for pediatrics UG teaching

1. CHRONIC DIARRHEA
Dr M.Sanjeevappa
M.D.(Paeds)
Asst.Professor,
Dept. of Paediatrics
Govt.Medical College
Ananthapuramu.

2.  Most diarrheal disorders resolve within the first
week of the illness.
 1 to 3% of acute diarrhoeas become chronic, With
a high mortality and morbidity.
 Chronic diarrhea has been defined as an episode
that begins acutely but lasts for 14 days or longer.
 Two entities :
1) Persistent diarrhea.
2) Chronic diarrhea.

3. PERSISTENT DIARRHEA
 starts as acute diarrhea, but instead of subsiding
in the usual time, the child goes on purging for a
period of more than 2 weeks.
risk factors :
 Protein-energy malnutrition
 Younger age < 18 months
 Lack of breast-feeding
 Bottle-feeding
 Cow's milk,Soy protein allergy.
 Inappropriate use of antibiotics

4. PERSISTENT DIARRHEA
Risk factors :
 Improper therapy of ADD.
 Use of antimotility drugs like loperamide.
 Starvation during ADD.
 Vitamin A deficiency.
 Zinc deficiency.
 Poor hygiene leading to reinfection.
 Certain extra intestinal infections, e.g :UTI

5. CHRONIC DIARRHEA
Definition :
 Chronic diarrhea is defined as diarrhea greater than
2 weeks duration, with an insidious onset and
usually due to noninfectious cause. Almost all
patients need a complete workup for underlying
malabsorptive state.
1. Inflammatory causes :
 Tuberculosis.
 Eosinophilic gastroenteritis.
 Crohn's disease.
 Necrotising enterocolitis.
 Allergic colitis.
 Henoch-Schonlein vasculitis.

6. CHRONIC DIARRHEA
2. Malabsorption states :
 Pancreatic diseases.
 Cystic fibrosis.
 Chronic pancreatitis.
 Hereditary pancreatitis.
 Congenital lipase deficiency.
 Congenital trypsin deficiency.

7. CHRONIC DIARRHEA
3.Intestinal diseases :
 Tropical sprue
 Coeliac disease
 Whipple's diseae
 Intestinal lymphangiectasia
 Enterokinase deficiency.
 Vitamin B12 malabsorption
 Juvenile pernicious anaemia.
 Transcobalamin II deficiency.
 Lactase deficiency-congenital/acquired.
 Sucrase-isomaltase deficiency.
 Glucose-galactose malabsorption.

8. CHRONIC DIARRHEA
4.Metabolic disorders :
 Darrow's syndrome (congenital chloride diarrhea).
 Abetalipoproteinaemia.
 Acrodermatitis enteropathica.
5.Endocrine causes :
 Hypoparathyroidism, Hyperthyroidism.
 Diabetes mellitus.
 Adrenal insufficiency.
6.Congenital alterations in electrolyte transport :
 Congenital chloride diarrhea

9. CHRONIC DIARRHEA
7.Immune defects :
 Agammaglobulinaemia.
 Isolated IgA deficiency.
 Defective CMI.
 Combined immunodeficiency.
8.Neoplasms :
 lmmunoproliferative small intestinal disease
(IPSID orMediterranean lymphoma).
 Western lymphoma.
 Ganglioneuroma.
 Vernor-Morrison syndrome (pancreatic cholera)
 Zollinger-Ellison syndrome.

10. CHRONIC DIARRHEA
Liver diseases :
 Cholestatic jaundice.
 Primary bile acid malabsorption.
Motility disorders :
 Toddler´s diarrhoea
 Hyperthyroidism
 Idiopathic bowel pseudo-obstruction
 Irritable bowel syndrome
Anatomical or surgical disorder :
 Necrotizing enterocolitis
 Short bowel syndrome
 Blind loop syndrome
 Hirschprung’s disease
 Intestinal lymphangiectasia

11. PATHOPHYSIOLOGY
OSMOTIC DIARRHEA
presence of nonabsorbable solutes.
colonic bacteria ferment the nonabsorbed sugar to
short-chain organic acids
osmotic load
water secreted

12. CAUSES FOR OSMOTIC DIARRHEA
 malabsorption of water-soluble nutrients
-glucose-galactose malabsorption
-congenital, acquired disaccharidase deficiencies.
 excessive intake of carbonated fluid.
 excessive intake of nonabsorbable solutes.
-sorbitol, lactulose, magnesium hydroxide.
 stops with fasting.
 has a low pH.
 positive for reducing substances

13. PATHOPHYSIOLOGY
SECRETORY DIARRHEA
activation cAMP, cGMP, and intracellular calcium.
active chloride secretion (crypt cells)+ inhibit
the neutral coupled sodium chloride absorption.
alter the paracellular ion flux( toxin-mediated
injury to the tight junctions)
secretory diarrhea

14. CAUSES OF SECRETORY DIARRHEA
ACTIVATION OF CYCLIC AMP
 Bacterial toxins: enterotoxins of cholera, Escherichia coli
(heat-labile), Shigella, Salmonella, Campylobacter jejuni,
Pseudomonas aeruginosa
 Hormones: vasoactive intestinal peptide, gastrin, secretin
 Anion surfactants: bile acids.
ACTIVATION OF CYCLIC GMP
 Bacterial toxins: E. coli (heat-stable) enterotoxin, Yersinia
enterocolitica toxin
CALCIUM-DEPENDENT
 Bacterial toxins: Clostridium difficile enterotoxin
 Neurotransmiters: acetylcholine, serotonin
 Paracrine agents: bradykinin

16. EVALUATION OF A CHILD WITH
CHRONIC DIARRHEA
STOOL HISTORY :
 SBD : profuse, watery, usually offensive stools,
without blood.
 LBD: small quantity, frequently with blood and
mucus.
 Odourless blood tinged stools - shigellosis
 Frequent mucoid stools in a healthy child without blood -
IBS
 Nocturnal diarrhoea favours organic disease over IBS.
 History of delayed passage of meconiurn and if
constipation preceded diarrhoea,- Hirschsprung's
disease

17. DIETETIC HISTORY
 It may provide vital clues to the aetiology, e.g., cow's milk
protein intolerance, lactose intolerance, gluten enteropathy,
soy protien intolerance, egg protien enteropathy.
 Overfeeding, concentrated formula feeds> osmotic
diarrhoea.
 Chewing gums and chocolates.
 plenty of undiluted fruit juices (e.g., pineapple juice has
an osmolality of 900 mOsm/L and apple juice 650 mOsm/L

18. TREATMENT HISTORY
 If achild on antibiotics develops diarrhea, -
pseudomembranous colitis.
 Drugs - neomycin, colchicine, cholestyrarnine, digitalis,
and propranolol.
 Laxatives abuse(Factitious diarrhoea by proxy)
 A family history- IBS.

19. DIAGNOSIS
 A complete clinical history is mandatory.
 Age of onset
 Nutritional assessment
 Associated symptoms: fever, vomiting, abdominal pain,
anorexia.
 Stool characteristics: blood, mucous, non digested
substances, steatorrhea.
 Physical examination: FTT, abdominal distension,
 visceromegaly, tenderness, presence of abdominal
masses.
 Other organs affected, e.g. skin, respiratory system.

20. DIAGNOSIS
 Hyperpigmentation- Addison's disease, coeliac
disease ,Whipple's disease.
 Generalized lymphadenopathy- lymphoma, AIDS or
Whipple's disease.
 In a child born of consanguinous parents with
malabsorption and chronic lung disease, cystic
fibrosis should be ruled out.

21. DIAGNOSIS
 Recurrent fever- tuberculosis, lynphoma, and IBD
 Marked loss of weight- malabsorption, lymphomas,
IBD, TB.
 periorifcial lesions : acrodermatitis emeropathica.
 perianal fistula - Crohn's disease.
 Clubbing - malabsorption syndromes, IBD.
 Chronic liver disease- IBD
 Hepatomegaly -lymphomas, metastatic carcinoid,
IBD and Whipple's disease.
 Ascites - TB and lymphoma.

22. INVESTIGATION
STOOL EXAMINATION
Microscopy :
 Polymorphs and RBCs - bacterial colitis, whipworm
colitis, amoebic colitis and in IBD.
 Eosinophils are seen in milk or soya protein intolerance.
pH and Reducing Substance :
 A stool pH < 5.5 (on cow's milk) or < 5 (on breast milk) is
suggestive of carbohydrate malabsorption and proximal
small bowel damage.
 Stool pH gives a clue to the amount of organic acids in
stool while the increased amounts of reducing substances
indicate the presence of unabsorbed sugars.

23. DEMONSTRATION OF REDUCING SUGARS IN STOOL
 Benedict's test : 1 ml of distilled water is added to 0.5
ml liquid stool and shaken well. 8 drops of this are
added to 5 ml of preboiled Benedict's solution and
boiled for 1 minute.The solution is cooled and the
precipitate is examined for colour change.
 Stool Culture :
Stool culture is positive only in 20% of patients with
acute diarrhoea and it is even lower in PD.
 Occult Blood :
In acute diarrhoea- bacterial or parasitic colitis.
Chronic diarrhoea- IBD like ulcerative colitis and
Crohn's colitis and IPSID(Immunoproliferative small
intestinal desease).

24. INVESTIGATION
Peripheral Blood Picture
 iron deficiency anaemia or dimorphic anaemia.
 abetalipoproteinaemia (acanthocytes)
Biochemical Investigations
 Serum electrolytes,
 blood urea,
 RBS and plasma proteins.
Blood and Urine Culture
 Systemic infections are important causes of CD in
infancy. Cultures from various sites, before starting
antibiotics, are extremely useful in detecting these
infections.

25. INVESTIGATION
 Barium meal follow through:
This will detect ulcers and strictures of small bowel.
 Small bowel biopsy:
tropicalsprue, coeliac disease, tuberculosis,
lymphoma,abetalipoproteinaetnia, Whipple's
disease, amyloidosis, lymphangicetasia.

26. INVESTIGATION
 Proctosigmoidoscopy:
 To differentiate SBD from LBD(colitis).
 To visualize pseudomernbrane/polyps/ulcers/tumours.
 Direct swabs for microscopy and culture.
 Rectal biopsy.
 Rectal Biopsy :
 Ulcerative colitis.
 Crohn's disease.
 Schistosomiasis.
 Trichuriasis.
 Amyloidosis.
 Whipple's disease

27. INVESTIGATION
Tests for Tuberculosis :
 Mantoux test.
 X-ray chest.
 Barium meal follow-through for ulcers, strictures,
malabsorption pattern etc.
 Barium enema-if colonic lesion is suspected.
 Duodenal, jejunal or colonic biopsy-for tissue
diagnosis.

28. MANAGEMENT
 About 30% of patients with PD require
hospitalization, if they have 1 or more of the
following:
 Age: Less than 4 months and not breast feed.
 Severe PEM.
 Dehydration
 Presence of systemic infections.

29. MANAGEMENT
The management of PD consists of 3 phases:
 Resuscitation phase (24-48 hours).
 Control of diarrhoea (up to 7 days).
 Rehabilitation phase (up to 8 weeks).

30. MANAGEMENT
RESUSCITATION PHASE
 IV line , vital signs monitored and blood group and
cross matching.
 Correction of dehydration, shock, electrolyte
disturbance, hypoglycaemia and renal failure.
 Appropriate antibiotics.
 first 24 hours the child is given iv fluids and nil
orally, except sips of ORS.

31. MANAGEMENT
CONTROL OF DIARRHEA
The major factors responsible for PD
 Bacterial contamination of the gut.
 Systemic infections.
 Food allergen (cow milk, soy protein, egg protein).
 Lactose intolerance.
 Toxins.
 Bile acids.

32. MANAGEMENT
 Many infants with PD are very sick and have features of
systemic infections like septicaemia and
bronchopneumonia.
 Combination of I.V. Amikacin and I.V. cefotaxime is
extremely effective in sick infants.
 In infants less than 3 months I.V. Amikacin and I.V.
Ampicillin are more effective.
 In a recent study cotrimoxazole was found to be very
useful in children with PD.
 Albendazole.
 Shigellosis – ciprofloxcacin.
 Amebiasis – metronidazole.

33. MANAGEMENT
REHABILITATION PHASE AND AIMS
 To improve the general health and nutritional
status.
 To correct nutritional deficiencies.
 For catch-up growth.
 To educate the parents, especially to prevent future
relapse.

34. MANAGEMENT
DIETARY MANAGEMENT AND GOALS :
 Small frequent feeds.
 Start with a high carbohydrate, low protein, and no fat
regime, as the patient improves, coconut oil may be
added.
 Always avoid those food substances, which may be
responsible for PD e.g., milk and milk products in
cow's milk allergy.
 Provide adequate micronutrients and vitamins.
 The diet should not be hyperosmolar.

35. MANAGEMENT

36. MANAGEMENT

37. MANAGEMENT

38. MANAGEMENT
INDICATORS OF TREATMENT FAILURE :
 Passage of >7 stools per day at the end of one
week.
 Weight loss or poor weight gain, in spite of an oral
intake of at least 100 ml/kg/day, over the previous
3 days.
 If the child develops dehydration at anytime.
 Significant increase in diarrhoea with in 48 hr

39. MANAGEMENT
Problems and Remedies :
 Anorexia - try nasogastric feeding.
 Intolerance - change diet, postpone alimentation.
 Poor weight gain - add fat and pancreatic enzymes.
 Trace element deficiency - oral zinc, Mg.
 Hypothermia - wrap the baby well.

40. THANK YOU