Acute and chronic diarrhoea

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

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.

Key points

Define true diarrhoea by increased stool liquidity and frequency, then clarify onset, duration, volume, blood, nocturnal stool, urgency, steatorrhoea, pain and fasting response.
Acute illness is commonly infectious, medicine-related or inflammatory; symptoms lasting four weeks or more require a structured chronic-diarrhoea pathway rather than repeated empirical antibiotics.
Ask about travel, food and water, sick contacts, antibiotics, hospital or care-home exposure, sexual exposure, immunosuppression and occupation because testing and public-health consequences differ.
Blood, fever, severe pain, systemic toxicity and dehydration alter urgency; anti-motility treatment can be unsafe when invasive infection, C difficile or acute severe colitis is plausible.
Review metformin, magnesium, antibiotics, laxatives, PPIs, NSAIDs, colchicine, orlistat and other medicines before labelling chronic diarrhoea idiopathic.
Faecal calprotectin addresses intestinal inflammation in an appropriate population, quantitative FIT addresses colorectal cancer risk, and neither test substitutes for the other.
Chronic watery diarrhoea may reflect bile acid diarrhoea or microscopic colitis even when colonoscopy looks normal; correct testing and colonic biopsies are essential.
Fatty, difficult-to-flush stool with weight loss directs assessment towards coeliac disease, pancreatic insufficiency and small-bowel malabsorption.
Oral rehydration replaces both salt and water more effectively than plain water during substantial gastrointestinal losses; intravenous replacement is needed when shock or oral failure develops.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Infection and medicines

Acute diarrhoea commonly follows enteric infection, antibiotics, laxatives or other medicines; travel, healthcare exposure, contacts and immune status alter likely organisms and consequences.

Inflammatory and malabsorptive

Inflammatory bowel disease, microscopic colitis, coeliac disease, pancreatic insufficiency and bile-acid diarrhoea are important causes when symptoms persist or nutritional features emerge.

Functional and systemic

Disorders of gut-brain interaction, endocrine disease, postoperative anatomy and altered motility can increase stool frequency or liquidity without primary mucosal inflammation.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Excess luminal water
Poorly absorbed solutes, active secretion or accelerated transit retain water within the bowel and reduce colonic time for fluid recovery.
2
Mucosal inflammation
Infection or immune injury disrupts epithelial absorption and releases blood, protein and inflammatory mediators, causing urgency, nocturnal stool and sometimes systemic illness.
3
Fluid and nutrient loss
Sustained high-volume stool depletes water, electrolytes and bicarbonate; chronic maldigestion or mucosal disease additionally causes weight loss and micronutrient deficiency.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Severe infectious diarrhoeaRed flag

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.

Clostridioides difficile infectionRed flag

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.

Inflammatory bowel phenotypeRed flag

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.

Bile acid diarrhoea

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.

Microscopic colitis

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.

Malabsorption pattern

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Stool culture or multiplex pathogen testingFirst step
Why
Identify bacterial, viral or parasitic infection when severity, duration, travel, outbreak or host factors make the result actionable.
Interpretation and limitations
Request the exposure-specific panel and tell microbiology about travel, blood and immunocompromise. A detected organism requires clinical interpretation and may trigger notification or clearance action.
02
C difficile laboratory algorithm
Why
Detect toxigenic organism and evidence of toxin activity in a patient with compatible diarrhoea.
Interpretation and limitations
Follow local GDH or nucleic-acid and toxin interpretation. Organism-positive toxin-negative results may represent colonisation or early disease and require clinical and microbiology review, not automatic treatment.
03
Full blood count, renal profile and CRP
Why
Measure dehydration, kidney injury, anaemia, inflammation and severity during acute or chronic diarrhoea.
Interpretation and limitations
Haemoconcentration may mask anaemia; falling platelets, haemolysis or kidney injury after bloody diarrhoea raises haemolytic uraemic syndrome and needs urgent specialist assessment.
04
Coeliac serology with total IgA
Why
Identify coeliac disease as a cause of chronic diarrhoea, bloating, weight loss or nutritional deficiency.
Interpretation and limitations
Test while gluten is consumed and use an IgG strategy in IgA deficiency. Positive results generally proceed through specialist confirmation rather than immediate unsupported lifelong exclusion.
05
Faecal calprotectin
Why
Estimate intestinal inflammatory activity and guide IBD assessment in suitable chronic lower gastrointestinal symptoms.
Interpretation and limitations
Infection, NSAIDs and other disease can raise values; use local repeat and referral thresholds. Severe bloody or systemic colitis should be admitted rather than waiting for a routine result.
06
Quantitative FIT
Why
Guide colorectal cancer referral for eligible symptoms under the current NICE NG12 pathway.
Interpretation and limitations
Use the commissioned assay and do not confuse a low value with exclusion of IBD. Persistent symptoms, mass, anaemia or strong concern can still require referral despite a low result.
07
Ileocolonoscopy with segmental biopsies
Why
Diagnose inflammatory bowel disease, colorectal neoplasia and microscopic colitis when chronic symptoms or markers justify direct assessment.
Interpretation and limitations
Biopsy right and left colon even if mucosa is normal when microscopic colitis is suspected. Acute severe colitis requires specialist selection of limited endoscopy to reduce perforation risk.
08
Bile acid and pancreatic testing
Why
Confirm bile acid diarrhoea or pancreatic exocrine insufficiency when the clinical phenotype supports either mechanism.
Interpretation and limitations
Use the locally available validated bile acid test. Faecal elastase is most useful on a formed sample because watery dilution can create a falsely low result; correlate with imaging and nutrition.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Infectious diarrhoea

Abrupt onset, fever, sick contacts, travel, recent antibiotics or institutional exposure favours infection; stool testing is selected according to severity and public-health implications.

Inflammatory bowel disease

Blood, nocturnal symptoms, weight loss, raised inflammatory markers or calprotectin and compatible endoscopy support inflammatory disease rather than uncomplicated functional diarrhoea.

Malabsorption or functional disease

Steatorrhoea, deficiencies and weight loss suggest malabsorption, whereas a chronic fluctuating pattern without alarm features or objective inflammation may support irritable bowel syndrome.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Acute assessmentHydrate, isolate and target samplingFirst stepDiarrhoea began recently and may be infectious.

1Assess perfusion, urine output, electrolytes, abdominal signs and host risk, giving oral rehydration or intravenous fluid according to severity.
2Institute appropriate enteric precautions and take an exposure history covering travel, food, contacts, antibiotics, healthcare, occupation and immune status.
3Send targeted stool testing for blood, systemic illness, persistence, high-risk exposure or public-health consequence; discuss severe cases with microbiology.
4Avoid routine antibiotics and anti-motility agents until invasive, toxin-mediated and C difficile risks are considered, then safety-net hydration and worsening features.

02C difficileTreat disease and remove driversCompatible diarrhoea has a supportive C difficile result or high clinical probability.

1Isolate, review and stop non-essential antibiotics, PPIs and laxatives, assess severity and abdominal distension, and involve infection specialists for severe or recurrent disease.
2Start NICE-recommended oral treatment appropriate to episode and severity, avoiding anti-motility medicine and ensuring prompt administration.
3Monitor stool frequency, abdominal examination, white count, creatinine and systemic state; urgent surgical and critical-care review is required for ileus, megacolon or deterioration.
4Plan recurrence advice, antimicrobial stewardship and environmental infection control rather than using repeat tests to prove routine cure.

03Chronic classificationUse phenotype to order testsLoose stool persists for at least four weeks or repeatedly returns.

1Classify watery, inflammatory or fatty features and review medicines, surgery, radiotherapy, travel, diet, endocrine symptoms and family history.
2Obtain baseline bloods, coeliac serology and appropriately selected FIT or calprotectin, while investigating nutritional deficits and thyroid disease where indicated.
3Arrange colonoscopy with biopsies for warning or inflammatory features and test specifically for bile acid diarrhoea, microscopic colitis or pancreatic insufficiency rather than diagnosing IBS by exclusion alone.
4Refer persistent unexplained, malnourishing or nocturnal diarrhoea to gastroenterology and maintain nutrition and hydration during investigation.

04Public healthPrevent onward transmissionInfectious diarrhoea is suspected in a healthcare, food-handling, education or outbreak context.

1Give handwashing, toilet-cleaning and food-preparation advice and exclude symptomatic people according to current UKHSA and workplace guidance.
2Notify the laboratory, infection team or health protection team when organism, occupation, cluster or setting requires enhanced action.
3Follow organism-specific clearance and return requirements for high-risk cases and contacts; generic 48-hour advice is not sufficient for every pathogen.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Replaces water and sodium through coupled intestinal absorption during acute gastrointestinal losses.

Oral rehydration solution

Give frequent small volumes of a correctly prepared glucose-electrolyte solution, increasing replacement after each loose stool and using intravenous therapy if oral intake fails.

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.

Treats symptomatic C difficile infection while precipitating antibiotics and infection-control risks are addressed.

Oral vancomycin for first C difficile episode

NICE recommends 125 mg orally four times daily for 10 days for a first episode of mild, moderate or severe infection; follow the current recurrent-disease table.

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.

Reduces stool frequency and urgency in selected uncomplicated or established chronic non-inflammatory diarrhoea.

Loperamide for selected non-inflammatory diarrhoea

Use the current BNF short-term regimen only after hydration and once invasive infection, C difficile, acute colitis and obstruction have been excluded.

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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Volume and renal injury

Large gastrointestinal losses cause orthostatic symptoms, hypovolaemia and acute kidney injury, especially in frailty, infancy or pre-existing renal disease.

Electrolyte and acid-base disturbance

Potassium, magnesium and bicarbonate loss can produce weakness, arrhythmia or metabolic acidosis; vomiting and renal dysfunction may modify the biochemical pattern.

Malnutrition and transmission

Persistent diarrhoea may cause protein-energy and micronutrient deficits, while infectious causes can spread to contacts and create occupational or institutional risk.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record stool frequency, volume, blood and nocturnal episodes together with intake, urine output, weight and postural physiology during significant acute losses.
Repeat renal function and electrolytes after replacement in dehydration and trend haemoglobin, platelets and haemolysis markers when HUS is possible.
For suspected C difficile, monitor abdominal distension, tenderness, white count, creatinine and systemic trajectory and escalate reduced stool output with worsening illness as possible ileus.
Track calprotectin, FIT, cultures and histology to a named reviewer, including public-health notifications and organism-specific clearance requirements.
In chronic disease, follow weight, albumin where appropriate, iron, folate, B12 and fat-soluble vitamin risk alongside treatment of the identified mechanism.
Review whether discontinued or newly introduced medicines change diarrhoea before escalating to repeated endoscopy or empirical antimicrobial courses.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Low stool output can worsen

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.

Normal colon can be microscopic

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.

Watery samples dilute elastase

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 and calprotectin diverge

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.

Bile acid diarrhoea is common

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.

11Common pitfallsFrequent interpretation and management errors.

01
Giving loperamide for bloody febrile diarrhoea or suspected C difficile before assessing invasive disease.
02
Treating a positive C difficile molecular test in an asymptomatic patient without toxin and clinical interpretation.
03
Using a normal-looking colonoscopy to exclude microscopic colitis without right- and left-sided biopsies.
04
Calling chronic diarrhoea IBS without coeliac testing, medicine review or consideration of inflammatory and cancer pathways.
05
Interpreting a low faecal elastase from a very watery sample as definitive pancreatic insufficiency.
06
Giving generic return-to-work advice without checking organism, occupation and UKHSA health-protection requirements.