SEMINAR 6

ACUTE DIARRHOEA
AND VOMITING
ACUTE DIARRHOEA
DEFINITION
EPIDEMIOLOGY
C L A S S I F I C AT I O N
CAUSES
PAT H O P H Y S I O L O G Y
SIGNS AND SYMPTOMS
P H Y S I C A L E X A M I N AT I O N
A S S E S S M E N T O F H Y D R AT I O N
C O M P L I C AT I O N
I N V E S T I G AT I O N
MANAGEMENT
DEFINITION
• The passage of 3 or more loose or liquid stools per day (or more frequent
passage than is normal for the individual).

• Frequent passing of formed stools or breastfed babies pass loose, ‘pasty’ stools
is not diarrhoea.

• Can cause rapid fluid and electrolyte loss through stools. The volume of fluid
loss can vary from 5ml/kg/day to ≥ 200 ml/kg/day.
Infants have higher risk to be dehydrated!

• The greater the surface area to weight ratio, the greater the insensible water
losses (15-17ml/kg/day)
• Higher basal fluid requirements (100-120ml/kg/day)
• Immature renal tubular reabsorption
• Unable to obtain fluid for themselves when thirsty
EPIDEMIOLOGY
• Second leading cause of death in children less than 5 years old
• Kills around 525,000 children every year
• WHO: 1.7 billion cases of childhood diarrhoeal disease globally every year
• Diarrhoea due to infection is widespread throughout developing countries
• In low income countries, children less than 3 years old had an average of 3
diarrhoeal episodes every year
• In Malaysia, a study conducted estimates at least 13 million episodes of acute
diarrhoea annually
Incidence of acute diarrhoea by sociodemographic profile
• By age, the four-weeks incidence of acute diarrhoea was the highest among
young adults aged 20-29 years old
• By educational level, those with tertiary education ranked the highest level of
incidence
• Those residing in rural areas had a higher level of incidence of acute diarrhoea
than urban areas
• Both gender had the same level of incidence
 CLASSIFICATION
• Clinical types of diarrhoea:
Acute diarrhoea Persistent diarrhoea Chronic diarrhoea

1) Acute Watery Diarrhoea Lasts more than 14 days • Last more than 4 weeks
(including Cholera) • Commonly a result of
- lasts several hours or intestinal disease or
days disorder
- Celiac disease
2) Acute Bloody Diarrhoea - Ulcerative colitis
- presence of blood and - Crohn’s disease
mucous in stools
- also called dysentery
CAUSES
• Viral – rotavirus, Norwalk virus, astrovirus, adenovirus
• Bacterial – E. coli, Shigella, Salmonella, V. cholera,
Campylobacter jejuni
• Parasite – Giardia, Cryptosporidium, Entamoeba histolytica
• Fungal – Candida, Aspergillus, Coccidioidomycoses
• Antibiotics – Ampicillin, Clindamycin
• Food poisoning
• Parenteral diarrhoea – inflammation at the other sites of the body causing
diarrhoea (e.g. UTI)
PATHOPHYSIOLOGY
There are numerous causes of diarrhoea, but in almost all cases, this disorder is a
manifestation of one of the four basic mechanisms
1. Osmotic Diarrhoea
2. Secretory Diarrhoea
3. Inflammatory and Infectious Diarrhoea
4. Diarrhoea Associated with Deranged Motility
 OSMOTIC DIARRHOEA
• 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 diarrhoea
will result.
• A distinguishing feature of osmotic diarrhoea is that it stops after the patient is fasted or stops
consuming the poorly absorbed solute
Ingestion of a poorly absorbed substrate:
• The offending molecule is usually a carbohydrate or divalent ion. Common examples include
mannitol or sorbitol.
Malabsorption:
• Inability to absorb certain carbohydrates is the most common deficit in this category of diarrhoea,
but it can result virtually any type of malabsorption. A common example of malabsorption,
afflicting many adults humans and pets is lactose intolerance resulting from a deficiency in the
brush border enzyme lactase. In such cases, a moderate quantity of lactose is consumed (usually as
milk), but the intestinal epithelium is deficient in lactase, and lactose cannot be effectively
hydrolysed into glucose and galactose for absorption. The osmotically-active lactose is retained in
the intestinal lumen, where it "holds" water.
SECRETORY DIARRHOEA
• Diarrhoea occurs when secretion of water into the intestinal lumen exceeds absorption.
• (e.g.) Vibrio cholerae produces cholera toxin  strongly activates adenylyl cyclase 
prolonged increase in intracellular concentration of cyclic AMP within crypt enterocytes 
prolonged opening of the chloride channels  uncontrolled secretion of water. Additionally,
cholera toxin affects the enteric nervous system, resulting in an independent stimulus of
secretion.
• 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 diarrhoea that is often lethal.
• In addition to bacterial toxins, a large number of other agents can induce secretory diarrhoea
by turning on the intestinal secretory machinery, including:
 Laxatives
 A broad range of drugs (e.g. some types of asthma medications, antidepressants, cardiac
drugs)
 Certain metals, organic toxins, and plant products (e.g. arsenic, insecticides, mushroom
toxins, caffeine)
INFLAMMATORY AND INFECTIOUS DIARRHOEA
• Disruption of the epithelium of the intestine due to microbial or viral pathogens is a very
common cause of diarrhoea.
• Destruction of the epithelium  exudation of serum and blood into the lumen and
widespread destruction of absorptive epithelium  inefficient absorption of water 
diarrhoea.
• Examples of pathogens frequently associated with infectious diarrhoea include:
 Bacteria: Salmonella, E. coli, Campylobacter
 Viruses: rotaviruses, coronaviruses, norovirus
 Protozoa: Coccidia species, Cryptosporidium, Giardia
DIARRHOEA 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 than accelerate transit time could decrease absorption,
resulting in diarrhoea even if the absorptive process was proceeding properly.
 In Summary: PATHOPHYSIOLOGY OF ACUTE DIARRHEA
Basis of all diarrhoea is the failure of normal absorption of water and electrolytes by the intestines, resulting in net loss of water and electrolytes in the stool
SECRETORY OSMOTIC INVASIVE MIXED SECRETORY-OSMOTIC

An active secretory state (secretion An osmotic forces exerted by Mucosal invasion / inflammation of Causes :
of fluid and electrolytes) induced in unabsorbed luminal solutes to drive the intestine. Rotavirus infection
the enterocytes & reduced water into the gut. Causes :
absorption. Causes : 1. Bacterial invasion : Pathophysiology :
Causes: 1. Lactose intolerance (d/t lactase • Shigella sp.
1. Intestinal infections deficiency) • Campylobacter
(gastroenteritis) 2. Pancreatic insufficiency (cystic • Toxin-producing E.coli Invade, replicate and release
 Viral : rotavirus, norovirus, fibrosis) • Salmonella sp. enterotoxin in intestinal epithelium
adenovirus 3. Osmotic laxatives cells
 Bact : V. cholera 4. Excessive intake of sorbitol and Pathophysiology :
 Parasitic : giardia, amoeba mannitol
Villous atrophy, Damage to
Pathophysiology :
Pathophysiology : flattened transport
mechanism
Pathogen directly invade the intestine
Disrupts the
Lack of enzymes / osmotic pull of water absorptive Alteration in the
Enterotoxin released Produce cytotoxin
in the lumen function water &
electrolytes fluxes
Stimulate CAMP (Affect secretory Nutrients/solutes cannot be Cause mucosal erosion and destruction across
solutes stay
system) digested into smaller form of blood vessels enterocytes
in the lumen
Absorption of Na+ by microvilli was Nutrients/solutes cannot be absorbed
(stays in the gut lumen) Loss of fluid and blood into the Secretory diarrhoea
blocked // water and Cl- secreted into Osmotic
lumen intestinal lumen
Increases intestinal luminal osmolality diarrhoea
Watery stool dysentery
Influx of water & electrolytes into
intestinal lumen
Diarrhoea
HISTORY TAKING & PHYSICAL EXAMINATION
History taking and physical examination serve 2 vital functions:
1. Differentiating causes of vomiting and diarrhoea in children
2. Estimating the degree of dehydration

In some cases, the history and physical examination can also aid in determining
the type of pathogen responsible.
TYPE OF STOOL
According to Bristol stool chart
 Physical Examination

• General: Weight, ill appearance, level of alertness, lethargy, irritability

• Presence or absence of tears, dry or moist mucous membranes, and whether the
eyes appear sunken.
• Cardiovascular: Heart rate and quality of pulses
• Respiratory: Rate and quality of respirations (The presence of deep, acidotic
breathing suggests severe dehydration.)
 Signs of Dehydration

• Lethargic or unconscious
• Sunken eyes & tearless
• Sunken anterior fontanelle
• Reduced skin turgor
• Dry mucosa
• Reduced capillary filling time (>2s)
• Oliguria
• Tachycardia , tachypnoea , hypotension
• Sudden loss of weight
 ASSESSMENT OF DEHYDRATION
• Child with dehydration needs acute
intervention to ensure adequate tissue
perfusion.
• The most accurate measure of dehydration is
degree of weight loss.
• All calculations in fluid therapy are only
approximations.
• Especially true for the assessment of
percentage dehydration.
• History and examination can be used to
assess the degree of dehydration
Convulsion: Loss of water and sodium
COMPLICATIONS
• Severe Dehydration with hypovolemic shock
• Acute kidney injury
• Electrolyte imbalance : Hyponatremia, hypokalemia
• Metabolic acidosis
• Hemolytic uremic syndrome
• Secondary lactose intolerance
INVESTIGATION
1. Blood test
Full Blood Count White Blood Cell
Hemoglobin
Platelet
Hematocrit
Renal Profile Urea and nitrogen
Creatinine
Electrolytes
Arterial Blood Gas pH, pCO2, pO2, HCO3
Blood Culture and Sensitivity Salmonella typhi
Escherichia coli

2. Stool examination
- Microscopic examination
- Culture and sensitivity
MANAGEMENT
• PLAN A: Treat diarrhoea at home
• PLAN B: Treat dehydration with ORS
• PLAN C: Treat severe dehydration quickly
 Plan A: Treat diarrhoea at home
Give extra fluid Continue feeding When to return (to
clinic/hospital)

• Breastfeed frequently and for longer at each • Breastfed infants : continue When the child :
feed breastfeed • Not able to drink or
• Exclusively breastfed : give Oral Rehydration • Formula fed infants : breastfeed or drinking
Salt (ORS) or cooled boiled water in addition continue usual formula poorly
to breastmilk immediate after rehydration • Becomes sicker
• Not exclusively breastfed : ORS, food-based • Children on semi-solid or • Develops a fever
fluids, or cooled boiled water (give one or solid foods : continue receive • Has blood in stool
more) usual food (avoid simple
sugar food as osmotic load
How to give ORS in addition to usual fluid can worsen diarrhea)
intake :
Up to 2 years 50 to 100ml
old after each loose
stool
2 years old or 100 to 200ml
more after each loose
stool
Plan B: Treat dehydration with ORS
• Recommended amount of ORS over 4-hour period :
Age Up to 4months 4-12months 12months-2yrs 2-5yrs
Weight Less than 6 kg 6 to 10 kg 10 to 12 kg 12 to 19 kg
Volume 200-400 ml 400-700 ml 700-900 ml 900-1400 ml

• After 4hours :
- Reassess the child and classify for dehydration
- Select appropriate plan to continue treatment (Plan A, B or C)
- Begin feeding the child
How to give ORS solution?
Give frequent small sips from cup or spoon
If child vomits, wait 10 minutes, then continue but
more slowly (e.g. a spoonful every 2-3 minutes)
Continue breastfeeding whenever the child wants
Plan C: Treat severe dehydration quickly
• Start intravenous (IV) or intraosseous (IO) fluid immediately. If patient can drink, give
ORS by mouth while drip is being set up.
• Initial fluid for resuscitation of shock :

20ml/kg of 0.9% Normal Saline (NS) or Hartmann’s Solution as rapid IV bolus

• Repeated if necessary until patient is out of shock or if fluid overload is suspected.
Review patient after each bolus.
• Calculate fluid needed over next 24 hours :

Fluid for rehydration (fluid deficit) + maintenance fluid

Fluid for rehydration :

Percentage of dehydration X body weight in gram

Maintenance fluid :
Weight Total fluids Infusion rate
First 10kgs 100ml/kg 4mls/kg/hr
Subsequent 10kg 50ml/kg 2mls/kg/hr
All additional kg 20ml/kg 1ml/kg/hr
• Reassess the hydration status frequently (e.g. at 1-2hourly), and adjust infusion as
necessary.
• Start giving more of the maintenance fluid as oral feed e.g. ORS as soon as the child can
drink
• Classify dehydration, then choose most appropriate plan (A,B or C) to continue treatment
Example :
A 6 kg child is clinically shocked and 10% dehydrated as a result of gastroenteritis. Calculate
fluid therapy?
1. Total fluid deficit:
% of dehydration x body weight (kg) x1000ml
=10/100 x 6kg x 1000ml
=600ml
2. Initial therapy (shock resuscitation) :
20ml/kg for shock
=20ml/kg x body weight(kg)
=20ml/kg x 6kg
=120ml
3. Fluid therapy for next 24 hours :
a) Remaining fluid deficit : Total fluid deficit – fluid of shock resuscitation
=600ml – 120ml
=480ml >>20ml/24hrs

b) Fluid maintenance : First 10kg : 100ml/kg x body weight (kg)

=100ml/kg x 6kg
=600ml >> 25ml/24hrs

Other management :
 Antibiotics if indicated : e.g. Salmonella gastroenteritis (amoxicillin, ceftriaxone),
Shigellosis (azithromycin, ceftriaxone), Cholera (doxycycline, azithromycin)
 Do not give antiemetics, anti-diarrhea, antimotility
 Zinc supplements during acute episode to reduce duration and severity of episode
 Correction of electrolyte imbalance if any
 Monitoring of vital signs
VOMITING
DEFINITION
CAUSES
H I S T O R Y TA K I N G
P H Y S I C A L E X A M I N AT I O N
I N V E S T I G AT I O N
MANAGEMENT
C O M P L I C AT I O N
DEFINITION
• Forceful ejection of gastric contents through the mouth
 HISTORY TAKING
• Onset
• Frequency
• Character – forceful or effortless
• Colour, Contents and amount of vomitus - undigested food/bilious/blood
• Nature : Projectile/non-projectile (projectile vomiting suggests intracranial pathology)
• Pattern – after meal, only with certain food, primarily in the morning/night
• Aggravating or relieving factors
• Associated symptoms – fever, abdominal pain, diarrhoea, high pitch cry, weight loss,
headache
• History of eating outside, recent travelling, history of head trauma or family members
having similar symptoms
 PHYSICAL EXAMINATION
VITAL SIGNS
– Fever : signs of infection (gastroenteritis, meningitis, urinary infection)
– Tachycardia and hypotension : signs of volume loss

GENERAL EXAMINATION
– altered level of consciousness due to dehydration or CNS causes
– Pale, jaundice, weight loss (cachexic)
– Look for any skin rashes – indicates food allergy or viral infection
– Hydration status : sunken eyes, skin turgor, prolonged capillary refill time, dry mucous
membrane, sunken fontanelle
– Assess the anterior fontanelle (sunken or bulging)
ABDOMINAL EXAMINATION
– Inspection : abdominal distension
– Palpation : tenderness, guarding or rigidity
– Auscultation : hyperactive or absent bowel sound

CNS EXAMINATION
– Signs of increase ICP : assessment of bulging fontanelle, papilledema, presence of
focal neurological signs

Growth parameters and signs of development progress

 INVESTIGATION
• Full blood count : evidence of infection
• Blood culture & sensitivity
• Blood urea & serum electrolytes (BUSE) : renal function/ hydration status/ electrolyte
abnormality
• ESR & CRP
• Urinalysis / urine culture: in suspected UTI
• Blood glucose: hypoglycaemia/ hyperglycaemia
• Liver function test : in suspected hepatitis/ metabolic disorder
• CSF analysis/culture : meningitis
• Stool C&S : occult blood suggests intestinal mucosal disease; viral or bacterial
pathogen detection
IMAGING
– Abdominal X-ray – for intestinal obstruction
– Abdominal ultrasound – to detect any mass, to confirm CHPS
– CT scan brain – if clinical history and PE is suspected of increased ICP
– Contrast study (Barium study) – for GERD, congenital hypertrophy pyloric
stenosis, other obstructive lesion in small and large bowel

ENDOSCOPY
– OGDS – atresia
 MANAGEMENT
 Maintain daily fluid requirement and replace the concurrent fluid losses
 Mild to moderate dehydration, able to tolerate orally: ORS, monitor hydration status
 Persistent vomiting or moderate to severe dehydration: IV fluid replacement
 Antiemetics: Reduce the risk of dehydration in children who vomit repeatedly
 Maintain nutritional needs (next slide)
 Treat underlying causes
 Prevention: Wash hands frequently, keep sick children out of school or daycare
 Children who are vomiting but are not dehydrated can continue to eat a regular diet as
tolerated. Dehydrated children require rehydration (replacement of lost fluid, ORT).
– Infants
Continue breastfeeding. Oral rehydration solutions (e.g. Pedialyte) are not usually
needed for infants who exclusively breastfeed, because breastmilk is more easily
digested.
If infant vomits immediately after nursing: breastfeed more frequently and for a
shorter time. (e.g. breastfeed every 30 minutes for 5 to 10 minutes)
– Older infants and children
Continue to eat, if desired. Remember, it is common for children to have little or no
appetite during a vomiting illness.
Monitor signs of dehydration and do not force the child to eat, especially during the
first 24 hours. Encourage the child to drink fluids.
The best fluids are the commercially prepared oral rehydration solutions (e.g.
Pedialyte). Other fluids, including water, diluted juice, or soda, can be given in small
quantities.
COMPLICATION
 Dehydration and shock
 Electrolyte imbalance (hyponatremia, hypokalaemia, hypochloraemia, metabolic
alkalosis)
 Aspiration of stomach content  aspiration pneumonitis/ pneumonia.
 Damage to teeth enamel: gastric acid that enters mouth, it erodes tooth enamel
 Mallory-Weiss tear: caused by violent/severe vomiting. Presents with haematemesis
and abdominal pain.