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Diarrhea

Definition

Diarrhea is a symptom, not a disease, defined as an increase in stool mass, frequency, or fluidity — typically >200 g/day. Patients most commonly describe increased stool fluidity as the key feature. It is further classified as:

Acute: <4 weeks duration
Chronic: liquid stools lasting ≥4 weeks (affects ~6.6% of the population annually)

— Sleisenger and Fordtran's Gastrointestinal and Liver Disease

Pathophysiology

There are three major mechanisms:

1. Osmotic Diarrhea

Caused by the malabsorption of ingested non-electrolytes (e.g., carbohydrates, osmotic laxatives such as Mg²⁺, PO₄³⁻, SO₄²⁻) that draw water into the intestinal lumen. Key feature: stops with fasting.

2. Secretory Diarrhea

Caused by the malabsorption or net secretion of electrolytes. Sources include:

Bacterial toxins (e.g., Vibrio cholerae, E. coli)
Congenital syndromes (e.g., congenital chloridorrhea)
Hormone-secreting tumors (VIPoma, carcinoid, gastrinoma)
Bile acid malabsorption Key feature: persists with fasting.

3. Complex (Motility-Related) Diarrhea

Fast transit ("intestinal hurry"): Insufficient mucosal contact time → incomplete absorption. Seen in hyperthyroidism, post-vagotomy states, IBS, and peptide-secreting tumors.
Slow transit: Promotes small intestinal bacterial overgrowth (SIBO), which disrupts digestion. Classic example: scleroderma.
Reduced intestinal blood flow: Mesenteric ischemia or radiation enteritis can produce secretory-type diarrhea via cytokine and neurotransmitter signaling.

The intestinal regulatory system (the "ALPINEs" system — Autocrine, Luminal, Paracrine, Immune, Neural, Endocrine, Secretory) integrates all these signals to modulate fluid transport, motility, and permeability. Maladaptive responses in this system underlie chronic diarrhea.

Clinical Classification

Category	Features
Watery / Osmotic	Carbohydrate malabsorption, Mg-laxatives; resolves with fasting
Watery / Secretory	Bacterial toxins, VIPoma, bile acid malabsorption; persists with fasting
Inflammatory	Blood/mucus in stool; IBD, invasive infections (Shigella, EIEC, Entamoeba histolytica)
Fatty (Steatorrhea)	Malabsorption; pale, greasy, floating stools; celiac, chronic pancreatitis

Differential Diagnosis

Acute diarrhea causes:

Viral gastroenteritis (most common)
Bacterial: Salmonella, Shigella, Campylobacter, E. coli O157:H7, C. difficile
Parasitic: Giardia lamblia, Entamoeba histolytica, Cryptosporidium
Medications: laxatives, antacids, digitalis, quinidine, colchicine, antibiotics
Graft-versus-host disease (post-transplant)

Chronic diarrhea causes:

IBS / functional diarrhea
Microscopic colitis
Bile acid-induced diarrhea (after cholecystectomy or ileal resection)
Celiac disease, IBD, SIBO
Hormone-secreting tumors
Diabetic autonomic neuropathy, postsurgical (post-vagotomy, short bowel)
Factitious (laxative abuse)

Evaluation

History: Duration, stool character (bloody, watery, fatty), timing (nocturnal diarrhea → organic cause), travel, medications, diet, family history.

Physical examination: Signs of dehydration, weight loss, abdominal tenderness, lymphadenopathy.

Workup:

Acute: Stool culture, O&P (ova and parasites), C. difficile toxin assay, fecal leukocytes
Chronic: Full labs (CBC, CMP, TSH, celiac antibodies), fecal fat, colonoscopy with biopsies, osmotic gap calculation

Osmotic gap = 290 − 2 × (stool [Na⁺] + stool [K⁺])

125 mOsm/kg → osmotic diarrhea
<50 mOsm/kg → secretory diarrhea

Treatment

Rehydration (most critical)

Oral rehydration salts (ORS) — WHO-recommended; optimizes water absorption
Avoid high-sugar beverages (worsen fluid losses without adequate salt)
IV hydration in severe cases

Symptomatic (Antidiarrheal) Agents

Agent	Mechanism
Loperamide	µ-opioid receptor agonist; reduces motility and secretion
Diphenoxylate/atropine (Lomotil)	Anticholinergic + opioid
Bismuth subsalicylate	Antibacterial, anti-secretory
Pectin/kaolin	Toxin binding
Cholestyramine	Bile acid-binding resin (bile acid diarrhea)
Octreotide	Somatostatin analogue; hormone-mediated secretory diarrhea

Antibiotics (Specific Infections)

C. difficile: Oral vancomycin or fidaxomicin (first-line); metronidazole IV added in fulminant disease; fecal microbiota transplant for recurrent cases
Amebiasis: Metronidazole → paromomycin or iodoquinol (to eliminate cysts)
Giardiasis: Metronidazole or tinidazole
Empiric antibiotics: Only in moderate-to-severe illness with systemic symptoms — avoid in suspected E. coli O157:H7 (increases hemolytic-uremic syndrome risk)

Special Populations

HIV/immunocompromised: Consider Cryptosporidium, Microsporidium, CMV as opportunistic pathogens
Hospitalized patients: High suspicion for C. difficile; antibiotic stewardship is key to prevention

Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease; The Washington Manual of Medical Therapeutics; Robbins, Cotran & Kumar Pathologic Basis of Disease

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