DIARRHEA

1. DIARRHEA Dr. Therese C. Macatula Section of Gastroenterology Department of Medicine The Medical City

2. What is diarrhea? • Diarrhea is caused by an imbalance in the physiologic mechanisms of the GI tract, resulting in impaired absorption and excessive secretion • Increased fluidity of stools • Difficult to quantitate • Visual scales

3. Bristol Stool Chart

4. What is diarrhea? • Increased fluidity of stools • Difficult to quantitate • Visual scales • ≥3 bowel movements/day • >200g of stool daily • “scientific definition” • however, dependent on amount of fiber in diet

5. What is diarrhea? • Objective determinants of decreased fecal consistency: • ability of water-insoluble fecal solids (derived from dietary fiber or bacterial cell walls) to hold or bind fecal water correlated well with fecal consistency •  water-holding capacity = loose stools  water-holding capacity = formed or thick stools • Fecal consistency correlated best with ratio of water-binding capacity of insoluble solids to the total amount of water present & not simply to the amount of fecal water

6.  Fecal Incontinence • “bad diarrhea” • Seen in older adults • Major problem is with the mechanisms of incontinence and not with intestinal fluid or electrolyte absorption  Pseudodiarrhea • Hyperdefecation • Increased stool frequency (≥3x daily) with a normal daily stool weight of <200g/d • often associated with rectal urgency and accompanies anorectal disorders such as proctitis

7. Categories of Diarrhea: pathophysiology • Osmotic • Malabsorptive • Secretory • Dysmotility • Exudative

8. Categories of Diarrhea: pathophysiology • Osmotic Diarrhea • Defintion: Increased amounts of poorly absorbed, • osmotically active solutes in gut lumen • • Interferes with absorption of water • • Solutes are ingested (fasting stops diarrhea) • – Mg sulfate or citrate or Mg-containing antacids • – Sorbitol • – Malabsorption • • mechanical and biochemical disturbances from • enzyme deficiencies (ie. lactase deficiency) • • Celiac sprue • • Variety of infectious organisms (viruses)

9. Categories of Diarrhea: pathophysiology SecretoryDiarrhea • Excess secretion of electrolytes and water across mucosal surface • Usually coupled with inhibition of absorption • Clinical features – stools very watery – stool volume large – fasting does not stop diarrhea • Bacterial or viral enterotoxins – Cholera, enterotoxigenic E. coli, B. cereus, S. aureus, Rotavirus, Norwalk virus • Hormonal secretagogues • Certain laxatives (castor oil, senna)

10. Categories of Diarrhea: pathophysiology ExudativeDiarrhea • Intestinal or colonic mucosa inflamed and ulcerated – Leakage of fluid, blood, pus – Impairment of absorption – Increased secretion (prostaglandins) • The extent and location of bowel involved determines: – Severity of diarrhea – Systemic signs and symptoms (abdominal pain, fever, WBC, etc) – Tenesmus, urgency • Infectious invasive organisms – Shigella, Campylobacter, Yersinia, E. histolytica, EIEC, C. difficile; CMV • Inflammatory bowel disease – Crohns disease, Ulcerative Colitis • Ischemia

11. Categories of Diarrhea: pathophysiology Dysmotility • Increased colonic motility – Irritable bowel syndrome • Increased small bowel motility – Hyperthyroidism, post-operative dumping • Decreased small bowel motility – Scleroderma, with bacterial overgrowth Factitial - administration of laxatives, adding water to stool bulk - psychiatric illness Steatorrheal - implies the disruption of fat solubilization, digestion or absorption in the small intestine (>7g of fat / day)

12. Types of Diarrhea: Duration  Acute • Diarrhea occurring for <2weeks • Commonly self-limited • 90% infectious in origin  Persistent • Diarrhea occurring for 2-4 weeks  Chronic • Diarrhea occurring >4weeks

13. ACUTE DIARRHEA Acute Diarrhea

14. ACUTE DIARRHEA Acute Diarrhea INFECTIOUS NON- INFECTIOUS

15. Acute Diarrhea • 10% are non-infectious: • Drug-induced • Toxin ingestion • Insecticides (organophosphates), heavy metals, house plants • Most poisonings are accompanied by vomiting and other signs • Antibiotics: Clindamycin, Ampicillin, Cephalosporins • Anti-helmintics • Antacids with Mg++ • • Anti-HTN Agents: Propranolol, Methyldopa, Hydralazine • • CV Agents: digitalis • NSAIDs • Antimetabolites • • Alcohol • • Nutritional Supplements • • Potent Diuretics: Furosemide, Bumetanide • Laxatives

16. Acute Diarrhea • 90% are infectious in origin

17. Clinical features of infection with most common diarrheal pathogens

18. Acute Infectious Diarrhea • Common syndromes of infectious diarrhea: • • Food poisoning • • Acute watery diarrhea – travelers’diarrhea • epidemics • Acute bloody diarrhea (dysentery)

19. Acute Infectious Diarrhea Acute food poisoning • Similar illness in 2 or more persons • Epidemiologic evidence of common food source • Onset of symptoms typically within 6 hours of ingestion • Nausea and vomiting prominent •

20. Acute Infectious Diarrhea • Travelers’Diarrhea • • Attack rates of as high as 25% • • 90% brief and self-limited • • Persistent diarrhea in 1-2% • Depends on destination, eating habits, length of stay

21. Acute Infectious Diarrhea Food-borne Illnesses

22. Acute Infectious Diarrhea Food-borne Illnesses

23. Acute Infectious Diarrhea Dysentery • Bloody stools • Usually with fever • Shigella, enterohemorrhagic E. coli (EHEC), enteroinvasive E. coli (EIEC) • Enteric fever (salmonella typhi) • Campylobacter jejuni • Amebiasis

24. Acute Infectious Diarrhea Pathogenic Mechanisms • Inoculum size • Adherence • Invasion • Toxin Production - Enterotoxin - Cytotoxin - Neurotoxin

25. Acute Infectious Diarrhea Host Defenses • Normal Flora – Anaerobes: acidic pH & fatty acid productionprevent colonization by bacterial pathogens • Gastric Acid – Increased frequency of Salmonella amongpatients with gastric bypass • Intestinal Motility – Impaired motility allows for bacterial overgrowth • Immunity – SecretoryIgA, systemic IgG and IgM – Cell-mediated immunity • • Binding of bacterial antigens to the luminal side of M cells in distal small intestines, subsequent presentation of antigen to subepithelial lymphoid tissue

26. ACUTE DIARRHEA Acute Diarrhea

27. Degree of Dehydration

28. Rehydration • Oral rehydration therapy (ORT) • administration of fluid by mouth to prevent or correct dehydration that is a consequence of diarrhea. • is the standard for efficacious and cost-effective management of AGE

29. Rehydration • Oral rehydration solution (ORS) is the fluid specifically developed for ORT. Water and electrolytes are administered to replace losses. • Maintenance fluid therapy (along with appropriate nutrition). • IV (RL, NSS) fluids must be given to those with severe dehydration

30. Antimicrobials Antibiotics not usually indicated but may be given for: • Dysentery (some cases) • Suspicion of cholera or enteric fever • Giardiasis or amebiasis

31. Antibiotics not usually indicated but may be given for: • Dysentery (some cases) • Suspicion of cholera or enteric fever • Giardiasis or amebiasis

32. Anti-diarrheals • None of these drugs addresses the underlying causes of diarrhea. • Antiemetics are usually unnecessary in acute diarrhea management. • Antimotility: Loperamide is the agent of choice for adults (4–6 mg/day) • Should be used mostly for mild to moderate traveler’sdiarrhea (without clinical signs of invasive diarrhea). • Inhibits intestinal peristalsis and has mild antisecretory properties. • Should be avoided in bloody or suspected inflammatory diarrhea (febrile patients). • Significant abdominal pain also suggests inflammatory diarrhea (this is a contraindication for loperamide use). • Antisecretory agents: Bismuth subsalicylate can alleviate stool output in children or symptoms of diarrhea, nausea, and abdominal pain in traveler’sdiarrhea.

33. Anti-diarrheals • Racecadotril is an enkephalinase inhibitor (nonopiate) with antisecretory activity, and is now licensed in many countries in the world for use in children. It has been found useful in children with diarrhea, but not in adults with cholera. • Adsorbents: • Kaolin-pectin, activated charcoal, attapulgite — Inadequate proof of efficacy in acute adult diarrhea

34. Complications • Dehydration: • Hypovolemic Shock • Electrolyte imbalance: • Hyponatremia, hypokalemia, hypochloridia • Acid-Base Imbalance: • metabolic acidosis pH < 7.35; bicarbonate < 22 mEq/L • Acute Renal Failure: • Pre-renal Azotemia •  BUN/crea • Sepsis .

35. Prevention • Since most are through the fecal-oral route, proper hygeine should always be emphasized. • Water, sanitation, and hygiene: • Safe water • Sanitation: houseflies can transfer bacterial pathogens • Hygiene: hand washing • Safe food: • Cooking eliminates most pathogens from foods • Exclusive breastfeeding for infants • Weaning foods are vehicles of enteric infection • Vaccines: Salmonella typhi, Shigella organisms, V. cholerae: ETEC vaccines, Rotavirus

36. Community Management

37. Chronic Diarrhea Evaluation of Chronic Diarrhea • History • Physical Exam • Endoscopy • Laboratory studies • Radiological studies • Other studies

38. Inflammatory Bowel Diseases • Group of chronic disorders that cause inflammation or ulceration in the small and large intestines. • Most often IBD is classified as: • Ulcerative colitis - causes ulceration and inflammation of the inner lining of the colon and rectum. • Crohn‘s disease - an inflammation that extends into the deeper layers of the intestinal wall, and also may affect other parts or layers of the digestive tract (from mouth to large intestines)

39. Inflammatory Bowel Diseases Epidemiology of IBD • Incidence: CD: 1-10 / 100,000 UC: 3-15 / 100,000 • Race: Whites > Blacks • Sex: Male = Female • Age: 20 - 40 yrs • Geography: Northern countries> south countries • Cause: unknown (genetic? immune? environmental?)

41. Diagnosis of IBD • Blood test: • CD: mild anemia, mild leukocytosis, elevated ESR • UC: anemia, leucocytosis, hypokalemia, hypoaluminemia, elevated ESR, elevated LFTs • Radiology • Endoscopy • Biopsy

42. Crohns Disease Ulcerative Colitis

45. Management of IBD The goals of therapy are • Relieve symptoms • Correct nutritional deficiencies • Control inflammation • Prevent colon cancer Treatment depends on • Type of disease • Site of disease • Disease severity Treatment may include drugs, nutrition supplements, surgery or a combination of these options

46. Irritable Bowel Syndrome • The Rome III criteria (2006) for the diagnosis of irritable bowel syndrome require that patients must have recurrent abdominal pain or discomfort at least 3 days per month during the previous 3 months that is associated with 2 or more of the following: • Relieved by defecation • Onset associated with a change in stool frequency • Onset associated with a change in stool form or appearance • Supporting symptoms include the following: • Altered stool frequency • Altered stool form • Altered stool passage (straining and/or urgency) • Mucorrhea • Abdominal bloating or subjective distention

47. Irritable Bowel Syndrome • No known cause • No actual treatment; may give symptomatic relief

48. Food Intolerance Lactose Intolerance • Deficiency/absence of the enzyme lactase in the brush border of the intestinal mucosa → maldigestion and malabsorption of lactose • Unabsorbed lactose draws water in the intestinal lumen • In the colon, lactose is metabolized by bacteria to organic acid, CO2 and H2; acid is an irritant and exerts an osmotic effect • Causes diarrhea, gaseousness, bloating and abdominal cramps

49. Lactose Intolerance • Inherited or acquired • Isolated lactase deficiency is most common in African Americans (50-80% prevalence) and in Asians (75-100% prevalence); 10-20% whites in the US • Onset of genetic disease is unpredictable and may not occur until adult life • Small amounts of lactose may produce symptoms in some while ingestion of large amounts may not affect others

50. Lactose Intolerance • Lactose tolerance test – measures changes in the concentration of serum glucose at 1 and 2 hours after ingestion of 50g lactose; rise in glucose of 20mg/100ml above fasting is normal; 30% false positive rate • Hydrogen breath test – easy to perform, more accurate. Unabsorbed lactose is fermented by colonic bacteria and the resultant hydrogen is absorbed and released in the breath where substantial levels are recorded. Requires 2-4 hours in ambulatory setting