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▰ Diarrhoea is defined as the passage of more than 200g of stool daily
and measurement of stool volume is helpful in confirming this.
▰ The most severe symptom in many patients is urgency of defecation,
and faecal incontinence is a common event in acute and chronic
▰ This is extremely common and is usually caused by faecal–oral
transmission of bacteria or their toxins, viruses or parasites.
▰ Infective diarrhoea is usually short-lived and patients who present with
a history of diarrhoea lasting more than 10 days rarely have an
▰ A variety of drugs, including antibiotics, cytotoxic drugs, PPIs and
NSAIDs, may be responsible.
▰ Acute diarrhoea, sometimes with vomiting, is the predominant
symptom in infective gastroenteritis.
▰ Acute diarrhoea may also be a symptom of other infectious and
▰ Stress, whether psychological or physical, can also produce loose
▰ Large volumes of water are normally secreted into the small intestinal
lumen, but a large majority of this water is efficiently absorbed before
reaching the large intestine.
▰ Diarrhea occurs when secretion of water into the intestinal lumen
▰ Many millions of people have died of the secretory diarrhea.
associated with cholera. The responsible organism, Vibrio cholerae,
produces cholera toxin, which strongly activates adenylyl cyclase,
causing a prolonged increase in intracellular concentration of cyclic
AMP within crypt enterocytes.
▰ This change results in prolonged opening of the chloride channels that
are instrumental in secretion of water from the crypts, allowing
uncontrolled secretion of water. Additionally, cholera toxin affects
the enteric nervous system, resulting in an independent stimulus of
▰ Exposure to toxins from several other types of bacteria (e.g. E.
coli heat-labile toxin) induce the same series of steps and massive
secretory diarrhea that is often lethal unless the person is aggressively
treated to maintain hydration.
▰ In addition to bacterial toxins, a large number of other agents can
induce secretory diarrhea by turning on the intestinal secretory
▰ some laxatives, hormones, drugs, certain metals, organic toxins, and
plant products (e.g. arsenic, insecticides, mushroom toxins, caffeine)
▰ In most cases, secretory diarrheas will not resolve
during a 2-3 day fast.
Inflammatory and Infectious Diarrhea
▰ The epithelium of the digestive tube is protected from insult by a
number of mechanisms constituting the gastrointestinal barrier, but
like many barriers, it can be breached.
▰ Disruption of the epithelium of the intestine due to microbial or viral
pathogens is a very common cause of diarrhea in all species.
▰ Destruction of the epithelium results not only in exudation of serum
and blood into the lumen but often is associated with widespread
destruction of absorptive epithelium.
▰ In such cases, absorption of water occurs very inefficiently and
Inflammatory and Infectious Diarrhea
▰ Examples of pathogens frequently associated with infectious diarrhea
▻ Bacteria: Salmonella, E. coli, Campylobacter
▻ Viruses: rotaviruses, norovirus
▻ Protozoa: Giardia, Cryptosporium,
Inflammatory and Infectious Diarrhea
▰ The immune response to inflammatory conditions in the bowel
contributes substantively to development of diarrhea.
▰ Activation of white blood cells leads them to secrete inflammatory
mediators and cytokines which can stimulate secretion, in effect
imposing a secretory component on top of an inflammatory diarrhea.
▰ Reactive oxygen species from leukocytes can damage or kill intestinal
epithelial cells, which are replaced with immature cells that typically
are deficient in the brush border enyzmes and transporters necessary
for absorption of nutrients and water. In this way, components of an
osmotic (malabsorption) diarrhea are added to the problem.
It is the diarrhea that occurs due to the ingestion of poorly absorbed
osmotically active substances that cause shifting of the water into the
▻ If you stop oral feeding the diarrhea will stop.
▰ Can be Occur in:
1.ingestion of high CHO diet.
2-Congenital Lactase deficiency (primary)
3.infection with rotavirus or Salmonella, Enter hemorrhagic E.coli
causes severe shedding of villi that contains Disaccharidases
enzyme (secondary lactase deficiency).
▰ Gut dysmotility may cause increased intestinal and colonic transit
time as well as decrease contact time with intestinal absorptive
▰ Functional syndromes such as irritable bowel syndrome (IBS) include
a pain component as well as a change in bowel habits.
▰ Diarrhoeal disease is the second leading cause of death in
children under five years old. It is both preventable and treatable.
▰ The World Health Organisation (WHO) estimates that there are
more than 1.7 billion cases of acute diarrhoea annually globally.
▰ Each year diarrhoea kills around
760 000 children under five.
▰ In developed countries, diarrhoea remains
an important problem, with the elderly being
▰ Gram –ve bacillus
▰ Normal commensal in human gut Virulent types-
▰ Enterotoxigenic - leading cause of watery diarrhea, most common
cause of travellers’ diarrhea
▰ Enteropathogenic- diarrhea with mucus
▰ Enteroinvasive- profuse diarrhea with fever
▰ Enterohemorrhagic - dysentery, can cause HUS Enteroaggregative-
▰ Caused by bacteria Vibrio cholerae Primarily affects small-intestine
▰ People with O blood group more affected, carriers of cystic fibrosis are
▰ Toxin leads to cAMP activation causing secretion of water, Na, K, Cl &
▰ Causes profuse diarrhea (rice water),
▰ with abdominal pain, ± vomiting
• Fever with chills
• Abdominal cramps
• Diarrhea often with blood and mucus
• Headache, malaise
• Direct person-to-person spread
• Tx Trimethoprim-
▻ sulfamethoxazole, ciprofloxin, levofloxacin, ampicillin
• Increasing resistance to antibiotics noted
• Azithromycin, 500mg orally on day 1 and 250mg orally one time a day
for 4 days, may be an effective alternative treatment
for resistant strains
• Clostridium difficile
• 20% chance after completing broad spectrum antibiotic
• The A and B toxins produced by C. difficile can cause severe diarrhea,
pseudomembranous colitis, or toxic megacolon.
• High risk pts: nursing home residents and employees, hospitalized pts and
• metronidazole (250mg orally four times a day or 500mg orally three times
a day for 10 days)
▰ The history should address foods ingested, duration and frequency of
diarrhoea, presence of blood or steatorrhoea, abdominal pain and
tenesmus, and whether other people have been affected.
▰ Fever and bloody diarrhoea suggest an invasive, colitic, dysenteric
▰ An incubation period of less than 18 hours suggests toxin-mediated
food poisoning, and longer than 5 days suggests diarrhoea caused by
protozoa or helminthes.
▰ Person-to-person spread suggests certain infections,
such asshigellosis or cholera.
Foods associated with infectious illness,
Foods associated with infectious illness,
▰ Examination includes assessment of the degree of dehydration.
▰ Assessment for early signs of hypotension, such as thirst, headache,
altered skin turgor, dry mucous membranes and postural hypotension,
is important, particularly in tropical regions where dehydration
▰ Signs of more marked dehydration include supine hypotension and
tachycardia, decreased urinary output, delirium and sunken eyes.
▰ The blood pressure, pulse rate, urine output and ongoing stool losses
should be monitored closely.
▰ The severity of diarrhoea may be assessed by reference to the Bristol
stool form scale (Bristol stool chart), which allows an objective
assessment of stool consistency by providing a verbal and visual
▰ The Bristol stool form scale was developed in the 1990s to monitor
patients with irritable bowel syndrome, but its main use (at least in UK
hospitals) is to monitor hospital inpatients with loose stool to assist in
decisions on stool sampling and infection prevention precautions,
especially in relation to C. difficile.
Bristol stool chart
▰ The stool is given a ‘score’ of 1–7 by
▰ reference to the verbal and visual
▰ This is recorded on a chart (usually known
as a ‘Bristol stool chart’) or in a patient
These include stool inspection for blood and microscopy for leucocytes,
and also an examination for ova, cysts and parasites if the history indicates
residence or travel to areas where these infections are prevalent.
▰ Stool culture should be performed and C. difficile toxin sought.
▰ FBC and serum electrolytes indicate the degree of inflammation and
▰ Where cholera is prevalent, examination of a wet film with dark-field
microscopy for darting motility may provide a diagnosis.
▰ In a malarious area, a blood film for malaria parasites
should be obtained.
▰ Blood and urine cultures and a chest X-ray may identify alternative
sites of infection, particularly if the clinical features suggest a
syndrome other than gastroenteritis.
▰ Structural examination by sigmoidoscopy, colonoscopy, or abdominal
computed tomography (CT) scanning (or other imaging approaches)
may be appropriate in patients with uncharacterized persistent
diarrhea to exclude IBD or as an initial approach in patients with
suspected noninfectious acute diarrhea such as ischemic colitis,
diverticulitis, or partial bowel obstruction.
▰ All patients with acute, potentially infective diarrhoea should be
appropriately isolated to minimise person-to-person spread of
▰ If the history suggests a food-borne source, public health measures
must be implemented to identify the source and to establish whether
other linked cases exist.
▰ Replacement of fluid losses in diarrheal illness is crucial and may be life-
▰ Although normal daily fluid intake in an adult is only 1–2 L, there is
considerable additional fluid movement in and out of the gut in
▰ Altered gut resorption with diarrhea can result in substantial fluid loss;
for example, 10–20 L of fluid may be lost in 24 hours in cholera.
▰ The fluid lost in diarrhea is isotonic, so both water and electrolytes need
to be replaced.
Fluid homeostasis in the gastrointestinal
• Absorption of electrolytes from the
gut is an active process requiring
• Infected mucosa is capable of very
rapid fluid and electrolyte transport
if carbohydrate is available as an
▰ Oral rehydration solutions (ORS) therefore contain sugars, as well as
water and electrolytes.
▰ ORS can be just as effective as intravenous replacement fluid, even in
the management of cholera.
▰ In mild to moderate gastroenteritis, adults should be encouraged to
drink fluids and, if possible, continue normal dietary food intake.
▰ If this is impossible – due to vomiting, for example – intravenous fluid
administration will be required.
▰ In very sick patients or
those with cardiac or
monitoring of urine
output and central
venous pressure may
The volume of fluid replacement required should be estimated based on
the following considerations:
▰ Replacement of established deficit
▰ Replacement of ongoing losses
▰ Replacement of normal daily requirement
Replacement of established deficit
▰ After 48 hours of moderate diarrhoea (6–10 stools per 24 hrs), the
average adult will be 2–4 L depleted from diarrhoea alone. Associated
vomiting will compound this.
▰ Adults with this symptomatology should therefore be given rapid
replacement of 1–1.5 L, either orally (ORS) or by intravenous infusion
(normal saline), within the first 2–4 hours of presentation.
▰ Longer symptomatology or more persistent/severe diarrhoea rapidly
produces fluid losses comparable to diabetic ketoacidosis and is a
metabolic emergency requiring active intervention.
Replacement of ongoing losses
▰ The average adult’s diarrheal stool accounts for a loss of 200 mL of
▰ Stool losses should be carefully charted and an estimate of ongoing
replacement fluid calculated.
▰ Commercially available rehydration sachets are conveniently produced
to provide 200 mL of ORS; one sachet per diarrhoea stool is an
appropriate estimate of supplementary replacement requirements.
Replacement of normal daily requirement
▰ The average adult has a daily requirement of 1–1.5 L of fluid in
addition to the previous calculations.
▰ This will be increased substantially in fever or a hot environment.
▰ In non-specific gastroenteritis, routine use of antimicrobials does not
improve outcome and may lead to antimicrobial resistance or side-
▰ They are usually used where there is systemic involvement, a host with
immunocompromise or significant comorbidity.
▰ Evidence suggests that, in Enterohaemorrhagic Escherichia coli (EHEC)
infections, the use of antibiotics may make the complication of
haemolytic uraemic syndrome (HUS) more likely due to increased toxin
release. Antibiotics should therefore not be used in
▰ Conversely, antibiotics are indicated in Shigella dysenteriae infection
and in invasive salmonellosis – in particular, typhoid fever.
▰ Antibiotics may also be advantageous in cholera epidemics, reducing
infectivity and controlling the spread of infection.
Antidiarrhoeal, antimotility and
▰ These agents are not usually recommended in acute infective
▰ Loperamide, diphenoxylate and opiates are potentially dangerous
in dysentery in childhood, causing intussusception.
▰ Antisecretory agents, such as bismuth and chlorpromazine, may
make the stools appear more bulky but do not reduce stool fluid losses
and may cause significant sedation.
▰ Adsorbents, such as kaolin or charcoal, have little effect.
▰ Good hygiene, hand washing,
safe food preparation, and
access to clean water are key
factors in preventing diarrheal
▰ Vaccine development remains
a high priority for disease
▰ Effective and safe vaccines
exist for rotavirus, typhoid
fever, and cholera, and are
under investigation for
enterotoxigenic E. coli,
and Shigella infections.
Take Home Message
▰ Infectious diarrhoea is due to faeco–oral transmission of viruses,
bacteria, bacterial toxins or parasites.
▰ Most cases are self-limiting and a pathogen is rarely identified.
▰ Viruses and toxins causes large-volume watery diarrhoea.
▰ Invasive intestinal pathogens (cause bloody diarrhoea)
▰ Clostridium difficile infection (CDI) (cause hospital-acquired diarrhoea).
▰ Diarrhoea that persists for >10 days is unlikely to be infective.
▰ Consider protozoal infections in patients who are immunocompromised
or have recently travelled to the tropics.