Acute Gastroenteritis in Children

Overview & Definition

Acute gastroenteritis (AGE) is an inflammation of the stomach and intestinal mucosa of infectious origin, producing diarrhoea (passage of 3 or more loose or watery stools in 24 hours, or a stool frequency/looseness exceeding the child's normal baseline) and/or vomiting, lasting under 14 days.[1]

The clinical definition is operational. WHO defines diarrhoea as the passage of 3 or more loose or watery stools in 24 hours, with the caveat that a single large, watery stool or any stool containing visible blood is also diarrhoea. Passage of formed stools, even when frequent, is not diarrhoea. Breast-fed neonates may pass 6 to 10 semi-formed stools daily; this is physiological and not gastroenteritis.[1]

Three temporal categories are recognised:[1]

• Acute diarrhoea — under 14 days. By far the commonest (over 90% of cases). Mostly infective and self-limiting.
• Persistent diarrhoea — 14 to 29 days. Implicated organisms include Giardia, Cryptosporidium, enteroaggregative E coli, and (in endemic regions) HIV. Persistent diarrhoea signals underlying malnutrition, immune compromise, or a non-infectious cause.
• Chronic diarrhoea — 30 days or more. Includes coeliac disease, cow's milk protein allergy, inflammatory bowel disease, cystic fibrosis, congenital chloride-losing or sodium-losing diarrhoea, and toddler's diarrhoea.[5]

AGE is fundamentally a volume and electrolyte disorder: the entire threat to life comes from fluid and electrolyte loss. Most deaths occur not from the pathogen but from dehydration, hypovolaemic shock, electrolyte disturbance (hypo- or hypernatraemia, hypokalaemia), metabolic acidosis, and hypoglycaemia. The defining therapeutic insight of the past 60 years — recognised in the discovery of sodium-glucose co-transport by Hirschhorn and others — is that enterotoxin-stimulated intestine retains the capacity to absorb sodium and water in the presence of glucose, which is the molecular basis of oral rehydration solution (ORS).[6]

Classification

AGE can be classified along three clinically useful axes.[6]

By duration

• Acute — under 14 days (the focus of this chapter).
• Persistent — 14 to 29 days. Carry a different workup: stool for ova/cysts/parasites, HIV test, anti-tTG for coeliac, sweat chloride.
• Chronic — 30 days or more (non-infectious causes dominate).[1]

By stool character — the most useful clinical split

By pathogen class

The mnemonic "Viruses, Bacteria, Parasites" with their relative frequency and key features is captured below in the Classification figure and Epidemiology section.[11]

Epidemiology & Risk Factors

Global burden

Acute gastroenteritis remains the second leading cause of death in children under 5 worldwide, behind only pneumonia. Estimates of global diarrhoeal mortality have fallen substantially with scale-up of ORS, zinc, rotavirus vaccine, clean water, and improved nutrition, but diarrhoea still kills in the order of half a million children under 5 every year.[11] Almost 90% of these deaths are due to dehydration — and are therefore preventable with simple fluids. The vast majority of deaths occur in sub-Saharan Africa and South Asia, where access to ORS, clean water, and timely care is constrained.

The GEMS study

The Global Enteric Multicenter Study (GEMS), a prospective case-control study of over 9,400 children under 5 in seven sites across Africa and Asia (Kotloff et al., 2013), is the most authoritative modern dataset on diarrhoeal aetiology in developing countries. GEMS identified four pathogens accounting for the majority of moderate-to-severe diarrhoea:[2]

1. Rotavirus — the leading cause overall (about 20% of moderate-to-severe cases pre-vaccine).
2. Cryptosporidium — particularly in infants under 12 months and in HIV-positive children.
3. Shigella — the leading cause of dysentery and a major cause of mortality.
4. Heat-stable enterotoxigenic E. coli (ST-ETEC) — the major cause of travellers' diarrhoea and a leading cause of paediatric watery diarrhoea in developing settings.[2]

Risk factors

• Age: peak incidence 6 to 24 months — loss of transplacentally acquired immunity, introduction of weaning foods, mouthing behaviour, immature gut mucosa.
• Malnutrition: the single most important risk modifier. A wasted child has 2 to 3× the mortality risk for an identical pathogen load; oedematous severe malnutrition reduces the clinical signs of dehydration.
• Immunocompromise: HIV, primary immunodeficiency, chemotherapy. Persistent Cryptosporidium, Cystoisospora, CMV.
• Lack of exclusive breastfeeding: bottle-feeding in low-resource settings introduces contaminated formula.
• Unsafe water and poor sanitation: faecal-oral transmission.
• Day-care attendance, household crowding, season: viral AGE peaks in winter (rotavirus, norovirus); bacterial AGE peaks in hot/wet season.
• No rotavirus vaccination: vaccine reduces severe rotavirus AGE by about 85% and rotavirus deaths dramatically.[10]
• Recent antibiotic exposure: risk of C. difficile.
• Travel: ETEC, cholera, amoebic dysentery.

Pathophysiology

The fundamental division of acute diarrhoea is between secretory and osmotic mechanisms. Understanding which mechanism is at work predicts the natural history, the response to fasting, and the choice of ORS.[11]

Secretory diarrhoea

The defining feature is active intestinal secretion of chloride and water that persists despite fasting. The stool is large-volume, watery, isotonic, and continues even when the patient takes nothing by mouth. The prototype is cholera, but rotavirus NSP4 also acts as an enterotoxin.[10]

Molecular cascade (cholera model):[6]

1. Vibrio cholerae elaborates cholera toxin (an A-B toxin). The B subunit binds GM1 ganglioside on the enterocyte; the A subunit enters the cell.
2. The A subunit ADP-ribosylates the stimulatory G-protein Gsα, locking it in the active (GTP-bound) state.
3. Constitutive activation of adenylate cyclase → sustained rise in intracellular cAMP.
4. cAMP opens the CFTR chloride channel on the apical membrane of the crypt enterocyte → massive Cl⁻ secretion into the lumen.
5. To maintain electroneutrality, Na⁺ follows, and water follows osmotically — producing "rice-water" stool.
6. Crucially, the absorptive villous cells remain intact. Sodium-glucose co-transport (SGLT1) on villous tips still functions. This is the molecular rationale for ORS: glucose-coupled sodium absorption bypasses the secretory defect and reclaims water.[6]

Rotavirus produces a similar picture through NSP4 (an enterotoxic viral protein), villous ischaemia, and transient malabsorption of disaccharidases (especially lactase — hence the temporary lactose intolerance that follows rotavirus infection).[10]

Osmotic diarrhoea

The defining feature is malabsorption of nutrients that remain in the lumen and draw water osmotically. The stool is smaller in volume, stops with fasting, has an osmotic gap (stool osmolality minus 2×(Na⁺ + K⁻) greater than 50 mOsm/kg), and may show reducing substances. Mechanisms:[6]

• Mucosal invasion and villous-tip destruction — Shigella, Campylobacter, Salmonella. Loss of mature absorptive enterocytes; transient brush-border enzyme deficiency; inflammatory exudate.
• Disaccharidase deficiency — lactase destroyed by rotavirus → undigested lactose ferments in the colon → osmotic load.
• Mucosal inflammation and protein loss — invasive bacteria produce mucosal ulceration and exudative, bloody stool.[10]

Fluid and electrolyte consequences

Stool losses in AGE are isotonic — roughly 90 mEq/L Na⁺, 80 mEq/L Cl⁻, 50 mEq/L K⁺, 30 to 40 mEq/L HCO₃⁻. The net result is:[6]

• Dehydration — predominantly isotonic (isonatraemic) in 70 to 80% of cases. Hypernatraemic dehydration (Na over 150 mmol/L) occurs in 10 to 15%, typically in infants fed concentrated feeds or with high insensible losses; presents with irritability, very doughy skin, tremor, seizures. Hyponatraemic (Na under 130 mmol/L) in 5 to 10%, presents with lethargy, seizures, oedema.
• Hypokalaemia — stool K⁺ loss, secondary hyperaldosteronism, intracellular shift with correction of acidosis. Presents with muscle weakness, ileus, paralytic ileus, cardiac arrhythmias (U waves, flat T, prolonged QT).
• Metabolic acidosis — bicarbonate loss in stool, lactic acidosis from shock, renal failure. Presents with tachypnoea (Kussmaul), sighing respiration, low pH, low bicarbonate, normal PaCO₂ (compensatory) on blood gas.
• Hypoglycaemia — fasted state, depleted glycogen, especially in malnourished infants. May cause seizures and coma; easily missed.[2]

Clinical Presentation

The presenting complaint is almost always one of: acute-onset diarrhoea, vomiting, fever, abdominal cramps, reduced oral intake, lethargy, reduced urine output, or in young infants, fewer wet nappies. The history must establish:[6]

• Stool frequency, volume, character: watery vs bloody, presence of mucus or pus, smell (foul-smelling, greasy suggests Giardia), colour (rice-water in cholera; redcurrant-jelly in intussusception).
• Vomiting: frequency, bilious (surgical cause), coffee-ground (haematemesis).
• Fever: high swinging fever favours bacterial; absent fever with profuse watery stool favours cholera.
• Ability to drink: a key WHO discriminator.
• Urine output: number of wet nappies in past 12 to 24 h — last wet nappy is the bedside proxy.
• Preceding illness, contacts, travel, day-care, recent antibiotics, food history, water source.
• Immunisation status: rotavirus vaccine; measles in the differential of diarrhoea with rash.[10]

Stool patterns by pathogen — the clinical "fingerprint"

• Rotavirus: vomiting precedes watery diarrhoea by 12 to 24 h; fever low-grade; lasts 3 to 8 days.
• Norovirus: explosive vomiting prominent; diarrhoea brief (1 to 3 days); outbreak setting.
• Enterotoxigenic E. coli: watery diarrhoea without fever; travellers.
• Shigella (shigellosis): high fever, abdominal cramps, tenesmus, then bloody mucoid stool with faecal leucocytes; may cause seizures in young children (Shigella encephalopathy / "Shigellosis-associated encephalopathy").[9]
• Salmonella (non-typhoidal): watery or bloody diarrhoea, fever, bacteraemia in infants under 3 months; risk of osteomyelitis in sickle-cell disease.
• Campylobacter jejuni: bloody diarrhoea, abdominal pain mimicking appendicitis; Guillain-Barré syndrome 1 to 3 weeks later (anti-GQ1b antibody).
• EHEC (O157:H7): afebrile, bloody diarrhoea, abdominal pain, then 5 to 10 days later pallor, oliguria, petechiae — HUS.
• Entamoeba histolytica: abdominal pain, bloody mucoid stool, may form amoebic liver abscess (right upper quadrant pain, fever).
• Giardia lamblia: foul-smelling, greasy, floating stools, bloating, flatulence; persistent; no fever; no blood.
• Vibrio cholerae: profuse rice-water stool, vomiting, rapid severe dehydration, no fever.

Dehydration — the cardinal physical finding

Signs to elicit and document at every assessment are in the WHO dehydration table (see Clinical Assessment). The bedside set is: general appearance / alertness, eyes (sunken?), fontanelle (sunken in infants), mouth/tongue (dry?), tears when crying, skin pinch (elasticity), capillary refill, peripheral pulse, warmth of extremities, urine output, weight (most useful when a recent pre-illness weight exists).[6]

Extra-intestinal / atypical presentations

• Neonate / young infant: may present with poor feeding, lethargy, hypothermia, or apnoea — atypical and easily missed.
• Severe malnutrition: oedema masks dehydration; sunken eyes and reduced skin turgor are unreliable. Use WHO's modified assessment (see Special Populations).
• Immunocompromised: persistent watery diarrhoea (Cryptosporidium, Cystoisospora, CMV colitis).
• Shigella in infants: seizures may precede the diarrhoea and be mis-attributed to febrile convulsion.[6]

Differential Diagnosis

The list is broad — "diarrhoea and vomiting" is one of the commonest paediatric presentations and includes surgical, metabolic, and extra-intestinal emergencies. A structured differential is mandatory.[4]

Key distinguishing questions

1. Is the child toxic / systemically unwell beyond the dehydration grade? — think sepsis, meningitis, DKA, surgical abdomen.
2. Is there bile-stained vomit? — malrotation / volvulus until proven otherwise.
3. Is there blood in the stool? — invasive bacterial, amoebic, cow's-milk-protein colitis, intussusception (redcurrant-jelly).
4. Has the urine output been normal? — picture of dehydration without reduced urine output suggests an alternative diagnosis (DKA, diabetes insipidus).[6]

Clinical & Bedside Assessment

The WHO dehydration grading is the single most important bedside tool in paediatric AGE and must be reproduced verbatim — every NEET-PG/INICET candidate is expected to recall it fluently.[1]

[6]

Two signs suffice for SOME dehydration

WHO operational rule: two or more of the following → classify as SOME dehydration (and treat with Plan B): restlessness/irritability, sunken eyes, drinks eagerly/thirsty, skin pinch goes back slowly.[6]

Two signs suffice for SEVERE dehydration

Two or more of the following → classify as SEVERE dehydration (treat with Plan C): lethargy/unconsciousness, sunken eyes, not able to drink, skin pinch goes back very slowly.[6]

The skin pinch test (abdominal wall)

Pinch a fold of skin and subcutaneous tissue over the mid-abdominal wall between thumb and forefinger, lift it, and release. Time the return to flat.[1]

• Under 1 second — normal / no dehydration.
• 1 to 2 seconds — slow → some dehydration.
• More than 2 seconds — very slow → severe dehydration.[6]

Avoid pinching over the chest wall (less reliable in malnourished or obese children).[1]

Capillary refill time

Press the nail-bed of a finger or toe for 5 seconds, release. Refill over under 2 seconds is normal; 2 to 3 seconds indicates moderate compromise; over 3 seconds indicates shock. CRT is sensitive but non-specific — febrile, cold, or anxious children may have prolonged CRT.[12]

Other bedside assessments

• Weight — most objective measure of dehydration if a recent pre-illness weight is available. Acute weight loss: under 5% mild, 5 to 9% moderate, 10% or more severe. These percentage categories do not map exactly to WHO grades (which use clinical signs, not percentages) but are useful in resuscitation monitoring.
• Vital signs — tachycardia (early), weak thready pulse (shock), tachypnoea (acidosis or compensation), hypotension (late, pre-terminal), hypothermia in severe sepsis or malnutrition.
• Anterior fontanelle (infants under 18 months) — sunken fontanelle is a reliable sign of significant dehydration.
• Mucous membranes, tears, eyes — dry tongue and absent tears support dehydration.
• Urine output — under 1 mL/kg/h indicates significant dehydration; anuria for 6 h or more suggests HUS or AKI.[6]

[6]

Investigations

AGE is, in the vast majority of cases, a clinical diagnosis. Routine laboratory tests are unnecessary. The choice of investigation is dictated by severity, host risk factors, and outbreak setting.[12]

Stool tests — when to send

• Stool culture — send if bloody diarrhoea, severe/prolonged illness, immunocompromise, suspected sepsis, day-care or hospital outbreak, suspected HUS, recent foreign travel, suspected cholera. Specifically request culture for Salmonella, Shigella, Campylobacter, E. coli O157:H7 (sorbitol-MacConkey), Yersinia, Vibrio.
• Stool microscopy for ova, cysts, parasites — if persistent diarrhoea (over 14 days), or suspected Giardia / amoebiasis. Send three serial samples (parasite shedding is intermittent).
• Stool for C. difficile toxin — if recent antibiotic exposure, hospital-acquired diarrhoea, or severe colitis with leucocytosis.
• Stool multiplex PCR panel — increasingly available; rapid, sensitive, but detects DNA, not necessarily viable organisms — over-diagnosis of co-infection is a real pitfall. Use selectively.
• Fecal calprotectin / faecal leucocytes / lactoferrin — surrogate markers of intestinal inflammation (invasive vs non-invasive diarrhoea); supportive but rarely change management in AGE.
• Stool reducing substances / pH — supports osmotic (carbohydrate malabsorption) diarrhoea when lactose intolerance is suspected.[6]

Blood tests — when to send

• Urea and electrolytes (U&E) and creatinine — essential in severe dehydration, when IV fluids are needed, when sodium abnormality is suspected, or before potassium replacement. Look for hyponatraemia/hypernatraemia, hypokalaemia, metabolic acidosis (low bicarbonate), pre-renal AKI (raised urea, raised creatinine).
• Venous blood gas — bedside in any severely dehydrated or acidotic child. Confirms metabolic acidosis (low pH, low HCO₃⁻, normal PaCO₂ with compensatory fall) and identifies hyper- or hyponatraemia.
• Blood glucose — every severely dehydrated or malnourished child. Hypoglycaemia is easily missed and rapidly fatal.
• Full blood count — leucocytosis and left shift in bacterial invasive disease; marked leucocytosis with fragmented red cells and falling platelets is the HUS signature; thrombocytopenia also in sepsis and dengue.
• Blood culture — before antibiotics if bacteraemia suspected, especially infants under 3 months and immunocompromised.
• CRP / procalcitonin — non-specific; may support bacterial cause but not diagnostic alone.[6]

Urine tests

• Urinalysis and culture — mandatory in any infant under 3 months with vomiting or unexplained fever, and in any child where urine output is hard to assess. UTI commonly co-presents with or mimics AGE.[2]

Imaging

• Abdominal ultrasound — if intussusception, appendicitis, malrotation, or HUS (to look for colonic wall thickening) is suspected.
• Chest X-ray — if pneumonia is in the differential.
• Abdominal X-ray — only if toxic megacolon, perforation, or Hirschsprung enterocolitis is suspected (pneumatosis intestinalis, free air).[1]

What is NOT routinely required

• Routine stool culture in simple watery AGE.
• Routine electrolytes in no-dehydration / some-dehydration managed at home.
• Routine imaging.
• Sigmoidoscopy in acute AGE (reserved for suspected IBD or C. difficile with diagnostic uncertainty).[6]

Management — Resuscitation

Resuscitation is dictated by the WHO dehydration grade. The key principle is that most children can and should be rehydrated orally — IV fluids are reserved for the severely dehydrated, those in shock, and those who cannot tolerate oral fluids.[6]

Plan C — severe dehydration (the resuscitation bundle)

Goal: restore intravascular volume and perfusion within 30 to 60 minutes, then correct the deficit, then maintain.[6]

Step 1 — confirm shock and start IV access immediately. If IV access cannot be obtained within minutes, use the intraosseous route (proximal tibia, distal femur). Do not delay fluids for access.[6]

Step 2 — give a 20 mL/kg bolus of isotonic crystalloid — normal saline (0.9% NaCl) or Ringer's lactate (Hartmann's) — over 10 to 20 minutes. Ringer's lactate is preferred by WHO because it buffers metabolic acidosis, but normal saline is the practical default in most settings. Avoid dextrose-containing solutions as the resuscitation fluid (dextrose is metabolised to free water; effectively hypotonic once the dextrose is metabolised, and may worsen cerebral oedema in hypernatraemia).[1]

Step 3 — reassess after each bolus. Recheck pulse, capillary refill, skin temperature, conscious level, blood pressure, urine output. Repeat the 20 mL/kg bolus (up to a total of 60 mL/kg in the first hour) until perfusion is restored (warm peripheries, CRT under 2 seconds, conscious and responding, urine output returns).[6]

Step 4 — once shock is reversed, switch to deficit correction with ORS where possible, or continue IV fluids at a slower rate calculated from the deficit and maintenance using the Holliday-Segar formula:

• First 10 kg body weight: 100 mL/kg/day = 4 mL/kg/h.
• Next 10 kg: 50 mL/kg/day = 2 mL/kg/h.
• Each subsequent kg: 20 mL/kg/day = 1 mL/kg/h.[6]

Add ongoing stool losses with ORS (not IV) wherever tolerated.[6]

Step 5 — check blood glucose and electrolytes early. Treat hypoglycaemia with 2 mL/kg of 10% dextrose IV bolus, then continue dextrose-containing maintenance. Correct hypernatraemia and hyponatraemia slowly (see Complications).[6]

Step 6 — switch to ORS as soon as the child is conscious and able to drink.[6]

Key resuscitation pitfalls

• Treating with 5% dextrose or 0.45% saline as the bolus — hypotonic; ineffective for volume; risks hyponatraemia and cerebral oedema.
• Not reassessing between boluses — fluid overload and pulmonary oedema in heart disease.
• Stopping ORS / feeds prematurely — prolongs the illness, worsens mucosal recovery.
• Failing to give zinc — zinc is part of standard WHO management, not optional.
• Forgetting glucose in the malnourished infant — hypoglycaemia.[3]

Shock / collapse

If the child is in undifferentiated shock, follow the standard paediatric sepsis bundle: high-flow oxygen, IV access, 20 mL/kg isotonic boluses, blood glucose check, antibiotics if sepsis suspected, and escalate to inotropes if fluid-refractory. AGE may co-present with sepsis (Salmonella bacteraemia) or be the misdiagnosis for sepsis, DKA, or surgical abdomen.[1]

Management — Definitive & Stepwise

The four pillars of definitive management of acute watery AGE, in order of importance:[1]

1. Rehydrate according to WHO Plan A/B/C (above).
2. Give zinc — 20 mg/day for 10 to 14 days.
3. Continue feeding (and breastfeeding).
4. Selective adjunctive therapy — ondansetron, probiotics, specific antibiotics.[5]

Plan A — no dehydration (home management)

Plan A is also the counselling plan given to every caregiver regardless of dehydration grade. The components are:[6]

1. Give extra fluids — ORS, breast-milk, plain water, soups, rice water, coconut water, lassi. Avoid sugary or carbonated drinks (osmotic diarrhoea), fruit juices (especially apple and pear — sorbitol), and avoid boiled milk (concentrated salts and protein worsen diarrhoea).
2. Give ORS for each loose stool:
   • under 2 years: 50 to 100 mL after each loose stool.
   • 2 to 10 years: 100 to 200 mL after each loose stool.
   • over 10 years: as much as wanted.
3. Give zinc 20 mg/day for 10 to 14 days (10 mg/day for infants under 6 months).
4. Continue feeding — never stop feeds; resume a normal age-appropriate diet as soon as rehydration is achieved; breastfeeding on demand.
5. Return immediately if danger signs develop (see below).[6]

Plan B — some dehydration (clinic management)

• Give ORS 75 mL/kg over 4 hours in the clinic.
• Method: small, frequent sips (5 mL every 1 to 2 minutes) by spoon or cup. If the child vomits, wait 5 to 10 minutes, then resume slowly.
• If unable to tolerate orally: NG tube with ORS at the same total volume over 4 hours.
• Continue breastfeeding throughout; do not give other foods during the 4-hour ORS phase (resume after).
• Reassess at 4 hours: re-classify dehydration and proceed to Plan A (improved), repeat Plan B (some dehydration persists), or escalate to Plan C (now severe).[6]

Zinc supplementation

Dose: 20 mg elemental zinc daily for 10 to 14 days (10 mg/day for infants under 6 months). The Cochrane systematic review and meta-analysis (Lazzerini & Wanzira, 2016, 25 trials, over 9,000 children) found that oral zinc shortens the duration of acute diarrhoea by about 0.5 day, reduces stool frequency at day 3, and reduces the proportion of episodes lasting over 7 days.[3] Benefits are greatest in children with stunting or zinc deficiency, who bear the highest mortality. WHO and UNICEF recommend zinc for every episode of acute diarrhoea in children, integrated with ORS.

ORS formulation

[6]

Antiemetics — ondansetron

A single dose of oral ondansetron (0.15 mg/kg, max 8 mg) reduces vomiting, the proportion who need IV fluids, and the proportion who need admission in children with mild-to-moderate AGE and vomiting. The evidence comes from Freedman's 2006 NEJM trial and a Cochrane / Bayesian network meta-analysis of antiemetics.[4][8] Cautions:

• Do not use in children with prolonged QT interval (congenital long QT, electrolyte disturbance, on QT-prolonging drugs). ECG if doubt.
• Do not repeat the dose routinely — risk of QT prolongation and osmotic diarrhoea from the oral dissolving vehicle.
• Do not substitute antiemetics for rehydration — they are an adjunct.
• Not recommended in children with surgical abdomen (may mask the diagnosis).[4]

Probiotics

Lactobacillus rhamnosus GG (and S. boulardii to a lesser extent) shorten the duration of acute viral diarrhoea by about 1 day when started early, with a Network Meta-Analysis confirming benefit primarily in viral, watery AGE.[5] Caution in immunocompromised and central venous catheter patients — probiotic bacteraemia and fungaemia are described.

Antibiotics — when (and when NOT)

[4]

Nutrition — continue feeding

WHO and ESPGHAN guidance: continue breastfeeding throughout and resume normal age-appropriate feeding as soon as rehydration is achieved (typically after the 4-hour Plan B period). Do not "rest the gut". Avoid routine dilution of formula, and avoid prolonged clear-fluid or restrictive diets. Lactose-free formula may be tried in the small subset who develop secondary lactose intolerance (persistent watery, acidic, frothy stool with reducing substances positive, perianal excoriation); resume standard formula once stools normalise.[6]

[6]

When to admit

• Severe dehydration (Plan C).
• Persistent vomiting unable to tolerate ORS despite ondansetron.
• Bloody diarrhoea with systemic toxicity, or suspected HUS.
• Infants under 6 months, malnourished, immunocompromised.
• High stool output (over 5 to 10 mL/kg/h) — manage in hospital with measured replacement.
• Social concerns — caregiver unable to manage Plan A reliably.[6]

When to discharge

• Adequate rehydration, tolerating oral fluids.
• Caregiver competent in Plan A and zinc administration.
• No red flags (no bloody diarrhoea, no high output, no HUS).
• Clear "return immediately" advice given.[6]

Specific Subtypes & Scenarios

Rotavirus AGE

The leading cause of severe AGE in children under 5 worldwide pre-vaccine, accounting for ~40% of AGE hospitalisations.[2] Causes destruction of mature villous enterocytes with transient lactase deficiency, NSP4-mediated secretion, and reduced disaccharidase activity. Clinical: vomiting precedes watery diarrhoea, low-grade fever, lasts 3 to 8 days. Vaccine (live-attenuated oral — Rotateq pentavalent, Rotarix monovalent): given at 6, 10, 14 weeks; the first dose must be given before 15 weeks and the last by 24 to 32 weeks (concern about intussusception with later dosing). The Cochrane review of rotavirus vaccines in use shows ~85% protection against severe rotavirus AGE in high-income settings, less (~40 to 60%) in low-income settings because of competing enteric disease, malnutrition, and interfering gut flora.[10] Contraindicated in severe combined immunodeficiency (SCID) and history of intussusception; caution in immunocompromised.

E. coli — the pathotypes

• ETEC (enterotoxigenic): heat-labile (cholera-like, ADP-ribosylation) and heat-stable toxins; watery diarrhoea, no fever; the major cause of travellers' diarrhoea. Self-limiting; ORS.
• EPEC (enteropathogenic): attaching-and-effacing lesions; infantile diarrhoea in developing countries; persistent watery diarrhoea.
• EAEC (enteroaggregative): stacked-brick adherence; persistent diarrhoea in malnourished and HIV-positive children.
• EIEC (enteroinvasive): invasive, dysentery-like, similar to Shigella.
• EHEC / STEC (enterohaemorrhagic / Shiga-toxin-producing): O157:H7 and non-O157 serotypes. Shiga toxin (Stx1, Stx2) damages vascular endothelium → HUS. Source: undercooked beef, unpasteurised milk, contaminated water, petting zoos. Antibiotics increase toxin release and HUS risk — avoid.[2]

Shigellosis

The prototype of bacillary dysentery. S. sonnei (mild), S. flexneri (developing countries), S. dysenteriae type 1 (most severe, produces Shiga toxin). Highly infectious — only 10 to 100 organisms. Clinical: high fever, abdominal cramps, tenesmus, bloody mucoid stool, faecal leucocytes. Complications: seizures (especially S. flexneri in infants — neurotoxic, may precede the diarrhoea), toxic megacolon, intestinal perforation, haemolytic-uraemic syndrome (with S. dysenteriae type 1), reactive arthritis, leukaemoid reaction. Treatment: azithromycin or ceftriaxone — multidrug resistance is now widespread.[9]

Non-typhoidal Salmonella

Food-borne (poultry, eggs, reptiles). Self-limiting watery diarrhoea, sometimes bloody, with fever and abdominal cramps; bacteraemia in infants under 3 months, immunocompromised, and sickle-cell disease (risk of osteomyelitis). Antibiotics reserved for high-risk groups; otherwise avoid (prolongs carriage).[10]

Campylobacter jejuni

Invasive; bloody diarrhoea with abdominal pain that may mimic appendicitis or surgical abdomen. Guillain-Barré syndrome in ~1 in 1,000 cases, 1 to 3 weeks after, mediated by anti-GQ1b antibodies. Treatment: azithromycin if severe; supportive otherwise.[3]

Vibrio cholerae

Profuse rice-water stool, vomiting, rapid and severe dehydration, no fever, hypokalaemia, acidosis. Endemic in South Asia and Africa; outbreaks after disasters. Treatment: aggressive ORS / IV (Plan C), azithromycin 20 mg/kg single dose (or doxycycline in older children and adults) shortens the illness. Hand-washing, safe water, and cholera vaccine (Shanchol/Euvichol) for outbreak control.[2]

Giardia lamblia

Foul-smelling greasy stool that floats, bloating, flatulence, no blood, no fever, persistent (> 7 to 14 days). Microscopy shows trophozoites or cysts. Antigen detection is more sensitive. Treatment: metronidazole 15 mg/kg/day tds for 5 to 7 days or tinidazole 50 mg/kg single dose.[1]

Entamoeba histolytica

Bloody mucoid diarrhoea with abdominal pain; risk of amoebic liver abscess (right upper quadrant pain, swinging fever). Treatment: metronidazole 30 to 50 mg/kg/day tds for 7 to 10 days followed by a luminal agent (paromomycin 25 to 35 mg/kg/day tds for 7 days) to clear cysts.[3]

C. difficile colitis

Recent antibiotics or hospitalisation; watery or bloody diarrhoea, abdominal pain, marked leucocytosis, hypoalbuminaemia, pseudomembranous colitis. Treatment: stop inciting antibiotic; oral metronidazole (mild–moderate) or oral vancomycin (severe) for 10 to 14 days; fidaxomicin in recurrent disease.[3]

Cryptosporidium

Common in HIV / immunocompromised children; persistent watery diarrhoea; acid-fast oocysts on modified Ziehl-Neelsen stain. Treatment: nitazoxanide; supportive + immune reconstitution in HIV.[3]

Surgical mimics — intussusception

Age 6 to 36 months; intermittent colicky abdominal pain, drawing up of legs, vomiting, eventually redcurrant-jelly stool (late sign). Sausage-shaped mass in right upper quadrant; empty right lower quadrant (Dance sign). Ultrasound shows target / doughnut sign. Treat with air or contrast enema reduction (radiology) or surgery if unstable / unsuccessful. Distinguish from AGE: intussusception has episodic pain and mass, AGE has continuous diarrhoea.[3]

Complications & Pitfalls

[6]

Prognosis & Disposition

• Overall mortality is very low in well-nourished children with access to ORS; severe dehydration untreated can be fatal within hours (especially cholera in infants).
• Most viral AGE resolves in 5 to 7 days; bacterial invasive disease 1 to 2 weeks.
• HUS mortality 3 to 5%; long-term renal sequelae (hypertension, proteinuria, CKD) in 10 to 30% of survivors of typical HUS.
• Persistent diarrhoea suggests alternative diagnosis; needs investigation.
• Disposition: home (Plan A, reliable caregiver); short-stay / clinic observation (Plan B); inpatient (Plan C, infants under 6 months, malnourished, immunocompromised, suspected HUS, surgical differential); ICU (shock, severe sepsis, HUS with multi-organ failure).[6]

Special Populations

Infants under 6 months

• Higher risk of dehydration per kilogram of stool loss.
• Breastfeed on demand; do not give plain water alone (hyponatraemia).
• Lower zinc dose — 10 mg/day (not 20 mg).
• Lower threshold to investigate — urinalysis and culture mandatory; consider sepsis workup.
• Avoid anti-motility agents and ondansetron in neonates (QT risk, limited data).[4]

Severe acute malnutrition (SAM)

• Oedema masks dehydration — use WHO's modified criteria: lethargy, sunken eyes, poor skin pinch are still valid; weight change is not reliable.
• Rehydrate with Resomal (Na 45, K 40 mmol/L, with magnesium) — 5 to 10 mL/kg/half-hourly for first 2 hours, then 5 to 10 mL/kg/h for up to 10 hours — slower than well-nourished children.
• Avoid rapid IV boluses — risk of fluid overload and heart failure.
• Check and treat hypoglycaemia, hypothermia, and severe infection — the standard WHO "10 steps".
• Empirical broad-spectrum antibiotics (parenteral ampicillin + gentamicin).[6]

Immunocompromised (HIV, chemotherapy, transplant)

• Persistent, atypical organisms: Cryptosporidium, Cystoisospora, Cyclospora, CMV colitis, Mycobacterium avium complex.
• Stool workup should include acid-fast staining, viral PCR (CMV), and special cultures.
• Avoid live rotavirus vaccine in SCID.
• Coordinate care with the immunology / infectious diseases team.[1]

Post-rotavirus vaccine era

In countries with high rotavirus vaccine coverage, norovirus has overtaken rotavirus as the leading cause of paediatric AGE hospitalisation; aetiology has shifted but management principles are unchanged.[10]

Travellers

• ETEC, Giardia, Entamoeba, cholera, hepatitis A, typhoid in the differential.
• Send stool microscopy and culture.
• Treat per organism.[2]

Children on long-term medications

• Steroids, immunosuppressants: invasive disease, CMV, atypical.
• Diuretics: electrolyte disturbance with AGE.
• Laxatives: confusion with cause of diarrhoea.
• Cardiac / renal: lower fluid-tolerance — manage in hospital.[3]

Evidence, Guidelines & Regional Differences

Landmark evidence

• GEMS (Kotloff 2013, Lancet) — defined the four leading pathogens of moderate-to-severe paediatric diarrhoea in developing countries: rotavirus, Cryptosporidium, Shigella, ST-ETEC.[2]
• Cochrane zinc (Lazzerini & Wanzira 2016) — confirmed that oral zinc shortens duration, reduces stool frequency, and reduces the proportion of episodes lasting over 7 days.[3]
• Reduced-osmolarity ORS (Hahn et al., Cochrane 2002) — established the superiority of 245 mOsm/L ORS over the original 311 mOsm/L for non-cholera AGE: less stool output, less vomiting, fewer IV fluids.[6]
• Freedman NEJM 2006 / Alhashimi Cochrane 2006 — single-dose oral ondansetron reduces vomiting, IV need, and admissions in AGE with vomiting.[4][7]
• Probiotics for acute infectious diarrhoea (Collinson Cochrane 2020) — probiotics (especially Lactobacillus rhamnosus GG) reduce duration of acute viral diarrhoea.[5]
• Cochrane rotavirus vaccines (Soares-Weiser 2019) — confirms ~85% vaccine effectiveness in high-income, ~40 to 60% in low-income settings.[10]

Guidelines

• WHO — Diarrhoea Treatment Manual (2005, periodically updated); recommends Plan A/B/C, ORS, zinc, continued feeding; defines reduced-osmolarity ORS (245 mOsm/L).[1]
• ESPGHAN / European — broadly aligned with WHO; supports ondansetron and probiotics in selected cases.
• AAP / NICE (UK) — emphasize ORS for rehydration, single-dose ondansetron for vomiting, anti-motility drugs discouraged, avoid routine antibiotics, antiemetic caution for QT.
• India (ICMR) — zinc 20 mg/day for 10 to 14 days in every episode of acute diarrhoea; integrated with the National Diarrhoeal Disease Control Programme; ORS plus zinc packets distributed free through ANM/Asha workers.

Regional / practice deltas

• India / South Asia: very high burden; cholera, Shigella, typhoid; rotavirus vaccine is part of the UIP (Rotavac / Rotasiil). Zinc-ORS co-packaging is government standard.
• Africa: high Cryptosporidium (HIV) and cholera outbreaks; ORS access a barrier; WHO programmes central.
• High-income / west: norovirus now leading cause of hospitalisation in post-rotavirus-vaccine era; lower mortality; stool PCR panels widely used (with over-diagnosis risk).
• WHO does not recommend routine antibiotics in AGE; anti-motility agents are not recommended in children under any WHO guideline.[10]

Controversies

• Stool PCR panels detect DNA, not viable organisms — risk of treating colonisation rather than disease.
• Antiemetics and probiotics are recommended by Western guidelines but less universally adopted in WHO programmes.
• Eculizumab in typical HUS remains controversial; reserved for severe / atypical HUS.
• Lactose-free formula in routine AGE — not required; trial only in proven secondary lactose intolerance.[5]

Exam Pearls

• Rotavirus = the leading cause of severe viral AGE in children under 5.[2]
• GEMS four: rotavirus, Cryptosporidium, Shigella, ST-ETEC.[2]
• WHO grades: no / some / severe dehydration — two signs suffice for each category.[1]
• Plan A (home): ORS after each stool, zinc, continue feeding. Plan B (clinic): ORS 75 mL/kg over 4 h. Plan C (severe): IV bolus 20 mL/kg NS or Ringer's lactate.[1]
• ORS — sodium 75, glucose 75, total osmolarity 245 mOsm/L (reduced-osmolarity WHO formula).[6]
• Zinc 20 mg/day for 10 to 14 days (10 mg/day for infants under 6 months).[3]
• Continue feeding and breastfeeding — never stop.
• Ondansetron 0.15 mg/kg single oral dose reduces vomiting, IV need, and admissions.[4]
• Loperamide is contraindicated in children under 2 years; not recommended in older children.
• EHEC (E coli O157:H7) → HUS: triad of microangiopathic haemolytic anaemia + thrombocytopenia + AKI; antibiotics increase the risk.[12]
• Antibiotics are NOT routine — only for Shigella, cholera, amoebic dysentery, Giardia, severe Salmonella in infants under 3 months, C. difficile, severe Campylobacter.[9]
• Bloody diarrhoea: think Shigella, Campylobacter, EHEC, EIEC, Entamoeba.
• Foul-smelling greasy floating stool: Giardia — treat with metronidazole.
• Rice-water stool, no fever, rapid dehydration: cholera — IV fluids and azithromycin.
• Severe dehydration: IV bolus 20 mL/kg NS; reassess; repeat until perfusion restored.[1]
• Metabolic acidosis from bicarbonate loss in stool; hypokalaemia from stool K⁺ loss.
• Hypernatraemic dehydration: doughy skin, irritability, tremor; correct slowly.[1]
• Skin pinch over 2 seconds + lethargic + cannot drink = severe dehydration (Plan C).[1]
• Hypoglycaemia — easy to miss in malnourished infants; check glucose, treat with 2 mL/kg 10% dextrose.
• Rotavirus vaccine reduces severe rotavirus AGE by ~85% in high-income settings.[10]
• Redcurrant-jelly stool with episodic colic and a sausage-shaped mass in a 6 to 36 month-old = intussusception, not AGE.
• Vomiting + acidotic breathing + weight loss in a young child = exclude DKA.
• Vomiting with no wet nappy for many hours and reduced oral intake: a febrile infant = UTI / sepsis until proven otherwise — urinalysis is mandatory.

Exam application bank (NEET-PG / INICET)

One-line answer

Acute gastroenteritis (AGE) = inflammation of stomach and intestines causing 3 or more loose/watery stools in 24 hours and/or vomiting, of infectious origin, lasting under 14 days. The 2nd leading cause of under-5 mortality worldwide. Most common pathogen globally is rotavirus (pre-vaccine); post-vaccine, norovirus is rising. WHO classifies dehydration as no / some / severe and treats with Plan A (home ORS), Plan B (ORS 75 mL/kg over 4 h), Plan C (IV bolus 20 mL/kg normal saline). Zinc 20 mg/day for 10 to 14 days shortens the episode. Continue feeding throughout. EHEC (E coli O157:H7) → HUS (microangiopathic haemolytic anaemia + thrombocytopenia + AKI). Antibiotics are reserved for Shigella, cholera, severe Salmonella in infants under 3 months, and amoebic dysentery.[1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard.[3]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes.[1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change.[1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each.[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory.[11]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Acute Gastroenteritis in Children.

References

1. [1]Guarino A, Ashkenazi S, Gendrel D, et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/European Society for Pediatric Infectious Diseases evidence-based guidelines for the management of acute gastroenteritis in children in Europe: update 2014. Journal of pediatric gastroenterology and nutrition, 2014.PMID 24739189
2. [2]Kotloff KL, Nataro JP, Blackwelder WC, et al. Burden and aetiology of diarrhoeal disease in infants and young children in developing countries (the Global Enteric Multicenter Study, GEMS): a prospective, case-control study. Lancet, 2013.PMID 23680352
3. [3]Lazzerini M, Wanzira H. Oral zinc for treating diarrhoea in children. Cochrane Database of Systematic Reviews, 2016.PMID 27996088
4. [4]Freedman SB, Adler M, Seshadri R, Powell EC. Oral ondansetron for gastroenteritis in a pediatric emergency department. New England Journal of Medicine, 2006.PMID 16625009
5. [5]Collinson S, Tarring N, Bhatnagar S, et al. Probiotics for treating acute infectious diarrhoea. Cochrane Database of Systematic Reviews, 2020.PMID 33295643
6. [6]Hahn S, Kim Y, Garner P Reduced osmolarity oral rehydration solution for treating dehydration due to diarrhoea in children: systematic review. BMJ (Clinical research ed.), 2001.PMID 11451782
7. [7]Fedorowicz Z, Jagannath VA, Carter B Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. The Cochrane database of systematic reviews, 2011.PMID 21901699
8. [8]Tomasik E, Szymanska I, Wysocki J, et al. Systematic review with meta-analysis: ondansetron for vomiting in children with acute gastroenteritis. Alimentary Pharmacology & Therapeutics, 2016.PMID 27401959
9. [9]Kotloff KL, Riddle MS, Platts-Mills JA, Pavlinac P, Zaidi AKM. Shigellosis. Lancet Infectious Diseases, 2018.PMID 29254859
10. [10]Soares-Weiser K, Bergman H, Henschke N, et al. Vaccines for preventing rotavirus diarrhoea: vaccines in use. Cochrane Database of Systematic Reviews, 2019.PMID 31684685
11. [11]Guarino A, Ashkenazi S, Lo Vecchio A, et al. Acute gastroenteritis in children of the world: what needs to be done? Journal of Pediatric Gastroenterology and Nutrition, 2020.PMID 32079974
12. [12]Freedman SB, Vandermeer B, Milne A, Hartling L. Acute infectious pediatric gastroenteritis: beyond oral rehydration therapy. Expert Opinion on Pharmacotherapy, 2007.PMID 17685883