DIARRHOEA AND IBD

KATE COLEMAN-SARFO(PhD, Pharm D)

(CONSULTANT CLINICAL PHARMACIST)

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DIARRHOEA

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 PRESENTATION OUTLINE
• INTRODUCTION
• DEFINITION
• EPIDEMIOLOGY
• AETIOLOGY
• PATHOPHYSIOLOGY
• TYPES OF DIARRHOEA
• ACUTE INFECTIOUS DIARRHOEA
• CLINICAL PRESENTATION
• DEHYDRATION: ASSESSING DEHYDRATION
• TREATMENT

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 INTRODUCTION
• Diarrheal diseases are one of the leading causes of death globally.
• Most cases of diarrhea are associated with contaminated food and water sources, and
more than 2 billion people globally have no access to basic sanitation.
• Diarrheal disease is the second leading cause of death in children under five years old,
and is responsible for killing around 525,000 children every year in Africa.
• In the past, for most people, severe dehydration and fluid loss were the main causes of
diarrhoea deaths.

• Now, other causes such as septic bacterial infections are likely to account for an
increasing proportion of all diarrhoea-associated deaths.

• Children who are malnourished or have impaired immunity as well as people living
with HIV are most at risk of life-threatening diarrhoea . (WHO 2017)
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 DEFINITION
The definition of diarrhoea is based on two characteristics of stool: frequency and
consistency, a third feature may be urgency.

• Diarrhoea can be defined as the abnormal passing of loose or liquid stools, with increased
frequency and/or increased volume.

• Increased frequency is defined as the presence of three or more abnormally loose or watery
stools in the preceding 24 hours.
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DEFINITION
• Frequent passing of formed stools is not diarrhoea, nor is the passing of
loose, "pasty" stools by breastfed babies.

• Loose watery bowel movements that may occur frequently and with a sense of
urgency

• The increased passage of loose or watery stools relative to person’s usual

bowel habit (3 or more liquid stools within 24 hrs). It is usually a symptom of
gastrointestinal infection which can be caused by a variety of bacterial, viral
and parasitic organisms. (WHO 2017)

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 DEFINITION

Diarrhea is defined as acute, persistent or chronic.

• Acute diarrhoea - lasts less than 2 weeks;

• Persistent diarrhoea – lasts from 2 to 4 weeks, and

• Chronic diarrhoea - lasts longer than 4 weeks

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 EPIDEMIOLOGY
•World: globally, there are nearly 1.7 billion cases of childhood
diarrhoeal diseases per year. Diarrhoea accounted for 9% of all deaths in
children under 5 years in 2019 (WHO, 2019).

• Africa: the second leading cause of death in children under five years old
and responsible for killing 525,000 children every year.

•Ghana: accounts for 25% of mortality and morbidity in children

under five years of age, with more than 9 million episodes occurring
annually

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EPIDEMIOLOGY

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 AETIOLOGY
Acute Diarrhoea

• Acute diarrhoea generally involves the sudden onset of three or more loose or liquid
stools above baseline in a 24-hour period.

• More than 90% of cases of acute diarrhea are caused by infectious agents.

• Acute diarrheal infection is also referred to as gastroenteritis.

• Most infectious diarrhoea are acquired by fecal–oral transmission or via ingestion of

food or water contaminated with human or animal fecal pathogens.

• Many of these cases are accompanied by abdominal pain and cramps, bloating,
flatulence, passage of bloody stools, tenesmus, fecal urgency, fever, and vomiting
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 AETIOLOGY
Viruses cause a large proportion of acute diarrhoea cases.

• Common culprits include Rotavirus, Norwalk (Norovirus), and adenovirus.

Bacterial causes include Escherichia coli, Salmonella species, Shigella species, Vibrio
cholerae, and Clostridium difficile (especially if antibiotics had been administered).

• The term dysentery describes some of these bacterial infections when associated with serious
occurrences of bloody diarrhea.

• Acute or persistent diarrheal conditions can also result from parasites and protozoa such as
Entamoeba histolytica, Microsporidium, Giardia lamblia, and Cryptosporidium parvum.

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 AETIOLOGY
• The remaining 10% of acute diarrhoea cases are non-infectious.

• Noninfectious causes of acute diarrhea include drugs and toxins, laxative abuse, food
intolerance, IBS, inflammatory bowel disease, ischemic bowel disease, lactase
deficiency, vitamin B12 deficiency anemia, diabetes mellitus, malabsorption, fecal
impaction, and diverticulosis

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 AETIOLOGY

Chronic Diarrhoea

• Chronic diarrhoea is much less likely to be infectious and usually results from
functional or inflammatory bowel disorders, endocrine disorders,
malabsorption syndromes, and drugs (including laxative abuse).

• Daily watery stools may not occur with chronic diarrhoea.

• Diarrhoea may be either intermittent or continual.

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 Drug-induced Diarrhoea
• Drugs are a common cause of diarrhoea.
• Drug-induced diarrhea can occur by several mechanisms.
First, water can be drawn into the intestinal lumen osmotically (eg, saline laxatives).
Second, the intestinal bacterial ecosystem can be upset leading to emergence of invasive
pathologic organisms triggering secretory and inflammatory processes (eg, antibiotic
use).
Third, some drugs increase intestinal motility (eg metoclopramide).
Other drugs produce diarrhea through undetermined mechanisms (eg, procainamide,
colchicine).
• Discontinuation of the offending drug may be the only measure needed to ameliorate
diarrhoea.

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 Examples of drugs known to cause
diarrhoea
• Antibiotics (all) • Theophylline
• Proton Pump Inhibitors • Digitalis
• Metformin, acarbose • Quinidine
• NSAIDs • Thyroid products
• Sorbitol, mannitol • Antihypertensives (Lisinopril,
• Colchicine Hydralazine)
• Laxatives • Acetylcholinesterase inhibitor (eg
rivastigmine, donepezil)
• Misoprostol

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 FOOD POISONING

• Food poisoning should be suspected if at least two individuals present with similar
symptoms after the ingestion of a common food in the prior 72 hours.

• Many bacterial and viral pathogens (eg, Salmonella, Shigella, Campylobacter, E. coli,
and noroviruses) can cause food poisoning.

• Other bacteria that can cause food-borne illness include Staphylococcus aureus, C.
perfringens, Clostridium botulinum, and Bacillus cereus

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 EXAMPLES OF COMMON CAUSES OF DIARRHOEA
BACTERIA VIRUS PARASITES OTHERS
Vibrio cholera Rotavirus Entamoeba histolytica Medical conditions:

Shigella Adenoviruses Gardia Lamblia Irritable bowel

syndrome
Inflammatory bowel
disease
Intestinal
Malabsorption

Escherichia coli Caliciviruses Cryptosporidium Medications:

Isospora
Salmonella Astroviruses Antibiotics
Cytotoxic drugs
Magnesium
Campylobacter jejuni Colchicine
Laxatives
Clostridium difficile
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 PATHOPHYSIOLOGY
• The fundamental process causing all diarrheal diseases is incomplete absorption of
water from intestinal luminal contents.

• Water itself is not actively transported across the intestinal mucosa but moves across
secondary to osmotic forces generated by the transport of solutes, such as electrolytes
and nutrients.
• Normally, absorption and secretion take place simultaneously, but absorption is
quantitatively greater.
• Either a decrease in absorption or an increase in secretion leads to additional water
within the lumen and diarrhea.
• Excess stool water then causes decreased stool consistency.
• Thus, diarrhea is a condition of altered intestinal water and electrolyte transport.
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 PATHOPHYSIOLOGY
• The pathophysiologic mechanisms of diarrhea include osmotic, secretory,
inflammatory, and altered motility.
• Osmotic diarrhea involves an unabsorbed substance that draws water from the
plasma into the intestinal lumen along osmotic gradients.
• Secretory diarrhea results from disordered electrolyte transport and, despite the
term, is more commonly caused by decreased absorption rather than net secretion.
• Inflammatory diseases cause diarrhea with exudative, secretory, or osmotic
components.
• Altered motility of the intestine or colon may alter fluid absorption by increasing or
decreasing the exposure of luminal content to intestinal absorptive surface.

However, from a pathophysiologic perspective, no single cause of diarrhea is truly

unifactorial. 19
 TYPES OF DIARRHOEA
• There are four types of diarrhoea;
Osmotic
Secretory
Inflammatory, and
Altered motility (or accelerated transit time) diarrhoea

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 PATHOPHYSIOLOGY
TYPE OF DIARRHEA MECHANISM

SECRETORY Secretion of water into the intestinal lumen

exceeds absorption
Eg: Vibrio cholera, Enterotoxigenic E.coli

OSMOTIC Excess amount of solutes is retained in the

intestinal lumen leading to reduced water
absorption
Eg Viral infection, Lactose deficiency
EXUDATIVE Destruction of the intestinal epithelium by
pathogens resulting in exudation of blood and
serum into the lumen
Eg Bacterial enteritis, Amoebiasis
MOTILITY DISORDER Diarrhea results from acceleration in transit
time leading to a decrease in absorption of
water and electrolytes. Eg. Irritable bowel
syndrome 1
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PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
 RISK FACTORS
Infectious Non-infectious

Poor sanitation Large amounts of cow milk

Urban slums & refugee camps Genetic factors

Unsafe drinking water Antibiotic use

Food hygiene

Travelling to endemic areas

Swimming in crowded pools

Immunocompromised individuals
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MODE OF TRANSMISSION

DIARRHOEA
•The “five F’s”
 Food
 Fluids
 Faeces
 Flies
 Finger
s

•Contaminated
fomites.

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 CLINICAL
PRESENTATION AND
DIAGNOSIS

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 CLINICAL PRESENTATION
History taking
• Getting a complete history of the patient is important.
• The duration of the diarrhoea, along with its severity and symptoms, will need to be
ascertained to establish whether referral is warranted.
• Warning (alarm) signs that warrant further investigation include blood in the stools,
persistent vomiting, unintentional and unexplained weight loss, or nocturnal
symptoms which disturb sleep.
• Patients should be questioned about whether other members of the family or other
people they have been in contact with are ill.
• They should also be questioned about the food they have eaten, any medicines they have
taken and if they have recently travelled abroad, because all of these factors are
important in assessing the condition.

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 Patient’s History
Patients with diarrhea should be
questioned about;
• recent travel
• the onset of symptoms
• Diet
• duration and severity of the diarrhea
• source of water
• the presence of abdominal pain or
• medication use;
vomiting;
• blood in the stool; • and weight loss.
• stool consistency, appearance, and
frequency;

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 CLINICAL PRESENTATION
Physical examination – (especially in children)
Look for:
• signs of dehydration
• blood in stools
• signs of severe malnutrition
• abdominal mass
• abdominal distension.
• There is no need for routine stool microscopy or culture in children with non-bloody
diarrhoea

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 CLINICAL PRESENTATION
Physical examination

• Findings on physical examination can assist in determining hydration status and

disease severity

• The presence of blood in the stool suggests an invasive organism, an

inflammatory process, or perhaps a neoplasm.

• Large-volume stools suggest a small- intestinal disorder, whereas small-volume

stools suggest a colon or rectal disorder

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 DEHYDRATION
• Dehydration can be a consequence of diarrhoea, and this can be exacerbated if the
patient is also vomiting.

• Signs and symptoms of dehydration should be reviewed when assessing a patient, and
particularly if the patient is very young or very old.

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Assessing Dehydration in Acute Diarrhoea
For all children with diarrhoea, their hydration status should be classified as;

• severe dehydration (>10%),

• some dehydration [mild-to-moderate] (5-10%)
• or no dehydration (<5%).

• In a child with diarrhoea, assess the general condition, look for sunken eyes, make a skin
pinch, and offer the child fluid to see if he or she is thirsty or drinking poorly.

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 1. SEVERE DEHYDRATION
Severe dehydration should be diagnosed if two or more of the following signs are
present in a child with diarrhoea:
• lethargy or unconsciousness
• sunken eyes
• unable to drink or drinks poorly
• skin pinch goes back very slowly (≥ 2 s) (WHO Guidelines for Childhood
illnesses, 2013)
• In addition, very dry mouth and tongue

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Assessing Dehydration

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 2. Some Dehydration (Mild-to-Moderate)

If the child has two or more of the following signs, he or she has some dehydration:
• restlessness or irritability
• thirsty and drinks eagerly
• sunken eyes
• skin pinch goes back slowly. (WHO Guidelines for Childhood illnesses, 2013)
• In addition, dry mouth and tongue (STG, 2017)

• Note that if a child has only one of the above signs and one of the signs of severe
dehydration (e.g. restlessness or irritable and drinking poorly), then the child also has
severe dehydration.

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 3. No dehydration
Diarrhoea with no dehydration should be diagnosed if the child does not
have two or more signs that characterize some or severe dehydration, as
described above (WHO Guidelines for Childhood illnesses, 2013).
In general;
• the child Looks well, alert
• The eyes are Normal
• Mouth and tongue are Moist
• Drinks normally, not thirsty
• Skin goes back quickly after pinching (STG 2017)
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 CLINICAL PRESENTATION
Usually, acute diarrhoeal epsidoses subside within 72 hours of onset, whereas chronic
diarrhoea involves frequent attacks over extended period.

Signs and Symptoms of acute diarrhoea

• Acute diarrhea presents abruptly as loose, watery, or semi-formed stools.

• Abdominal cramps and tenderness, rectal urgency, nausea, bloating, and fever may be
present.

• Patients infected with invasive organisms may have bloody stools and severe abdominal
pain. 38
 SYMPTOMS
+ mild ++ moderate +++
severe
CAUSATIVE ORG FEVER ABDOMINAL NAUSEA BLOOD MUCOID STOOL
PAIN VOMITING Y STOOL NATUR
STOOL E
Campylobacter +++ +++ ++ + _

E.Coli ++ +++ ++ _ - Very watery

Vibrio cholerae - _ +++ _ _ Rice watery

(voluminous)

Shigellosis +++ ++ _ +++ _ Extremely

voluminous
(bacillary )
Entaemoeba + _ _ + +++ Offensive/
histolytica bulky

Gardia lamblia + + _ + ++

C.difficile + ++ ++ +

Salmonella +++ ++ ++ + _

cyclospora ++ +++ + _ _

Travellers ++ ++ ++ _ _ Very watery

(severe cases)
 CLINICAL PRESENTATION
Laboratory Tests in Acute Diarrhea

• Stool cultures can help identify infectious causes. Methods using real-time polymerase
chain reaction shorten the reporting time.

• Stool may be analyzed for mucus, fat, osmolality, fecal leukocytes, and pH.

• Mucus fragments suggest colonic involvement; fat in the stool suggests malabsorption.

• Fecal leukocytes are present in inflammatory diarrheas including bacterial infections.

• Stool pH (normally > 6) is decreased by bacterial fermentation processes .

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 CLINICAL PRESENTATION
• Assessment of stool volume and electrolytes in large- volume watery stools may identify
osmotic or secretory diarrhea.
• FBC and blood chemistries to determine extent of vitamin and electrolyte deficiencies may
be helpful when symptoms persist.
• Findings of anemia, leukocytosis, or neutropenia offer further clues to the underlying
cause.

Signs and Symptoms of Chronic Diarrhea

• Presenting symptoms may be severe or mild.
• Weight loss can be demonstrated, and weakness may be present.
• Dehydration may manifest as decreased urination, dark-colored urine, dry mucous
membranes, increased thirst, and tachycardia.

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 CLINICAL PRESENTATION
Laboratory Tests in Chronic Diarrhea

• Tests described for acute diarrhea are also useful to diagnose chronic diarrhea; the
differential diagnosis is more complicated.

• Results can help categorize the diarrhea as watery, inflammatory, or fatty, narrowing
the focus on a primary disorder.

• Colonoscopy allows visualization, and biopsy of the colon and is preferred when there
is blood in the stool or if the patient has acquired immune-deficiency syndrome.

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 DIAGNOSIS
DIAGNOSTIC CLUES FOR DIARRHOEA

• Diarrhoea WITH vomiting, low grade fever with no mucus in stools: consider viral
infection

• Diarrhoea WITH vomiting, fever, abdominal cramps, blood and mucus in stools:
consider bacterial infection

• Diarrhoea WITH blood and mucus in stool WITHOUT fever: consider amoebiasis

• Profuse diarrhoea present (rice water stools) WITH vomiting: consider cholera

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 DIAGNOSIS
• Diarrhoea WITH excessive vomiting (especially if in more than one member of the
household or group): consider food poisoning

• Diarrhoea presenting with oral and/or skin lesions, weight loss etc. over long period:
consider HIV

• Diarrhoea alternating with constipation in adults: consider bowel malignancy

(STG, 2017)

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 PREVENTION
Acute diarrheal diseases can be prevented with a variety of measures focused on
preventing the spread of organisms from person to person and within the community.

These include:
• Hand washing with soap
• Ensuring the availability of safe drinking water
• Appropriate disposal of human waste
• Breastfeeding of infants and young children
• Safe handling and processing of food
• Control of flies

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TREATMENT
(ACUTE DIARRHOEA)

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 TREATMENT
• Acute diarrhea is generally self-limited, lasting 3 to 4 days even without treatment.

• Most healthy adults with diarrhea do not develop significant dehydration or other
complications and can self-medicate symptomatically if necessary.

• Dehydration can occur when diarrhea is severe and oral intake is limited, particularly in
older persons and infants.

• Other complications of diarrhea resulting from fluid loss include electrolyte disturbances,
metabolic acidosis, and cardiovascular collapse.

• Children are more susceptible to dehydration (particularly when vomiting occurs) and may
require medical attention early in the course, especially if younger than 3 years.
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 TREATMENT
Treatment objectives:
• To prevent dehydration
• To replace lost fluid
• To maintain nutrition by ensuring adequate dietary intake during illness
• To maintain personal hygiene
• To eliminate infecting organisms where appropriate

(STG, 2017)

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 TREATMENT
• The interventions of greatest impact on acute diarrhea are hydration and nutrition
(Brandt et al., 2015).

• Because diarrhoea results in fluid and electrolyte loss, it is important to prevent or

reverse any fluid and electrolyte depletion.

• Most patients can be advised to increase their intake of fluids.

• Young children and the frail and elderly are prone to diarrhoea induced dehydration,
and the use of an oral rehydration solution (ORS) is recommended.

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 ORS
The formula recommended by the WHO consists of the ff;
• Sodium – 75mmol/L
• Glucose – 75 mmol/L
• Chloride – 65mmol/L
• Potassium – 20mmol/L
• Citrate – 10mmol/L
• This solution is almost isotonic with body fluid.
• A number of similar preparations are available commercially in the form of sachets
that require reconstitution in clean water before use.

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 ORS
The reasoning behind the ingredients within ORS are that;

• Sodium and potassium are needed to replace the body losses of these essential ions during
diarrhoea (and vomiting)

• The glucose facilitates the absorption of sodium (and hence water) on a 1:1 molar basis in the
small intestine.

• Some preparations replace glucose with rice powder.

• The citrate corrects the acidosis that occurs as a result of diarrhoea and dehydration.

• Other preparations contain bicarbonate instead of citrate

• Some commercial products include Pedialyte, Rehydralyte, and CeraLyte.

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 ORS
A simple solution can be prepared with six teaspoonfuls of sugar and half teaspoonful of
table salt in 1L of clean drinking water or boiled water and then cooled (Dipiro J.T et al,
2019).

How to prepare ORS

• Dissolve the contents of one sachet of ORS in 600 ml or 1000 mls depending on type of
ORS.
• To get 600 ml, use 2 small (300 ml) soft drink bottles or 1 big beer bottle
• To get 1000 ml, use 1L mineral water bottle
• The child or adult should drink AS MUCH of it as he/she wants. If the child vomits, the
mother should wait about 10 minutes and give it again (STG 2017).
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Home made ORS recipe

Ingredients:
•half level teaspoon of salt.
•six level teaspoons of sugar.
•one litre of clean drinking or
boiled water and then cooled.
That is
5 cupfuls (each cup about
200 ml.)
 OTHER FLUIDS USED IN DEHYDRATION

• Cholera replacement fluid (5g sodium chloride, 4g sodium bicarbonate, 1g potassium

chloride) 5:4:1

• Ringer’s lactate (Hartmann’s solution) [sodium-130mmol/L; Potassium – 4mmol/L;

Chloride–107 mmol/L; calcium-2.7 mmol/L; Lactate-28mmol/L]

• Half strength Darrow’s infusion (sodium-61mmol/L; Potassium-17mmol/L; Chloride

52mmol/L; lactate – 27mmol/L)

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 DEHYDRATION TREATMENT
A. NO DEHYDRATION (PLAN A)
• Child can be treated safely at home
• Instruct mother to give home-based fluids like rice water, koko, soup, water, and Oral
Rehydration Salt (ORS).
• Breastfed babies should be given breast milk and ORS
• Give as much as child wants of all the fluids;
• for children < 2 years, about 50–100 ml after each loose stool
• for children ≥ 2 years, about 100–200 ml after each loose stool.
• Child should continue to feed
• Mother should return to the health facility if the child gets worse, passes more watery stools,
vomits repeatedly, becomes very thirsty, eats or drinks poorly or is not better in 2 days

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 DEHYDRATION TREATMENT
B. SOME DEHYDRATION (MILD-TO-MODERATE) – PLAN B
• Child to be treated in the health facility
• Give ORS over the first 4 hours;
• 0-4 months (<6kg): 200-400 ml
• 4-12 months (6-10kg): 400-700 ml
• 1-2 years (10-12kg): 700-900 ml
• 2-5 years (12-19kg): 900-1400 ml
• If child vomits, wait 10 minutes and start again
• Continue with other fluids the child will accept
• Instruct mother to continue breast feeding if child is breastfeeding
• If eyes become puffy, it means too much fluid has been given so stop ORS and re-evaluate

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 DEHYDRATION TREATMENT

B. SOME DEHYDRATION (MILD-TO-MODERATE) – PLAN B

• Check for signs of worsening dehydration
• Reassess state of dehydration after 4 hours
• If clinical state has improved with no dehydration - go to plan A
• If there is still mild-moderate dehydration repeat plan B
• If condition is worsening - go to plan C

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 DEHYDRATION TREATMENT
C. SEVERE DEHYDRATION (PLAN C)

• A child with severe dehydration requires urgent treatment with IV fluids in hospital

• If the child can drink, give ORS by mouth while the IV line is being set up

• Start IV fluids immediately.

• Note: The best IV fluid solutions for rehydration are isotonic solutions: Ringer’s lactate
solution (called Hartmann’s solution for Injection) and normal saline solution (0.9% NaCl).
Cholera replacement fluid (5:4:1) can also be given

• Do not use 5% glucose (dextrose) solution or 0.18% saline with 5% dextrose solution, as
they increase the risk for hyponatraemia, which can cause cerebral oedema. 58
 DEHYDRATION TREATMENT
• C. SEVERE DEHYDRATION (PLAN C)
• Give 100 ml/kg Ringer’s lactate solution or, if not available, normal saline or
cholera replacement fluid (5:4:1), divided as shown below:
• <12 months: First give 30ml/kg in 1 hour, then 70ml/kg in 5 hours
• >12 months: First give 30ml/kg in 30 mins, then 70ml/kg in 2.5 hours
• If you cannot give the above treatment and cannot pass a nasogastric tube, refer to a
health facility that can do so.
• Reassess the child every 1-2 hours. If hydration status is not improving, give the IV
fluid more rapidly
• Also give ORS (about 5 ml/kg body weight/hour) as soon as the child can drink:
usually after 3-4 hours (infants) or 1–2 hours (children)

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 DEHYDRATION TREATMENT
C. SEVERE DEHYDRATION (PLAN C)
• Severe diarrhoea may be complicated by marked fluid loss accompanied by loss of
potassium (hypokalaemia) or on the other hand, impaired renal function leading to acidosis
and elevated blood potassium (hyperkalaemia)
• When the patient is passing adequate amounts of urine, probably indicating good renal
function, start potassium containing foods such as coconut water and fresh fruits (e.g.
banana)
• If there is clinical and/or laboratory evidence of severe hypokalaemia, potassium should be
given by the intravenous route using potassium chloride but only in a hospital. Potassium
containing fluids such as half strength Darrow’s solution or Ringer’s lactate may be added
• If possible infants and children should continue to breastfeed or eat during the period of
diarrhoea

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PHARMACOLOGIC
TREATMENT

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 1. ANTIMOTILITY AGENTS
• Examples include loperamide (Imodium), diphenoxylate (lomotil) and codeine
• They act by binding to opiate receptors in the gut wall, reducing propulsive peristalsis,
decreasing intestinal transit time and enhancing the reabsorption of water and
electrolytes.
• In uncomplicated acute diarrhoea (noninfectious diarrhoea), antimotility agents are
occasionally useful for symptomatic control in adults.
• These should be discontinued in patients whose diarrhea worsens despite therapy
• Antimotility agents are not recommended for use in children because they provide
small benefits with unacceptable levels of side effects observed.
• Antimotility agents should be avoided in severe gastroenteritis or dysentery.

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 1. ANTIMOTILITY AGENTS
• Loperamide
• Loperamide is a synthetic opioid analogue.
• It should have an effect within 1 hour of oral administration.
• For acute diarrhoea in adults, 4 mg of loperamide is taken initially followed by 2 mg after
every loose stool, up to a maximum of 16 mg each day for 5 days.

• Diphenoxylate.
• Diphenoxylate is a synthetic opioid available as co-phenotrope in combination with a
subtherapeutic dose of atropine.
• The atropine is included only as an abuse deterrent; when taken in large doses, the
unpleasant anticholinergic effects of atropine negate the euphoric effect of diphenoxylate.

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 2. ADSORBENTS AND BULK AGENTS
• Examples of adsorbents: Attapulgite and calcium polycarbophil
• Attapulgite adsorbs excess fluid in the stool with few adverse effects.
• Calcium polycarbophil is a hydrophilic polyacrylic resin that also works as an
adsorbent, binding about 60 times its weight in water and leading to formation of a gel
that enhances stool formation.
• Neither attapulgite nor polycarbophil is systemically absorbed.
• Calcium polycarbophil is effective in reducing fluid in the stool.
• However, caution must be exercised because it can also adsorb nutrients and other
medications, thereby reducing their benefits.
• Its administration should be separated from other oral medications by 2 to 3 hours.

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 2. ADSORBENTS AND BULK AGENTS
Examples of bulk agents: Methylcellulose and psyllium

• These products may also be used to reduce fluid in the stool and relieve chronic
diarrhea

Note: Methylcellulose can be used to treat both diarrhoea and constipation

• Dose: 3-6 tablets twice daily (500mg/tablet)
• In constipation, the dose should be taken with at least 300mL liquid
• In diarrhoea, avoid liquid intake for 30 minutes before and after dose (BNF 80, 2020)

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 3. Antisecretory agents
• Bismuth subsalicylate (BSS) [Kaopectate]
• BSS appears to have antisecretory, anti-inflammatory and antimicrobial effects and is used
to treat acute diarrhea.
• The antimicrobial and anti-inflammatory action is provided by the bismuth and the
antisecretory effect is by the salicylate.
• Patients taking BSS should be informed that their stool will turn black.

Octreotide
• Octreotide, a synthetic octapeptide analog of endogenous somatostatin, is an antisecretory
agent used for severe secretory diarrhea associated with cancer chemotherapy, human
immunodeficiency virus, diabetes, gastric resection, and GI tumors.

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 4. ENKEPHALINASE INHIBITORS
• Eg. Racecadotril and thiorphan

• Enkephalins are endogenous opioid substances which regulate fluid movement across the
mucosa by stimulating absorptive processes.

• Racecadotril is a pro-drug of thiorphan. Thiorphan, an enkephalinase inhibitor, inhibits the

breakdown of endogenous opioids (enkephalins), thereby reducing intestinal secretions. It
does not change intestinal transit time.

• Racecadotril can be used as an adjunct to rehydration for the symptomatic treatment of

acute uncomplicated diarrhoea.
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 5. PROBIOTICS
• Probiotics are dietary supplements containing bacteria that may promote health by
enhancing the normal microflora of the GI tract while resisting colonization by potential
pathogens.

• Probiotics can stimulate the immune response and suppress the inflammatory response.

• Probiotics can be taken in tablets, gummies, capsules, powders, and liquids.

• Well known probiotics include Bacillus clausii (Enterogemina), Lactobacillus species,

Saccharomyces, Bifidobacterium species, etc

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 5. PROBIOTICS
• Yogurt may provide relief from diarrhea due to lactose intolerance.

• The Lactobacillus acidophilus in yogurt, cottage cheese, and acidophilus milk

improve digestion of lactose and may prevent or relieve diarrhea related to
lactose deficiency and milk intake.

• Although lactase is not a probiotic, lactase tablets may also be used to prevent
diarrhea in susceptible patients.

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5. PROBIOTICS

70
 6. ZINC
• Zinc is an important micronutrient for a child’s overall health and development but is lost in
greater quantities during diarrhoea.

• Zinc supplementation is important because it;

• Helps the child’s recovery

• Reduces the duration and severity of the episode

• lowers the incidence of diarrhoea in the following 2–3 months.

• Restores mucosal barrier integrity increasing absorption of fluids and enterocyte brush
border activity

• Also promotes the production of antibodies and lymphocytes against intestinal pathogens
71
 6. ZINC
• Zinc should be given as follows:
• ≤ 6 months: half tablet (10 mg) per day for 10–14 days
• ≥ 6 months: one tablet (20 mg) per day for 10–14 days

• The mother should be shown how to give the zinc supplement:

• For infants, dissolve the tablet in a small amount of clean water, expressed milk or
ORS.
• Older children can chew the tablet or drink it dissolved (WHO Guidelines for
Childhood Illnesses, 2013).

72
 7. ANTIMICROBIALS
• Antibiotics are generally not recommended in diarrhoea associated with acute infective
gastroenteritis.

• This is because the cause is more commonly viral, and the symptoms tend to resolve
quickly on their own.

• Inappropriate treatment of diarrhoea with antibiotics will only further contribute to the
problem of resistant organisms.

• Antibiotics should be reserved for patients who produce a positive stool culture for
bacteria and where the symptoms are not receding or for traveller’s diarrhoea
73
 7. ANTIMICROBIALS
PATHOGEN / TYPE OF THE ENTERITIS ANTIMICROBIAL
Shigellosis (bacillary dysentery) Ciprofloxacin, Levofloxacin, Azithromycin, Ceftriaxone
Salmonellosis Gastroenteritis: Supportive
Typhoid fever: Ciprofloxacin, Azithromycin, Ceftriaxone

Campylobacteriosis Azithromycin, Ciprofloxacin, Tetracycline/Doxycycline, Ceftriaxone,

Gentamicin, ampicillin, carbapenem

. Enterohemorrhagic E.coli gastroenteritis Antibiotics are currently contraindicated; give ORS

Cholera (Vibrio cholera) Azithromycin, Ciprofloxacin, Doxycycline, Rice based ORS

Traveler’s diarrhoea Levofloxacin, Ciprofloxacin, Azithromycin, Rifaximin, Bismuth

subsalicylate
Clostridium difficile gastroenteritis Metronidazole, Vancomycin, fidaxomocIn
Amoebic dysentery (Entamoeba histolytica) (Metronidazole/Tinidazole +Diloxanide/Paramomycin
74
 8. VACCINES
A. Rotavirus
• Two oral rotavirus vaccines are currently approved for use;
• Rotarix (monovalent) and RotaTeq (pentavalent)
• Vaccination for Rotarix is recommended at 2 and 4 months and that of RotaTeq is at 2, 4
and 6 months

B. Cholera
• An oral vaccine for cholera (Vaxchora®) is licensed and available in the United States.
• The vaccine is recommended for adults aged 18-64 years old who are traveling to an
endemic area

75
 8. VACCINES
C. Typhoid
• There are two newer typhoid vaccine formulations, one a parenteral inactivated
whole-cell vaccine and the other an oral live-attenuated (Ty21a) vaccine that is
administered in four doses on days 1, 3, 5, and 7, to be completed at least 1 week
before exposure.

D. Shigella
• Oral Shigella vaccine, although effective under field conditions, requires five weekly
oral doses and repeat booster doses, thereby limiting its practicality for use in
developing nations.

76
INFLAMMATORY BOWEL
DISEASE
Dr(Mrs) Kate Coleman-Sarfo
 INFLAMMATORY BOWEL
DISEASES
(IBD)
• IBD describes a group of intestinal disorders that cause a prolonged
inflammation of the digestive tract.
Classification:
Chron’s Dx (CD): This is a chronic , relapsing and remitting inflammatory
disease of the GIT affecting any site from mouth to the rectum.

Ulcerative colitis (UC): This is a condition that causes mucosal

inflammation and ulcers in the lining of the large intestines
 Etiology
1) Infectious Agents: Viruses (measles), Bacteria (mycobacteria)
2) Genetics
3) Environmental factors: Diet, Smoking
(Non-smokers have a higher risk of UC, whilst smoking increases the
risk of CD)
4) Psychological factors: Stress, Emotional or physical trauma
(Stress induces activation of HPA axis, ANS,ENS leading to dysbiosis)
Male to female ratio for UC is 1:1 and for CD is 1.1-1.8
The risk of CD in smokers is 40% that of nonsmokers.
 Pathophysiology
• Altered mucosal immune response
Dietary and bacterial antigens penetrate into the intestinal wall and activates the
immune system causing increased production of pro-inflammatory mediators
which will lead to inflammation of the mucosal layer.
• Defects in epithelial cells have been described in IBD.
• These defects result in influx of components like macrophages and dendritic
cells which activate CD4 cells.
• Activated CD4 cells activate other inflammatory cells like B- cells and T-cells by
stimulating of receptors on leucocytes and vascular epithelium.
• Inflammation in IBD is maintained by an influx of leucocytes from the vascular
system into sites of active disease.
NORMAL. CHRONS AND ULCERATIVE
COLITIS
 Similarities between UC and CD
• Both diseases affect men and women almost equally.
• Both often develop in teenagers and young adults although the
disease can occur at any age.
• Symptoms are quite similar
• The causes of both UG and Crohn’s are not known, but they have
similar contributing factors such as environmental, genetic and
inappropriate immune system response
Differences between UG and CD
• CD can occur anywhere between the mouth and rectum (more in the
small intestines) whilst UC is limited to the colon.

• In CD, the intestines has healthy parts interspersed between inflamed

areas whilst the UC shows continuous inflammation of the colon.

• UC only affects the inner most lining of the colon whilst crohn’s dx
can occur in all the layers of the bowel walls
 ASSOCIATED SYMPTOMS
• IBD may be associated with low albumin levels mostly due to
malabsorption.
• There may be low potassium levels probably as a result of the
diarrhoea experienced in IBD, although note that corticosteroids can
also cause hypokalaemia.
EXTRA INTESTINAL
MANIFESTATIONS
 Diagnosis
• Physical Examination: Abdominal tenderness, oral aphthous, anal tags,
fissures and fistulae.
• Endoscopy: Upper gastro intestinal, Colonoscopy, sigmoidoscopy
• Radiological: CT scan, MRI (exclude toxic dilation of the colon or bowel
perforation)
• Blood tests: CBC, ESR, C-reactive protein, Serum ferritin
• Biopsy
• Stool examination: ( C. diff., occult blood etc )
• Barium swallow
• Endoscopic procedure with tissue biopsy: confirmation of UC
 Goals of Therapy
• To relieve symptoms eg. Abdominal pain
• To treat acute disease
• Prevent complications eg perforation, hospitalization and surgery
• Maintain good nutritional status
• Improve and maintain patients’ general well-being.
Approach to treatment must be individualized. Factors to consider
include 1) Dx severity, 2) anatomic location of dx, 3) Previous response
to medication, 4) co-morbidities
 Pharmacologic Management
AMINOSALICYLATES IMMUNE MODIFIERS
• Anti-inflammatory agents • Thiopurines
*5- aminosalicylic acid (5-ASA) *Azathioprine, Mercaptopurine
e.g. Mesalazine, Sulfasalazine • Calcineurin Inhibitors
ANTIBIOTICS *Cyclosporine A (CSA)
*Metronidazole *Tacrolimus
*Ciprofloxacin • Methotrexate (MTX)
Pharmacological Management
CORTICOSTERIODS BIOLOGICS
*IV Methylprednisolone, • Anti-tumor necrosis factor (anti-
Hydrocortisone TNF) agents.
*Oral: Prednisone, Prednisolone, *Infliximab
Budesonide, Dexamethasone *Adalimumab
*Enema *Certolizumab
PROBIOTICS • Adhesion molecule antagonists
*VSL#3 (Visbiome) *Vedolizumab
 AMINO SALICYLATE
(MESALAZINE)
• Mesalazine is useful in maintaining remission in patients with ulcerative colitis.

• Mesalazine has only been shown to be of benefit in mild to moderate flares of

ulcerative colitis

• Although significant adverse effects (e.g. Stevens Johnson syndrome,

pancreatitis and agranulocytosis) are rare, all patients should be advised to
report any unexplained symptoms such as bleeding, bruising, purpura (small
areas of haemorrhage), sore throat, fever or malaise. These may be indicative of
agranulocytosis and warrant urgent investigation.
Pharmacologic Management
 Symptomatic Therapy and
Supplements
• Antidiarrheals: Loperamide, cholestyramine if patient has previously
undergone resection.
• Analgesics: Acetaminophen, Codeine
• Nutritional Supplements: In malnutrition or reduced intake
• Vitamin B12 : Replenish if deficient
• Vitamin D and Calcium supplementation: For steroid users
 NON PHARMACOLOGICAL INTERVENTIONS/MANAGEMRNT

• Avoid smoking
• Reduce alcohol consumption
• Avoid NSAIDS
• Avoid spicy and fried /oily foods
• Eat Fiber rich diet
• Eat small meals
• Eat more foods containing omega 3 fatty acids eg fish (anti-
inflammatory)
• Drink plenty of fluids
• Include whole fresh foods in your diet
• Include low-fat foods
Foods to avoid:
• Foods that worsen your symptoms
• Spicy foods
• Foods containing caffeine such as tea and coffee
• Limit dairy products
• Avoid processed foods
 MANAGEMENT OF FLARES
• Tests: Stool culture, U&E, FBC, ESR/CRP, faecal calprotectin.
• Stop NSAIDs(if on NSAIDS). Consider self-care for mild symptoms
including dietary advice and reducing stress.
• Acute Severe colitis: 6 or more bowel movements plus two or more
features of systemic upset: Visible blood in stool, Pyrexia (temperature
greater than 37.8°C) Pulse rate greater than 90 bpm Anaemia )
• Pancolitis/extensive disease: Maximize oral 5-ASA (mesalazine)
• If still symptomatic: Consider adding topical therapy (eg predsol
enemas)
Assess response after 2 weeks :If still symptomatic then consider;
• Oral prednisolone 40mg od for 7 days then 35mg od for 7 days.
Reducing by 5mg each week over 8 weeks = 252 x 5mg prednisolone
tablets in total. Remember GI and bone protection. Counsel on side
effects (crohnsandcolitis.org.uk/steroids)
• If no better after 2 weeks, switch to IV corticosteroids like IV
Hydrocortisone.
 Use of cyclosporine?

• Several studies have been conducted, including some small

randomized studies, to assess the use of cyclosporine in Crohn’s
disease.
• The evidence suggests that intravenous cyclosporine can induce
disease remission in severe flares of ulcerative colitis that are
unresponsive to corticosteroids.
• Oral cyclosporine has only been shown to be useful as a bridging
treatment between intravenous cyclosporine and more long-term
maintenance strategies.
 POINTS TO DISCUSS WITH
PATIENT BEFORE CYCLOSPORIN
ADMINISTRATION
• Reason for using cyclosporine: Disease modifying. Last resort but has good
reviews. Although it may avoid the need for surgery in some patients it
doesn’t always work and surgery may still be needed.
• IV administration: Cyclosporine is Initially given through a drip. If it is
successful in controlling the disease formulation can be switched to oral.
Possible adverse effects: Altered electrolyte levels ,
• Increases in blood pressure( treated with BP tablets, or by stopping the
medicine).
• Tingling in the hands and feet, cramps and muscle pains.
• Altered periods in ladies
• Renal impairments (with high doses)
 DISCHARGE MEDICATIONS
AFTER FLARES
• Cyclosporin 6–8 mg/kg per day (target blood level 100–200 ng/mL).
• Prednisolone 40–60 mg daily, with a reducing course over several
weeks (regimens vary, but reductions should not be more than 10 mg
and will need to be smaller and slower towards the tail end of
treatment. Many patients end up taking long-term steroids.
• Antibiotics may be necessary especially in Pouchitis surgery
(Metronidazole, ciprofloxacin)
• Mesalazine 800 mg three times daily.
 SURGERY FOR IBD
• Proctocolectomy (Removing colon and rectum)
• Ileostomy: If UC is severe, after proctocolectomy, the ilium is brought
through an opening (stoma) in the abdominal to allow intestinal
waste out of the body. Stoma is connected to an external bag to
collect waste.
• Restorative proctocolectomy (Ileal pouch- anal anastomosis):
Removing colon and rectum and connecting ilium directly to the anus.
 SURGERY FOR CD
• Strictureplasty: Widening a narrowed portion of bowel
• Resection: Removing affected sections of the intestines and joining
healthy portions together (Anastomosis)
• Abscesses and fistulas: Removal of pus filled mass
• Colectomy: Removal of the colon. Sometimes a proctocolectomy may
be necessary.
Patient with a colostomy bag
Patient with Ileostomy bag
 When is surgery likely?

• Surgery is undertaken in patients not responding to medical treatments

• Surgery may also be used when patients have poorly controlled
frequently relapsing disease.
• In ulcerative colitis, surgery (a colectomy) offers the hope of a cure, by
removing the diseased portion of the gastrointestinal tract. This
contrasts with Crohn’s disease, where surgery is undertaken for
symptomatic relief.
• However, as Crohn’s disease can affect the whole of the gastrointestinal
tract it is not curative, and the disease often recurs in a different area
following surgery.
 TERMS TO KNOW
• Perforated Bowel: Chronic inflammation of the intestine may weaken the
intestinal wall to such an extent that a hole develops.
• Toxic Mega colon: Severe inflammation that leads to rapid enlargement of
the colon.
• Fistula: Ulcers on the wall of the intestine that extend and cause a tunnel
(fistula)
• Stricture: A narrowing of a section of intestine caused by scarring which can
lead to an intestinal blockage.
• Clostridium difficile: Bacteria that can infect the bowel and cause
diarrhoea. The infection most commonly affects people who have recently
been treated with antibiotics. It can spread easily to others.
 REFERENCES
• . Talley NJ, Vakil N; Practice Parameters Committee of the American Col_x0002_lege of Gastroenterology. Guidelines for the management of dyspepsia.
Am J Gastroenterol. 2005;100(10):2324-2337.

• 2. Malfertheiner P, Megraud F, O’Morain CA, et al.; European Helicobacter Study Group. Management of Helicobacter pylori infection—the
Maas_x0002_tricht IV/ Florence Consensus Report. Gut. 2012;61(5):646-664.

• 3. Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol.
2007.102(8):1808-1825.

• 4. Ford AC, Delaney BC, Forman D, Moayyedi P. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database
Syst Rev. 2006;19(2):CD003840.

• 5. Papatheodoridis GV, Sougioultzis S, Archimandritis AJ. Effects of Heli_x0002_cobacter pylori and nonsteroidal anti-inflammatory drugs on peptic
• ulcer disease. Clin Gastroenterol Hepatol. 2006;4(2):130-142.

• 6. Sánchez-Delgado J, Gené E, Suárez D, et al. Has H. pylori prevalence in bleeding peptic ulcer been underestimated? A meta-regression. Am J
Gastroenterol. 2011;106(3):398-405.

• ACG Clinical Guideline: Management of Patients with Ulcer Bleeding