Gastroenterology & Internal Medicine & Family Medicine
Chronic diarrhea
Chronic diarrhea is defined as the presence of loose or watery stools (consistency less than type 5-6 on the Bristol scale) at a frequency greater than 3 per day, or a fecal weight greater than 200-250 g per day, persisting for more than 4 weeks. It affects 3-5 % of the adult population in industrialized countries, and is one of the most frequent gastrointestinal complaints to seek medical attention. Unlike acute diarrhea - the cause of which is most often infectious and self-limiting - chronic diarrhea requires a structured diagnostic approach, as it may be the manifestation of a serious systemic disease (chronic inflammatory bowel disease, celiac disease, colorectal cancer, hyperthyroidism, exocrine pancreatic insufficiency). Pathophysiological classification distinguishes three main, often interrelated mechanisms: secretory diarrhea (active hypersecretion of fluids and electrolytes into the intestinal lumen - persists on an empty stomach - large, watery stools - secretory tumors, bacterial toxins, bile acids) ; osmotic diarrhea (presence of unabsorbed osmotically active solutes in the intestinal lumen - ceases on an empty stomach - fecal osmotic gap >125 mOsm/kg - carbohydrate malabsorption, osmotic laxatives, pancreatic insufficiency) ; and inflammatory diarrhea (exudation of mucus, blood and proteins from an inflamed or ulcerated mucosa - fever, rectorrhagia, tenesmus - chronic inflammatory bowel disease, invasive infections, microscopic colitis). The diagnostic approach should be guided by the clinical distinction between small bowel diarrhea (large, fatty, infrequent stools - malabsorption - no blood) and colonic diarrhea (frequent, small stools - mucus and blood may be present - tenesmus - large bowel pathology).
Main etiologies and clinical features
| Etiology | Mechanism and clinical presentation | Key diagnostic elements |
|---|---|---|
| Irritable bowel syndrome (IBS) with diarrhea predominance - IBS-D Functional cause - most frequent |
Intestinal functional disorder (IFD) - central and visceral sensitization, altered intestinal motility, microbiome dysbiosis, intestinal hyperpermeability, disturbed brain-gut axis; Rome IV criteria: recurrent abdominal pain ≥1 day/week × last 3 months + ≥2 of the criteria: related to defecation, associated with change in stool frequency, associated with change in consistency; IBS-D: soft/liquid stool ≥25 % + hard stool <25 % of defecations; prevalence 10-15 %; female predominance (F:H 2:1); no organic red flags (no blood, no fever, no weight loss) | Diagnosis of exclusion - negative organic workup (CBC, CRP, TSH, celiac, coprocultures, colonoscopy if >50 years or red flags); fecal calprotectin <50 µg/g (quasi-excludes IBD - negative predictive value 93 %); normal biological markers; triggers: stress, meals, certain foods (FODMAP - fermentable oligosaccharides, disaccharides, monosaccharides and polyols) |
| Celiac disease Gluten-sensitive autoimmune enteropathy |
Adaptive immune response (Th1 + Th17 - HLA-DQ2 and HLA-DQ8) to gluten (gliadin from wheat, secalin from rye, hordein from barley) → villous inflammation + villous atrophy + crypt hyperplasia → malabsorption of fats, carbohydrates, fat-soluble vitamins (A, D, E, K) and B12, iron and calcium ; prevalence 1 % of population (iceberg - 70-80 undiagnosed %); classic presentation: chronic fatty diarrhea (steatorrhea), abdominal pain, meteorism, weight loss, iron-deficiency or mixed anemia (iron + B12/folates); frequent atypical forms: constipation, reflux, fatigue, osteoporosis, infertility, peripheral neuropathy, dermatitis herpetiformis (pruritic vesicular lesions - knees, elbows, buttocks) | Anti-transglutaminase IgA antibodies (anti-tTG IgA) - sensitivity 95 %, specificity 95 % - to be measured before gluten-free diet; total IgA (to exclude IgA deficiency - 2-3 % of general population - anti-tTG IgA false negative); if IgA deficient : anti-tTG IgG or anti-DGP IgG (deamidated gliadin peptides); histological confirmation: endoscopic D2 duodenal biopsies (Marsh 3a-3c: villous atrophy + crypt hyperplasia) - perform during gluten-containing diet; HLA-DQ2/DQ8: negative predictive value >99 % (if negative, excludes celiac disease). |
| Inflammatory bowel disease (IBD) - Crohn's and UC Crohn's disease and ulcerative colitis |
Immune dysregulation of the intestinal mucosa (Th1/Th17 Crohn's - Th2 UC) → transmural segmental inflammation with skip lesions the entire digestive tract from mouth to anus (Crohn's) or continuous superficial inflammation limited to the colon beginning at the rectum (UC); Crohn's: diarrhea ± blood depending on location (ileal: bulky malabsorptive diarrhea without blood; colonic: bloody diarrhea with tenesmus), IDF pain, palpable mass, fistulas, abscesses, extra-intestinal manifestations (uveitis, arthritis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis); UC: rectorrhagia + tenesmus + frequent glairo-bloody diarrhea (10-20 stools/day in severe forms) + abdominal cramps; incidence Crohn's ≈ 10-15/100,000/year in Canada (among the highest in the world) + UC ≈ 15-20/100,000/year | Fecal Calprotectin >200 µg/g (active inflammation - sensitivity 83 % for IBD - correlates with endoscopic activity); elevated CRP, accelerated ESR, normochromic anemia; peri-nuclear ANCA (pANCA): UC 65 %; ASCA (Saccharomyces cerevisiae): Crohn's 60 % - combination pANCA+/ASCA- → probable UC, ASCA+/pANCA- → probable Crohn's; colonoscopy with ileoscopy + staged biopsies: gold standard (epithelioid granulomas → Crohn's); enteroclysis MRI and entero-MRI: assessment of small intestine in Crohn's |
| Microscopic colitis (collagenous or lymphocytic) Frequent under-diagnosed cause - women >50 years old |
Chronic inflammation of the colon without macroscopic abnormality on colonoscopy (normal mucosal appearance - histological diagnosis only) - two subtypes: collagenous colitis (band of subepithelial collagen >10 µm) and lymphocytic colitis (intraepithelial lymphocytic infiltrate >20 lymphocytes/100 epithelial cells); profuse non-bloody watery diarrhea (10-20 stools/day), nocturnal abdominal cramps, fecal incontinence; predominantly female F:H 5:1; peak incidence 60-70 years; association with NSAIDs (ibuprofen, naproxen) - major drug cause; other drugs implicated: PPIs (lansoprazole, omeprazole), serotonin reuptake inhibitors (sertraline, paroxetine), acarbose, ranitidine | Colonoscopy: normal macroscopic appearance (diagnosis impossible without biopsies); systematic biopsies of right colon + transverse colon + left colon mandatory in any woman >50 years old with chronic watery diarrhea even if colonoscopy normal - nocturnal watery diarrhea waking the patient is quasi-pathognomonic of microscopic colitis (vs IBS: nocturnal exceptional); discontinuation of suspect drugs → often spontaneous resolution in weeks |
| Exocrine pancreatic insufficiency (EPI) Steatorrhea - fat maldigestion |
Pancreatic lipase, amylase and protease deficiency → maldigestion of lipids, protides and carbohydrates → steatorrhea (fatty, pale, floating, foul-smelling stools - fecal fat score >7 g/24h) + weight loss + nutritional deficiencies (vitamins ADEK + B12 + zinc); causes: chronic alcoholic pancreatitis (1st cause - pancreatic calcifications on CT scan); cystic fibrosis (CFTR); total or partial pancreatectomy; pancreatic cancer with ductal obstruction; autoimmune pancreatitis type 1 (IgG4); Zollinger-Ellison syndrome (lipase-inactivating acid hypersecretion) | Fecal elastase-1 (FE-1): non-invasive screening test - sensitivity 73 % for mild PEI, 93 % for severe PEI - value 7 g/24h - but restrictive test); abdominal CT scan: pancreatic calcifications, dilatation of Wirsung's duct, pancreatic atrophy; secretin-CCK test (Lundh test - limited availability) |
| Lactose and FODMAP malabsorption Frequent enzyme intolerance |
Intestinal lactase deficiency (adult primary hypolactasia - physiological acquired enzyme deficiency affecting 70 % of the adult world population - variable prevalence: 15-25 % in Northern Europe vs. 65-90 % in Asia, Africa, Latin Americas) → unabsorbed lactose fermented by the colonic microbiome → AGCC + H₂ + CO₂ → osmotic diarrhea + bloating + flatulence + abdominal cramps within 30 min-2h after lactose ingestion ; FODMAP (fermentable oligosaccharides - excess fructose, fructans, galacto-oligosaccharides, sorbitol, mannitol): same mechanism; fructose malabsorption: apples, pears, honey, high-fructose corn syrup | Lactose breath test (hydrogen breath test): sensitivity 77-94 %, specificity 89-100 % - elevation of exhaled H₂ by >20 ppm after loading with 25-50 g lactose at 90-120 min; diagnostic exclusion diet: elimination of milk and dairy products for 2 weeks → resolution of symptoms → reintroduction → reappearance = clinical diagnosis; low FODMAP diet (Monash University): efficacy 50-80 % in IBS-D (elimination for 4-6 weeks then gradual reintroduction) |
| Chronic infectious and parasitic causes Giardia, Cryptosporidium, recurrent C. difficile |
Giardia lamblia (giardiasis): flagellate protozoan - faecal-oral contamination (water, food, traveller) - adherence to proximal duodenum → fat and carbohydrate malabsorption → watery diarrhoea or steatorrhoea, bloating, sulphurous eructations - chronic if immunodepressed ; Cryptosporidium apicomplexan protozoa - profuse diarrhea in the immunocompromised (HIV CD4 <100) - self-resolving in the immunocompetent ; Clostridium difficile recurrent: toxins A + B → pseudomembranous colitis - bloody diarrhea after recent antibiotics or repeated hospitalizations; ; Blastocystis hominis controversial - discussed opportunistic pathogen; strongyloidiasis (Strongyloides stercoralis): tropical endemic - chronic self-infestation persisting for decades after exposure - recurrent diarrhea + urticaria | Parasitological examination of stools (EPS) × 3 on 3 consecutive days (increased sensitivity); Giardia fecal antigens (ELISA or immunochromatography): sensitivity 94-97 % - test of choice for giardiasis; multiplex stool PCR (FilmArray GI panel): simultaneously detects 22 bacterial + viral + parasitic pathogens - modern gold standard; C. difficile A+B toxins (ELISA + GDH (glutamate dehydenase) + tcdB PCR; strongyloidiasis serology (IgG ELISA if previous travel history). difficile A+B toxins (ELISA) + GDH (glutamate dehydrogenase) + PCR tcdB; strongyloidiasis serology (ELISA IgG) if history of tropical travel. |
Structured diagnostic workup
- 1st-line assessment (all chronic diarrhea) : CBC + formula (iron-deficiency anemia → celiac/MICI; eosinophilia → parasites); CRP + VS; ionogram + creatinine + albumin (malnutrition); TSH (hyperthyroidism); glycemia (diabetic autonomic neuropathy) ; anti-tTG IgA + total IgA (celiac disease); coprocultures + EPS × 3 + Giardia antigens; fecal calprotectin (discriminates IBD vs IBS with PPV 67 % and NPV 93 % - threshold 50-200 µg/g)
- 2nd-line assessment (depending on orientation) : colonoscopy with systematic biopsies (right + left colon - microscopic colitis, IBD, colorectal cancer) if >50 years, red flags or elevated calprotectin; gastroscopy + D2 duodenal biopsies if celiac suspected; fecal elastase-1 if steatorrhea ; lactose/fructose breath test if malabsorption is suspected; entero-MRI if Crohn's is suspected; bile acid scintigraphy (SeHCAT) or fasting serum bile acids if malabsorption of bile salts (post-cholecystectomy, ileal resection, ileal Crohn's).
- 3rd-line test (refractory secretory diarrhea): plasma VIP (vasoactive intestinal peptide) - VIPome (pancreatic tumor): profuse watery diarrhea (Verner-Morrison syndrome - WDHA: Watery Diarrhea, Hypokalemia, Achlorhydria); fasting serum gastrin - Zollinger-Ellison syndrome (gastrinoma): multiple ulcers + acid diarrhoea; urinary chromogranin A + 5-HIAA (5-hydroxyindoleacetic acid) - carcinoid tumour / neuroendocrine tumour (NET): carcinoid syndrome (flush, diarrhoea, bronchospasm - liver metastases); urinary cortisol / dexamethasone test - Cushing's syndrome; calcitonin - medullary thyroid carcinoma
ℹ️
Visit fecal calprotectin is a calcium- and zinc-bound protein released by neutrophils during intestinal inflammation - its measurement in stool (ELISA - normal value 200 µg/g) from a functional cause such as IBS (calprotectin <50 µg/g - VPN 93 %). Between 50 and 200 µg/g: grey zone - to be interpreted with the clinical context (a recent infection, NSAID intake or microscopic colitis may moderately elevate calprotectin). It is reimbursed by the RAMQ in certain indications (suspicion of IBD) and available at our points of service.
Treatments by etiology
| Treatment / Etiology | Treatment modalities and mechanisms | Effectiveness and precautions |
|---|---|---|
| Gluten-free diet (RSG) Celiac disease - single treatment |
Total and definitive exclusion of gluten (wheat, rye, barley - and oats if cross-contamination) → resolution of villous inflammation + regeneration of intestinal villi (6-24 months depending on initial severity) + normalization of anti-tTG antibodies (serological follow-up at 6 and 12 months); authorized foods: rice, corn, quinoa, potatoes, legumes, meat, fish, eggs, dairy products; vigilance for hidden sources of gluten: sauces, seasonings, medications, cross-contamination in the kitchen; follow-up by a dietician specialized in celiac disease. | Strict GFD cures symptoms in 90-95 % celiac cases; monitoring: anti-TTG serology at 6 and 12 months post-GFD (normalization = adherence) + bone densitometry (osteoporosis common in undiagnosed celiac) + iron, folate, vitamin D, B12 supplementation if documented deficiencies; complications of refractory celiac (persistence of symptoms despite strict GFD >12 months): refractory T-cell-associated enteropathy (EATL) → assessment in specialized center (biopsies, endoscopic videocapsule, CT scan) |
| Budesonide 9 mg/day Microscopic colitis - 1st line |
Topical glucocorticoid with local action and significant hepatic first-pass effect (reduced systemic bioavailability - 10-15 % vs. 80 % for prednisone) → mucosal anti-inflammatory with limited systemic side effects; dosage: budesonide 9 mg/day (Entocort 3 mg × 3/day) for 6-8 weeks → resolution of diarrhea in 85 % of microscopic colitis (Bonderup 2016 meta-analysis) → gradual tapering over 4-8 weeks to avoid relapse (frequent on discontinuation - 60-80 % relapse within a year) | In case of relapse on discontinuation: maintenance treatment with budesonide 6 mg/day - long-term if frequent relapses (discuss benefit/risk ratio of chronic treatment); alternatives if budesonide unavailable or ineffective: bismuth subsalicylate (Pepto-Bismol) 2 tablets × 3/day × 8 weeks (collagenous colitis); cholestyramine (bile acid sequestrator) if biliary component; fundamental treatment: discontinuation of suspect drugs (NSAIDs, PPIs, SRIs) → resolution in 50-70 % of drug-induced cases |
| Treating IBS-D: antidiarrheals, antispasmodics and neuromodulators Irritable bowel syndrome - diarrhea |
Loperamide (Imodium) 2 mg before meals or as PRN: peripheral µ-opioid agonist - reduces motility and increases reabsorption → less frequent, firmer stools - effective in controlling defecatory urgency (0.5-0.8 mg/episode in some) - do not exceed 16 mg/day; antispasmodics (mebeverine 135 mg × 3/day, pinaverium Dicetel 100 mg × 3/day): relaxation of intestinal smooth muscle → reduction of abdominal cramps; tricyclic antidepressants (amitriptyline 10-25 mg at bedtime): visceral neuromodulation + slowing of transit - NNT ≈ 4 (Ford 2014 meta-analysis); rifaximin (Xifaxan) 550 mg × 3/day × 14d: non-absorbable antibiotic → reduction in dysbiosis (Small Intestinal Bacterial Overgrowth - SIBO) - effective in IBS-D: TARGET 1 and 2 (Pimentel 2011 - NEJM) - lasting reduction in symptoms of 40-50 % | Low FODMAP diet (Monash University Protocol): elimination for 4-6 weeks → gradual reintroduction of subgroups → identification of individual triggers - symptom reduction of 50-80 % in IBS-D (Marsh 2016 meta-analysis); alosetron (Lotronex): 5-HT3 antagonist - severe refractory female IBS-D - ischemic colitis rare (restricted use - not available in Canada); eluxadoline (Viberzi): mixed µ/κ agonist and δ opioid receptor antagonist - available in Canada (RAMQ - prior authorization); CBT and gastrointestinal hypnotherapy: efficacy comparable to pharmacotherapy in refractory IBS |
| Pancreatic enzymes Exocrine pancreatic insufficiency |
Pancreatin (Creon, Cotazym) - porcine pancreatic extracts standardized in lipase units (Lip IU): cover main meals (25,000-80,000 Lip IU) + snacks (10,000-40,000 Lip IU) - take at the beginning of the meal (or in two doses - beginning and middle of the meal) to coincide with the arrival of chyme in the duodenum; objective: reduce steatorrhea + improve fat digestion + regain weight + correct ADEK vitamin deficiencies. | Efficacy: reduce steatorrhea by 80-90 %; do not crush gastro-protected capsules (destruction of lipase by gastric acidity); if insufficient response despite high doses: add a PPI (omeprazole 20 mg before meals) to reduce gastric acidity → better activation of lipases in the duodenum; systematic supplementation: ADEK vitamins (including vitamin D 1,000-2,000 IU/day) + vitamin B12 if associated ileal resection |
| Cholestyramine and analogues Bile salt malabsorption |
Sequestering bile acids in the intestinal lumen (cholestyramine 4-8 g × 2-3/day, colestipol) → prevention of the laxative effect of unabsorbed bile acids on the right colonic mucosa (bile acid-induced secretory diarrhea - BAD); causes of bile salt malabsorption: ileal resection or Crohn's ileitis (active reabsorption of bile salts in the terminal ileum disrupted); post-cholecystectomy (continuous bile flow without vesicular regulation); idiopathic biliary malabsorption (primary BAD - under-diagnosed cause of functional diarrhea in 25-30 % of patients labeled IBS-D) | Reference diagnostic test: SeHCAT (selenium homocholic acid taurine) scintigraphy - available in some Canadian centers - retention <10 % at 7 days = severe bile salt malabsorption; alternative non-invasive test: fasting serum bile acids (7αC4) + plasma C4 (marker of hepatic synthesis); response to cholestyramine within 48-72h = virtually sufficient diagnostic therapeutic test in routine practice; caution: cholestyramine may interfere with absorption of other drugs (digoxin, levothyroxine, warfarin) - administer 2-4h after other drugs |
Red flags - Urgent investigation and/or specialist referral
Consult your doctor without delay (gastroenterology referral in <4 weeks) if chronic diarrhea is accompanied by any of the following signs: rectorrhagia or melena (bright red or black blood in the stool); ; involuntary weight loss >5 % in 3 months ; persistent or nocturnal fever; diarrhoea awakening the patient (organic diarrhoea - virtually impossible in functional IBS); ; unexplained iron-deficiency anemia ; palpable abdominal mass; family history of colorectal cancer or IBD; age >50 with recent change in transit.
These elements require a colonoscopy as a priority to eliminate a colorectal cancera Severe IBD or a gastrointestinal malignancy - don't attribute chronic diarrhea to IBS without first ruling out serious organic causes in patients over 50 or with red flags.
Consult at Clinique Omicron
Clinique Omicron's doctors carry out the initial structured work-up for chronic diarrhea - CBC, CRP, TSH, celiac, fecal calprotectin, coprocultures and parasitology - and refer to gastroenterology for colonoscopy or specialized explorations, depending on the results. Identified causes (IBS, lactose malabsorption, microscopic colitis) can be managed directly, including nutritional education, prescription of first-line treatments and biological follow-up. Consultations are available at our points of service in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The contents of this page are provided for information purposes only and do not replace the advice of a qualified healthcare professional. Any chronic diarrhea persisting beyond 4 weeks should be referred to a physician to determine the cause.
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