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Stool is 60 to 90% water. In Western society, stool amount is 100 to 200 g/day in healthy adults and 10 g/kg/day in infants, depending on the amount of unabsorbable dietary material (mainly carbohydrates). Diarrhea is defined as stool weight > 200 g/day. However, many people consider any increased stool fluidity to be diarrhea. Alternatively, many people who ingest fiber have bulkier but formed stools but do not consider themselves to have diarrhea.
Complications may result from diarrhea of any etiology. Fluid loss with consequent dehydration, electrolyte loss (Na, K, Mg, Cl), and even vascular collapse sometimes occur. Collapse can develop rapidly in patients who have severe diarrhea (eg, patients with cholera) or are very young, very old, or debilitated. HCO 3 loss can cause metabolic acidosis. Hypokalemia can occur when patients have severe or chronic diarrhea or if the stool contains excess mucus. Hypomagnesemia after prolonged diarrhea can cause tetany.
Normally, the small intestine and colon absorb 99% of fluid resulting from oral intake and GI tract secretions—a total fluid load of about 9 of 10 L daily. Thus, even small reductions (ie, 1%) in intestinal water absorption or increases in secretion can increase water content enough to cause diarrhea.
There are a number of causes of diarrhea ( Some Causes of Diarrhea*). Several basic mechanisms are responsible for most clinically significant diarrheas: increased osmotic load, increased secretions, and decreased contact time/surface area. In many disorders, more than one mechanism is active. For example, diarrhea in inflammatory bowel disease results from mucosal inflammation, exudation into the lumen, and from multiple secretagogues and bacterial toxins that affect enterocyte function.
Diarrhea occurs when unabsorbable, water-soluble solutes remain in the bowel and retain water. Such solutes include polyethylene glycol, Mg salts (hydroxide and sulfate), and Na phosphate, which are used as laxatives. Osmotic diarrhea occurs with sugar intolerance (eg, lactose intolerance caused by lactase deficiency). Ingesting large amounts of hexitols (eg, sorbitol, mannitol, xylitol) or high fructose corn syrups, which are used as sugar substitutes in candy, gum, and fruit juices, causes osmotic diarrhea because hexitols are poorly absorbed. Lactulose, which is used as a laxative, causes diarrhea by a similar mechanism. Overingesting certain foodstuffs ( Some Causes of Diarrhea*) can cause osmotic diarrhea.
Diarrhea occurs when the bowels secrete more electrolytes and water than they absorb. Causes of increased secretions include infections, unabsorbed fats, certain drugs, and various intrinsic and extrinsic secretagogues.
Infections (eg, gastroenteritis—discussed in Gastroenteritis) are the most common causes of secretory diarrhea. Infections combined with food poisoning are the most common causes of acute diarrhea (< 4 days in duration). Most enterotoxins block Na + -H+ exchange, which is an important driving force for fluid absorption in the small bowel and colon.
Unabsorbed dietary fat and bile acids (as in malabsorption syndromes and after ileal resection) can stimulate colonic secretion and cause diarrhea.
Drugs may stimulate intestinal secretions directly (eg, quinidine, quinine, colchicine, anthraquinone cathartics, castor oil, prostaglandins) or indirectly by impairing fat absorption (eg, orlistat).
Various endocrine tumors produce secretagogues, including vipomas (vasoactive intestinal peptide), gastrinomas (gastrin), mastocytosis (histamine), medullary carcinoma of the thyroid ( calcitonin and prostaglandins), and carcinoid tumors (histamine, serotonin, and polypeptides). Some of these mediators (eg, prostaglandins, serotonin, related compounds) also accelerate intestinal transit, colonic transit, or both.
Rapid intestinal transit and diminished surface area impair fluid absorption and cause diarrhea. Common causes include small-bowel or large-bowel resection or bypass, gastric resection, and inflammatory bowel disease. Other causes include microscopic colitis (collagenous or lymphocytic colitis) and celiac disease.
Stimulation of intestinal smooth muscle by drugs (eg, Mg-containing antacids, laxatives, cholinesterase inhibitors, SSRIs) or humoral agents (eg, prostaglandins, serotonin) also can speed transit.
Some Causes of Diarrhea*
Dietary Factors That May Worsen Diarrhea
History of present illness should determine duration and severity of diarrhea, circumstances of onset (including recent travel, food ingested, source of water), drug use (including any antibiotics within the previous 3 mo), abdominal pain or vomiting, frequency and timing of bowel movements, changes in stool characteristics (eg, presence of blood, pus, or mucus; changes in color or consistency; evidence of steatorrhea), associated changes in weight or appetite, and rectal urgency or tenesmus should be noted. Simultaneous occurrence of diarrhea in close contacts should be ascertained.
Review of systems should seek symptoms suggesting possible causes, including joint pains (inflammatory bowel disease, celiac disease); flushing (carcinoid, vipoma, mastocytosis); chronic abdominal pain (irritable bowel, inflammatory bowel disease, gastrinoma); and GI bleeding (ulcerative colitis, tumor).
Past medical history should identify known risk factors for diarrhea, including inflammatory bowel disease, irritable bowel syndrome, HIV infection, and previous GI surgical procedures (eg, intestinal or gastric bypass or resection, pancreatic resection). Family and social history should query about simultaneous occurrence of diarrhea in close contacts.
Acute, watery diarrhea in an otherwise healthy person is likely to be of infectious etiology, particularly when travel, possibly tainted food, or an outbreak with a point-source is involved.
Acute bloody diarrhea with or without hemodynamic instability in an otherwise healthy person suggests an enteroinvasive infection. Diverticular bleeding and ischemic colitis also manifest with acute bloody diarrhea. Recurrent bouts of bloody diarrhea in a younger person suggest inflammatory bowel disease.
In the absence of laxative use, large-volume diarrhea (eg, daily stool volume > 1 L/day) strongly suggests an endocrine cause in patients with normal GI anatomy. A history of oil droplets in stool, particularly if associated with weight loss, suggests malabsorption.
Diarrhea that consistently follows ingestion of certain foods (eg, fats) suggests food intolerance. Recent antibiotic use should raise suspicion for antibiotic-associated diarrhea, including Clostridium difficile colitis.
The symptoms can help identify the affected part of the bowel. Generally, in small-bowel diseases, stools are voluminous and watery or fatty. In colonic diseases, stools are frequent, sometimes small in volume, and possibly accompanied by blood, mucus, pus, and abdominal discomfort. In irritable bowel syndrome (IBS), abdominal discomfort is relieved by defecation, associated with more loose or frequent stools, or both. However, these symptoms alone do not discriminate IBS from other diseases (eg, inflammatory bowel disease). Patients with IBS or rectal mucosal involvement often have marked urgency, tenesmus, and small, frequent stools (see Irritable Bowel Syndrome (IBS) : Symptoms and Signs).
Extra-abdominal findings that suggest an etiology include skin lesions or flushing (mastocytosis), thyroid nodules (medullary carcinoma of the thyroid), right-sided heart murmur (carcinoid), lymphadenopathy (lymphoma, AIDS), and arthritis (inflammatory bowel disease, celiac disease).
Acute diarrhea (< 4 days) typically does not require testing. Exceptions are patients with signs of dehydration, bloody stool, fever, severe pain, hypotension, or toxic features—particularly those who are very young or very old. These patients should have a CBC and measurement of electrolytes, BUN, and creatinine. Stool samples should be collected for microscopy, culture, fecal leukocyte testing, and, if antibiotics have been taken recently, C. difficile toxin assay.
Chronic diarrhea (> 4 wk) requires evaluation, as does a shorter (1 to 3 wk) bout of diarrhea in immunocompromised patients or those who appear significantly ill. Initial stool testing should include culture, fecal leukocytes (detected by smear or measurement of fecal lactoferrin), microscopic examination for ova and parasites, pH (bacterial fermentation of unabsorbed carbohydrate lowers stool pH < 6.0), fat (by Sudan stain), and electrolytes (Na and K). If no standard pathogens are found, specific tests for Giardia antigen and Aeromonas, Plesiomonas, coccidia, and microsporidia should be requested. Sigmoidoscopy or colonoscopy with biopsies should follow to look for inflammatory causes. Chronic diarrhea develops in 10% of patients after an acute enteric infection (postinfectious irritable bowel syndrome).
If no diagnosis is apparent and Sudan stain is positive for fat, fecal fat excretion should be measured, followed by small-bowel enteroclysis or CT enterography (structural disease) and endoscopic small-bowel biopsy (mucosal disease). If evaluation still yields negative findings, assessment of pancreatic structure and function (see Laboratory tests) should be considered for patients who have unexplained steatorrhea. Infrequently, capsule endoscopy may uncover lesions, predominantly Crohn disease or NSAID enteropathy, not identified by other modalities.
The stool osmotic gap, which is calculated 290 − 2 × (stool Na + stool K), indicates whether diarrhea is secretory or osmotic. An osmotic gap < 50 mEq/L indicates secretory diarrhea; a larger gap suggests osmotic diarrhea. Patients with osmotic diarrhea may have covert Mg laxative ingestion (detectable by stool Mg levels) or carbohydrate malabsorption (diagnosed by hydrogen breath test, lactase assay, and dietary review).
Undiagnosed secretory diarrhea requires testing (eg, plasma gastrin, calcitonin , vasoactive intestinal peptide levels, histamine, urinary 5-hydroxyindole acetic acid [5-HIAA]) for endocrine-related causes. A review for symptoms and signs of thyroid disease and adrenal insufficiency should be done. Surreptitious laxative abuse must be considered; it can be ruled out by a fecal laxative assay.
Severe diarrhea requires fluid and electrolyte replacement to correct dehydration, electrolyte imbalance, and acidosis. Parenteral fluids containing NaCl, KCl, and glucose are generally required. Salts to counteract acidosis (Na lactate, acetate, HCO 3 ) may be indicated if serum HCO 3 is < 15 mEq/L. An oral glucose-electrolyte solution can be given if diarrhea is not severe and nausea and vomiting are minimal (see Practical Example : Solutions). Oral and parenteral fluids are sometimes given simultaneously when water and electrolytes must be replaced in massive amounts (eg, in cholera).
Diarrhea is a symptom. When possible, the underlying disorder should be treated, but symptomatic treatment is often necessary. Diarrhea may be decreased by oral loperamide 2 to 4 mg tid or qid (preferably given 30 min before meals), diphenoxylate 2.5 to 5 mg (tablets or liquid) tid or qid, codeine phosphate 15 to 30 mg bid or tid, or paregoric (camphorated opium tincture) 5 to 10 mL once/day to qid.
Because antidiarrheals may exacerbate C. difficile colitis or increase the likelihood of hemolytic-uremic syndrome in Shiga toxin–producing Escherichia coli infection, they should not be used in bloody diarrhea of unknown cause. Their use should be restricted to patients with watery diarrhea and no signs of systemic toxicity. However, there is little evidence to justify previous concerns about prolonging excretion of possible bacterial pathogens with antidiarrheals.
Psyllium or methylcellulose compounds provide bulk. Although usually prescribed for constipation, bulking agents given in small doses decrease the fluidity of liquid stools. Kaolin, pectin, and activated attapulgite adsorb fluid. Osmotically active dietary substances ( Dietary Factors That May Worsen Diarrhea) and stimulatory drugs should be avoided.
In patients with acute diarrhea, stool examination (cultures, ova and parasites, C. difficile cytotoxin) is only necessary for those who have prolonged symptoms (ie, > 1 wk) or red flag findings.
Be cautious when using antidiarrheals if C. difficile colitis, Salmonella infection, or shigellosis is possible.
Postinfectious IBS develops in 10% of patients after acute infectious enteritis.
Drug NameSelect Brand Names
quinidineNo US brand name
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