Diarrhoea

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"diarrhea"[MeSH Terms] AND management

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Diarrhoea

Definition

Diarrhoea is defined as the passage of 3 or more loose or watery stools per day, or more frequently than is normal for the individual. A more precise stool-weight definition used in clinical research is >200 g/day in Western populations. The term derives from the Greek "to run through."

Duration defines the clinical subtype:

Acute diarrhoea - <2 weeks
Persistent diarrhoea - 2-4 weeks
Chronic diarrhoea - >4 weeks (affects ~6.6% of the adult population at any given time)

(Sleisenger and Fordtran's Gastrointestinal and Liver Disease)

Pathophysiology

Normal intestinal fluid balance involves approximately 9 litres entering the gut daily (2 L oral intake + 7 L secretions), with all but ~100-200 mL being absorbed. Diarrhoea results from any disruption in this balance. Four major mechanisms operate:

1. Osmotic Diarrhoea

Non-absorbable solutes in the lumen retain water osmotically. Classic example: lactase deficiency, where undigested lactose remains in the gut and draws water in. Key feature: stops with fasting. The osmotic gap is elevated (stool osmotic gap >125 mOsm/kg).

2. Secretory Diarrhoea

Active ion secretion into the lumen exceeds absorptive capacity. The prototype is cholera, where the toxin enters crypt epithelial cells, activates adenylyl cyclase via the Gs protein, raises cAMP, and opens apical Cl⁻ channels. Na⁺ and H₂O follow passively:

Cl⁻ secretion in the intestine - mechanism of secretory diarrhoea

Fig: Mechanism of Cl⁻ and fluid secretion. Cholera toxin activates adenylyl cyclase, raises cAMP, and opens apical Cl⁻ channels. VIP and other hormones use the same pathway. (Costanzo Physiology, 7th Ed.)

Key feature: persists with fasting, large-volume, no osmotic gap.

3. Reduced Absorptive Surface Area

Infection, inflammation (celiac disease, IBD), or surgical resection reduces surface area available for absorption. Ileocecal resection permanently impairs NaCl absorption against a concentration gradient that no other bowel segment can compensate for.

4. Abnormal Motility

Rapid transit ("intestinal hurry") - oral-cecal transit may be as short as 10 minutes, preventing adequate absorption. Seen in diabetic autonomic neuropathy, post-vagotomy, hyperthyroidism
Slow transit - promotes small intestinal bacterial overgrowth (SIBO), causing secondary secretory diarrhoea (e.g., scleroderma)

(Sleisenger and Fordtran's)

Electrolyte Consequences

Diarrhoeal fluid is rich in HCO₃⁻ (from pancreatic/intestinal secretions) and K⁺ (colonic flow-rate-dependent secretion). Consequences:

Metabolic acidosis - hyperchloraemic, normal anion gap (loss of HCO₃⁻)
Hypokalemia - K⁺ loss in stool
Volume depletion / circulatory collapse - in severe cases (e.g., cholera)

Clinical Classification

By Duration

Type	Duration	Common Causes
Acute	<2 weeks	Infection (viral, bacterial, parasitic), food poisoning, medications
Persistent	2-4 weeks	May indicate ongoing infection or early chronic disease
Chronic	>4 weeks	IBD, IBS, malabsorption, endocrinopathy, neoplasia

By Stool Character (Watery / Fatty / Inflammatory)

Watery diarrhoea - either osmotic or secretory. Large-volume if small bowel origin; small-volume if colonic.

Fatty (steatorrhoeic) diarrhoea - pale, bulky, offensive, floats. Indicates:

Malabsorption: celiac disease, Whipple disease, short bowel syndrome
Maldigestion: pancreatic exocrine insufficiency, inadequate bile acids, SIBO

Inflammatory diarrhoea - mucus, pus, blood ("dysentery"). Indicates mucosal ulceration:

IBD (Crohn disease, ulcerative colitis)
Infectious: Shigella, Campylobacter, C. difficile, CMV, E. histolytica, tuberculosis
Ischaemic colitis, colon cancer

Differential Diagnosis

Acute Diarrhoea

Infections (most common): rotavirus, norovirus, Salmonella, Shigella, Campylobacter, C. difficile, E. coli (ETEC, EHEC)
Food allergies / food poisoning
Medications (antibiotics, laxatives, metformin, NSAIDs, immune checkpoint inhibitors)
Initial presentation of a chronic disorder

Chronic Watery Diarrhoea

Secretory causes:

Endocrinopathies: VIPoma, gastrinoma (ZES), carcinoid syndrome, medullary thyroid carcinoma, phaeochromocytoma, Addison disease, hyperthyroidism
Microscopic colitis (collagenous or lymphocytic)
IBD
Ileal bile acid malabsorption
IBS-D, functional diarrhoea
Brainerd (epidemic secretory) diarrhoea

Osmotic causes:

Carbohydrate malabsorption (lactase deficiency, fructose)
Osmotic laxatives (Mg²⁺, PO₄³⁻, SO₄²⁻)

Chronic Fatty Diarrhoea

Malabsorption: celiac disease, tropical sprue, Whipple disease, short bowel syndrome, SIBO
Maldigestion: chronic pancreatitis, cystic fibrosis, cholestasis

Chronic Inflammatory Diarrhoea

Crohn disease, ulcerative colitis
Microscopic colitis
Radiation enteritis
Vasculitis
Colon carcinoma, lymphoma

(Sleisenger and Fordtran's, Box 16.2)

Evaluation

History

Key questions: onset and duration, stool frequency/consistency/volume, blood or mucus, associated symptoms (fever, vomiting, weight loss, tenesmus), travel history, dietary history, medications, immunosuppression, sexual history, family history of IBD.

"Alarm features" prompting urgent workup:

Blood in stool
Nocturnal diarrhoea (waking from sleep)
Unintentional weight loss >5 kg
Fever >38.5°C
Duration >4 weeks
Age >50, or family history of colorectal cancer/IBD

Physical Examination

Hydration status (skin turgor, mucous membranes, capillary refill, BP/HR)
Abdominal tenderness, distension, bowel sounds
Rectal examination
Signs of systemic disease (goitre, flushing, lymphadenopathy)

Investigations

Acute diarrhoea (most is self-limited - no tests needed):

Stool culture + microscopy if: bloody stool, fever, immunocompromised, traveller, >7 days duration, community outbreak
C. difficile toxin PCR if: recent antibiotics or hospitalisation

Chronic diarrhoea:

Investigation	Purpose
FBC, CRP, ESR	Inflammation
TSH	Hyperthyroidism
Coeliac serology (anti-TTG IgA)	Celiac disease
Stool calprotectin	IBD vs functional
Stool fat / 72-hr collection	Steatorrhoea
Colonoscopy + biopsy	IBD, microscopic colitis, neoplasia
Upper GI endoscopy + duodenal biopsy	Celiac disease, Whipple disease
Hydrogen breath test	SIBO, lactose intolerance
Urine 5-HIAA, serum VIP, gastrin, calcitonin	Secreting tumours
CT abdomen/pelvis	Pancreatic disease, lymphoma, neoplasia

Treatment

Acute Diarrhoea

Rehydration is the cornerstone. Oral rehydration solution (ORS) replaces fluid, Na⁺, K⁺, and HCO₃⁻. WHO/UNICEF standard ORS contains 75 mmol/L sodium, 75 mmol/L glucose, 20 mmol/L potassium, 30 mmol/L bicarbonate.

Loperamide (opioid receptor agonist at myenteric plexus): reduces motility and secretion. Use in non-bloody, non-febrile traveller's diarrhoea. Avoid in suspected inflammatory/invasive diarrhoea (risk of toxic megacolon).

Antibiotics: indicated for:

Traveller's diarrhoea (azithromycin, rifaximin)
Suspected Shigella (azithromycin, ciprofloxacin)
C. difficile - oral vancomycin or fidaxomicin (metronidazole no longer first-line for severe disease)
Giardia - metronidazole or tinidazole
E. histolytica - metronidazole 750 mg q8h + luminal amebicide (iodoquinol or paromomycin)
Cryptosporidium in immunocompetent - nitazoxanide 500 mg BD
Cyclospora - trimethoprim-sulfamethoxazole

Zinc supplementation in children (20 mg/day x 10-14 days) - reduces duration and severity, recommended by WHO. A recent systematic review (Ali et al., 2024) confirms benefit for acute and persistent watery diarrhoea.

Probiotics - a 2025 meta-analysis (Alsabri et al.) found probiotics reduce duration and severity of acute gastroenteritis in children.

Chronic Diarrhoea

Treatment is directed at the underlying cause:

IBD: mesalazine, corticosteroids, immunomodulators, biologics
Celiac disease: gluten-free diet
Microscopic colitis: budesonide
Bile acid diarrhoea: cholestyramine, colesevelam
IBS-D: low-FODMAP diet, loperamide, rifaximin, tricyclic antidepressants
VIPoma/carcinoid: somatostatin analogues (octreotide)
Pancreatic exocrine insufficiency: pancreatic enzyme replacement
SIBO: rifaximin, rotating antibiotics

Special Scenarios

Diarrhoea in HIV/AIDS

Pre-HAART: occurred in up to 90% of patients. Now more often HAART-induced or unrelated to HIV. Main pathogens depend on CD4 count: Cryptosporidium, Microsporidium, MAC, CMV, C. difficile. (Sleisenger and Fordtran's)

Traveller's Diarrhoea

Most common illness in travellers. Usually ETEC, but also Campylobacter, Shigella, norovirus. Self-limited in 3-5 days. Azithromycin is preferred (ciprofloxacin resistance rising in South/SE Asia).

Paediatric Diarrhoea

Leading cause of death in children under 5 in low-income countries. Rotavirus is the most common severe cause globally; rotavirus vaccine has dramatically reduced burden. Management: ORS + zinc + continued feeding. (Rosen's Emergency Medicine)

Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease; Costanzo Physiology, 7th Ed.; Rosen's Emergency Medicine; Harriet Lane Handbook, 23rd Ed.

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