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Diarrheal diseases have quite different prevalences and outcomes in developed and developing countries (Fig. 5-1, Fig. 5-2, Fig. 5-3). Infant and child mortality rates decreased in developing nations from 5 million a year in 1987 to 3.5 million a year in 1995. The infant mortality rate from diarrheal diseases in the United States is stable at 300-500 deaths per year over the same period. In the United States, the death rate from diarrhea among persons older than 74 years is nearly 10 times that of infants, children, and younger adults.
Diarrhea (stool volumes greater than 200 mL/24 h) results from alterations in water and electrolyte transport mediated through changes in intracellular messengers (Fig. 5-4 and Fig. 5-5) or from unabsorbed osmotic solutes that retain fluid within the intestinal lumen. Inflammatory diarrhea causes systemic symptoms through the release of cytokines (Fig. 5-6).
Acute diarrhea is defined as that less than 2 to 3 weeks in duration. The most common causes are infections
(Table 5-1). The incidence of diarrhea is high in daycare centers (Table 5-2) and hospitals (Table 5-3). Consolidation of the food industry, the increased number of and use of fast-food restaurants and a change in eating habits in industrialized nations has led to a marked increase in food-borne illness and diarrheal disease. The illnesses may be caused by ingestion of toxins (Table 5-4, Table 5-5, Table 5-6) or infection with microorganisms (Fig. 5-7). Various algorithms have been made to guide physicians in the investigation and management of acute diarrhea (Fig. 5-8). A key feature in most diagnostic algorithms is the presence or absence of fecal leukocytes (Table 5-7). Management of diarrhea can be symptomatic and primarily involves rehydration (Table 5-8 and Table 5-9); in specific instances, antimicrobial therapy may be used (Table 5-10 and Table 5-11). The various bacteria are most sensitive to specific antibiotics; however, trimethoprim-sulfamethoxazole and fluoroquinolones are effective management of most enteric organisms. Campylobacter infections require erythromycin. Traveler’s diarrhea (Fig. 5-9; Table 5-12) and acquired immunodeficiency syndrome diarrhea (Fig. 5-10; Table 5-13) are special forms of diarrheal disease that require a different approach.
Chronic diarrhea is that which lasts longer than 3 to 6 weeks. It may be caused by malabsorption, intestinal secretory states, or intestinal inflammation. The classic example of a malabsorptive disease is celiac sprue (Table 5-14). In infancy and childhood, the manifestations are recognized with chronic severe malnutrition and include abnormal hair growth as seen in the eyelashes (Fig. 5-11). Whipple disease is another malabsorptive disease. Like celiac sprue, it has an inflammatory component that causes many systemic symptoms, including arthritis (Table 5-15). The infectious agent of Whipple disease can invade the central nervous system and cause severe and drastic complications (Table 5-16). The steatorrhea of celiac sprue sometimes can be differentiated from that of pancreatic exocrine insufficiency on clinical grounds alone (Table 5-17). Steatorrhea is the clinical hallmark of malabsorption (Fig. 5-12). Abnormal qualitative stool-fat findings, if the examination is properly performed (Fig. 5-13 and Fig. 5-14) lead the physician to initiate an evaluation for malabsorption. Severe diarrhea of any type (e.g., secretory diarrhea or osmotic diarrhea from MgOH ingestion) can cause mild steatorrhea and mislead the clinician to a diagnosis of generalized malabsorption (Fig. 5-15). Endoscopic duodenal biopsy (Fig. 5-16) may be the best way to differentiate intestinal from pancreatic malabsorption. A d-xylose absorption test is much less frequently used now in adult medicine because of the various factors that affect its interpretation (Table 5-18). Radiography of the small intestine is of only limited value in the diagnosis of intestinal malabsorptive diseases (Fig. 5-17).
Malabsorption of carbohydrate alone causes watery diarrhea. The most common cause of carbohydrate malabsorption is lactose intolerance, a condition prevalent throughout the world (Fig. 5-18). The use of the nonabsorbable carbohydrate sorbitol to sweeten dietetic chewing gum and candy also can cause diarrhea (Table 5-19 and Table 5-20). Sorbitol also is present in some fruits (Table 5-19) and medicines (Table 5-21). Diarrhea caused by the high sorbitol content of liquid medicine is called elixir diarrhea. Fructose is the primary sugar in fruit juice and is often used as a sweetener for soft drinks; some persons also malabsorb fructose.
Secretory diarrhea may be caused by factitious ingestion of laxatives, use of drugs, or endocrine tumors. Factitious diarrhea is the most common of the secretory type and may be recognized with several characteristic clinical features (Table 5-22 and Table 5-23), including the finding of melanosis coli at sigmoidoscopy (Fig. 5-19). When secretory diarrhea is suspected, a cathartic screening test should be performed on the stool specimen. Such screening tests lead to a search for the agents listed in Table 5-24 and for magnesium and PO4. The docusates (dioctyl sodium sulfosuccinate) may not be available in the screen, and phenolphthalein is off the market now in the United States. Neuroendocrine tumors are fairly rare, but they result in devastating, high-volume secretory diarrhea because of the elaboration of secretory hormones (Table 5-25). Pancreatic endocrine tumors that secrete vasoactive intestinal polypeptide (VIP) are a cause of secretory diarrhea. Suspicion of these tumors can be confirmed with various blood and urine tests (Table 5-26).
Stool electrolyte measurements and the response to fast often are helpful in sorting out the cause of diarrhea (Fig. 5-20). Secretory diarrheas generally do not decrease on fast to volumes less than 200 mL/24 h unless the secretory state is mild, as in collagenous or microscopic colitis. Determination of the osmotic gap in the stool can be useful in differentiating secretory from osmotic diarrhea. Fermentation of nonabsorbed carbohydrate by intestinal bacteria increases the osmolality of stool after it is passed into the container and during storage before testing (Table 5-27). Because of their effect on colonic bacteria, antibiotics also alter stool electrolyte content. Stool sodium concentrations less than 50 mEq/L with osmotic gaps more than 100 mOsm are characteristic of osmotic diarrhea, whereas stool sodium concentrations greater than mEq/L and osmotic gaps less than 50 to 100 mOsm are classic for secretory diarrhea (Table 5-28). Specific congenital diarrhea can be suspected in infants and children because of changes in stool chloride or sodium content (Table 5-29). A more recently recognized type of congenital secretory diarrhea, microvillus inclusion disease (Fig. 5-21), causes stool electrolyte excretion like that of the adult pancreatic cholera syndrome. Inflammatory diarrhea may be caused in part by ulceration of the mucosa, malabsorption due to crypt hyperplasia, and intestinal secretion stimulated by inflammatory mediators (Fig. 5-22).
Many causes of diarrhea can be diagnosed on the basis of history, physical examination, and routine blood tests (Fig. 5-23). A stool examination for microorganisms, blood, and fat and a colonic biopsy bring the diagnostic yield to 75% to 80%. The remaining 20% of cases are elusive diarrhea that necessitate hospitalization and extensive testing.
The management of mild diarrhea is best accomplished with drugs, such as opiates, that alter intestinal motility. The somatostatin analog octreotide has been shown to be useful in the management of neuroendocrine tumors. Somatostatin inhibits secretion of peptide hormones by the tumor (Fig. 5-24), and this is accompanied by marked reduction in the secretory diarrhea (Fig. 5-25).


RECOMMENDED READINGS

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