see also General Surgery

British Society of Gastroenterology Guidelines

ALARMS symptoms in GI Disease
A Anaemia
L weight Loss
A Anorexia
R Refractory problems
M Melaena
S Swallowing


Difficulty transferring food to the pharynxneurological disorderslocal inflammatory conditionsaffects liquids > solids with reguritation, cough aspiration
  • Intrinsic
  • tumour
  • stricture
  • rings and webs
  • Extrinsic
  • Tumour
  • Osteophytes
  • Vascular Lesions
  • Motility disorders
  • Achalasia
  • Diffuse Oesophageal Spasm
  • Scleroderma

Solids > liquids.



Degeneration of  myenteric ganglion cells supplying lower oesophagus  causing loss of peristalsis and failure of lower oesophageal sphincter to relax.

Intermittent dysphagia, wt loss, reflux, indigestion.


Oesophageal stricture

Oesophageal stricture Medscape


Strictures Webs and Rings PUK


Reflux of gastric contents into the oesophagus usually due to transient laxity of LOS
Symptoms heatburn, water brash, dysphagia, halitosis. Worse lying flat.may also cause respiratory symptoms – chronic cough, wheeze, hoarseness.
Risk factors  – obesity, HH, smoking, salty diet, fatty foods, alcohol, peppermints, citrus fruits.
GORD Management
General Measures Elevate head of bed, avoid late eating, smaller meals  advice on healthy eating, weight reduction and smoking cessation
Antacids See below
PPIs More effective than H2 antagonists

Patients with severe reflux oesophagitis may require specialist follow-up, and often require long term maintenance therapyUse the lowest dose that maintains control of symptoms.Patients with a normal endoscopy should stop drug therapy. If symptoms recur consider further anti-reflux therapy. See “step down/step/off” advice below for patients continued on PPIs

Surgery Severe +/- resistant +/- requiring long term maintainance


Antacids and Alginates Tayside
Co-magaldrox 195/220 (Mucogel®) suspension10-20ml, 20 minutes to 1 hour after meals and at bedtime or when required.low in sodium (<1mmol per 10ml) and sugar-free
Peptac® compound alginate suspension10-20ml after meals and at bedtimeContains sodium alginate, sodium bicarbonate, and calcium carbonateForms a viscous gel (‘raft’) that floats on the surface of the stomach contents and can protect the oesophageal mucosa from acid reflux.Sugar-free but high sodium content (6.2mmol per 10ml)
Gaviscon® Advance and Gastrocote® preparations are alginate-based alternatives not containing calcium.Gaviscon® Advance tablets and suspension contain sodium alginate and potassium bicarbonate.Gastrocote® tablets contain alginic acid, aluminium hydroxide, magnesium trisilicate and sodium bicarbonateGastrocote® liquid contains aluminium hydroxide, magnesium trisilicate, sodium alginate and sodium bicarbonateGastrocote® tablets have high sugar content and should be used with caution in diabetic patients.
Antacids reduce absorption of a number of drugs. Administration times should be separated by 1 to 2 hours to minimise the effect. Similarly, the administration times of an antacid and enteric coated tablets should be separated so that that the pH-sensitive coating is not destroyed in the stomach


Barrett’s oesophagus

Metaplastic replacement of squamous epithelium of distal oesophagus with intestinal type columnar epithelium.

Due to recurrent irritation from  GORD (affects up to 15%)  smoking and alcohol.

May become dysplastic (3%) and malignant (adenocarcinoma 9%).

Needs surveillance +/- radiofrequency ablation +/- oesophagectomy.


Dyspepsia and PUD 
GORD LOS dysfunction with acid reflux(or sometimes respiratory symptoms)
Dyspepsia epigastric discomfort
Functional Dyspepsia
  • 1 reflux-like symptoms
  • 2 ulcer-like symptoms.

Note that there may be overlap and as noted above, GIT symptoms are not well localized in some patients.

Gastritis (erosive)
  • Alcohol
  • Drugs
  • RadioRX
  • SRMD (stress ulcer)
Gastritis (nonerosive)
  • H pylori
  • lymphocytic
  • atrophic
H pylori Bacterium colonising the stomach causing a non-erosive gastritis which may be asymptomatic or present as dyspepsia, duodenal and gastric ulceration
PUD Gastric and Duodenal Ulcers


H pylori testing
Serologydoes not distinguish between old and active infection  – IgG antibodies can remain in the circulation for up to nine months after eradicationHigher false positive rate than either stool antigen tests or urea breath tests
Carbon-13 urea breath testDetects CO2 from H. pylori hydrolysis of urea CO2 and ammoniaCan be done inhouse (kit on FP10) but does still have to be sent to the lab)Can have false negatives if done whilst taking antacids/PPIsBecomes negative once H. pylori is eradicated.More expensive than serology but may reduce the need for endoscopy, so may be more cost effective in the long run.
Stool antigen testneed a pea-sized piece of stoolAntibiotics should be stopped at least four weeks before testing, PPIs at least two weeks before, and H2 receptor antagonists at least one day before testing
Endoscopy and biopsyAllows histopathology/culture/urease enzyme testing


 endoscopy vs. empirical treatment in dyspepsia
Treat and Test younger patients without ALARM symptoms‘test and treat’ for Helicobacter pylori, or give a proton pump inhibitor empirically rather than referring immediately
Test and Treat  Refer endoscopy if symptoms persist for 4-6 weeks despite initial interventions especially if there has been a previous gastric ulcer, or increased concern about the risk of gastric cancer
NICE CG17 Dyspepsiahttp://343/bmj.d6234.full


Drugs causing dyspepsia (McGavock)
2 nitrates
3 oral steroids
4 bisphosphonates
5 theophylline/aminophylli
7 calcium-channel blockers
Check for drug causes and stop/replace potential offenders


Helicobacter pylori eradication in functional dyspepsia? NeLM Nov 2011

H pylori eradication
omeprazole 20 mg bd + amoxycillin 500 mg tds + metronidazole 500 mg tds for 7 days
lansoprazole 30 mg + amoxicillin 1 g bd + clarythromycin 500 mg bd for 7 days


Tests of eradication (at least 1m after Rx)

complicated patients eg a duodenal ulcer which has previously bled, a gastric ulcer or a duodenal ulcer remaining symptomatic

H pylori MIMS

H pylori PUK


H pylori quadruple therapy better than gold standard

28 Feb 11 Pulse The Lancet February 22

Quadruple therapy with a proton-pump inhibitor plus a single three-in-one capsule is better than the gold-standard treatment regimen of omeprazole, amoxicillin, and clarithromycin in adults with Helicobacter pylori infection


PU Disease

Gastric or duodenal ulceration most frequently due to H pylori infection.

Presents with dyspepsia



PPI Discontinuation JAGS Sep 2011

EEP Infopeoms Surgery and esomeprazole equally effective for chronic GORD

There is an association between acid suppression therapy, particularly with PPIs, and increased rates of Clostridium difficile Campylobacter enteritis and pneumonia



Seen in to DM (or smooth muscle disorders -scleroderma, dermatomyositis).

Gastric stasis with bloating, satiety, nausea and vomitting.

Treated by improving glycaemic control +/- prokinetic agents (metoclopromide, domperidone).



Intestinal and metabolic complication post gastric resection plus drainage procedures where excess partially digested food is delivered to the small intestine.

Hypotension Sweating dizzyness tachycardia.

Early Dumping (1hr) hyperosmolar food draws water into SI stimulating peristallsis and relaease of VIPs.

Late Dumping (1-3 hrs) Rapid absorption of large ammounts glucose causes spike f insulin release with rebound hypoglycaemia.


Epigastric Mass
Ca stomach
Ca transverse colon
Pancreatic tumour or pseudocyst
Retropreitoneal Lymphadenopathy


Coeliac disease
Gluten-sensitive enteropathy – inflammatory immunolgical reaction to gluten in wheat causing proximal small bowel mucosal damage and chronic malabsorptionPrevalence is 0.5-1% diagnosis is often delayed or missed.
  • dermatitis herpetiformis
  • recurrent aphthous ulcers
  • iron deficiency anaemia
  • irritable bowel
  • increased risk of diabetes mellitus
  • small bowel lymphoma
  • small bowel adenocarcinoma and carcinoma of the colon or oesophagus
  • ulcerative jejuno-ileitis and colitis
Children FTT, diarrhoea, irritability and anorexia may appear following weaning, with presentation between 9 months and 3 yearsChildren over 3 years may also present with short stature, anaemia or during workup following diagnosis of diabetes mellitus
Adults Symptoms are often less acute. The peak incidence of diagnosis is in the third decade, with smaller peaks in the fifth and sixth decades

  • general lassitude
  • diarrhoea
  • iron/folate deficiency
  • vitamin D deficiency
  • vitamin K deficiency
Tests coeliac screen (EMA/TTG)Serological tests for antibodies to tTG, gliadin and endomysiumIgG anti-gliadin (AGA)IgA and IgG antiendomysial transglutaminase antibodiesanti-transglutaminase antibodyDxylose test to confirm small bowel malabsorption

Formal diagnosis requires a small intestinal biopsy – ileal and jejunal villous atrophy, duodenal crypt hyperplasia

Repeat biopsy should be performed after 3–6 months on a gluten free diet (GFD) to assess adequate histological response

Supportive investigations

A number of routine blood tests, including haemoglobin, vitamin B12, folate, iron, serum albumin and calcium, should be carried out as part of workup, during symptomatic relapse, and during pregnancy

Diet Gluten exclusion – all foods containing wheat, rye, barley and oatsGluten-free foods (flour, bread, biscuits and pasta) can be prescribed on FP10 endorsed with ACBS
Supplements Many people will have dietary deficiencies at the time of diagnosis Fe B12 folate CaThese usually resolve spontaneously once on a GFD, but  it seems reasonable to ensure rapid correction with appropriate supplements
Pregnancy Folate supplements if planning conception
Hyposplenism Pneumococcal vaccination recommended for  patients over two years of age
Bone abnormalities Many patients develop  osteopenia and osteoprosisBone densitometry scanning should be considered on presentation and may be repeated after 1–2 years of dietary therapy if the initial value is low, after menopause in women or after 55 in men. If a fragility fracture occurs at any age then a scan should be done. (PCSG)Osteoporosis in post-menopausal women may warrant hormone replacement therapy and the use of bisphosphonatesCalcium supplementation (1500 mg a day) may be considered
Compliance 70% of adults, and a greater proportion of children, respond promptly to a GFD, showing improvement of symptoms within weeks or days.Adherence should be life-long – complications including nutritional deficiencies, osteoporosis, DM and small intestinal lymphoma are more likely in  coeliac patients who continue to ingest gluten.If the diagnosis is in doubt, gluten challenge and repeat jejunal biopsy should be undertakenFailure to respond:

  • assess dietary compliance
  • confirm diagnosis
  • exclude other coincident disease
Follow-up In patients with a satisfactory response to diet, follow-up should be at 6–12 month intervals to assess symptomatic improvement, nutritional state and dietary compliance, and to check routine blood tests.Patients should be referred back to a consultant clinic if any abnormalities are found by the blood testsIt is important to review patients at times of stress, whether this be physical or emotional, particularly during pregnancy


Gluten Free Foods


Inflammatory bowel disease
Ulcerative colitis 
bloody diarrhoea, sometimes with colicky abdominal pain, urgency or tenesmus

affects only the colon

diagnosis on clinical suspicion plus typical results of sigmoidoscopy/colonoscopy and biopsy

(with negative stool tests for infection)youtu.be/HcSmVKGnGPEyoutu.be/2n_B0cfiFgU

abdominal pain, diarrhoea, weight loss, malaise, anorexia, fever or intestinal obstruction

not limited to a particular part of the GI tract

diagnosis on demonstration of focal, asymmetric and often granulomatous inflammationyoutu.be/k_6AsumRnU0

Both diseases are relapsing and remitting

Crohn’s often more disabling

Disease extent location and activity determines therapy


Inflammatory bowel disease assessment
  • recent travel
  • medication
  • smoking status
  • family history
  • stool frequency and consistency
  • urgency
  • rectal bleeding
  • abdominal pain,
  • malaise
  • fever
  • weight loss
  • extra-intestinal symptoms e.g. joint/cutaneous/eye problems
  • general wellbeing
  • heart rate
  • blood pressure
  • temperature,
  • checks for anaemia
  • fluid depletion
  • weight loss
  • abdominal tenderness/distention
  • palpable masses
  • perineal involvement
  • full blood count
  • urea and electrolytes
  • liver function tests
  • microbiology,
  • abdominal radiography
  • if diarrhoea present: rigid sigmoidoscopy + rectal biopsy
  • mild to moderate disease:colonoscopy
  • terminal ileal biopsy if Crohn’s  suspected
  • others small bowel radiology, ultrasound, CAT, MRI, laparoscopy



Drug treatment of inflammatory bowel disease (Tayside)
Aminosalicylates (‘5 – ASA’ preparations)
Oral aminosalicylates are of great value in the maintenance of remission of ulcerative colitis.Less effective in the maintenance of remission of Crohn’s disease though some  formulations of mesalazine are licensed for this in Crohn’s ileo-colitis.In the treatment of acute ulcerative colitis and Crohn’s disease, diffuse disease or disease that does not respond to local therapy requires oral treatment.Mild disease affecting the proximal colon can be treated with an oral aminosalicylate alone;a combination of a local and an oral aminosalicylate can be used in proctitis or distal colitis.
Oral Treatments

The release characteristics of e/c mesalazine preparations may vary, therefore preparations should not be considered interchangeable.When prescribing, the brand name should be specified.

Formulation choice should be patient specific and related to the severity and position in the bowel of their disease, however efficacy may depend more on adherence with the prescribed dose than the delivery system.Of the available e/c mesalazine preparations, Mesren® MR 400mg and Asacol®MR 400mg are bioequivalent and considered to be identical with regards to clinical, pharmaceutical, pharmacokinetic and manufacturing profile.Mesren® MR 400mg is currently the most cost effective e/c mesalazine preparation.Mesalazinee/c tablets (Mesren® MR 400mg) or (Asacol®MR 400mg)Dose: acute attack, 2.4g daily in divided doses; maintenance 1.2g – 2.4g daily in divided dosese/c tablets (Asacol®MR 800mg)Dose: acute attack, 2.4 – 4.8g daily in divided doses; maintenance up to 2.4g daily in divided dosesm/r tablets 500mg (Pentasa®)Dose: acute attack, up to 4g daily in 2-3 divided doses; maintenance 2g once daily.Tablets may be dispersed in water, but should not be chewed.m/r granules 1g, 2g (Pentasa Sachet®)Dose: acute attack, up to 4g daily in 2-4 divided doses; maintenance 2g once daily.Granules should be placed on tongue and washed down with water or orange juice without chewing.m/r, e/c tablets 1.2g (Mezavant® XL)Dose: acute attack, 2.4g once daily, increase if necessary to 4.8g once daily (review treatment at 8 weeks); maintenance, 2.4g once daily.Pentasa Sachet® should be considered first line for maintenance in patients with compliance problems.


750mg tabs

Acute attack 2.25g tds until remission for a maximum of twelve weeks

Maintenance 1.5g bd adjusted according to response. Max 6g daily.


standard and e/c tablets 500mg

Acute attack, 1-2g qds, until remission, reducing to a maintenance dose of 500mg qds

Both formulations of sulfasalazine, standard and enteric coated, are licensed in inflammatory bowel disease but only the e/c version is licensed in rheumatoid arthritis

Sulfasalazine may cause staining of soft contact lenses and may colour urine

FBC WCC LFTs U&Es should be performed in all patients before starting therapy with an oral aminosalicylate

and checked at regular intervals during treatment eg:

FBC and LFTs: 4 weekly for the first 12w then every 12w for the first year, if blood results stable then 6 monthly during the second year then discontinue if stable

Renal function: every 3 months for the first year; every 6 months for the next 4 years and annually thereafter

Topical Treatments
Acute mild to moderate disease affecting the rectum (proctitis) or the recto-sigmoid is treated initially with local application of aminosalicylate.

if not tolerated or ineffective, considet local corticosteroid


foam enema (Asacol®) 1g/metered application

Acute attack affecting rectosigmoid region, 1 application (1g mesalazine) daily

affecting descending colon, 2 metered applications daily for 4-6 weeks

retention enema (Pentasa®) 1g in 100ml

1 enema at bedtime.

suppositories(Pentasa®) 1g

ulcerative proctitis, acute attack, 1 suppository daily for 2-4 weeks;

maintenance, 1 suppository daily.

These drugs are mainly specialist initiated.

However, in the event of acute relapse the above preparations are recommended, choice may be influenced by the success of previous therapies. For severe relapse advice from a specialist may be required

Patients receiving aminosalicylates should be advised to report any unexplained bleeding, bruising, purpura, sore throat, fever or malaise that occurs during treatment. FBC/WCC should be performed and the drug stopped if there is suspicion of a blood dyscrasia.

Oral steriods
Refractory or moderate inflammatory bowel disease usually requires adjunctive use of an oral corticosteroid (prednisolone) for 4-8 weeks.

Use of enteric coated tablets to prevent peptic ulceration is speculative only.

Budesonidee/c, m/r capsules 3mg (Entocort®)

Mild to moderate Crohn’s disease affecting the ileum or ascending colon9mg once daily in the morning, before breakfast for up to 8 weeks; reduce dose for the last 2-4 weeks of treatment.

Poorly absorbed but has therapeutic benefit with reduced systemic toxicity in ileocaecal Crohn’s or UC.It therefore may offer advantages for patients requiring frequent courses of prednisolone and those at particular risk of adverse effects

Topical Steroids
indicated in acute mild to moderate disease affecting the rectum (proctitis) or the recto-sigmoid where local application of an aminosalicylate is not tolerated or not effective

Prednisolone (Predfoam®) foam 20mg/metered application

Proctitis and distal ulcerative colitis in adults, 1 metered application (20mg prednisolone) inserted into the rectum once or twice daily for 2 weeks, continued for further 2 weeks if good response.

Topical Hydrocortisone (Colifoam®) 10% foam

Ulcerative colitis, proctosigmoiditis and granular proctitis, Initially 1 metered application (125mg of hydrocortisone acetate) inserted into the rectum once or twice daily for 2 to 3 weeks, then once on alternate days.

Budesonide (Budenofalk®) foam

Ulcerative colitis involving rectal and recto-sigmoid disease in adults over 18 years, one enema at bedtime for 4 weeks

Disease Modifying Treatments
eg azathioprine methotrexate mercaptopurine infliximab

Initiated by specialists and continued according to local shared care agreement

BSG Guidelines for the management of inflammatory bowel disease 2004

BSG Guidelines for osteoporosis in IBD and Coeliac disease 2007


Other considerations ***
smoking stop
analgesia treat underlying cause if possibleopioid, e.g. tramadol, for non-specific pain
antibiotics metronidazole


Fistulating and perianal disease


PPIs gastroduodenal Crohns
nutrition regular assessment of nutritional status is essential esp in Crohn’s disease

nutritional support may be needed

pregnancy plan conception during remission

if acute severe colitis/life-threatening complications manage as if no pregnancy

methotrexate contraindicated

Other sites eg oral Crohns – requires specialist management

Extraintestinal manifestations usually respond to IBD therapy if associated with active disease, but follow their own course when disease is not active

Ca Surveillance inform patient of risks and benefits and decide together whether surveillance is appropriate
Surgery Ulcerative colitis

surgery advisable if no response to intensive medical therapy

Crohn’s disease

surgery advisable only for symptomatic disease as symptoms are likely to recurdiffuse small bowel disease



UC Management
severe admit to hospital
mild/moderate treat as outpatient
proctitis/disease extending to the sigmoid topical management
more widespread oral or parenteral treatment; additional topical therapy may help
Active left-sided or extensive ulcerative colitis: oral aminosalicylates or corticosteroids
Active distal ulcerative colitis topical mesalazine or topical steroid plus oral mesalazine or corticosteroids
Severe ulcerative colitis admit to hospital
Maintenance of remission aminosalicylates, azathioprine or mercaptopurine



Gall bladder disease





Biliary Colic


Pancreatitis I get smashed
autoimmune disease
scorpion bites


Liver Disease

Liver disease Merck Professionals      Merck Home Health


Yellow discolouration of skin due to deposition of elevated bilirubin from RBC breakdown
Prehepatic – haemolytic – overproduction
RBC lysis exceeds the livers capacity to conjugate bilirubin

  • uncojugated hyperbilirubinaemia
  • raised urine urobilinogen but no urinary no bilirubin
  • liver enzymes normal
  • Haemolysis (sickle cell anemia, thalassemia, transfusion reactions and autoimmune disease), reticulocytosis anaemia
  • Impaired conjugation (reduced UDPGT activity)
  • Congenital hyperbilirubinaema (Gilberts, Crigler Nagler)
  • Breast Milk Jaundice
Hepatic – hepatocellular – failure of excretion
Hepatocyte damage renders liver unable to conjugate or excrete bilirubin

  • conjugated and unconjugated hyperbilirubinaemia
  • bilirubin in urine
  • AST/ALT/GGT raised markedly
  • alk phosph minimally raised or normal


  • congenital hyperbilirubinaemias (Dubin-Johnson, Rotor)
  • viral hepatitis
  • hepatotoxic drugs (paracetamol, ABs, ChemoRx, aspirin, warfarin, anticonvilsants, statins, hypoglycaemics)
  • (some drugs may cause a cholestatic or mixed picture)
  • alcohol
  • cancer
  • cirrhosis
  • haematochromatosis and Wilsons disease
Post hepatic – obstructive – failure of elimination
Obstruction of bile outflow within the liver or down the common bile duct due to calculi or tumour – liver can conjugate bilirubin but this can’t reach the small intestine

  • conjugated hyperbilirubinaemia
  • increased urine bilirubin
  • alk phosph and GGT markedly raised
  • clinicaly jaundiced
  • pale stools (no bile pigments) + dark urine (increased bile pigments)




  • Transaminases aspartate aminotransferase (AST)
  • Alanine aminotrasferase (ALT)
  • Antimitochondrial antibodies
  • Cholesterol screening
  • Total bilirubin
  • Coomb’s test
  • Alkaline phosphatase
  • Albumin
  • Viral hepatitis screening
  • Abdominal ultrasound or CT
  • Drug toxicology


Gilberts syndrome

Gilberts syndrome.org.uk

Gilberts syndrome British Liver Trust

Gilberts syndrome BMJ


Fatty Liver

fatty liver British Liver trust

Fatty liver and cardiovascular risks NEJM 2010;363:1341


Chronic liver disease and cirrhosis



Liver and GI Seattle Pacific University iTunes U

some aspects of liver disease and liver failure are currently in “general surgery





Portal hypertension





clinicalexam.com hepatosplenomegaly



Ascites Medscape


Liver Failure

Acute Liver Failure Medscape

Chronic liver failure and cirrhosis AAFP 2006

Liver failure dwp.gov.uk


Autoimmune hepatitis


Hepatitis ABCDE




Hepatitis B management



Hepatitis C management



Irritable Bowel Syndrome

Variable and varying abdominal pain, often poorly localised, bloating, diarrhoea, constipation or a sense of incomplete defecation.

IBS Rome III Criteria
Presence in any 12 weeks in last 12 months of abdominal discomfort or pain with at least two of the following features
relieved with defaecation
onset associated with a change in the frequency of stool
onset associated with a change in form (appearance) of stool.





NDDIC Diverticulitis/Diverticulosis

InfoPoems antibiotics in diverticulitis

Diverticulitis Medscape


Constipation in adults



  • inadequate dietary fibre
  • enforced inactivity (e.g. elderly patients and bedbound)
  • hypothyroidism
  • drugs
Drugs Causing Constipation
Codeine Morphine Opiates
Tricyclic antidepressants
Phenothiazine antipsychotics
Some antacids (calcium carbonate or aluminium hydroxide)
Anticholinergic Anti-parkinsonian drugs (e.g. benzotropine, orphenadrine)
Chronic laxative use/abuse

RED flags: e.g. colorectal cancer or inflammatory bowel disease

  • 1 a change in bowel habit to looser stools and/or increased frequency, lastingmore than 6 weeks
  • 2 rectal bleeding (excluding bleeding piles)
  • 3 iron-deficiency anaemia, particularly if the haemoglobin concentration is < 8 gldl
  • 4 a palpable mass in the abdomen or rectum.

Constipation is in fact not often due to colorectal cancer, unless the intestinal lumen has been obstructed by the tumour

Chronic constipation Clinical review BMJ 2009;338:b831


GIT Often vomiting related to GI disorders is due to gastroenteritis caused a virus or bacteria, gastritis due to ingestion of caffeine, alcohol, spicy or irritating foods or food poisoning from the ingestion of undercooked spoiled foods.   A more serious cause of vomiting is intestinal obstruction; vomiting is more common in obstruction of the upper small intestine.  Severe steady pain, abdominal distention and possibly visible peristaltic waves and palpable abdominal mass are associated symptoms with intestinal obstruction and vomiting.  Vomiting seen with weight loss and anorexia is also seen with gastric cancer, and ulcerative colitis.  Peptic ulcers are associated with hematemesis and epigastric pain after ingestion of alcohol, caffeine or aspirin.The characteristics of the patient’s vomit can be a useful clue in detecting the cause as well:Bile-stained vomit is indicative of an obstruction below the pylorus, as seen with duodenal lesions.Hematemesis is indicative of an upper GI bleed, bright red may be caused by gastritis or peptic ulcer, dark red may be due to esophageal or gastric varices.Brown vomit with a fecal odor could be due to intestinal obstruction or infarction.Coffee-ground emesis is due to digested blood from a slow GI bleed or duodenal lesion.Burning bitter tasting emesis is caused  by excessive acid in the gastric contents.Undigested food in the emesis may be caused by gastroenteritis, gastric tumor or ulcer
Pregnancy Pregnancy in the first trimester is a common cause of vomiting typically peaking around 8-12 weeks and disappearing after the 20th week.  Hyperemesis gravidarum occurs in 1-2% of pregnancies and commonly associated with multiple pregnancies or hydatiform moles.  Vomiting after the 20th week should be investigated for different causes.  Preeclampsia and ectopic pregnancies can also present with vomiting.
CVS Myocardial infarct will often present with vomiting, immediately assess patient for other associated symptoms and don’t delay treatment and transfer of patient to emergency room.
CNS Patients with projectile vomiting not preceded by nausea, altered level of consciousness, severe headache should considered for central nervous system disorders such as concussion from a recent head injury, meningitis, or lesions of the central nervous system.
Renal FB Cystitis, pyelonephritis, calculi, and other renal and urologic disorders are commonly associated with vomiting.  Cholecystitis can present with vomiting and right upper quadrant pain.
Drugs antineoplastics, opiates, ferrous sulfate, estrogens, oral potassium, antibiotics, NSAID’s or anesthetics and radiotherapy
Psychological Fear, stress, severe emotions, bulimia
Infants more likely to present with dehydration. Intussusceptions may lead to vomiting bile and fecal matter in an infant or toddler, while pyloric obstruction is a common cause of projectile vomiting in a neonate
Elderly Beware intestinal ischemia. Close monitoring of the elderly patient is required during periods of electrolyte imbalance and rehydration due to pre-existing conditions such as cardiac or renal failure




Frequent passage of loose liquid faeces. The most common UK cause is acute self-limiting gastroenteritis (food poisoning)  but it is important to consider more serious underlying causes.

It can lead to rapid fluid and electrolyte losses and severe dehydration particularly in elderly and infants.

Red Flags in diarrhoea


Systemic Features (weight loss fevera anorexia malaise sweats)

Persistant altererd bowel habit

Blood or mucous in the stool

Severe abdominal pain, fever or toxic patient.

Hypotension, including postural hypotension altered mental status or other signs of profound dehydration


Acute diarrhoea is typically caused by infectious agents viral, bacterial or parasitic – ask about foreign travel.

Diarrhoea can be a feature of Irritable or Inflammatory bowel disease, malabsorption syndromes, celiac disease alcohol or laxative abuse, drug withdrawal, hyperthyroidism, autonomic neuropathy (eg diabetes) bowel cancer, constipation with overflow antibiotic and other drugs.

Most cases of acute diarrhoea resolve with conservative therapy such as anti-motility drugs and fluid replacement.

Chronic diarrhoea may be a symptom of chronic infections, motility disorders, inflammatory bowel disease or food intolerances.

Campylobacter jejuni
Source food/water/poultry
Incubation 2-7 days
Notes Campylobacter Enteritis- Produces an inflammatory bloody diarrhoea or dysentery syndrome but may also be watery in nature.  Improper preparation of chicken, unpasteurized milk or contaminated water can cause campylobacter.


E coli 0157 H7
Source milk raw meat
Incubation 12-48 hrs
Duration 8 days
Notes Escherichia Coli (E. coli) – Is caused by a bacterium found in the colon that becomes a contaminant when found in food or water supplies.  E. coli accounts for the majority of bacterial diarrhoea deaths globally in children.  An uncommon but serious complication of E.coli is hemolytic uremic syndrome and eventually acute renal failure.


Source poultry eggs
Incubation 24 hrs
Duration 5 days
Notes children and elderlyheadache fever abdo pain dysentry sepsis (5-10%)Salmonellosis- Infection usually occurs from eating contaminated meat, eggs, and poultry.  The incubation period is 12-48 hours. Diarrhoea can be mild or up to 20-30 stools per day can occur, it usually resolves after 5-7 days.


Source FOT toxin
Incubation 48 hrs
Notes children and institutionsmucoid dysentery dehydration febrile seizuresRx ciprofloxacinabdo pain fever bleeding toxic megacolontoxin in stoolRx metronidazole /vancomycinShigellosis- Produces an acute colitis, characterized by diarrhoea, dysentery, fever, abdominal pain, and tenesmus.  Children between the ages of 1 and 4 are at the highest risk for acquiring the infection.  Complications include dehydration, seizures, septicemia, hemolytic-uremic syndrome, Reiter’s syndrome and peritonitis.


Clostridium difficile
Source pseudomembranous colitis
Notes clindamycin and BSA use PPisClostridium difficile – C difficile diarrhoea is characterized by foul smelling, greenish watery stools accompanied by lower abdominal cramping.  It is more common in elderly infirm  patients who have been recently hospitalized or have received antibiotic therapy especially cephalosporins.  Patients may present with mild symptoms or with an acute abdomen secondary to toxic megacolon and perforation. Note C Difficile are found in 5% of normal individuals.


Norwalk Virus Noravirus
Incubation 24 hrs
Duration 1-3 days
Notes Acute outbreaks of gastroenteritis in adults, school children and contacts.  Outbreaks have occurred in diverse locations from cruise ships to nursing homes.  The incubation period is 24 hours, with the symptoms lasting for 1-3 days.Viral Gastroenteritis can also be caused by astrovirus, adenovirus, or coxsackievrous.  A history of other people in the family, at work or school with diarrhoea suggests viral gastroenteritis.Rotavirus- Causes severe diarrhoea primarily in infants and young children ages 6-24 months.


Entoemeba histolytica
Source food/water/travel/sexual
Incubation variable
Notes dysentry colitis toxic megacolon perforation peritonitis liver abcess flask ulcersfluorescent antibody test microscopyRx metronidazole dolixanid

Food Poisoning and  Enterocolitis

Diarrhoea occurring 2-6 hours after a meal containing milk, pies, salad or mayonnaise can be caused by Staphylococcal food poisoning.

Diarrhoea appearing 8-14 hours after a meal can be caused by Salmonella, Shigella, Vibrio cholera, or E. coli.  Mushrooms, fish, vegetables, meat, poultry, and shellfish can also cause diarrhoea.

Bloody Diarrhoea

Can be caused by infectious agents, inflammatory bowel disease, peptic ulcer disease, or bleeding from anywhere in the gastrointestinal tract.

Melena, or black tarry stools may indicate upper GI bleeding.  Hematochezia, or maroon stools may indicate lower GI bleeding.

A small amount of bright red blood may indicate localized bleeding such as hemorrhoids or anal fissures.

The bleeding associated with intussusception is described as red currant jelly stools.

Additional Causes

include traveler’s diarrhoea, medications, and stress.  Chronic diarrhoea can be due to long term use of laxatives, sorbitol, diets rich in fruit/fiber/carbohydrates, irritable bowel syndrome, poorly controlled diabetes, and chronic alcohol abuse.


Usually Nil Required

Stool culture, for persistant or unusual cases

Giardia antigen, Clostridium dificile toxin assay

Hemoccult testing

Routine Bloods (FBC UEs RBS if indicated)

History of travel, meals, and recent antibiotic use

Fluid and electrolyte replacement

Bismuth subsalicylate or loperamide for patients without fever or bloody stools

Antibiotics for diarrhoea due to Shigella, cholera, pseudomembranous enterocolitis, parasites

Analgesics for abdominal pain if indicated

Refer hospital/ GP for further FU treatmen as appropriate. to gastrointestinal specialist

Encourage proper oral fluid intake (clear water); consider electrolyte replacement fluids

Increase dietary soluble fiber; eat smaller more frequent meals

Avoid alcohol, caffeine, insoluble fiber, fatty and spicy foods

Proper cleaning and protection of perianal area

Discontinue any diarrhoea causing medications.

Extra protection not usually needed with contraceptive pill

Instruct on signs of dehydration in children.

Instruct on importance of and proper technique for hand washing



Flatulence @ CORE


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