Introduction and Epidemiology
This chapter discusses the general assessment of patients with diarrhea and the special considerations of acute infectious and traveler’s diarrhea, Clostridium difficile diarrhea and colitis, inflammatory bowel disease, ileitis and colitis, and ulcerative colitis.
Acute diarrhea is the sudden onset of an increase in the normal water content of stool. In general, humans lose approximately 10 mL/kg/day of fluids in stool. The increased water content of diarrhea results in an increased frequency of stools from 3 or more times daily to more than 20 bowel movements in a 24-hour period. Diarrhea is an increased frequency of defecation, usually greater than 3 bowel movements per day for a daily stool weight exceeding 200 grams.1,2 Practically speaking, however, diarrhea is present when the patient is making more stools of lesser consistency more frequently.
There are four basic mechanisms of diarrhea: increased intestinal secretion, decreased intestinal absorption, increased osmotic load, and abnormal intestinal motility. Normally, the jejunum receives between 6 and 8 L per day of fluid in the form of oral intake and gastric, pancreatic, and biliary secretions. Dietary intake actually constitutes a small portion of the jejunal load (1.5 L). A healthy small intestine absorbs nearly 75% of the fluid to which it is exposed. The 2 L of fluid not absorbed by the small intestine then enters the colon, where fluid is absorbed at an even higher rate. The absorptive power of the colon approaches 90% efficiency and far exceeds that of the small intestine. In fact, the colon can make up for a decrease in small intestinal absorption. Under normal conditions, very little fluid (<100 mL) is lost in the stool each day.3
In diarrheal states, normal intestinal physiology is disrupted. At a cellular level, intestinal absorption occurs through the villi, and secretion occurs through the crypts. Fluids are absorbed by two mechanisms: passively with the transport of sodium and actively with the absorption of glucose. Selected enterotoxins block the passive sodium resorption and specifically stimulate sodium excretion, resulting in a net loss of fluid. The glucose-dependent mechanism of water absorption, however, is unaffected by these toxins and can be exploited by including glucose in the rehydration treatments. The composition of oral rehydration therapies recommended by the World Health Organization is based largely on this physiology. In addition, diarrheal states, enterotoxins, inflammation, or ischemia disrupt the structure of the intestinal villi preferentially with less involvement in the crypts. As a result, diarrhea occurs because of diminished intestinal villi absorption and unopposed crypt secretion (the crypts are more resilient after injury).4
Another mechanism by which disease processes cause diarrhea is by the delivery of an osmotic load to the intestine. For example, administration of a laxative results in the collection of an osmotically active, nondigestible agent within the intestinal lumen. Other substances such as diet products and medications (e.g., colchicine) have similar effects. Osmosis occurs, drawing fluid into the intestinal lumen, and results in diarrhea. Increased intestinal motility also causes diarrhea. This mechanism is responsible for diarrhea in patients with irritable bowel syndrome, neuropathies, or a shortened intestine secondary to surgery.
Diarrheal illness is primarily a viral infection (norovirus), but can also be caused by bacteria and parasites. Antibiotic and nosocomial diarrhea is most often caused by C. difficile. Many drugs affect gastrointestinal function. Erythromycin accelerates gastric emptying. Clavulanate stimulates small bowel motility. Other drugs that cause diarrhea are laxatives, sorbitol, lactose, nonsteroidal anti-inflammatory drugs, and cholinergics. Inflammatory bowel disease, ulcerative colitis, and Crohn’s disease are characterized by diarrhea. If patients have fecal evidence of inflammation and Shigella, Salmonella, Campylobacter, C. difficile, or Entamoeba histolytica have been excluded, suspect inflammatory bowel disease. Less common causes of severe diarrhea include gastrointestinal bleeding, thyrotoxicosis, toxin exposure, and mesenteric ischemia, which are addressed elsewhere in the text.
After confirming a diarrheal illness, focus on identifying the cause. Determine whether the diarrhea is acute (<3 weeks) or chronic (>3 weeks). The acute diarrheas are of greatest concern to the emergency physician as they are more apt to be a manifestation of an immediately life-threatening illness (infection, ischemia, intoxication, or inflammation).2 In the United States, most infectious diarrheal illnesses are caused by noroviruses or rotaviruses and occur in the winter.5
Ask directed questions to characterize the diarrhea: Is the diarrhea bloody or melenic? Is it associated with possible food poisoning or the ingestion of certain foods, such as milk or sorbitol? Does it resolve or persist with fasting? If so, this can indicate an osmotic or secretory diarrhea, respectively. Are the stools of smaller volume, localizing to the large intestine, or of larger volume, indicating small intestine pathology? What symptoms accompany the diarrhea? Is there fever or abdominal pain, which may suggest diverticulitis, infectious gastroenteritis, or inflammatory bowel disease? Seizures accompanying diarrhea often point toward shigellosis but could also indicate theophylline toxicity or hyponatremia. Does the patient have heat intolerance and anxiety, suggesting thyrotoxicosis, or paresthesias and reverse temperature sensation, suggesting ciguatera poisoning?
Next, define the host by obtaining the medical and surgical history. The differential diagnosis for diarrhea is broadened if the patient is immunocompromised. Is the patient taking medication that may cause diarrhea? Has the patient recently traveled outside the United States or to a rural area? Rural hiking places the patient at risk for Giardia, particularly if water-purification procedures were not strictly followed, and travel to third-world countries increases the chances of parasitic infection and traveler’s diarrhea. A patient’s occupation may be a clue to a diagnosis of organophosphate poisoning.
Some examination findings helpful for diagnosis include thyroid enlargement, masses, oral ulcers, erythema nodosum, episcleritis, or an anal fissure, which would point toward inflammatory bowel disease. Reiter’s syndrome, the triad of arthritis, conjunctivitis, and urethritis or cervicitis, should cause concern for Salmonella, Shigella, Campylobacter, or Yersinia infection.
Abdominal and rectal examinations are critical. Especially in the elderly, fecal impaction may result in diarrhea as liquid stool passes around the impaction. Pay attention to the presence or absence of surgical scars, tenderness, masses, or peritoneal signs. Check the stool for blood, because bloody diarrhea can be caused by inflammation, infection, or ischemia. An elderly patient with bloody diarrhea and abdominal pain out of proportion to the physical examination may have mesenteric ischemia—a true emergency.
Diagnostic Stool Evaluation
Diagnostic testing is rarely immediately helpful in the ED, but it can be helpful at patient follow-up. Since most diarrheal illnesses are self-limited, viral, or last less than 24 hours, most patients who present within 24 hours of onset need no microbiologic examination. Patients who have severe abdominal pain, fever, and diarrhea that is voluminous, purulent, or bloody may have acute infectious diarrhea associated with the following pathogens: Salmonella, Campylobacter, Shigella, shiga toxin-producing Escherichia coli, Yersinia, Vibrios, or C. difficile. 5 Patients fitting this subset will require microbiologic evaluation, as described next.
When applied to a stool sample, Wright’s stain allows detection of fecal leukocytes. A positive Wright’s stain has a sensitivity of 52% to 82% and a specificity of 83% for the presence of bacterial pathogens by stool culture.6 Historically, Wright’s stain for fecal leukocytes has been used to differentiate invasive from noninvasive infectious diarrheas. In the past, this was an important distinction: physicians were reluctant to prescribe antibiotics for patients with infectious diarrhea because of the fear of prolonging the Salmonella carrier state. They therefore reserved antimicrobial treatment for the toxic patients who they felt truly had invasive diarrhea. Many physicians now treat patients with diarrheal illness with antibiotics regardless of whether or not the diarrhea is invasive or bacterial in origin.7
Bacterial stool culture is expensive and labor intensive and plays a minor role in the ED evaluation of diarrhea. The diagnostic yield of stool cultures is probably <5%, unless there is careful patient selection.1 Obtain stool cultures for bacteria in ill children; toxic, dehydrated, or febrile patients; patients with a diarrheal illness >3 days; patients with blood or pus in the stool; and the immunocompromised. For systemic illness, fever, or bloody stools, test for Salmonella, Shigella, Campylobacter, Shiga toxin-producing E. coli, or amoebic infection.1,4,5 Many laboratories culture for only three common bacterial pathogens: Salmonella, Shigella, and Campylobacter. If other enteric pathogens are suspected, notify the laboratory so that appropriate testing may be performed.
Ova and Parasite Evaluation
Suspect parasitic infection and evaluate stool for ova and parasites in travelers exposed to untreated water and those presenting with diarrhea for more than 7 days. Stool tests for ova and parasites lack sensitivity, because many parasites are fastidious, and shedding of the organisms is intermittent. Multiple samples may need to be collected for a positive result. Direct immunofluorescence staining improves the sensitivity for detecting Giardia and Cryptosporidium.8
Clostridium difficile Toxin Assay
C. difficile infection is the commonest cause of antibiotic-associated or nosocomial diarrhea. Diagnosis is by the C. difficile toxin assay. Unfortunately, this assay has a 10% false-negative rate, and the turnaround time on the test approaches 24 hours.9
If diarrhea is not infectious in origin, data acquisition should be dictated by the differential diagnosis. Severely dehydrated patients need serum electrolyte and renal function measurements. Serum drug levels can assist the physician in making the diagnosis of theophylline, lithium, or heavy metal intoxication. In patients with a history of abdominal surgery, abdominal films may help rule out partial obstruction as a cause of diarrhea. A chest radiograph may help diagnose Legionella pneumonia in a patient with diarrhea and a cough. For patients in whom mesenteric ischemia is suspected, obtain a serum lactate, IV contrast CT scan, or mesenteric angiography.
Severely dehydrated patients need IV hydration. Oral rehydration with a glucose-based electrolyte solution can be initiated in patients without associated nausea or vomiting and without severe dehydration. Glucose-containing, caffeine-free beverages are the fluids of choice. The glucose transport mechanism is unaffected by enterotoxins, allowing for water absorption in the small intestine. For patients who can afford to buy it, Gatorade® is a good rehydration choice for patients with mild dehydration. The World Health Organization recommends a solution with a higher sodium concentration for more extensive dehydration. Mildly dehydrated patients should aim to drink 30 to 50 mL/kg over the first 4 hours. For moderate dehydration, patients should drink 100 mL/kg over the next 4 hours.2
Counsel patients to avoid caffeine, which stimulates gastric motility, and sorbitol-containing chewing gum or raw fruits, which can worsen osmotic diarrhea. Initially, avoid lactose until the colonic villi are able to recover and produce the necessary digestive enzymes. Encourage patients to attempt early solid food intake, but with the previously mentioned restrictions, because eating expedites the recovery from diarrheal illnesses.10