Diarrhea & Constipation by dr Mohammed Hussien. Ass. Lecturer of Gastroenterology & Hepatology Kafrelsheik University Membership at American Collage of Gastroenterology (ACG) Membership at Egyptian association for Research and training in Hepatogastroentrology

1. Dr/ Mohammed Hussien
Ass. Lecturer of Gastroenterology & Hepatology
Kafrelsheik University
Membership at American Collage of Gastroenterology
(ACG)
Membership at Egyptian association for Research and
training in Hepatogastroentrology
Diarrhea

2. Normal bowel frequency
Ranges from three times a day to three
times a week in the normal population
3-21/week

3. Definitions:
Acute Diarrhoea
Increase stool frequency or increased fluidity
sudden onset and lasts less than two weeks
90% are infectious in etiology
Chronic Diarrhoea
More than four weeks and/or a daily stool weight greater than 200 g/day.
Most of the causes are non-infectious
Persistent Diarrhoea
 -Diarrhoea lasting between 2 to 4 weeks

4. Dysentery:
A triad of diarrhea + pathological stool (blood, mucus, or polymorphs) +
tenesmus.
So, bloody diarrhea is not equal to dysentery.
Tenesmus (which is a sense of urgency and incomplete evacuation) results
from irritation of rectum. So, presence of dysentery points to rectal affection.
Causes of Dysentry:
1- Amoebic dysentry.
2- Bacillary dysentry.
3- Schistosomal dysentry.
4- Ulcerative colitis.
5- Crohn’s disesae (if affecting the rectum).

5. Pathophysiology
• Approximately 7 L of fluid enter the intestines daily—2 L represents food and liquid
intake, and the rest is from endogenous sources such as salivary, gastric, pancreatic,
biliary, and intestinal secretions. Most of the fluid, about 7.5 L, is absorbed in the
small intestine, and only about 1.5 L is presented to the colon. 1.3 absorbed as it
passes through the colon, leaving a stool output of about 200g/day.
Although many organisms simply impair the normal absorptive processes in the
small intestine and colon, others, organisms, such as Vibrio cholera, secrete a toxin
that causes the colonic mucosa to secrete, rather than absorb, fluid and electrolytes.
Voluminous diarrhea may result.

6. Causes of Acute Diarrhea
• -Viral infection:Norovirus, rotavirus, CMV
• -Bacterial infection:Salmonella,Campylobacter, Shigella, Escherichia coli,
Clostridium difficile, V.cholera
• -Parasitic infection: Giardia, Entamoeba histolytica, B.coli,
Cryptosporidia,C.phlepinensis, S.stercolaris
• -Food poisoning: Staphylococcus, Bacillus cereus, Clostridium perfringens
• -Drugs:Laxatives, Mg-containing antacids, caffeine, antineoplastic drugs, many
antibiotics, colchicines.

7. Diagnosis
• Acute diarrheas are usually infectious in origin and, for the most part, resolve with or without
intervention before a diagnosis is made.
• The presence of blood is a useful clue, suggesting infection by invasive organisms,
inflammation, ischemia, or neoplasm.
• Large-volume diarrhea suggests small bowel or proximal colonic disease, whereas small frequent
stools associated with urgency suggest left colon or rectal disease.
• All current and recent medications should be reviewed, specifically new medications, antibiotics,
antacids, and alcohol abuse.
• The physical examination
Vital signs and signs of dehydration.
Abdominal examination to evaluate tenderness and distention.

8. Diagnosis
• When to investigate:
• Failed empirical therapy.
• Passage of many small-volume stools containing blood and mucus
• Temperature higher than 38.5° C (101.3° F)
• Passage of more than six unformed stools in 24 hours
• Duration of illness longer than 48 hours
• Diarrhea with severe abdominal pain in a patient older than 50 years
• Stool analysis:
• Fecal leukocyte (or lactoferrin, a by-product of white blood cells) determination:
support a diagnosis of inflammatory diarrhea
• Stool culture for enteric pathogens.
• Stool examination for ova and parasites: Multiple fresh stool collections should be
collected at different times because shedding of parasites may be intermittent.
• Flexible sigmoidoscopy with biopsy: IBD

9. Treatment:
Pharmacologic Measures:
Antidiarrheal Agents: These can be useful for the improvement of symptoms. The most effective agents
are the opioid derivatives—Loperamide (Imodium ), Diphenoxylate (Lomotil )— and tincture of opium.
Mechanism : inhibit intestinal peristalsis, facilitating intestinal absorption, and antisecretory
properties.
Loperamide may reduce the duration of diarrhea in those with traveler's diarrhea and bacillary
dysentery. These agents should be avoided in patients with fever, bloody diarrhea, and possible
inflammatory diarrhea because they may be associated with prolonged fever in patients with shigellosis,
toxic megacolon in patients with C. difficile infection,
Rehydration. ---Electrolyte replacement--Dietary modifications,--drug
therapy.

10. Bismuth subsalicylate ( Pepto-Bismol®, Kaopectate) somewhat less effective than loperamide, used in traveler's diarrhea.
Antimicrobial Treatment:
• Empirical treatment is indicated for
▪ Patients with suspected invasive bacterial infection
▪ Traveler's diarrhea
▪ Immunosuppressed patients
▪ More than eight loose stools per day, dehydration, symptoms that continue for more than one week and in those who
require hospitalization.
Specific therapy:
• Shigella or Salmonella speices: Quinolone therapy twice daily for 5 days.
• Giardia lamblia infection: Metronidazole drug 250 mg tds for 7 days
• Intestinal amoebiasis: Metronidazole 750mg tds for 10 days.
• Enteropathogenic E.coli: Quinolone therapy.
• Campylobacter infection: Erythromycin 500mg for 5 days twice daily.

11. Chronic Diarrhea
Pathophysiology Of Diarrhea:
• Osmotically active solutes in the intestinal lumen (Osmotic
diarrhea).
• Active ion secretion (Secretory diarrhea).
• Abnormal ( Deranged ) intestinal motility.
• Altered mucosal morphology or loss of absorptive surface.

12. Osmotic Diarrhea
• Mechanism :
Retention of water in the bowel as a result of an accumulation of
non‐absorbable water‐soluble compounds
Improved with fasting
Causes :
-Purgatives like magnesium sulfate or magnesium containing antacids
-especially associated with excessive intake of sorbitol and mannitol.
-Disaccharide intolerance
-Generalized malabsorption

13. Secretory Diarrhoea
• Mechanism :
• Active intestinal secretion of fluid and electrolytes as well as decreased absorption.
• Persist with fasting
• Causes :
• Cholera enterotoxin, heat labile E.coli enterotoxin
• Neuroendocrine tumours:-
✓Vasoactive Intestinal Peptide hormone ~ VIPoma in Verner-Morrison
syndrome (Clinical syndrome: watery diarrhoea, hypokalemia, metabolic acidosis)
✓ Zollinger Ellison syndrome
✓ Somatostatinoma (Diabetes mellitus and diarrhoea/steatorrhoea)
✓ Carcinoid syndrome ( Wheezing ( bronchoconstriction)-- Diarrhea --Facial flushing-Cardiac
involvement)
✓ Medullary carcinoma of thyroid (Parafollicular C cells---Produce calcitonin & also 5HT—diarrhea)

14. Inflammatory Diarrhea (loss of absorptive surface)
• Mechanism :
-damage to the intestinal mucosal cell leading to a loss of fluid
and blood
-pain, fever, bleeding, inflammatory manifestations
• Causes :
-- Immunodeficiency patient
• Infective conditions like Shigella dysentary
• Inflammatory conditions
• Ulcerative colitis and Crohns disease

15. Abnormal Motility Diarrhoea
• Mechanism :
-Increased frequency of defecation due to underlying diseases
-large volume, signs of malabsorption (steatorrhoea)
• Causes :
• Diabetes mellitus- autonomic neuropathy
• Post vagotomy
• Hyperthyroid diarrhoea
• Irritable Bowel Syndrome

16. CAUSES:
Chronic
Diarrhea
Infections
Endocrine
Chronic
nonspecific
diarrhea.
Carbohydrat
es
malabsorptio
n
Dietary
Immune
defects
Metabolic
defects
Pancreas
Small
intestine
IBS
IBD
Viral, parasitic, bacterial,..
•Hyperthyroidism.
•Adrenal insufficiency.
•Lactase deficiency.
•Glucose-glactose
malabsorption.
 Cow’s Milk/soy protein
intolerance.
 Agammaglobulinemia
 IgA deficiency.
 AIDS.
 Familial chloride diarrhea.
 Cystic fibrosis.
 Celiac disease.

17. Diagnosis:
• History
a. When the stools are consistently large in volume, the underlying cause of diarrhea is likely to be located in the
small bowel or in the proximal colon. By contrast, small- volume diarrhea, in which the patient has frequent
urges to defecate but passes only small amounts of feces or mucus, the disorder is usually in the left portion of
the colon and rectum.
b. Passage of blood mixed with the diarrheal stool usually indicates inflammation of the mucosa, less often a
neoplasm.
c. Passage of non bloody mucus suggests irritable bowel syndrome, as does a history of small-volume diarrhea
alternating with constipation.
d. Excessively bad odour stools suggest putrefaction of unabsorbed amino acids and amoebiasis .
e. Visible oil or fat indicates severe steatorrhoea.
f. Fecal soiling (incontinence) suggests an anal sphincter defect.
g. Diarrhea in a patient with features of anorexia nervosa suggests laxative abuse.

18. • Clinical examination
a) Fever: bacillary dysentery amoebiasis, lymphoma, tuberculosis
b) Hypotension: Diabetic diarrhea, Addison’s disease,
c) Marked weight loss: Malabsorption, IBD, cancer, thyrotoxicosis
d) Flushing, large liver: Malignant carcinoid
e) Purpura: Celiac disease
f) Lymphadenopathy: Lymphoma, Whipple’s disease, AIDS
g) Arthritis: Ulcerative colitis, Crohn’s disease, Whipple’s disease
h) Liver disease: Ulcerative colitis, Crohn’s disease, GIT cancer with liver 2ndries
i) Neuropathy: Diabetic diarrhea, amyloidosis

19. •Diagnostic Tests:-
•1. Routine Examination Of Stool.
• Microscopic examination: pus, parasite
• Occult Blood: Occult (or gross) blood in association with diarrhea usually indicates inflammation
• Stain for Fat (Sudan stain).
• Alkalinization: A pink color following alkalinization of a stool or urine sample indicates
phenolphthalein ingestion
•2. Other Tests.
• Biochemical tests: serum glucose,T3,T4 ,serum amylase
• Complete blood count
• Determination of urinary 5-hydroxyindole acetic acid
• Search for Infectious and Parasitic Organisms. Duodenal or jejunal biopsy or aspirate for Giardia,
cryptosporidium.

20. • Proctosigmoidoscopy is helpful in establishing the presence or absence of mucosal
inflammation.
• Rectal Biopsy. Amyloidosis, Whipple's disease, microscopic colitis.
• Quantitative Fecal Fat. Collected stools (usually for 72 hours)
• Twenty-four-hours Stool Volume
• Vasoactive Intestinal Polypeptide (VIP) and other secretory hormones in blood.
• Therapeutic Trials.
• These trials may include pancreatic enzymes, antibiotics, Metronidazole or anti-T.B
drugs, cholestyramine, indomethacin (for prostaglandin synthetase inhibition), and
various diets (lactose free, carbohydrate free, low fat, gluten free)

21. Enterocolitides
•Definition:
• Enterocolitides is a group of diseases that affect colon or colon and small intestine. The most frequent symptoms are
diarrhea (which may be bloody) and abdominal pain. There may be extra-intestinal manifestations as arthritis hepatic
affection
•Causes:
•I. Infectious:
• Amoebic colitis
• Bacillary dysentery
• Bilharzial colitis
• T.B. enterocolitis
•II. Inflammatory bowel diseases:
• Ulcerative colitis
• Crhon’s disease
III. Pseudomembranous colitis
IV. Ischemic colitis
V. Radiation enterocolitis.
•

22. Epidemiology of
Constipation

23. Chronic constipation is one of the most common gastrointestinal disorders, affecting
about 15% of all adults and 30% of those over the age of 60.
Constipation is more prevalent in women and in elderly people.
It is associated with lower socioeconomic status, depression, less self-reported
physical activity, certain medications, and stressful life events.

24. Constipation Defined By Rome IV
Criteria

25. According to the Rome IV criteria, chronic constipation is defined by the presence of the
following for at least 3 months (with symptom onset at least 6 months prior to diagnosis):
(1) Two or more of the following for more than 25% of defecations:
• Straining
• Lumpy or hard stools
• Sensation of incomplete evacuation
• Sensation of anorectal obstruction or blockage
• Manual maneuvers to facilitate evacuation
• Fewer than 3 spontaneous bowel movements per week
(2) Loose stools are rarely present without the use of laxatives.
(3) The patient does not meet the criteria for diagnosis of irritable bowel syndrome.

26. Defecation is complex

27. Primary Constipation
Disorders

28. The American Gastroenterological Association classifies constipation into 3
groups on the basis of colonic transit time and anorectal function.
Normal-transit constipation
Stool normally takes 20 to 72 hours to pass through the colon, with transit time
affected by diet, drugs, level of physical activity, and emotional status.
Normal-transit constipation is the most common type of constipation.

29. Slow-transit constipation
Slow-transit constipation—also called delayed-transit constipation, colonoparesis,
colonic inertia, and pseudo-obstruction—is defined as prolonged stool transit in the
colon, ie, for more than 5 days.
It can be the result of colonic smooth muscle dysfunction, compromised colonic
neural pathways, or both, leading to slow colon peristalsis.
Factors that can affect colonic motility such as opioid use and hypothyroidism
should be carefully considered in these patients.

30. Outlet dysfunction
Outlet dysfunction, also called pelvic floor dysfunction or defecatory disorder, is associated
with incomplete rectal evacuation.
It can be a consequence of weak rectal expulsion forces (slow colonic transit, rectal
hyposensitivity), functional resistance to rectal evacuation (high anal resting pressure,
anismus, incomplete relaxation of the anal sphincter, dyssynergic defecation), or structural
outlet obstruction (excessive perineal descent, rectoceles, rectal intussusception).
About 50% of patients with outlet dysfunction have concurrent slow-transit constipation.
Dyssynergic defecation is the most common outlet dysfunction disorder. It is defined as a
paradoxical elevation in anal sphincter tone or less than 20% relaxation of the resting anal
sphincter pressure with weak abdominal and pelvic propulsive forces. Anorectal
biofeedback is a therapeutic option for dyssynergic defecation.

31. Secondary Constipation

32. Constipation can be secondary to several conditions and factors, including:
• Neurologic disorders that affect gastrointestinal motility (eg, Hirschsprung
disease, Parkinson disease, multiple sclerosis, spinal cord injury, stroke, spinal or
ganglionic tumor, hypothyroidism, amyloidosis, diabetes mellitus, hypercalcemia)
• Drugs used to treat neurologic disorders
• Mechanical obstruction
• Diet (eg, low fiber, decreased fluid intake)
• Organic disease of the gastrointestinal tract: colorectal cancer or polyps

34. Evaluation of Constipation

35. Red flags such as unintentional weight loss, blood in the stool, rectal pain, fever, and iron-
deficiency anemia should prompt referral for colonoscopy to evaluate for malignancy,
colitis, or other potential colonic abnormalities.
A detailed perineal and rectal examination can help diagnose defecatory disorders and
should include evaluation of the resting anal tone and the sphincter during simulated
evacuation.
Laboratory tests of thyroid function, electrolytes, and a complete blood cell count should
be ordered if clinically indicated.
Evaluation of chronic constipation begins with a thorough History (Stool consistency,
a better indicator of colon transit than stool frequency) and physical examination to
rule out secondary constipation.

36. Further diagnostic tests can be considered if symptoms persist despite conservative
treatment or if a defecatory disorder is suspected. These include anorectal
manometry, colonic transit studies, defecography, and colonic manometry.
Anorectal manometry and the rectal balloon expulsion test
These tests measure the function of the internal and external anal sphincters at rest
and with straining and assess rectal sensitivity and compliance. Anorectal
manometry is also used in biofeedback therapy in patients with dyssynergic
defecation.

39. Colonic transit time
can be measured if anorectal manometry and the balloon expulsion test are normal. The
study uses radiopaque markers, radioisotopes, or wireless motility capsules to confirm slow-
transit constipation and to identify areas of delayed transit in the colon.
Defecography is usually the next step in diagnosis if anorectal manometry and balloon
expulsion tests are inconclusive or if an anatomic abnormality of the pelvic floor is
suspected. It can be done with a variety of techniques. Barium defecography can identify
anatomic defects, scintigraphy can quantify evacuation of artificial stools, and magnetic
resonance defecography visualizes anatomic
landmarks to assess pelvic flor motion without exposing the patient to radiation.
Colonic manometry is most useful in patients with refractory slow-transit constipation and
can identify patients with isolated colonic motor dysfunction with no pelvic flor dysfunction
who may benefit from subtotal colectomy and end-ileostomy.

40. Management of
Constipation

42. Serotonin Receptor Agonists
Activation of serotonin 5-HT4 receptors in the gut leads to release of acetylcholine, which
in turn induces mucosal secretion by activating submucosal neurons and increasing gut
motility.
Two 5-HT4 receptor agonists were withdrawn from the market (cisapride in 2000 and
tegaserod in 2007) due to serious cardiovascular adverse events (fatal arrhythmias, heart
attacks, and strokes) resulting from their affinity for hERG-K+ cardiac channels.
The newer agents prucalopride ( Resolar) , velusetrag, and naronapride are highly selective
5-HT4 agonists with low affinity for hERG-K+ receptors and do not have proarrhythmic
properties, based on extensive assessment in clinical trials.

43. Prucalopride has been shown to accelerate gastrointestinal and colonic transit in patients
with chronic constipation, with improvement in bowel movements, symptoms of chronic
constipation, and quality of life.
Adverse effects reported with its use have been headache, nausea, abdominal pain, and
cramps.
Prucalopride is approved in Europe and Canada for chronic constipation in women but is
not yet approved in the United States.
Dosage is 2 mg orally once daily. Caution is advised in elderly patients, in whom the
preferred maximum dose is 1 mg daily, as there are only limited data available on the safety
of this medication in the elderly.

44. Antidepressant therapy: For constipation-predominant irritable bowel syndrome, selective
serotonin reuptake inhibitors are preferred over tricyclics because of their additional
prokinetic properties. Starting at a low dose and titrating upward slowly avoids potential
adverse effects. Cognitive behavioral therapy has also been beneficial in treating irritable
bowel syndrome.
Adjunctive therapies: including peppermint oil, probiotics (eg, Lactobacillus,
Bifiobacterium), and acupuncture have also shown promise in managing irritable bowel
syndrome.
Other emerging pharmacologic therapies are plecanatide and tenapanor.