Download mechanism of diarrhea

DIARRHOEA in INFANCY &
CHILDHOOD
By
Dr. Athal Humo
2015-2016
Objectives of Lec.1
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To define diarrhea (& gastroenteritis).
To differentiate between the types of diarrhea.
To know the mechanism of each type.
To know the etiologies of GE.
To know the risk factors of GE.
To know the clinical features of GE & how
clinically evaluate the degree of dehydration.
How can investigate a patient with GE?
Acute Gastroenteritis in
Children
The term gastroenteritis captures the
bulk of infectious cases of diarrhea. The
term diarrheal disorders is more
commonly used to denote infectious
diarrhea in public health settings,
although several noninfectious causes of
gastrointestinal illness with vomiting
and/or diarrhea are well recognized.
The term gastroenteritis
denotes
infections of the gastrointestinal tract
caused by bacterial, viral, or parasitic
pathogens
Diarrhea
Refers to:
 Abnormal increase in frequency and
liquidity of fecal discharges.
OR
 Stool output >10 g/kg/24 hr, or more than
the adult limit of 200 g/24 hr.
EPIDEMIOLOGY OF
CHILDHOOD DIARRHEA
Diarrheal disorders in childhood account for
a large proportion (18%) of childhood
deaths.
with an estimated 1.5 million deaths per year
globally, making it the second most common
cause of child deaths worldwide..
Global trends in diarrhea incidence
TYPES OF DIRRHEA
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Acute watery diarrhea (<14
days).
Dysentery (visible blood in
stool).
Persistent diarrhea (>14 days).
MECHANISM OF DIARRHEA
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The basis for all diarrhea is disturbed
intestinal solute transport; water movement
across intestinal membranes is passive and
is determined by both active and passive
fluxes of solutes, particularly sodium,
chloride, and glucose.
The pathogenesis of most episodes of
diarrhea can be explained by secretory,
osmotic, or motility abnormalities or a
combination of these
Mechanisms of Diarrhea
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Secretory:
Defect:
Increased secretion
Decreased absorption
Examples:
Activation of cAMP: Cholera, toxinogenic E.coli(LT),
Shigella, Salmonella, Campylobacter jejuni,
Pseudomonas aeruginosa.
Activation of cGMP: E. coli (ST) , Yersinia
enterocolitica
toxin
Comments:
Persists during fasting
No stool leukocytes
Mechanisms of Diarrhea
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Osmotic
Defect present:
Digestive enzyme deficiencies
Ingestion of unabsorbable solute
Examples:
Malabsorption: Disaccharidase deficiencies (lactase )(rota virus cause
lactase def)
Excessive intake of carbonated fluid
Excessive intake of non absorbable solute: Lactulose
Comments:
Stop with fasting
No stool WBCs
•Stool volme
• Moderately increase
• Large volume
•Stool Na
•Fasting
•Ion gap
•Stool PH
•Reducing subst
<200ml/24h
•< 70mEq/l
• diarrhea stop
• >100mosm/kg
•< 5
• +ve
>200ml/24h
•>70
•Diarrhea continue
•< 100
•>6
• -ve
Mechanisms of Diarrhea
NOTE
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The stool osmolality is indicated by the
electrolytes and the ion gap is
100 mOsm/kg or less.
The ion gap is calculated by subtracting
the concentration of electrolytes from total
osmolality:
Ion gap = Stool osmolality – [ (stool Na + stool K) ×
2]
PATHOLOGY
I.
Noninflammatory Diarrhea
Through:
enterotoxin production by some bacteria
destruction of villus (surface) cells by
viruses
adherence by parasites, and by bacteria.
II. Inflammatory Diarrhea
usually caused by bacteria that:
directly invade the intestine
produce cytotoxins with consequent
fluid, protein, and cells (erythrocytes,
leukocytes) that enter the intestinal
lumen.
Some enteropathogens possess more
than one virulence property
ETIOLOGY OF DIARRHEA
DIARRHEA
Infectious diarrhea
(GE)
Non infectious diarrhea
Infectious Diarrhea
Gastroenteritis is due to infection
acquired through the feco-oral route
or by ingestion of contaminated food
or water.
Gastroenteritis is associated with
poverty and poor environmental
hygiene.
GE
Viral
Bacteri
a
Parasite
Viral gastroenteritis (“stomach flu”)
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rotavirus
noroviruses (small round viruses such as
Norwalk-like virus and caliciviruses)
sapovirus
enteric adenoviruses
astroviruses
noroviruses
noroviruse
s
Rotavirus
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Rotavirus invades the epithelium and damages villi
of the upper small intestine and in severe cases
involves the entire small bowel and colon.
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Rotavirus is the most frequent cause of diarrhea
during the winter months. Vomiting may last 3 to 4
days, and diarrhea may last 7 to 10 days.
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Dehydration is common in younger children.
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Usually cause watery diarrhoea ,
no blood and pus in stool
Escherichia Coli :
gram-negative bacilli
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5 major groups of diarrheagenic E. coli:
(1) enterotoxigenic E. coli (ETEC)
(2) enteroinvasive E. coli (EIEC)
(3) enteropathogenic E. coli (EPEC)
(4) Shiga toxin–producing E. coli (STEC)also known
as enterohemorrhagic E. coli (EHEC)
(5) enteroaggregative E. coli (EAEC).
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Clinical Characteristics of Diarrheagenic Escherichia
coli
Shiga Toxin–Producing E. coli.
HUS
E-coli 0157-h7
Shigella
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Four species of Shigella are responsible for
bacillary dysentery:
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S. dysenteriae
S. flexneri
S. boydii
S. sonnei
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It is most common in the 2nd and 3rd year of life,
infection in the 1st 6 mo of life is rare (may be due to
Breast feeding)
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The colon is the target organ for shigellae
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Symptoms:
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generalized toxicity
urgency, and painful defecation characteristically occur.
watery → bloody mucoid stools
Convulsions, headache, lethargy, confusion, nuchal
rigidity, or hallucinations may be present before or after
the onset of diarrhea.
Pathogenesis of Shigella infection and diarrhea
Salmonella
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Salmonella causes 2 clinical syndromes
in humans: a GE that is usually selflimited, and typhoid fever that is a
relatively severe systemic illness
classically caused by S. typhi.
Nontyphoidal strains of Salmonella can
also cause a severe bacteremic illness
in some circumstances.
CLINICAL MANIFESTATIONS.
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Acute Enteritis:
 mild to severe watery diarrhea
 Bloody diarrhea
Campylobacter
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The organism invades the mucosa of the jejunum, ileum,
and colon, producing enterocolitis.
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DISEASES IN HUMANS: Gastroenteritis, bacteremia,
Guillain-Barré syndrome
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Acute Gastroenteritis.
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Watery or bloody diarrhea
The abdominal pain is periumbilical; cramping but may mimic
appendicitis or intussusception.
Yersinia Enterocolitica
Infants
&
young
children
characteristically have a diarrheal disease,
whereas older children usually have acute
mesenteric lymphadenitis mimicking
appendicitis or Crohn disease. Arthritis,
rash, and spondylopathy may develop.
Entamoeba histolytica
Clinical
presentations
range
from
asymptomatic cyst passage to amebic colitis,
amebic
dysentery,
ameboma,
and
extraintestinal disease as amebic liver disease.
Amebic colitis, gradual onset of colicky
abdominal pains and frequent bowel
movements (6–8/day). Diarrhea is frequently
associated with tenesmus. Stools are blood
stained and contain a fair amount of mucus
with few leukocytes. Generalized constitutional
symptoms and signs are characteristically
absent, with fever documented in only ⅓ of
patients.
Giardia Lamblia
It infects the duodenum and small intestine
Clinically:
asymptomatic, acute infectious
diarrhea (insidious onset of progressive
anorexia, nausea, gaseousness, abdominal
distention, watery diarrhea) or chronic diarrhea
with persistent GIT signs and symptoms,
including FTT and abdominal pain or cramping.
There is usually no extraintestinal spread.
Non-infectious diarrhoea
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Allergy to milk or its components
Malabsorption
Endocrinopathies
Poisoning
Neoplasia e.g.: neuroblastoma
IBD
Drugs / medications
DIARRHEA
WATERY
BLOODY
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Viral enteritis
Enterotoxin producing bacteria:
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s.
aureus
Parasitic GE:
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Escherichia coli
Klebsiella organisms
Clostridium perfringens
Vibrio species
vibrio
Giardia
Cryptosporidium
cryptosporidium
Extraintestinal Infections:
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Parenteral Diarrhea e.g.: otitis media & urinary tract infection .
S.aureus
Cl.perferingen
s
BACTERIAL
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Shigella
Salmonella
Campylobacter
Yersinia enterocolitica
Invasive E. coli
NON-BACTERIAL
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Amoebic dysentery
Pseudomembranous enterocolitis (C. difficile
toxin)
Ulcerative or granulomatous colitis (acute
presentation)
Necrotizing enterocolitis in neonates
RISK FACTORS FOR GASTROENTERITIS
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Major risks include environmental contamination
and increased exposure to enteropathogens.
Additional risks include:
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Lack of exclusive or predominant breast-feeding.
Young age
Immune deficiency
Measles
Malnutrition, malnutrition increases severalfold the risk
of diarrhea and associated mortality.The risks are
particularly higher with micronutrient malnutrition; in
children with vitamin A deficiency, the risk of dying
from diarrhea, measles, and malaria is increased by 20–
24%. Zinc deficiency increases the risk of mortality
from diarrhea, pneumonia, and malaria by 13–21%.
CLINICAL MANIFESTATIONS
Clinical Manifestation of GE
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Diarrhea, vomiting ,nausea, anoroxia,
abdomenal distension, abdominal cramps.
Manifestation of complications:
dehydration & electrolyte disturbance.
Extra intestinal: Fever, malaise, reactive
arthritis, systemic spread of M.O.,
Guillain- Barre Synd, HUS, hemolytic
anaemia.
DIAGNOSIS OF GE
DIAGNOSIS OF GE
The diagnosis of gastroenteritis is based
on clinical recognition, an evaluation of its
severity by rapid assessment, and
confirmation by appropriate laboratory
investigations, if indicated.
CLINICAL EVALUATION OF DIARRHEA
Assess the degree of dehydration
and acidosis and provide rapid
resuscitation and rehydration with
oral or intravenous fluids as
required
Obtain appropriate contact or
exposure history. This includes
information on exposure to contacts
with similar symptoms, intake of
contaminated foods or water, childcare center attendance, recent
travel to a diarrhea-endemic area,
and use of antimicrobial agents.
Clinically determine the etiology of
diarrhea for institution of prompt
antibiotic
therapy,
if
indicated.
Although nausea and vomiting are
nonspecific
symptoms,
they
are
indicative of infection in the upper
intestine. Fever is suggestive of an
inflammatory process but also occurs as
a result of dehydration or co-infection
(e.g., urinary tract infection, otitis
media).
Fever is common in patients with
inflammatory diarrhea. Severe abdominal
pain and tenesmus are indicative of
involvement of the large intestine and
rectum. Features such as nausea and
vomiting and absent or low-grade fever
with mild to moderate periumbilical pain
and watery diarrhea are indicative of
small intestine involvement and also
reduce the likelihood of a serious bacterial
infection.
<5
<3
5-10
3-6
>10
>6
LABORATORY STUDIES
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Initial laboratory evaluation of moderate to severe diarrhea includes:
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GSE for:
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electrolytes
Blood sugar.
BUN, creatinine
Blood pH , S. [HCO3]
urinalysis for specific gravity as an indicator of hydration.
CBP.
Macroscopical
Microscopical.: mucus, blood, and leukocytes
Chemical
Stool cultures are recommended for patients with:
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fever
profuse diarrhea
if HUS is suspected.
bloody diarrhea.
in immunosuppressed children with diarrhea.
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ELISA for rotavirus..
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The diagnosis of E. histolytica is based on identification of the organism in the stool. Serologic
tests are useful for diagnosis of extraintestinal amebiasis, including amebic hepatic abscess.
Giardiasis can be diagnosed by identifying trophozoites or cysts in stool; less often a duodenal
aspirate or biopsy of the duodenum or upper jejunum is needed.
GUE
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