section epub:type=”chapter” id=”c0015″ role=”doc-chapter”> After studying this chapter, the student should be able to: Normally, about 100 to 200 g of fecal material is passed each day. The feces consist of undigested foodstuffs (e.g., cellulose), sloughed intestinal epithelium, intestinal bacteria, GI secretions (e.g., digestive enzymes), bile pigments, electrolytes, and water. Because of the slow movement of fecal material in the large intestine, it normally takes 18 to 24 hours for the contents presented to it by the small intestine to be excreted as feces. The function of the small intestine includes the digestion and absorption of foodstuffs, whereas the principal function of the large intestine is the absorption of water, sodium, and chloride. Approximately 9000 mL of fluid enters the GI tract from food, water, saliva, gastric secretions, bile, pancreatic secretions, and small intestinal secretions. Only 500 to 1500 mL actually enters the large intestine each day, however, with a final excretion of only about 100 mL of fluid in normal feces. Because the large intestine has a limited ability to absorb liquid (up to about 4000 mL), a volume of fluid presented to it that exceeds this capacity causes watery stools (diarrhea). Similarly, if water absorption is inhibited, or if inadequate time is allowed for the absorption process, diarrhea results. In contrast, stationary bowel contents (or decreased intestinal motility) permit increased water absorption, resulting in constipation. Fecal specimens from constipated individuals are typically small, hard, often spherical masses (scybala) that are often difficult and painful to pass. Fermentation by intestinal bacteria in the large intestine results in the production of intestinal gas or flatus and is normally produced at a rate of about 400 to 700 mL/day. Some carbohydrates are not digested completely by intestinal enzymes (e.g., brown beans) and are readily metabolized by intestinal bacteria to produce large amounts of gas. Increased gas production and its incorporation into the feces can result in foamy and floating stools. Although these stools can be normal, they are often produced by patients with lactose intolerance and steatorrhea. Diarrhea is defined as an increase in the volume, liquidity, and frequency of bowel movements compared to an individual’s normal bowel movement pattern. The mechanisms that cause diarrhea can be classified into three types: secretory, osmotic, and intestinal hypermotility (Table 15.1). Note that diarrhea can result from one or a combination of these mechanisms. With secretory and osmotic diarrhea, the presence of an unabsorbed solute draws and retains water in the intestinal lumen. The origin of this osmotically active solute differs. Secretory diarrhea results from increased intestinal secretion of a solute, whereas osmotic diarrhea results from the ingestion of an osmotically active solute (e.g., lactose). Table 15.1 Differentiating these two mechanisms requires a determination of the fecal osmolality, fecal sodium, and fecal potassium levels. Using the fecal sodium and potassium results, a “calculated” fecal osmolality is determined using Equation 15.1. If the osmotic gap (i.e., difference between the measured and calculated fecal osmolality) exceeds 20 mOsm/kg, the patient is experiencing osmotic diarrhea. If measured and calculated fecal osmolalities agree within 10 to 20 mOsm/kg, the patient is experiencing secretory diarrhea. Secretory diarrhea is characteristic of infestation with various enterotoxin-producing organisms. These microbes release substances that stimulate electrolyte-rich intestinal secretions. Similarly, damage to intestinal mucosal caused by drugs or disease can also cause secretory diarrhea. Osmotic diarrhea accompanies conditions characterized by maldigestion or malabsorption. Maldigestion, the inability to convert foodstuffs into readily absorbable substances, most often results from various pancreatic and hepatic diseases. With these disorders, the pancreatic digestive enzymes or bile salts needed for fat emulsification and lipase activation are deficient or lacking. The absence of other digestive enzymes, such as disaccharidases (e.g., lactase) in the small intestine, can also result in maldigestion. In contrast, intestinal malabsorption is characterized by normal digestive ability but inadequate intestinal absorption of the already processed foodstuffs. Some parasitic infestations, mucosal diseases (e.g., celiac disease [sprue], tropical sprue, ulcerative colitis), hereditary diseases (e.g., disaccharidase deficiencies), surgical procedures, and drugs can cause malabsorption and osmotic diarrhea. In summary, maldigestion and malabsorption present an abnormally increased quantity of foodstuffs to the large intestine. These osmotically active substances (i.e., the foodstuffs) cause the retention of large quantities of water and electrolytes in the intestinal lumen and the excretion of a watery stool or diarrhea. Intestinal hypermotility results in diarrhea when the transit time for intestinal contents is too short to allow normal intestinal absorption to occur. Normally, intestinal motility is stimulated by intestinal distention. Foodstuffs that are bulky, such as dietary fiber, produce a natural laxative effect because of the intestinal distention they cause. Intestinal motility can also be altered by chemicals, nerves, hormones, and emotions. Laxatives (e.g., castor oil) and parasympathetic nerve activity increase intestinal motility, whereas sympathetic nerve activity decreases intestinal motility. During secretory and osmotic diarrhea, the increased lumen fluid causes intestinal distention, thereby increasing intestinal motility and compounding the diarrheal condition. When severe, diarrhea decreases the blood volume (hypovolemia) and disrupts the acid-base balance of the body. The large fluid loss and accompanying electrolyte depletion (particularly sodium, bicarbonate, and potassium) can result in metabolic acidosis. Acute diarrhea has a sudden onset and usually resolves in less than 1 to 2 weeks; however, it may persist for up to 4 weeks. The majority of cases of acute diarrheas are resulting from toxin ingestion or infections with a variety of pathogens—bacteria, viruses, or parasites. The remaining cases are caused by medications which can be osmotically active, stimulate intestinal secretions, or damage intestinal epithelium and cause inflammation and malabsorption or maldigestion. The clinical presentation of acute diarrhea aids the health care provider in determining the cause and the treatment course to take. Based on a thorough patient history, symptoms, and a few fecal tests, diarrhea can be identified as noninflammatory or inflammatory. Table 15.2 provides an overview of acute diarrheas, including symptoms, pathogens, diarrheal mechanisms involved, and laboratory tests that can assist in differentiation. It is important to note that despite testing, 20% to 40% of acute infections remain undiagnosed.1 Because an in-depth discussion of these infections is beyond the intent and scope of this text, for more information a microbiology textbook or journal should be consulted. Table 15.2 FOBT, Fecal occult blood test. aE. coli O157:H7 is the most important enterohemorrhagic E. coli (EHEC) serotype. Chronic diarrhea lasts for more than 4 weeks and often 8 weeks or longer. It can be classified as inflammatory or noninflammatory and further characterized by the volume and appearance of the stool, see Table 15.3. Chronic bloody diarrhea is often caused by inflammatory bowel disease (IBD), such as ulcerative colitis or Crohn’s disease, whereas other inflammatory conditions such as celiac disease (celiac sprue), tropical sprue, and microscopic colitis typically present with chronic watery diarrhea. Table 15.3 Noninflammatory conditions that cause chronic diarrhea can be subcategorized by the effect of fasting on the diarrhea. When diarrhea ceases upon fasting, it suggests that malabsorption or maldigestion is the issue. This presentation is seen with various pancreatic diseases such as chronic pancreatitis and pancreatic cancer, or when there is intolerance for carbohydrates. When a carbohydrate, such as lactose, fructose, or sorbitol, cannot be metabolized and absorbed, these osmotically active solutes are retained in the intestinal tract and cause diarrhea. This occurs with various disaccharidase deficiencies, of which the most common is lactose intolerance resulting from lack of the enzyme lactase. Bacterial overgrowth in the GI tract impairs absorption of solutes by the intestinal mucosa, whereas irritable bowel syndrome (IBS) is associated with increased intestinal motility and secretion. When diarrhea persists despite fasting, the mechanism is secretory. The volume of feces excreted daily is significantly increased (2–3 times more), and patients complain that they need to get up during the night to defecate. Various hormones and hormone-secreting tumors are causes, as well as the abuse of laxatives. Diarrhea characterized by a fat content that exceeds 7 g per day is called steatorrhea and is a common feature of patients with malabsorption syndromes. This fat originates from several sources: the diet, GI secretions, bacterial byproducts of metabolism, and sloughed intestinal epithelium. Note that the amount of dietary fat ingested has a minor effect on the total quantity of fecal lipids excreted, in addition, the types of lipid (fatty acid salts, neutral fat) excreted can vary significantly from the dietary fat ingested.2 In health, the fat content of fecal material can reach 6 g daily. Steatorrhea fecal specimens are characteristically pale, greasy, bulky, spongy, or pasty and are extremely foul smelling. They vary in fluidity and may float or be foamy because of the presence of large amounts of gas within them. This latter feature is not particularly significant because normal stools may also contain gas. Differentiation of steatorrhea from diarrhea is clinically important. Although macroscopic examination of the feces can be highly suggestive of steatorrhea, some diarrheal conditions can make differentiation difficult. Therefore, to diagnose steatorrhea, a fecal fat determination is performed (see section “Chemical Examination”). Any condition that alters fat digestion or fat absorption will present with steatorrhea (Table 15.4). Table 15.4 Conditions producing steatorrhea can occur simultaneously with diarrhea. For appropriate patient management to begin, the cause of the diarrhea, steatorrhea, or both must be identified. Usually, this is achieved by following an algorithm similar to that in Fig. 15.1. Because a definitive diagnosis may not be readily apparent, a good patient history is invaluable. The patient history can provide information that directly relates to the cause of the patient’s condition (e.g., diet, environment, recent exposure or contacts). For example, following the algorithm in Fig. 15.1 to a negative stool culture rules out specific bacteria but does not exclude parasites, viruses, or other inflammatory conditions. A good patient history can reveal significant information, such as a visit to a foreign country, exposure to a contaminated water source, ingestion of herbs that can be cathartic, or recent intake of fresh oysters. Unlike urination, individuals have limited control in the timing of their fecal excretion. In addition, collecting fecal specimens is considered highly undesirable by most individuals, and it is postulated to be at least partially responsible for the high noncompliance rate (50%–90%) in collecting fecal specimens for occult blood testing observed in studies of colorectal cancer.3 In light of these facts, patient education regarding the importance of testing and proper collection of fecal specimens is of utmost importance. Verbal and written instructions should be provided to patients, along with an appropriate specimen container. Note that providing written instructions in the languages of the local ethnic communities will also aid in decreasing the unease of patients with language backgrounds other than English. Fecal specimen containers vary depending on the amount of specimen to be collected. Essentially any clean, nonbreakable container that is sealable and leakproof is acceptable. For specimen collections over multiple days, large containers such as paint cans frequently are used. Single, random collections can be placed in routine urine collection cups or other suitable containers. For some tests, the entire stool is not required for analysis, and the patient must be instructed regarding the portion of the stool to sample or transport to the laboratory. Some commercial fecal collection kits are available for the recovery of feces after they are passed into the toilet onto a sheet of floating tissue paper. These kits have greatly facilitated fecal collection by patients. After sampling a portion of the feces, the patient can flush the remainder. The type and amount of specimen collected vary with the test to be performed. Fecal analysis for occult blood, white blood cells, or qualitative fecal fat requires only a small amount of a randomly collected specimen. In contrast, quantitative tests for the daily fecal excretion of any substance usually require a 2- or 3-day fecal collection. Multiple-day collections are necessary because the daily excretion of feces does not correlate well with the amount of food ingested by the patient in the same 24-hour period. In addition, to ensure an optimum fecal specimen, dietary restrictions may be necessary before the collection (e.g., in tests for occult blood and quantitative fecal fat). Contamination of the fecal specimen with urine, toilet tissue, or toilet water must be avoided. The detection of protozoa can be adversely affected by contaminating urine, and the strong cleaning or deodorizing agents used in toilets can interfere with chemical testing. Patients must also be instructed to avoid (1) contaminating the exterior of collection containers, and (2) applying too much sample to a collection device or slide. Fecal specimens produce gas because of bacterial fermentation in vivo and in vitro. Therefore closed containers of fecal specimens should be covered with a disposable tissue or toweling and slowly opened. This covering retards spattering of fecal matter should gas buildup cause the sudden release of fecal contents when the container is opened. The macroscopic examination of feces involves visual assessment of color, consistency, and form. Other notable substances within the feces include mucus and undigested matter. The normal brown color of feces results from bile pigments. When conjugated bilirubin is secreted as bile into the small intestine, it is hydrolyzed back to its unconjugated form. Intestinal anaerobic bacteria subsequently reduce it to the three colorless tetrapyrroles collectively called the urobilinogens: stercobilinogen, mesobilinogen, and urobilinogen. These urobilinogens spontaneously oxidize in the intestine to produce the urobilins—stercobilin, mesobilin, and urobilin—which are orange-brown and impart color to the feces. With conditions in which bile secretion into the small intestine is inhibited partially or completely, the color of the feces changes. Pale or clay-colored stools, also termed acholic stools, are characteristic of these posthepatic obstructions. Be aware that similarly colored fecal specimens resulting from barium sulfate contamination can be obtained after a diagnostic procedure to evaluate GI function (e.g., barium enema). Unusual fecal colors can also be encountered after the ingestion of certain foodstuffs or medications, or as a result of the presence of blood. Table 15.5 summarizes macroscopic characteristics of feces, and Table 15.6 provides reference intervals for various tests performed. Table 15.5
Fecal Analysis
Key Terms1
Fecal Formation
Diarrhea
Type
Mechanism
Secretory diarrhea
Increased solute secretions by the intestine cause increased fluid volume sent to the large intestine; the resultant fluid volume exceeds the absorptive capacity of the large intestine.
Osmotic diarrhea
Increased quantities of osmotically active solutes remain in the intestinal lumen, causing additional secretions of water and electrolytes into the lumen; the resultant fluid volume exceeds the absorptive capacity of the large intestine.
Intestinal hypermotility
An increase in intestinal motility decreases the time allowed for the intestinal absorptive processes.
Equation 15.1
Acute Diarrhea
Duration
<2–4 weeks
Noninflammatory Acute Diarrhea
Symptoms
Large volume of stool; nausea and vomiting (varies with pathogen)
Diarrheal mechanisms
Predominantly malabsorption (osmotic) and secretory diarrhea; intestinal hypermotility
Laboratory tests
Pathogens
Epidemiology
Preformed toxins
“Food poisoning”
Viruses
Norovirus
Rotavirus
Person-to-person contact; predominantly infants (day-care centers) or elderly
Bacteria
Escherichia coli (toxigenic)
Cholera-like toxin; foreign travel
Vibrio cholerae
Contaminated water; seafood, shellfish
Parasites
Giardia lamblia
Contaminated water (drinking, swimming); foreign travel; animal-to-person contact
Cryptosporidium
Cyclospora
Contaminated produce, fresh berries
Medications
Can become chronic diarrhea if agent not discontinued
Inflammatory Acute Diarrhea
Symptoms
Normal to small volume of stool, bloody; lower abdominal cramps; tenesmus; fever
Diarrheal mechanisms
Predominantly secretory diarrhea (due to colonic invasion); intestinal hypermotility
Laboratory tests
Pathogens
Epidemiology
Bacteria
Campylobacter
Food such as undercooked poultry, unpasteurized milk; animal-to-person contact (puppies, kittens); foreign travel (Asia)
Salmonella sp.
Food such as poultry, eggs, milk, sprouts, seafood, shellfish; person-to-person contact; animal-to-person contact; foreign travel (S. typhi—Asia)
Shigella
Food such as poultry, seafood, shellfish; person-to-person contact; animal-to-person contact; foreign travel
Clostridium difficile
Hospitalization, antibiotics, chemotherapy, day-care centers
Enterohemorrhagic Escherichia coli (EHEC)a
Vibrio parahaemolyticus, Vibrio vulnificus
Food such as raw or undercooked seafood
Parasites
Entamoeba histolytica
Contaminated water (drinking, swimming); foreign travel (rare in the United States); person-to-person contact
Tapeworms
Raw or undercooked beef, pork, seafood
Medications
Gold therapy
Chronic Diarrhea
Fecal Features
Disease
Diarrheal Mechanism
Inflammatory
Ulcerative colitis
Osmotic (malabsorption)
Crohn’s disease
Osmotic (malabsorption)
Food allergy (cow’s milk, soy protein)
Osmotic (malabsorption); predominantly infants
Radiation enteritis
Osmotic (malabsorption)
Watery
Celiac disease
Osmotic (malabsorption) diarrhea decreases with fasting; increased fecal fat
Tropical sprue
Osmotic (malabsorption); diarrhea decreases with fasting
Microscopic colitis
Combined: osmotic (malabsorption) and secretory
Noninflammatory
Normal to small volume (<1 L/day); diarrhea usually ceases with fasting
Pancreatic disease: chronic pancreatitis, pancreatic cancer
Osmotic (malabsorption); increased fecal fat
Lactose intolerance (lactase deficiency), sorbitol intolerance, fructose intolerance
Osmotic (malabsorption)
Bacterial overgrowth
Osmotic (malabsorption); increased fecal fat
Irritable bowel syndrome
Secretory and intestinal hypermotility
Large volume (1–3 L/day or greater); diarrhea persists with fasting
Hormones and hormone-secreting tumors (e.g., vasoactive intestinal peptide, prostaglandin, gastrinoma, thyroid medullary cancer)
Secretory; often nocturnal diarrhea
Laxative abuse
Secretory; often nocturnal diarrhea
Steatorrhea
Type
Cause
Maldigestion
Decreased pancreatic enzymes
Pancreatitis
Cystic fibrosis
Pancreatic cancer
Zollinger-Ellison syndrome
Ileal resection
Decreased bile acid micelle formation
Hepatocellular disease (severe)
Bile duct obstruction; biliary cirrhosis
Bile acid deconjugation caused by stasis (e.g., strictures, blind loop syndrome, diabetic visceral neuropathy)
Malabsorption
Damaged intestinal mucosa
Celiac disease
Tropical sprue
Biochemical defect: abetalipoproteinemia
Lymphatic obstruction
Lymphoma
Whipple’s disease
Specimen Collection
Patient Education
Specimen Containers
Type and Amount Collected
Contaminants to Avoid
Gas Formation
Macroscopic Examination
Color
Characteristic
Cause
Color
Clay-colored or gray, pale yellow, or white
Posthepatic obstruction
Barium (ingestion or enema)
Red
Blood (from lower GI tract)
Beets
Food dyes
Drugs (e.g., BSP dye, rifampin)
Brown
Normal
Black
Blood (from upper GI tract)
Iron therapy
Charcoal ingestion
Bismuth (e.g., medications, suppositories)
Green
Green vegetables (e.g., spinach)
Biliverdin (during antibiotic therapy)
Consistency
Formed
Normal
Hard
Constipation (i.e., scybalum)
Soft
Increased fecal water
Watery
Diarrhea, steatorrhea
Form
Cylindrical
Normal
Narrow, ribbon–like
Bowel obstruction
Intestinal narrowing (e.g., strictures)
Small, round
Constipation
Bulky
Steatorrhea
Other
Foamy, floating
Increased gas incorporated into feces
Greasy, spongy
Steatorrhea
Mucus
Constipation, straining
Disease (e.g., colitis, villous adenoma)
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
Fecal Analysis
Learning Objectives
