Category Archives: Gastro

Irritable Bowel Syndrome

Rome IV classification gives definition as:

Recurrent abdominal pain, at least once per week for at least 3 months, associated with at least 2 of:

  • Associated with defecation
  • Change in bowel frequency
  • Change in stool form/appearance

Bloating has been removed from diagnostic criteria as it has no predictive value, being common across all kinds of GI issues.

Subtypes then based on stool form on symptomatic days – predominantly constipation, predominantly diarrhoea, mixed constipation/diarrhoea.

Normal physical examination supports diagnosis. Tests should include FBC to exclude iron deficiency anaemia, CRP for IBD, TTG antibody for coeliac disease.


Trial of lactose, fructose and wheat free diet if suspected link to consumption of these foods (non coeliac gluten sensitivity occurs).

Low FODMAP diet is challenging but can help – should be supervised by dietician.

Reassurance – making diagnosis helps justify not investigating fruitlessly.

[J Clin Med 2017]


Substantial evidence that alterations in the gut microbiome early in life “imprint” gut mucosal immunity, which is probably important for development of food allergy.

Maternal factors, timing and how solids introduced all likely to be important.

Experimental studies have shown that faecal transplants or other attempts to modify bacterial commenals can prevent or treat food allergy.

Mechanisms include restoration of gut immune regulatory checkpoints (eg retinoic orphan receptor gamma T+ regulatory T cells), the epithelial barrier, and healthy immunoglobulin A responses to gut commensals.

[Rima Rachid, JACI 2021]


Common cause of bloody diarrhoea. As with other causes of bloody diarrhea, often associated with fever and abdominal cramps.

Usually self resolving within a week. Antibiotics help if symptoms severe enough.

Excretion continues for a number of weeks, although risk of spreading infection after diarrhoea has settled of course much less, assuming decent hygiene.

Chronic excretion can occur with continuous symptoms rarely, certainly in immunosuppressed patients. Asymptomatic carriers exist, although seems to be more common in developing countries (so malnutrition probably a factor) and reinfection can also occur, of course.

About 1 in 1000 cases develop Guillain Barre syndrome after the infection. Inflammatory bowel disease seems more common after campylobacter infection?

Acute pancreatitis

Incidence increasing, approaching that of adults!? INSPPIRE international study. 


Amylase 3x upper limit, radiology positive. 

Cullen’s and Grey Turner signs (umbilical and flank bruising respectively).

Amylase level not prognostic. False positive liver/renal impairment, GI inflammation.  False negative in 10%, esp drug induced!

Lipase more specific, only done in Huddersfield?! Stays high for longer.

Low calcium, high glucose seen.

Diagnosis mostly clinical. USS usually sensitive, else CT – more for complications (focal or diffuse enlargement, heterogeneous enhancement, irregular or shaggy outline, oedema of surrounding fat).

AXR may show sentinel loop, free gas (loss of psoas shadow). CXR for effusion.



  • idiopathic (25% in children)
  • gall stones
  • ethanol
  • trauma
  • steroids – and other drugs, esp anti-epileptics, immunosuppressants eg azathioprine, cancer drugs.
  • mumps (even without parotitis), malignancy
  • autoimmune
  • scorpion sting!

But misses IBD, sepsis, Mycoplasma (early or late), genetic causes! 


Prognosis good in children. Scoring systems in adults eg Modified Glasgow-Imrie not applicable, various paediatric versions, of debatable value. 

Fluid resuscitation then 1.5-2x maintenance requirements (not much evidence – don’t be afraid of positive balance! Keep urine output at 1ml/kg/hr), analgesia, early enteral nutrition if possible (to avoid bacterial translocation) else parenteral.

Antibiotics only for suspected sepsis.

Surgery eg necrosectomy. 

1/3 acute recurrent (defined as recurrence after full recovery). Often anatomical problems. Chronic associated with genetic disorders, metabolic, autoimmune.

ERCP for anatomical causes. Pancreatic enzymes. Non opiate pain management eg tricyclics. 

[NASPGHAN 2018 Guidelines]


According to NICE, 3 or more loose or liquid stools in a day (or more frequently than is normal for the individual) counts as diarrhoea.

Persisting for more than 14 days makes it chronic.

Acute typically gastroenteritis. Presence of blood and/or mucus suggests more invasive inflammation, viz colitis.

In kids, can occur with pretty much any illness!

Vomiting with diarrhoea makes a primary gut cause more likely, but still not specific.

Enteral feeding

Freka PEG tube can only be removed orally.  Good if v active, combative patient.  But risk of mucosal burying, so weekly push and pull.  Corflo can be removed by traction.  Need replacing every 18 months. 

Button preferred now, tube can be disconnected as required, replace every 12-18 months.  40% mortality at 5yrs post fundoplication where CP. 40% had no improvement in gagging symptoms.  Only 1 in 8 need subsequent fundo if PEG only done first, so tend not to be done at same time.

Alternatives – jejunal tube via PEG (needs continuous feeds) or jejunal button (less retching but more tube problems eg blockage).

Jejunostomy via Roux en Y potentially primary procedure.  Risk of volvulus.

Oesophagogastric disconnection – (Manchester) stomach detached from oesophagus, which gets plumbed on to Roux en Y instead. 

Bridles for NG/NJ skin fixation issues.

Blended diet for growth issues, feeding tolerance issues, failed jejunal, to avoid fundoplication. Currently not done via NG/NJ.


A functional gastrointestinal problem, where food or other stomach contents effortlessly comes up into the mouth, where it is either then vomited, spat or swallowed. Odour may be a clue.

Diagnosis is on history, but often misdiagnosed as reflux (and resistant to reflux treatment). Typically no nausea, no nocturnal symptoms, no dysphagia but these do not necessarily exclude the diagnosis.

Treatment is diaphragmatic breathing! Baclofen has been used.

Rome IV criteria. Beware eating disorder.

Prolonged Jaundice

Physiological is because Long chain FAs in breast milk compete with Glucuronyl transferase! Dehydration and poor feeding contribute (jaundice FOLLOWS, does not cause). But can also be seen in bottle fed babies.

Prolonged jaundice defined as 21/7 if well, term according to American Academy of Pediatrics. After that, investigation probably appropriate.

Unconjugated vs Conjugated bilirubin is important – do direct bilirubin. Conj bili >20 may indicate significant disease, esp if unconj not high. Low albumin suggests prenatal onset.


  • Haemolysis (so liver function tests normal): eg rhesus disease (diagnosis: Direct Coombs Test Positive), ABO, irregular antibodies (Kell, Duffy; varying significance), hereditary sphero/elliptocytosis, G6PD deficiency, DIC. G6PD in baby can be precipitated by maternal drugs/infection. Enzyme assay false negative because of high retic count, so test mother for carrier status.
  • Crigler Najjar is unconjugated. Uridine Di Phos Glucuronyl transferase deficiency (Dubin Johson/Rotor only present >2 yr). Recessive form is severe, assoc with kernicterus; dominant can be treated with phenobarb.
  • Hypothyroidism
  • Galactosaemia – in the first week of life can be unconjugated but always features liver dysfunction cf Crigler Najjar so unlikely to be any confusion.


Suggests hepatitis. Note that Alk phos in normal neonates is often high in isolation. See BSPGHAN protocol.

  • Congenital Biliary Atresia
  • Choledochal cyst: assoc with East Asians, PKD (Caroli’s disease). Cystic mass below liver. Can rupture and cause ascites, cause obstruction +/or cholangitis. Late carcinoma risk.
  • Spont CBD perforation – discoloured umbilicus, paracentesis diagnostic. Rx Surg
  • Gallstones – possible!
  • Congenital viral infection (TORCH), enteroviruses (esp ECHO, assoc with fulminant hepatitis), sepsis (eg UTI, listeria assoc with hepatic abscesses).
  • Cystic fibrosis and bile plug syndrome
  • Inherited Metabolic Disorders: galactosaemia, Zellweger’s, haemochromatosis, etc.
  • Alpha -1 antitrypsin deficiency
  • Alagille’s syndrome
  • Endocrine disorders: congenital hypothyroidism (1 in 60 000), pituitary/adrenal underactivity.

Biliary atresia

Wasting of biliary tree +/- gall bladder in early months of life (LANDING’s theory). Premature babies get it less (as wasting hasn’t progressed as much) but can still get it!

Stool colour chart

Presents with prolonged jaundice. Dark urine, pale (white!) stools distinguish it from common, benign breast feeding jaundice, but often missed. Parental reporting of stool/urine colour is unreliable! Stool colour chart available from Children’s Liver Disease Foundation.

Normally distal but 20% proximal.

Associated with SPLENIC MALFORMATION syndrome (poly or asplenia, situs inversus, malrotation, absent IVC).

Lanarkshire incidence 1.26 per 10 000, significantly higher than rest of Scotland!  NO evidence of genetic factors.  Pigweed in pregnant ewes in Australia – “biliatresone” toxin. Industrial waste…?


Colour of stool!

Fasting (4hrs) USS essential, but sensitivity is operator dependent

Treat by Kasai Porto-enterostomy before 6 weeks ideally (16% normal LFTs, 18% portal hypertension, 94% survival @5yr +/- transplant), else liver transplant.

1yr phenobarb, urso, Vit K.  Long term Dalivit.

Consider varicella vaccination if likely for transplant!


Prognosis related to clearing of jaundice, established cirrhosis/fibrosis, cholangitis, biliary stricture, portal hypertension (degree of – most have).

60% clear jaundice, up to 60% require transplant in first 2yrs.  Of the rest, half need transplant in childhood, leaving just 20% getting to transition with native liver.Most mortality due to transplant complications.

New Japanese data suggests length of jaundice more important than age (traditionally 45-60 days low risk for liver failure)

Outcomes from Kasai operation are better in centres doing more than 5/yr, so only 3 supra-regional centres in England.  But outcomes in Scotland seem to have got worse, even though overall better!  Up to surgeon whether feasible or not for an individual patient.

Increased sepsis due to gut organisms from Roux-en-Y loop.

Cholangitis – features can be seen on USS.  Characteristically unwell, febrile with rise in bilirubin and LFTs (but not always).  Rx Tazocin.  Some require antibiotic prophylaxis.

Portal hypertension can develop early or late.  May present with variceal bleeding, low platelets, splenomegaly. Managed by banding of varices, TIPS shunt, transplant.

Strictures present with biliary stasis, itch, pain, coagulopathy. 

[Rachel Tayler]

Bloody Stools

Bloody stools, think VTEC rules!

Acute bloody diarrhoea usually infective –

  • Shigella/salmonella (non typhoid strains)
  • Campylobacter
  • E coli (some, eg EHEC)

Usually worse abdominal pain than usually seen in gastroenteritis, can also be high fever. If severe, shigella/campylobacter can be treated with antibiotics.

If chronic, consider

Some serious causes: