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Acute and chronic diarrhea summary
 

Acute and chronic diarrhea summary

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    Acute and chronic diarrhea summary Acute and chronic diarrhea summary Presentation Transcript

    • Acute and Chronic Diarrhea
      Crystal Byerly, MEd., PA-C
      Seton Hill University PA Program Assistant Professor
      And Family Practice PA
    • Learning Objectives
      Define acute vs. chronic diarrhea etiologies
      Create a differential diagnosis for each type of diarrhea
      Differentiate when further testing,  including a colonoscopy,  should be ordered
      Discuss treatment options including symptom management
    • Definitions of diarrhea
      Symptomatic:
      Increased frequency
      Increased fluidity
      Increased volume
      Or any combination of above
      Physiologic definition:
      Decreased absorption or increased secretion, or both, causing > 200 mL liquid BM excretion/day
    • Normal stool frequency ranges from three times a week to three times a day
      Acute diarrheas are those lasting less than 2 to 3 weeks or, rarely, 6 to 8 weeks.
      The most common cause of acute diarrhea is infection. Learn infectious vs. non-infectious.
      Chronic diarrheas are those lasting at least 4 weeks, and more usually 6 to 8 weeks or longer.
      There are three categories of chronic diarrhea:
      osmotic (malabsorptive) diarrhea
      secretory diarrhea,
      and inflammatory vs. non-inflammatory diarrhea.
    • Approximately 80% of acute diarrheas are due to infections with viruses, bacteria, helminths, and protozoa.
      The remainder are secondary to the ingestion of medications, poorly absorbed sugars (fructose polymers or sorbitol), fecal impaction, pelvic inflammation.
      Diarrhea results from imbalance of the intestines to handle water and electrolytes
    • Acute Diarrhea
      Bloody
      Must evaluate ALL bloody diarrhea.
      C & S stool
      Sigmoidoscopy
      Maybe CT
      Non-bloody
      Most are viral
      Most resolve on own without definite dx
      Rarely further complications unless remission of a chronic condition
      If sx progress to fever, pus, dehydration, then needs more evaluation.
    • Big Clinical Clues to Infectious vs. Noninfectious
      Infectious!
      Fever
      Pus
      Blood
      Epidemic
      Travel
      Bacterial: Sx onset WHILE IN visited country
      Parasitic: Sx onset AFTER RETURN
      Noninfectious
      AFEBRILE
      Non-pus stool
      Nonbloody
      Sporadic
      No travel
    • Acute infectious diarrhea
      Most infectious diarrheas are acquired through fecal-oral transmission from water, food, or person-to-person contact
      Patients with infectious diarrhea often complain of nausea, vomiting, and abdominal pain and have watery, malabsorptive, or bloody diarrhea and fever (dysentery)
    • Some of the short-lived watery diarrheas diagnosed as “viral gastroenteritis” are likely to be mild, sporadic, food-borne bacterial infections.
      Since diagnostic work up is not always indicated, you may not be able to label the exact etiology of the acute diarrhea.
    • Get a thorough history from your patient!
      Nutritional supplements should be reviewed, including
      the intake of “sugar-free” foods (containing nonabsorbable carbohydrates),
      fat substitutes,
      milk products,
      and shellfish,
      and heavy intake of fruits, fruit juices,
      or caffeine.
    • Diarrhea is one of the most frequent adverse effects of prescription medications;
      it is important to note that drug-related diarrhea usually occurs after a new drug is initiated or the dosage increased.
      Especially antibiotics
      Augmentin, EES
    • Food- or waterborne outbreaks of diarrhea are becoming more common.
      The history should include
      place of residence,
      drinking water (treated city water or well water),
      rural conditions,
      with consumption of raw milk,
      consumption of raw meat or fish
      Fish can become contaminated in their own environment (especially the filter-feeding bivalve mollusks, such as mussels, clams, oysters, and scallops) or by food handlers,
      and exposure to farm animals that may spread Salmonella or Brucella organisms
      Unwashed vegetables
      outbreaks of E. coli O157:H7 have been associated with petting zoos and unwashed lettuce.
    • Sexual history is important, because specific organisms can cause diarrhea in homosexual men and HIV-infected patients.
    •  
      Symptoms that begin within six hours suggest ingestion of a preformed toxin of Staphylococcus aureus or Bacillus cereus
      Symptoms that begin at 8 to 16 hours suggest infection with Clostridium perfringens
      Symptoms that begin at more than 16 hours can result from viral or bacterial infection (eg, contamination of food with enterotoxigenic or enterohemorrhagic E. coli).
    •  
      It is also important to ask about recent antibiotic use (as a clue to the presence of C. difficile infection, although it is possible for community-associated C. difficile infection to occur in patients without antibiotic exposure), other medications, and to obtain a complete past medical history (eg, to identify an immunocompromised host or the possibility of nosocomial infection)
    • Syndromes that may begin with diarrhea but progress to fever and more systemic complaints such as headache, muscle aches, stiff neck may suggest infection with Listeriamonocytogenes, particularly in pregnant woman.
      Women who are pregnant have a 20-fold increased risk of developing listeriosis from meat products or unpasteurized dairy products (such as soft cheeses).
    • PE
      The physical examination in acute diarrhea is helpful in determining the severity of disease and hydration status.
      Vital signs (including temperature and orthostatic evaluation of pulse and blood pressure)
      and signs of volume depletion (including dry mucous membranes, decreased skin turgor, and confusion) should be carefully evaluated.
      A careful abdominal examination to evaluate for tenderness and distention
      and a stool examination to evaluate for grossly bloody stools are warranted. Nonbloody stools should be evaluated for heme positivity.
    • Viral acute diarrhea
      “Acute Viral Gastroenteritis”
      Sx onset
      Self-limited illnesses commonly due to
      Norovirus
      Rotovirus
      Adenovirus
      Astrovirus
    • Bacterial acute diarrhea
      Even though bacteria is the cause, many of these acute outbreaks are self-limited. Often patient will not even present for treatment and will never need antibiotic.
    • Salmonella
      consuming food that is contaminated with animal feces
      8-48 hours incubation
      Fever with chills
      Nausea and vomiting
      Cramping and abdominal pain
      Diarrhea often grossly bloody 3-5 days
      Tx if not self-limited: Trimethoprim-sulfamethoxazole, ampicillin, ciprofloxin
    • Campylobacter
      typically caused by Campylobacter jejuni or C. coli; it is largely a foodborne disease.
      Primarily uncooked poultry
      Diarrhea (bloody ~10%), abdominal pain
      Azithromycin (500 mg orally one time a day for 3 days) should be first line Rx therapy for symptoms lasting >7days, otherwise self-limited symptomatic therapy recommended.
    • Shigellosis
      Fever with chills
      Abdominal cramps
      Diarrhea often with blood and mucus
      Headache, malaise
      Direct person-to-person spread
      TxTrimethoprim-sulfamethoxazole, ciprofloxin, levofloxacin, ampicillin
      Increasing resistance to antibiotics noted
      Azithromycin, 500 mg orally on day 1 and 250 mg orally one time a day for 4 days, may be an effective alternative treatment for resistant strains
    • E. Coli/Enterohemorrhagic Escherichia coli (EHEC)
      Sx abdominal pain and bloody diarrhea
      No fever
      Two strains now
      0157:H7 (since 1982)
      O104:H4 (May 2011)
      Antbiotictx is not recommended at present,
      the incidence of complications (hemolytic-uremic syndrome) may be greater after antibiotic therapy
      Hemolytic-uremic syndrome (HUS) is the major systemic complication, and is characterized by the triad of acute renal failure, microangiopathic hemolytic anemia and thrombocytopenia; these typically begin 5 to 10 days after the onset of diarrhea.
    • C. diff
      Clostridium difficile
      20% chance after completing broad spectrum antibiotic
      The A and B toxins produced by C. difficile can cause severe diarrhea, pseudomembranous colitis, or toxic megacolon.
      High risk pts: nursing home residents and employees, hospitalized pts and employees
      metronidazole (250 mg orally four times a day or 500 mg orally three times a day for 10 days)
    • Cholera
      History of travel to endemic areas
      Vibriocholerae
      Ingestion in contaminated food
      Massive diarrhea-nonbloody, liquid, gray, “rice water diarrhea”, No odor
      Dehydration occurs quickly
      Vaccine available but short-lived
      Tx with hydration and antibiotics
      Tetracycline, ampicillin, azithromycin, trimethoprim-sulfamethoxazole, fluoroquinolones
    • Protozoa induced diarrhea
    • Giardia
      Giardia protozoa infection (giardiasis) is one of the most common causes of diarrhea in the United States.
      Giardia infection can be transmitted through water, food, and person-to-person contact.
    • Watery yellow, sometimes foul-smelling diarrhea that may alternate with soft, greasy stools
      Fatigue
      Abdominal cramps and bloating
      Nausea
      Weight loss — as much as 10 percent of your body weight
    • Infections usually clear up within six weeks. But you may have recurrent episodes or have intestinal problems long after the parasites are gone.
      Several drugs are generally effective against giardia parasites, but not everyone responds to them.
      Tinidazole 2 g orally as a single dose
      Metronidazole (Flagyl) 250mg potidx 5d
    • Noninfectious causes of diarrhea include
      inflammatory bowel disease,
      irritable bowel syndrome,
      ischemic bowel disease,
      partial small bowel obstruction,
      pelvic abscess in the rectosigmoid area,
      fecal impaction,
      and the ingestion of poorly absorbable sugars, such as lactulose and acute alcohol ingestion.
    • Diagnostic evaluation
      A medical evaluation of acute diarrhea is not warranted in the previously healthy individual if
      symptoms are mild, moderate,
      spontaneously improve within 48 hours,
      and are not accompanied by fever, chills, severe abdominal pain, or blood in the stool.
    • evaluation is indicated if
      symptoms are severe or prolonged,
      the patient appears “toxic,”
      there is evidence of colitis (occult or gross blood in the stools, severe abdominal pain or tenderness, and fever),
      Hospitalized patients or recent use of antibiotics,
      Diarrhea in the elderly (≥70 years of age) or the immunocompromised,
      Systemic illness with diarrhea, especially in pregnant women (in which case listeriosis should be suspected),
      or empirical therapy has failed.
    • Diagnostic evaluation of diarrhea
      The use of the laboratory to make the diagnosis of infectious diarrhea of Campylobacter, Salmonella, Shigella, and C. difficile and if only liquid stools are cultured.
      “C & S” = culture and sensitivity of stool
      “C diff” = needs requested separately in local labs
    • Organisms that can cause diarrhea but are not sought routinely by most clinical microbiology laboratories unless specifically requested include
      Yersinia,
      Plesiomonas,
      enterohemorrhagic E. coli serotype O157:H7,
      Cryptosporidium,
      Cyclospora,
      Microsporidia,
      and noncholeraVibrio.
    • “O & P” stool study
      Parasites such as Giardia and Strongyloides and enteroadherent bacteria can be difficult to detect in stool but may be diagnosed by intestinal biopsy.
      Even with the use of all available laboratory techniques, the cause of 20 to 40% of all acute infectious diarrheas remains undiagnosed.
    • Stool evaluation for fecal leukocytes “Fecal WBCs” is a useful initial test, because it may support a diagnosis of inflammatory diarrhea.
      If the test is negative, stool culture may not be necessary, but culture is indicated if the test is positive.
    • Tx
      The treatment of diarrhea can be symptomatic (fluid replacement and antidiarrheal agents) or specific (antimicrobial therapy) or both.
      Because death in acute diarrhea is caused by dehydration, the first task is to assess the degree of dehydration and replace fluid and electrolyte deficits.
    • Severely dehydrated patients should be rehydrated with intravenous Ringer's lactate or saline solution, to which additional K+ and NaHCO3− may be added as necessary.
      In mild-to-moderate dehydration, ORS (oral rehydration solution) can be given to infants and children in volumes of 50 to 100 mL/kg over 4 to 6 hours; adults may need to drink 1000 mL/hr.
    • Diet
      Total food abstinence is unnecessary and not recommended.
      Foods providing calories are necessary to facilitate renewal of enterocytes.
      Patients should be encouraged to take frequent feedings of fruit drinks, tea, “flat” carbonated beverages, and soft, easily digested foods such as bananas, applesauce, rice, potatoes, noodles, crackers, toast, and soups.
    • Dairy products should be avoided, because transient lactase deficiency can be caused by enteric, viral, and bacterial infections.
      Caffeinated beverages and alcohol, which can enhance intestinal motility and secretions, should be avoided.
    • Bismuth subsalicylate (Pepto-Bismol, 525 mg orally every 30 minutes to 1 hour for five doses, may repeat on day 2) is safe and efficacious in bacterial infectious diarrheas.
    • Anxiolytics (e.g., diazepam 2 mg orally two to four times daily) and antiemetics (e.g., promethazine 12.5 to 25 mg orally once or twice daily) that decrease sensory perception may make symptoms more tolerable and are safe.
      Some foods or food-derived substances (green bananas, pectins [amylase-resistant starch], zinc) lessen the amount and/or duration of diarrhea.
      Zinc supplementation (20 mg of elemental zinc orally once a day) is effective in preventing recurrences of diarrhea in malnourished children.
    • Probiotics are live, nonpathogenic, human microorganisms that provide a health benefit. Level 1 evidence has been reported for the therapeutic use of probiotics.
      Most species are lactic acid bacteria. Lactobacillus GG (1010 colony-forming units [CFU]/250 mL ORS daily until diarrhea stops) added to an ORS decreases the duration of diarrhea in children with acute diarrhea, particularly with rotavirus infection.
    • Who you must treat!
      Regardless of the cause of infectious diarrhea, patients should be treated if they are
      immunosupressed;
      have valvular, vascular, or orthopedic prostheses;
      have congenital hemolytic anemias (especially if salmonellosis is involved);
      or are extremely young or old.
    • If you must tx empirically without significant suspicion of cause...
      While the clinician is awaiting stool culture results to guide specific therapy the fluoroquinolones (e.g., ciprofloxacin 500 mg orally two times a day for 5 days) are the treatment of choice.
      Trimethoprim-sulfamethoxazole is second-line therapy.
    • Chronic Diarrhea >4 weeks
      Stool culture and examination may detect organisms that often cause protracted infectious diarrhea in adults:
      enteropathogenic(enteroadherent) E. coli,
      Giardia,
      Entamoeba,
      Cryptosporidium,
      Aeromonas, and
      Yersiniaenterocolitica.
    • Chronic diarrhea eval
      Fecal WBCs
      Stool C&S
      O&P
      C. difficile stool test
      TSH
      CBC
    • Fecal WBCs
      Present fecal WBCs:
      C. difficile colitis
      Chrohn’s disease
      Ulcerative colitis
      Shigellosis
      Salmonellosis
      Typhoid fever (s. typhi)
      Invasive e. coli
      Y. enterocolitica
      Absent fecal WBCs:
      Giardiasis
      Amebiasis
      Viral enteritis
      Toxigenicecoli
      Microscopic colitis
      Drug-induced diarrhea
    • Malabsorption
      caused by many different diseases, drugs, or nutritional products that impair intraluminal digestion, mucosal absorption, or nutrient delivery to the systemic circulation.
      Steatorrhea (excess fat in the stool) is the hallmark of malabsorption; a stool test for fat is the best screening test for malabsorption.
    • A careful history is crucial in guiding further testing to confirm the suspicion of malabsorption and to make a specific diagnosis
      The goals of treatment are to correct or treat the underlying disease and to replenish water, electrolyte, and nutritional losses.
    • Conditions of malabsorption include:
      Celiac sprue
      Bacterial overgrowth
      Lactase deficiency
    • Malabsorption Clinical presentation
      Individuals typically present with:
      bulky, fat-laden stools
      (usually >30 g of fat per day),
      abdominal pain,
      and diabetes,
      although some present with diabetes in the absence of gastrointestinal symptoms.
    • Diagnostic evaluation for malabsorption
      Quantitative stool fat test
      Gold standard test of fat malabsorption, with which all other tests are compared.
      Requires ingestion of a high-fat diet (100 g) for 2 days before and during the collection.
      Stool is collected for 3 days.
    • Qualitative stool fat test
      Sudan stain of a stool sample for fat.
      determines the percentage of fat in the stool (normal, <20%).
      The test depends on an adequate fat intake (100 g/day).
      There is high sensitivity (90%) and specificity (90%) with fat malabsorption of >10 g/24 hr.
    • Acid steatocrit
      Reliable screening test for fat malabsorption that is inexpensive and easy to perform.
      Centrifugation of acidified stool in a hematocrit capillary yields solid, liquid, and fatty layers.
      Results are expressed as volumetric percentages (lipid phase on solid phase); normal, <10%.
      High sensitivity (100%) and specificity (95%) compared with the 72-hr stool quantitative fat test.
      Depends on adequate fat intake (100 g/day).
    • D-Xylosetest
      A test of small intestinal mucosal absorption, used to distinguish mucosal malabsorption from malabsorption due to pancreatic insufficiency.
      An oral dose of D-xylose (25 g/500 mL water) is administered, and D-xylose excretion is measured in a 5-hr urine collection
    • Hydrogen breath test
      Most useful in the diagnosis of lactase deficiency.
      An oral dose of lactose (1 g/kg body weight) is administered after measurement of basal breath H2 levels.
      A late peak (within 3–6 hr) of >20 ppm of exhaled H2 after lactose ingestion suggests lactose malabsorption.
      Absorption of other carbohydrates (e.g., sucrose, glucose, fructose) also can be tested.
    • Small-bowel biopsy
      Obtained for a specific diagnosis when there is a high index of suspicion for small intestinal disease.
      Several biopsy specimens (4–5) must be obtained to maximize the diagnostic yield.
      Small intestinal biopsy provides a specific diagnosis in some diseases
      intestinal infection,
      Whipple's disease
      lymphoma,
      Amyloidosis
      celiac disease and tropical sprue
    • Tx
      Pancreatic enzyme replacement and analgesics are the mainstays of treatment.
    • Celiac Sprue
      Aka: gluten enteropathy, celiac disease
      Diffuse damage to proximal small intestinal mucosa causes malabsorption of most nutrients
      Present more commonly in infancy, but also between 20-40 and again > 60
    • Removal of gluten from the diet results in disappearance of symptoms and healing in most
      Gluten is a protein component of some grains, wheat, rye, oats, barley.
      Not in rice or corn
      Thought to elicit both humoral and cellular inflammatory responses in the mucosal lining
      Inflammation leads to destruction
    • Celiac dx
      Small bowel biopsy showing is blunting and flattening of villi.
      First line labs:
      IgA tissue transglutaminase antibodies
      IgAendomysial antibodies
    • Lactose deficiency
      Lactase is a brush border enzyme that breaks down lactulose to glucose to galactose
      Deficiency may be from:
      congenital prematurity < 30 wks gestation
      A decline in quantity as person matures
      Secondary to conditions that effect the proximal small bowel
    • Lactose deficiency
      Clinical findings
      Symptomatology depends on
      the amount of deficiency
      And the amount of lactose ingestion
      Bloating, cramping
      Flatus
      Osmotic diarrhea
      No weight loss
    • Lab tests
      Hydrogen breath test
      Trial of lactose free diet
    • TRUE SECRETORY DIARRHEAS
      Endocrine Tumor Diarrheas
      Nonendocrine malignancies
      Factitious diarrhea
      Diabetic diarrhea
      Alcoholic diarrhea
      Clinical clue: Secretory diarrheas continue with fasting and osmotic diarrheas cease with fasting!
    • Endocrine tumor diarrhea
      Carcinoid Syndrome
      Patients with metastatic carcinoid tumors of the gastrointestinal tract may develop a watery diarrhea and cramping abdominal pain in addition to other symptoms
      Because one third of these patients do not have other symptoms at the time the diarrhea begins, carcinoid should be considered in patients with secretory diarrhea.
    • Nonendocrine malignancies
      Villous Adenomas-Large (4 to 10 cm) villous adenomas of the rectum or rectosigmoid may cause a secretory form of diarrhea (500 to 3000 mL/24 hours) characterized by hypokalemia, chloride-rich stool, and metabolic alkalosis
    • Radiation Enteritis
      Patients receiving pelvic radiation for malignancies of the female urogenital tract or the male prostate may develop chronic radiation enterocolitis 6 to 12 months after total doses of radiation
      Symptoms can develop 20 years after treatment
    • Questions?
      Thank You!
    • References
      Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap.
      DuPont HL. Guidelines on acute infectious diarrhea in adults. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol 1997; 92:1962.
      Thielman NM, Guerrant RL. Clinical practice. Acute infectious diarrhea. N Engl J Med 2004; 350:38.
      Fine KD, Schiller LR. AGA technical review on the evaluation and management of chronic diarrhea. Gastroenterology 1999; 116:1464.