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ACUTE DIARRHOEAL DISEASE
1
AIMS OF THE LECTURE
o Definitions
o Risk factors
o Pathogenesis and mechanisms
o Consequences of watery diarrhea
o Site / duration of infective diarrhea
o Risk factors for persistent diarrhea
o Principles of ORT
o Composition of ORT
o Advantages/ Limitations of ORT
2
WHAT IS DIARRHEA?
• Increase in frequency, fluidity & volume of feces, for
the age of the child.
• In epidemiological studies:
The passage of three or more loose or watery stools in
a 24‐hour period, a loose stool being one that would
take the shape of a container.
3
MAGNITUDE OF THE PROBLEM
 In developing countries
1.3 thousand million episodes
4 million deaths each year in under‐fives.
Economic burden: occupy 1/3 hosp beds
 80% of diarrheal deaths occur < 2 yrs of age.
 Is an important cause of under nutrition.
Eat less during diarrhea
Ability to absorb nutrients is reduced;
Nutrient requirements are increased.
4
DEFINITIONS
1.Acute watery diarrhea
Diarrhea that begins acutely, lasts less than 14 days
(most episodes last less than seven days), and
involves the passage of frequent loose or watery
stools without visible blood. Vomiting and fever may
be present.
2.Dysentery
Diarrhea with visible blood in the feces. Important
effects of dysentery include anorexia, weight loss, and
damage to intestinal mucosa by the invasive bacteria
5
RISK FACTORS FOR ACUTE DIARRHEA
• Failure to breast‐feed exclusively for 4‐ 6 months.
• Failure to breast‐feed until at least one year of age.
• Using infant feeding bottles.
• Storing cooked food at room temperature.
• Drinking water contaminated with fecal bacteria.
• Failing to dispose off infant feces hygienically.
6
PREDISPOSING HOST FACTORS
• Under nutrition.
• Recent measles (In previous four weeks).
• Immunodeficiency
• Age: First two years of life, maximum at 6‐11
months Why ? Weaning period
‐ Declining levels of maternal antibodies.
‐ Lack of active immunity in the infant.
‐ Infant starts to crawl.
• Seasonal : Rotavirus throughout the year.
Bacterial in summer & rainy season.
• Epidemics: Vibrio cholera, Shigella.
7
WHAT CAUSES DIARRHOEA?
Infectious Disease Agents Causing Diarrhoea.
BACTERIA
1. Escherichia coli
It produces heat labile (LT) and heat stable (ST) entertoxins.
E.COLI - COULD BE
 Enteropathogenic- Causes infantile diarrhoea.
 Entero toxigenic – Causes travellers diarrhoea.
 Enteroinvasive- Dysentery type of diarrhoea.
 Enteroadherent
 Enterohaemorrhagic
VIBRIO CHOLERAE- produces enterotoxins
 Vibrio para haemolyticus- Invasive.
 Non-Cholerae vibrios
WHAT CAUSES DIARRHOEA?
Infectious Disease Agents
SHIGELLAE–Invasive, produce bloody diarrhoea or Dysentery.
 CAMPYLOBACTER JEJUNI – invasive.
 SALMONELLAE OTHER THAN S.TYPHI- invasive.
 STAPHYLOCOCCUS AUREUS- entrotoxins
 CLOSTRIDIUM PERFRINGENS- enterotoxins.
3. VIRUSES
 Rotavirus – invasive.
4. PARASITES
 E. histolytica- invasive.
 Giardia Lamblia- non invasive.
TYPES OF DIARRHOEA
 Acute watery diarrhoea.
 Acute bloody dairrhoea (blood in stools)aka dysentry
 Persistent diarrhoea.
 Dairrhoea with severe malnutrition (marasmus and
kwashiorkar)
PATHOGENESIS OF VIRAL DIARRHEAS
• Replicate within the villous epithelium,
causing patchy epithelial cell destruction
and villous shortening.
• Normally absorptive villous cells replaced
by immature, secretory, crypt‐like cells .
• Loss of disaccharidase enzyme ‐lactose
malabsorption
• Recovery occurs when the villi regenerate and the
villous epithelium matures E.g. : Rota virus
11
PATHOGENESIS OF BACTERIAL DIARRHOEAS
Mucosal adhesion:
• Prevents organism being swept away.
• Fimbriae bind to mucosal receptors.
• Results in reduced absorptive capacity.
E.g. : Enteropathogenic/ Enteroadherent
E Coli.
Secretory toxins:
• Toxins alter epithelial cell function absorption of sodium
by the villi is decreased
increased secretion of chloride in the crypts.
• Recovery occurs when “intoxicated cells” are replaced
by healthy cells.
E.g. : Enterotoxigenic E. coli, V. cholerae, Salmonella.
12
PATHOGENESIS OF BACTERIAL DIARRHOEAS
Mucosal invasion:
• Direct invasion & destruction of mucosal cells.
• Usually in the colon and distal ileum.
• Invasion micro abscesses & superficial ulcers.
• Toxins cause tissue damage and possibly also
mucosal secretion of water and electrolytes.
E.g. : Shigella, enteroinvasive E. coli
13
PATHOGENESIS OF PROTOZOAL DIARRHOEAS
• Production of micro‐abscesses:
Occurs only when the infecting
Entamoeba histolytica is virulent.
strain
In
of the
90% of
human infections, the strains are not virulent; in
which case there is no mucosal invasion and no
symptoms, although amoebic cysts are present in
the feces.
14
FLUID BALANCE IN THE GUT
 Absorption & secretion of water &
electrolytes occur throughout intestine.
 They are simultaneously absorbed by
the villi & secreted by the crypts of the
mucosa.
Water
Electrolytes
 Change in this two‐directional flow more fluid
enters large intestine. If this exceeds colonic absorptive
capacity, diarrhea occurs.
Normally fluid absorption>>fluid secretion
15
MECHANISMS OF DIARHEA
o Osmotic diarrhea
o Secretory diarrhea
o Inflammatory diarrhea
16
OSMOTIC DIARRHEA
• Small bowel mucosa is a porous epithelium; water and
salts move across it rapidly to maintain osmotic balance
• Diarrhea occurs when a poorly absorbed, osmotically
active substance is present in the gut .
• If substance is isotonic, the water and solute will simply
pass through the gut unabsorbed, causing diarrhea.
E.g. ; magnesium sulfate, lactose.
• If it is a hypertonic solution, water will move from the ECF
into the gut lumen until osmolality is equalized ‐ volume of
stool &dehydration.
17
OSMOTIC DIARHOEA
Features:
Stooling stops on fasting.
Stool pH acidic.
Reducing substance positive.
E.g.. Rota virus diarrhea.
Disaccharide malabsorption.
 Monosaccharide
malabsorption. Lactulose
ingestion.
Treatment :
Remove offending agent from diet.18
SECRETORY DIARHOEA
ACTIVE SECRETION
 Caused by the abnormal secretion (water and salt)
into the small bowel.
 Occurs when
Sodium absorption by the villi is impaired.
Chloride secretion in crypts
continues/increased.
 Mediators .. Cyclic A.M.P of Cholera
.. Cyclic G.M.P of E.T.E.C
19
SECRETORY DIARHOEA
Features:
 Stooling continues on fasting.
 Stool pH alkaline.
 Reducing substance – Negative.
Treatment:
 Treat underlying cause.
 Correct fluid & electrolyte deficits.
 Limited role for antibiotics.
20
CONSEQUENCES OF WATERY DIARRHOEA
1. Dehydration
.. Isotonic dehydration : commonest
‐ Net losses of water & sodium are in
proportion.
.. Hypernatremic dehydration
‐ Net loss of water in excess of sodium.
‐ Severe thirst out of proportion to the dehydration.
.. Hyponatremic dehydration
‐ Replacement with fluids of low salt
concentration
‐ Rare, usually iatrogenic
21
CONSEQUENCES OF WATERY DIARRHOEA
2. Metabolic acidosis
Causes : Loss of bicarbonate in the stool.
Poor renal blood flow, production of lactic acid.
Low bicarb, arterial pH < 7.10, deep/rapid
breathing.
3. Potassium depletion
Due to large fecal losses (esp. in infants)
Signs : Muscular weakness, Paralytic ileus.
22
RECAP OF IMPORTANT POINTS
• Diarrhea is an important cause of malnutrition and death in
children below 2 yrs.
• Acute uncomplicated watery diarrhea settles in 7 ‐14 days
• Normally H2O absorbed by villi >> secreted by crypt cells
• Secretory diarrhea occurs when Na+ absorption by the villi is
impaired, while Cl‐ secretion in cryptscontinues
• Osmotic diarrhea occurs when a poorly absorbed, osmotically
active substance is present in the gut
• Dehydration, acidosis and hypokalemia are complications
23
MECHANISMS OF DIARRHEA
3. Inflammatory diarrhea
A. Infective – Shigellosis, Amoebiasis.
B. Non infective – Ulcerative colitis.
How to diagnose ?
A. Fever.
B. Blood in stool. Increased fecal leucocytes.
C. Abdominal pain, cramps, tenesmus.
24
MANAGEMENT OF DYSENTERY
 Antibiotics : Depends on local sensitivity pattern
.. Nalidixic acid, Norflox, Cefixime
Given for 5 days.
 Fluids:
Oral replacement enough, unless vomiting present.
 Feeding :
Continue breast‐feeding
Give energy & nutrient‐rich foods six times a day.
One extra meal a day for two weeks follow‐up.
25
MORE ON INFECTIVE DIARRHEA……
3 to 6 days1. Cholera
2. Shigella
3. Rota Virus
4. ETEC
5. EIEC
6. Salmonella
7. Giardia
8. Amoebiasis ‐ Large Bowel
‐ Small Bowel ‐
‐ Large Bowel ‐
‐ Small Bowel ‐
‐ Small Bowel ‐
‐ Large Bowel ‐
‐ Small & Large ‐
‐ Small Bowel ‐
‐
7 to 14 days
5 to 7 days
5 to 10 days
? ?
3 ‐ 7 days
Chronicity
Chronicity
SITE DURATIO
N
26
TERMINOLOGIES IN DIARRHEA
•Persistent Diarrhea
An episode of diarrheal of presumed infectious
etiology that begins acutely and lasts for more than
14 days.
• Chronic diarrhea
Diarrhea that is recurrent/lasting more than 14 days,
is due to non‐ infectious cause & associated
with malabsorption. E.g. Celiac disease
27
PERSISTENT DIARRHEA
RISK FACTORS
 Infants below 6 months
 Malnourished infants
 Multiple antibiotics
 Multiple physicians
 Not breast fed
 Repeated diarrhea
 Enteropathogenic E. coli infection
28
ORAL REHYDRATION THERAPY
What is it?
Administration of fluid & electrolytes orally to
treat or prevent dehydration.
Why?
– Correction of water & electrolyte deficit is
possible orally
– Reduce mortality
– Cheap, easy and scientific
29
STORY OF ORAL REHYDRATION THERAPY
• Developed in the late 1960’s
• Life saver in cholera epidemic in east India in 70’s
• In the last 40 yrs , has saved more lives than any
other medical invention.
• In 1980 : 5 million deaths < 5 yrs from diarrhea
• In 2000 : Only 1.8 million deaths !!!
The problem today : low ORS usage by health
workers
30
SCIENTIFIC BASIS OF ORT
• Absorption of H2O/Na/K/HCO3 near normal in
diarrhea
• Glucose coupled sodium absorption promotes water
absorption across intestinal mucosa
• Maximal absorption, when Na to glucose ratio is 1.0
• Potassium absorption occurs by passive diffusion
• Water/electrolyte losses in diarrhea can be
effectively corrected by ORT 29
32
COMPOSITION OF CURRENT ORS
Gm
1.5
13.5
2.6
CONTENTS
• K Cl
• Glucose
• Na Cl
• Trisodium citrate 2.9
TOTAL 20.5
OSMOLARITY
• Na 75
• Cl 65
• Glucose 75
• K 20
• Citrate 10
TOTAL 245
33
DIARRHEA MANAGEMENT IN IMNCI
• Assessment of dehydration
• Mixing of ORS and details of administration
• Treatment of diarrhea at home ( Plan A)
• Treating some dehydration in clinic ( Plan B)
• Treating severe dehydration in an emergency (Plan C)
• Management of dysentery
• Diet in acute diarrhea
34
RICE BASED ORS
• Rice powder when digested releases twice the amount of
glucose than in ORS. This is enough to support the absorption
of water & electrolytes in ORS
• Protein in rice adds to this effect by release & absorption of
amino acids.
• Osmotic activity of rice‐ORS ( 220 mOsm/l) is lower than that
of blood or other tissues (290 mOsm/l).
• Calories in rice may help prevent malnutrition
• Trials show lower rate of stool volume in cholera.
More studies needed in non‐cholera diarrhea.
33
ADVANTAGES OF ORT
• Low cost
• Eliminates need for IV line placement
• Treatment can be done/continued at home
• Safe and few side effects
36
LIMITATIONS OF ORT USE
• Difficult when mental status is altered
(aspiration)
• Difficult when there is paralytic ileus
• Severe dehydration
• High failure rate if stool output remains excessive
• Difficult in severe/persistent vomiting, when ORS
37
ASSESSMENT OF A CHILD WITH DIARRHOEA
HISTORY
• Acute watery D
• Dysentery
• Persistent D.
• Watery, large ,frequent
• Vomiting‐ 6‐8hrs
• Urine
• Nature of fluids
• Feeding before illness
PHYSICAL EXAM.
• Signs of Dehydration
• Nutritional Status of
child
• Pneumonia,
Otitis Media
Other infections
38
ASSESSMENT OF A CHILD WITH
DIARRHOEA
NO DEHYDRATION
LOOK AT
• Condition
• Eyes
• Tears
• Mouth & Tongue
•Thirst
FEEL
Skin Pinch
• Well Alert
• Normal
• Present
• Moist
• Drinks Normally Not Thirsty
• Goes back quickly
39
ASSESSMENT OF A CHILD WITH DIARRHOEA (CONT)
SOME DEHYDRATION
Two of following signs
Restless, Irritable
Sunken
Absent
Dry
Thirsty, Drinks eagerly
Goes back slowly
Look at
•Condition
•Eyes
•Tears
•Mouth & Tongue
•Thirst
Feel
•Skin Pinch
40
ASSESSMENT OF A CHILD WITH DIARRHOEA
(CONT) SEVERE DEHYDRATION
LOOK AT
• Condition
• Eyes
• Tears
• Mouth & Tongue
• Thirst
FEEL
Skin Pinch
Lethargic or unconscious, floppy
Very sunken & dry
Absent
Very dry
Drinks poorly or not able to drink
Goes back very slowly
41
• No Dehydration
MANAGEMENT
• PLAN ‐ A
• Some Dehydration • PLAN ‐ B
• Severe Dehydration • PLAN – C
42
ORS FOR PREVENTION OF DEHYDRATION
(PLAN‐A)
Age
Amt . of ORS after
each loose stool
Amt of ORS to
provide for use at
home
<24 months 50‐100 ml 500 ml /day
2‐10 years 100‐200ml
1000 ml /day
10 years/more As much as wanted 2000 ml /day
43
TREATMENT PLAN B
(FOR SOME DEHYDRATION)
• Rehydration Therapy‐75 ml/Kg ORS in 1st 4 hours
• Maintenance Therapy
• Provision of Normal daily fluid requirements
44
TREATMENT PLAN C
SEVERE DEHYDRATION : IV FLUID THERAPY
RINGER LACTATE/N.SALINE
Age First‐30 ml/kg Then 70 ml / kg
<12 months 1 hour 5 hours
Older children 30 minutes 2 1/2hours
45
NUTRITIONAL MANAGEMENT OF ACUTE
DIARRHOEA
Diarrhea Worsens Nutritional status
a) Decreased food intake –
Anorexia /
Maternal food withholding
b) Intestinal malabsorption –
Macronutrients & Some micronutrients
46
RECOMMENDATIONS
•Continue Feeding
•Continue Breast Feeding even during
rehydration
•Animal milk need not be diluted
•Enrich staple foods – fats & oil /sugar
•High fiber content foods–avoided
•Routine lactose free feeds‐not needed
•During recovery‐125% intake
47
RECAP ……
 Persistent diarrhea lasts > 14 days. Infants < 6
months, malnourished and not breast fed are at high
risk.
 High fever, blood in stool & abdominal cramps
suggest dysentery
 ORT is life saving in diarrheal dehydration.
 Principle of ORT is that glucose coupled sodium
transport promotes water absorption across
intestinal mucosa
 Total osmolarity of current ORS is only 245 mOsm/L
 Advantages of ORT are more than the limitations.
48
THANK YOU
49

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Acute diarrhoeal diseases

  • 2. AIMS OF THE LECTURE o Definitions o Risk factors o Pathogenesis and mechanisms o Consequences of watery diarrhea o Site / duration of infective diarrhea o Risk factors for persistent diarrhea o Principles of ORT o Composition of ORT o Advantages/ Limitations of ORT 2
  • 3. WHAT IS DIARRHEA? • Increase in frequency, fluidity & volume of feces, for the age of the child. • In epidemiological studies: The passage of three or more loose or watery stools in a 24‐hour period, a loose stool being one that would take the shape of a container. 3
  • 4. MAGNITUDE OF THE PROBLEM  In developing countries 1.3 thousand million episodes 4 million deaths each year in under‐fives. Economic burden: occupy 1/3 hosp beds  80% of diarrheal deaths occur < 2 yrs of age.  Is an important cause of under nutrition. Eat less during diarrhea Ability to absorb nutrients is reduced; Nutrient requirements are increased. 4
  • 5. DEFINITIONS 1.Acute watery diarrhea Diarrhea that begins acutely, lasts less than 14 days (most episodes last less than seven days), and involves the passage of frequent loose or watery stools without visible blood. Vomiting and fever may be present. 2.Dysentery Diarrhea with visible blood in the feces. Important effects of dysentery include anorexia, weight loss, and damage to intestinal mucosa by the invasive bacteria 5
  • 6. RISK FACTORS FOR ACUTE DIARRHEA • Failure to breast‐feed exclusively for 4‐ 6 months. • Failure to breast‐feed until at least one year of age. • Using infant feeding bottles. • Storing cooked food at room temperature. • Drinking water contaminated with fecal bacteria. • Failing to dispose off infant feces hygienically. 6
  • 7. PREDISPOSING HOST FACTORS • Under nutrition. • Recent measles (In previous four weeks). • Immunodeficiency • Age: First two years of life, maximum at 6‐11 months Why ? Weaning period ‐ Declining levels of maternal antibodies. ‐ Lack of active immunity in the infant. ‐ Infant starts to crawl. • Seasonal : Rotavirus throughout the year. Bacterial in summer & rainy season. • Epidemics: Vibrio cholera, Shigella. 7
  • 8. WHAT CAUSES DIARRHOEA? Infectious Disease Agents Causing Diarrhoea. BACTERIA 1. Escherichia coli It produces heat labile (LT) and heat stable (ST) entertoxins. E.COLI - COULD BE  Enteropathogenic- Causes infantile diarrhoea.  Entero toxigenic – Causes travellers diarrhoea.  Enteroinvasive- Dysentery type of diarrhoea.  Enteroadherent  Enterohaemorrhagic VIBRIO CHOLERAE- produces enterotoxins  Vibrio para haemolyticus- Invasive.  Non-Cholerae vibrios
  • 9. WHAT CAUSES DIARRHOEA? Infectious Disease Agents SHIGELLAE–Invasive, produce bloody diarrhoea or Dysentery.  CAMPYLOBACTER JEJUNI – invasive.  SALMONELLAE OTHER THAN S.TYPHI- invasive.  STAPHYLOCOCCUS AUREUS- entrotoxins  CLOSTRIDIUM PERFRINGENS- enterotoxins. 3. VIRUSES  Rotavirus – invasive. 4. PARASITES  E. histolytica- invasive.  Giardia Lamblia- non invasive.
  • 10. TYPES OF DIARRHOEA  Acute watery diarrhoea.  Acute bloody dairrhoea (blood in stools)aka dysentry  Persistent diarrhoea.  Dairrhoea with severe malnutrition (marasmus and kwashiorkar)
  • 11. PATHOGENESIS OF VIRAL DIARRHEAS • Replicate within the villous epithelium, causing patchy epithelial cell destruction and villous shortening. • Normally absorptive villous cells replaced by immature, secretory, crypt‐like cells . • Loss of disaccharidase enzyme ‐lactose malabsorption • Recovery occurs when the villi regenerate and the villous epithelium matures E.g. : Rota virus 11
  • 12. PATHOGENESIS OF BACTERIAL DIARRHOEAS Mucosal adhesion: • Prevents organism being swept away. • Fimbriae bind to mucosal receptors. • Results in reduced absorptive capacity. E.g. : Enteropathogenic/ Enteroadherent E Coli. Secretory toxins: • Toxins alter epithelial cell function absorption of sodium by the villi is decreased increased secretion of chloride in the crypts. • Recovery occurs when “intoxicated cells” are replaced by healthy cells. E.g. : Enterotoxigenic E. coli, V. cholerae, Salmonella. 12
  • 13. PATHOGENESIS OF BACTERIAL DIARRHOEAS Mucosal invasion: • Direct invasion & destruction of mucosal cells. • Usually in the colon and distal ileum. • Invasion micro abscesses & superficial ulcers. • Toxins cause tissue damage and possibly also mucosal secretion of water and electrolytes. E.g. : Shigella, enteroinvasive E. coli 13
  • 14. PATHOGENESIS OF PROTOZOAL DIARRHOEAS • Production of micro‐abscesses: Occurs only when the infecting Entamoeba histolytica is virulent. strain In of the 90% of human infections, the strains are not virulent; in which case there is no mucosal invasion and no symptoms, although amoebic cysts are present in the feces. 14
  • 15. FLUID BALANCE IN THE GUT  Absorption & secretion of water & electrolytes occur throughout intestine.  They are simultaneously absorbed by the villi & secreted by the crypts of the mucosa. Water Electrolytes  Change in this two‐directional flow more fluid enters large intestine. If this exceeds colonic absorptive capacity, diarrhea occurs. Normally fluid absorption>>fluid secretion 15
  • 16. MECHANISMS OF DIARHEA o Osmotic diarrhea o Secretory diarrhea o Inflammatory diarrhea 16
  • 17. OSMOTIC DIARRHEA • Small bowel mucosa is a porous epithelium; water and salts move across it rapidly to maintain osmotic balance • Diarrhea occurs when a poorly absorbed, osmotically active substance is present in the gut . • If substance is isotonic, the water and solute will simply pass through the gut unabsorbed, causing diarrhea. E.g. ; magnesium sulfate, lactose. • If it is a hypertonic solution, water will move from the ECF into the gut lumen until osmolality is equalized ‐ volume of stool &dehydration. 17
  • 18. OSMOTIC DIARHOEA Features: Stooling stops on fasting. Stool pH acidic. Reducing substance positive. E.g.. Rota virus diarrhea. Disaccharide malabsorption.  Monosaccharide malabsorption. Lactulose ingestion. Treatment : Remove offending agent from diet.18
  • 19. SECRETORY DIARHOEA ACTIVE SECRETION  Caused by the abnormal secretion (water and salt) into the small bowel.  Occurs when Sodium absorption by the villi is impaired. Chloride secretion in crypts continues/increased.  Mediators .. Cyclic A.M.P of Cholera .. Cyclic G.M.P of E.T.E.C 19
  • 20. SECRETORY DIARHOEA Features:  Stooling continues on fasting.  Stool pH alkaline.  Reducing substance – Negative. Treatment:  Treat underlying cause.  Correct fluid & electrolyte deficits.  Limited role for antibiotics. 20
  • 21. CONSEQUENCES OF WATERY DIARRHOEA 1. Dehydration .. Isotonic dehydration : commonest ‐ Net losses of water & sodium are in proportion. .. Hypernatremic dehydration ‐ Net loss of water in excess of sodium. ‐ Severe thirst out of proportion to the dehydration. .. Hyponatremic dehydration ‐ Replacement with fluids of low salt concentration ‐ Rare, usually iatrogenic 21
  • 22. CONSEQUENCES OF WATERY DIARRHOEA 2. Metabolic acidosis Causes : Loss of bicarbonate in the stool. Poor renal blood flow, production of lactic acid. Low bicarb, arterial pH < 7.10, deep/rapid breathing. 3. Potassium depletion Due to large fecal losses (esp. in infants) Signs : Muscular weakness, Paralytic ileus. 22
  • 23. RECAP OF IMPORTANT POINTS • Diarrhea is an important cause of malnutrition and death in children below 2 yrs. • Acute uncomplicated watery diarrhea settles in 7 ‐14 days • Normally H2O absorbed by villi >> secreted by crypt cells • Secretory diarrhea occurs when Na+ absorption by the villi is impaired, while Cl‐ secretion in cryptscontinues • Osmotic diarrhea occurs when a poorly absorbed, osmotically active substance is present in the gut • Dehydration, acidosis and hypokalemia are complications 23
  • 24. MECHANISMS OF DIARRHEA 3. Inflammatory diarrhea A. Infective – Shigellosis, Amoebiasis. B. Non infective – Ulcerative colitis. How to diagnose ? A. Fever. B. Blood in stool. Increased fecal leucocytes. C. Abdominal pain, cramps, tenesmus. 24
  • 25. MANAGEMENT OF DYSENTERY  Antibiotics : Depends on local sensitivity pattern .. Nalidixic acid, Norflox, Cefixime Given for 5 days.  Fluids: Oral replacement enough, unless vomiting present.  Feeding : Continue breast‐feeding Give energy & nutrient‐rich foods six times a day. One extra meal a day for two weeks follow‐up. 25
  • 26. MORE ON INFECTIVE DIARRHEA…… 3 to 6 days1. Cholera 2. Shigella 3. Rota Virus 4. ETEC 5. EIEC 6. Salmonella 7. Giardia 8. Amoebiasis ‐ Large Bowel ‐ Small Bowel ‐ ‐ Large Bowel ‐ ‐ Small Bowel ‐ ‐ Small Bowel ‐ ‐ Large Bowel ‐ ‐ Small & Large ‐ ‐ Small Bowel ‐ ‐ 7 to 14 days 5 to 7 days 5 to 10 days ? ? 3 ‐ 7 days Chronicity Chronicity SITE DURATIO N 26
  • 27. TERMINOLOGIES IN DIARRHEA •Persistent Diarrhea An episode of diarrheal of presumed infectious etiology that begins acutely and lasts for more than 14 days. • Chronic diarrhea Diarrhea that is recurrent/lasting more than 14 days, is due to non‐ infectious cause & associated with malabsorption. E.g. Celiac disease 27
  • 28. PERSISTENT DIARRHEA RISK FACTORS  Infants below 6 months  Malnourished infants  Multiple antibiotics  Multiple physicians  Not breast fed  Repeated diarrhea  Enteropathogenic E. coli infection 28
  • 29. ORAL REHYDRATION THERAPY What is it? Administration of fluid & electrolytes orally to treat or prevent dehydration. Why? – Correction of water & electrolyte deficit is possible orally – Reduce mortality – Cheap, easy and scientific 29
  • 30. STORY OF ORAL REHYDRATION THERAPY • Developed in the late 1960’s • Life saver in cholera epidemic in east India in 70’s • In the last 40 yrs , has saved more lives than any other medical invention. • In 1980 : 5 million deaths < 5 yrs from diarrhea • In 2000 : Only 1.8 million deaths !!! The problem today : low ORS usage by health workers 30
  • 31. SCIENTIFIC BASIS OF ORT • Absorption of H2O/Na/K/HCO3 near normal in diarrhea • Glucose coupled sodium absorption promotes water absorption across intestinal mucosa • Maximal absorption, when Na to glucose ratio is 1.0 • Potassium absorption occurs by passive diffusion • Water/electrolyte losses in diarrhea can be effectively corrected by ORT 29
  • 32. 32
  • 33. COMPOSITION OF CURRENT ORS Gm 1.5 13.5 2.6 CONTENTS • K Cl • Glucose • Na Cl • Trisodium citrate 2.9 TOTAL 20.5 OSMOLARITY • Na 75 • Cl 65 • Glucose 75 • K 20 • Citrate 10 TOTAL 245 33
  • 34. DIARRHEA MANAGEMENT IN IMNCI • Assessment of dehydration • Mixing of ORS and details of administration • Treatment of diarrhea at home ( Plan A) • Treating some dehydration in clinic ( Plan B) • Treating severe dehydration in an emergency (Plan C) • Management of dysentery • Diet in acute diarrhea 34
  • 35. RICE BASED ORS • Rice powder when digested releases twice the amount of glucose than in ORS. This is enough to support the absorption of water & electrolytes in ORS • Protein in rice adds to this effect by release & absorption of amino acids. • Osmotic activity of rice‐ORS ( 220 mOsm/l) is lower than that of blood or other tissues (290 mOsm/l). • Calories in rice may help prevent malnutrition • Trials show lower rate of stool volume in cholera. More studies needed in non‐cholera diarrhea. 33
  • 36. ADVANTAGES OF ORT • Low cost • Eliminates need for IV line placement • Treatment can be done/continued at home • Safe and few side effects 36
  • 37. LIMITATIONS OF ORT USE • Difficult when mental status is altered (aspiration) • Difficult when there is paralytic ileus • Severe dehydration • High failure rate if stool output remains excessive • Difficult in severe/persistent vomiting, when ORS 37
  • 38. ASSESSMENT OF A CHILD WITH DIARRHOEA HISTORY • Acute watery D • Dysentery • Persistent D. • Watery, large ,frequent • Vomiting‐ 6‐8hrs • Urine • Nature of fluids • Feeding before illness PHYSICAL EXAM. • Signs of Dehydration • Nutritional Status of child • Pneumonia, Otitis Media Other infections 38
  • 39. ASSESSMENT OF A CHILD WITH DIARRHOEA NO DEHYDRATION LOOK AT • Condition • Eyes • Tears • Mouth & Tongue •Thirst FEEL Skin Pinch • Well Alert • Normal • Present • Moist • Drinks Normally Not Thirsty • Goes back quickly 39
  • 40. ASSESSMENT OF A CHILD WITH DIARRHOEA (CONT) SOME DEHYDRATION Two of following signs Restless, Irritable Sunken Absent Dry Thirsty, Drinks eagerly Goes back slowly Look at •Condition •Eyes •Tears •Mouth & Tongue •Thirst Feel •Skin Pinch 40
  • 41. ASSESSMENT OF A CHILD WITH DIARRHOEA (CONT) SEVERE DEHYDRATION LOOK AT • Condition • Eyes • Tears • Mouth & Tongue • Thirst FEEL Skin Pinch Lethargic or unconscious, floppy Very sunken & dry Absent Very dry Drinks poorly or not able to drink Goes back very slowly 41
  • 42. • No Dehydration MANAGEMENT • PLAN ‐ A • Some Dehydration • PLAN ‐ B • Severe Dehydration • PLAN – C 42
  • 43. ORS FOR PREVENTION OF DEHYDRATION (PLAN‐A) Age Amt . of ORS after each loose stool Amt of ORS to provide for use at home <24 months 50‐100 ml 500 ml /day 2‐10 years 100‐200ml 1000 ml /day 10 years/more As much as wanted 2000 ml /day 43
  • 44. TREATMENT PLAN B (FOR SOME DEHYDRATION) • Rehydration Therapy‐75 ml/Kg ORS in 1st 4 hours • Maintenance Therapy • Provision of Normal daily fluid requirements 44
  • 45. TREATMENT PLAN C SEVERE DEHYDRATION : IV FLUID THERAPY RINGER LACTATE/N.SALINE Age First‐30 ml/kg Then 70 ml / kg <12 months 1 hour 5 hours Older children 30 minutes 2 1/2hours 45
  • 46. NUTRITIONAL MANAGEMENT OF ACUTE DIARRHOEA Diarrhea Worsens Nutritional status a) Decreased food intake – Anorexia / Maternal food withholding b) Intestinal malabsorption – Macronutrients & Some micronutrients 46
  • 47. RECOMMENDATIONS •Continue Feeding •Continue Breast Feeding even during rehydration •Animal milk need not be diluted •Enrich staple foods – fats & oil /sugar •High fiber content foods–avoided •Routine lactose free feeds‐not needed •During recovery‐125% intake 47
  • 48. RECAP ……  Persistent diarrhea lasts > 14 days. Infants < 6 months, malnourished and not breast fed are at high risk.  High fever, blood in stool & abdominal cramps suggest dysentery  ORT is life saving in diarrheal dehydration.  Principle of ORT is that glucose coupled sodium transport promotes water absorption across intestinal mucosa  Total osmolarity of current ORS is only 245 mOsm/L  Advantages of ORT are more than the limitations. 48