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ACUTE GASTROENTERITIS

Outline
1. Epidemiology
2. Etiology
3. Pathogenesis
4. Pathophysiology
5. Clinical Features
6. Prevention
7. Investigations
8. Diagnosis
9. Classification
10. Differential Diagnosis
11. Principle of Management
12. Complication
13. Prognosis
• In developing countries, acute gastroenteritis (AGE) is a
major cause of child mortality and morbidity due to
dehydration.
• AGE is one of frequent causes of hospitalization in children
under age of five in the hospital setting, both in Malaysia
and throughout the world, especially in developing
countries.
• It is estimated that approximately 440,000 annual deaths in
children <5 years of age worldwide due to diarrhoea related
illness, with rotavirus as the main cause.
• In Malaysia, recent study by Lee et al, the financial burden
of providing inpatient care for rotavirus GE range (US0.6
million to 7.5 million) annualy.
Based on Malaysian Journal of Medicine and
Health Sciences Vol. 7 (2) June 2011 :

 Acute gastroenteritis among indigenous paediatric


patients – A descriptive Study in a Rural District
Hospital, Sarawak (2011) [at Serian District Hospital]
 Carried out by Unimas with UPM
 234 indigenous children between 2006-2007
VIRUS (about 70%)
 Rotavirus
 Norovirus
 Enteric adenoviruses
 Caliciviruses
 Astroviruses
 Enteroviruses

BACTERIA (10-20%)
 Campylobacter jejuni
 Non-typhoid Salmonella spp
 Enteropathogenic Escherichia coli
 Shigella spp
 Yersinia enterocolitica
 Shiga toxin producing E coli
 Salmonella typhi and S paratyphi
 Vibro cholerae
PROTOZOA (<10%)
Crptosporidium
Giardia Lamlia
Entamoeba histolytica

HELMINTS
Strongtloides stercoralis
Research study : Best Approaches to Acute Gastroenteritis
(February, 2016)
Research study : Best Approaches to Acute Gastroenteritis
(February, 2016)
Ingestion of pathogenic organism will
cause : Adherence, mucosal invasion,
enterotoxin/cytotoxin production

Interference of intestinal function


leading to increased fluid
secretion/decreased absorption

Increased luminal fluid content


leading to dehydration, loss of
electrolytes & nutrients.
 Acute gastroenteritis occur when the fluid balance between secretion
and reabsorption of fluid in the intestinal tract become damage.
 The most common presentation of AGE is diarrhea.
 Diarrhea occurs when intestinal fluid output overwhelms the
absorptive capacity of the gastrointestinal tract.
 The 2 primary mechanisms responsible for acute gastroenteritis are :
 Damage to the villous brush border of the intestine, causing
malabsorption of intestinal contents and leading to an osmotic
diarrhea
 The release of toxins that bind to specific enterocyte receptors and
cause the release of chloride ions into the intestinal lumen, leading
to secretory diarrhea.

Osmotic Diarrhea : Small (generally less than 200ml/24 hours)


Secretary Diarrhea : Large (>200ml/24 hours)
DIARRHEA

Acute (<7 days) Chronic (>14 days)

•Gastroenteritis •Post infectious secondary lactase


•Food poisoning deficiency
•Systemic infection •Cow’s milk/soy protein intolerance
•Antibiotic associated •Toddler’s diarrhoea
•Celiac disease
•Cystic fibrosis
•Irritable bowel syndrome
•Inflammatory bowel disease
•Lactose intolerance
•Giardiasis
•Laxative abuse
• Type 1-2: constipation
• Type 3-4: ideal stools
• Type 5-7: leading towards
diarrhea.
Severe symptoms :
• High fever
• Vomiting more than 48 hours
• Blood in vomit or stool
• Severe abdominal pain
• Dehydration – loss of weight, weakness, light-
headedness, decreased urination, dry skin, dry
mouth and lack of sweat and tears are
characteristic findings
Common Symptoms :
• Low grade fever
• Nausea with/without vomiting
• Mild to moderate diarrhoea
• Abdominal pain
• Lethargy

 Most of the clinical manifestations and clinical syndromes


of diarrhea are related to the infecting pathogen and the
dose or inoculum
 Additional manifestations depend on the development of
complications and the nature of the infecting pathogen
Increased risk for dehydration :
1. Infants (<6 months)
– Greater surface area : weight ratio – greater insensible
water losses
– Higher basal fluid requirements
– Immature renal tubular reabsorption
– Unable to obtain fluid by themselves when thirsty
2. Low birthweight
3. Passed ≥ 6 diarrhoeal stools in previous 24 hours
4. Vomited ≥ 3 times in previous 24 hours
5. Unable to tolerate extra fluids
6. Malnutrition
Hydration Assessment
Bacterial
Campylobacter Shigella Salmonella Vibrio Cholera Enterotoxigenic
Jejuni (toxin) E. coli (ETEC)
• Diarrhoea • Abdominal S. typhi and S. • Profuse • Watery
(may be cramps paratyphi produce watery diarrhea
bloody) • High fever typhoid with diarrhea • Abdominal
• Severe • Diarrhoea insidious onset • Vomiting cramps
abdominal • Stools characterized by: (Can lead to • Vomiting
pain (may contain • Fever severe
• Fever blood and • Headache dehydration
• Vomiting mucus) • Constipation and death
• Malaise within hours)
• Chills
• Myalgia
• Diarrhoea
(uncommon)
• Vomiting (not
severe)
Viral
Rotavirus Hepatitis A Calicivirus Astrovirus,
adenovirus,
parvovirus
• Vomiting • Diarrhea • Nausea • Nausea
• Watery diarrhea • Dark urine • Vomiting • Vomiting
• Low-grade fever • Jaundice (more prominent in • Diarrhoea
• Temporary • Flu-like children) • Malaise
lactose symptoms • Abdominal • Abdominal pain
intolerance (fever, headache, cramping • Headache
(Infants & children, nausea) • Diarrhoea • Fever
elderly and • Abdominal pain (more prominent in
immunocompromise adult)
d are especially • Fever
vulnerable) • Myalgia
• Headache
• Prolonged
asymptomatic
excretion possible
Parasitic
Entamoeba histolytica Giardia lamblia Cryptosporidium Parvum

• Diarrhoea (often • Diarrhoea • Diarrhea (usually


bloody) • Stomach cramps watery)
• Frequent bowel • Gas • Stomach cramps
movements • Weight loss • Upset stomach
• Lower abdominal pain • Slight fever
• Maintain good hygiene in preparing foods
• Food should be cooked appropriately
• Immunization against rotavirus (children at 6
weeks age)
• Typhoid and polio vaccination
• Public education on the risk of AGE and cross
contamination
• Prophylaxis with bismuth subsalicyclate
• Breastfeeding newborn
Full Blood Count Urinalysis Stool culture BUSE Blood culture

• Increase in WBC • Specific gravity as •Done if: •To check if IV fluid is •To rule out septicemia
(Infection) indicator of hydration •Child appears septic required •Done if - antibiotics are
•Presence of blood or •Done if - features started
mucus in stool suggestive of
•Immunocompromised hypernatremia present
state
•Recent foreign travel
•Diarrhoea not improved
by day 7
•Diagnosis uncertain
Based on :
• Clinical recognition
• Evaluation of its severity by rapid assessment
• Confirmation by appropriate laboratory
investigations (if indicated)
History Taking for Diarrhoea
• Obtain appropriate contact, travel, or exposure
history
• Exposure to contacts with similar symptoms
• Intake of contaminated foods or water
• Child-care center attendance
• Recent travel of patient
• Contact with a person who traveled to a diarrhea-
endemic area
• Use of antimicrobial agents
Clinically determine the etiology of
diarrhoea
• Although nausea and vomiting are nonspecific symptoms,
they indicate infection in the upper intestine.
• Fever suggests 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 diarrhoea.
• Severe abdominal pain and tenesmus indicate involvement
of the large intestine and rectum.
• Nausea, vomiting and absent/low-grade fever with mild to
moderate periumbilical pain and watery diarrhoea indicate
small intestine involvement and also reduce the likelihood
of a serious bacterial infection.
Systemic infection i. Septicaemia
ii. meningitis
Local infections i. Respiratory tract infection
ii. otitis media
iii. hepatitis A
iv. urinary tract infection
Surgical disorders i. Pyloric stenosis
ii. Intussusception
iii. acute appendicitis
iv. necrotising enterocolitis
v. Hirschsprung disease
Metabolic disorder i. Diabetic ketoacidosis
Renal disorder i. Haemolytic uraemic syndrome
Other i. Coeliac disease
ii. cow’s milk protein intolerance
iii. adrenal insufficiency
• Dehydration
• Shock
• Death
Clinical features of shock from dehydration in an infant
Treatment of dehydration and shock
Risk of dehydration :
• Infants (particularly those under 6 months of age
or those born with low birth weight)

• If they have passed ≥6 diarrhoeal stools in the


previous 24 hours

• If they have vomitted ≥3 in the previous 24 hours

• If they have been unable to tolerate (or not been


offered) extra fluids

• If they have malnutrition


Isonatraemic Hyponatraemic Hypernatraemic

The losses of sodium and water are There is a greater net loss of sodium than Water loss exceeds the relative sodium loss
proportional and plasma sodium remains water , leading to a fall in plasma sodium and plasma sodium concentration increases.
within the normal range. (when children with diarrhoea drink large
quantities of water or hypotonic solutions). Usually results from high insensible water
losses (high fever or hot, dry environment)
Water shifts from extra- to intracellular or from profuse, low sodium diarrhoea.
compartments :
1. Increase in intracellular volume > Water shifts from intra- to extracellular
increase in brain volume compartments.
(convulsions)
2. Marked extracellular depletion > a Signs of extracellular fluid depletion :
greater degree of shock per unit of 1. Depression of fontanelle
water loss 2. Reduced tissue elasticity
3. Sunken eyes (less obvious)
More common in poorly nourished infants in More difficult to recognise in an obese
developing countries. infant.

A dangerous form of dehydration (water is


drawn out of the brain > cerebral shrinkage
within a rigid skull) :
1. Jittery movements
2. Increased muscle tone with
hyperreflexia
3. Altered consciousness
4. Seizures‘
5. Multiple, small cerebral
haemorrhages

Transient hyperglycemia occurs in some


patients (self-correcting and does not
require insulin).
Is the child in shock?
(any child with shock go straight to treatment Plan C)

Signs of shock :
Tachycardia
Weak peripheral pulses
Delayed capillary refill time (>2 seconds)
Cold peripheries
Depressed mental state with or without hypotension
OR

you can also use the WHO chart to


assess the degree of dehydration
and then choose the treatment plan
A, B or C, as needed.
Assessment of dehydration according
to WHO classification
Plan C (treat severe dehydration quickly) :
• Start intravenous (IV) or intraosseous (IO) fluid immediately. If patient can
drink, give ORS by mouth while the drip is being set up.

 Initial fluids for resuscitation of shock : 20 ml/kg of NaCl 0.9% or Hartmann


solution as a rapid IV bolus.
 Repeated if necessary until patient is put of shock or if fluid overload is
suspected. Review patient after each bolus.
 Calculate the fluid needed over the next 24 hours : Fluid for rehydration (also
called fluid deficit) + Maintenance (minus the fluids given for resuscitation).
 Fluid for rehydration : percentage dehydration × body weight in grams
 Maintenance fluid (NaCl 0.45 / D5%)
1st 10 kg = 100ml/kg
10-20 kg = 1000 ml/day + 50 ml/kg for each kg above 10 kg
>20 kg = 1500 ml/day + 20 ml/kg for each kg above 20 kg
The cornerstone of management is to reassess the hydration status
frequently (e.g. at 1-2 hourly), and adjust the infusion as necessary.

• Start giving more of the maintenance fluid as oral feeds (e.g. ORS
about 5 ml/kg/hour as soon as the child can drink, usually after 3 to
4 hours for infants, and 1 to 2 hours for older children, this fluid
should be administered frequently in small volumes).

• Generally normal feeds should be administered in addition to the


rehydration fluid, particularly if the infant is breastfed.

• Once a child is able to feed and not vomitting, oral rehydration


according to Plan A or b can be used and the IV drip reduced
gradually and taken off.
If you cannot or fail to set up IV or IO line, arrange for the child to be sent to
the nearest centre that can do so immediately. Meanwhile as arrangements
are made to send the child (or as you make further attempts to establish IV or
IO access,
Other indications for intravenous therapy :
• Unconscious child

• Continuing rapid stool loss (>15-20 ml/kg/hour)

• Frequent, severe vomitting, drinking poorly

• Abdominal distension with paralytic ileus, usually caused by some antidiarrhoeal


drugs (e.g. codeine, loperamide) and hypokalaemia

• Glucose malabsorption, indicated by marked increase in stool output and large


amount of glucose in the stool when ORS solution is given (uncommon)

IV regime as for Plan C but the replacement fluid volume is calculated according to
the degree of dehydration. (5% for mild, 5-10% for moderate dehydration)
Management of hypernatraemic dehydration :

• Can be particularly difficult.

• ORS can be used to rehydrate hypernatraemic children with


clinical dehydration.

• If IV fluids are required, a rapid reduction in plasma sodium


concentration and osmolality will lead to a shift of water
into cerebral cells and may result in seizures and cerebral
oedema. Therefore, reduction in plasma sodium should be
slow.

• The fluid deficit should be replaced over at least 48 hours


and the plasma sodium measured regularly, aiming to
reduce it at <0.5 mmol/L per hour.
Indications for admission to hospital :
• Moderate to severe dehydration

• Need for intravenous therapy

• Concern for other possible illness or uncertainty of diagnosis

• Patient factors (e.g. young age, unusual irritability/drowsiness,


worsening symptoms)

• Caregivers not able to provide adequate care at home

• Social or logistical concerns that may prevent return evaluation if


necessary
Non pharmacological / nutritional strategies :

• Undiluted vs diluted formula


no dilution of formula is needed for children taking milk
formula

• Soy based or cow milk-based lactose free formula


not recommended routinely, indicated only in child with
suspected intolerance
Pharmacological agents :
• Antimicrobials
 Antibiotics should not be used routinely. They are reliably helpful only in children with bloody
diarrhoea, probable shigellosis, and suspected cholera with severe dehydration.

• Antidiarrhoeal medications
 The locally available diosmectite has been shown to be safe and effective in reducing stool
output and duration of diarrhoea. It acts by restoring integrity of damaged intestinal
epithelium, also capable to bind to selected bacterial pathogens and rotavirus. Other
antidiarrhoeal agents like kaolin (silicates), loperamide (anti-motility) and diphenoxylate
(anti-motility) are not recommended.

• Antiemetic medication
 Not recommended, potentially harmful.

• Probiotics
 Probiotics has been shown to reduce duration of diarrhoea in several randomized controlled
trials. However, the effetiveness is very strain and dose specific. Therefore, only probiotic
strain or strains with proven efficacy in appropriate doses can be used as an adjunct to
standard therapy.

• Zinc supplements
 It has been shown that zinc supplements during an episode of diarrhoea reduce the duration
and severity of the episode and lower the incidence of diarrhoea in the following 2-3 months.
WHO recommends zinc supplements as soon as possible after diarrhoea has started. Dose up
to months of age is 10 mg/day, and age 6 months and above 20 mg/day, for 10-14 days.
• In developing countries,
ORS saves the lives of millions of children
worldwide each year.

• In developed countries,
ORS is effective in most, but IV fluid is
required for shock, ongoing vomitting or
clinical deterioration.
Electrolyte imbalance
Paediatric Fluid and Electrolyte
Guideline
• Paediatric Protocol for Malaysian Hospitals ,
3rd ed.
Sodium disorder
Hypernatriemia
• Defined as serum Na+ > 150 mmol/L
• Moderate = 150-160 mmol/L ; Severe = >160
mmol/L
• Due to :
Water loss in excess of sodium
Water deficit
Sodium gain
• Clinical sign of Hypernatremia dehydration
Irritability
Doughy skin
Ataxia, tremor, hyperreflexia
Seizure
Reduce awareness, coma
• Look of sign of hypernatremia dehydration
• Shock occurs late
Management – refer to paediatric
protocol
• Treat underlying cause
• Shock – bolus resuscitation with 0.9% NS
• Avoid rapid correction – cerebral edema
• Aim of correction – serum Na+ falls not more
than 0.5 mmol/L/hr
• Repeat BUSE 6 hourly
• Check calcium and glucose level
Hyponatriemia
• Definition : serum Na+ < 135 mmol/L
• Causes
Administration of hypotonic fluid – D5%
GI loss
Adrenal insufficiency
Impaired water secretion – SIADH
Cerebral salt wasting
Renal tubular disorder
Psychogenic polydipsia
Diuretics
• Symptomatic < 125 mmol/L
 apathy, nausea, vomiting, weakness, lethargy, malaise
Headache
Muscle cramps, hyperreflexia, restlessness
Convulsion
• Complication
 seizure , coma, permanent brain damage , respiratory
arrest
Hyponatraemia encephalopathy (EMERGENCY!)
• Diagnosis – based on osmolality ( Serum Osm = 2(Na) =
Glucose + Urea)

1. Normal osmolality (275-295) = isotonic


pseudohyponatriemia
2. High osmolality ( > 295) = hypertonic
hyponatraemia
3. Low osmolality (< 275) = hypotonic
hyponatremia
• Management
 fluid restriction
Replace Na ( mmol of sodium required = [(135- Na
level) x 0.6 x BW(kg)]
Correction – not more than 0.8 mmol/day ( to
prevent osmotic demyelination syndrome)
Potassium Disorder
The daily potassium requirement is 1-2mmol/L
Normal values of potassium are :

Birth – 2 weeks : 3.7 – 6.0mmol/L


2 weeks – 3 months : 3.7 – 5.7 mmol/L
3 months and above : 5.5- 5.0mmol/L

Hyperkalemia is defined as K > 5.5mmol/L


• > 98 % of total potassium is intracelluar
• Potassium disorder are more significant than
sodium disorder
• Hyperkalemia is more cardiac toxicity than
hypokalemia. Fortunately, hyperkalemia is less
prevalent
• Persistent hyperkalemia require impaired
urinary potassium excretion
Clinical Manifestation
• Patients are always without significant
manifestations until serum K > 6.5mEq/L
• Symptoms are usually limited to :
- Muscle – weakness (legs –
arms)
- Cardiac conduction
abnormalities - various ECG
changes, arrhythymias
Typical progression in ECG Changes

Serum ( K ) 5.5 – 6.5 6.5-8.0 8.0-10.0 >10


(mEq/L)
Typical ECG Tall, peaked T QRS widens P waves flatten “Sine wave”
changes waves and dissapear
Bundle branch (blending of
block QRS complex
with T wave)
AV block
Etiologies

Increased oral intake Increase released from Decreased urinary


the cell excretion

• IV bolus of potassium • Metabolic acidosis • Adrenal


penicillin • Insulin deficiency, insuficiency
Hyperglycemia/ • Spironolactone
hyperosmalality • Reduced distal
• Tumor lysis delivery of sodium
syndrome and water
• Drugs : Beta • Acute and chronic
blockers, kidney disease
succinycholine
Pseudohyperkalemia
• Occurs when K out of the cells either during or
after the blood is drawn
• Can be due to:
- Blood drawing technique
- Hematologic disorders
Diagnostic Evaluation
Step 1 - Exculde pseudohyperkalemia

Step 2- Evaluate renal function and medication


list

Step 3 - Evaluate for hypoaldosteronism by


checking renin, aldosterone
Treatment
• Treatment of underlying cause

• Therapies that are rapidly acting, but trasient

• Therapies that remove potassium from the


body
Hypokalemia
• Patients are almost always without
manifestations until serum (K) <3.0mEq/L
• Symptoms are usually limited

Muscle – weakness (legs –arms),


cramps, ileus and rhabdomyolysis

Cardiac conduction abnormalities


Etiologies

Decreased oral Increased loss


intake
Increase Translocation
into the call • Vomitting
Daily intake is • Diarrhea
normally 1-2mmol/l • Diurectics
• Exogenous insulin • Renal tubular
• Salbutamol acidosis
• Alkalosis • Hypomagnesium
• Hypothermia
water

Aldosterone
Na

Hypokalemia
Vomiting Cl

Metabolic
H
alkalosis

K
ECG changes of hypokalemia
These occur when K < 2.5mmol/l
• Prominent U wave
• ST segment depression
• T wave inversion
• Prolonged PR interval
• Sinoatrial block
Treatment
Urgency of repletion is dependent upon
• Rate at which hypokalemia is develop
• Presence of high co-morbidity

Treatment should involve both addresing


underlying etiology, and repleting potassium

Oral KCL/ IV KCL