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03 GI AND HEPATOLOGY > Ddx: Diarrhea > Flashcards

Flashcards in Ddx: Diarrhea Deck (49):
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Diarrhea

Diarrhea is defined as more than three loose stools per day.

Many patients confuse true diarrhea with three other conditions: pseudodiarrhea (the frequent passage of small volumes of stool), fecal incontinence, and overflow diarrhea caused by fecal impaction. 

Acute diarrhea is present for less than 14 days, persistent diarrhea has been present for at least 14 days but 4 weeks or less, and diarrhea is considered to be chronic if it has been present for more than 4 weeks.

Although the vast majority of episodes of acute diarrhea are caused by viruses and are self-limited, further clinical evaluation is indicated in those who have bloody stools, body temperature greater than 38.5°C (>101.3°F), significant abdominal pain, severe diarrhea causing symptomatic dehydration, recent antibiotic use, a history of inflammatory bowel disease, or immunocompromised states; food handlers; the elderly; or pregnant women.

Because most episodes of diarrhea are self-limited, diagnostic testing generally is reserved for patients with severe diarrheal illness characterized by fever, blood in the stool, or signs of dehydration (weakness, thirst, decreased urine output, orthostasis) or patients with diarrhea lasting >7 days.

 

 

 

 

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Causes of Noninfectious (Chronic) Diarrhea:

Frequent, high-volume, watery stools suggest a disease process affecting the small intestine. Whereas high-volume diarrhea that is exacerbated with eating and relieved with fasting or a clear liquid diet suggests carbohydrate malabsorption, persistent or nocturnal diarrhea suggests a secretory process. The presence of persistent, severe or aching abdominal pain suggests an invasive process associated with inflammation or destruction of the mucosa. Oral ulcers and arthritis could indicate IBD. Skin findings, when present, may provide significant diagnostic clues. For example, flushing may indicate carcinoid syndrome, dermatitis herpetiformis (grouped, pruritic, erythematous papulovesicles on the extensor surfaces of the arms, legs, central back, buttocks, and scalp) may occur in patients with celiac disease, and erythema nodosum or pyoderma gangrenosum.  may suggest underlying inflammatory bowel disease. Bloody diarrhea typically indicates an invasive process with loss of intestinal mucosal integrity. An oily residue or evidence of undigested food in the toilet bowl is more suggestive of malabsorption, which can be seen in pancreatic insufficiency or malignancy.

Tx: Symptoms may be controlled with stool-modifying agents (eg, fiber, psyllium), opiate-based medications (loperamide), bile acid–binding agents (cholestyramine), and bismuth-containing medications.

Medications

Carbohydrate intolerance

Irritable bowel syndrome (diarrhea predominant)

Inflammatory bowel disease (ulcerative colitis, Crohn disease)

Microscopic colitis

Celiac disease

Pancreatic insufficiency

Enteral feedings

Dumping syndrome

Small bowel bacterial overgrowth

Bile acid malabsorption

Bile acid deficiency

Radiation exposure

Whipple disease

Common variable immune deficiency

Factitious diarrhea

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Medications

Acarbose, antibiotics, antineoplastic agents, magnesium-based antacids, metformin, misoprostol, NSAIDs, proton pump inhibitors, quinidine

Withhold suspected medications

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Carbohydrate intolerance

Presence of poorly absorbed solutes in the lumen of the gut (eg, lactose)

Lactose or fructose intake, use of artificial sweeteners (sorbitol, mannitol), bloating, excess flatus

Diet history may reveal large quantities of indigestible carbohydrates 

Dietary exclusion, hydrogen breath test, stool osmotic gap

Dx:

Qualitative fecal fat (Sudan stain): Sensitivity >90% for significant steatorrhea

Quantitative fecal fat (48- or 72-h collection): Values >10 g/24 h indicate fat malabsorption

A fecal fat study is usually indicated for evaluating a patient with noninvasive diarrhea. However, test results are valid only if the patient ingests an adequate amount of dietary fat (>100 g/d). Any cause of diarrhea may mildly elevate fecal fat values (6–10 g/24 h), but values in excess of 10 g/24 h almost always indicate primary fat malabsorption.

Stool electrolytes (sodium, potassium): Osmotic gap (290 – [2 × (stool Na+ + stool K+)]); A gap greater than 100 mOsm/kg (100 mmol/kg) indicates an osmotic cause of diarrhea. Lactose malabsorption is the most common cause of a stool osmotic gap. 

<50 mOsm/kg (50 mmol/kg) suggests secretory diarrhea. 

Stool pH: pH <6.0 suggests carbohydrate malabsorption

Hydrogen breath test: Lactose metabolized by bacterial flora in distal small intestine releases hydrogen, which is excreted by lungs

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Irritable bowel syndrome (diarrhea predominant)

No weight loss or alarm features

Chronic bloating, abdominal discomfort relieved by bowel movement

Consider IBS in patients with a long-standing history of abdominal pain, complaints of increased mucus in the stool, and abnormal bowel habits (constipation, diarrhea, or variable bowel movements) in the absence of other defined illnesses. The presence of weight loss, blood in the stool, or nocturnal diarrhea almost always indicates that the patient does not have IBS.

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Inflammatory bowel disease (ulcerative colitis, Crohn disease)

Disruption in the mucosal barrier secondary to infection or inflammation (eg, ulcerative colitis)

Hx: Association with stress, and the pattern of alternating diarrhea and constipationBloody diarrhea, tenesmus, weight loss, anemia, hypoalbuminemia; alarm symptoms, weight loss and anemia.

Dx: Colonoscopy is the preferred initial diagnostic study, as it allows direct visualization of the colonic mucosa and terminal ileum, which may be sufficient to diagnose both ulcerative colitis and Crohn disease. Colonoscopy also enables biopsy samples to be obtained that may help distinguish which form of inflammatory bowel disease is present.

Patients with ulcerative colitis with disease extending beyond the rectum are at an increased risk of developing colorectal cancer. Based on this increased cancer risk, routine surveillance colonoscopy with biopsies every 1 to 2 years is warranted beginning 8 to 10 years after diagnosis. Because cancers associated with ulcerative colitis tend to arise from the mucosa, as opposed to the usual adenoma-cancer sequence, biopsies are taken from flat mucosa throughout the colon and are evaluated for dysplastic changes. A finding of flat, high-grade dysplasia warrants recommending colectomy because of the high rate of concomitant undetected cancer. A finding of flat, low-grade dysplasia warrants either colectomy or continued surveillance colonoscopy at more frequent intervals.

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Microscopic colitis

Chronic relapsing–remitting watery diarrhea

Hx: Sudden onset of mild crampy abdominal pain and bloody diarrhea

Dx: Normal colonoscopy, abnormal biopsy (includes collagenous colitis, lymphocytic colitis).

 

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Celiac disease

Celiac disease (gluten-sensitive enteropathy) is an immunologic response to dietary gliadins in patients who are genetically at risk as determined by the presence of HLA-DQ2 or HLA-DQ8. 

Hx: Classic symptoms include steatorrhea and weight loss, but many patients have only mild or nonspecific symptoms that often result in an erroneous diagnosis of IBS.

intolerance to wheat products 

Iron deficiency anemia is a common finding, as are associated autoimmune diseases such as Hashimoto thyroiditis and type 1 diabetes mellitus.  Patients with celiac disease may have difficulty absorbing supplemental iron and levothyroxine

Dx:

Anti Tissue transglutaminase antibody IgA (tTG IgA): Sensitivity (69%–93%), specificity (96%–100%) Patients with a positive tTG IgA antibody assay should undergo upper endoscopy with small bowel biopsy showing intraepithelial lymphocytes, crypt hyperplasia, and partial to total villous atrophy (reduced mucosal surface area).

Extraintestinal Manifestations:

Hematologic: Anemia (low iron, vitamin B12, folate), functional asplenia

Musculoskeletal: Osteopenia or osteoporosis, osteomalacia, arthropathy

Neurologic: Seizures, peripheral neuropathy, ataxia

Reproductive: Infertility, recurrent miscarriages

Skin: Dermatitis herpetiformis

Renal: Glomerular IgA deposition

Other: Enamel defects, abnormal liver chemistry tests, vitamin-deficient states

Tx: Gluten-free diet.

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Pancreatic insufficiency

Malabsorption of fat from pancreatic or bile salt insufficiency (eg, chronic pancreatitis

Hx: Steatorrhea, chronic pancreatitis, pancreatic resection, weight loss

Tests for excess fecal fat, features of chronic pancreatitis on imaging (eg, pancreatic calcification on CT)

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Enteral feedings

Osmotic diarrhea

Modify enteral feeding

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Dumping syndrome

Postprandial flushing, tachycardia

History of gastrectomy or gastric bypass surgery

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Small bowel bacterial overgrowth

Excessive bacterial colonization of the small bowel lumen

Hx: May manifest with bloating, diarrhea, and features of malabsorption.

Intestinal dysmotility (eg, systemic sclerosis), bloating, excess flatus, malabsorption

Duodenal aspirate for bacterial culture, response to empiric antibiotics, hydrogen breath testing

A clue to the presence of bacterial overgrowth is finding a low serum vitamin B12 level (bacteria bind vitamin B12and cleave it from intrinsic factor) and a high serum folate level (intestinal bacteria synthesize folate).

Hx: Common conditions that predispose patients to bacterial overgrowth include diabetes, systemic sclerosis, and surgically created blind loops (ie, gastrojejunostomy). Although the gold standard is aspiration of duodenal luminal contents for quantitative culture at the time of upper endoscopy, many clinicians first attempt a trial of empiric antibiotics to assess if the patient's symptoms improve.

Having segments of small intestine excluded from the usual stream of gastric acid, bile, and proteolytic enzymes, which all act to decrease excess bacterial growth in the small intestine, is a risk factor for bacterial overgrowth. The diarrhea in bacterial overgrowth can be from deconjugation of bile salts from the intestinal bacteria, leading to fat malabsorption, as well as from decreased disaccharidase levels, leading to carbohydrate malabsorption.

Duodenal aspirate: Quantitative bacterial culture; responds to empiric antibiotic trial

Culture of the normally sterile small intestine or carbohydrate (lactulose, glucose, or d-xylose) breath testing can be done to substantiate the diagnosis; alternatively, in some patients an empiric trial of antibiotic therapy can be considered.

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Bile acid malabsorption

Resection of <100 cm of terminal ileum

Empiric response to cholestyramine

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Bile acid deficiency

Cholestasis, resection of >100 cm of terminal ileum

Tests for excess fecal fat, response to medium-chain triglyceride diet

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Radiation exposure

History of radiation therapy (may begin years after exposure)

Bowel imaging, characteristic biopsy findings

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Whipple disease

Arthralgia, neurologic or ophthalmologic symptoms, lymphadenopathy

Polymerase chain reaction for Tropheryma whippelii, small bowel biopsy

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Common variable immune deficiency

Pulmonary disease, recurrent Giardia infection

Immunoglobulin assay

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Factitious diarrhea

Psychiatric history, history of laxative abuse; diagnosis of exclusion

A patient's fixation on body image and weight loss may be a clue to laxative abuse.

Low stool osmolality; stool magnesium >90 meq/L may be diagnostic

Dx: Stool osmolarity: <250 mOsm/kg (250 mmol/kg) suggests factitious diarrhea

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Causes of Infectious (Acute) Diarrhea:

The most common cause of acute diarrhea is an infectious agent (>90% of cases).

Dx: Stool culture: Used selectively because of low yield (<3%);detects Salmonella, Shigella, and Campylobacter spp.; specify if needed to test for Escherichia coli O157:H7 (if visible or occult blood)

Stool ova and parasites: Microscopic examination for Giardia, Entamoeba, Cryptosporidium, Cyclospora, and Isospora spp. and microsporidia if suspected

Stool enzyme immunoassays: Detect Shiga toxins 1 and 2 and antigens for Giardia, Entamoeba, Campylobacter, Cryptosporidium spp. if suspected

Preformed toxin:

Staphylococcus aureus

Bacillus cereus

Clostridium perfringens

Enterotoxin:

Vibrio cholerae

Enterotoxigenic Escherichia coli

Klebsiella pneumonia

Aeromonas spp.

Enteroadherent:

E. coli

Giardia lamblia

Cryptosporidiosis

Helminths

Enteroinvasive:

Norovirus?

Rotavirus

Salmonella spp.

Campylobacter spp.

Aeromonas spp.

V. parahaemolyticus

Yersinia spp.

Shigella spp.

Enteroinvasive E. coli

Entamoeba histolytica

Cytotoxin production:

Clostridium difficile

Enterohemorrhagic E. coli

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Preformed toxin:

Ingestion of preformed bacterial toxins results in nausea and vomiting followed by diarrhea within 12 hours.

(Toxins are ingested, and no intestinal microbial growth is required; symptoms occurs rapidly, within 2–12 hours)

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Staphylococcus aureus

Potato salad, mayonnaise, ham

1–8 h

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Bacillus cereus

Fried rice

1–8 h

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Clostridium perfringens

Beef, poultry

8–24 h

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Enterotoxin:

(Toxins produced by intestinal microbes that act directly on secretory mechanisms in the intestinal mucosa, causing watery diarrhea)

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Vibrio cholerae

Disruption of intestinal mucosal ion transport and subsequent water secretion (eg, cholera)

Hx: Shellfish

8–72 h

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Enterotoxigenic Escherichia coli

Hx: Salads, cheese, meats

8–72 h

Tx: Although prophylactic antibiotics are not recommended for traveler's diarrhea, empiric antibiotics (quinolones) may be appropriate for patients with symptoms.  Untreated traveler's diarrhea usually resolves in 3 to 5 days, but treatment can improve symptoms and shorten the course.

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Klebsiella pneumonia

8–72 h

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Aeromonas spp.

8–72 h

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Enteroadherent:

(Infecting organisms adhere to the gastrointestinal mucosa and compete with normal bowel flora)

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E. coli

Travel history

1–8 d

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Giardia lamblia

1–8 d

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Cryptosporidiosis

Acute or chronic watery diarrhea in an immunocompromised patient; outbreak in a nursing home or day care center or on a cruise ship

1–8 d

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Helminths

1–8 d

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Enteroinvasive:

(Infecting organisms invade and destroy intestinal mucosa, resulting in bloody diarrhea)

Minimal Inflammation

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Norovirus

Minimal inflammation

Outbreaks of diarrhea in families; on cruise ships and airplanes; and in day care centers, extended care facilities, or schools are commonly associated with norovirus.

Acute diarrhea for 1–3 d

For most patients, this finding represents a self-limited gastroenteritis.

Features or clinical characteristics that require additional evaluation for acute diarrhea include fever; bloody stools; diarrhea in pregnant, elderly, or immunocompromised patients; hospitalization; employment as a food handler; recent antibiotic use; volume depletion; or significant abdominal pain.

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Rotavirus

Moderate Inflammation

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Salmonella spp.

Beef, poultry, eggs, dairy, travel history

12 h–11 d

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Campylobacter spp.

Poultry, raw milk, travel history

Reactive arthritis can occur after Shigella, Salmonella, and Campylobacter infections.

Guillain-Barré syndrome is associated with Campylobacter and Yersinia infections.

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Aeromonas spp.

Travel history

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V. parahaemolyticus

?

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Yersinia spp.

Raw milk

Severe inflammation

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Shigella spp.

Routine stool culture cannot distinguish pathogenic E. coli from normal fecal flora. Therefore, in the setting of blood in the stool, test specifically for shiga toxin.

If symptoms have persisted beyond 7 days, stool should be examined for ova and parasites. 

Travel history

12 h–8 d

Hemolytic uremic syndrome (hemolytic anemia, thrombocytopenia, acute kidney injury) can occur with Shiga toxin–producing E. coli or Shigella infection.

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Enteroinvasive E. coli

Routine stool culture cannot distinguish pathogenic E. coli from normal fecal flora. Therefore, in the setting of blood in the stool, test specifically for E. coli O157:H7

If symptoms have persisted beyond 7 days, stool should be examined for ova and parasites. 

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Entamoeba histolytica

?

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Cytotoxin production:

(Toxins produced by intestinal organisms cause destruction of mucosal cells and associated inflammation, resulting in dysentery: bloody stools containing inflammatory cells)

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Clostridium difficile

C. difficile infection is an inflammatory condition of the colon caused by the ingestion of the spore-forming, anaerobic, gram-positive bacillus. The inflammatory response is secondary to toxin-induced cytokines (toxins A and B) in the colon. Findings can range from watery diarrhea to ileus and life-threatening conditions (toxic megacolon, perforation, sepsis). 

Disruption in the mucosal barrier secondary to infection or inflammation (Clostridium difficile infection)

Health care facility or antibiotic exposure.  For health care–related diarrhea, test for C. difficile toxin. Fecal specimens collected after 3 days of hospitalization have a very low yield for standard bacterial pathogens, and routine stool culture is not indicated for inpatients with diarrhea unless there is evidence of a specific outbreak.

1–3 d

Patients with CDI and associated colitis typically have diarrhea up to 10 to 15 times daily, lower abdominal pain, cramping, fever, and leukocytosis that often exceeds 15,000/µL (15 × 109/L)

Clostridium difficile polymerase chain reaction and stool culture should be considered in patients with any features that require additional evaluation

Antidiarrheal agents should be avoided in patients with suspected inflammatory diarrhea (eg, diarrhea due to ulcerative colitis, C. difficile infection, or Shiga toxin–producing E. coli) because of the association with toxic megacolon. 

Clostridium difficiletoxin enzyme immunoassay: Should be performed if recent antibiotic use or hospitalization; sensitivity 70%–80% and specificity >97% for toxins A and B

Tx: Oral vancomycin and intravenous metronidazole.

Recommended treatment of severe disease is oral vancomycin

 

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Enterohemorrhagic E. coli

Ground beef, raw vegetables

12–72 h

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Mycobacterium Avium Complex

In an immunocompromised patient, test for Mycobacterium avium complex (MAC) by sending stool for acid-fast bacillus stain and culture because disseminated MAC infections often involve the GI tract and cause diarrhea; also test for viruses (cytomegalovirus, adenovirus, herpes simplex virus) and protozoa (cryptosporidium, Isospora spp., microsporidia).

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