| 10. Acute Diarrhea | page 221 |
With a complaint of "diarrhea,"
the physician must establish if this represents a change in the patient's bowel habit and
if the complaint arises from a perception of increased frequency of stool, increased
volume or both.
If the diarrhea is acute (i.e., lasting less than two weeks), the
malabsorption of fluid and electrolytes probably has an infectious or toxic cause (Table 8). When diarrhea lasts for a
longer period of time, other explanations need to be considered. In the absence of prior
gastric surgery, the four most common causes of chronic diarrhea are (1) the irritable
bowel syndrome; (2) inflammatory bowel disease; (3) malabsorption; and (4) carcinoma of
the colon. The physician also must consider altered bowel function due to drug or alcohol
abuse (see Section 11). Bacteria (toxin-mediated, cytotonic) Viruses Protozoa Parasites Associated tenesmus, urgency or a sense of
incomplete evacuation suggests involvement of the rectum or sigmoid colon. The passage of
blood, pus and mucus suggests bowel inflammation, ischemic bowel disease or cancer.
Malassimilation syndromes (discussed in the previous section) are suspect if there is
passage of food and oil droplets, or if the patient develops symptoms suggestive of
nutrient deficiency, particularly weight loss.
In Western societies, stool weight is
approximately 200 g/day. Since stools are 70-90% water, regardless of their consistency,
excess fecal water must accompany diarrheal diseases with elevated stool weight. This
concept leads directly to consideration of the mechanisms responsible for the
malabsorption or stimulated secretion of water.
Two caveats need to be remembered. First,
fecal bulk varies with the diet, being influenced most notably by the content of
indigestible carbohydrates (dietary fiber). Stools are smaller in developed countries than
they are among societies whose members regularly ingest large amounts of dietary fiber.
Second, disease of the distal colon or rectum can lead to the frequent, often painful
passage of small stools (due to limited capacity as a reservoir), yet there may be little
fecal water and no increase in stool weight. In fact, "constipation" may be
common in patients with proctitis.
Acute diarrhea is thus defined as stool weight > 200
g/day for less than 14 days' duration. It always will represent a change in bowel habit
for the individual and will often be associated with an increased frequency of bowel
movements. Most enteric infections are self-limiting
and resolve in less than two weeks. Acute bacterial diarrheas can be classified into
toxigenic types, in which an enterotoxin is the major pathogenic mechanism, and invasive
types, in which the organism penetrates the enterocyte as a primary event, although an
enterotoxin may be produced as well. Enterotoxins are either cytotonic (producing
intestinal fluid secretion by activation of intracellular enzymes, without damage to the
epithelial surface) or cytotoxic (causing injury to the enterocyte as well as inducing
fluid secretion). Three major clinical syndromes caused by bacterial infections are (1)
food poisoning, (2) infectious gastroenteritis and (3) traveler's diarrhea. 10.1.1 FOOD POISONING The food poisoning syndrome
characteristically features the development of a brief but explosive diarrheal illness in
subjects following exposure to a common food source contaminated with bacteria or
bacterial toxins. Staphylococcus aureus, Salmonella, Clostridium perfringens and Bacillus
cereus are responsible for 90% of these outbreaks.
Staphylococcus aureus produces a
heat-stable, odorless and tasteless enterotoxin that is generated in poorly refrigerated
desserts and seafoods. Ingestion of the preformed enterotoxin causes nausea, vomiting and
profuse diarrhea within 4 to 8 hours. Spontaneous resolution occurs within 24 hours. No
specific therapy is available or necessary.
Clostridium perfringens produces a preformed
toxin from spores that germinate in contaminated meats cooked to less than 50ºC. Symptoms
are diarrhea and crampy abdominal pain without vomiting, beginning 8 to 24 hours after the
meal. The illness lasts less than 24 hours. No specific therapy is indicated.
Bacillus
cereus produces either a diarrheal syndrome or a vomiting syndrome, depending upon the
enterotoxin. The vomiting syndrome is always associated with ingestion of rice and is
caused by a preformed toxin that is elaborated when rice is left to cool unrefrigerated.
Flash-frying later does not generate enough heat to destroy the toxin. The diarrheal
syndrome occurs after ingestion of the organism itself. Both illnesses are short-lived and
require no specific therapy.
The diagnosis of food poisoning is usually made by history.
Except in special circumstances (e.g., botulism), isolation of the toxin is not
cost-effective. 10.1.2 GASTROENTERITIS The organisms responsible for bacterial
gastroenteritis exert their predominant effects by invading and destroying the intestinal
epithelium or by producing various enterotoxins. 10.1.2.1
Toxin-mediated, cytotoxic bacterial gastroenteritis Vibrio cholerae is the prototypic cause of
toxigenic diarrhea. The Vibrio cholerae organisms elaborate a toxin that attaches to the
inner cell membrane and activates adenylate cyclase (formerly "adenyl cyclase").
The presence of adenylate cyclase then elevates cyclic AMP (cAMP) levels. Cyclic AMP then
stimulates the enterocyte to secrete fluid and electrolytes while at the same time
impairing their absorption. Stool output can exceed 1 L/hour. Treatment is based on
restoring fluid and electrolyte balance and maintaining intravascular volume. Even though
fluid and electrolyte transport is impaired, glucose transport is intact. Since glucose
absorption carries Na+ (and thus water with it), an oral rehydration solution containing
glucose, sodium and water will enhance water absorption during the profound dehydration
stage of cholera.
Several types of Escherichia coli (E. coli) are intestinal pathogens.
Each exerts its effects through different mechanisms (Table 9). Invasive forms of E. coli may cause colitis
that resembles colitis from other bacterial infections and also may resemble ischemia
clinically, endoscopically and histologically.
Enterotoxigenic E. coli (ETEC) colonizes the
upper small intestine after passing through the acid barrier of the stomach. The organisms
colonize the surface without penetrating the mucus layer. Like cholera, ETEC causes no
mucosal damage and no bacteremia. Two types of enterotoxins are produced by ETEC: the
heat-labile toxin (also called "labile toxin" or LT) and the heat- stable toxin
(also called "stable toxin" or ST). ETEC can elaborate LT only, ST only, or both
toxins. ST produces diarrhea by stimulating intestinal secretion through guanylate cyclase
and subsequently cyclic GMP. LT produces diarrhea by a similar mechanism, except that it
acts through adenylate cyclase and cyclic AMP. After a 24- to 48-hour incubation period,
the disease begins with upper abdominal distress followed by watery diarrhea. The
infection can be mild (with only a few loose movements) or severe (mimicking cholera).
Treatment is symptomatic. Antibiotic therapy is ineffective and favors the emergence of
resistant ETEC strains.
Vibrio parahaemolyticus causes acute diarrheal disease after
consumption of seafood: raw fish or shellfish. The common factor in most outbreaks appears
to be storage of the food for several hours without proper refrigeration. Explosive,
watery diarrhea is the cardinal manifestation, along with abdominal cramps, nausea and
vomiting. Fever and chills occur in 25% of cases. The duration of illness is short, with a
median of three days. Treatment is symptomatic; there is no role for antimicrobial
therapy.
After ingestion, Shigella dysenteriae organisms attack the colon, sparing the
stomach and small bowel. Shigella organisms adhere to the mucosal surface, penetrate the
mucosal surface, and then multiply within epithelial cells, moving laterally through the
cytoplasm to adjacent cells by filopodium-like protrusions. Shigella organisms rarely
penetrate below the intestinal mucosa and almost never invade the bloodstream. Both
attached and intracellular organisms elaborate toxic products.
Even a small inoculum of 200
organisms (as contrasted with Salmonella, which requires greater than 107 organisms) will
lead to crampy abdominal pain, rectal burning and fever associated with multiple
small-volume bloody mucoid bowel movements. Intestinal complications include perforation
and severe protein loss. Extraintestinal complications include respiratory symptoms,
meningismus, seizures, the hemolytic uremic syndrome, arthritis and rashes. Ampicillin 500
mg q.i.d. or co-trimoxazole 2 tablets b.i.d. for 5 days is the treatment of choice.
Amoxicillin, interestingly, is not effective therapy for shigellosis.
Salmonella food
poisoning has been attributed to an enterotoxin similar to that of Staphylococcus aureus,
but none has been clearly identified. Within 12 to 36 hours after ingestion of
contaminated foods (usually poultry products), there is a sudden onset of headaches,
chills and abdominal pain, with nausea, vomiting and diarrhea. These symptoms may persist
for one to four days before subsiding. Antibiotic therapy of nontyphoidal Salmonella
gastroenteritis fails to alter the rate of clinical recovery. In fact, antibiotic therapy
will increase the duration of intestinal carriage of the Salmonella and is thus
contraindicated.
Campylobacter jejuni-induced diarrhea is more common than diarrhea from
either Salmonella or Shigella. Infection is from consumption of improperly cooked or
contaminated foodstuffs. Campylobacter attaches to the mucosa and releases an enterotoxin
that destroys the surrounding epithelia. Clinically, there is often a prodrome of
constitutional symptoms along with headache and generalized malaise. A prolonged diarrheal
illness follows - often with a biphasic character, with initial bloody diarrhea, slight
improvement, then increasing severity. The illness usually lasts less than one week,
although symptoms can persist for a longer period, and relapses occur in as many as 25% of
patients. Erythromycin 500 mg q.i.d. for 7 days is optimal therapy.
Yersinia enterocolitica
is often transmitted to humans from pets or food sources. The organism invades epithelial
cells and produces an enterotoxin. Clinically, the spectrum of illness ranges from simple
gastroenteritis to invasive ileitis and colitis. This organism causes diarrheal illness
most frequently in children less than 5 years of age. Children over 5 years of age develop
mesenteric adenitis and associated ileitis, which mimic acute appendicitis. Yersinia is
less likely to cause disease in adults; if it does, the illness is an acute diarrheal
episode that may be followed two to three weeks later by joint symptoms and a rash
(erythema nodosum). Treatment is symptomatic. There is no evidence that antibiotics alter
the course of the gastrointestinal infection.
Clostridium difficile causes
antibiotic-associated colitis (Section 10.4). Certain strains of E. coli are invasive,
producing an illness indistinguishable from shigellosis. Isolates of E. coli 0157:H7 have
been identified in the stools of patients with a diarrheal illness clinically designated
as "hemorrhagic colitis." Infection has been traced to contaminated hamburger
meat obtained from a variety of sources, including large national restaurant
chains.
Ingestion of this organism results in severe crampy abdominal pain and fever,
followed within 24 hours by bloody diarrhea that lasts five to seven days. Since the
organism is shed in the stool for only a short period of time, early stool collections are
critical for the diagnosis. Treatment is symptomatic, as antibiotics do not appear to
alter the disease course. In severe cases with possible toxic megacolon, systemic
antibiotics may be in order.
Approximately 1,700 serotypes and variants of Salmonella are
potential pathogens for humans. A dose of approximately 107-109 organisms is required to
produce a clinical illness. Salmonella organisms invade the mucosa of the small intestine
and (particularly) the colon. This form of gastroenteritis produces nausea and vomiting
followed by abdominal cramps and diarrhea that lasts three to four days and then gradually
subsides. In 10% of the cases bacteremia of the Salmonella organism occurs, and in
approximately 5% there are disseminated infections to bones, joints and meninges. Certain
conditions increase the risk of salmonellosis: hemolytic anemia, malignancy,
immunosuppression, achlorhydria and ulcerative colitis. With uncomplicated Salmonella
gastroenteritis, treatment is symptomatic. In fact, antibiotic therapy increases the
duration of intestinal carriage of these organisms. Patients with complicated Salmonella
gastroenteritis (e.g., those with predisposing conditions or sepsis, or who are very young
or very old) should be treated with ampicillin or co-trimoxazole.
TABLE 8. Common causes of
acute diarrhea
Drugs
Laxatives
Antacids
Antibiotics
Cholinergic drugs
Lactose
Guanethidine
Quinidine
Digitalis
Colchicine
Potassium supplements
Lactulose
Enterotoxigenic Escherichia coli
(both heat-labile and heat-stable toxins)
Vibrio cholerae
Vibrio parahaemolyticus
Clostridium perfringens
Bacillus cereusBacteria (toxin-mediated,
cytotoxic)
Clostridium difficile
Staphylococcus aureus
Shigella dysenteriae
Campylobacter jejuni
Yersinia enterocolitica
Bacteria (invasive)
Salmonella
Enteroinvasive Escherichia coli
Bacteria (unknown mechanism)
Enteropathogenic Escherichia coli
Enteroadherent Escherichia coli
Parvovirus (Norwalk agent)
Reovirus (rotavirus)
Cryptosporidia
Giardia lamblia
Entamoeba histolytica
Strongyloides
Trichuris
10.1 Bacterial
Diarrhea
page 223
TABLE 9.
Types of Escherichia coli intestinal pathogens
Name
Toxin
Mechanism
Enteropathogenic
(EPEC)
Shiga-like toxin
Adherence
Enterotoxigenic
(ETEC)
Labile toxin (LT)
Stable toxin (ST)Activates adenylate
cyclase
Activates guanylate cyclase
Enteroinvasive (EIEC)
Shiga-like toxin
Penetrates epithelium
Enteroadherent (EAEC)
-
Adherence
Enterohemorrhagic
(EHEC)
Shiga-like toxin
(verotoxin)
Unknown
Enterohemorrhagic E. coli-induced diarrhea tends to occur in neonates and young children. Only occasionally does it affect older children and adults. The pathogenic mechanism of this diarrhea is unclear; adherence of the organism to the intestinal epithelial cell seems to cause intestinal damage. There is no indication for specific treatment except for neonates in a nursery epidemic. In this case, oral nonabsorbable aminoglycosides should be used.
10.1.3 TRAVELER'S DIARRHEA
Traveler's diarrhea is a syndrome characterized by an increase in frequency of unformed bowel movements, typically four to five loose stools per day. Associated symptoms include abdominal cramps, nausea, bloating, urgency, fever and malaise. Traveler's diarrhea usually begins abruptly, during travel or soon after returning home, and is generally self-limiting, lasting three to four days. Ten percent of cases persist longer than one week, approximately 2% longer than one month and very few beyond three months. Enterotoxigenic E. coli (ETEC) is the most common causative agent of traveler's diarrhea. These organisms adhere to the small intestine, where they multiply and produce an enterotoxin that causes fluid secretion and hence diarrhea. Salmonella gastroenteritis, Shigella dysentery, and viral enteric pathogens (rotavirus and Norwalk-like virus) are less common causes of traveler's diarrhea.
Since traveler's diarrhea is usually mild and self-limiting, with complete recovery even in the absence of therapy, therapy should be considered optional (Table 10).
TABLE 10. Traveler's diarrhea: recommendations for treatment
General
Avoid ice cubes, raw vegetables and fruits, raw fish and shellfish, unrefrigerated food.
Drink canned pop and beer, boiled water.
Drink oral replacement solutions for acute attacks.
Avoid over-the-counter preparations sold locally for acute attacks.
Specific To decrease severity of acute attack:
To provide symptomatic relief of acute attack:
Prophylaxis:
Not recommended except for persons who are immunosuppressed or suffer chronic illness. If
indicated, then:
The value of prophylaxis for travelers is unclear. Bismuth preparations are helpful, but their use is limited by the large volumes necessary and by their taste. Antibiotic prophylaxis can reduce the likelihood of developing diarrhea, but carries its own risks.
| 10.2 Viral Gastroenteritis | page 229 |
At least two groups of viruses are capable of producing an acute diarrheal illness.
10.2.1 NORWALK VIRUS
The Norwalk virus causes a self-limiting syndrome that affects children and adults, mainly in winter. An incubation period of 24 to 48 hours is followed by a variable combination of fever, anorexia, nausea, vomiting, myalgia, abdominal pain and diarrhea. Spontaneous recovery occurs two to three days later. Immune electron microscopy of fecal filtrates demonstrates a characteristic 27 nm viral particle (the Norwalk agent). No specific treatment is available. The vomiting represents delayed gastric emptying; there are no morphologic features of gastritis.
10.2.2 ROTAVIRUSES
Rotaviruses are the most common causes of acute nonbacterial gastroenteritis in infancy and childhood. Rotaviruses invade mucosal epithelial cells. The resulting illness is more severe than that caused by the Norwalk virus. Rotavirus infection commonly requires hospital admission and intravenous fluids. Infection occurs mainly in children from 6 to 24 months old, and almost always in winter. Virus excretion is maximum three to four days after the onset of symptoms and disappears after a further three to four days. The stability of the virus and the large number of viral particles excreted make environmental contamination inevitable, with a high risk of secondary infection in susceptible contacts. For example, 20% of the rotavirus infections diagnosed in pediatric hospitals are acquired in the hospital. Most older children and adults have antibodies to rotaviruses, so any subsequent infection is generally mild.
| 10.3 Parasitic Enteritis | page 229 |
The parasites that infect the intestine may be divided into three broad groups. These include protozoa, roundworms and flatworms. The flatworms may be further divided into cestodes (tapeworms) and trematodes (flukes). This chapter will focus upon only a few relevant protozoa.
10.3.1 GIARDIA LAMBLIA
Giardia lamblia is endemic in many areas of the world, including Canada. Some patients with giardiasis present with an abrupt, self-limiting illness that develops one to three weeks after infection and lasts three to four days. Others may develop chronic and episodic diarrhea associated with bloating and, at times, steatorrhea and a malabsorption syndrome clinically like celiac disease. Diagnosis is made by recovery of the organism; it is found in the stool of approximately 50% of patients and in 90% of histologically examined smear preparations obtained from small bowel biopsy specimens (Figure 16A, B). The treatment of choice in both asymptomatic and symptomatic patients is metronidazole 250 mg t.i.d. for 7 days. Repeat therapy will occasionally be needed to totally eradicate the organism. Quinacrine 100 mg t.i.d. for 7 days also is effective.
10.3.2 AMEBIASIS
This is an acute and chronic disease caused
by the organism Entamoeba histolytica. Although there are numerous species of ameba that
inhabit the human intestinal tract, E. histolytica seems to be the only variety that is
pathogenic for humans. Its manifestations vary from the asymptomatic carrier state to a
severe fulminating illness with mucosal inflammation and ulceration. Asymptomatic patients
harbor only cysts in their stools and have no evidence of tissue invasion. Since the cysts
are resistant to the outside environment, the disease can be transmitted by individuals
unaware of their infective potential. This is in contrast to patients with acute or
chronic invasive disease, who harbor a trophozoite that cannot survive outside the
host.
The acute illness is characterized by diarrhea with the passage of blood and mucus,
and by variable degrees of abdominal pain. In its most severe form it may mimic
fulminating ulcerative colitis and may progress to a toxic dilation (toxic megacolon) and
perforation of the colon. During the acute illness, trophozoites may be recovered in the
stool, from biopsies of shallow ulcers in the rectum, or from smears of rectal
mucus.
Chronic infectious features may develop many years after the patient has left an
endemic area. Patients present with nonspecific bowel complaints and may show radiologic
changes in the distal small bowel and colon that mimic Crohn's disease, cancer or
tuberculosis. Diagnosis necessitates recovering trophozoites from the stool. As an
adjunct, the indirect hemagglutination test can help detect patients with invasive
disease.
Intestinal complications of amebiasis include massive intestinal hemorrhage, which
is rare; ameboma formation in any part of the colon, which may lead to obstruction or
intussusception; permanent stricture formation during the healing stage; and
postdysenteric colitis, which usually resolves over several weeks or months without
specific therapy.
Systemic dissemination of the ameba may involve other organs, such as the
brain, lung, pericardium and liver. Liver abscess is the most common extraintestinal
infection by the ameba.
Therapeutic agents used for the treatment of amebiasis act at
selected sites: intraluminally, intramurally or systemically. Treatment must therefore be
individualized to the location of the disease. Asymptomatic carriers are treated with
iodoquinol 650 mg t.i.d. for 20 days; this effective agent acts against amebas located
intraluminally. Acute or chronic intestinal disease is treated with metronidazole 750 mg
t.i.d. for 10 days. However, because metronidazole is less effective against organisms
within the bowel lumen, iodoquinol (650 mg t.i.d. for 20 days) must be added.
10.3.3 CRYPTOSPORIDIA
Cryptosporidia are a genus of protozoa
classified within the subclass Coccidia. Cryptosporidia infection has been recognized as a
diarrheal disease in humans only since 1979. In immunocompetent persons it presents as a
transient, self-limiting diarrheal state lasting from one to seven days. Adults are less
commonly affected than young children. In most, the illness is mild and medical help is
not sought. With immunological incompetence (e.g., AIDS, neoplasia, hypogammaglobulinemia
or concurrent viral infection), a persistent chronic watery diarrhea may occur. Diagnosis
is made by demonstrating Cryptosporidia oocysts in the stool or, better still, by mucosal
biopsy and examination of the microvillus border for embedded Cryptosporidia oocysts (Figure 17).
A successful treatment for Cryptosporidia
has not yet been found. Spiramycin and hyperimmune bovine colostrum remain experimental. Since almost every drug can cause diarrhea,
the first question to ask a patient is "What medications, both prescribed and
over-the-counter, are you currently taking?" Discontinuing the drug is often the only
therapeutic move required in nonantibiotic diarrhea; even in patients with
antibiotic-associated diarrhea, with or without colitis, this may be the only step
necessary. Although many drugs can cause diarrhea, little is understood about the ways in
which they do so. The common causes of drug-induced diarrhea with pathogenic mechanisms
follow. 10.4.1
ANTIBIOTIC-ASSOCIATED DIARRHEA AND PSEUDOMEMBRANOUS COLITIS Antibiotics are the most common cause of
drug-induced diarrhea. In many cases, the condition is self-limiting. The development of
pseudomembranous colitis (PMC) in association with antibiotics may be a serious and
sometimes life-threatening condition.
PMC secondary to antibiotics was first recognized
during the 1950s. Initially, it was thought to be caused by overgrowth with Staphylococcus
aureus, but later research revealed that the colitis was usually caused by an enterotoxin
produced by Clostridium difficile.
PMC can follow virtually any antibiotic use. It may
occur months after antibiotic exposure, and may rarely occur without a past history of
antibiotic use. The frequency of diarrhea or colitis does not appear to be related to dose
or route of administration. Symptoms can occur while the patient is on the antibiotic or
within six weeks following its discontinuation. Only increasing age is clearly
identifiable as a risk factor. The diarrhea is usually loose with a blood-streaked mucus.
Frank bleeding is uncommon. The diarrhea can be devastating, with up to 30 bowel movements
in a 24-hour period. The diarrhea may be associated with varying degrees of abdominal pain
and low-grade fever. Depending on the severity of the diarrhea and the amount of fluid
loss, hypotension, shock and even death have been reported. In many patients the problem
is self-limiting and resolves spontaneously with discontinuation of the antibiotic.
Further investigation is required in those patients who have severe diarrhea associated
with systemic symptoms and those whose diarrhea persists despite discontinuing the
implicated antibiotic.
An accurate history is usually sufficient to suggest the diagnosis
of PMC, and a sigmoidoscopy may be all that is required for confirmation. The presence of
copious amounts of mucus and typical raised white pseudomembrane plaques are
characteristic features on sigmoidoscopy. Biopsies help confirm the diagnosis (Figure 18A, B). The distal
colon is involved in most cases so that sigmoidoscopy is usually adequate. Lesions may be
restricted to the right colon, necessitating colonoscopy.
Isolation of C. difficile plus
toxin in the stools provides the diagnosis. If it is certain that there can be no other
cause for the diarrhea, treatment can be undertaken while awaiting assay results.
Treatment depends upon the condition of the patient. If symptoms are resolving with
discontinuance of the antibiotic, no further therapy may be indicated. In mild cases,
metronidazole 250 mg p.o. t.i.d. for 14 days is effective. In severe hospitalized cases
the drug of choice is vancomycin 125 mg p.o. q.i.d. for 14 days. Vancomycin is poorly
absorbed and central nervous system and renal toxic effects are uncommon. The high cost of
this medication limits its use, even though the eradication rate is quite high. If oral
therapy cannot be used, as with severe ileus or recent surgery, parenteral metronidazole
is preferred. Some 20% of treated patients will have a recurrence of symptoms, PMC or C.
difficile, usually within 4 to 21 days of stopping treatment. In this case, another course
of metronidazole or vancomycin should be given. Cholestyramine (Questran®) binds the
toxin and can provide symptomatic relief even though it will not eliminate the
microorganism. 10.4.2
MAGNESIUM-CONTAINING ANTACIDS Usually, the osmotic diarrhea produced by
Mg++ is mild; it may even be welcomed by previously constipated patients. A change to a
magnesium-free aluminum-containing antacid is all that is required to control the
situation in some. (Magnesium can be used to induce diarrhea by the rare patient with the
Münchausen syndrome seeking medical attention for self-induced problems.) 10.4.3 ANTIARRHYTHMIC
DRUGS The antiarrhythmic drugs most commonly
associated with diarrhea include quinidine, procainamide and disopyramide. The mechanism
involved is unknown. Changing the antiarrhythmic drug may halt the diarrhea. 10.4.4 OTHER
MEDICATIONS Colchicine, often administered for acute
gout, produces diarrhea as a common side effect. It resolves with discontinuance of the
medication. The mechanism of the diarrhea is unknown, but may relate to an intestinal
cytotoxic effect of colchicine. Antimetabolites (e.g., methotrexate) often cause diarrhea
as a result of damage to the small or large bowel mucosa. This type of diarrhea can be
devastating and difficult to control. Except for rehydration and stopping the drug, little
can be done.
10.4 Drug-Related
Diarrhea
page 231
