Approach to chronic diarrhea

1. Acute <2 weeks
Persistent: acute diarrhea with late recovery: 2-4 weeks
Chronic: > 4 weeks

2. Organic vs functional diarrhea:
FEATURES FUNCTIONAL ORGANIC
Onset Insidious Usually abrupt
Duration Long Short
Constitutional symptoms Less marked Marked
Weight loss No Yes
Appetite Normal Decrease
Nocturnal diarrhea No Yes
GCR Yes No
Anxiety symptoms Yes No

3. Small vs Large intestinal diarrhea
FEATURE SMALL BOWEL
DIARRHEA
LARGE BOWEL
DIARRHEA
Volume Large Small
Excessive flatulence +- -
Steatorrhea + -
Malabsorption + -
Blood/ pus in stool Rare Common
Abdominal pain Mid abdominal colic, central,
not relieved with defecation
Lower abdomen, usually
improves with defecation
Tenesmus/urgency Absent Present

4. Large vs Small volume diarrhoea
Differentiation of the cause of diarrhea by the volume of individual stools (rather than total
daily stool output) rests on the premise that the normal rectosigmoid colon functions as a
storage reservoir.
Reservoir capacity is compromised by
an inflammatory or motility disorder
involving the left colon
Frequent,small-volume, painful bowel
movements
If the source of diarrhea is in the right colon
or small bowel and if the rectosigmoid
reservoir is intact,
Bowel movements are less frequent
Painless,large volume stools

5. CHRONIC DIARRHEA

6. History
Duration: acute vs chronic
Onset: abrupt/ gradual
Pattern: continuous / intermittent
Epidemiology: travellers/ epidemics/ DM/ AIDS/Institutionalised patients
Stool appearance
Volume
Nocturnal episodes
Iatrogenic factors
Factitious diarrhea

7. Family history: neoplastic, IBD, celiac disease
Systemic diseases: endocrine, collagen vascular, neoplastic, immunologic
Presence of fecal incontinence
Abdominal pain
Weight loss
Aggravating factors like diet/ stress
Alleviating factors

8. Physical examination:
-Volume status
-Nutrient deficiencies- BMI, vitamin deficiencies.
-Cutaneous manifestations: urticaria pigmentosa/ dermatographism/ migratory necrotising
erythema/ hyperpigmentation/ flushing/ dermatosis herpetiformis/Muscle wasting/ edema
/ thyroid nodule/ lymphadenopathy/ tremors/ lid lag
-Right sided heart murmer/ wheezing
-Arthritis
-Abdominal examination:; bowel sounds/ distension/ tenderness/ mass/ hepatomegaly/
abdominal bruit
--Anal sphincter weakness

12. How to investigate??
CBC: Hb, MCV, TLC, Differential count, platelet
P.smear: characterise anemia, acanthocytes
Renal function test
Serum electrolytes
LFT: albumin, globulin, ALP
Specific nutrient deficiencies: iron, folate, vit B12
HIV status when indicated

13. Stool analysis:
Macroscopy
Microscopy -
- leucocytes
- wet smears or after concentration technique for ova and cysts
- Special stains- sudan or Acid fast for coccidian parasites
- Occult blood to exclude ulcerative conditions
- Fetal calprotectin
- pH, reducing substances
- Fecal fat estimation

14. Comprehensive metabolic panel
IgA tissue transglutaminase Ab
IgA level

16. Osmotic vs Secretory Diarrhoea

17. Stool osmotic gap
Serum osmolality- stool osmolality
290-2x (Na+ + K+)
<25mOsm/kg >50mOsm/kg

18. Osmotic diarrhoea
● Ingestion of poorly absorbed cations and anions (magnesium, sulfate, and phosphate)
or poorly absorbed sugars or sugar alcohols (mannitol, sorbitol) .

19. ● Osmotic diarrhea results from the presence of osmotically active, poorly absorbed
solutes in the bowel lumen that inhibit normal water and electrolyte absorption.
● About 3.5 mL of water (1000 mL/kg ÷ 290 mOsm/kg) are retained for every 1
mOsm of retained ions or molecules.

20. Osmotic diarrhoea by sugars or sugar alcohols
● Monosaccharides can be absorbed intact across the apical membrane of the
intestine.
● Disaccharides are not absorbed.
● When disaccharides like sucrose and lactose are ingested, absence of the
appropriate disaccharidase will preclude hydrolysis of the disaccharide and
absorption of its component monosaccarides.
● The most common clinical syndrome of disaccharidase deficiency is acquired
lactase deficiency, which accounts for lactose intolerance in many adults

21. Congenital sucrase and trehalase deficiencies are rare and prevent adequate digestion
of sucrose (table sugar) and trehalose (a disaccharide found in mushrooms and
lobsters and used as an additive in processed foods), respectively.
The spectrum of foods that potentially contribute to osmotic diarrhea has been
expanded with the recognition of a group of foods containing poorly absorbed,
fermentable oligosaccharides, disaccharides, monosaccharides, and polyols
(FODMAPs).

22. Features of osmotic diarrhea
● The essential characteristic of osmotic diarrhea is that it resolves with fasting or
cessation of ingestion of the offending substance.
● Electrolyte absorption is not impaired in osmotic diarrhea and electrolyte
concentrations in stool water are usually low.

23. Fecal osmotic gap :
– if elevated: stool Mg output, stool PEG output
– If negative:nstool phosphorous/ sulfate output
Stool pH: <6 - carbohydrate malabsorption
– diet review
– breath hydrogen test with lactose
– measurement of stool reducing substance: anthrone reaction

24. OSMOTIC DIARRHEA
Osmotic diarrhea
Stool analysis
Low pH
Carbohydrate
malabsorption
High Mg output
Inadvertent ingestion
Laxative abuse
Dietary review
Breath H2 test( lactose)
Lactase assay

25. Secretory diarrhoea
● The mechanism of this type of diarrhea is
➔ net secretion of anions (chloride or bicarbonate)
➔ net secretion of potassium
➔ net inhibition of sodium absorption.
● The stimuli for altered electrolyte transport arise from the intestinal lumen,
subepithelial space, or systemic circulation and substantially alter the messenger
systems that regulate ion transport pathways.

26. Causes of secretory diarrhoea
1. Infections: enterotoxins interact with receptors and lead to anion secretion.
2. Tumors- peptides produced by endocrine tumors
3. Genetic causes: congenital chloridorrhea, congenital sodium diarrhea etc
4. Exogenous agents: drugs and toxins
5. Decrease in absorptive surface - celiac disease/ IBD/ resective surgeries
6. Abnormal motility - rapid transit / slow transit
7. Reduced intestinal blood flow - mesenteric ischemia/ Radiation eneteritis

27. Exclusion of infections: Bacterial cultures, Tests for other pathogens (microscopy for ova
and parasites, Giardia, Cryptosporidium antigens, special techniques for Cyclospora,
coccidia, microsporidia), and/or multiplex PCR assay
:short bowel syndrome, fistulas, mucosal diseases, tumors including lymphoma
- CT or MRI of abdomen and pelvis
- Sigmoidoscopy or colonoscopy with mucosal biopsies
- Small bowel mucosal biopsy and aspirate for quantitative culture
- Capsule enteroscopy

28. - TSH, serum cortisol, diabetic status
When indicated…
- Plasma peptides: calcitonin, chromogranin A, gastrin, somatostatin,
vasoactive intestinal polypeptide
- Urine autacoids and metabolites: histamine, 5-hydroxyindoleacetic
acid, metanephrines
- Other tests: ACTH stimulation, immunoglobulins, serum protein
electrophoresis, TSH
- Glucose hydrogen breath test for SIBO
Others:
- Serum protein electrophoresis/ immunoglobulin electrophoresis
- Food exclusion diets (e.g., low-FODMAP diet)
- Bile acid–binding agent
- Antibiotic for SIBO

29. SECRETORY DIARRHEA
Secretory diarrhea
Exclude infection
Small bowel biopsy with
aspirate culture
Others
Plasma peptides:
Gastrin
Calcitonin
VIP
Somatostatin
Exclude structural diseases
Specific tests
Small bowel
radiographs
CT scan
Bacterial
sigmoidoscopy/
colonoscopy
with biopsy
Urine:
5- HIAA
Metanephrines
Histamines
Others:
-TSH
-ACTH
stimulation
-Serum protein
electrophoresis
-Ig
Cholesteramine trail
for bile acid diarrhea

30. CHRONIC INFLAMMATORY DIARRHA
Mucosal disruption and inflammation
IBD
Infections
Mesenteric ischemia
Peudomembranous enterocolitis
Radiation enteritis
Neoplasia.
Exclusion of structural disease by CT/MRI/scopies
Exclusion of TB/ parasites/ viruses

31. INFLAMMATORY DIARRHEA
Inflammatory diarrhea
Exclude structural diseases
Exclude infection
Small bowel radiographs
Sigmoidoscopy or colonoscopy with
biopsy
Small bowel biopsy
Bacterial:
Aeromonas
TB
Others:
Parasites/ viral

32. FATTY DIARRHEA
Steatorrhea - disruption of fat solubilisation, digestion, or absorption in small intestine.
– Defective mixing- gastric resection/GI motility disorders
– Reduced solubilisation of fat- low luminal concentration of conjugated bile acids
– Decreased lipolysis- exocrine pancreatic function
– Decreased mucosal absorption- celiac disease
– disturbance of intracellular formation of chylomicrons or accumulation of lipids-
abetalipoprotenemia, hypobetalipoprotenemia
Exclude structural disease
Exclude pancreatic insufficiency
Exclude duodenal bile acid deficiency

33. Endoscopy:
Duodenal mucosa - scalloping of mucosa, reduction in number of mucosa folds- celiac
disease
Aphthae- chrons
Small, diffuse, white yellowish lesions in primary/ secondary lymphangiectasia
Endocrine tumors- duodenal gastrinoma/ somatostatinoma/ ampullary tumors
obstructing pancreratic duct
Duodenal biopsy

34. Duodenal biopsy:
Abetalipoproteinemia,
hypobetalipoproteinemia
Lipid accumulation and
vacuolization of enterocytes
Collagenous sprue Collagenous band below atrophic
epithelium
Mycobacterium avium complex
infection
Acid-fast bacilli, foam cells
Amyloidosis Congo red–stained deposits
with apple-green birefringence
in polarized light

35. Crohn disease Epithelioid granulomas and
characteristic focal inflammation
Eosinophilic gastroenteritis Eosinophilic infiltration
Lymphangiectasia Ectatic lymph vessels
Lymphoma Clonal expansion of lymphocytes
Mastocytosis Diffuse infiltration with mast cells
Parasites and worms (Giardia
lamblia, Strongyloides stercoralis,
coccidia)
Some parasites may be seen on
histologic examination

36. Aspiration: giardia , SIBO
Imaging:
Small bowel follow through/ enteroclysis:
- mucosal/ mural irregularity
- Focal / diffuse abnormalities that predispose to SIBO
Abdominal CT:
- Focal lesions
- Lymphnodes - whipples, lymphoma, chrons
- Pancreatic structural disorders
- PD obstruction/ hormone secreting neuroendocrine tumors

37. MRI:
- segmental bowel wall thickening/ mesentric inflammation/ cobblestoning/ ulceration
- chrons
- small intestinal dilatation, mucosal thickening, and an increased
- number of folds in the ileum (ileal jejunization) with flattening of duodenal and
jejunal folds (jejunoileal fold pattern reversal)- celiac disease
Abdominal USG:
- obstruction of the biliary tract, pancreatic calcifications, dilatation of the pancreatic
- duct, or stones within the pancreatic duct may be demonstrated.
- celiac disease, Crohn disease, mycobacterial infections, Whipple disease etc

38. Exocrine pancreatic insufficiency: empirical trial of pancreatic enzyme replacement,
quantitative fecal fat estimation, fecal elastase or chymotryspsin, secretin test
Semi quantitative fat analysis: Acid steatocrit test
Stool microscopy:glacial acetic acid and sudan III stain- presence of fat globules
*number : 100 *size: RBC/<4mm per HPF
Bile acid malabsorption- serum levels of C4, FGF 19, SeHCAT test
Incomplete fructose absorption- fructose hydrogen breath test
Lactose malabsorption- lactose hydrogen breath test, lactose tolerance test
SIBO- glucose pr lactulose hydrogen breath test
van de Kamer test- fecal fat <7gms/ day with a fat intake of 100g/day- normal

39. FATTY DIARRHEA
Fatty diarrhea
Exclude structural
diseases
Exclude pancreatic
exocrine
insufficiency
Small bowel radiographs CT abd
Small bowel biopsy and aspirate
fluid for culture
Secretin test
Stool chymotrypsin
activity

40. Thank you..