Diarrhoea
Diarrhoea is clinically characterized by the frequent passage of unformed stools. Episodes that are brief, self-limited, and well tolerated do not require medical attention, but when diarrhoea becomes severe or chronic, a thoughtful evaluation is needed to ensure proper management. The primary care physician needs to know how to conduct an expeditious assessment of acute severe diarrhoea and coordinate a cost-effective approach to the evaluation of chronic diarrhoea. Diarrhoea in the HIV-infected patient requires special attention.
The pathophysiologic common denominator is increased stool water content, which may be a consequence of increased fluid secretion, decreased water absorption, or altered bowel motility. At times, several mechanisms are operative. Increased fluid secretion can be triggered by inflammation, hormones, or enterotoxins. The resulting secretory diarrhoea has a stool volume that remains in excess of 500 mL/24 h despite fasting, a low stool osmolality, and a normal stool electrolyte concentration. Decreased reabsorption of fluid occurs with abnormalities of the bowel mucosa, loss of re-absorptive surface, or the presence of unabsorbable, osmotically active materials in the bowel lumen, such as lactose in patients with lactase deficiency. Patients with diarrhoea resulting from decreased re-absorption typically respond to fasting with a decrease in stool volume to less than 500 mL/24 h; stool osmolality is increased, and its sodium and potassium concentrations are low. Increased bowel motility decreases the contact time with the bowel mucosa, limiting fluid reabsorption; it can ensue after vagotomy or may be chemically stimulated, as in hypergastrinemia or with the use of laxatives.
A diarrhoea is categorized as “acute” if its duration is less than 2 weeks. Infectious causes dominate and include viral, bacterial, and parasitic agents. Bacteria may cause diarrhoea by producing a toxin in contaminated food or after ingestion, or by invading the bowel mucosa. Some parasites invade the bowel wall, whereas others cling to it and coat the absorptive surface.
Viruses. Viral gastroenteritis has long been the most common cause of acute diarrhoea in the United States, although it was not until the late 1970s that the responsible organisms were finally isolated and identified. Epidemics of viral gastroenteritis are particularly common. More than 40% of outbreaks of nonbacterial gastroenteritis investigated by the Centers for Disease Control and Prevention (CDC) during a 5-year period were linked to the Norwalk virus. In children, rotavirus infection is a common cause. Outbreaks have been found to occur during all seasons and involve water-borne, food-borne, and person-to-person modes of transmission. They last about a week. Vomiting is the prominent symptom in children, diarrhoea in adults. After an incubation period of 48 to 72 hours, symptoms usually begin abruptly with diarrhoea, nausea, vomiting, headache, low-grade fever, abdominal cramps, and malaise; they resolve spontaneously within 24 to 96 hours. The diarrhoea tends to be predominantly secretory in quality. Abdominal examination reveals diffuse tenderness (without guarding) and hyperactive bowel sounds. The white blood cell count is usually normal but may be elevated. Stools are usually free of leukocytes, but occasionally white cells are found, as in an invasive etiology.
Staphylococcus Aureus is a common contaminant of custard-filled pastries and processed meats. The organism produces an enterotoxin that causes nausea, vomiting, abdominal cramps, and diarrhoea within 2 to 8 hours after contaminated food has been eaten. Symptoms usually last less than 12 hours. A common-source pattern and lack of fever are typical.
Clostridium Perfringens is another common food contaminant, especially of foods that have been warmed on steam tables. The organism releases an enterotoxin after sporulation in the intestine. Consequently, the incubation period of 8 to 24 hours is a bit longer than that for staphylococcal food poisoning. Symptoms include diarrhoea, abdominal cramps, and occasionally some vomiting. It, too, has a common-source epidemiology, and fever is absent.
Escherichia Coli 0157:H7. This pathogen is increasingly recognized as responsible for much food-borne diarrhoea. It accounts for up to 2.5% of all cases of acute diarrhoea and up to a third of cases of bloody acute diarrhoea. Transmission to humans is usually by ingestion of contaminated meat (typically hamburger) that is undercooked. Person-to-person transmission also occurs. Peak incidence is in the summer months. The organism does not directly invade the bowel wall, but the two Shiga-like toxins it produces cause mucosal edema, ulceration, and hemorrhage. The mean incubation period is 3 days (range, 1 to 9 days). Among those who become symptomatic, presentations range from mild, crampy, nonbloody diarrhoea to life-threatening hemorrhagic colitis complicated by hemolytic–uremic syndrome or thrombotic thrombocytopenic purpura. The typical presentation starts with crampy abdominal pain followed within hours by watery diarrhoea that progresses to grossly bloody stools. Children, the elderly, and compromised hosts are at greatest risk.
Salmonella species cause diarrhoea by invading the bowel wall. Achlorhydric patients who lack the antibacterial action of normal gastric acidity are at increased risk. The most common form of Salmonella infection is a self-limited diarrhoeal illness resulting from ingestion of contaminated food (eggs and poultry are the major sources). Children are at greatest risk; late summer and fall are the times of peak incidence. Although most episodes of salmonellosis are mild, debilitated patients are at risk for serious bacteremia. In the typical outpatient case, symptoms begin 12 to 36 hours after ingestion and resolve within 5 days, although diarrhoea may persist for up to 2 weeks. The initial presentation is rather nonspecific, although indicative of a small-bowel process: watery diarrhoea, cramps, nausea, vomiting, and fever. In addition to colonization, an enterotoxin is released that stimulates the secretory diarrhoea. In later stages, invasion spreads to the large bowel, and leukocytes may be noted in the stool. A distinguishing feature of salmonellosis is that the leukocytes are often mononuclear cells. In severe cases, dysentery can develop.
Typhoid fever, a rare but “must-not-miss” form of Salmonella disease, is caused by infection with Salmonella typhi. About 500 cases occur in the United States each year, mostly among young people. Infections are both water-borne and food-borne. Although diarrhoea develops in only a small percentage of patients with typhoid fever, it does occur. The classic and most severe form is a “pea soup” diarrhoea developing in the third week of illness. Early symptoms suggestive of the condition are progressive fever, relative bradycardia, evanescent rash on the trunk (“rose spots”), splenomegaly, cough, headache, and right lower quadrant abdominal pain.
Shigella infection produces an invasive diarrhoeal illness. Transmission is by the fecal–oral route, and stubborn reservoirs include day care centers, Indian reservations, urban ghettos, and rural villages in developing countries. Young children are at greatest risk and often the source of infection within a family. The illness proceeds in two stages. First, colonization takes place in the small bowel, resulting in a watery diarrhoea and periumbilical pain, followed in a few days by invasion of the large bowel, associated with frequent small stools, tenesmus, and polymorphonuclear leukocytes on smear. In florid cases, the patient has fever, toxicity, bloody diarrhoea, nausea, vomiting, and cramps. Most often, the disease is more subtle and may be difficult to distinguish from other diarrhoeal illnesses accompanied by fever.
Campylobacter Jejuni infection is responsible for more cases of diarrhoea in the United States than is either Salmonella or Shigella. Infection derives most often from animal sources, such as poultry and household pets; fecal transmission between people also occurs. The incubation period is 2 to 7 days. Clinically, the illness resembles that caused by Salmonella or Shigella; however, symptoms may persist longer. The relapse rate is as high as 20%, although the illness is usually self-limited and resolves within a week. In half of all cases, a Gram’s stain of the stool shows characteristic curved, gram-negative rods arranged in “sea gull wing” fashion. The organism grows best on a special medium incubated at 42°C; it will not grow on plates customarily used for isolation of Salmonella and Shigella.
Yersinia Enterocolitica also causes an illness that resembles salmonellosis. Patients become infected by eating contaminated meat or dairy products. The incubation period is 12 hours to 3 days. An intense, regional lymphoid reaction may arise in the terminal ileum (the portal of entry for the organism) and result in a clinical picture of fever, right lower quadrant abdominal pain, and diarrhoea that can simulate the onset of Crohn’s disease. In 10% to 40% of patients, fever, arthralgias, polyarthritis, or erythema nodosum develops. The illness is usually self-limited.
Vibrio Parahaemolyticus and non–toxin-producing Vibrio cholerae are pathogenic species that have caused outbreaks of diarrhoeal disease among people eating raw seafood, particularly oysters and sushi-style red snapper and salmon. The incubation period is measured in hours to several days. The illness that ensues is usually mild and self-limited, although an occasional patient may present with fever, nausea, vomiting, and crampy diarrhoea.
Listeria Monocytogenes is another of the food-borne pathogens found increasingly in tainted processed meats and poultry products and also in unpasteurized milk products. Person-to-person transfer does not occur. About 2,000 cases per year occur in the United States. Deaths are common, with mortality rates of 20% to 30% reported. The elderly and the immunocompromised are at greatest risk. Onset of symptoms is typically 1 to 2 days after exposure. Initial symptoms resemble those of a viral gastroenteritis (fever, cramps, myalgias, diarrhoea, headache). Days to weeks later, meningitis and bacteremia may ensue, especially in the immunocompromised host.
Vibrio Cholerae causes the prototypical toxin-mediated secretory diarrhoeal disease that results from drinking water contaminated with the organism. Most outbreaks are pandemic in the Indian subcontinent, Southeast Asia, Africa, and the Middle East. Isolated outbreaks have been reported in Mediterranean countries. In the United States, rare outbreaks sometimes occur along the Gulf coast. The disease ranges in severity from a mild illness to fulminant, life-threatening diarrhoea with copious production of gray, watery, mucoid (“rice water”) stool. In severe cases, fluid losses may exceed 1 L/h and are accompanied by vomiting, muscle cramps, and severe thirst. Because it is a noninvasive diarrhoea involving the small bowel, cholera does not cause tenesmus, and the stool contains no leukocytes. Dehydration, serious volume depletion, and a metabolic acidosis may ensue. In mild cases, the patient reports painless, nonbloody diarrhoea of abrupt onset.
Bacillus Cereus is a toxin-producing bacterial contaminant of rice and bean sprouts. One form of toxin-induced illness leads to vomiting but no diarrhoea; another is characterized by severe abdominal cramping and diarrhoea. The incubation period is 8 to 16 hours after ingestion of contaminated food. The symptoms are self-limited.
Entamoeba Histolytica usually exists in a commensal relationship with its host, and most patients harboring the protozoan are asymptomatic carriers. Occasionally, this relationship breaks down and the ameba invades the colonic wall; an acute bloody diarrhoea is the result. The clinical presentation ranges from mild to fulminant illness. Occasionally, the illness is mistaken for inflammatory bowel disease and may have a protracted course with exacerbations and remissions. Asymptomatic carriers such as returning tourists and immigrants are often the source of infection in developed countries. Because the organism does not have a soil phase, amebiasis is not restricted to warmer climates. Well-documented outbreaks have occurred in the United States and Europe, in addition to those that originate in developing countries. Amebiasis can be spread by sexual contact and is prevalent among promiscuous homosexuals.
Giardia Lamblia ranks as a leading parasitic cause of diarrhoea, especially overseas but also in the United States. Infection with the flagellated protozoan is particularly common where water supplies are contaminated by human sewage, but the organism is also endemic to such areas as the Rocky Mountains and St. Petersburg, Russia. The exact means by which Giardia causes diarrhoea remains unsettled, although heavy infestations can lead to malabsorption by coating large areas of the small bowel, particularly the lower duodenum and upper jejunum. The majority of patients with giardiasis are asymptomatic, but the organism is being recognized more frequently as an important cause of acute, intermittent, and chronic diarrhoeas in the United States. The ensuing loose stools may be watery or greasy; mucus is often present, but blood is rare. The patient may complain of epigastric or periumbilical discomfort. Mild steatorrhea and malabsorption occur with heavy parasite burdens.
Cryptosporidium, Microsporidia, and Other Protozoans are increasingly recognized as causes of acute watery diarrhoea (and sometimes of chronic disease). Point-source outbreaks occur in addition to sporadic cases. Transmission is by person-to-person contact through stool or by water or food contaminated with the spore or oocyst forms of the organism. Intestinal inflammation may develop. Children and immunocompromised adults are at greatest risk for severe and prolonged illness. A profuse, watery diarrhoea can develop, with stool volumes that may exceed 3 L daily. Although the illness is usually self-limited, it may persist in immunocompromised hosts. A mild illness develops in otherwise healthy, immunocompetent patients; they may become infected during occupational contact (e.g., animal dung). For them, symptoms resolve spontaneously within 5 to 21 days.
Diarrhoea in HIV-infected Patients is a major problem, with a host of possible etiologies. In HIV-infected persons who engage in receptive anal intercourse, the presentation may be one of diarrhoea, tenesmus, and rectal pain. In this setting, polymicrobial etiologies are not uncommon and may include Neisseria, Giardia, E. histolytica, Campylobacter, Chlamydia, Shigella, Salmonella, and protozoans.
Patients traveling from industrialized to developing nations are at considerable risk for the development of diarrhoea. Etiologic agents include E. coli, Salmonella, Shigella, E. histolytica, G. lamblia, S. typhi, and V. cholerae. Invasive E. coli strains can also cause a dysentery syndrome. Although most cases of traveler’s diarrhoea are associated with travel to developing nations, this is not always true. For example, there is substantial risk of giardiasis with travel to St. Petersburg, Russia, or even to the Rocky Mountains of the United States.
Toxigenic Escherichia coli is responsible for a large proportion of cases labeled as “traveler’s diarrhoea” or “turista.” The agent is transmitted by poor food-handling practices and contaminated water. With enterotoxin production, a watery diarrhoea ensues because the toxin promotes fluid secretion in the small bowel.
Acute Diarrhoea. Mechanisms of acute diarrhoea include excessive fluid secretion (alcohol, phenolphthalein, and castor oil), reduction of fluid absorption (magnesium-containing antacids), and stimulation of bowel motility (caffeine-containing beverages and herbal teas). An osmotic diarrhoea with crampy pain and watery stools may follow oral or parenteral use of broad-spectrum antibiotics, which disrupt the salvage of unabsorbed carbohydrate by killing normal colonic flora.
Chronic Diarrhoea: Pseudomembranous Colitis. Broad-spectrum antibiotics can cause chronic diarrhoea by promoting overgrowth of toxin-producing species such as Clostridium difficile. The antibiotics most often responsible are ampicillin and clindamycin, but other broad-spectrum agents have also been implicated. Immunocompromised patients, the elderly, and those with underlying bowel disease are most susceptible. Pseudomembranous colitis is characterized by fever, abdominal pain, profuse watery stools, and fecal leukocytes. Symptoms may range from mild to severe, usually starting after the initiation of a course of antibiotics, but onset can be delayed for as much as 4 to 8 weeks after cessation of antibiotics. Symptoms may persist for months, mimicking inflammatory bowel disease. The sigmoidoscopic finding of nodular, inflammatory ulcers or yellow-white mucosal plaques is characteristic.
Although the number of etiologies is vast, consideration of a few exemplary conditions provides a good sense of the range and types of presentations.
Irritable Bowel Syndrome is the most common of the motility disorders responsible for chronic diarrhoea or hyperdefecation. It can present as diarrhoea alternating with constipation, or as chronic, recurrent diarrhoea. Some studies report a high frequency of associated psychiatric disease. In addition to diarrhoea and constipation, patients may complain of distention, cramping, and mucus-laden stools. The condition waxes and wanes over many years. Neither fever nor fecal leukocytes are present. Any rectal bleeding that may occur is secondary to anal trauma resulting from straining and passage of hard stool.
Inflammatory Bowel Diseases are typical of the diarrhoeas that result from inflammatory destruction of the bowel wall . Abdominal pain, bloody stools, purulent discharge, and fever are seen in patients with active disease affecting the large bowel. Extraintestinal manifestations may involve the skin, joints, liver, and heart. Microscopic examination of the stool reveals red cells and leukocytes.
Diabetic Enteropathy results from diabetes-induced autonomic neuropathy. When the small bowel is involved, the ensuing stasis allows bacterial overgrowth. The bacteria deconjugate bile acids, which leads to fat malabsorption. With involvement of the large bowel, the patient experiences distressing nocturnal diarrhoea. Postural hypotension, impotence, and other symptoms and signs of autonomic insufficiency may accompany the diarrhoea and suggest the diagnosis.
Dumping Syndrome is another motility disorder, seen most commonly in patients who have undergone vagotomy and gastroenterostomy. Patients complain of sweating, postural light-headedness, tachycardia, and diarrhoea following meals. Concentrated carbohydrates are most likely to trigger symptoms. Lying down minimizes symptoms, as does avoidance of concentrated sweets. Onset of the syndrome is shortly after surgery, and symptoms usually subside within 12 months, although they may persist. Besides dysmotility, osmotic factors may contribute, but their precise role remains unclear.
Villous Adenoma of the rectosigmoid causes a secretory, noninflammatory chronic diarrhoea. Watery diarrhoea, independent of food and fluid intake, is typical; severe potassium depletion can result. In some patients with this tumor, excessive secretion of mucus occurs, with loss of sufficient protein to produce hypoalbuminemia and a protein-losing enteropathy syndrome.
Malabsorption of Fat or Carbohydrate can lead to an osmotic diarrhoea, as occurs in patients with pancreatic inefficiency, sprue, and short-bowel syndrome. Some of the osmotically active substances may also stimulate increased bowel secretion of fluids and electrolytes. Malabsorption of fat characteristically presents as steatorrhea (foul, bulky, greasy stools). Patients may note that the stools seem to be “sticky” and difficult to flush down the toilet. Steatorrheic stools “float,” not because of their fat content but because of an increase in trapped gas. Associated symptoms are a function of the severity of the caloric and vitamin deficiencies that ensue and may include weight loss, ecchymoses, bone pain, glossitis, muscle tenderness, and peripheral neuropathy. Cramping lower abdominal pain typically precedes bowel movements. Early concerns about severe diarrhoea and abdominal pain associated with the regular use of Olestra, a nonabsorbable sucrose ester fat substitute used in snack foods, have not been confirmed in randomized, prospective, controlled trials.
Lactase Deficiency (Milk Intolerance) leads to malabsorption of lactose and an osmotic diarrhoea. It is particularly common among African-Americans, Indians, Asians, and Jews. Onset is typically in adulthood. A secondary form of the disease may develop in patients with extensive disease of the small bowel. Patients report nausea, bloating, cramps, and diarrhoea after ingesting more than their customary intake of milk products. Weight loss and steatorrhea are absent or mild; appetite remains good. Avoidance of milk products (except for yogurt containing live cultures, which provide lactase) terminates symptoms. Diagnosis may be confirmed by a trial of abstinence and by abnormal results on lactose tolerance testing or hydrogen breath testing (which detects excessive hydrogen production resulting from bacterial metabolism of undigested lactose).
Laxative Abuse is an important etiology of chronic diarrhoea. Patients with bulimia tend to use laxatives constantly and surreptitiously in a relentless attempt to lose weight. Depending on the type of agent used, either a secretory or osmotic diarrhoea may develop. Agents associated with secretory diarrhoeas include castor oil and phenolphthalein preparations. Osmotic diarrhoeas occur when the patient takes a preparation that contains magnesium (e.g., milk of magnesia) or another poorly absorbable substance. These substances appear in the stool and can be tested for if laxative abuse is suspected. Patients who abuse laxatives may present with unexplained dehydration, electrolyte depletion, or preoccupation with weight loss.
Lymphocytic Colitis and Collagenous Colitis. These two new conditions associated with refractory chronic diarrhoea have recently been recognized. They occur predominantly in women and cause chronic watery diarrhoea, often complicated by steatorrhea and malabsorption. The colonic appearance is grossly normal, but biopsy reveals collagenous or lymphocytic infiltrates. The small bowel usually is normal but may show spruelike changes in patients with lymphocytic disease, and persons with the condition may present with spruelike malabsorption unresponsive to a gluten-free diet.
Bile Acid Diarrhoea is seen after cholecystectomy and ileal reaction. It is an irritant diarrhoea caused by the action of excessive bile acids on the bowel and responds to bile acid sequestrants (e.g., cholestyramine).
A number of patients who complain of “diarrhoea” actually suffer from incontinence. Typically, their stool volumes are normal (< 2.5 mL/d), although their stools may be soft poor sphincter tone and evidence of stool incontinence are found on physical examination.
Acute Diarrhoea. The differential diagnosis for acute diarrhoea is dominated by infectious agents. Viruses are the single most important frequent cause. Staphylococcal toxin, clostridial toxin, and ingestion of Campylobacter, Salmonella, Shigella, and enteropathogenic E. coli are common bacterial etiologies. Of increasing importance are the potentially life-threatening outbreaks of food-borne disease caused by toxin-producing E. coli 0157:H7, Listeria, and protozoans such as Cryptosporidium. Giardia and amebae are less frequent sources of acute diarrhoea in the United States. Drug-induced acute disease is associated with the use of antibiotics, laxatives, magnesium-containing antacids, and agents such as quinidine. Alcohol and caffeine-containing beverages should be considered. Most causes of chronic diarrhoea are also capable of causing acute presentations.
Traveler’s Diarrhoea. In more than 50% of acute cases, the cause is exposure to enterotoxigenic E. coli. Most of the remainder are accounted for by Salmonella, Shigella, Giardia, or Campylobacter.
Chronic Diarrhoea. The differential diagnosis is even more extensive and includes causes of acute disease that may become chronic (e.g., laxative abuse, pseudomembranous colitis, protozoan infections, amebic infestations) in addition to a host of intrinsic bowel diseases. A malabsorption picture may be the consequence of sprue, bile salt deficiency, lactase deficiency, intestinal lymphoma, Whipple’s disease, pancreatic insufficiency, or the newly recognized collagenous and lymphocytic forms of colitis. Postsurgical diarrhoea may reflect postgastrectomy dumping syndrome, fistulas, blind loops, loss of parasympathetic innervation, extensive bowel resection, or excessive bile acid. Diarrhoea with bleeding may herald neoplasms and inflammatory bowel disease. Diarrhoea alternating with constipation may be caused by irritable bowel syndrome, Crohn’s disease, or diverticular disease of the bowel. A variety of extraintestinal conditions may be responsible, including cirrhosis, alcoholism, pellagra, and heavy metal intoxications from lead, mercury, or arsenic. Endocrinopathies also must be considered (e.g., diabetes mellitus, Addison’s disease, hyperthyroidism).
Diarrhoea of Unknown Etiology. In studies of patients referred for chronic diarrhoea of unknown etiology, the vast majority turn out to be abusing laxatives or to have a subtle form of inflammatory bowel disease (including collagenous or lymphocytic varieties) or irritable bowel syndrome. Most of the remainder have a more readily diagnosed condition that was overlooked on initial evaluation.
Diarrhoea in the HIV-Infected Patient. The common infectious causes are frequently seen, but such uncommon causes as Cryptosporidium, Mycobacterium avium–intracellulare, herpes simplex virus, cytomegalovirus, Neisseria gonorrhoeae, Giardia, and Chlamydia trachomatis must also be considered.
Before embarking on a workup, one needs to confirm that the problem is indeed diarrhoea and not simply an occasional loose stool or frequent defecation of formed stools. Stool volume, frequency, and water content should all be increased.
History. The nature of the bowel movements should be determined, including their frequency, consistency, volume, and the presence of gross blood, pus, or mucus, and the presence of any associated symptoms, such as fever, rash, and abdominal pain, should be noted. Late onset of neurologic deficits or meningeal symptoms should suggest listeriosis.
Epidemiologic Information is critical because the clinical
presentation is often nonspecific. Reviews of travel (both international and
domestic), personal contacts, and food intake are essential. Among the foods to
consider are custard-filled pastries, undercooked processed meats, foods warmed
on steam tables, eggs, poultry, raw seafood, unpasteurized milk and fruit
juices, rice, and bean sprouts. Important contacts include children who attend
day care centers because they may contract rotavirus, Giardia, Shigella,
Cryptosporidium, or Campylobacter. A sexual history is
indicated if there is concern about polymicrobial infection.
Onset and Associated Symptoms. Diarrhoea occurring within hours of ingestion of a potentially contaminated food is suggestive of food poisoning, which is confirmed if others have been similarly affected. Food-borne illness with a short incubation period and no fever indicates ingestion of a preformed enterotoxin. Fever and a slightly longer incubation period are characteristic of an infectious etiology. Some toxin-producing organisms (e.g., E. coli 0157:H7) require a few days of incubation.
Drug History. It is particularly important to question about the use of laxatives, magnesium-containing antacids, excess alcohol, caffeine-containing beverages, herbal teas, antibiotics, digitalis, quinidine, loop diuretics (furosemide, ethacrynic acid), antihypertensive agents, and excessive intake of sorbitol-containing “sugar-free” gums and mints.
Physical Examination. Vital signs must be checked. Postural hypotension is a sign of significant volume depletion and an indication for prompt IV repletion. Any elevation in temperature or loss of weight also needs to be noted. The patient who appears markedly dehydrated or toxic is a candidate for hospital admission. The skin is examined for manifestations of sepsis; the macular “rose spot” rash on the trunk is an important clue for typhoid. The lymph nodes are checked for enlargement, and the abdomen for tenderness, guarding, rebound, abnormal bowel sounds, organomegaly, and masses. A rectal examination and fecal occult blood test complete the physical evaluation. When listeriosis is suspected epidemiologically, a careful neurologic examination is in order, with a search for focal deficits and meningeal signs.
Laboratory Studies: Initial Evaluation. The laboratory workup should be individualized. The patient who feels well except for frequent loose stools requires no immediate laboratory testing. On the other hand, the patient who is ill with fever, nausea, abdominal cramps, or other systemic symptoms requires more extensive evaluation, beginning with a stool test for leukocytes, which indicates a potentially serious etiology.
Stool Testing for Leukocytes. A drop of the sample is placed on a microscope slide, mixed thoroughly with two drops of methylene blue solution (or Wright’s or Gram’s stain), and topped with a cover slip for viewing under the microscope. Finding large numbers of white cells suggests an inflammatory or invasive diarrhoea, such as occurs with Shigella, Salmonella, Campylobacter, invasive or certain toxigenic E. coli, and Entamoeba. The presence of mononuclear cells is characteristic of salmonellosis. An occasional white cell is of no pathologic significance. Leukocytes may be absent from the stool in the early phases of shigellosis and pseudomembranous colitis.
Gram’s Stain of the Stool will provide etiologic information in selected instances, such as suspected Campylobacter infection. In about half of cases, the Gram’s stain will demonstrate gram-negative rods arranged in a characteristic sea gull wing configuration.
Stool Cultures. Cultures are usually not necessary in acute diarrhoea because most cases are self-limited. However, if the patient appears ill and either occult blood or leukocytes are present in the stool, then bacterial cultures should be obtained. Detection of Campylobacter or Yersinia requires plating on specific medium at 42°; the usual medium for Salmonella and Shigella will not suffice. The laboratory should be notified when E. coli 0157:H7 is a consideration because special growth media and other procedures are required to identify the pathogen.
Sigmoidoscopy. Patients with gross blood or large numbers of leukocytes in the stool and severe illness should undergo sigmoidoscopy to examine the appearance of the colonic mucosa; samples of the mucosa and cultures can also be obtained (see following section on the workup for chronic diarrhoea for details). Preparatory enemas and cathartics should be avoided so as not to distort the appearance of the bowel wall.
Laboratory Studies: Subsequent Evaluation. If the diarrhoea persists for 2 weeks or more, a secondary evaluation is indicated. Stools should once again be examined for blood and leukocytes. A second stool should be sent for bacterial culture, and a fresh specimen should be examined for ova and parasites.
Stool for Ova and Parasites. Ova and parasite examinations are fraught with limitations that must be kept in mind. If giardiasis is a consideration, at least three stool samples are necessary because excretion of the organism is intermittent. Many primary care physicians use a therapeutic trial of metronidazole when they strongly suspect giardiasis. Identifying E. histolytica trophozoites by stool examination can be difficult; their visualization is easily impaired by the presence of barium, bismuth, and kaolin compounds. False-negative results of stool examinations also can be caused by the use of preparatory enemas (which lyse the organism) and antibiotics (tetracycline and sulfonamides reduce shedding of trophozoites into the stool).
Other Studies. If symptoms persist and the diagnosis remains uncertain, the patient requires further assessment for a chronic or recurrent diarrhoeal syndrome (see below). Persons in whom neurologic deficits or meningeal signs develop after a diarrhoeal illness require culturing of the blood and cerebrospinal fluid for Listeria.
Suggestive Patterns. A few patterns are suggestive. Frequent passage of small volumes of loose stools in association with left lower quadrant crampy abdominal pain or tenesmus points to rectosigmoid pathology. Large volumes of loose stools in conjunction with periumbilical or right lower quadrant pain indicate disease of the small bowel, as does diarrhoea occurring shortly after a meal or ingestion of certain foods. Diarrhoea following meals should also lead to a search for malabsorption, an osmotic etiology, the dumping syndrome, or a fistula. The presence of foul, bulky, greasy stools further supports the diagnosis of fat malabsorption. Bloody stools require investigation for neoplasm, invasive infection, and inflammatory bowel disease. The presence of fever has similar diagnostic implications. Frothy stools and excessive flatus are signs of fermentation of unabsorbed carbohydrates, as occurs in giardiasis. Alternating diarrhoea and constipation point to irritable bowel syndrome, as does mucus in the stool. The absence of intermittent constipation in a patient with chronic diarrhoea does not rule out the diagnosis.
Travel in conjunction with diarrhoea that persists for more than 2 weeks raises the possibilities of giardiasis and amebiasis; pseudomembranous colitis is a consideration if the traveler has recently taken antibiotics. The slow resolution of traveler’s diarrhoea suggests postdysentery lactase deficiency and postdysentery irritable bowel syndrome.
Drugs. A thorough review of drug intake is mandatory; especially important is a check for antibiotic use, even if it was a few months before the onset of symptoms. A history of surreptitious laxative abuse may be hard to elicit, but inquiring gently and nonjudgmentally about feelings of low self-esteem and a poor body image may provide suggestive information when a young, intense woman presents with chronic diarrhoea and wasting.
Prior Surgery. Previous abdominal surgery should be specified, with any procedures that may have produced blind loops and allowed for bacterial overgrowth noted.
Physical Examination. Any fever, dehydration, postural hypotension, or cachexia should be noted. The skin should be inspected for jaundice, pallor, rash, and manifestations of inflammatory bowel disease. The abdomen is examined for distention, ascites, hepatomegaly, tenderness, rebound, and masses. Rectal examination may reveal fecal impaction, perirectal fistula, or a patulous anal sphincter. Stool is tested for occult blood.
Laboratory. Blood tests are helpful but rarely diagnostic. They should include a complete blood cell count for evidence of anemia and leukocytosis and determinations of serum electrolytes to detect serious losses and imbalances, amylase for pancreatic disease, liver function tests and prothrombin time for hepatobiliary disease, and serum calcium and glucose for metabolic conditions that can lead to diarrhoea. Eosinophil counts are normal in most parasitic infections that cause diarrhoea. (The only gastrointestinal parasites that stimulate peripheral eosinophilia are worms.)
Examination of Stool for White and Red Blood Cells. See above. If blood or pus is in the stool, or other evidence of rectosigmoid pathology is present, then one should proceed to sigmoidoscopy (see below).
Other Stool Tests. Additional stool testing can be helpful in selected instances. For suspected laxative abuse, one alkalinizes the stool; if it contains phenolphthalein (a common ingredient of many over-the-counter laxatives), it will turn pink. For suspected fat malabsorption, a stool sample is subjected to Sudan stain for qualitative detection of fat. Those with a positive result on qualitative study are candidates for a 72-hour quantitative stool fat determination. Normally, stool fat should not exceed 6% of the daily fat intake. Stool fat in excess of 6 g/d while the patient is on a test diet of 100 g of fat per 24 hours indicates fat malabsorption.
Sigmoidoscopy performed without cleansing enemas is a potentially definitive procedure in persons suspected of having inflammatory bowel disease and amebiasis and helps differentiate such conditions from irritable bowel syndrome. The presence of mucosal ulceration, plaques, friability, and bleeding should be noted. The finding of mucus in the absence of evidence of inflammation helps confirm the diagnosis of irritable bowel syndrome, whereas the presence of pus directs the evaluation toward infection and inflammation. Nodular inflammatory ulcers and yellow-white mucosal plaques are characteristic of pseudomembranous colitis. Ulceration is also noted with inflammatory bowel disease and amebic colitis. If Crohn’s disease or chronic neoplasia is suspected, colonoscopy should be substituted for sigmoidoscopy. Pseudomembranous colitis and amebic disease may produce an endoscopic appearance similar to that of inflammatory bowel disease, so that additional testing is necessary (see below).
Barium Enema and Upper Gastrointestinal Series best demonstrate anatomic abnormalities (blind loops, fistulas, and tumors). A barium enema is an alternative to colonoscopy when inflammatory bowel disease and malignancy are being considered, but the test is not as sensitive and does not allow for biopsy or mucosal sampling. Moreover, amebiasis can simulate inflammatory bowel disease. Because barium obscures the identification of ova and parasites, stool collections must be complete before a barium study is obtained.
Stool for C. difficile Toxin. Patients with recent antibiotic exposure and an inflammatory exudate on sigmoidoscopy require evaluation for pseudomembranous colitis. Up to three stool samples should be assayed for C. difficile toxin to maximize sensitivity, although it must be understood that some patients without disease harbor the organism and might show detectable amounts of toxin in the stool.
Mucosal Smears and Stool for Ova and Parasites. If ulceration of the rectosigmoid mucosa is present and amebic disease is suspected on the basis of epidemiologic data, fresh mucosal smears should be prepared. Proper technique for the identification of trophozoites involves sampling the periphery of the ulcers with a glass rod or metal spatula; cotton swabs are inadequate because the organisms adhere too firmly and do not readily transfer to a slide. Multiple stool examinations for ova and parasites can also be ordered. False-negative results of examinations for trophozoites are common and can be associated with the administration of preparatory enemas, recent exposure to antibiotics, and the concurrent use of barium, bismuth, or kaolin. To detect spore-forming organisms (i.e., Cryptosporidium, others), one needs to request that the stool be examined specifically for spores and oocysts.
Other patients who should have their stools examined for ova and parasites include those who have traveled to areas endemic for Giardia, homosexual men, and immunocompromised hosts, including persons with AIDS (who are at risk for harboring a host of pathogens, including Cryptosporidium; see below). Fresh loose stools are needed for identification of trophozoites; less fresh specimens can be used for detection of ova. Several stool examinations may be necessary.
Serologic Testing for Amebic Disease. When amebic disease is seriously suspected clinically and epidemiologically, yet results of examinations for ova and parasites are negative, serologic testing is indicated. The standard test is an indirect hemagglutination assay. A positive titer is in excess of 1:128. It takes 2 to 4 weeks for seroconversion to occur. By the time most patients with amebic disease present with diarrhoea, they are seropositive. The test is 85% sensitive in the setting of intestinal disease and 95% sensitive with extraintestinal spread. The test works best in nonendemic areas, where most people are seronegative.
Additional Testing for Giardia. Sometimes, small-bowel aspiration or even biopsy may be necessary to establish the diagnosis of giardiasis or cryptosporidiosis. Immunologic assay of the stool based on ELISA (enzyme-linked immunosorbent assay) technology can identify Giardia antigen with high sensitivity and specificity (92% and 98%, respectively); the test is rapidly obviating the need for biopsy and aspiration.
Therapeutic Trials sometimes substitute for more elaborate studies. As noted above, cessation of diarrhoea in response to restriction of milk products strongly supports the diagnosis of lactose intolerance. Other recognized empiric trials include a course of antibiotic therapy in patients suspected of blind loop syndrome, and use of pancreatic enzymes in patients believed to have pancreatic insufficiency. The once common trial of metronidazole for patients with suspected giardiasis is being deferred in favor of sensitive ELISA stool testing for Giardia antigen. Some patients are given empiric trials of a gluten-free diet, but bowel biopsy is preferred.
Often, patients with AIDS experience acute or chronic diarrhoea. They especially are susceptible not only to the common pathogens but also to such uncommon ones as Cryptosporidium, M. avium–intracellulare, herpes simplex virus, cytomegalovirus, N. gonorrhoeae, and C. trachomatis. Evaluation should focus on finding the pathogen and may require sigmoidoscopic biopsy to obtain tissue for viral or mycobacterial culture .
The leading possibilities are surreptitious laxative abuse, subtle forms of inflammatory bowel disease, and irritable bowel syndrome. Laxative abuse should be considered in young, professional women who are preoccupied with their weight and have low self-esteem and a poor body image. An otherwise unexplained hypokalemia is also suggestive. Collagenous and lymphocytic forms of colitis must be considered in women who present with chronic watery diarrhoea complicated by steatorrhea and malabsorption, especially those who are thought to have sprue but fail to respond to a gluten-free diet. Irritable bowel syndrome is suggested by the presence of abdominal pain in addition to diarrhoea. Although inpatient assessment is often needed, outpatient evaluation can be tried and may obviate the need for hospitalization. Stool analysis and colonoscopy with biopsy are the two most helpful studies.
Stool Analysis. One attempts to characterize the type of diarrhoea further by determining stool volume, osmolality, and electrolyte content. A stool volume of less than 200 mL/d is strongly suggestive of irritable bowel syndrome. Osmotic diarrhoeas show increased stool osmolality and low sodium and potassium concentrations. The differential diagnosis of osmotic diarrhoea includes ingestion of nonabsorbable solutes (magnesium, bran), maldigestion of food, and malabsorption of osmotically active substances (e.g., carbohydrates). Stool volumes in excess of 1 L/d indicate a secretory diarrhoea. Occult causes include surreptitious laxative abuse, villous adenoma, carcinoid syndrome, pancreatic cholera (from secretion of vasoactive intestinal peptide), and other rare conditions.
Bowel Biopsy. Because the appearance of the bowel in collagenous colitis and lymphocytic colitis is grossly normal on endoscopic examination, biopsy is required for diagnosis. Biopsy should be considered in women with unexplained watery diarrhoea, especially if complicated by steatorrhea and malabsorption. The small bowel usually is normal but may show spruelike changes in patients with lymphocytic disease.
Inpatient Study. The next step for patients whose condition remains undiagnosed is inpatient evaluation with imposition of a 24- to 72-hour fast and IV hydration. The fast helps to differentiate between osmotic and secretory causes; with the former, diarrhoea ceases or is markedly reduced during fasting. Stool analysis is repeated under conditions of fasting and standardized diets.
Hydration. The vast majority of cases of acute diarrhoeal illness should be managed by maintaining hydration and waiting for the spontaneous resolution of symptoms. Often, hydration can be maintained with oral fluids, even in cases of profuse diarrhoea. Solutions rich in electrolytes and sugar facilitate absorption of water. An 8-oz glass of fruit juice to which are added a pinch of table salt and half a teaspoon of honey or a teaspoon of table sugar makes a well-tolerated replacement solution. Nondiet cola drinks that have been allowed to stand and lose their carbonation are a reasonable substitute. Either can be taken along with a similarly sized glass of water containing one fourth of a teaspoon of baking soda to replenish losses in stool electrolytes, which in acute infectious diarrhoea are sodium (125 mEq/L), potassium (20 mEq/L), bicarbonate (45 mEq/L), and chlorine (90 mEq/L). If adequate hydration cannot be maintained orally, IV therapy is necessary.
Absorbent Preparations are commonly used for symptomatic therapy of simple acute diarrhoea. Solutions of kaolin and pectin have no proven benefit but seem to be harmless; however, they should not be relied on for the treatment of severe diarrhoea. Doses of bismuth subsalicylate (Pepto-Bismol) in excess of those recommended on the bottle (e.g., 2 to 3 tablespoons every 3 hours) are sometimes effective (see below).
Inhibition of Motility. Opiates such as diphenoxylate (dispensed as a combination with small amounts of atropine [Lomotil] to discourage abuse) and loperamide (Imodium) are effective in the symptomatic treatment of diarrhoea by directly inhibiting the motility of the intestinal smooth muscle. Diphenoxylate and loperamide are derived from meperidine but have less effect on the central nervous system. They should be used cautiously, if at all, in conditions in which toxic megacolon is possible (e.g., inflammatory bowel disease). Their use should also be restricted in certain bacterial diarrhoeas, such as shigellosis, to avoid prolonging the clinical course. There is also concern for their use in outbreaks of E. coli 0157:H7 infection, in which an increased risk for complications has been noted.
The usual dosage of diphenoxylate is 2.5 to 5 mg every 4 hours, up to 20 mg daily. Loperamide is given as 2 or 4 mg every 4 hours, up to 16 mg daily. Lower maintenance doses are often sufficient after initial control has been achieved. Other opiates are potent antidiarrhoeal agents but carry a higher risk for addiction; they are useful when their coincident analgesic activity is needed. Deodorized tincture of opium (0.5 to 1 mL), paregoric (4 mL), or codeine (30 to 60 mg) can be given orally every 4 hours. Anticholinergics are useful only for irritable bowel syndrome.
Antibiotics. The empiric use of antibiotics is not recommended routinely for acute bacterial diarrhoeas because most infections are self-limited. Empiric antibiotics have a minimal effect on the course of illness (with the exception of shigellosis outbreaks) and may prolong the asymptomatic bacterial carrier state, especially with Salmonella infection. Moreover, one risks triggering an antibiotic-induced diarrhoea and inducing antibiotic resistance (e.g., in Campylobacter). Antibiotics may also be counterproductive in E. coli 0157:H7 infection, in which their use has been associated in some instances with an increased risk for complications.
Antibiotics are best reserved for very ill patients who demonstrate positive stool cultures or other evidence for a specific bacterial etiology (e.g., typhoid fever, salmonellosis, shigellosis, pseudomembranous colitis, Campylobacter infection, and Yersinia infection).
Salmonella. Elderly patients and others who would be endangered by a Salmonella bacteremia (persons with vascular prostheses or sickle cell anemia) should receive a course of antibiotics to limit metastatic infection. Bacteremia and typhoid fever can be treated with parenteral ampicillin or oral chloramphenicol; in milder cases, oral trimethoprim/sulfamethoxazole (one double-strength tablet of TMS twice daily for 2 weeks) suffices.
Shigella. Patients with severe dysentery caused by shigellosis can be treated with oral amoxicillin (500 mg three times daily for 3 to 5 days), but antibiotic sensitivity testing is needed because amoxicillin-resistant strains are common. TMS (one double-strength tablet twice daily for 3 to 5 days) is an excellent alternative. Pending stool culture results, a few days of empiric therapy for shigellosis is reasonable if the epidemiologic history is suggestive and the patient is experiencing severe bloody diarrhoea. Antiperistaltic drugs are contraindicated.
Campylobacter is sensitive to oral erythromycin (500 mg four times daily for 7 days). Most patients with Yersinia infection have a self-limited illness, but toxic patients are candidates for oral chloramphenicol (50 mg/kg daily in four divided doses for 7 days) or parenteral therapy.
Pseudomembranous Colitis usually resolves without antibiotic treatment, but oral vancomycin in a liquid suspension (as little as 125 mg four times daily for 7 to 10 days) and metronidazole (250 mg three times daily for 5 to 10 days) have proved equally capable of controlling the disease, although relapses occur in 10% to 20%, so that retreatment is necessary. Metronidazole is preferred for initial use because it is far less expensive. Cholestyramine (one packet in water three times daily) is used in conjunction with antibiotics to help bind the enterotoxin; it has proved useful in difficult cases, as have rifampicin and bacitracin.
Parasitic Infection. Symptomatic patients with diarrhoea caused by parasitic infection also benefit from definitive antimicrobial therapy. E. histolytica responds to metronidazole (750 mg three times daily for 5 to 10 days) for treatment of trophozoites and diiodohydroxyquin (650 mg three times daily for 21 days) for elimination of cysts. Giardiasis is treated with quinacrine (100 mg three times daily for 7 days) or metronidazole (250 mg three times daily for 7 to 10 days). Retreatment is often necessary.
Prevention. Although much attention has been given to pharmacologic agents for prophylaxis, care in what one eats and drinks remains the single most important means of preventing traveler’s diarrhoea. Use of local water supplies should be avoided when they are in question. This includes foregoing fresh vegetables, which may have been washed in such water, and even ice cubes. Drinking bottled water is preferable.
Chemoprophylaxis. Because the majority of “turista” cases are caused by enterotoxigenic E. coli, chemoprophylaxis has been directed at this organism. TMS (one double-strength tablet daily) and ciprofloxacin (500 mg daily) can reduce the risk for diarrhoea, which ranges from 20% to 30%. For symptomatic relief of acute diarrhoea, ciprofloxacin (500 mg twice daily for 3 days) is effective, as is TMS (one double-strength tablet twice daily). Some resistance to TMS is emerging, making ciprofloxacin the preferred agent. Doxycycline, a tetracycline derivative, taken on the day of travel (200 mg) and daily (100 mg) while away has also proved useful, although as many as 40% of the toxigenic E. coli strains are resistant to the drug, and the drug often causes gastrointestinal upset and photosensitivity. The prophylactic use of antibiotics had been in vogue, but the growing awareness of antibiotic-induced diarrhoea, the high frequency of bacterial resistance to some agents, and the efficacy of bismuth subsalicylate is leading to less reliance on antimicrobials.
Treatment. Although antibiotics are sometimes used, their disadvantages (see above) suggest the use of other measures first, if possible.
Bismuth Subsalicylate (Pepto-Bismol) has proved effective as both prophylaxis and treatment for traveler’s diarrhoea when given in large doses (60 mL four times daily). Unlike antibiotics, it has the advantage of not altering the normal bowel flora. Its mechanism of action is believed to involve inhibiting colonization by toxigenic bacterial strains. Bismuth turns the stools black; it is useful to alert patients to this side effect so its occurrence does not cause alarm.
Diphenoxylate or Loperamide is often more convenient for symptomatic relief of traveler’s diarrhoea than are other measures. In most instances, these agents can be used for brief periods with safety, except when Shigella or Salmonella infection is a serious consideration (i.e., when fever or rectal bleeding is present). Loperamide has also been a useful adjunct to the antibiotic treatment of symptomatic disease.
Antibiotics are indicated in acute, severe cases. Ciprofloxacin (500 mg twice daily) and TMS (one double-strength tablet twice daily) are both effective, especially when used with loperamide (2 mg after each loose stool, up to 16 mg/d). A 3-day course of antibiotics usually suffices. Giving travelers a 3-day antibiotic supply plus loperamide to carry with them is reasonable and appreciated. Ciprofloxacin is probably preferred because of the emergence of TMS-resistant strains of E. coli.
Unlike the treatment of acute diarrhoea, in which many cases are self-limited and non-specific measures aimed at symptomatic relief are appropriate, the effective management of chronic diarrhoea requires an etiologic diagnosis and specific therapy. Simply suppressing symptoms without identifying a cause may delay identification of a serious underlying condition (e.g., colon cancer or inflammatory bowel disease). Empiric trials are limited to use in diagnosis (see above).
Many causes are treatable. For example, exacerbations of inflammatory bowel disease respond to steroids and sulfasalazine; collagenous and lymphocytic forms appear to benefit from a course of bismuth subsalicylate. Malabsorption associated with pancreatic insufficiency improves with the use of enzyme supplements. Steatorrhea caused by sprue responds to a gluten-free diet, but not all patients repond to the dietary change because often a concurrent contributing factor is present. Lactase deficiency requires limitation of milk products or the use of exogenous lactase. The dumping syndrome can be controlled with small feedings. Persistent pseudomembranous colitis is an indication for antibiotic therapy (see above). Cessation of surreptitious laxative abuse cures the diarrhoea that accompanies it. In the setting of irritable bowel syndrome, a high-fiber diet is indicated if the clinical picture is predominantly one of constipation interspersed with brief episodes of diarrhoea, but if diarrhoea predominates, loperamide can be useful for symptomatic relief.
Chronic Diarrhoea of Unknown Etiology. For patients whose condition remains undiagnosed after an extensive workup yet who appear otherwise well, a trial of therapy for irritable bowel syndrome is reasonable. Many such patients with unexplained diarrhoea turn out to have a bowel motility disorder and associated psychosocial stresses. Clues to the diagnosis include an absence of weight loss, normal findings on laboratory studies, and a suggestive psychosocial history. Failure to respond after 4 weeks of management should lead to a gastroenterologic consultation. One should not resort to nonspecific antidiarrhoeal agents to treat patients who have not been given a diagnosis.
Admission. Most patients with diarrhoea can be managed on an outpatient basis. However, for those who are unable to maintain their hydration orally and become significantly volume-depleted (with postural hypotension), hospital admission and parenteral fluid replacement must be seriously considered. Sometimes, several hours of IV fluids given in the emergency department will suffice and obviate an admission. Infants, elderly persons, and persons with chronic or debilitating illnesses such as diabetic renal failure are particularly vulnerable to the complications of volume depletion and warrant close monitoring. Patients with inflammatory diarrhoea manifested by bloody, purulent stools and fever are also candidates for admission, as are those with neurologic deficits and meningeal signs following a diarrhoeal illness, who require assessment for listeriosis. Patients with undiagnosed chronic diarrhoea may benefit from the observation and testing possible only during hospitalization.
Referral to a gastroenterologist is indicated for patients who have complicated acute disease (e.g., hemorrhagic diarrhoea), poorly controlled inflammatory bowel disease, undiagnosed chronic diarrhoea, or who require colonoscopy or intestinal biopsy.
Because most cases of acute diarrhoea are self-limited, the patient with no evidence of serious underlying pathology can be reassured and advised to concentrate on maintaining hydration. The sugar and electrolyte preparations described in this Chapter are easy to take and should be encouraged. Many people think that taking fluids will seriously worsen their diarrhoea, and they request opiates or antibiotics; the proper role for such agents needs to be reviewed and their unrestricted use should be limited. Many ask if kaolin and pectin preparations are helpful; there is no evidence that they alter symptoms or the course of the illness, but neither are they harmful. Although antibiotics have been in vogue for prophylaxis of traveler’s diarrhoea, patients should be informed of the emergence of resistant strains, the potential complications of antibiotic use, and the efficacy of bismuth preparations. A few bottles of a bismuth preparation (e.g., Pepto-Bismol), a few tablets of diphenoxylate for “emergencies,” and advice to use bottled water and avoid foods likely to be contaminated (e.g., raw vegetables washed with local water) represent reasonable alternatives to antibiotic prophylaxis. Patients with chronic undiagnosed diarrhoea need to be prepared for a potentially extensive evaluation. In the meantime, advice on perianal care is much appreciated and ought not to be overlooked while investigation proceeds.
Perianal Hygiene. Much can be done to relieve the perianal discomfort that accompanies severe, unrelenting diarrhoea. Sitz baths for about 10 minutes two or three times a day can be soothing, followed by gentle drying with absorbent cotton (not toilet paper or towels). Washing with warm water on absorbent cotton after each bowel movement is also helpful in lieu of using toilet paper, which can be irritating. Also important is avoidance of soap. Desitin may be effective, and a short course of hydrocortisone cream may be useful when considerable anal inflammation is present. Some patients report that cleaning gently with cotton pads soaked in witch hazel (Tucks) provides considerable relief. Ointments containing topical anaesthetics should be avoided; they can be irritating in themselves.
Recovery Phase. After resolution of diarrhoea, it is best to avoid milk and dairy products for approximately another 7 to 10 days because mild lactose intolerance commonly accompanies many cases. The best foods to begin eating are easily digested, high-carbohydrate substances such as bananas, rice, baked potato, and apple sauce. Continued repletion of fluid is important