Professional Documents
Culture Documents
And management
Dr. s. s. yadav
Dr jyoti prajapati
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.
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.
Abetalipoproteinaemia.
Acrodermatitis enteropathica.
Endocrine causes
Hypoparathyroidism, Hyperthyroidism.
Diabetes mellitus.
Adrenal insufficiency.
Neoplasms
lmmunoproliferative small intestinal disease (IPSID or
Mediterranean lymphoma).
Western lymphoma.
Ganglioneuroma.
Vernor-Morrison syndrome (pancreatic cholera or
VIPoma).
Zollinger-Ellison syndrome.
Motility disorders
Toddler´s diarrhoea
Hyperthyroidism
Hirschprung’s disease
Intestinal lymphangiectasia
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
PATHOPHYSIOLOGY
osmotic diarrhea
secretory diarrhea,
osmotic load
water secreted
CAUSES
MALABSORPTION OF WATER-SOLUBLE
NUTRIENTS -Glucose-galactose
malabsorption Congenital , Acquired
Disaccharidase deficiencies.
EXCESSIVE INTAKE OF CARBONATED FLUID
secretory diarrhea
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
DIFFERENTIAL DIAGNOSIS OF OSMOTIC
VS SECRETORY DIARRHEA
SECRETORY
OSMOTIC DIARRHEA DIARRHEA
Volume of stool <200 mL/24 hr >200 mL/24 hr
Immune-Cytokines
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.
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.
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)
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).
Occult Blood
In acute diarrhoea- bacterial or parasitic colitis
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.
Tests for Tuberculosis
Mantoux test.
X-ray chest.
systemic infections,
lactose intolerance,
toxins,
bile acids
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.
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 cotrimoxazole was found to be very
useful in children with PD.
nitrazoxanide
Albendazole
Shigellosis – ciprofloxcacin
Emebiasis -metronidazole
REHABILITATION PHASE
Aims
To improve the general health and nutritional status.
GOALS
Avoid all feeds till diarrhoea is at least partially controlled-
(2nd day of treatment).
Small frequent feeds
Not palatable
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.
Indications for TPN
Persistent diarrhoea with intolerance to oral
realimentation diets after 10 days.
Severe forms of IBD and resistant colitis.
Sepsis
NaHCO3: 20 ml
KCI: 5 ml
MVI: 2 ml
Short gut
recovery Failure
SUMMARY