GASTROENTERITIS


DEFINITION
An acute disruption in gut function characterised by vomiting and/or diarrhoea and associated symptoms, caused by the infection of the gut by a bacterium, virus or parasite.
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INCIDENCE
Very common.
1 billion cases in children per year worldwide.
Viral causes predominate in children.
Very common in developing world, mostly due to poor sanitation and hygiene linked with malnutrition.

Risk Factors
Malnutrition.
Being breastfed is protective in neonates.
Poor hygiene.
Viral gastroenteritis predominates in winter.
Nurseries, daycare centres etc.
Immunocompromised individuals.
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AETIOLOGY

Viral
Rotavirus (most common)
Enteric adenovirus.
Norwalk virus (norovirus)

Bacterial

i) enteroinvasive organisms

proliferate, invade and destroy mucosal epithelial cells.
- eg shigella, salmonella, shigella, amoebiasis, yersinia, campylobacter, enteroinvasive and enterohaemorrhagic E coli.

ii) infection by toxigenic organisms
- proliferate in gut, elaborate enterotoxin
- eg cholera, toxigenic e. coli, c. diff, cryptosporidium

iii) ingestion of preformed toxin

eg Staph aureus, vibrios, clostridium perfringens, clostridium botulinum.

Also note some subacute infections like Yersinia, mycobacterium TB.

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BIOLOGICAL BEHAVIOUR
See also diarrhoea card, and individual disorders.

Pathophysiology
Key virulence factors
- adherence (eg fimbriae, pili)
- enterotoxins (eg cholera toxin)
- capacity to invade (eg Yersinia penetrates ileum, multiplies in Peyer's patches; Salmonella causes bacteraemia in 5-10%)

Specific examples
Shigella --> distal colon, mucosal inflammation and erosion.
Campylobacter --> small intesting and colon, ulcers, inflammation, villus blunting.
Salmonella --> ileum and colon, invade peyers patches, typhimurium can cause bacteremia, fever and systmic unwellness
- and may chronically infect biliary treem joints, bones, meninges
Yersinia --> ileum, appendix, colon, with mucosal haemorrhage, gulceration and granulomas.
Vibrio cholerae --> small intestine
Clostridium --> like cholera, but with some epithelial damage.

Natural History
Almost always self-limiting.

Complications
Transient lactose intolerance.
Post-infective irritable bowel syndrome.
Reiter's syndrome (with Salmonella or Yersinia).
Erythema nodosum.

Necrotising Enterocolitis
Acute necrotising inflammation of small and large intestines: emergency in neonates, especially prems.
From immaturity, release of cytokins from initiation of oral feeding, bugs mucosal injury and deranged intestinal blood flow.
--> fulminant illness with shock and underlying gangrene & perforation.

Pseudomembranous colitis
Acute colitis with an inflammatory exudate overlying sites of mucosal injury (a pseudomembrane; merely a coagulum)
- C diff makes two exotoxins A ad B --> inflammation, denuding of surface epithelium, and a membrane of debris and mucus.
- often in patients with some chronic GI disease after a course of broad spectrum antibiotics.

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MANIFESTATIONS

Symptoms
Local
Watery diarrhoea or bloody dysentery (depends on infective agent).
Vomiting (most commonly with Rotovirus, Norwalk virus).

Systemic
Thirst, generally feeling rotten.

Signs
Observe
Signs of dehydration.
Apart from this, examination is often entirely normal.
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INVESTIGATIONS
Stool examination
Can distinguish mechanism.
Excess osmolality indicates malabsorption or laxative abuse.
Blood, mucus and leukocytes is dysentery, and indicates mucosal invasion.

Biochemistry
Metabolic acidosis.
Hyponatraemia.
Hypokalaemia.

Microbiology
Stool often contains traces of offending pathogen.
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MANAGEMENT
3 Principles:
1. Manage shocked patients aggressively with fluid resuscitation – IV, IO bolus doses.
2. Rehydrate orally or via NG tube if patient is not in shock.
- Review frequently.
3. Begin feeding early with simple foods.

Antibiotics
Can reduce length of illness with some E. coli, Shigella, Yersinia, giardia, amoeba, C. difficile, according to sensitivities.
See local guidelines / contact public health as required.

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