Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Separate acute infection and dehydration from chronic inflammatory, malabsorptive, secretory and functional diarrhoea, select stool and endoscopic tests by consequence, and protect patients and contacts through appropriate public-health action.
Acute diarrhoea is first a severity and transmission problem. Estimate intake, urine output, postural symptoms and comorbidity; examine perfusion, hydration, temperature, abdominal tenderness and mental state. Most uncomplicated community gastroenteritis is self-limiting and does not require a broad stool panel or antibiotics. Testing becomes useful when illness is bloody, severe, persistent, travel-associated, outbreak-linked, immunocompromised, post-antibiotic or occupationally significant. Infection-control precautions and clear advice about work, school, food handling and healthcare settings prevent secondary cases; the health protection team sets enhanced clearance requirements for high-risk organisms and groups.
Chronic diarrhoea is classified by phenotype. Watery stool can be secretory, osmotic, bile-acid related, microscopic colitis or a disorder of gut-brain interaction. Inflammatory diarrhoea brings blood, urgency, nocturnal symptoms, weight loss, fever, raised calprotectin or extra-intestinal disease. Malabsorptive diarrhoea causes bulky pale or oily stool, weight and micronutrient loss. A high-volume pattern continuing during fasting raises secretion, whereas improvement during fasting supports osmotic intake, although real presentations overlap. Previous ileal disease or resection, cholecystectomy, pelvic radiotherapy, pancreatic disease and thyroid or endocrine symptoms redirect the work-up.
Acute diarrhoea commonly follows enteric infection, antibiotics, laxatives or other medicines; travel, healthcare exposure, contacts and immune status alter likely organisms and consequences.
Inflammatory bowel disease, microscopic colitis, coeliac disease, pancreatic insufficiency and bile-acid diarrhoea are important causes when symptoms persist or nutritional features emerge.
Disorders of gut-brain interaction, endocrine disease, postoperative anatomy and altered motility can increase stool frequency or liquidity without primary mucosal inflammation.
Poorly absorbed solutes, active secretion or accelerated transit retain water within the bowel and reduce colonic time for fluid recovery.
Infection or immune injury disrupts epithelial absorption and releases blood, protein and inflammatory mediators, causing urgency, nocturnal stool and sometimes systemic illness.
Sustained high-volume stool depletes water, electrolytes and bicarbonate; chronic maldigestion or mucosal disease additionally causes weight loss and micronutrient deficiency.
High fever, bloody stool, severe pain, dehydration, sepsis, recent travel, outbreak exposure or immunocompromise raises invasive infection and justifies urgent sampling, isolation and specialist or public-health discussion before empirical treatment.
New unexplained diarrhoea after antibiotics, healthcare exposure or in frailty raises C difficile. Severity includes clinical and laboratory features; ileus or toxic megacolon may reduce stool output despite fulminant disease.
Blood, urgency, nocturnal diarrhoea, weight loss, fever, perianal disease, extra-intestinal inflammation and raised calprotectin support IBD, while acute severe colitis requires immediate hospital and gastroenterology assessment.
Chronic watery urgency after ileal disease or resection, sometimes after cholecystectomy or without an obvious cause, supports excessive colonic bile acids. Positive diagnosis is preferred to an unstructured long-term empirical trial where testing is available.
Chronic watery non-bloody diarrhoea, often nocturnal and associated with older age or selected medicines, may have normal endoscopic appearance. Histology from appropriate right and left colonic biopsies establishes diagnosis.
Weight loss, bulky pale oily stool, iron or folate deficiency, low albumin and bloating suggests coeliac, pancreatic or small-bowel disease. The exact deficiency pattern and surgical history guide focused testing.
Abrupt onset, fever, sick contacts, travel, recent antibiotics or institutional exposure favours infection; stool testing is selected according to severity and public-health implications.
Blood, nocturnal symptoms, weight loss, raised inflammatory markers or calprotectin and compatible endoscopy support inflammatory disease rather than uncomplicated functional diarrhoea.
Steatorrhoea, deficiencies and weight loss suggest malabsorption, whereas a chronic fluctuating pattern without alarm features or objective inflammation may support irritable bowel syndrome.
Large gastrointestinal losses cause orthostatic symptoms, hypovolaemia and acute kidney injury, especially in frailty, infancy or pre-existing renal disease.
Potassium, magnesium and bicarbonate loss can produce weakness, arrhythmia or metabolic acidosis; vomiting and renal dysfunction may modify the biochemical pattern.
Persistent diarrhoea may cause protein-energy and micronutrient deficits, while infectious causes can spread to contacts and create occupational or institutional risk.
Fulminant C difficile may progress from diarrhoea to ileus and toxic megacolon. A falling stool count alongside increasing distension and systemic toxicity is deterioration, not recovery.
Microscopic colitis often leaves the mucosal surface visually unremarkable. The diagnosis depends on biopsies from appropriate colonic segments, which must be requested despite normal appearance.
Faecal elastase concentration can look low because a liquid stool contains more water. Repeating on a formed sample and correlating pancreatic imaging avoids false exocrine-insufficiency labels.
FIT measures human haemoglobin to support colorectal cancer triage; calprotectin reflects intestinal neutrophilic inflammation. Using one as a substitute for the other creates predictable missed diagnoses.
It can occur without major ileal surgery and may be mislabelled diarrhoea-predominant IBS. A positive diagnostic test permits treatment intensity to reflect severity and improves adherence.
Giving loperamide for bloody febrile diarrhoea or suspected C difficile before assessing invasive disease.
Treating a positive C difficile molecular test in an asymptomatic patient without toxin and clinical interpretation.
Using a normal-looking colonoscopy to exclude microscopic colitis without right- and left-sided biopsies.
Calling chronic diarrhoea IBS without coeliac testing, medicine review or consideration of inflammatory and cancer pathways.
Interpreting a low faecal elastase from a very watery sample as definitive pancreatic insufficiency.
Giving generic return-to-work advice without checking organism, occupation and UKHSA health-protection requirements.
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A patient being treated for C difficile has fewer stools today but develops increasing abdominal distension, tachycardia and rising inflammatory markers. What is the safest interpretation?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
The investigation plan needs an action for each result. Baseline blood count, renal and liver profiles, inflammatory markers, thyroid testing and coeliac serology identify systemic consequences and treatable causes. Stool microbiology is chosen from the exposure; C difficile diagnosis uses the local multistep laboratory algorithm and must be interpreted with symptoms because colonisation occurs. Calprotectin directs inflammatory evaluation. Colonoscopy with ileoscopy and right- and left-colon biopsies can diagnose IBD, cancer and microscopic colitis; visually normal mucosa does not exclude the latter. Bile acid testing, faecal elastase and small-bowel imaging follow specific phenotypes. Treatment targets cause while protecting hydration, nutrition and antimicrobial stewardship.
Commercial or pharmacy-approved preparation avoids dangerous home concentration errors. Fluid, sodium and potassium plans need adjustment in significant kidney or heart disease and severe dehydration.
Seek specialist advice for life-threatening or recurrent disease, ileus or treatment failure. Do not use anti-motility agents, and do not treat asymptomatic colonisation merely because a molecular assay is positive.
Avoid with bloody stool, fever, severe colitis, abdominal distension or suspected toxin-mediated disease. Excess dosing can cause serious cardiac toxicity and prolonged unsupervised use can conceal deterioration.