; ~25% continue into adulthood as IBS, migraine, or functional dyspepsia.

What is coeliac disease? Describe its aetiology, classical and non-classical presentations, diagnosis, and management.

Coeliac disease is an immune-mediated systemic disorder triggered by gluten and related prolamines (found in wheat, barley, and rye) in genetically susceptible individuals (HLA DQ2 and DQ8 haplotypes). It causes progressive villous shortening and flattening of the small intestinal mucosa. Prevalence is approximately 1 in 100. Classical presentation occurs at 8–24 months after introduction of wheat-containing weaning foods: profound malabsorption syndrome, faltering growth, abdominal distension, buttock wasting, abnormal stools, recurrent abdominal pain, and general irritability. Non-classical presentation (now more common): mild non-specific GI symptoms, anaemia, growth faltering, short stature, delayed puberty, arthritis, neuropathy, dermatitis herpetiformis, or osteoporosis. Screening is performed in high-risk groups (type 1 diabetes, autoimmune thyroid disease, Down syndrome, first-degree relatives). Diagnosis: serology (IgA anti-tTG and IgA EMA — highly sensitive and specific); confirmed by endoscopic duodenal biopsy (flat mucosa); diagnosis can be made on blood tests alone if IgA anti-tTG is markedly raised AND IgA EMA is positive. Management: lifelong strict gluten-free diet (remove all wheat, rye, barley); dietician supervision essential; non-adherence risks micronutrient deficiency (especially osteopenia) and small bowel lymphoma.

What is lactose intolerance? Describe its mechanism, clinical features, causes, epidemiology, and management.

Lactose intolerance is a form of malabsorption in which lactase enzyme is not expressed on the intestinal microvilli. Without lactase, lactose is not broken down into glucose and galactose, causing recurrent bloating, abdominal pain, and foul-smelling 'yeasty' stool whenever dairy products are consumed; some patients experience nausea and vomiting. The most common cause in children is secondary (post-infectious) lactose intolerance following viral gastroenteritis, which damages microvilli and reduces lactase expression — this typically resolves after several months of a dairy-free diet. From early adulthood, primary lactose intolerance varies widely by ethnicity: <10% in Northern Europe to 95% in parts of Asia and Africa. Congenital lactase deficiency (genetic inability to produce lactase) is rare. Management: dairy exclusion diet; lactase supplements are available but can be denatured by stomach acid and are not always effective.

What are the causes of vomiting in infants, preschool children, and school-age/adolescent children?

In infants: gastro-oesophageal reflux, feeding problems, infection (gastroenteritis, respiratory tract infection/otitis media, whooping cough, urinary tract infection, meningitis), food/milk allergy or intolerance, intestinal obstruction (pyloric stenosis, atresia, intussusception, malrotation, volvulus, strangulated inguinal hernia, Hirschsprung disease), inborn errors of metabolism, congenital adrenal hyperplasia, and renal failure. In preschool children: gastroenteritis, infections (including pyelonephritis, septicaemia, meningitis), peptic ulceration/H. pylori, appendicitis, migraine, raised intracranial pressure, coeliac disease, eosinophilic oesophagitis, renal failure, and inborn errors of metabolism. In school-age/adolescents: gastroenteritis, diabetic ketoacidosis, alcohol/drug ingestion, cyclical vomiting syndrome, bulimia/anorexia nervosa, pregnancy, and torsion of the testis.

What are the red flag signs suggesting a surgical cause of acute abdominal pain, and what initial assessment steps are taken?

Red flag signs suggesting a surgical cause include: sudden onset of severe pain; pain that interrupts sleep; bilious vomiting; haematemesis and haematochezia; hypotension; tachycardia; patient writhing in pain; jaundice; guarding and rigidity; absent or tinkling bowel sounds; and gross abdominal distension. Initial assessment and stabilisation aims for: rapid cardiopulmonary assessment; exclusion of life-threatening surgical conditions; and assessment of severity of illness. Steps include: (1) child's appearance; (2) assessment of airway, breathing, circulation, and vital signs; (3) neurological status; (4) blood sugar; (5) food and fluid intake. Investigations to consider include CBC and CRP, urinalysis, stool analysis and occult blood, liver function tests, amylase/lipase, abdominal X-rays (for small bowel obstruction), abdominal ultrasound, and CT abdomen (high sensitivity and specificity).

What are the when-to-return warning signs that should be given to parents of a child with acute gastroenteritis managed at home?

Parents should be advised to return immediately if: the baby is not able to drink or breastfeed; the child becomes sicker with no improvement; the child develops a fever; blood appears in the stool; the child has repeated vomiting; or the child shows signs of increased thirst (suggesting worsening dehydration). Additionally, for prevention, parents should be counselled on thorough hand washing; not sharing towels used by the infected child; and keeping the child out of childcare facilities or school until 48 hours after the last episode of vomiting or diarrhoea. Immunisation against rotavirus is recommended to prevent severe gastroenterit