GI Flashcards
What is gastroenteritis?
What are the types / causes?
GI tract inflammation secondary to infection (bacterial, viral or protozoa – usually ingested).
Viral: most common (especially rotavirus), particularly children <5. Rotavirus vaccination is reducing disease burden, but others include adenovirus, enterovirus + norovirus.
Bacterial: Camplyobacter jejuni most common, other bacteria that can cause gastroenteritis are E. coli, Salmonella & Shigella
Parasites: Yersinia enterocolitica, Cryptosproidium, Entamoeba histolytica & Giardia
What is the pathophysiology of gastroenteritis?
Symptoms?
Responsible pathogen damages the villi > malabsorption of intestinal contents and osmotic diarrhoea. Can also be caused by toxins from bacteria (bind to receptors in intestine > release of Cl⁻ ions > secretory diarrhoea). The most common toxins are from Staphylococcus aureus, Bacillus cereus & Clostridium perfringens.
Sudden onset diarrhoea + vomiting (severity often depends on degree of dehydration)
Depending on infective agent, other symptoms include: o Fever o Headache o Lethargy o Abdominal pain o Poor feeding o Dysuria o Weight loss
Which children with gastroenteritis are more likely to be dehydrated?
Dehydration is more likely if:
• <1 year (especially <6 months)
• Low birth weight
• Stopped breastfeeding
• Not been offered, or not tolerated, fluids pre-presentation
• >5 episodes of diarrhoea, or 2 episodes of vomiting in 24 hours
• Signs of malnutrition
Investigations for gastroenteritis?
Most cases mild with clear history (if so, no further investigations needed). History may identify source (seafood, unwashed vegetables, unpasteurised milk, contaminated water, uncooked meats, takeaways / unusual foods, recent travel + exposure to other individuals with gastroenteritis).
Stool sample if: • Diagnostic doubt • Septic • Blood or mucus in stool • Immunocompromised • Unusual infective organism suspected • Diarrhoea has continued >2 weeks
If definitive focus cannot be found, other sources of infection should be investigated e.g. urine MC&S, CXR, LP.
If appears significantly dehydrated, monitor urine output + U&Es to look for electrolyte disturbances + AKI.
Other useful blood tests in potentially septic or significantly shocked patient: blood gas, inflammatory markers, blood cultures.
Management of gastroenteritis?
Clinical assessment of dehydration
If no signs: home treatment (continue feeding + adequate clear fluid intake). ORS can be supplemented to reduce risk of dehydration (small frequent fluid intake, 50ml/kg ORS over 4 hours + maintenance fluids). If not orally tolerated can potentially be given by NG feed.
Restart normal diet after rehydration, in those at risk of dehydration consider 5ml/kg of ORS after large watery stools (younger children more likely to need admission to hospital, as are those with no improvement on ORS). Isolate child as much as possible to prevent spread
IV fluids only if: shock suspected, red flag symptoms and clinical deterioration persist despite oral fluids, or there is persistent vomiting whilst on ORS, given orally or NG
(Bolus: 20ml/kg 0.9% NaCl, followed by isotonic maintenance (e.g. 0.9% NaCl / 5% dextrose). Fluid deficit (100ml/kg if initially shocked, 50ml/kg if not initially shocked), should be replaced on top of maintenance therapy. Consider adding K⁺ once plasma levels are known. Regular bloods should monitor kidneys, glucose + electrolytes. If hypernatraemic at presentation, replace fluids cautiously over 48 hours, with regular monitoring of sodium level, aiming to reduce it a rate of <0.5mmol/L/hour)
Abx: not routine (majority viral), but consider in special circumstances
Prognosis / complications of gastroenteritis?
Most are mild (no significant complications).
Self-limiting illness which rarely causes severe or lasting adverse effects.
More severe cases may lead to electrolyte imbalances or AKI.
Other complications include: • Acquired lactose intolerance • Persistent diarrhoea • IBS • Systemic infection • Haemolytic uraemic syndrome (associated with E. Coli O157:H7).
Gastroenteritis: criteria for no dehydration, clinical dehydration and clinical shock?
No Clinical Dehydration: appears well, alert + responsive, normal urine output + skin colour, warm extremities, eyes not sunken, moist mucous membranes, normal HR, RR, peripheral pulses, cap refill, skin turgor + BP
Clinical Dehydration: Appears unwell or deteriorating, altered responsiveness, decreased urine output, normal skin colour, warm extremities, sunken eyes, dry mucous membranes, tachycardia, tachypnoea, normal peripheral pulses, normal cap refill, reduced skin turgor, normal BP
Clinical Shock: Appears unwell or deteriorating, decreased level of consciousness + urine output, PALE OR MOTTLED, COLD extremities, sunken eyes, dry mucous membranes, tachycardia, tachypnora, WEAK peripheral pulses, PROLONGED CAP refill, reduced skin turgor, HYPOTENSION (decompensated shock)
In what circumstances can you consider Abx for gastroenteritis?
- Salmonella gastroenteritis if immunocompromised, malnourished, or <6 months
- Suspected septicaemia
- Extra-intestinal spread of bacterial infection
- C DIFF associated pseudomembranous colitis, giardiasis, dysenteric shigellosis, dysenteric amoebiasis or cholera.
IBD - ADD IN.
efa
How common is coeliac / who does it affect
What is the pathophysiology?
UK Prevalence 0.8-1.9%. In children: peak diagnosis 6 months – 3 years (however, about 1/3 are undiagnosed).
Autoimmune disorder: inflammatory response to gliadin (protein in gluten i.e. wheat, barley, rye) damage to mucosa of small intestine malabsorption. β-lymphocytes from gut-associated lymphoid tissue (GALT) produce antibodies to gliadin, endomysial cells (connective tissue around muscle fibres) & tissue transglutaminase.
Risk and protective factors for coeliac?
Family history
- Complex polygenetic mechanism: HLA-DR3-DQ2 in 95% and HLA-DR4-DQ8 in 5%, only occurs in those with genetic susceptibility
Women > men
Rotavirus in childhood
Related conditions: routine coeliac screening if present o Dermatitis herpetiformis o Autoimmune thyroid disorders o Addison’s disease o T1DM
Protective factors:
• Continuing breastfeeding while introducing gluten
• Introducing gluten between 4-6 months of age
Symptoms / signs of coeliac disease?
Presents at any age but can be asymptomatic, most common symptoms: • Unintentional weight loss, anorexia • Fatigue • Chronic diarrhoea or constipation • Flatulence • Pale stools • Severe recurrent abdominal pain • Mouth ulcers • Vomiting
Signs: unexplained anaemia, faltering growth, low impact fractures, motor weakness, vitamin deficiencies. Children may have abdominal distention with faltering growth.
wasting buttocks
Investigations for coeliac disease?
Due to non-specific symptoms
• FBC: anaemia due to iron or folate deficiency
• Iron studies, B12, folate
• U+Es, bone profile, magnesium: e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia
• LFTs: elevated transaminases which should revert to normal on changing to gluten free diet, however, persistently elevated levels may warrant further investigation for autoimmune liver conditions (associated with coeliac disease). Low albumin is associated with malnutrition.
Tissue transglutaminase antibody (tTGA) and IgA endomysial antibodies (EMA)
- patient needs to include gluten in their diet (daily) over the previous 6 weeks
- if positive serology: refer for endoscopy and intestinal biopsy (histological diagnosis, with patient continuing gluten-containing diet until then)
- if serology is negative, IgA serology to check for IgA deficiency (may mask a positive test – IgA response unlikely if patient IgA deficient, therefore IgG testing can be done instead – if also negative, unlikely to have coeliac disease
Endoscopy: upper GI endoscopy enables biopsies, histological findings include atrophic villi + crypt hyperplasia (gold standard for diagnosis). Recent guidelines suggest that diagnosis can be made without endoscopy if:
• Child is symptomatic
• tTGA 10x normal on two occasions
• Child HLA DR3-DQ2 or DR4-DQ8 positive (confirmed on genetic testing)
Management of coeliac disease?
Child, nurseries + schools informed: strict, lifelong gluten free diet (products can be prescribed). Referred to dietician for advice on optimising diet. All patients should have lifelong follow up appointments:
- Check adherence to diet (tTGA + EMA levels decrease 6-12 months after a gluten-free diet has been initiated + can be used to monitor adherence, generally poorest in adolescents as starting to take control own diet, increasing chance of complications)
- Ensure adequate growth + nutrition
- Osteoporosis screening with dual energy X-ray absorptiometry (DEXA) scan every 3 years in patients on a gluten-free diet
- As some patients have splenic dysfunction, offer vaccinations against pneumococcus, Hib + influenza.
- Assessment of psychosocial wellbeing.
Complications and prognosis of coeliac disease?
Complications due to malabsorption (decreases after 12 months gluten free): o IDA o B12 deficiency o Folate deficiency o Calcium or vitamin D deficiency o Faltering growth
Absolute increase in risk of some conditions, including:
o Bone fragility > fractures
o Adverse pregnancy outcomes: miscarriages, low birth weight, IGR
o Cancers e.g. oesophageal, intestinal, Hodgkin’s and non-Hodgkin’s lymphoma
o Splenic dysfunction
Prognosis: normal life expectancy if adhere to gluten-free diet
In some situations, refractory coeliac disease is present, characterised by persistent or recurrent malabsorption and villous atrophy despite removal of gluten from diet after 6-12 months.
GORD - add in
add in
What is pyloric stenosis?
risk factors
symptoms
Gradual thickening of pyloric muscle, eventually resulting in complete gastric outlet obstruction. Unclear aetiology but ?neurogenic cause: neural nitric oxide synthase gene linked to the condition.
Incidence: 1-3 per 1000 live births.
Condition more prevalent in:
• Males (4x more common)
• Firstborns
• Strong family history
Typically, non-bilious vomiting (usually projectile) that commences at 3-4 weeks, can be associated with haematemesis secondary to oesophagitis.
Prolonged vomiting typically leads to:
• Lethargy
• Weight loss (or failure to gain weight) despite being a hungry baby
• Constipation
Pyloric stenosis - examination findings and investigations?
Infants appear thin but hungry + may show signs of dehydration. Occasionally, visible gastric peristalsis can be seen. Palpable pyloric tumour (olive-shaped mass) in epigastrium or RUQ is diagnostic but often difficult to feel + can often only be detected by experienced clinician
If unsure, ‘test feed’ should be performed by offering dextrose water - relaxes the abdominal muscles, allowing deep palpation + stimulating pylorus to contract (examining hand in RUQ to appreciate thickened pylorus)
Investigations:
• Blood gas: hypochloraemic, hypokalaemic metabolic alkalosis
• As dehydration worsens, patients also develop paradoxical aciduria (renal tubules reabsorb sodium in exchange for K+ and H+ > acidic urine).
• Electrolytes regularly monitored
• Abdo USS recommended if test feed inconclusive (if positive test feed i.e. pylorus was palpable - no further investigations are needed).
• Contrast studies: reserved for cases where USS inconclusive: ‘string sign’ = delayed passage of small amount of contrast through thin pyloric canal (also allows detection of other conditions e.g. malrotation).
To confirm IPS on USS, following 3 criteria:
• Pyloric muscle thickness >4mm
• Pyloric muscle length >18mm
• Failure of fluid passage beyond pylorus despite vigorous gastric peristalsis
Pyloric stenosis - management and prognosis?
Medical: pre-op rehydration + correction of electrolyte imbalances (v important: surgery deferred until corrected)
Oral feeds stopped: NG tube for decompression of stomach, measurement of losses + accurate replacement.
Fluids:
o Saline bolus for initial rehydration
o Maintenance: 100ml/kg 5% dextrose / 0.9% NaCl. K added as per serum levels + Na may need adjusting.
o Replacement: to replace NG tube losses e.g. 0.9% NaCl with 10% KCl. Must be K⁺ rich due to high K⁺ content of gastric fluid. Infusion rate is adjusted according to the rate of gastric losses + therefore higher concentrations of K⁺ are not recommended due to the high risk of hyperkalaemia.
Surgical: definitive treatment is Ramstedt’s pyloromyotomy (via right RUQ or supraumbilical incision). Laparoscopic approach recently advocated but not yet widely practiced. In all approaches, incision made along length of pyloric swelling down to the mucosa.
Complications: main presurgical issues are electrolyte imbalance + dehydration – complications of Ramstedt’s pyloromyotomy include bleeding, perforation and wound infection.
Prognosis: recovery usually uneventful, infants discharged 24-48 hours following the procedure once feeding re-established. Usually no long-term complications.
What is the difference between normal rotation, malrotation and volvulus?
- Normal rotation: gut develops + matures outside the abdominal cavity in the foetus, intestines rotate 270 degrees counter clockwise whilst returning into the abdominal cavity during the 11th week of gestation
- Malrotation: can happen to various degrees, but classically duodenal-jejunal (DJ) flexure comes to lie on the right side of the midline instead of the left
- Midgut volvulus: in patients with malrotation, the gut mesentery has a narrow base + can twist on its own axis > midgut volvulus. Mesentery contains the superior mesenteric blood vessels – leads to compromise of the blood flow and a mechanical obstruction > catastrophic consequences (dead gut can cause pt death in a few hours).
