approach to diarrhoe modified chronic diarrhoea.pptx

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

9. 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

10. 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

11. Comprehensive metabolic panel IgA tissue transglutaminase Ab IgA level

12. Osmotic vs Secretory Diarrhoea

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

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

15. 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.

16. 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

17. 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).

18. 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.

19. 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

20. 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

21. 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.

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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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

36. Thank you..