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BY DR: RAMY A. SAMY Definition: abnormal increase in stool liquidity, stool frequency, and stool weight (more than 200 grams per day). Diarrhea : < 2 weeks: acute > 2 weeks: chronic Traveler’s diarrhea Infection: non-inflammatory Inflammatory Other medical disease: Drugs: Acute diverticulitis, superior mesenteric arterial/venous thrombosis, Ischemic bowel disease, IBD Virtually all medications ◦ magnesium- or phosphate-containing antacids or supplements, antiarrhythmics, broad-spectrum antibiotics, antineoplastics, antihypertensives, bile acids, cholinergic agents, laxatives, NSAID, potassium supplements, and prostaglandins. ◦ Medicinal elixirs contain high amounts of sorbitol, which can have a cathartic effect on the bowel (1 dose….) eg. acetaminophen, theophylline, and cimetidine (not listed) Immunocompromised and food allergy Whenever a person travels from one country to another—particularly if the change involves a marked difference in climate, social conditions, or sanitation standards and facilities—diarrhea is likely to develop within 2–10 days There may be up to ten or even more loose stools per day, often accompanied by abdominal cramps, nausea, occasionally vomiting, and rarely fever. The stools do not usually contain mucus or blood, and aside from weakness, dehydration, and occasionally acidosis, there are no systemic manifestations of infection. The illness usually subsides spontaneously within 1–5 days, although 10% remain symptomatic for a week or longer, and in 2% symptoms persist for longer than a month . Bacteria cause 80% of cases of traveler's diarrhea, with enterotoxigenic E coli, Shigella species, and Campylobacter jejuni being the most common pathogens. Less common causative agents include Aeromonas, Salmonella, noncholera vibrios, Entamoeba histolytica, and Giardia lamblia. Contributory causes may at times include unusual food and drink, change in living habits, occasional viral infections (adenoviruses or rotaviruses), and change in bowel flora Watery, nonbloody diarrhea associated with periumbilical cramps, bloating, nausea, or vomiting (singly or in any combination) suggests small bowel enteritis caused by either a toxin-producing bacterium (enterotoxigenic E coli [ETEC], Staphylococcus aureus, Bacillus cereus, C perfringens) or other agents (viruses, Giardia) that disrupt the normal absorption and secretory process in the small intestine. Prominent vomiting suggests viral enteritis or S. aureus food poisoning. Though typically mild, the diarrhea (which originates in the small intestine) may be voluminous (ranging from 10 to 200 mL/kg/24 h) and result in dehydration with hypokalemia and metabolic acidosis due to loss of HCO3– in the stool (eg, cholera). Because tissue invasion does not occur, fecal leukocytes are not present. A severe systemic illness manifested initially by prolonged high fevers, prostration, confusion, respiratory symptoms followed by abdominal tenderness, diarrhea, and a rash is due to infection with Salmonella typhi or Salmonella paratyphi, which causes bacteremia and multiorgan dysfunction In over 90% of patients with acute diarrhea, the illness is mild and self-limited and responds within 5 days to simple rehydration therapy or antidiarrheal agents Patients with signs of inflammatory diarrhea manifested by any of the following require prompt medical attention: high fever (> 38.5 °C), bloody diarrhea, abdominal pain, or diarrhea not subsiding after 4–5 days. Similarly, patients with symptoms of dehydration must be evaluated (excessive thirst, dry mouth, decreased urination, weakness, lethargy) Physical examination should note the patient's general appearance, mental status, volume status, and the presence of abdominal tenderness or peritonitis Peritoneal findings may be present in C difficile and enterohemorrhagic E coli. Hospitalization is required in patients with severe dehydration, toxicity, or marked abdominal pain. Stool specimens should be sent in all cases for examination for fecal leukocytes and bacterial cultures Most cases of acute diarrhea are selflimited, and specific therapy is not necessary. Preventing dehydration and restoring fluid losses. IV/PO Oral intake should be encouraged to minimize the risk of dehydration. The misconception that the bowel needs to be at rest or that oral intake will worsen the diarrheal illness should be abandoned. Avoid milk and other lactose-containing products, Caffeine-containing products Glucose-containing electrolyte solutions Clostridium difficile ¼ of antibiotic- associated diarrhea. ¾ no etiologic agent is identified, diarrhea– mild– abdominal pain(-). respond to... Antibiotics :clindamycin, ampicillin, amoxicillin, and cephalosporins The clinical presentation varies The diagnostic test: Treatment Prevention ? Pus cell, stool OB ? Gram stain ? Culture ? Tissue culture assay for the cytotoxicity of toxin B ◦ ? ELISA: detect toxin ◦ ◦ ◦ ◦ ◦ Oral metronidazole(500mg po tid or 250mg po qid ) or oral vancomycin hydrochloride for 10 to 14 days ◦ oral metronidazole is preferred ◦ Approximately 15% of patients experience relapse… Inflammatory, bloody diarrhea Severe volume depletion High fever Sever abdominal pain Duration > 3 days Community outbreak Impaired host Antibiotics Antiretroviral agents Antineoplastic agents Anti-inflammatory agents (NSAIDs, gold, 5-ASA) Antiarrhythmics (quinidine) Antihypertensives (β blockers) Oral hypoglycemics (metformin, acarbose) Antacids (magnesium-containing) Acid-reducing agents (H2 blockers, PPIs) Colchicine Prostaglandin analogs (misoprostol) Theophylline Vitamin and mineral supplements Herbal products Heavy metals Etiology The causes of chronic diarrhea may be grouped into six major pathophysiologic categories As stool leaves the colon, fecal osmolality is equal to the serum osmolality, ie, approximately 290 mosm/kg. Under normal circumstances, the major osmoles are Na+, K+, Cl–, and HCO3–. The stool osmolality may be estimated by multiplying the stool (Na+ + K+) × 2 (multiplied by 2 to account for the anions) The most common causes of osmotic diarrhea are disaccharidase deficiency (lactase deficiency), laxative abuse, and malabsorption syndromes . Osmotic diarrheas resolve during fasting. Osmotic diarrheas caused by malabsorbed carbohydrates are characterized by abdominal distention, bloating, and flatulence due to increased colonic gas production. The major causes of malabsorption are small mucosal intestinal diseases, intestinal resections, lymphatic obstruction, small intestinal bacterial overgrowth, and pancreatic insufficiency In patients with suspected malabsorption, quantification of fecal fat should be performed Increased intestinal secretion or decreased absorption results in a watery diarrhea that may be large in volume (1–10 L/d) but with a normal osmotic gap Major causes include: endocrine tumors (stimulating intestinal or pancreatic secretion), bile salt malabsorption (stimulating colonic secretion), and laxative abuse Diarrhea is present in most patients with inflammatory bowel disease (ulcerative colitis, Crohn's disease, microscopic colitis). A variety of other symptoms may be present, including abdominal pain, fever, weight loss, and hematochezia Abnormal intestinal motility secondary to systemic disorders or surgery may result in diarrhea due to rapid transit or to stasis of intestinal contents with bacterial overgrowth resulting in malabsorption Cyclospora, and the intestinal nematodes Immunocompromised patients, especially those with AIDS, are susceptible to a number of infectious agents that can cause acute or chronic diarrhea Chronic diarrhea in AIDS is commonly caused by Cryptosporidium, cytomegalovirus, Isospora belli, Cyclospora, and Mycobacterium avium complex. Approximately 15% of patients with chronic diarrhea have factitial diarrhea caused by laxative abuse or factitious dilution of stool Rome Criteria: Recurrent abdominal pain or discomfort at least 3 days per month for the past 3 months, associated with 2 or more of: - Improvement wih defecation - Onset associated with a change in frequency of stool - Onset associated with a change in form (appearance) of stool Periods of constipation common Long history, passage of mucus, exacerbation by stress Diarrhea during waking hours, urgency Coexistence with other functional disorders Against IBS: Recent onset, nocturnal diarrhea, bleeding, weight loss, voluminous or greasy stool, abnormal blood tests Rule out celiac sprue! Functional diarrhea: Recurrent loose stools without pain. • History • Physical examination • Routine laboratory tests (CBC, albumin, ESR/CRP) • Stool analysis • Categorize: • Watery diarrhea • Inflammatory diarrhea • Fatty diarrhea Secretory Osmotic Define patient’s complaint of diarrhea (change in consistency, presence of urgency or incontinence) Stool characteristics (blood, mucus, oil, pus, food particles) and volume Duration, pattern of onset Relation to prandial state Nocturnal diarrhea Weight loss Travel history Risk factors for HIV infection Dietary profile and medication review Family history of IBD Other systemic symptoms Physical finding Diagnosis More helpful to determine severity rather than etiology Skin changes Celiac sprue (dermatitis herpetiformis) Hemodynamics, temperature, signs ofpigmentosa) toxicity Mastocytosis (urticaria Amyloidosis (macroglossia, purpura) Helpful clues: Addison’s disease (hyperpigmentation) Glucagonoma (migratory necrolytic erythema) Carcinoid syndrome (flushing) Degos’ disease (malignant atrophic papulosis) Peripheral neuropathy, orthostatic hypotension Amyloidosis Thyroid nodule Medullary carcinoma of the thyroid Right-sided cardiac murmur, hepatomegaly Carcinoid syndrome Arthritis IBD, Whipple’s, infections Lymphadenopathy AIDS, lymphoma Peripheral vascular disease/abdominal bruits Mesenteric vascular insufficiency Directed testing for confirmation based on clinical suspicion, or “broad net” cast in difficult cases Categorize diarrhea into watery, inflammatory, fatty Timed collection is best, spot tests on random stool sample more practical - Occult blood - White blood cells - pH - Sudan stain for fat - Cultures - Laxative screen - Electrolytes, osmolality Occult blood and white blood cells: - Primarily define inflammatory diarrhea - Wright stain: Sensitivity 70%, specificity 50% for leukocytes - Fecal calprotectin and lactoferrin less operator dependent, but test characteristics in chronic diarrhea not well defined pH: - Low pH (< malabsorption 6) generally indicative of carbohydrate Sudan stain: - Fatty diarrhea (steatorrhea) - Gold standard: Quantitative estimation of stool fat on collected specimen - Qualitative estimation feasible on random sample, - Semiquantitative methods (number and size of fat globules) correlate well with quantitative collection Stool cultures: - Infection: Usually inflammatory diarrhea - Bacterial infection rarely cause of chronic diarrhea in immunocompetent host - Routine cultures are low yield and not recommended (but done anyway!) - Special techniques for Aeromonas and Plesiomonas - Ova and Parasites - Always consider giardiasis (stool ELISA for Giardia antigen) Stool electrolytes: Stool osmotic gap: 290 – 2([Na+] + [K+]) - Gap < 50 mOsm/Kg: Pure secretory diarrhea - Gap > 125 mOsm/Kg: Pure osmotic diarrhea - Gap 50-125 mOsm/kg: Mixed or mild carbohydrate malabsorption Measured stool osmolality: - Not used to calculate gap - Useful in cases of unexplained diarrhea - Low measured stool osmolality (< 290 mOsm/Kg) suggestive of contamination with water or dilute urine