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DR.V.PADMA
M.D,FRCP(Glasgow).
PROFESSOR OF MEDICINE
SREE BALAJI MEDICAL COLLEGE
Epidemiology of Diarrhoea
Leading cause of illness and death among children in
developing countries.
estimated 1.3 thousand million episodes and 4 million
deaths occur each year in under-fives.
Main cause of death from acute diarrhoea is
dehydration. Other important causes of death are
dysentery and undernutrition.
Definitions
Acute Diarrhoea
 sudden onset and lasts less than two weeks
 90% are infectious in etiology
 10% are caused by medications, toxin ingestions, and
ischemia
Chronic Diarrhoea
 Diarrhoea which lasts for more than 4 weeks
 Most of the causes are non-infectious
Persistent Diarrhoea
-Diarrhoea lasting between 2 to 4 weeks
Classifications of Diarrhoea
Duration-
( Acute, Chronic)
Causes-
( infectious, post-infectious, drugs, endocrine,
factitious)
Chronic Dirrhoea-
Pathophysiologic mechanism
(osmotic, secretory, inflammatory, abnormal
motility)
Mechanism of Diarrhoea
Osmotic Diarrhoea
Secretory Diarrhoea
Inflammatory Diarrhoea
Abnormal Motility Diarrhoea
Osmotic Diarrhoea
Mechanism :
-retention of water in the bowel as a result of an
accumulation of non-absorbable water-soluble
compounds
-cease with fasting, discontinue oral agents
Causes :
-Purgatives like magnesium sulfate or magnesium
containing antacids
-especially associated with excessive intake of sorbitol
and mannitol.
-Disaccharide intolerance
-Generalized malabsorption
Secretory Diarrhoea
Mechanism :
Active intestinal secretion of fluid and electrolytes as
well as decreased absorption.
Large volume, painless, persist with fasting
Causes :
Cholera enterotoxin, heat labile E.coli enterotoxin
Vasoactive Intestinal Peptide hormone in Verner-
Morrison syndrome
Bile salts in colon following ileal resection
Laxatives like docusate sodium
Carcinoid tumours
Inflammatory Diarrhoea
Mechanism :
-damage to the intestinal mucosal cell leading to a loss of
fluid and blood
-pain, fever, bleeding, inflammatory manifestations
Causes :
-- Immunodeficiency patient
Infective conditions like Shigella dysentry
Inflammatory conditions
 Ulcerative colitis and Crohns disease
Abnormal Motility Diarrhoea
Mechanism :
-Increased frequency of defecation due to underlying
diseases
-large volume, signs of malabsorption (steatorrhoea)
Causes :
Diabetes mellitus- autonomic neuropathy
Post vagotomy
Hyperthyroid diarrhoea
Irritable Bowel Syndrome
Etiology
Non- inflammatory :
enterotoxin production
Villus destruction
Adherence to surface
Inflammatory:
Direct invasion
cytotoxins
Mucosal adherence
- Bacteria adhere to specific receptors
on the mucosa, e.g. adhesions at the
tip of the pili or fimbriae
- Mode of action: effacement of
intestinal mucosa causing lesions,
produce secretory diarrhoea as a
result of adherence
- Causing moderate watery diarrhoea
- e.g. enteropathogenic E.coli
Mucosa Invasion
- The bacteria penetrate into the intestinal mucosa,
destroying the epithelial cells and causing dysentery
- e.g. Shigella spp.
Enteroinvasive E.coli
Campylobacter spp
Toxin Production
i) Enterotoxins
- toxin produced by bacteria adhere to the intestinal epithelium,
induce excessive fluid secretion into the bowel lumen, results in
watery diarrhoea without physically damaging the mucosa.
- Some enterotoxin preformed in the food can cause vomiting
- e.g Staph.aureus (enterotoxin B)
Bacillus cereus
Vibrio cholerae
ii) Cytotoxins
- damage the intestinal mucosa and sometimes vascular
endothelium, leads to bloody diarrhoea with inflammatory cells,
decreased absorptive ability.
- e.g. Salmonella spp.
Campylobacter spp.
Enterohaemorrhagic E.coli 0157
Bacterial
Campylobacter jejuni
Salmonella sp.
Shigella
Escherichia coli
Staphylococcal enterocolitis
Bacillus cereus
Clostridium perfringens
Clostridium botulinum
Gastrointestinal tuberculosis
Viral
Rotavirus
Norovirus
Adenovirus
Protozoa
• Entamoeba histolytica
• Cryptosporidium
• Giardia intestinalis
• Schistosomiasis
1. Travelers
Tourists to Latin America, Africa, and
Asia develop “traveler's diarrhea”
commonly due to enterotoxigenic
Escherichia coli, Campylobacter, Shigella,
and Salmonella.
Visitors to Russia may have increase risk
of Giardia-associated diarrhea.
Visitors to Nepal may acquire Cyclospora.
Campers, backpackers, and swimmers in
wilderness areas may become infected
with Giardia.
Consumers of Certain Food
Diarrhea closely following food
consumption may suggest infection with
Salmonella or Campylobacter from chicken;
Enterohemorrhagic Escherichia coli (O157:H7)
from undercooked hamburger
Bacillus aureus from fried rice
S. aureus from mayonnaise or creams
Salmonella from eggs
Vibro species, acute hepatitis A or B from (raw)
seafood
Clinical Features
Diarrhoea
Watery
Bloody
Cramping abdominal pain
Nausea, +/- Vomiting
Fever
Loss of appetite
Lethargy
Shock
Extraintestinal manifestation
Reactive arthritis :Salmonella ,shigella , Yersinia,
campylobacter C.difficile
Guillain-Barre Syndrome: campylobacter
Glomerulonephritis:Shigella , campylobacter
,Yersinia
IgA nephropathy :campylobacter
Erythema nodosum: Yersinia ,campylobacter,
salmonella
Hemolytic anemia : Yersinia ,campylobacter
HUS: shigella , E. coli
Bacterial causes of
watery diarrhoea and dysentery
Watery diarrhoea Dysentery
- Vibrio cholerae - Shigella spp
- Enterotoxigenic E.coli (ETEC) - Yersinia enterocolitica
- Enteropathogenic E.coli (EPEC) - Campylobacter spp
- Salmonella spp. - Salmonella spp.
- Clostridium difficile - Clostridium difficile
- Clostridium perfringens - Enteroinvasive E.coli
- Campylobacter jejuni - Enterohaemorrhagic
- Bacillus cereus E.coli (EHEC)
- Staphylococus aureus
+ profuse vomiting
Diurnal variation
 No relationship to time of day: Infectious Diarrhea
 Morning Diarrhea and after meals
 Gastric cause
 Functional bowel disorder (e.g. irritable bowel)
 Inflammatory Bowel Disease
 Nocturnal Diarrhea (always organic)
 Diabetic Neuropathy
 Inflammatory Bowel Disease
Weight Loss
 Despite normal appetite
 Hyperthyroidism
 Malabsorption
 Associated with fever
 Inflammatory Bowel Disease
 Weight loss prior to Diarrhea onset
 Pancreatic Cancer
 Tuberculosis
 Diabetes Mellitus
 Hyperthyroidism
 Malabsorption
Acute Diarrhoea
Viral,Bacterial,
Protozoa (90%)
Medications
Laxatives or diuretic
abuse
Ingestion of
environmental
preformed toxin such as
seafood
Ischemic Colitis
Graft versus Host
Chronic Diarrhoea
Irritable Bowel
Syndrome
Diverticular disease
Colorectal Cancer
Bowel Resection
Malabsorption
Inflammatory Bowel
Disease
Celiac Disease
Carcinoid tumour
DIFFERENTIAL DIAGNOSIS
Food intolerance e.g. Lactose intolerance,
Inorganic agents like Sodium nitrite,
Organic substances like Mushrooms and shellfish,
Drugs e.g. Laxatives and Antibiotics,
Emotional stress.
Diagnostic Methods
Stool samples :
 fresh collected
Mucous,bld,white cells
Ova & parasites:
Recent travel to endemic area,-ve stool cultures,diarrhea > 1wk
Part of an outbreak
Immunocompromised
Stool cultures:
As early as possible
Suspected HUS
Bloody diarrhea
outbreaks
Diagnostic Methods
Stool cultures :
Routine : Salmonella, shigella,yersinia,campylobacter.
Toxin assays: C. difficle,E.coli
Special stains:Aeromonas, cryptosporidium & vibrio sp.
Duodenal aspirate & Biopsy: Giardia,
Isospora,cryptosporidium.
ELISA
E.M.
Colonoscopy & sigmoidoscopy.
DRUG INDUCED DIARRHOEA
Antibiotics
Laxatives
Antihypertensives
Lactulose
Antineoplastics
Antiretroviral drugs
Magnesium containing
compounds
Anti arrhythmics
NSAIDs
Colchicine
Antacids
Acid reducing agents
Prostaglandin analogs
Antibiotic-induced diarrhea
unexplained onset of diarrhea that occurs with the
administration of any antibiotic
due to disruption of normal intestinal flora, which
leads to
either proliferation of pathogenic microorganisms or
impairment of the metabolic functions of the
microflora
Endocrine causes
Diabetic autonomic neuropathy
Thyrotoxicosis
Neuroendocrine tumours
~ Zollinger Ellison syndrome
~ VIPoma
~ Somatostatinoma
~ Carcinoid syndrome
~ Medullary carcinoma of thyroid
 Hypokalaemia
 Depletional hyponatraemia
 Hypernatraemia
 Hypophosphataemia
 Hypomagnesemia
 Dehydration
 Hypovolaemic shock
Acute Diarrhoea : Management
Access Hydration Status
Encourage fluids intake
Consider antibiotics if ill or frail
Consider referring if very ill, diabetic on insulin or
metformin
Children and Elderly are especially prone to
dehydration.
A child should be encouraged by their preferred diet.
Breastfeeding should be continued and alternate with
ORS
Oral Rehydration Therapy
Sodium chloride 3.5 g
Trisodium citrate dehydrate 2.9 g
(or sodium bicarbonate 2.5g)
Potassium chloride 1.5g
Glucose 20 g
To be dissolved in one litre of clean drinking water
encourage fluid intake e.g. salt + glucose drink to assist
in co-transport of sodium into the epithelial cells via
the SGLT1 protein, which enhances water and sodium
re-absorption in small intestines.
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea
Epidemiology and Management of Diarrhoea

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Epidemiology and Management of Diarrhoea

  • 2. Epidemiology of Diarrhoea Leading cause of illness and death among children in developing countries. estimated 1.3 thousand million episodes and 4 million deaths occur each year in under-fives. Main cause of death from acute diarrhoea is dehydration. Other important causes of death are dysentery and undernutrition.
  • 3. Definitions Acute Diarrhoea  sudden onset and lasts less than two weeks  90% are infectious in etiology  10% are caused by medications, toxin ingestions, and ischemia Chronic Diarrhoea  Diarrhoea which lasts for more than 4 weeks  Most of the causes are non-infectious Persistent Diarrhoea -Diarrhoea lasting between 2 to 4 weeks
  • 4. Classifications of Diarrhoea Duration- ( Acute, Chronic) Causes- ( infectious, post-infectious, drugs, endocrine, factitious) Chronic Dirrhoea- Pathophysiologic mechanism (osmotic, secretory, inflammatory, abnormal motility)
  • 5. Mechanism of Diarrhoea Osmotic Diarrhoea Secretory Diarrhoea Inflammatory Diarrhoea Abnormal Motility Diarrhoea
  • 6. Osmotic Diarrhoea Mechanism : -retention of water in the bowel as a result of an accumulation of non-absorbable water-soluble compounds -cease with fasting, discontinue oral agents Causes : -Purgatives like magnesium sulfate or magnesium containing antacids -especially associated with excessive intake of sorbitol and mannitol. -Disaccharide intolerance -Generalized malabsorption
  • 7. Secretory Diarrhoea Mechanism : Active intestinal secretion of fluid and electrolytes as well as decreased absorption. Large volume, painless, persist with fasting Causes : Cholera enterotoxin, heat labile E.coli enterotoxin Vasoactive Intestinal Peptide hormone in Verner- Morrison syndrome Bile salts in colon following ileal resection Laxatives like docusate sodium Carcinoid tumours
  • 8. Inflammatory Diarrhoea Mechanism : -damage to the intestinal mucosal cell leading to a loss of fluid and blood -pain, fever, bleeding, inflammatory manifestations Causes : -- Immunodeficiency patient Infective conditions like Shigella dysentry Inflammatory conditions  Ulcerative colitis and Crohns disease
  • 9. Abnormal Motility Diarrhoea Mechanism : -Increased frequency of defecation due to underlying diseases -large volume, signs of malabsorption (steatorrhoea) Causes : Diabetes mellitus- autonomic neuropathy Post vagotomy Hyperthyroid diarrhoea Irritable Bowel Syndrome
  • 10. Etiology Non- inflammatory : enterotoxin production Villus destruction Adherence to surface Inflammatory: Direct invasion cytotoxins
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  • 13. Mucosal adherence - Bacteria adhere to specific receptors on the mucosa, e.g. adhesions at the tip of the pili or fimbriae - Mode of action: effacement of intestinal mucosa causing lesions, produce secretory diarrhoea as a result of adherence - Causing moderate watery diarrhoea - e.g. enteropathogenic E.coli
  • 14. Mucosa Invasion - The bacteria penetrate into the intestinal mucosa, destroying the epithelial cells and causing dysentery - e.g. Shigella spp. Enteroinvasive E.coli Campylobacter spp
  • 15. Toxin Production i) Enterotoxins - toxin produced by bacteria adhere to the intestinal epithelium, induce excessive fluid secretion into the bowel lumen, results in watery diarrhoea without physically damaging the mucosa. - Some enterotoxin preformed in the food can cause vomiting - e.g Staph.aureus (enterotoxin B) Bacillus cereus Vibrio cholerae ii) Cytotoxins - damage the intestinal mucosa and sometimes vascular endothelium, leads to bloody diarrhoea with inflammatory cells, decreased absorptive ability. - e.g. Salmonella spp. Campylobacter spp. Enterohaemorrhagic E.coli 0157
  • 16. Bacterial Campylobacter jejuni Salmonella sp. Shigella Escherichia coli Staphylococcal enterocolitis Bacillus cereus Clostridium perfringens Clostridium botulinum Gastrointestinal tuberculosis
  • 17. Viral Rotavirus Norovirus Adenovirus Protozoa • Entamoeba histolytica • Cryptosporidium • Giardia intestinalis • Schistosomiasis
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  • 19. 1. Travelers Tourists to Latin America, Africa, and Asia develop “traveler's diarrhea” commonly due to enterotoxigenic Escherichia coli, Campylobacter, Shigella, and Salmonella. Visitors to Russia may have increase risk of Giardia-associated diarrhea. Visitors to Nepal may acquire Cyclospora. Campers, backpackers, and swimmers in wilderness areas may become infected with Giardia.
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  • 24. Consumers of Certain Food Diarrhea closely following food consumption may suggest infection with Salmonella or Campylobacter from chicken; Enterohemorrhagic Escherichia coli (O157:H7) from undercooked hamburger Bacillus aureus from fried rice S. aureus from mayonnaise or creams Salmonella from eggs Vibro species, acute hepatitis A or B from (raw) seafood
  • 25. Clinical Features Diarrhoea Watery Bloody Cramping abdominal pain Nausea, +/- Vomiting Fever Loss of appetite Lethargy Shock
  • 26. Extraintestinal manifestation Reactive arthritis :Salmonella ,shigella , Yersinia, campylobacter C.difficile Guillain-Barre Syndrome: campylobacter Glomerulonephritis:Shigella , campylobacter ,Yersinia IgA nephropathy :campylobacter Erythema nodosum: Yersinia ,campylobacter, salmonella Hemolytic anemia : Yersinia ,campylobacter HUS: shigella , E. coli
  • 27.
  • 28. Bacterial causes of watery diarrhoea and dysentery Watery diarrhoea Dysentery - Vibrio cholerae - Shigella spp - Enterotoxigenic E.coli (ETEC) - Yersinia enterocolitica - Enteropathogenic E.coli (EPEC) - Campylobacter spp - Salmonella spp. - Salmonella spp. - Clostridium difficile - Clostridium difficile - Clostridium perfringens - Enteroinvasive E.coli - Campylobacter jejuni - Enterohaemorrhagic - Bacillus cereus E.coli (EHEC) - Staphylococus aureus + profuse vomiting
  • 29. Diurnal variation  No relationship to time of day: Infectious Diarrhea  Morning Diarrhea and after meals  Gastric cause  Functional bowel disorder (e.g. irritable bowel)  Inflammatory Bowel Disease  Nocturnal Diarrhea (always organic)  Diabetic Neuropathy  Inflammatory Bowel Disease
  • 30. Weight Loss  Despite normal appetite  Hyperthyroidism  Malabsorption  Associated with fever  Inflammatory Bowel Disease  Weight loss prior to Diarrhea onset  Pancreatic Cancer  Tuberculosis  Diabetes Mellitus  Hyperthyroidism  Malabsorption
  • 31. Acute Diarrhoea Viral,Bacterial, Protozoa (90%) Medications Laxatives or diuretic abuse Ingestion of environmental preformed toxin such as seafood Ischemic Colitis Graft versus Host Chronic Diarrhoea Irritable Bowel Syndrome Diverticular disease Colorectal Cancer Bowel Resection Malabsorption Inflammatory Bowel Disease Celiac Disease Carcinoid tumour
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  • 33. DIFFERENTIAL DIAGNOSIS Food intolerance e.g. Lactose intolerance, Inorganic agents like Sodium nitrite, Organic substances like Mushrooms and shellfish, Drugs e.g. Laxatives and Antibiotics, Emotional stress.
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  • 36. Diagnostic Methods Stool samples :  fresh collected Mucous,bld,white cells Ova & parasites: Recent travel to endemic area,-ve stool cultures,diarrhea > 1wk Part of an outbreak Immunocompromised Stool cultures: As early as possible Suspected HUS Bloody diarrhea outbreaks
  • 37. Diagnostic Methods Stool cultures : Routine : Salmonella, shigella,yersinia,campylobacter. Toxin assays: C. difficle,E.coli Special stains:Aeromonas, cryptosporidium & vibrio sp. Duodenal aspirate & Biopsy: Giardia, Isospora,cryptosporidium. ELISA E.M. Colonoscopy & sigmoidoscopy.
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  • 47. DRUG INDUCED DIARRHOEA Antibiotics Laxatives Antihypertensives Lactulose Antineoplastics Antiretroviral drugs Magnesium containing compounds Anti arrhythmics NSAIDs Colchicine Antacids Acid reducing agents Prostaglandin analogs
  • 48. Antibiotic-induced diarrhea unexplained onset of diarrhea that occurs with the administration of any antibiotic due to disruption of normal intestinal flora, which leads to either proliferation of pathogenic microorganisms or impairment of the metabolic functions of the microflora
  • 49. Endocrine causes Diabetic autonomic neuropathy Thyrotoxicosis Neuroendocrine tumours ~ Zollinger Ellison syndrome ~ VIPoma ~ Somatostatinoma ~ Carcinoid syndrome ~ Medullary carcinoma of thyroid
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  • 51.  Hypokalaemia  Depletional hyponatraemia  Hypernatraemia  Hypophosphataemia  Hypomagnesemia  Dehydration  Hypovolaemic shock
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  • 53. Acute Diarrhoea : Management Access Hydration Status Encourage fluids intake Consider antibiotics if ill or frail Consider referring if very ill, diabetic on insulin or metformin Children and Elderly are especially prone to dehydration. A child should be encouraged by their preferred diet. Breastfeeding should be continued and alternate with ORS
  • 54. Oral Rehydration Therapy Sodium chloride 3.5 g Trisodium citrate dehydrate 2.9 g (or sodium bicarbonate 2.5g) Potassium chloride 1.5g Glucose 20 g To be dissolved in one litre of clean drinking water encourage fluid intake e.g. salt + glucose drink to assist in co-transport of sodium into the epithelial cells via the SGLT1 protein, which enhances water and sodium re-absorption in small intestines.