The prevalence of chronic diarrhea is directly related to hygiene and sanitation practices and, therefore, varies widely throughout the world. The prevalence of chronic diarrhea in developed countries is 3–5 % but has been reported in up to 18 % of the population when “diarrhea” was more loosely defined. According to the World Health Organization, diarrhea affects 17 billion people annually and is the second leading cause of death worldwide in children less than 5 years of age. Within industrialized countries, chronic diarrhea is not associated with high mortality rates but is associated with decreased quality of life and significantly increased work and activity impairment compared to population norms. The economic impact of chronic diarrhea is difficult to measure; however, data from 1994 suggested that $350 million was lost annually due to time away from work. This amount is much greater today, especially if one adds the financial loss associated with diagnostic testing and management. The indication of “diarrhea” or “malabsorption” accounts for approximately 3 % of upper endoscopies, 7 % of colonoscopies, and 15 % of flexible sigmoidoscopies performed in the United States, not including those performed for a “change in bowel habits.” In 2009, the symptom of diarrhea accounted for over four million outpatient visits in the United States, second only to abdominal pain as a gastrointestinal complaint, and was the leading gastrointestinal symptom used as a search term by Internet users.

Stool weight and fluidity are directly related to the amount of water in the stool. The underlying pathophysiology in chronic diarrhea is either due to an increase in intestinal secretion of water or a decrease in net absorption of water. The amount of intestinal fluid is also inversely proportional to intestinal transit time, so any alteration that decreases intestinal transit time will increase stool frequency and fluidity.

Diarrhea is commonly divided into osmotic and secretory types based upon the pathophysiology. Osmotic diarrhea results from either the ingestion of nonabsorbable, osmotically active substances or the lack of small bowel mucosal disaccharidases that aid in carbohydrate absorption. Since the small bowel works to maintain an iso-osmolar state (290 mOsm/kg), any osmotically active substance within the small bowel creates an efflux of water into the intestinal lumen resulting in diarrhea. Osmotic diarrhea improves with fasting or discontinuation of the offending agent. Secretory diarrhea can be caused from many things, but in the case of infectious etiologies with toxin production (a common phenomenon), stimulation of cAMP, cGMP, or calcium-mediated pathways results in a transition from net absorption to net secretion within the small bowel. This results in a large volume of liquid stool reaching the colon, overwhelming its absorptive capacity. In secretory diarrhea, stool volume tends to be high and is not affected by fasting.

Diarrhea can also be characterized on the basis of its underlying pathophysiology. Inflammatory causes of diarrhea typically cause either macroscopic or microscopic damage to the intestinal mucosa surface, decreasing the overall absorptive surface area of the bowel. Carbohydrate malabsorption causes an osmotically mediated diarrhea. Bacterial fermentation of undigested carbohydrates also causes an increase in intestinal gas production. Fat malabsorption can result from pancreatic lipase deficiency (e.g., chronic pancreatitis), inactivation of pancreatic enzymes as occurs with Zollinger–Ellison syndrome, small bowel mucosal diseases, or impairment in the enterohepatic circulation of bile (e.g., hepatic dysfunction, biliary obstruction, extensive terminal ileal resection or disease). With resection of <100 cm of terminal ileum, excess bile spills into the colon causing a secretory diarrhea, with subsequent liver upregulation of bile production to counteract intestinal loss and maintain an adequate bile salt pool. In contrast, as alluded to previously, with >100 cm of resected terminal ileum, the hepatic production of bile is inadequate to compensate for the degree of intestinal loss, resulting in bile salt deficiency and fat malabsorption from impaired micelle production, which is required for intestinal transport of long-chain triglycerides. Protein malabsorption rarely occurs in isolation, but can be seen with mucosal erosive diseases (e.g., inflammatory bowel disease [IBD], ischemia, graft-versus-host disease), nonerosive diseases with increased permeability (e.g., eosinophilic gastroenteritis, and celiac, Whipple’s, and Menetrier’s disease), or conditions with altered lymphatic drainage (e.g., right heart failure, constrictive pericarditis, lymphoma, retroperitoneal fibrosis, lymphangiectasia).

Despite the ability to characterize diarrhea based on pathophysiology, this characterization is rarely pure, and many conditions will often have more than one mechanism involved in causing diarrhea.

The diagnostic approach to the patient with chronic diarrhea (see Fig. 18.1) begins with a detailed clinical history, noting the timing and features at onset, and the relationship to other events (e.g., surgery, new medications, self-limited illness, ingestion of specific foods). The frequency and pattern (e.g., postprandial, nocturnal) of bowel movements should be obtained. Details on stool characteristics should be reviewed including the presence of blood, which may indicate an infectious or inflammatory condition, or an oily appearance, which may be evidence of fat malabsorption. Small, low-volume frequent stools may imply a distal colonic or rectal disorder, while large-volume watery stools imply a small bowel disorder. Patients should be asked about the presence of fecal incontinence, although it should be noted that not all patients with fecal incontinence have a primary diarrheal condition, as spinal cord injuries and anal sphincter defects may also cause incontinence. The presence of associated gastrointestinal and systemic symptoms should be noted. The patient’s past medical history should be reviewed for evidence of autoimmune diseases (e.g., celiac disease, thyroid dysfunction, diabetes mellitus, adrenal insufficiency, microscopic colitis), immunosuppression (e.g., human immunodeficiency virus, chemotherapy, medication-induced), abdominopelvic radiation (e.g., colorectal, cervical, or prostate cancer), and psychiatric conditions. Medications should be scrutinized, paying attention to timing of medication initiation, antibiotic use, and over-the-counter products (e.g., magnesium-containing antacids, herbal products containing laxatives, nonsteroidal anti-inflammatory drugs [NSAIDs]). The patient’s surgical history should be reviewed for prior intestinal resections (including bowel segment and length removed), creation of blind loops of bowel (a risk factor for SIBO (small intestinal bacterial overgrowth)), and pancreaticobiliary surgeries. A family history of gastrointestinal and other relevant disorders should be obtained. Social history should focus on excessive alcohol consumption (pancreatic insufficiency), infectious exposures (e.g., daycare setting, animals, water sources), travel history, sexual preference, and dietary behavior patterns (e.g., excessive caffeine intake or gum chewing, ingestion of sugar-free foods or sugar substitutes). Review of systems should include asking about fever, which may indicate an inflammatory or infectious condition; weight loss; extraintestinal manifestations of IBD (e.g., pyoderma gangrenosum, erythema nodosum, ankylosing spondylitis, sacroiliitis, uveitis, or episcleritis); and celiac disease (e.g., dermatitis herpetiformis, infertility, premature metabolic bone disease, iron deficiency anemia).

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