Transcript Etiology of Acute Diarrhea

Diarrhea
Department of Pediatrics
Soochow University Affiliated Children’s Hospital
Aim and Claim
• Understanding the incidence and aetiology
of gastroenteritis
• Familiar with clinical featurs and diagnosis of
gastroenteritis
• Get hold of the management of dehydration
Definition
In epidemiological studies,
Diarrhea is defined as:
Passage of three or more loose or watery
stools in a 24-hour period,
a loose stool being one that would take
the shape of a container.
Definition
In Pediatrics,
Diarrhea is defined as an increase in the :
• Fluidity
• Volume
of stools
• Number
relative to the usual habits of each individual.
Importance of Diarrhea
In under five children
Diarrhea is a leading cause of:
–Mortality(死亡率)
–Morbidity（发病率）
–Malnutrition（营养不良）
High Childhood Mortality
3.2 million deaths/ year in <5y Children
High Childhood Morbidity
1.3 billion episodes / year in <5y children
Diarrhea
Malnutrition
Major Contributor to Malnutrition
If: Diarrhea + Malnutrition
In Malnourished Children
the RISK of DEATH form
Diarrhea is:
4 fold
that of well nourished children
Types of Diarrhea
• Acute watery
diarrhea
10
• Dysentery (Bloody
diar.)
• Persistent diarrhea
10
80
Acute Watery
Dysentery
Persistent
Morphology of Intestinal Mucosa
The small intestinal mucosa
comprises 2 main structures:
 Villi（刷状缘）:
Covered mainly (90%) by tall
columnar absorptive cells
(enterocytes) having a
microvillar brush border, and
Goblet cells
Crypts of Lieberkuhn（隐窝）:
Covered mainly by short
columnar secretory cells without
brush border
Brush border
(microvilli)
Tight junction
“Niche”for bacteria between cells
Mucus layer
Goblet cell
Enterocyte
Small Intestinal Mucosa
Defense barriers of the enterocytes:
1-Physical barrier: mucus
2-Bacteriological (flora)
3- Immunological : Secretory IgA
Defense Barriers of
Enterocytes
1.
Physical Barrier:
– The mucus secreted by goblet cells
opposes penetration of pathogens
– Tight junctions between enterocytes
2. Bacteriological Barrier:
– Saprophytic Flora occupy enterocytic
“niches” thus preventing their occupation
by foreign pathogens
3. Immunological Barrier:
– Secretory IgA included in the mucus
neutralizes the action of bacteria and
Viruses
Etiology of Acute
Diarrhea
Etiology of Acute Diarrhea
 Viruses: Rotavirus（轮状病毒）, Enteric Adenovirus（腺病毒）,
Calicivirus(杯状病毒), Astrovirus（星状病毒）(70 – 80% of
infectious diarrhea cases)
 Bacteria: Salmonella（沙门氏菌）, Shigella（志贺氏菌）,
Campylobacter jejuni（空肠弯曲菌） Yersinia Enterocolitica（耶尔
森氏菌） Escherichia coli (ETEC,EAEC, EIEC,EHEC,EPEC)
Clostridium difficile（艰难梭菌）(10 – 20% of cases)
 Parasites: Entamoeba histolytica（阿米巴滋养体）, Giardia Lamblia
（梨形鞭毛虫）, Cryptosporidium（隐孢子虫）(10% of cases)
Etiology: Fecal-Oral Transmission
Infected Animal
Infected Person
Food
Water
Susceptible person
Etiology of Acute Diarrhea
The most important causes of acute diarrhea
in developing countries are:
• Rotavirus
• Enterotoxigenic Escherichia coli
• Shigella
• Campylobacter jejuni
• Cryptosporidium
Rotavirus
Pathogenesis of Rotavirus
Diarrhea
Rotavirus invades the absorptive enterocytes of villi but spares crypt
cells. The viruses replicates and infected enterocytes are destroyed
Pathogenesis of Rotavirus
Diarrhea
11
2
1- Infected absorptive ente-
rocytes are killed causing
patchy epithelial cell destruction and villous shortening
2- Destroyed absorptive cells
are rapidly replaced by cells
that migrate from the crypts.
Villi become covered with
immature non-absorptive
secretory cells having:
-no brush border
- no brush border enzymes
Rotavirus
No brush border
Osmotic diarrhea
Enterotoxigenic Organisms
Vibrio
Cholerae
Enterotoxigenic E.Coli
Pathogenesis of Enterotoxigenic Diar.
1-Enterotoxigenic Bacteria
secrete an Enterotoxin
2-Toxin stimulates the
production of C-AMP (cyclic
adenosine mono-phosphate)
3-Increased C-AMP leads to:
Inhibition of absorption of
Na+ & Cl- from the cells of villi
Stimulation of secretion of
Cl- from crypt cells
Enterotoxigenic E. coli
Secretory diarrhea
Pathogenesis of Secretory
Diarrhea
X
NET SECRETION
+++++
Entero-Invasive Organisms
Shigella
Pathogenesis of Invasive Diarrhea
Invasive organisms like Shigella, Campylobacter jejuni,
enteroinvasive E.coli, etc.:
 Invade and destroy the mucosal epithelial cells in colon and
distal part of ileum（回肠）.
 Formation of micro-abscesses and superficial ulcers; hence the
presence of:
Red and white blood cells in stools
Visible blood in the stools.
 These organisms produce also toxins that lead to:
Tissue damage
Increased mucosal secretion of water and electrolytes
Entero-Invasive Organisms
Enterotoxin
Destruction
Clinical Features
 Viral infection may cause a prodromal illness followed
by vomiting and diarrhea.
 The vomiting may precede diarrhea and is not usually
bile or bloodstained.
 Abdominal pain and blood or mucus in the stools
suggests an invasive bacterial pathogen.
 The severity of diarrhea may be underestimated if it
pools in the large bowel watery stool is mistaken for
urine in the nappy.
Stool Characteristics and
Determining Their Source
Stool Characteristics
•
•
•
•
•
•
•
•
Appearance
bloody
Volume
Frequency
Blood
bloody
Ph
Reducing substances
WBCs
power
Serum WBCs
Small Bowel
Watery
Large
Increased
Possibly positive but
never gross blood
Possibly <5.5
Possibly positive
<5/high power field
Normal
Large Bowel
Mucousy and/or
Small
Increased
Possibly grossly
>6.5
Negative
Possibly >10/high
field
Possible leukocytosis,
bandemia
Stool Characteristics and Determining
Their Source
Stool Characteristics
Organisms
Small Bowel
Large Bowel
Viral
Rotavirus
Adenovirus
Calicivirus
Astrovirus
Norwalk virus
Invasive bacteria
E Coli
Shigella species
Salmonella species
Campylobacter species
Yersinia species
Aeromonas species
Toxic bacteria
Toxic bacteria
E coli
Clostridium difficile
Clostridium perfringens
Cholera species
Vibrio species
Parasites
Parasites
Giardia species
Entamoeba organisms
Cryptosporidium species
Clinical Findings of Dehydration
mild
Lose of body
5(%)
weights
Thirst
+
of tears
+
Sunken eyes
Sunken fontanel
Skin and mucous slightly dry
membranes
Urine output
normal
status
intact
moderate
6～9(%)
+
+
+
+
dry
decreased
irritable
severe
>10(%)
+
+
+
+
Absence
parched
decreased Mental
lethargy
coma,shock
signs
Assessment
Of
Dehydration
Assessment of Dehydration
4 Important Signs:

General condition (sensorium):
Lethargic / irritable / normal

Eyes :
Sunken / normal

Mouth (offer a drink & watch the child):
Drinking poorly / drinking eagerly / drinking
normally

Skin turgor (skin pinch):
Returns very slowly / returns slowly / returns
immediately
Assessment of Dehydration
SIGNS
G General
condition
Eyes
E
M Mouth &
S
No signs of
dehydration
well,
alert
normal
Some (mod.)
Severe
dehydration dehydration
restless,
lethargic,
irritable
unconscious
sunken
sunken
normal
thirsty, drink poor or unaDrinking
eagerly
ble to drink
Skin pinch returns rapidly returns slowly very slowly
Always start from Red Column
2 or more signs in 1 column indicate that the
child falls in that column
Assessment of Dehydration
• Severe dehydration will have two of these
signs:
– Sensorium(general condition): lethargic or
unconscious
– Sunken eyes
– Drinking poorly or not at all
– Very slow skin pinch (more than 2 seconds)
Assessment of Dehydration
• Some dehydration will have two of these
signs:
– Restlessness or irritability
– Sunken eyes
– Drinking eagerly
– Slow skin pinch
• No dehydration
– No signs or less than 2 signs
Assessment of Dehydration
Severity
Infants (weight <10 kg) Children (weight
>10 kg)
Mild dehydration
5% or 50 mL/kg
3% or 30 mL/kg
Moderate dehydration
6%-9% or 60-90
mL/kg
6% or 60 mL/kg
Severe dehydration
＞10% or ＞100
mL/kg
9% or 90 mL/kg
Differential Diagnosis(1)
 Young infants(aged 2-12weeks)—pyloric stenosis—
vomiting
 Older infant and toddlers(aged 1-2years)—
intussusception—vomiting ,abdominal pain and
redcurrant jelly
Differential Diagnosis(2)
Appendicitis
Crohn Disease
Irritable Bowel Syndrome
Malabsorption Syndromes
 Meckel Diverticulum
 Protein Intolerance
Short Bowel Syndrome
 Ulcerative Colitis
Management
Objectives
 Prevent dehydration, if there are no signs of dehydration;
 Preat dehydration, when it is present;
 Prevent nutritional damage, by feeding during and after
diarrhoea; and
 Reduce the duration and severity of diarrhoea, and the
occurrence of future episodes, by giving supplemental
zinc.
ORT
 OR therapy(ORT) is the cornerstone of treatment,
especially for small bowel infections that produce a large
volume of watery stool output.
 A 5-cc or 10-cc syringe without a needle is a very useful
tool. The syringe can be used to quickly place small
amounts of fluid in the mouth of a child who is
uncooperative.
Diet
A strong body of evidence now suggests that
resuming the prediarrhea diet is perfectly safe
and must be encouraged,
In an incident of worsening of diarrhea proven to
be secondary to a clinically important lactose
malabsorption in infants positive for rotavirus, a
very transient use of lactose-free formulas (5-6 d)
can be considered.
Strong evidence in the literature demonstrates
that the continued use of breast milk is actually
beneficial in children with acute diarrhea.
Special Information
 Anti-diarrheal agents and antiemetics are notrecommended for use
in children with AGE.
 Antimicrobial therapies are recommended only for selected children
with AGE who present with special risks or evidence of a serious
bacterial infection (SBI).
 Probiotics (Lactobacillus GG) have been shown to reduce the
duration of diarrhea and the duration of shedding of rotavirus.
Lactobacillus GG may be considered as adjunctive therapy.
Summary
 The causes of GE are viruses(70—80%),bacteria(10—20%)and
parasites(10%)
 Patients may present diarrhoea,vomiting,abdominal pain and
fever
 The stool may be watery,mucuous ,bloody or pyic
 Dehydration is classed as mild,moderate and severe.According
to dehydration,you can estimate fluid deficit.
 GE need to differentiate varieties of diarrhoea
 Management of GE
Quiz
 Physical parameters associated with degree of
dehydration( Table: Clinical Findings of
Dehydration )
 How to estimate fluid deficit (Table: Assessment of
Dehydration)