1. CHRONIC DIARRHOEA
And management
Dr. s. s. yadav
Dr jyoti prajapati

2. CHRONIC DIARRHOEA
 Despite considerable advances in the understanding and
management of diarrheal disorders in childhood, they are
still responsible for a major burden of childhood deaths
globally, with an estimated2.5 million deaths.
 More recent reviews of studies published in the past 10
years indicate that, while global mortality may have
reduced, the incidence remained unchanged at about 3.2
episodes/child year.
 These findings indicate the continuing need to focus on
prevention and management of childhood diarrhea in
developing countries.

3. 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.
Persistent diarrhea has been defined as an episode that
begins acutely but lasts for 14 days or longer.
Classification of chronic Diarrhoea (CD)
 Type I—chronic diarrhoea in a previously normal child-
90%
 Type Il—chronic diarrhoea in a child with inherent
defect-10%

4. type 1 (persistent or protracted)
starts as acute diarrhoea, but instead of subsiding in the usual time, the child
goes on purging for a period of more than 2 weeks.
The various risk factors for this are:
 Protein-energy malnutrition
 Younger age < 18 months
 Lack of breast-feeding
 Bottle-feeding
 Cow's milk.,Soy protein
 Inappropriate use of antibiotics
 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., septi-cacmia, UTI

5. TYPE II CHRONIC DIARRHOEA
1. Inflammatory causes
 Tuberculosis.
 Eosinophilic gastroenteritis.
 Crohn's disease.
 Behcel's syndrome.
 Necrotising enterocolitis.
 Allergic colitis.
 Henoch-Schonlein vasculitis.
2. Malabcription states
 Pancreatic diseases
 Cystic fibrosis.
 Diamond-Shwachman syndrome.
 Chronic pancreatitis.
 Hereditary pancreatitis.
 Congenital lipase deficiency.
 Congenital trypsin deficiency.

6. Liver diseases
 Cholestatic jaundice.
 Primary bile acid malabsorption.
Intestinal diseases
 Tropical sprue
 Coeliac disease
 Whipple's diseae
 Intestinal lymphangiectasia
 Anderson's disease (chylornicron reten-tion disease)
 Bassen-Kornzweig syndrome (abetal-ipoproteinaemia
 Enterokinasc deficiency
 Vitamin B12 malabsorption
 Juvenile pernicious anaemia.
 Transcobalamin II deficiency.
 Lactase deficiency-congenital/ac-quired.
 Sucrase-isomaltase deficiency.
 Glucose-galactose malabsorption.

7. Metabolic disorders
 Darrow's syndrome (congenital chloride diarrhoea).
 Abetalipoproteinaemia.
 Acrodermatitis enteropathica.
Endocrine causes
 Hypoparathyroidism, Hyperthyroidism.
 Diabetes mellitus.
 Adrenal insufficiency.
Congenital alterations in electrolyte transport
 Congenital chloride diarrhoea

8. Immune defects
 Agammaglobulinaemia.
 Isolated IgA deficiency.
 Defective CMI.
 Combined immunodeficiency.
Neoplasms
 lmmunoproliferative small intestinal dis-ease (IPSID or
Mediterranean lym-phoma).
 Western lymphoma.
 Ganglioneuroma.
 Vernor-Morrison syndrome (pancreatic cholera or
VIPoma).
 Zollinger-Ellison syndrome.

9. 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

10. COMMON CAUSES OF CHRONIC DIARRHEA
INFANCY
 Postgastroenteritis malabsorption syndrome (persistent)
 Cow's milk/soy protein intolerance
 Secondary disaccharidase deficiencies
 Cystic fibrosis
CHILDHOOD
 Chronic nonspecific diarrhea
 Secondary disaccharidase deficiencies
 Giardiasis
 Postgastroenteritis malabsorption syndrome
 Celiac disease
 Cystic fibrosis
ADOLESCENCE
 Irritable bowel syndrome
 Inflammatory bowel disease
 Giardiasis
 Lactose intolerance

11. PATHOPHYSIOLOGY
 osmotic diarrhea
 secretory diarrhea,
 mutations in apical membrane transport
proteins,
 reduction in anatomic surface area
 alteration in intestinal motility, and
 inhibition of transport of electrolytes by
inflammatory mediators

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

13. CAUSES
 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

14. 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

15. 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, ricinoleic acid
ACTIVATION OF CYCLIC GMP
 Bacterial toxins: E. coli (heat-stable) enterotoxin, Yersinia
enterocolitica toxin
CALCIUM-DEPENDENT
 Bacterial toxins: Clostridium difficileenterotoxin
 Neurotransmitters:acetylcholine, serotonin
 Paracrine agents: bradykinin

16. DIFFERENTIAL DIAGNOSIS OF OSMOTIC VS
SECRETORY DIARRHEA
OSMOTIC DIARRHEA SECRETORY DIARRHEA
Volume of stool <200 mL/24 hr >200 mL/24 hr
Response to fasting Diarrhea stops Diarrhea continues
Stool Na+ <70 mEq/L >70 mEq/L
Reducing substances[*] Positive Negative
Stool pH <5 >6

17. CHRONIC NONSPECIFIC DIARRHEA (TODDLER'S
DIARRHEA)
 well-appearing toddlers (1 and 3 yr )
 morning
 brown and watery, undigested food particles.
MANAGEMENT- fluid intake should be reduced to no
more than 90 mL/kg/24 hr.
-Dietory history
-0ffending food should be decreased( apple, pear, and
prune juices)

18. PATHOGENESIS OF PERSISTENT
DIARRHOEA
final common pathway to persistent diarrhoea is `prolonged
small intestinal mucosal injury' or PSIMI.
PSIMI is caused, intensified and perpetuated by the following
factors:
 Malnutrition
 Ineffective villous repair.
 Persistent infection with one or more enteric pathogens.
 Malabsorption of nutrients, especially carbo-hydrates and fats.
 Increased absorption of foreign proteins.
 Deficient enteric hormones.
All these factors contribute to the vicious cycle of mucosal injury
and malabsorption, leading to PD.

19. ROLE OF MALNUTRITION IN PSIMI
 Normally, in the epithelium of the small bowel, absorptive
cells are continuously lost from the villous tip and
replaced by newer cells produced by the crypts of
Lieberkuhn, once in 4-5 days.
 In a child with malnutrition, the production of the
absorptive cells of the villi is decreased, as it requires
energy and nutrients.
 These cells are responsible for the synthesis of
disacchari-dase enzymes like lactase and hence their
concentration in the gut decreases. This leads to osmotic
diarrhoea.

20.  The absorption of nutrients, which also re-quires energy,
is decreased in malnutrition,
 Malnutrition can depress the immune functions, leading
to infections of the gut
 gastrin and cholecystokinin are proteins in nature, their
secretion is decreased in malnutrition.
 gastric HCI and pancreatic enzymes are also decreased
leading to maldigestion and diarrhoea.

21. MALNUTRION

22. ROLE OF BACTERIAL OVERGROWTH IN
PSIMI
Bacterial contamination of the small gut causes PSIMI by
the following mechanisms:
 release toxins
 directly invade and damage the small bowel mucosa >
malabsorption
 deconjugate bile acids, --releasing free bile acids in the
small gut.

23. ROLE OF DECREASED ENTERIC HORMONES
IN PSIMI
Gastrin
- decreased ,HCI, pepsin secretion is decreased,
-increased colonisation of the small bowel with bacteria
-protein macromolecules are able to reach intact small
bowel
-increased absorption by the damaged smalI bowel
mucosa
These proteins are highly antigenic thus resulting in the
formation of circulating immune complexes. These are
deposited in the damaged mucosa as well as the normal
mucosa, perpetuating PSIMI.

24. CCK-PZ
 Decreased> maldigestion, malabsorption and
steatorrhoea.
Gastric inhibitory polypeptide
 decreased in small bowel damage.
 essential for the release of insulin and for glucose
utilization
 energy supply to the gut mucosa is decreased and hence
the cell turnover and production of enzymes are
decreased.

25. ROLE OF BILE ACIDS IN PSIMI
abnormal bacterial flora of the small bowel deconjugates
BA. The unconjugated bile acids cause diarrhoea by two
mechanisms:
 directly damage the small bowel mucosa, causing
malabsorption and osmotic diarrhoea.
 secretory diarrhoea.
 fat malabsorption and steatorrhoea

26. INCREASED ABSORPTION OF FOREIGN
PROTEINS
 in PD, the small bowel mucosa is damaged and hence
large protein molecules are absorbed intact into the
blood-stream.
 This leads to the formation of circulating immune
complexes that aggravate PSIMI.
 Classic examples of this phenomenon are cow's milk
protein intolerance and soya protein intolerance.

27. ROLE OF PINE REGULATORY SYSTEM IN
THE BOWEL
In a child with PD, there are mechanisms other than
osmotic and secretory, as pure osmotic and pure secretory
diarrhoea are uncommon. These include:
 Paracrine-bradykinin, histamine
 Immune-Cytokines
 Neural serotonin, acetylcholine
 Endocrine-gastrin, vasoactive intestinal peptide
This regulatory system is referred to as the "PINE" system.
It produces coordinated changes in mucosal and muscular
functions, which permit adaptive responses to changing
conditions.

28. Acting simultaneously, these mechanisms regulate
mucosal permeability, intestinal trans-port, and the
motility and metabolism of the gut.
Acute diarrhoea may be an appropriate response to acute
infections.
A maladaptive response may be responsible for chronic
diarrhoea.

29. EVALUATION OF A CHILD WITH CHRONIC
DIARRHOEA
Stool history
- -site of pathology, i.e.,
- -whether it is a SBD or LBD, and
- -the nature of the disease process.
 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.

30.  persistent profuse watery diarrhoea soon after birth,
==congenital microvillusatrophy & Darrow's syndrome
(congenital chloride diarrhoea).
 Such picture in a 6-month-old baby- autoimmune
enteropathy,
 Infant having chronic diarrhoea, with a history of delayed
passage of meconiurn and if constipation preceded
diarrhoea,-Hirschsprung's disease
 A strong family history and Down syndrome are
additional points for HD.

31. Dietetic history
 record a detailed history of feeding, prior to the onset of
the disease and during the disease.
 It may provide vital clues to the aetiology, e.g., cow's milk
protein in-tolerance, lactose intolerance, gluten
enter-opathy. 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 osmolali-ty of 900 mOsm/L and apple juice 650
mOsm/L

32.  Patients with gluten enteropathy, usually become
symptomatic several months after the introduction of the
offending food, but occasionally it may take even years.
 In cystic fibrosis, the appetite is voracious, unlike coeliac
disease, where it is poor.

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

34. DIAGNOSIS
A complete clinical history is mandatory. Some clinical
signs
and symptoms are relevant for a diagnostic approach
 Age of onset
 Nutritional assessment
 Associated symptoms: fever, vomiting, abdominal pain,
anorexia.
 Stool characteristics: blood, mucous, nondigested
substances, steatorrhoea.
 Physical examination: FTT, abdominal distension,
visceromegaly, tenderness, presence of abdominal
masses.
 Other organs affected, e.g. skin, respiratory system.

35. degree of dehydration and malnutrition should be assessed.
General examination in a child with CD may give vital clues to
the diagnosis.
 Hyperpigmentation- Addison's disease, coeliac disease
or 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

36.  recurrent fever- tuberculosis, lynphoma, and IBD
 marked loss of weight- malabsorption, lymphomas,
IBD, TB
 flushing,- malignant carcinoid syndrome and Vernor-
Morrison syndrome (pancreatic cholera)
 ageusia -zinc deficiency
 periorifcial and acral vesicular and scaly lesions,
acrodermatitis emeropathica

37.  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.

38. INVESTIGATION
A meticulous history and a thorough physical examination,
supplemented by a few simple in-vestigations are usually
sufficient in the majority of cases. A few cases may
require more sophisticated tests.
STOOL EXAMINATION
Microscopy
 Polymorphs and RBCs - bacterial colitis, whipworm
colitis, amoebic colitis and in IBD.
 Eosinophils are seen in milk or soya protein intolerance.

40. Stool 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.

41.  If in a neonate, the stool pH is low and reducing
substance is present, a diagnosis of primary lactase
deficiency or glucose-galactose malabsorption is
probable.
 If a similar picture is found shortly after the
introduction of cereals or sucrose, sucrase-
isomaltase deficiency should be suspected.

42. 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 I
minute.The solution is cooled and the precipitate is
examined for colour change.
 To detect non reducing sugars like sucrose and
trehalose, I nil of N/10 HCl (instead of distilled water) is
added to 0.5 ml of liquid stool and boiled for 1 minute.
(hydrolysation test)

43. Stool Culture
 Stool culture is positive only in 20% of patients with
acute diarrhoea and it is even lower in PD.
Alkalinisation of Stool
 If, in a child with unexplained chronic diarrhoea,
alkalinisation of the stool produces a pink colour, the
possibility is phenolphthalein ingestion and the most
probable diagnosis is Laxative abuse (Factitious
diarrhoea by proxy).

44. Occult Blood
 In acute diarrhoea- bacterial or para-sitic colitis
 chronic diarrhoea- IBD like ulcerative colitis and Crohn's
colitis and IPSID(Immunoproliferative small intestinal
desease).
CBC
 Haemoglobin
 bacterial infections like septicaemia, urinary tract
infection etc.
 ESR - very high in septicaemia and lymphoma of the
bowel.

45. Peripheral Blood Picture
 iron deficiency anaemia or dimorphic anaemia.
 abetalipoproteinaemia (acanthocytes)
Biochemical Investigations
 Serum electrolytes,
 blood urea,
 sugar 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.

46. D-xylose Test
This helps to find out whether there is damage to the small
bowel mucosa.
5 g of D-xylose is given orally and the urine con-tent
estimated for the next 5 hours. if it is less than I g, there
is a defect in the absorption from small bowel and the
further tests to be done are:
 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, lymphang-icetasia

47. If the D-xylose test is normal, the site of pathology could be
pancreas. pancretic func-tion tests and USG will be useful.
Proctosigmoidoscopy-
 To differentiate SBD from LBD(colitis).
 To visualize pseudomernbrane/polyps/ulcers/tumours.
 Direct swabs for microscopy and culture.
 Rectal biopsy.
Rectal Biopsy Helps in the Diagnosis Of
 Ulcerative colitis.
 Crohn's disease.
 Schistosonniiasis.
 Trichuriasis.
 Amyloidosis.
 Whipple's disease.

48. Tests for Tuberculosis
 Mantoux test.
 BCG test, if the chili has PEM.
 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.
It is important, to screen all patients with PD for AIDS

49. MANAGEMENT OF PERSISTENT
DIARRHOEA
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.
Patients with PD and malnutrition are highly prone to systemic
infections, including septicaemia. Infection should be ruled out if the
child has any of the following signs or symptoms:
 Fever.
 Hypothermia.
 Inability to drink.
 Abdominal distension.
 Lethargy or drowsiness.
 Cold skin.
 Dyspnoea.

50. 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).

51. RESUSCITATION PHASE
 Correction of dehydration, shock, electrolyte disturbance,
hypoglycaemia and renal failure.
 IV line , vital signs monitored and blood group and cross-
matching.
 Appropriate antimicrobials
 first 24 hours the child is given iv fluids and nil orally,
except sips of ORS.
 This helps to differentiate osmotic diarrhoea (when
diarrhoea may decrease) from secretory diarrhoea (when
diarrhoea persists).
 This also provides some time for the crypt cells to replace
the damaged villus cells.

52. CONTROL OF DIARRHOEA
The major factors responsible for PD
 bacterial contamination of the gut,
 systemic infections,
 food allergen (cow milk, soy protein, egg protein etc.
 lactose intolerance,
 toxins,
 bile acids

53.  In several studies it was shown that by using a
combination of high-dose oral gentamicin,
cholestyramine & metronidazole,(―bowel cocktail”)
diarrhoea subsides rapidly in about 90% pt.
 Gentamicin - bactericidal action,
 Cholestyrarnine- bind bile acids and bacterial toxins and
 metronidazole - antianaerobic effect.
supports the hypothesis that bacterial overgrowth is major
factor responsible,
 `bowel cocktail' has been studied in different
combinations in various studies and it was found that
the response was equally good without
cholestyramine.

54.  Many infants with PD are very sick and have features of
systemic infections like septicaemia and
bronchopneumonia.
 -combination of oral gentamicin (50 mg/kg of the
parenteral preparation in 6 divided doses for 3-5 days)
and parenteral cefotaxime (100 mg/kg) is extremely
effective in sick infants
 In a recent study co-trimoxazole was found to be very
useful in children with PD.
 nitrazoxanide
 Albendazole
 Shigellosis – ciprofloxcacin
 Emebiasis -metronidazole

55. REHABILITATION PHASE
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.
These patients should be followed up regularly, as they are
predisposed to develop PD again.

56. DIETARY MANAGEMENT
GOALS
 Avoid all feeds till diarrhoea is at least partially controlled-(2nd
day of treatment).
 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; gluten-containing food in coeliac disease.
 Provide adequate micronutrients and vitamins.
 The diet should not be hyperosmolar and should not produce
adverse effects or worsen the diarrhoea.

57. 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.

58. DIET IN PERSISTENT DIARRHOEA
The small bowel mucosa of a child with PD is extensively
damaged due to
bacterial contamination,
ineffective villous repair,
Malnutrion etc.
Hence, one should be very cautious in introducing food.
 There is a lot of controversy and confusion whether cow's
milk can be given or not in PD.

59. It should be remembered that in a child with severe
malnutrition and PD, PSIMI has already set in.
If such a child is given cow's milk, the following may occur:
 There is deficiency of lactase as the enterocytes are
damaged> osmotic diarrhoea
 Cow's milk proteins maybe absorbed intact into the
bloodstream through the damaged mucosa, thereby
aggravating PSIMI.
Hence when the child is very sick, it is better to avoid cow's
milk.

60. LOW LACTOSE DIET(PLAN A)
many children tolerate milk feeds in reduced amounts, and child
is not very sick, he may be given a low lactose diet, containing
50 ml/kg/day of milk.
Water should not be added, it can be mixed with cereals like rice,
and sugar.
 Yoghurt (curd) -contains lactase enzyme which digests
lactose and so the lactose content of yogurt is only 70% of that
of milk.
 rice-lentil + yoghurt
 Yoghurt mixed + mashed potatoes + coconut oil
Feeding should be started after the resuscitation phase.
Initially 6--7 feeds /d (110 kcal/day. )
Then 150 ml/kg/day, to achieve weight gain.
Nasogastic tube feeding may be necessary, if the child has
severe anorexia.

61. 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

62. LACTOSE FREE DIET(PLAN B)
if a child does not respond to low lactose diet: These patients may
be given milk-free diet.
Rice-Bengal gram-fat mixture
A diet containing rice, Bengal gram, glucose and coconut oil
 Roasted Bengal gram powder: 25 g.
 Rice powder: 20 g.
 Glucose: 20 g.
 Coconut oil: 15 ml.
 Salt to taste.
 Water to make up to 400 ml.
This gives:
Protein: 7 g.
Calories: 400.
Approximate cost: 2/-

63. Advantages of rice, Bengal grain, fat gruel
 Cheap
 Easily available and acceptable.
 Well tolerated.
 Appreciable weight gain.
 High nutritional value.
Rice-moong dal gruel
 50 g of raw rice, 30 g moong dal, water, 30 g sugar
coconut oil. It provides 67 calories/l00 ml.
plan c or monosaccharide diet
Chicken-glucose puree diet
 100 g of boneless chicken ,40 g glucose and coconut oil.
( 72 calories/1 00 ml)

64. Role of Lactose-free Milk
 if. a patient has significant lactose intolerance (isolated) ,
they may be tried, otherwise not helpful.
 S’d not be given in acute diarrhoea.
 cost is horrible taste is terrible.
 Not palatable
 aggravate diarrhoea by ―soy protein intolerance‖.

65. Vitamin and Mineral Supplementation
 vitamin A
 Folic acid, vitamin B12 and iron (have a tropic action on
the intestinal epithelium should be given.)
 Zinc , mild zinc deficiency may aggravate the severity
and duration of diarrhoea. It may be given in the dose of
50-100 mg/day..
Parenteral Nutrition
 The severely affected digestive tract of the child may not
tolerate even the most theoretically perfect diet, given in
the most careful manner.

66. Indications for TPN
 Persistent diarrhoea with intolerance to oral
realimentation diets after 10 days.
 Severe forms of IBD and resistant colitis.
 Severe necrotising enteritis.
Some of the Problems of' TPN
 Needs trained personnel and round the clock monitoring
and team work.
 Very high cost
 Sepsis
 Cholestasis which may lead to cirrhosis.

67. Partial Parenteral Nutrition
if TPN is not feasible, a partial parenteral nutrition
(combined parenteral and oral) may be tried in selected
patients.
The Composition of PPN Fluid is as Follows
 Paediatric maintenance solution: 250 ml (Isolyte P)
 25% dextrose: 150 nil
 Amino acid solution: 100 ml
 NaHCO3: 20 ml
 KCI: 5 ml
 MVI: 2 ml
 Dose 50-75 ml/kg'day; 54 ml provides 300 cals

68. INTRACTABLE DIARRHEA SYNDROME
 permanent defect in the the structure or function of
intestine , leading to progressive ,often irreversible
intestinal failure, requiring parenteral nutrition for
survival.
 Structural enterocyte defect
 Immune based disorders
 Short gut
 Multiple food intolerance

70. Persistent
diarrhoea
In a
malnourished
child
recovery Failure

72. SUMMARY
 Diarrhoea and malnutrion interaction is a vicious
cycle and is a leading cause of morbidity and
mortality.
 Persistent diarrhea lasts for 14 days or longer.
 final common pathway to persistent diarrhoea is
`prolonged small intestinal mucosal injury' or PSIMI.
 A meticulous history and a thorough physical
examination, supplemented by a few simple
in-vestigations are usually sufficient in the majority
of cases.
 degree of dehydration and malnutrition should
always be assessed.

73.  Patients with PD and malnutrition are highly
prone to systemic infections.
 Avoid all feeds till diarrhoea is at least partially
controlled
 when the child is very sick, it is better to avoid
cow's milk.
 Always avoid those food substances, which
may be responsible for PD.
 Give as per plan A,B,C change when necessory.
 Give TPN or PPN
 Lactose free milk is not much helpful, s’d be
avoided.