APPROACH TO

CHRONIC DIARRHEA
Moderator-Dr.Ramesh M
Presenter-Dr.Deena Kumari S
 CONTENTS
◦ Introduction
◦ Types and predisposing factors
◦ Etiology
◦ Pathogenesis
◦ Evaluation
◦ Investigation
◦ Treatment
 Definition
◦ Diarrhea –condition characterized by an increase in the frequency ,fluidity and weight of the
stool, compared to the normal bowel habit of the child.
◦ According to stool weight-In infants >10g/kg/day
-1-3 years >15g/kg/day
-In older children >200g/day
-In adolescent >300g/day

◦ Liquidity of stool is also important –stool taking the shape of the container
◦ Acute diarrhea-usually subsides by 1 week , but may go upto 2 weeks
◦ Chronic diarrhea is diarrhea lasts for more than 2 weeks.
(According to Nelson 21st edition-duration >4 weeks)
Non specific diarrhea
◦ Most benign and common etiology of chronic diarrhea is non specific diarrhea
which encompasses functional diarrhea or toddler’s diarrhea in children
younger than 4 years of age and irritable bowel syndrome in those 5 year of
age and older.

◦ Toddler’s diarrhea is defined by the daily painless recurrent passage of 4 or

more large unformed stools,for 4 (or )
4 weeks with onset in infancy or pre-school years.(Night time defecation is
usually absent)
Diagnostic criteria for functional diarrhoea
◦ Must include all of the following:
1.Daily painless, recurrent passage of 4 or more large,unformed stools
2.> 4 weeks
3.Between 6-60 month of age
4.No failure to thrive if caloric intake adequate

Evaluate diet
o Assess for infections and growth
o Watch for antibiotic or laxative use
o Rule out fecal impaction and encopresis by digital rectal examination
 Chronic diarrhea
Classification

Type 1/Persistent Type II 10%

diarrhea 90%

In a previously normal child In a child with inherent defect

Simple persistent Persistent protracted

Predisposing factors -Age <18 months
-Feeding practices –bottle feeding ,lack of breast feeding and not feeding
during acute episode of diarrhea
-Cow’s milk protein allergy
-Soy protein
-Measles
-Malnutrition ,Vitamin A and zinc deficiency
-Poor hygiene
-Contamination of food
-Galactose malabsorption and intolerance of food
-Inappropriate use of antibiotics
-Improper therapy or starvation of ADD
Types
◦ Type 1 chronic diarrhea-Seen in a previously normal child .
◦ acute onset
◦ infective etiology
◦ 90% of chronic diarrhea
◦ Also known as persistent diarrhea
1.Simple Persistent diarrhea –Lasts for >14 days and responds to diet modification
Etiology- Usually the most common infectious with Giardia lamblia
Agents that predispose to simple disaccharide intolerance

◦ Healthy looking child without dehydration or toxic symptoms

◦ No weight loss
◦ Appetite preserved
◦ Perianal excoriation

◦ Treatment-modification of diet –avoiding sugars in the diet

-treatment of giardiasis/infestations
2.Persistent protracted diarrhea-Lasts for >14 days, which does not respond to diet
modification.
◦ Etiology –infections (bacteria, virus, fungi or parasites ) cause small bowel bacterial
over growth
Bacteria Virus Fungi Parasites
Shigella HIV Candida albicans Giardia lamblia
Salmonella Herpes simplex Cryptococcus Cryptosporidium
Enteroadherent E.coli CMV neoformans

-post-infective sequelae like malabsorption (dietary protein intolerance)

-Extraintestinal infections such as UTI and CSOM
◦ Common in malnourished and young children –Loose stools,growth failure
◦ Does not respond to diet modification
Type II chronic diarrhea
◦ 1.Inflammatory causes
Tuberculosis
Eosionophillic gastroenteritis
Crohn’s disease
Behcet’s syndrome
Necrotising enterocolitis
Allergic colitis
Henonch –Schonlein vasculitis
◦ 2.Malabsorption states
a)Pancreatic diseases-
Cystic fibrosis
Diamond –shwachman syndrome
Chronic pancreatitis
Hereditary pancreatitis
Congenital lipase deficiency
Congenital trypsin deficiency

b).Liver disease
Cholestatic jaundice
Primary bile acid malabsorption
c).Intestinal diseases
Tropical spure
Coeliac disease
Whipples disease
Intestinal lymhangiectasia
Anderson’s disease(chylomicron retention disease)
Bassen –Kornzweig syndrome (Abetalipoproteinemia)
Enterokinase deficiency
Vitamin B12 malabsorption-Juvenile pernicious anaemia
-Transcobalamin II deficiency
-Immerslund-Grasbeck syndrome(cubilin receptor defect)
Lactase deficiency-congenital /acquired
Sucrase-isomaltase deficiency
Glucose-galactose malabsorption
3.Metabolic disorders
Darrows syndrome (congenital chloride diarrhea )
Abetalipoproteinemia
Wolman’s disease
Acrodermatitis enteropathica

4.Endocrine causes
Hypoparathyroidism
Hyperthyroidism
Diabetes mellitus
Adrenal insufficiency
◦ 5.Immune defects
Agammaglobulinaemias
Isolated IgA deficiency
Defective CMI
Combined immunodeficiency

◦ 6.Anatomic defects
Short bowel syndrome
Congenital microvillus atrophy
Biliary atresia
Intestinal duplication
o 7. Neoplasms

Immunoproliferative small intestine disease(IPSID or Mediterranean lymphoma)

Western lymphoma
Ganglioneurona
Vernor-Morrison syndrome(Panctreatic cholera or VIPoma)
Zollinger –Ellison syndrome

◦ 8.Miscellaneous

Protein losing enteropathy

Antibiotric associated diarrhea-C.difficile
Autoimmune enteropathy
Pathogenesis of persistent diarrhea
◦ Prolonged small intestinal mucosal injury(PSIMI)
◦ Caused,intensified and perpetuated by –
PEM
 Ineffective villous repair
Persistent infection with one or more enteric pathogens
Malabsorption of nutrients, especially carbohydrates and fats
Increased absorption of foreign proteins
Deficient enteric hormones
Role of PEM in PSIMI
◦ Normal-Epithelium of the small intestine replaced every 4-5
days and takes 36-48 hours for migration from crypts to the villi.
◦ In PEM-production of absorptive cells of the villi is decreased as
it requires energy and nutrition which are responsible for the
synthesis of disaccharide enzymes like lactase leading to
osmotic diarrhea
◦ Absorption of nutrients also decreased in PEM
◦ PEM depresses immune system especially cell mediated
immunity ,humoral and complement function ,thus leading
infections of the gut
◦ Secretions of gastrin and cholecystokinin decreased leading to
decreased HCl and pancreatic enzymes.
Role of bacterial overgrowth in PSIMI
◦ Release of toxins causing secretory diarrhea
◦ Invade and damage the small bowel mucosa
leading to malabsorption of nutrients and
hence chronic diarrhea
◦ Deconjugate bile acids ,releasing free bile
acids in the small gut directly increasing fluid
and electrolyte secretions
Role of decreased enteric hormones
1.Gastrin 2.CCK-PZ(Cholecystokinin proteozyme)
◦ HCl secretion decreased ◦ Decreased secretion of pancreatic enzymes
◦ Increased colonization of bacteria and contraction of gall bladder
◦ Maldigestion ,malabsorption and steatorrhea
◦ Decreased breakdown of macromolecules and
increased absorption by the damaged mucosa
◦ Antigenic proteins cause formation of
circulating immune complexes
3.GIP(Gastric intestinal
pepetide)
◦ Release of insulin and
glucose utilization
◦ Decreased energy supply to
the gut mucosa leading to
decreased cell turnover and
production of enzymes
◦ Malabsorption-aggravating
diarrhea
Role of bile acids in PSIMI
◦ The abnormal bacterial flora of small intestine deconjugate bile acids
◦ The unconjugated bile acids cause direct damage to the mucosa causing malabsorption and
osmotic diarrhea
◦ Increased secretion of water and electrolytes by colon causes secretory diarrhea
◦ Decreased CCK –decreased bile acids leading to fat malabsorption and steatorrhea
Increased absorption of foreign proteins
◦ Damaged mucosa absorbs the large intact protein molecules into the blood stream causing
leading to formation of circulating immune complexes that aggravate PSIMI.
◦ Eg:Cow’s milk protein allergy
Soy protein intolerance
Role of PINE regulatory system in the bowel
◦ Paracrine –bradykinin ,histamine
◦ Immune-Cytokines
◦ Neural- serotonin , acetylcholine
◦ Endocrine-gastrin , vasoactive intestinal peptide

◦ The paracellular pathway that controls passive transmucosal permeation of electrolytes is

widened or narrowed by PINE system
◦ Contract and relax muscle layers changing mucosal blood flow.
◦ Both act simultaneously to regulate mucosal permeability ,intestinal transport , motility and
metabolism of the gut .
Age Causes
Newborn • Congenital short bowel syndrome
• Neonatal lymphangiectasia
• Inherited transport defect such as cystic fibrosis
• Glucose-galactose malabsorption
• Congenital chloridorrhoea
• Bile salt malabsorption
• Milk enterocolitis
• Exocrine pancreatic insufficiency
• Primary or secondary lymphangiectasia
• Hypo/abetalipoproteinemia

1 month to 2 years • Lactose intolerance

• Cow’s milk ,soy and other allergies
• Celiac disease
• Irritable colon of infancy (Chronic specific diarrhea)
• Cystic fibrosis
• C.Difficile(antibiotic usage)
• VIP-secreting tumours
>2 years • Celiac disease
• Inflammatory bowel disease
• Chronic non specific diarrhea(IBS)
• Primary acquired lactase deficiency
• Chronic pancreatitis/exocrine pancreatic deficiency
• Primary or secondary lymphangiectasia
• Hypo/abetaipoproteinaemia
 Evaluation
o History –Age of onset
Range of possible etiologies depends on child’s age
◦ Early onset neonatal period: Congenital diarrhoeas
Infections, GI malformations

◦ Later infancy and upto 2 years of age: Infections

Allergies
◦ Older children and adolescents: Inflammatory diseases

◦ Independent of age: Coeliac and functional diarrhea

specific diarrhoea
o Stool history –Frequency
o Quantity
o Bulky ,difficult to flush
o Associated with blood/mucus
o Site of pathology (SBD or LBD)
o SBD-profuse watery ,usually offensive ,without blood
o LBD-small quantity,frequent ,with blood and mucus stools
o Encopresis: Voluntary or involuntary passage of faeces in inappropriate places atleast once a month for 3
consecutive months once a chronological or development age of 4 years has been reached.
Characteristics of stools
Loose stools with undigested particles: Toddler’s diarrhoea
◦ Frequent loose watery stools: Carbohydrate intolerance
◦ Foul smelling,: Fat malabsorption
oily appearance Giardiasis
◦ Bloody stools: Protein sensitivity
syndromes

Timing
◦ Nocturnal diarrhoea: Malabsorption
Colitis
Inflammatory bowel diseases
Associated symptoms and signs:
◦ Signs of generalised inflammation:
(fever,mucoid or bloody stools)
◦ Abdominal pain:
◦ Eczema or asthma:
◦ Arthritis, diabetes, thrombocytopenia:
◦ Vesicobullous dermatitis:
◦ Recurrent respiratory tract infections:
◦ Pyoderma gangrenosum:
Infection,Inflammatory bowel disease
Tuberculosis, IBD,IBS,
Ischemia, Neoplasm
Allergic
Autoimmune enteropathy
Acrodermatitis enteropathica
Cystic fibrosis
Inflammatory bowel disease
2.Dietary history
Prior to onset and during the disease
CMPA(Cow’s milk protein allergy)
Lactose intolerance
Gluten enteropathy
Egg protein enteropathy
Overfeeding
Chewing gum diarrhea
Cystic fibrosis(Voracious appetite)
Celiac disease(Poor appetite)
Increased consumption of undiluted fruit juices

3.Treatment history
On antibiotics-Pseudomembranous colitis
Drugs-propranolol,PPI,H2 blockers,Quinine,Magnesium containing antacids
Past history:
◦ History of systemic diseases (hyperthyroidism, AIDS)
◦ Immune suppression therapy
◦ Repeated exposure to antibiotics
◦ Recent history of acute diarrhoea , travel

Birth history:
◦ History of polyhydramnios: Congenital chloride sodium diarrhoea
(USG- dilated fetal bowel loops)
Prematurity
Timing of meconium passage
4.Family history
IBD
IBS
Hereditary pancreatitis AD
MEN
Tuberculosis History of
recurrent fever
Lymphoma
Carcinoid syndrome
History of flushing
Vernor-Morrison syndrome(Pancraetic cholera)
 Physical examination
◦ Anthropometry –Extent of malnutrition in
terms of wasting and stunting
◦ Signs of dehydration-Acute exacerbation of
diarrhea,vomiting,poor intake
◦ Signs of deficiency-pallor,koilonychia,flat or
spooning of
nails,rickets,chelitis,glossitis,bitot’sspots,con
junctiva/corneal xerosis,cutaneous bleed and
peripheral neuropathy
o Icterus
o Oral ulcers,oral thrush-
HIV,antibiotics ,severe malnutrition
o Pedal edema associated with
hypoproteinemia
o Clubbing –Cystic fibrosis,chron’s
disease,celiac disease,tuberculosis
o Skin-dry,scaly,phrynoderma,dermatosis
o Hyperpigmentation –Addison’s
disease,celiac disease
o Generalised lymphadenopathy-
Lymphoma,AIDS,Whipple’s disease
Abdominal examination:
◦ Gaseous distension
◦ Ascites
◦ Organomegaly
◦ Mass
◦ Previous surgical scars

Anal examination:
Prolapse- Cystic fibrosis, Coeliac
Skin tags, fissures, fistulas: Crohn’s disease

◦
Other systemic Examination
◦ Respiratory system-bronchiolitis in early
infancy ,Nasal polyps,recurrent LRI

◦ Central nervous system –ataxia,

Glove and stocking neuropathy
Investigation
◦ Hematology-
◦ Anaemia-microcytic,hypochromic,macrocytic,megaloblastic or dimorphic
◦ High platelets in iron deficiency like celiac disease and in IBD
◦ Acanthocytes in peripheral smear –abetalipoproteinemia
◦ ESR and leucocytes raised in inflammatory conditions whereas lymphopenia suggests
lymphangiectasia
◦ Raised PT,INR-Vitamin K deficiency in Malabsorption syndrome
Biochemistry

o Biochemistry
o Anemia: S. Iron, TIBC, S. Ferritin, Vit. B12, Folic acid
o Malnutrition assessment: Albumin, Prealbumin
o Renal function tests
o Electrolytes
Stool examination
◦ Naked eye-watery,bulky,with or without undigested matter,greasy(oil
in stools),blood and mucus
◦ Microscopic-detection of ova and cysts done for 3 consecutive days
to increase pick rate 80-90%
◦ Polymorphs and RBC present in Bacterial colitis,whipworm
colitis,amoebic colitis,IBD
◦ Polymorphs absent in IBS,Non invasive organisms producing
toxins,viral enteritis,malabsorption and laxative abuse
◦ Eosinophils in milk or soy protein allergy
◦ Stool osmolar gap: >100: osmotic
<50: secretory
Measured stool osmolality –
[2 * (stool Na + K)]

◦ The distinction between osmotic and secretory diarrhoea can be performed as clinical assessment
under 24 hour enteral starving and parenteral nutrition with rehydration. This approach will limit
stool analysis to selected cases.

◦ Keeping the child nil by mouth for 24 hours will stop the diarrhoea if it is osmotic, reduce the
amount if it is mixed, and leave unchanged if it is secretory.
o Parasites-best sample-duodenal aspirate

o Best method-Kinyoun’s Acid fast staining

o C.Difficile -toxin assay and culture

o Giardia-Antigen detection by ELISA

oStool pH-amount of organic acids in stools
o <5.5 on cow’s milk or <5 on breast milk is suggestive of carbohydrate malabsorption and proximal bowel
damage
o Colonic salvage mechanism

oStool reducing substances

o 1ml of distilled water us added to 0.5ml of liquid stool
o 8 drops are added to 5ml of benedicts solution and boiled for 1 minute

Colour change %of sugar

No change Nil
Green 0.5
Yellow 1
Orange 1.5
Brick red >2
o Stool culture –Positive in 20% of patients and lesser in persistent diarrhea
o E.coli and Klebsiella

o Alkalinisation of stool –Pink colour indicates phenolphthalein ingestion

o Chloride conc.:
o Occult blood:
o Fecal elastase and chymotrypsin
o Fecal calprotectin
o Fecal alpha 1 antitrypsin
High chloride fecal loss in Congenital
chloride diarrhoea
when anemia can’t be explained
Pancreatic insufficiency
Inflammatory bowel disease
Protein losing enteropathy
o Imaging:
o Xray abdomen: Intestinal obstruction and Increased retention of
faeces
◦ USG: Liver
Pancreatic abnormalities
Increase in distal ileal wall thickness (inflammatory bowel
disease)
o Barium meal or small bowel follow through:Structural and motility
disorders
o Capsule endoscopy: >10 kg patient
Explores intestinal tract for structural
changes,inflammation, bleeding
o Smart Pill: Pressure,Ph,Temp, motility
Hydrogen breath test
◦ Hydrogen is produced by the bacteria by fermentation of unabsorbed carbohydrates normally in case of
bacterial overgrowth
◦ Measured by gas chromatography
◦ Estimation of fasting breath hydrogen before performing breath test
◦ Lactulose,glucose,fructose,lactose is used
◦ All samples of breath analysed for hydrogen and methane every 15minutes for 2-4 hours
◦ Small intestinal bacterial growth shows rise above 12ppm above basal.
Fecal fat
◦ Malabsorption of fat globules on sudan III stain are more than 100 per HBF in the stool
◦ Fecal fat excretion is determined by supplementing fat 2g/kg per day <2 years of age and 50g daily for
children >2 years for 3 days
◦ Fat excretion >4.5g/day in children and >6.5g/day in adolescents
◦ Steatocrit-centrifuging and calculating fat layer
◦ Gold standard is van de Kramer
D-Xylose absorption test
◦ Abnormal in mucosal disease
◦ Test done after overnight fasting-0.5g od D-xylose is given orally and patient encouraged to drink fluids
to maintain adequate urine output
◦ Urine collected for 5 hours and venous sample after 1 hour to detect D-xylose in the blood
◦ D-Xylose more than 1.25 g or >20% of total urine or <20mg/dl –mucosal malabsorption
◦ Falsely negative in presence of dehydration,renal dysfunction,delayed gastric clamping,ascites and
improper collection of urine.
Endoscopy:
Upper GI
changes in duodenum: etiology
Eg.
Coeliac: decreased height of folds and mosaic pattern
Crohn’s disease: deep linear ulceration
Lymphangiectasia: white pearl like punctate lesions or vesicles
Giardiasis: nodular mucosa

Lower GI
To make diagnosis of CMPA,UC,Crohn’s disease, TB,amoebiasis, Strongyloides, CMV, HSV, Microscopic
colitis.
◦ Proctosigmoidoscopy –Uses
◦ To differentiate SBD from LBD
◦ To visualise pseudomembrane/polpys/ulcers/tumors
◦ Rectal biopsy –ulcerative colitis
-Crohns disease
-Schistosomiasis
-Trichuriasis
-Amyloidosis
-Whipple’s disease

◦ Tests for TB-Barium enema

-duodenal,jejunal or colonic biopsy
Approach to Chronic secretory diarrhea
Approach to Chronic osmotic diarrhea
Approach to fatty diarrhea
Approach to chronic inflammatory diarrhea
Management of persistent diarrhea
◦ Age <4 months and not on breast feeds
◦ Severe PEM
◦ Dehydration
◦ Presence of systemic infections

◦ Children with persistent diarrhea and malnutrition are highly prone to systemic infections ,including
septicemia
◦ Infections should be ruled out if there is presence of fever, Hypothermia, Inability to drink,Abdominal
distension, Lethargy/Drowsiness,Cold skin, dyspnea
3 phases od management
Resuscitation phase(24-48 hours)
◦ Correction of dehydration,shock,electrolyte disturbance,hypoglycemia and renal failure
◦ Intravenous fluid for 24 hours to provide time for replacement of damaged villus cells and to differentiate
between secretory and osmotic diarrhea
◦ Bowel cocktail as a major factor for persistent diarrhea is bacterial overgrowth of small bowell

Oral gentamycin Cholestyramine to

Metronidazole for
for bactericidal bind to bile acids
its anti-anaerobic
action and bacterial toxins
effect
Control of diarrhea
o upto 7 days

Rehabilitation phase

◦ 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.
Diet in rehabilitation phase
◦ Avoid feeds till partial contraol of diarrhea
◦ Small frequent feeds to reduce gastrocolic reflex
◦ High carbohydrate, low protein and no fat regime
◦ Avoid milk and milk products in Cow’s milk allergy,gluten in coeliac disease
◦ Micronutrients and vitamins
◦ Avoid hyperosmolar diet
 Initial diet A
◦ Reduced lactose diet,milk rice gruel,milk sooji gruel,rice with curds,dalia
Constituents
◦ Milk (1/3 katori/50ml)
◦ Puffed rice powder/cooked rice or sooji (2tsp/6g)
◦ Sugar(11/2 tsp/7g)
◦ Oil(1tsp/4.5g)
◦ Water(2/3 katori/100ml)
Preparation
◦ Mix milk ,sugar and rice,add boiled water and mix well,add oil
Nutrient content
◦ 85 cal and 2 g protein per 100g
Second diet B
◦ Lactose –free diet with reduced starch
◦ Impaired digestion of starch and disaccharides other than lactose
◦ Milk protein replaced by chiken,egg or protein hydrosylate
◦ Reducing starch content and partial replacement with glucose
◦ Constituents
Egg white(3tsp/half egg white)
Puffed rice powder/cooked rice(3tsp/9g)
Glucose(1 tsp/7g)
Oil(1 ½ tsp/7g)
Water 3 ½ katori/120ml)
◦ After whipping the egg white,add rice,glucose and oil ,mix well.Add boiled water and mix rapidly to avoid clumping
◦ 90kcal and 2.4 g protein/100g
Third diet C
◦ Monosaccharide based diet
◦ Glusose,egg white protein,protein gylycosylate with adding oil
◦ Green unripe banana-fermentation of the undigestable soluble fibres by colonic bacteria generates short
chain fatty acids absorbed along with sodium
◦ Constituents –Chicken puree(5tsp/15g) or egg white(3tsp/half egg white)
Glucose(1 ½ tsp/7g)
Oil(1 ½ tsp/7g)
Water (1 katori/500ml)
◦ Boil chicken and make puree after removing bones,mix it with glucose and oil,add boiled water to make
a smooth flowing feed
◦ 67kcals and 3 g protein per 100g
Change to next level diet when
◦ Marked increase in stool frequency (usually more than 10 watery stools/day) after 48 hours of initiating
diet
◦ Features of dehydration any time after initiating treatment
◦ Failure to gain weight by day 7 in absence of initial or hospital acquired systemic infection
References
◦ 1.Nelson textbbok of Paediatrics (21st edition)
◦ 2.PG Paediatric textbook of Paediatrics -Piyush Gupta
◦ 3.Ghai Essential Paediatrics
◦ 4.Paediatric gastroenterology and Hepatology-Riyaz
◦ 5.Nutrition and child development –KE Elizabeth
Next class
◦ Aapproach to pain abdomen by Dr.Hamsa on 01/06/2021
Lactose intolerance
◦ Inability to digest and absorb lactose resulting in gastrointestinal symptoms when milk or products
containing milk is consumed
◦ Primary-Congenital absence of the lactase enzyme due to a mutation in the gene
◦ Secondary –More common and self limiting.
Pathophysiology -
Secretory diarrhea

◦Active electrolyte and water fluxes toward intestinal lumen

◦Inhibits absorption of NaCl
◦Increase in electrogenic chloride secretion (CFTR)
◦Na-K-2Cl cotrasporter
◦Na-K pump(decreases intracellular Na)
◦K selective channel (K back to ECF)
◦Induced by CMP,CGP,Ca by micronial enterotoxins,inflammatory cytokines
◦Defects in genes of Na+/H+ and Cl-/HCO3- exchangers
Osmotic diarrhea
◦ Due to non-absorbed nutrients in the intestinal lumen
◦ Non absorbed solutes create an osmotic force to drive water back into the lumen
◦ Due to
1. Intestinal damage (Enteric infection )
2. Reduced absorptive surface area (active celiac disease )
3. Defective digestive enzyme or nutrient (lactase deficiency –lactose not fermented reaches large
intestine and converted into short chain organic acids releasing hydrogen )
4. Decreased intestinal transit time (functional diarrhea )
5. Nutrient overload, exceeding the digestive capacity ( Overfeeding, sorbitol )
◦ Diarrhea associated IBS are foods containing FODMAPs(fermentable oligo-di-monosaccharides
and polyols)