ACUTE DIRRHOEAL
DISEASES
BY DR CHEROP
FACILITATOR – DR AGNES
OUTLINE
• INTRODUCTION
• AETIOLOGY
• PATHOPHYSIOLOGY
• DIRRHOEA CLASSIFICATION
• CLINICAL FEATURES
• DIAGNOSIS
• MANAGEMENT OF ACUTE DIRRHOEAL ILLNESS
• COMPLICATIONS
INTRODUCTION/DEFINITIONS
•
Diarrhea is defined as the passage of three or more loose or liquid stools per day, or
more frequent passage than is normal for the individual (WHO DEFINITION)
• Can also be defined as stool volume of more than 20 grams/kg/day in infants and toddlers
(<10 kg) or more than 250 grams/day in older children or teenagers
• Acute diarrhea- Diarrhea that lasts several hours to days (upto 13 days)
• Persistent diarrhea- Any diarrhea with a duration>=14 days
• Prolonged diarrhea- Used to describe diarrhea that lasts between >7 days and <
14 days
• Chronic diarrhea — Chronic diarrhea is generally defined as diarrhea lasting
greater than four weeks
• Dysentery or invasive diarrhea- Diarrhea with visible blood, in contrast with watery
diarrhea, is commonly associated with fever and abdominal pain. Most common cause is
shillega
ETIOLOGY
• More than 90% of cases of acute diarrhea are caused by infectious agents
• These cases are often accompanied by vomiting,fever, and abdominal pain
• The remaining 10% or so are caused by medications. Toxic ingestions, ischemia, food
indiscretions, and other conditions
ETIOLOGY

Bacterial:
 Escherichia coli
 Salmonella
 Shigella
 Campylobacter jejuni
 Vibrio parahaemolyticus
 Vibrio cholerae
 Yersinia enterocolitica
 Clostridium difficile
 Staphylococcus aureus
 Bacillus cereus



Viral:

Rotavirus- most common pathogen in children

Norwalk-like virus (Norovirus)

Adenovirus

Astrovirus

calciviruses
Protozoal:

Giardia lamblia

Cryptosporidium

Entamoeba histolytica

Isospora belli
Others

overfeeding,

medications,- antibiotics

cystic fibrosis,

malabsorption
PATHOPHYSIOLOGY OF DIARRHOEA
• Normal fluid absorption and secretion in the gastrointestinal tract
• Pathophysiology of fluid transport in diarrheal disease
• Mechanisms of diarrhea
• Normal fluid
absorption and
secretion in the
gastrointestinal tract
• Diarrhea occurs when
excessive amounts of
fluid remain within the
lumen of the intestine
• This can occur because
of increased secretion
into the intestinal
lumen or reduced
absorption of water
from the lumen to the
body through the
MECHANISMS OF DIRRHOEA
• Loss of nutrient absorption or the presence of
nonabsorbable solutes
• Increased secretion or reduced absorption of
electrolytes
• Rapid intestinal transit
(A) Normal — During normal function, Na+ and
nutrient absorption drives fluid absorption, with a
small basal amount of electrolyte (Cl–)-driven fluid
secretion, allowing efficient reabsorption of fluid,
leading to minimal fluid loss via feces.
(B) Loss of nutrient absorption, or the
presence of nonabsorbable solutes (diet-induced
or "osmotic" diarrhea) — Loss of nutrient
absorption because of damage or loss of the
required transporter, or the presence of
nonabsorbable osmoles in the lumen (eg, PEG 3350),
prevents fluid absorption and promotes fluid
secretion into the intestinal lumen, leading to
diarrhea.
(C) Increased secretion or reduced absorption
of electrolytes (electrolyte transport-related or
"secretory" diarrhea) — Excessive anion-driven fluid
secretion and reduced electrolyte-driven fluid
absorption, as occurs in certain infections such as
cholera, leads to accumulation of fluid in the
intestinal lumen and diarrhea.
(D) Rapid intestinal transit (motility-related
diarrhea) — Increased intestinal motility results in
reduced time to absorb electrolytes and nutrients,
leading to excessive unabsorbed substrates in the
intestine and reduced fluid absorption, leading to
diarrhea
DIRRHOEA CLASSIFIACTION
• Diet induced (osmotic)
• Electrolyte transport related (secretory diarrhoea)
• Dirrhoea associated with deranged motility
• Inflammatory and infectious diarrhoea
DIET-INDUCED (OSMOTIC)
• Absorption of water in the intestines is dependent on adequate absorption of solutes.
• If excessive amounts of solutes are retained in the intestinal lumen, water will not be absorbed and diarrhea
will result.
• Osmotic diarrhea typically results from one of two situations:
• Ingestion of a poorly absorbed substrate: The offending molecule is usually a carbohydrate or divalent
ion. Common examples include mannitol or sorbitol, epson salt (MgSO4) and some antacids (MgOH2).
• Malabsorption: Inability to absorb certain carbohydrates. A common example is lactose intolerance
resulting from a deficiency in the brush border enzyme lactase
• Lactose cannot be effectively hydrolyzed into glucose and galactose for absorption.
• The osmotically-active lactose is retained in the intestinal lumen, where it "holds" water.
• Because this form of diarrhea is driven by osmotically active ingested nutrients (eg, carbohydrates) or
exogenous substances (eg, osmotic laxative), the diarrhea will abate during fasting.
• Trial of fasting (>12 hours) is a useful diagnostic test
ELECTROLYTE TRANSPORT-RELATED (SECRETORY)
• secretory diarrhea occurs as a result of alterations in ion transport mechanisms in
epithelial cells.
• persist unabated during fasting because it is independent of ingested osmotically active
nutrients.
• Several types of diarrheal diseases fall into this category:
…CT
• Enterotoxigenic bacteria• Infection with the pathogen Vibro cholerae. V. 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 secretion
• Other examples of bacterial enterotoxins include the enterotoxins produced by Clostridia
perfringens and C. difficile, and the heat-stable enterotoxin of E. coli.
• Enterotoxigenic viruses –
• Viral enterotoxins also may cause secretory diarrhea. As an example, rotavirus
produces a viral enterotoxin, the nonstructural glycoprotein (NSP4). NSP4 causes
Ca2+-dependent transepithelial Cl- secretion from the crypt cells, resulting in
secretory diarrhea
• Other secretory diarrheas – Noninfectious causes of secretory diarrhea include:
Diarrheas mediated by gastrointestinal peptides (such as vasoactive intestinal
peptide and gastrin),
DIARRHEA ASSOCIATED WITH DERANGED
MOTILITY
• In order for nutrients and water to be efficiently absorbed the intestinal contents must
be adequately exposed to the mucosal epithelium and retained long enough to allow
absorption.
• Disorders in motility that accelerate transit time could decrease absorption, resulting in
diarrhea even if the absorptive process per se was proceeding properly. E.g-irritable
bowel syndrome
• Hypomotility, or the severe impairment of intestinal peristalsis, results in stasis with
subsequent bacterial overgrowth and secondary bile acid deconjugation, bile acid
malabsorption, and activation of colonic secretion
INFLAMMATORY AND INFECTIOUS DIARRHEA
• Intestinal inflammation leads to diarrhea through multiple mechanisms.;
• The diarrhea can have a diet-induced component because the inflammatory process causes
destruction or impairment of epithelial cells, resulting in loss of surface area and transports,
resulting in impaired nutrient absorption and increased osmotic load in the intestinal lumen(Dietinduced (osmotic)
• The inflammatory process also can lead to the breakdown in intestinal barrier function, resulting in
the exudation of mucus, protein, and blood into the gut lumen (eg protein-losing enteropathy
• Inflammation can also cause electrolyte transport-related diarrhea by inducing active Cl- secretion
and a loss of Na+ absorption (Electrolyte transport-related (secretory))
The most common cause of inflammatory diarrhea is infection. (eg, Salmonella, Campylobacter, C.
difficile) cause primarily inflammatory responses, resulting in either watery or often bloody diarrhea
(dysentery)
TRASMISSION
• : Acute diarrhea is primarily transmitted through the fecal-oral route.
• This can occur due to the ingestion of contaminated food or water, poor sanitation
practices, inadequate hand hygiene, or close contact with an infected individual.
• Contaminated surfaces, utensils, or objects can also contribute to the spread of
pathogens
CLINICAL FEATURES
• Frequent, loose watery stools
• Loss of appetite
• Nausea and vomiting
• Fever
• Abdominal pains
• Abdominal cramps
• Dehydration- dry mouth or skin, excessive thirst, severe weakness, dark colored urine, dizziness
• Urgent need to have a bowel
• Bloody stools
CLINICAL FEATURES
• E- coli
• Rotavirus
• Watery stools
• Insidious onset
• Vomiting is common
• Prodromal symptoms, including fever, cough, and vomiting
precede diarrhea
• Dehydration moderate to severe
• Fever often of moderate
• Mild abdominal pain
• Cholera
• Rice –water stools
• Vomiting
• Abdominal cramping
grade
• Stools are watery or semi-liquid; the color is greenish or
yellowish typically looks like yoghurt mixed in water
• Mild to moderate dehydration
• Fever— moderate grade
-
Shigellosis
-
Frequent passage of scanty
amount of stools, mostly mixed
with blood and mucus
-
Moderate to high grade fever
-
Severe abdominal cramps
-
Tenesmus— pain around anus
during defecation
-
Usually no dehydration
Amoebiasis
-
Offensive and bulky stools
containing mostly mucus and
sometimes blood
-
Lower abdominal cramp
Mild grade fever
No dehydration
Watery stools of <14 days duration, with no visible blood constitutes acute watery diarrhea.
(A) Green watery stool. Green colored stool, often seen in rotavirus gastroenteritis.
(B) Rice water stool. White colored stool characteristic of severe cholera.
CLINICAL ASSESSMENT
• Evaluation of a child with diarrhea should begin with a detailed clinical history of
the duration, frequency, and character of the diarrhea
• Clinical assessment should include Assessing hydration and nutrition status
• Nutritional status –Children with acute diarrhea and malnutrition are at increased
risk for fluid overload and heart failure during rehydration; therefore, such
children require an individualized approach to rehydration and nutritional
repletion.
ASK IS THE CHILD HAVING DIARRHEA?
• Look and feel:
• If yes, ask: For
• how long?
• Is there blood in
stool ?
• Look at the child's general ,condition. Is the child:
• Lethargic or, unconscious? Restless and
irritable?
• Look for sunken eyes.
• Offer the child fluid. Is the child:
• Not able to drink or drinking poorly?
• Drinking eagerly, thirsty?
• Pinch the skin of the abdomen. Does it go back:
• Very slowly (longer than 2 secs)
• slowly? Less than 2 sec but not immediately
• immediately?
WHO GUIDELINES FOR ASSESSMENT OF
DEHYDRATION
Some dehydration (5 to 10%)
Severe dehydration (>10%)
Two or more of the following
signs:
Two or more of the following
signs:
•Well, alert
•Restlessness, irritability
•Lethargy or unconsciousness
•Normal eyes
•Sunken eyes
•Sunken eyes
•Drinks normally, not thirsty
•Thirsty, drinks eagerly
•Unable to drink or drinks poorly
•Skin pinch goes back quickly
•Skin pinch goes back slowly
•Skin pinch goes back very slowly
(≥2 seconds)
•Estimated fluid deficit: <50 mL/kg
•Estimated fluid deficit: 50 to 100
mL/kg
•Estimated fluid deficit: >100 mL/kg
No dehydration (<5%)
MANAGEMENT
• In absence of severe malnutrition treatment of children with acute diarrhea
consists of
• Correcting fluid and electrolyte losses
• Administering appropriate nutrition
• Managing associated comorbid conditions
• Antibiotic therapy is warranted in some circumstances,.
FLUID AND ELECTROLYTES
• Rehydration therapy is critical for management of diarrhea
• Fluid management consists of two phases: replacement and maintenance.
• Replacement – Initial phase of treatment .Corrects existing water and electrolyte imbalance. continues
until all signs and symptoms of volume depletion have resolved and the patient has urinated; ideally,
this is achieved during the first four hours of treatment.
• Maintenance – The maintenance phase counters ongoing losses of water and electrolytes; this phase
continues until diarrhea and other signs and symptoms of illness have resolved.
• The approach to fluid and electrolyte management depends on the degree of dehydration.
• The WHO provides definitions and treatment guidelines along a continuum that includes "no
dehydration" (Plan A), "some dehydration" (Plan B), and "severe dehydration" (Plan C)
HOW SEVERE ISTHE DEHYDRATION
DUE TO DIARRHOEA?
Hpovolaemic shock
(Severely impaired circulation)
All of the four (4) below are present:
 Not alert, AVPU < A
 Weak or absent peripheral pulse
 Cold periphery & temp gradient
 Capillary refill > 3 secs
PLUS
sunken eyes and
slow skin pinch > 2secs
Y
Ringer’s
20mls/kg
bolus max 2.
then Plan C
part 2
Transfuse urgently if
Hb <5g/dl
Treat hypoglycaemia
MANAGEMENT OF DIARRHOEA /
DEHYDRATION WITH SEVERELY
IMPAIRED CIRCULATION
=
‘HYPOVOLAEMIC SHOCK’
A ,B &C, start oxygen, then if signs of severely
impaired circulation & dehydration =
Hypovolaemic Shock
Exclude Sever Acute Malnutrition
Establish IV /IO access.
20mls/kg Ringer’s bolus
(<15min)
Reassess ABCD, give
max 2 boluses, then
Plan C step 2
HOW SEVERE ISTHE DEHYDRATION
DUE TO DIARRHOEA?
 Not alert, AVPU < A
 Weak or absent peripheral pulse
 Cold periphery and temperature
gradient
 Capillary refill > 3 secs
PLUS sunken eyes and skin pinch > 2
secs
Y
Severely Impaired
Circulation
‘Hypovolaemic
Shock’
N
Severe dehydration
AVPU < A plus / unable to drink
Plus
Sunken Eyes
Skin pinch ≥ 2 secs
Y
Severe
Dehydration
Plan C
TREATMENT OF SEVERE
DEHYDRATION
Step 1*
Step 2
30 mls / kg over 30 mins
(>12m) or over
60min if (< 12m)
70 mls / kg over 2.5
hours( >12m) or
over 5 hours
(<12m)
NGT rehydration-120ml/kg ORS over 6hours can be
used instead of steps 1 and 2
Re-assess at least hourly and after 3-6hrs, reclassify as
severe, some or no dehydration and treat accordingly
.
Give 5ml/kg of ORS once the child can drink
* Go to step 2 if child has received bolus for shock
IV FLUID REPLACEMENT
Existing fluid
Fluid deficit
Na+, 140 mmol/l
K+, 4.5 mmol/l
Replacement fluids
should be similar to
body fluids
All
concentrations
are in mmol/l
Na+
K+
Ringer’s
Lactate
(Hartmann’s)
130
5.4
But the iv fluids don’t contain glucose....
HOW SEVERE ISTHE DEHYDRATION DUETO
DIARRHOEA?
 Not alert, AVPU < A
 Weak or absent peripheral pulse
 Cold periphery and temperature
gradient
 Capillary refill > 3 secs
unable to drink or AVPU < A
plus:
Sunken Eyes
Skin pinch ≥ 2 secs?
Able to drink plus ≥ 2 of:
Sunken Eyes and / or
Skin pinch 1 - 2 secs
Restlessness / Irritability
Y
Y
Y
Severely Impaired
Circulation
‘Hypovolaemic
Shock’
Severe
Dehydration
Some
Dehydration
SOME DEHYDRATION IS BEST
TREATED WITH ORS
• Oral rehydration is associated with FEWER deaths and
convulsions
• ORS contains glucose and potassium
• ORS can safely be given down an NG tube if needed
• Very rarely an ileus (bowel stops working = absent sounds
with distension) is a reason to stop oral fluids
PRESCRIBING ORS-SOME DEHYDRATION
• 75 mls / kg of ORS over 4 hours.
• Continue breastfeeding as tolerated
• After 4 hours reassess and reclassify;
• Severe, Some or no dehydration?
Counseling the mother / caretaker?
• What do you tell the mother of an 8kg child?
COMPOSITION OF LOW OSMOLALITY ORS
Mmol/l
Sodium
75
Replaces Na lost in stool
Chloride
65
Glucose
75
Facilitates absorption of Na (and hence
water) in the small intestine
Potassium
20
Replace K+ lost in stool
Citrate
10
Corrects acidosis
Total Osmolality
245
ORS is based on the discovery that glucose greatly increases the
patient's capacity to absorb salts and water.
More than 90% of the diarrhea diseases irrespective of the cause
respond to ORS
PRESCRIBING ORS
• 75 mls / kg for an 8kg child?
600 mls in 4 hours
2 large cups / 2 soda
bottles in 4 hours
3 small cups in 4 hours.
ORS IN PRACTICE.
300 mls
200 mls
HOW SEVERE ISTHE
DEHYDRATION?
 Not alert, AVPU < A
 Weak or absent peripheral pulse
 Cold periphery and temperature
gradient
 Capillary refill > 3 secs
unable to drink / AVPU <A plus
Sunken Eyes &
Skin pinch ≥ 2 secs?
Able to drink plus 2 or more of:
Sunken Eyes and / or
Skin pinch 1 - 2 secs
Restlessness / Irritability
Not classified above?
Y
Severely Impaired
Circulation
‘Hypovolaemic
Shock’
Y
Severe
Dehydration
Y
Some Dehydration
Y
Diarrhoea
with no
Dehydration
PRESCRIBING ORSTO PREVENT
DEHYDRATION (PLAN A)
• After correction of dehydration
• Give required feeds and fluids
• In addition, ORS 10ml/kg for every loose stool
In a child with diarrhea and NO
dehydration give usual foods (appropriate
for nutritional status ) and fluids &
breastfeeds more frequently
PLUS
10ml/kg after every loose stool
TAKE HOME
• Severely Impaired Circulation caused by severe
diarrhoea likely indicates Hypovolaemic Shock requires immediate management
• Ability to drink is an important indicator of severity.
If they can drink then use oral or oral + ngt fluids.
• Sunken Eyes and Skin Pinch are the most reliable
signs of dehydration
• Signs which work poorly include:
• Dry mucous membranes
• Absence of tears
• Poor urine output
VOMITINGAND FEEDING?
• Vomiting is NOT a contra-
indication to oral rehydration
• Careful counseling about, slow,
steady administration of ORS is
helpful.
• Breast feeding and other forms of
feeding can and should continue
ROLE OFANTIBIOTICS & ZINC.
• Antimicrobials only indicated for bloody
diarrhoea or proven amoebiasis, cholera or
giardiasis
• Blood diarrhoea– Ciprofloxacin for 3 days
• If a child has another severe illness then treat
with appropriate antibiotics eg. If has
pneumonia, malnutrition
• Zinc should be given to all children with
diarrhoea as it speeds resolution of
symptoms:
• 10mg od (half tab) for 14 days if age <6 months
• 20mg od (one tab) for 14 days if age >=6 months
ZINC SULPHATE
• Reduces duration of diarrhea episodes by 25%
• Decreases by 25% the proportion of episodes lasting more than 7 days
• It is associated with a 30% reduction in stool volume
• Conclusion: significant beneficial impact on the clinical course of acute diarrhea:reduces
both severity and duration, also decrease in diarrhoea episodes 2-3 months
QUESTIONS?
SUMMARY
• A small number of signs are most useful in
classifying the severity of dehydration.
• IV fluids only used to treat children who cannot
drink.
• ORS is often more safe and effective even in
hospital.
• Give Zinc to all
• Reassess response to treatment.
COMPLICATIONS OF DIRRHOEA
•
Dehydration and electrolyte disturbances — Dehydration is an important cause of mortality in resource-limited settings;
•
Electrolyte disturbances may include hypokalemia, hyponatremia, and hypernatremia
•
Malnutrition — Recurrent diarrhea may be associated with malnutrition, which can contribute to delays in physical and
cognitive development;
•
Central nervous system (CNS) involvement — include seizures and encephalopathy. These have been described in patients
with severe disease due to Shigella and less commonly in systemic Salmonella infection [20-23].
•
The presence of seizures should prompt consideration of hypoglycemia, hyponatremia, and hypernatremia.
• Stool sample:
• Occult blood present in inflammatory bowel disease, bowel ischemia, bacterial infections
• Fecal leukocytes present in diarrhea caused by Salmonella, Campylobacter,Yersinia
• For community-acquired or traveler's diarrhea >1 day or accompanied by fever or bloody stools:
Culture or test for Salmonella, Shigella, Campylobacter, E. coli O157:H7. If antibiotics or
chemotherapy in recent weeks, C. difficile toxin A and B (1)[B]
• For nosocomial diarrhea (onset ≥3 days in hospital): Test for C. difficile toxins A and B. Also
consider bacterial cultures listed above in patients with bloody stools or infants (1)[B].
• For diarrhea >7 days: Stool ova and parasites plus bacterial cultures if immunocompromised (1)[B]
• Giardia ELISA: >90% sensitive in at-risk population, consider prior to O&P
DIAGNOSIS
• LAB-CBC:
• Increased WBC with a left shift may indicate an infectious process.
• A decreased hemoglobin/hematocrit may indicate anemia from blood loss.
Serum electrolytes
• Increased sodium from dehydration
• Decreased potassium from diarrhea
• BUN, creatinine: Elevated in dehydration
• pH: Hyperchloremic acidosis
IMAGING
• Abdominal radiographs (flat plate and upright) indicated with abdominal pain or evidence
of obstruction to rule out toxic megacolon and bowel ischemia
DIAGNOSTIC PROCEDURES/SURGERY
• Sigmoidoscopy indicated with bloody diarrhea or suspected pseudomembranous or
ulcerative colitis