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.
Frequent passage of small volumes of stool, as may occur in patients with tenesmus (rectal urgency), should be distinguished from diarrhea. Similarly, fecal incontinence can be confused with diarrhea. However, diarrhea can cause a marked worsening of fecal incontinence.
( See also Overview of Malabsorption and see Overview of Inflammatory Bowel Disease. Diarrhea in children is discussed elsewhere.)
Complications of diarrhea
Complications may result from diarrhea of any etiology. Fluid loss with consequent dehydration, electrolyte loss (sodium, potassium, magnesium, chloride), 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. Bicarbonate 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.
Etiology of Diarrhea
Normally, the small intestine and colon absorb 99% of fluid resulting from oral intake and gastrointestinal (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 ( see Table: Some Causes of Diarrhea*). Several basic mechanisms cause most clinically significant diarrheas. The three most common are increased osmotic load, increased secretions/decreased absorption, 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.
Osmotic load
lactose intolerance see Table: Some Causes of Diarrhea*) can cause osmotic diarrhea.
Increased secretions/decreased absorption
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) 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 sodium-potassium 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.
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.
Impaired absorption of bile salts, which can occur with several disorders, can cause diarrhea by stimulating water and electrolyte secretion. The stools have a green or orange color.
Reduced contact time/surface area
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. Hyperthyroidism may cause diarrhea due to rapid transit.
Stimulation of intestinal smooth muscle by drugs (eg, magnesium-containing antacids, laxatives, cholinesterase inhibitors, selective serotonin reuptake inhibitors) or humoral agents (eg, prostaglandins, serotonin) also can speed transit.
Evaluation of Diarrhea
History
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 months), 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. Physicians should ask specifically about any changes in drugs that may cause diarrhea.
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.
Physical examination
Fluid and hydration status should be evaluated. A full examination with attention to the abdomen and a digital rectal examination for sphincter competence and occult blood testing are important.
Red flags
Certain findings raise suspicion of an organic or more serious etiology of diarrhea:
Blood or pus in stool
Fever
Signs of dehydration
Chronic diarrhea
Weight loss
Interpretation of findings
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 tumor 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 Clostridioides difficile colitis (formerly Clostridium difficile).
Diarrhea with green or orange stools suggests impaired absorption of bile salts.
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 pain is related to defecation, associated with changes in stool frequency or consistency, or both. However, these symptoms alone do not discriminate IBS from other diseases (eg, inflammatory bowel disease). Functional diarrhea is characterized by loose or watery stools with onset at least 6 months before diagnosis and present during the previous 3 months. These patients do not meet the criteria for IBS; they may have abdominal pain and/or bloating, but these are not predominant symptoms (1). IBS with diarrhea sometimes develops in patients after an acute enteric infection (postinfectious IBS).
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).
Testing
Acute diarrhea (<C. difficile toxin assay.
Chronic diarrhea (> 4 weeks) requires evaluation, as does a shorter (1 to 3 weeks) bout of diarrhea in immunocompromised patients or those who appear significantly ill. Diagnostic evaluation should be directed by the history and physical examination when possible. If this approach does not provide a diagnosis or direction, a broader approach is needed. Initial testing should include stool for occult blood, fat (by Sudan stain or fecal elastase), electrolytes (to calculate the stool osmotic gap), and Giardia antigen or polymerase chain reaction test; complete blood count with differential; celiac serology (IgA tissue transglutaminase); thyroid-stimulating hormone (TSH) and free thyroxine (T4); and fecal calprotectin or fecal lactoferrin (to screen for inflammatory bowel disease [IBD]). The 2019 American Gastroenterological Association's guidelines on the laboratory evaluation of functional diarrhea and diarrhea-predominant IBS (IBS-D) recommend a threshold value of 50 mcg/g for fecal calprotectin or a range of 4.0 to 7.25 mcg/g for fecal lactoferrin to optimize sensitivity for IBD. Microscopic examination for ova and parasites should be done for patients with recent travel history to or recent immigration from high-risk areas. Stool tests for C. difficile should be done in patients with recent antibiotic exposure or suspected C. difficile infection. Sigmoidoscopy or colonoscopy with biopsies should follow to look for inflammatory causes.
If no diagnosis is apparent and Sudan stain or fecal elastase is positive for fat, fecal fat excretion should be measured. Additional testing, including small-bowel CT enterography (structural disease) and endoscopic small-bowel biopsy (mucosal disease), can be considered (eg, if symptoms persist or are severe such as weight loss). 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 nonsteroidal anti-inflammatory drug enteropathy, not identified by other modalities.
The stool osmotic gap, which is calculated 290 − 2 × (stool sodium + stool potassium), indicates whether diarrhea is secretory or osmotic. An osmotic gap <
Undiagnosed secretory diarrhea requires testing (eg, plasma gastrin, calcitonin
Evaluation reference
1. Lacy BE, Mearin F, Chang L, et al: Bowel disorders. Gastroenterology 150(6):1393–1407, 2016. doi: 10.1053/j.gastro.2016.02.031
Treatment of Diarrhea
Fluid and electrolytes for dehydration
Possibly antidiarrheals for nonbloody diarrhea in patients without systemic toxicity
< 15 mEq/L (< 15 mmol/L). An oral glucose-electrolyte solution can be given if diarrhea is not severe and nausea and vomiting are minimal ( see Solutions). Oral and parenteral fluids are sometimes given simultaneously when water and electrolytes must be replaced in massive amounts (eg, in cholera).
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.
Dietary Factors That May Worsen Diarrhea) and stimulatory drugs should be avoided.
Key Points
In patients with acute diarrhea, testing is only necessary for those who have prolonged symptoms (ie, > 1 week), have red flag findings, are very young, or are very old.
Be cautious when using antidiarrheals if C. difficile colitis, Salmonella infection, or shigellosis is possible.
Postinfectious inflammatory bowel syndrome develops in 10% of patients after acute infectious enteritis.
More Information
The following English-language resource may be useful. Please note that THE MANUAL is not responsible for the content of this resource.
American Gastroenterological Association: Guidelines on the laboratory evaluation of functional diarrhea and diarrhea-predominant irritable bowel syndrome in adults (IBS-D) (2019)
