|ALARMS symptoms in GI Disease|
|Difficulty transferring food to the pharynxneurological disorderslocal inflammatory conditionsaffects liquids > solids with reguritation, cough aspiration|
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.
|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.|
|General Measures||Elevate head of bed, avoid late eating, smaller meals advice on healthy eating, weight reduction and smoking cessation|
|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|
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.
- Barrett’s BMJ 2010
- Thermal Ablation Barretts oesophagus.co.uk
- Barretts campaign.org.uk
- Barrett’s PUK
- Barrett’s Macmillan.org
|Dyspepsia and PUD|
|GORD||LOS dysfunction with acid reflux(or sometimes respiratory symptoms)|
Note that there may be overlap and as noted above, GIT symptoms are not well localized in some patients.
|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)|
|3 oral steroids|
|7 calcium-channel blockers|
|Check for drug causes and stop/replace potential offenders|
|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 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
Gastric or duodenal ulceration most frequently due to H pylori infection.
Presents with dyspepsia
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.
|Ca transverse colon|
|Pancreatic tumour or pseudocyst|
|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.|
|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
|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
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:
|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 products Coeliac UK
- mims gluten glutafin
- mims juvela
- psnc gluten free toolkit
- bbc.co.uk gluten free
- coeliac.org.uk gluten free faqs
|Inflammatory bowel disease|
|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
|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|
|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.|
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.
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
|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.
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.
|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
|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 ***|
|analgesia||treat underlying cause if possibleopioid, e.g. tramadol, for non-specific pain|
Fistulating and perianal disease
|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
|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 advisable if no response to intensive medical therapy
surgery advisable only for symptomatic disease as symptoms are likely to recurdiffuse small bowel disease
|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 Penn Surgery
- Gallbladder disease SATT
- Cholecystitis and Biliary Colic in Emergency Medicine Medscape
- Analgesics in Biliary Colic BestBets
- Colecystitis vs Biliary Colic Mr Jason Smith
- Primary Surgery
|Pancreatitis I get smashed|
|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
|Hepatic – hepatocellular – failure of excretion|
|Hepatocyte damage renders liver unable to conjugate or excrete bilirubin
|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
- Transaminases aspartate aminotransferase (AST)
- Alanine aminotrasferase (ALT)
- Antimitochondrial antibodies
- Cholesterol screening
- Total bilirubin
- Coomb’s test
- Alkaline phosphatase
- Viral hepatitis screening
- Abdominal ultrasound or CT
- Drug toxicology
some aspects of liver disease and liver failure are currently in “general surgery“
- Autoimmune liver disease BMJ 2009
- British liver trust org.uk
- Autoimmune hepatitis.co.uk
- PBC foundation.org.uk
- PSC support.org.uk
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.|
- inadequate dietary fibre
- enforced inactivity (e.g. elderly patients and bedbound)
|Drugs Causing Constipation|
|Codeine Morphine Opiates|
|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.
|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|
|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.|
|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.|
|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.|
|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|
|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.|
|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.
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.
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
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