Introduction and Epidemiology
This chapter discusses the general assessment of patients with diarrhea and the special considerations of acute infectious and traveler’s diarrhea, Clostridium difficile diarrhea and colitis, inflammatory bowel disease, ileitis and colitis, and ulcerative colitis.
Acute diarrhea is the sudden onset of an increase in the normal water content of stool. In general, humans lose approximately 10 mL/kg/day of fluids in stool. The increased water content of diarrhea results in an increased frequency of stools from 3 or more times daily to more than 20 bowel movements in a 24-hour period. Diarrhea is an increased frequency of defecation, usually greater than 3 bowel movements per day for a daily stool weight exceeding 200 grams.1,2 Practically speaking, however, diarrhea is present when the patient is making more stools of lesser consistency more frequently.
There are four basic mechanisms of diarrhea: increased intestinal secretion, decreased intestinal absorption, increased osmotic load, and abnormal intestinal motility. Normally, the jejunum receives between 6 and 8 L per day of fluid in the form of oral intake and gastric, pancreatic, and biliary secretions. Dietary intake actually constitutes a small portion of the jejunal load (1.5 L). A healthy small intestine absorbs nearly 75% of the fluid to which it is exposed. The 2 L of fluid not absorbed by the small intestine then enters the colon, where fluid is absorbed at an even higher rate. The absorptive power of the colon approaches 90% efficiency and far exceeds that of the small intestine. In fact, the colon can make up for a decrease in small intestinal absorption. Under normal conditions, very little fluid (<100 mL) is lost in the stool each day.3
In diarrheal states, normal intestinal physiology is disrupted. At a cellular level, intestinal absorption occurs through the villi, and secretion occurs through the crypts. Fluids are absorbed by two mechanisms: passively with the transport of sodium and actively with the absorption of glucose. Selected enterotoxins block the passive sodium resorption and specifically stimulate sodium excretion, resulting in a net loss of fluid. The glucose-dependent mechanism of water absorption, however, is unaffected by these toxins and can be exploited by including glucose in the rehydration treatments. The composition of oral rehydration therapies recommended by the World Health Organization is based largely on this physiology. In addition, diarrheal states, enterotoxins, inflammation, or ischemia disrupt the structure of the intestinal villi preferentially with less involvement in the crypts. As a result, diarrhea occurs because of diminished intestinal villi absorption and unopposed crypt secretion (the crypts are more resilient after injury).4
Another mechanism by which disease processes cause diarrhea is by the delivery of an osmotic load to the intestine. For example, administration of a laxative results in the collection of an osmotically active, nondigestible agent within the intestinal lumen. Other substances such as diet products and medications (e.g., colchicine) have similar effects. Osmosis occurs, drawing ...