Dr Anurag ppt.pptCHRONIC AND ACUTE DIARRHEA

ACUTE AND CHRONIC DIARRHEA

1. DRANURAG TAJNE
MBBSDCH
ARIHANT HOSPITAL
NAGPUR
9579510161
APPROACH TO
DIARRHEA

2. OBJECTIVES
INTRODUCTION/ DEFINITION
CAUSES
ETIOPATHOGENESIS
CLINICAL FEATURES AND COMPLICATIONS
DIAGNOSIS
EVALUATION OF DEHYDRATION
TREATMENT
PREVENTION

3. Introduction
Commoncauseofdeathindevelopingcountries
Secondmostcommoncauseofinfantdeaths
worldwide.

4. DIARRHOEA
Diarrhoea defined as excessive loss of fluid and electrolyte in
stool.
For infants stool output >10 ml/kg/24 hr and >200g/24hr for
older children.
When there is an in frequency, volume or liquidity ( Recent
change in consistency) of the bowel movement relative to the
usual habit of each individual
Nelson Textbook of Pediatrics,20th ed

5. DEFINITIONS
•Acute diarrhea
Duration <2 wks, usually of infectious origin
•Prolonged diarrhea
Diarrhea of duration 7-14 days of presumed infectious etiology. It
may be an indicator for children with a high risk of progression to
Persistent diarrhea
•Chronic diarrhea
Diarrhea of more than 2 weeks duration.
•Dysentry
Bloody diarrhea, visible blood and mucus present.
Nelson Textbook of Pediatrics,20th ed

6. Persistent diarrhea
Persistentdiarrhea(PD)isanepisodeofdiarrheaofpresumed
infectiousetiology,whichstartsacutelybutlastsformorethan14
days,andexcludeschronicorrecurrentdiarrhealdisorderssuchas
tropicalsprue,glutensensitiveenteropathyorotherhereditary
disorders[WHO] (INDIANPEDIATRICS,JAN2011)
passageof>=3waterystoolsperdayfor>2weeksinachildwho
eitherfailstogainweightorlosesweight.(ESPGHAN)

7. WHAT IS NOT A DIARRHOEA?
1.Frequent formed stools
2.Pasty stools in breastfed child
3.Stools during or after feeding
4.PSEUDODIARRHOEA:Small volume of stool frequently
(IBS)

9. ETIO-PATHOGENESIS
OSMOTIC DIARRHOEA
LOSS OF MATURE ABSORPTIVE CELLS
INVADE S.I. MUCOSA
VIRAL -MC
ROTA ADENO

10. SECRETORY DIARRHOEA
ULCERATION –SYNTHESIS OF SECRETAGOGUES
ACUTE INFLAMMATION
INVADE LARGE INTESTINE
BACTERIAL -INVASIVE
SHIGELLA, SALMONELLA, YERSINIA, V.PARAHEMOLYTICUS

11. DECREASE ABSORPTIVE SURFACE
CELL INFLAMMATION, CELL DEATH
ELABORATION OF CYTOTOXIN
BACTERIA -CYTOTOXIC
SHIGELLA,EPEC,V.HEMOLYTICUS,C.DIFFICILE

12. ALTERED SALT AND WATER TRANSPORT
ENTEROTOXIN-INCREASE THE CONC. OF INTRACELLULAR
MEDIATORS
COLONISE SMALL INTESTINE
BACTERIA -TOXIGENIC
SHIGELLA,ETEC,VIBRIO

13. DECREASE INTESTINAL ABSORPTIVE SURFACE
FLATTENING OF MICROVILLI
COLONISE & ADHERE SMALL INTESTINE
BACTERIAL ADHERENTS
EPEC,EHEC

14. CLINICAL FEATURES
BLOODY STOOLS –BACTERIAL ETIOLOGY
HUS
ABDOMINAL PAIN –GE
PERITONEAL SIGNS -APPENDICITIS

15. DIAGNOSIS
ATLEAST 3 STOOLS PER 24H
ASSESSING DEHYDRATION
-H/O NORMAL FLUID INTAKE AND OUT PUT
-PHYSICAL EXAMINATION
-PERCENTAGE OF BODY WT LOSS

16. EVALUATING DEHYDRATION
GENERAL CONDITION -MENTAL STATUS*
THIRST*
EXTREMITIES
CAPILLARY REFILL TIME
SKIN TURGOR
BREATHING
HEART RATE
B.P
PULSE QUALITY
EYES*
TEARS*
MUCOUS MEMBRANES*
ANTERIOR FONTANELLE
URINARY OUTPUT

17. SIGNS NONE /MINIMAL
DEHYDRATION(<3
%
LOSS OF BODY WT)
SOME/ MILD
TO
MODERATE(3 -
9% LOSS OF
B.WT)
SEVERE ( >9%
LOSS OF B.WT)

18. CLINICAL DEHYDRATION SCORE

19. No Dehydration: PLAN-A
Some Dehydration: PLAN-B
Severe Dehydration: PLAN-C
Plan of Treatment

20. Treat Diarrhea at Home.
4 Rules of Home Treatment:
GIVE EXTRA FLUID
CONTINUE FEEDING
WHEN TO RETURN [ADVICE TO MOTHER]
GIVE ORAL ZINC FOR 14 DAYS
PLAN –A

21. TELL THE MOTHER:
Breastfeed frequently and for longer at each feed
If exclusively breastfeed give ORS for replacement of stool
losses
If not exclusively breastfed, give one or more of the following:
ORS, food-based fluid (such as soup, rice water,
coconut water and yogurt drinks), or clean water.
TEACH THE MOTHER HOW TO MIX AND GIVE
O.R.S
AMOUNT OF FLUID TO GIVE IN ADDITION TO THE
USUAL FLUID INTAKE:
Up to 2 years: 50 to 100 ml after each loose stool.
2 years or more: 100 to 200 ml after each loose stool.
Give extra fluid

22. Continue usual feeding, which the child was
taking before becoming sick 3-4 times
(6 times)
Up to 6 months of age:
Exclusive Breast feeding
6 months to 12 months of age:
add Complementary Feeding
12 months and above:
Family Food
Continue feeding

23. Advise mother to return immediately if the
child has any of these signs:
Not able to drink or breastfeed or drinks poorly
Becomes sicker
Develops a fever
Blood in stool
[IF IT WAS NOT THERE EARLIER]
When to Return
[Advice to mother]

24. Plan-B is carried out at ORT Corner in
OPD/clinic/ PHC
Treat ‘some’ dehydration with ORS (50-100
ml/kg
Give 75 ml/kg of ORS in first 4 hours
If the child wants more, give more
After 4 hours:
Re-assess and classify degree of dehydration.
PLAN –B

25. PLAN -C
Signs of sever dehydration
Child not improving after 4 hours
Refer to higher center –give ORS on way /keep
warm /BF
When child comes back follow up as other children

26. Start I. V. Fluid immediately
Give 100 ml/kg of Ringer’s Lactate
Age First give
30ml/kg in
Then give
70 ml/kg in
Under 12 months 1 hour 5 hours
12 months and
older
½ hour 2½ hour
PLAN –C

27. Use intravenous or intraosseusroute
Ringers Lactate with 5% dextrose or ½ normal saline with 5% dextrose
at 15 ml/kg/hour for the first hour
* do not use 5% dextrose alone
Fluid therapy in severe dehydration
Continue monitoring every 5-10 min.
Assess after 1 hour
If no improvement or worsening If improvement(pulse slows/faster
capillary refill /increase in blood pressure)
Consider septic shock Consider severe dehydration with shock
Repeat Ringers Lactate 15 ml/kg over 1 h
Switch to ORS 5-10ml/kg/hr orally or by
nasogastric tube for up to 10 hrs

28. What Is ORS

29. Safe & effective
Can alone successfully rehydrate 95-97% patients with
diarrhea,
Reduces hospital case fatality rates by 40 -50%
Cost saving
Reduces hospital admission rates by 50% and cost of
treatment by 90%
BUT
WHO-ORS:“potentially the most important medical advance of this
century”’ The Lancet

30. > 50% Goa, Himachal, Meghalaya, Tripura,
Manipur
> 40% West Bengal, J&K, Mizo, Chhattisgarh
>20% Bihar, Orissa, Uttaranchal, Punjab, Gujarat,
MP, Southern States
< 20% Rajasthan, UP,Assam, Jharkhand,
Nagaland
Recent NFHS 3 data
ORS use rates are dismally low in some regions

31. STANDARD ORS SOLUTION LOW
OSMOLARITY ORS
(MEQOR MMOL/L)
GLUCOSE 111 75
SODIUM 90 75
CHLORIDE 80 65
POTASSIUM 20 20
CITRATE 10 10
OSMOLARITY 311 245
Composition of standard and low osmolarity
ORS solutions

32. LAB.EVALUATION AND IMAGING
STOOL CULTURE-salmonella
shigella
yersinia
campylobacter
pathogenic E.coli-serotyping
RAPID STOOL TEST: for inflammatory markers
Hematological tests: white blood cell band count >100/mm
3.
C-reactive protein cut point of >12
milligrams/dl
Biochemical tests: BUN
Ser.bicarbonate <17 mEq/L
GRBS
USG

34. TREATMENT
ANTIEMETIC-Ondansetron0.5mg/kg/dose
NO ANTIMOTILITY MEDICATION :
Diarrhea may function as an evolved expulsion
defense mechanism
Can cause HUS in EHEC infection.
ADSORBANTS AND ANTISECRETORY AGENTS:
Bismuth –inc.salicylate levels
PROBIOTICS -LactobacillusGGand
Saccharomyces boulardii
ANTIBIOTICS FOR A/C GE

35. PREVENTION
Good Hygiene
Vaccines
Prevent global warming
Global warming αfood borne infections
αcontamination of water
ENRICH –( December 2011Bulletin from IAP )

36. CHRONIC DIARRHOEA
•Diarrhoea lasting for more than 2 weeks
•Mainly non infections causes

37. Causes of chronic diarrhea
Inflammatory & immune
Celiac disease
Primary/sec immunodeficiency
Eosinophilicgastroenteritis
food allergy-cow milk protein, soy
protein
IBD
Infectious diarrhea
Parasites (e.g., Giardialamblia,
Isospora)
Helminths(e.g., Strongyloides)
Bacterial (e.g., MAI, Clostridium
difficile
SI bacterial overgrowth
Whipple disease
Abnormal digestive processes
Pancreatic-
Cystic fibrosis
Shwachman-Diamond syn
Isolated pancreatic enzyme
deficiency
Chronic pancreatitis
Pearson syndrome
Bile acid disorders-
Chronic cholestasis
Terminal ileum resection
Bacterial overgrowth
Primary bile acid
malabsorption

38. Causes of chronic diarrhea
Nutrient malabsorption
Lactase def-cong/ acquired
Sucrase-isomaltasedef
Glucose-galactosemalabsorption
fructose malabsorption
Short bowel syndrome
Structural defects
Microvillus inclusion disease
Tufting enteropathy
Motility disorders
Chronic intestinal pseodobstruction
Thyrotoxicosis
Electrolyte & metabolite
transport defect
Cong cldiarrhoea, Cong Na diarrhoea
Acrodermatitisenteropathica
Abetalipoproteinemia
Carbonated fluid
Sorbitol, mannitol
Laxatives-lactulose, Mg
Methylxanthines-tea coffee
Neoplastic
APUDomas-VIPomas
Zollinger-ellison
Pheochromocytoma
Chronic nonspecific diarrhea
Functional
Toddler’s diarrhea
Irritable bowel
syndromeAssociated with
exogenous subs

39. osmotic
secretory
Motility
disorder
Reduced
surface area
Mutational
defects in ion
transport
proteins
CHRONIC
DIARRHEA
PATHOGENESIS OF CHRONIC DIARRHEA

40. EVALUATION OF PATIENT
History
Examination
Investigations including tests of malabsorption

41. HISTORY TAKING
What is the complaint
Onset –sudden? Gradual?
Duration
Stool-frequency, consistency, volume, presence of blood or mucus, pain
Relation to particular food stuff
Fever
Abdominal pain –peri-umblical? Left lower quadrant?
Features of any systemic diseases
History of weight loss
Any known systemic disease
Food taken & History of gastroenteritis in others sharing same food
history of food allergy/ abdominal surgery

42. HISTORY
Confirmthisisdiarrhea(comparewithusualhabitofchild)
Onsetacuteorinsidious–infectious,acutesecretorydiarrhea
Age of onset
Neonatal –lactose intolerance, congenital diarrhea
-Cow milk protein intolerance
Early childhood-Celiac disease
late childhood -IBD, IBS
Durationofsymptom
Doesthechildhaveweightlossorfailuretogainweight-malabsorption,
pancreaticenzymeinsufficiency

43. Natureofdiarrhea
Urinelikestool-Congenitalchloridediarrhea
-Microvillusinclusiondisease
Explosivewaterydiarrhea-Carbohydratemalabsorption
Loosebulkystool-Celiacdisease
Pastyandyellowishoffensive–Exocrinepancreaticinsufficiency
Fatty,floatingstools-Malabsorptionsyndromes
Blood,pus,mucous-chronicinflammatorydiarrhea
Relation with diet/ dietary history
Carbonated drink and fruit juice –Chronic non specific diarrhea
Sucrose diet –sucrose intolerance
Wheat diet –Celiac disease
Fatty diet –Pancreatic insufficiency
Milk –Lactose intolerance, Cow milk protein intolerance
HISTORY

44. HISTORY
Abdominal pain –IBD, IBS
Patient undergo abdominal surgery –Short gut or bacterial over growth
syndrome
Fever, red eye, oral ulcer –IBD
Arthritis –IBD, Whipple disease
Drug history –Laxative (Factitious diarrhea)
Recurrent respiratory and skin infection -immunodeficiency, Cystic fibrosis
Family history of food allergy, asthma or allergic rhinitis.
Family history of celiac disease, crohn’s disease, cystic fibrosis
Prolonged use of antibiotic, pseudomembranous colitis

45. PHYSICAL EXAMINATION
Level of hydration
Look for tongue
Sunken eyes
Skin turger
Temperature, Blood pressure, Pulse rate, rr
Pallor
features of malnourishment -Anthropometry ,Loss of subcutaneous fat,
Muscle wasting, Loose skin appearance
Abdominal tenderness
Features of liver / pancreatic disease
Other features of relevant systemic diseases

46. Abdominal distension –Gas -due to bacteria
–Ascites –protein loss
Oedema –Protein lossing enteropathy
Clubbing –Coeliac diseae, cystic fibrosis
Perianal excoriation –carbohydrate malabsorption
Perianal and circumoral rash –acrodermatitis enteropathica
Hepatosplenomegaly with lymphadenopathy –HIV
Oral thrush –Immunodeficiency
Features of associated vitamin deficiencies
Glossitis, Cheilosis, Stomatitis, Vit B deficiency
Peripheral neuropathy -Vit B
12 and Thiamine deficiency
Ricketic change, osteomalacia, easy fracture –vit. D and Ca deficiency
Koilonychia –Iron deficiency

47. EXAMINATION -NUTRITION, CAUSE
Anthropometry
Anemia, bitot spots
aphthous ulcers, bleeding
gums, tongue goitre
Lymph
nodes
clubbing
Hyperpigmentation skin, pyoderma, dermatitis
herpetiformis
Rickets
Pedal edema
Wasting, loss of s/c fat
Hepatomegaly, Bowel sounds,
distension, perianal & rectal o/e
arthritis
flushing

48. INVESTIGATIONS
CBC
Anemia (microcytic or macrocytic)
Lymphopenia (lymphangiectasia)
Neutropenia (Shwachman syndrome)
Increased platelet –IBD
PBF
Acanthocytosis (A beta lipoproteinemia)
ESR
Increased in inflammatory pathology
RFT, LFT
Serum iron, TIBC, B12
STP, S. alb

49. Stool examination-
Take liquid contents
Stored in refrigerator
Blood or mucus colonic inflammation
Microscopic examination->20 wbc/hpf
Fecal calprotectinconcentration-100ug/gm stool
PH <5 .5 & presence of reducing substance –carbohydrate malabsorption
Stool electrolytes and osmolality-Secretorydiarrhea
Microscopy for ova and parasite-in endemic areas
Acid fast staining
Cryptosporidium/cyclospora
Stool culture-dysentry, fecal leucocytes +, HUS, immunocompromised
children.

50. FAT MALABSORPTION TESTS
1. STOOL FOR FAT GLOBULES
Qualitative test
Rapid and inexpensive
SudanIIIstain-DRUMMEY’S method
Orange fat globule -seen in microscope
<100 globule with diameter <4-8 u / HPF –moderate steatorrhoea
>100 globule with diameter <6-75 u / HPF –severe steatorrhoea
2. 72 hours fat extraction test (quantitative)
“Gold standard”
however cant differentiate between pancreatic and intestinal causes
Before the test, the patient is put on a high fat diet, consuming between 50-150 g/day of fat
for three days. Stool fat is estimated by VAN DE KAMER METHOD.
Steatorrhoeaif >15% fat output (<6 mo of age) >7%(>6 mo of age)
Limited use in clinical practice due to issues with
collection/processing

51. 3. Classical steatocrit
Semi-quantitative screening test
Steatocrit>2.1% indicates steatorrhoeaof >10gm/d
4. Fat soluble vitamin–Vit. D –Ca, Po
4,
AlkPO
4,
–VitK –PT INR
S. carotene-Dietary carotene is the only source and serum level
depends on normal fat absorption.
normal-100IU/dl

52. CARBOHYDRATE MALABSORPTION TEST
1. D-XYLOSE ABRORPTION TEST
Indicates malabsorption secondary to mucosal dysfunction (proximal small
intestinal-jejunum)
After overnight fasting-Oral load with 25 g D-xylose(adult dose) 5gm(children)
5 hr urine collection done ( atleast25% excretion <4g/ <15%-abnormal)
1 hr and 2 hr serum samples (normal > 20 mg/dl at 1 hr, > 25 mg/dl at 2 hr)
Normal-in pancreatic insufficiency
Abnormal-CD, Tropical sprue, Chron’sdisease, pellagra, advanced AIDS
Falsely low-vomiting, gastric stasis, ascites, edema, bacterial overgrowth, impaired
renal functions
Drugs that decrease urinary excretion of D xylose-aspirin, indomethacin,digitalis,
neomicin, opiates.
Almost obsolete test.

53. 2. Breath Hydrogen test
For specific carbohydrate malabsorption and bacterial overgrowth
Overnight fast
Suspected sugar 1-2 gm/kg max. 50 gm given
Not digest or absorb in small intestine
In colon by fermentation hydrogen and carbon dioxide isformed, absorbed
into blood and excreted in breath.
<20 ppm is normal. 20-80 ppm indeterminate. >80ppm-malabsorption.
Unreliable results-smokers, pulmonary disease, hyperventilation.
False negatives-Hydrogen non excretors, antibiotics 2 weeks prior.

54. PROTEIN MALABSORPTION TESTS
Indirect methods
Fecal -1 antitrypsin concentration
normal-0.8 mg/gm stool.
Protein losing enteropathy->2.6mg/gm stool
cant be done in < 1 week of age
Hypoalbuminemia
Serum proteins with short half lives can be used as nutritional markers.
Prealbumin(transthyretin)
Somatomedin C
Retinal binding protein
Transferrin

55. TESTSFORPANCREATIC INSUFFICIENCY
Serum trypsinogen
Fecal chymotrypsin <150 mg/kg in older children
Fecal elastase-1
Gold standard-Direct estimation of bicarbonate (secretin) or
amylase/lipase/trypsin (CCK) after stimulation using either secretin or CCK
or test (Lundh) meal
Limited by availability, invasiveness, expense
Cystic fibrosis is most common cause of exocrine pancreatic insufficiency in
children so a sweat chloride test must be performed.

56. IMAGING STUDIES & ENDOSCOPY
Plain X-ray abdomen
Air fluid levels-ileus, obstruction
Calcification-Chr. Pancreatitis
USG-e/o cholestasis, cirrhosis, thickening of small
bowel –crohn’s disease
Barium contrast small bowel series
Anatomical lesions, transit time
stenosis, decreased folds, segmentation, dilation
CT/MR abdomen
Detect bowel and pancreatic lesions
Small bowel endoscopy with jejunal aspirate and culture,
Colonoscopy
ERCP / MRCP-Detect ductal abnormalities

57. ENDOSCOPY ANDSMALLBOWELBIOPSY
-when SI mucosal disease is suspected
-when d-xylose test is abnormal
Visual assessment
Decreased folds, scalloping, mosaic
pattern, inflammatory changes

58. MANAGEMENT OF CHRONIC DIARRHEA
Nutritional management
Specific treatment
Drugs & probiotics
General supportive treatment

59. •Definitetreatment-celiacdisease,acrodermatitis
enteropathica
•Spontaneousimprovementwithnutritionalrehabilitation
seenin-Secondarylactoseintolerance,shortbowel
syndrome
•Nutritionalsupportisanessentialcomponentoflongterm
managementofotherdisorderswithchronicdiarrheaand
malabsorption- Pancreatic insufficiency,
abetalipoproteinemia,intestinallymphangiectasia
•Inmoderatetoseveremalnutrition,caloricintakeis
progressivelyincreasedto>=50%aboverecommended
dietaryallowances.
NUTRITIONAL MANAGEMNT

60. oElementaldiets-overcomefoodintoleranceandfacilitate
nutrientabsorption
oIncasethechildcantbefedbyoralroute,enteralnutrition
maybedeliveredbynasogastricorgastrostomytube.
oContinuousenteralnutritioniseffectiveinchildrenwith
reducedabsorptivefunction,suchasshortbowel
syndrome,becauseitextendsthetimeofnutrient
absorptionthroughthestillfunctionalsurfacearea.
oInextremewasting-parenteralnutritionmayberequired.
•Supplementwithminerals,vitaminsespZn-promotesion
absorption,restoresepithelialproliferation,stimulates
immuneresponse

61. SPECIFIC THERAPY
•Gluten free diet-Celiac disease
•Pancreatic enzyme supplementation -suspected pancreatic
insufficiency-pancreatin tablets
•Lactose free formula-Primary lactase deficiency
•Sucrose free formula-Sucrase-isomaltase deficiency
•CMPA-Extensively hydrolised 100% bovine casein infant
formulas or elemental amino acid formulas

62. DRUG THERAPY
ANTIBIOTICS
PROBIOTICS
ANTIMOTILITY DRUGS & ANTISECRETORY DRUGS
ABSORBANTS
IMMUNE SUPRESSION
Autoimmune enteropathy, IBD
Azathioprine, methotrexate, cyclosporine
PROMOTION OF CELL GROWTH
Zn, growth hormone-promote enterocytegrowth

63. ANTIBIOTICS
Antimicrobial therapy is required for
•Clostridium difficileenterocolitis
•Giardia-Metronidazole, nitrazoxanide
•Cryptosporidium-Nitrazoxanide
•If bacterial agent is detected-specific antibiotic treatment
Small intestinal bacterial overgrowth-metronidazolewith ampicillinor
trimethoprim-sulfamethoxazole.
Empericallygiven antibiotics in the treatment of associated systemic
infections that are seen in almost 30% to 40% of such children
Oral-Cefixime
Ciprofloxacin
Azithromycin
IV-Cefotaxim
Ceftriaxone

64. PROBIOTICS
•DEFINITION-Live micro-organisms that, when administered in
adequate amounts, confer a health benefit on the host
Promote
intestinal
growth
Toxin
degradation
adhesion
Boost
immunity
Antibacterial
Host cell
signalling
Competition
MECHANISM OF ACTION

65. INDICATIONS:
•Persistent diarrhea: The use of probioticsappear to hold promise as
adjunctive therapy but there is insufficient evidence to recommend
their use. (Cochrane reviews. 2010)
•Chronic diarrhea:
•Cl. Difficileassociated diarrhea prevention: level B evidence
•IBS: level B evidence
•IBD: role in UC, no role in CD

66. ANTIMOTILITY DRUGS & ANTISECRETORY DRUGS
Antimotilitydrug-LOPERAMIDE.
4mg f/b 2 mg (adult dose)
MOA-reduces gastric motility.
not recommended in under 4 yr age
Indications:
•Chronic diarrhoeain HIV/AIDS-can still be used, with greater emphasis
placed on adjunct therapies [Cochrane Database of Systematic Reviews
2008]
•Treatment of diarrhea-predominant IBS [Digestion 2006]
•S/E: Abdominal cramps, rashes, paralytic ileus, toxic megacolon
•Antimotilitydrug-CODEINE
Opium alkaloid
MOA-acts on u receptors and decreases stool frequency by peripheral action
on small intestine and colon.
S/e-nausea, vomiting, dizziness, dependanceproducing liability is low but
present

67. Enkephalinase inhibitors-RACECADOTRIL
enkephalinase
Enkephalins inactive
delta receptors
Decrease c-AMP
Decreases electrolyte
and water secretion
•Decreases intestinal secretion . No
effect on motility
•The advantage over standard opiates
is no rebound constipation or
prolonged intestinal transit time. [GUT
2002]
•INDICATION
Short term treatment of secretory
diarrheas
S/E-nausea, flatulance, drowsiness
Dose-1.5 mg/kg TDS

68. Somatostatin analogue-OCTREOTIDE
MOA-reduce intestinal secretion by decreasing gut hormones e.g. VIP and
direct effect, either on the ENS or on the enterocyte itself.[GUT 2002]
Antimotility action
Indications:
•HIV enteropathy
•IBS
•Hormone secreting tumors-VIPoma, carcinoid tumours, and gastrinoma
[Aliment Pharmacol Ther. 2001]
Adrenergic agonist-CLONIDINE
MOA-antisecretory and antimotility effects
Indications:
•Moderate and severe diarrhea-predominant IBS. [Clin Gastroenterol
Hepatol. 2003]
•Short bowel syndrome and high-output proximal jejunostomy that
require chronic parenteral fluid infusion. [J Parenter Enteral Nutr. 2006]

69. ABSORBANTS
Ispaghula / Psyllium
•They contain a natural colloidal mucilage and form a
gelatinous mass by absorbing water.
•They modify the consistency and frequency of stools and
give an impression of improvement without actually
decreasing water or electrolyte loss.
•No good evidence to support the use of bulking agents
(eg, psyllium) or adsorbents(eg, charcoal, kaolin plus
pectin) in chronic diarrhea-. [Aliment Pharmacol Ther. 2001]
•Irritable bowel syndrome –useful in both constipation and
diarrhea phases of IBS and also decrease abdominal pain