DIARRHOEAL DISEASE IN CHILDHOOD

DR. EKE
GASTROENTEROLOGY FIRM
DEPT. OF PAEDIATRICS, UNEC

DEFINITIONS:
• An intestinal dz characterised by abnormal fluidity and frequency of
faecal evacuations, generally the result of ↑ed colonic motility.

• Diarrhoea can also be defined as an increase in the number and volume

of stools with an alteration in the consistency, mainly due to increased
water content.

• Passage of watery or loose stools of 3 or more times in a 24 hours

period after infancy is generally considered abnormal.

• For exclusively breast fed infants, who normally pass several soft semi -
liquid “pasty” stools each day, it is practical to define diarrhoea as an
↑e in stool frequency or liquidity considered abnormal by the mother.
EPIDEMIOLOGY:
• The infectious agents that cause diarrhoea are spread by faeco-oral route,
which is facilitated by poor personal and food hygiene and lack of
portable water.
• Major cause of morbidity and mortality in children especially in the less
developed countries of the world including Nigeria.
• Account for a large proportion (18%) of childhood deaths, with an
estimated 1.8million deaths per year globally. The WHO suspects that
there are >700million episodes of diarrhoea annually in children < 5yr. of
age in developing countries. While global mortality may be declining, the
overall incidence of diarrhoea remains unchanged at about 3.2episodes
per child.

• Diarrhoea is a leading cause of malnutrition.

• Many children suffer from repeated episodes of diarrhoea which lead to

malnutrition as a result of anorexia, inadequate calorie and protein
intake, and ↑ed catabolism from infection.
• Malnutrition on its own impairs defence mechanism, predispose to gut infection and gut
mucosal damage with subsequent diarrhoea.

• Malnutrition: associated with an ↑ed frequency of enteral infections, increased bile acid
synthesis, pancreatic enzyme output, and disaccharidase activity; altered
motility, and changes in the intestinal flora- all of which may cause diarrhoea.

• Significantly malnutrition increases several fold the risk of diarrhoea & associated
mortality. Each episode of diarrhoea deprives the child of the nutrition necessary for
growth. As a result diarrhoea is a major cause of malnutrition, & mal-nourished children
are more likely to fall ill from diarrhoea. There is an inverse relationship b/w
appropriate, safe, complimentary feeding & severity of diarrhoea.

. Also risk of diarrhoeal disease deaths are particularly higher in micronutrient deficiency
esp. vitamin A and zinc.

• Acute diarrhoea kills by causing dehydration, which leads to hypovolaemia and

metabolic acidosis.
• With the advent of ORT the mortality due to diarrhoea has changed in many parts of the
world.
• Early & repeated episodes of childhood
diarrhoea during periods of critical
development especially when associated with
malnutrition, co- infections, and anaemia may
have long term effects on linear growth as
well as physical and cognitive functions.
AETIOLOGY
1. Infectious Agents
Viruses:
- Rotavirus (Reoviridae): Commonest cause of severe dehydrating acute watery
diarrhoea in under 5 children.
- Astroviruses
- Caliciviruses e.g. Norwalk and Norwalk - like agents
- Adenoviruses 40 & 41
- Hepatitis A
- Parvoviruses

Bacteria:
- Shigellae: (Sh. Sonnei, flexneri, dysenteriae and boydii). Most important cause
of acute bloody diarrhoea or dysentery.
- Salmonellae
- Escherichia coli (ETEC, EPEC,EIEC, EHEC)
- Staphylococcus aureus
- Yersinia enterocolitica
- Campylobacter jejuni/coli
- Clostridium perfringens and difficile
- Vibrio cholerae 01
Parasites:
(a) Protozoa
- Giardia lamblia
- Entamoeba histolytica
- Crytosporidium parvum  zoonotic protozoan associated with acute watery
diarrhoea or persistent diarrhoea in severely malnourished and immuno-
compromised children.

(b) Helminths:
- Enterobius
- Strongyloides stercoralis
- Trichuris trichuria

II. Non- Infections

- Antibiotic therapy: Altered bowel flora & abnormal colonisation; antibiotic
associated colitis and pseudo-membranous colitis in Clostridium difficle.

- Extra- intestinal infections (Parenteral diarrhoea): – This is diarrhoea which is not

associated with bowel infection, but is an alimentary response to some conditions,
often an infection elsewhere in the body. UTI, URTI (esp. otitis media), acute pyelitis and
malaria are at times associated with diarrhoea. The mechanism remains obscure.
- Diet: over-feeding in young infants, fruit juices (high in fructose/sorbitol) 
osmotic diarrhoea, intestinal irritants (spices and foods high in roughage) etc.

- Allergic Diarrhoea: protein allergy is more common in infants under 12 months of

age, who may experience mild to severe colitis.

- A family history of atopy is common in infants with protein allergy. Other forms of
allergic diarrhoea include celiac-like syndrome.

- Chronic Non- Specific Diarrhoea: Commonest cause of loose stools in thriving

children. It clears spontaneously at about 3½ year of age (usually coincident with
toilet training). No organic dz is discoverable. Possible causes include
abnormalities of bile acid absorption in the terminal ileum, incomplete
carbohydrate absorption (excessive fruit juice ingestion seems to worsen the
condition), and abnormal motor function.

- Excessive purgatives
- Protein energy malnutrition

- Primary lactose intolerance

- Psychosocial, irritable bowel syndrome

- Surgical – stenosis, mal-rotation, blind loop

etc
Risk Factors
- Young Age: infants and toddlers get diarrhoea more frequently than adults.
This is mainly b/c they have never b/4 encountered the common causative
organisms and had the chance to build up an immunity.

- Gender: in the 1st few months of life boys are more vulnerable than girls to
diarrhoeal dz.

- Seasonal Patterns: In tropical countries including Nigeria, viral diarrhoea

tends to occur throughout the year, with an increase during the drier, cooler
mouths while bacterial diarrhoea tend to occur more during the warmer
rainy season. ? Rotavirus season and possibility of increased diarrhoeal cases
in the drier cooler months of the year.
 Risk Factors Continued :
- Failure to breastfeed /feeding bottles
- Malnutrition
• Immuno-suppressive/deficiency states
• Measles
• HIV/AIDS
• Zinc deficiency
- Poor personal hygiene
- Poverty
- Lack of clean water
- Contaminated food supplies
- Over – crowding esp. in urban slums
- Illiteracy/ignorance

Pathophysiological Mechanisms of Diarrhoea:

There are several mechanisms which may be operative in acute diarrhoea.
• Stimulation of intestinal secretions- toxin induced secretary diarrhoea e.g.
V. cholera, ETEC. Bacterial pathogens after ingestion proliferate and
elaborate neurotoxins within the intestinal lumen which act on the
morphologically intact mucosa.
These entero-toxins stimulate receptors at the intestinal mucosal surface and induce the
production of excess c - AMP by stimulating the action of adenyl- cyclase. c-AMP inhibits the
influx of NaCl and H20 into the villous cells and also induces secretion of NaCl and water by
the crypt cells. The net result of these 2 changes is the secretion of large amounts of water
and electrolytes in the intestinal lumen. This process of secretion of fluid and electrolyte and
thus diarrhoea persists even during fasting.
enterotoxin
ATP C-AMP
adenyle cyclase

Na+ Cl -
H20

Villus Tip
Blocks Influx
C-
AMP Na+
Cl-
Stimulates H20
secretion

Crypt

Figure 1: Pathogenesis of Diarrhoeal Stool in Enteric Infection

ii. Mucosal adherence with local cytopathic effect e.g. enteroadherent E. Coli or
EPEC, G. lamblia, cryptosporidium. These organisms adhere tightly to the
mucosa and cause effacement of the microvilli without invading the microvilli.

ii. Mucosal invasion e.g. Shigella, EIEC, campylobacter, salmonella. These agents
invade and destroy the mucosal epithelial cells resulting in shedding of the cells
with formation of micro-ulcers and overlying bloody exudates. The stool
usually contains blood, mucus and leucocytes. Rotavirus replicates within the
villous epithelium and causes patchy mucosal damage.

ii. Increase in the osmolality of the intestinal luminal content (osmotic diarrhoea):
occurs following ingestion of osmotically active substances e.g. lactose by
children with lactase deficiency. Other causes include ingestion of non-
absorbable solutes such as lactulose or in laxative abuse. In osmotic diarrhoea,
there is no leucocytes in the stool unlike in secretory diarrhoea, the diarrhoea
stops with fasting. Other mechanisms which operate in the non-infectious
diarrhoea include:
- Alteration in intestinal motility

- Inhibition of active transport in the colon (congenital defects)- rare

and give rise to very watery diarrhoea from birth.
CLINICAL FEATURES
1. Diarrhoea

2. Other relevant features include:

- Prodromal illness with URT symptoms is common with viral

pathogens.

- Vomiting often common, may precede the diarrhoea.

- Fever.

- Abdominal pain, blood and mucus in the stool suggest invasive

organisms.

- Urine output: no urine passed for several hours is suggestive of

severe dehydration.

CLINICAL TYPES OF DIARRHOEA

- Acute Diarrhoea (Gastro-Enteritis) - commonest type of diarrhoea.
The main danger is dehydration/electrolyte imbalance
- Acute bloody Diarrhoea (Dysentery)
* The diarrhoea with visible blood in the stool
* The main dangers are intestinal damage, sepsis and malnutrition.
Dehydration may occur. Common agents include: Shigella, Campylobacter
Jejuni, EIEC and Salmonella.

- Persistent Diarrhoea- applies to diarrhoea (3 or more stools) that lasts 14 days or

longer. The main danger is malnutrition and serious non-intestinal infection;
dehydration may occur. Persistent diarrhoea may be associated with enteropathy,
with impaired mucosal healing and diminished digestive and absorptive capacity.
- Malabsorption or maldigestion results. In developing countries, persistent
diarrhoea is most common in children younger than two years of age, and
especially in children under one but can occur in older children.
- In developing countries persistent diarrhoea usually follows an acute episode of
diarrhoea and typically is associated with serial enteric infections without time to
recover between episodes.
- Children are at risk of malnutrition and often have intercurrent illnesses such as
respiratory infections.
- In developed countries, children are less likely to be exposed to serial enteric
infections.
• Among them chronic diarrhoea is more likely
to be caused by underlying disease, such as
celiac dx or food allergy.
• However, enteric infections (particularly in
immunocompromised patients), malnutrition,
and dietary factors (eg. Excessive
consumption of juice or with holding feeding
during diarrhoea and delaying in returning to
normal feeding), play a role in some cases.
- Chronic Diarrhoea- applies to diarrhoeal
episodes which have lasted more than 4 weeks
for which no known cause can be found and
which does not respond to specific or non-
specific form of tx.

- Toddler’s Diarrhoea- means recurrent episodes

of mild to moderate diarrhoea of variable
duration in toddlers, for which no cause can be
found and without associated constitutional
symptoms or nutritional impairment.
INVESTIGATIONS
1) STOOLS May confirm the diagnosis &
clues to’ the aetiology. M/C/S : -
Mucus, blood, leucocytes, parasites
- Faecal leucocytes: indicative of bacterial colonic mucosal
invasion.

Stool biochemistry- pH estimation & tests for sugars or reducing sugars

as in lactose intolerance.

2) FBC + Blood film for MP

3) S E U Cr

MANAGEMENT
The management of each type of diarrhoea should prevent or treat the main dangers
that each clinical type presents.

General principles include:

Assessment for dehydration, bloody diarrhoea, persistent diarrhoea, malnutrition,

severe non-intestinal infections e.g. pneumonia, sepsis, malaria. In addition to
institution of appropriate tx plan and regular re-assessment of the patient.
II. Enhancement of Control of Diarrhoeal Disease (CDD) through a combined
prevention and tx strategy incorporating rotavirus vaccine; new low- osmolality
formulations of ORS, and Zinc supplementation during diarrhoea episodes.

III. Use of probiotics in selected cases.

Metabolic consequences of Acute Diarrhoeal disease

1. Dehydration = larger BSA/ body weight ratio; higher body water content per
unit body weight, higher BMR. Also, the malnourished subjects are more at risk
of having dehydration following diarrhoea.
2. Electrolyte imbalances
3. In severe cases: vascular collapse, shock, metabolic acidosis
4. Effect of the on nutrition
5. Effect of the infection on the body’s metabolism

ANTIBIOTIC THERAPY
- Most micro- organisms that cause diarrhoea in children are either not affected
by antimicrobial drugs, like the rotavirus, or the natural history of the infection
is little influenced by the administration of an antibiotic, for eg. Campylobacter
jejuni. Unnecessary antibiotics can damage the bowel (eg. neomycin), prolong
faecal excretion of a pathogen (e.g. Non –typhoid salmonellosis), or destroy
many of the useful commensal flora (e.g. All wide – spectrum antibiotics).
- H/e timely antibiotic therapy in selected cases of diarrhoea may reduce
the duration and severity of diarrhoea and prevent complications.

- Anti- microbial should be used prudently, eg. In suspected cholera or

dysentery or preferably when there is microbial confirmation of invasive
pathogens in the stool or systemic illness. They are of proven efficacy only
for V. cholera, acute intestinal amoebiasis, acute giardiasis & shigellosis.

ANTI-MOTILITY AGENTS (Opiates and their analogues e.g. Loperamide)

- Contraindicated in children with dysentery and probably have no role in
the management of acute watery diarrhoea in healthy children.

- Also, anti-emetic agents such as phenothiazines are of little value and are
associated with potentially serious side effects (like respiratory depression
hypotension, lethargy, reduced motility, dystonia, malignant
hyperpyrexia).

- Nonetheless, ondansetron (selective serotonin- 3 receptor antagonist) is

an effective and less toxic anti emetic agent when persistent vomiting
ensues.
ORAL REHYDRATION THERAPY
The use of ORS is based on 2 scientific facts:
1. Sodium and glucose transport in the small intestine are coupled and
thus represent active transport mechanism while water follows
passively. Many small organic molecules e.g. glucose polymers,
neutral amino acids, dipeptides and short chain fatty acids could also
enhance absorption of electrolyte (and thus water) in the intestinal
epithelium. This is referred to as super ORS.

2. More importantly, the sodium/glucose co- transport mechanism and

other absorptive mechanisms in the gut are maintained during
diarrhoea, even in considerable intestinal damage.

An ideal ORS should be isotonic with plasma. Its glucose concentration should
be 2-3%, for optimal water & electrolyte absorption. It should be palatable
and cheap. In addition to the ORS, in many developing countries, Salt Sugar
Solution (SSS) are also available. It can be prepared by: 1level teaspoon (3ml)
of salt (1.6- 2.4g) and 10 level teaspoon or 5cubes of sugar (25g) are dissolved
in 1beer bottle or 2 soft drink bottles of water (600mls).
STRATEGIES FOR THE PREVENTION/CONTROL OF DIARRHOEAL DISEASE
1. Health education is very important in the CDD in children. During ORT
mothers should be educated on personal and environmental hygiene
(including proper hand washing practices, improved excreta disposal
system), the causes of diarrhoea in children, how to recognise simple
signs of dehydration and how to prepare the standard SSS at home.
2. Promotion of Exclusive Breast Feeding- protects young infants from
diarrhoeal disease through promotion of passive immunity and
reduce intake of potentially contaminated food and water. B/milk
contains all the nutrients needed in early infancy, and when
continued during diarrhoea, also diminishes the adverse impact on
nutritional status.
3. Improved complimentary feeding practices.

4. Improved immunisation services: Rotavirus immunisation/measles

immunisation and cholera immunisation in selected communities.

5. Improved water supply and sanitary facilities.

6. Enhancement of Control of Diarrhoeal Disease through a combined
prevention & tx strategy incorporating rotavirus vaccine; new low – osmolality
formulations of ORS; and Zinc supplementation during diarrhoeal episodes.

RECENT ADVANCES IN THE MGT. OF ACUTE WATERY DIARRHOEA IN CHILDREN

1. NEWS ORS FORMULATION

The standard “WHO” ORS has a Na+ concentration of 90mEq/L, K =

20mmol/L, Cl = 80mmol/L, glucose 110mmo/L, Osmolality 311 mosm/L (NaCl
3.5g/L , anhydrous glucose 20.0g/L,KCl = 1.5g/L,Trisodium citrate = 2.9g/L).

Recent researches reveal that lower osmolality solutions (sodium 60mmol/L,

glucose 80 – 120mmol/L, osmolality 240mosm/L) promote water and
sodium absorption more efficiently than the WHO ORS.

A new improved universal ORS was recommended by the WHO which

contains sodium 75mmol/L, glucose – 75mmol/L and osmolality
245mosmol/L (suitable for all ages).
2. ZINC IN THE Rx OF ACUTE DIARRHOEA
– The therapeutic effects of Zn are attributed to effects on the various
components of the immune system and its direct GIT effects. Zinc
deficiency is associated with lymphoid atrophy, decreased
cutaneous delayed HSR, lowered thymic hormone activity, a
decreased number of antibody forming cells and impaired T-killer
cell activity.

– Zinc supplementation in children with diarrhoea in developing

countries leads to reduced duration and severity of diarrhoea and
could potentially prevent 300,000 deaths. WHO and UNICEF
recommend that all children with acute diarrhoea in at risk areas
should receive oral Zinc in syrup or dispersible tablets for 10 – 14
days during and after diarrhoea (10mg per day for <6mo of age &
20mg/day for those >6mo). In addition to improving diarrhoea,
administration of Zinc in community settings leads to increased use
of ORS and reduction in the use of antimicrobials.
3. PROBIOTICS :
- These are non-pathogenic micro-organisms that
when ingested exert a positive influence on the health or
physiology of the host.

- They consist of either yeast (Saccharomyces

boulardii) or bacteria predominantly- Bifidobacterium and
lactobacillus. These are several mechanisms by which
probiotics may exert their clinical effects; can protect the
intestine by competing with the pathogens for attachment,
strengthening tight junctions between enterocytes and
enhancing the mucosal immune response to
pathogens.

- Recent probiotic studies showed significant

reduction of duration of diarrhoea/hospitalization.
 Stool electrolyte losses

Infection Stool sodium

Cholera 88.9 mMol/L
ETEC 53.7 mMol/L
Rotavirus 37.2 mMol/L
 History of Oral Rehydration

1910 Intestinal absorption in patients with cholera

Sellards, Phillip J Sci

1953 186 patients with cholera treated without iv lfuids

Chatterjee, Lancet

1960’s Identification of glucose-solute co-transport

1971 WHO recommended the use of ORS

intestinal sodium co-transport
“Oral rehydration is potentially the most important

medical advance in the 20th century”

Lancet, 1978
 Is This Child Dehydrated?
• The best measure of dehydration is the
percentage loss of body weight.
• Classification into subgroups with no or
minimal dehydration, mild or moderate
dehydration, and severe dehydration is an
essential basis for appropriate treatment

ESPGHAN/ESPID Guidelines, JPGN 2008

 Assess Dehydration by Clinical History?

• Parental reports on dehydration symptoms

are low in specificity. They may not be
clinically useful.
• Parental report of normal urine output
decreases the likelihood of dehydration.
• Infants and young children with frequent high
output diarrhea and vomiting are most at risk.

ESPGHAN/ESPID Guidelines, JPGN 2008

 Assess Dehydration Based on Signs and
Symptoms?
• Clinical tests for dehydration are imprecise.
• Historical points are moderately sensitive as a
screening test for dehydration.
• The best 3 individual examination signs for
assessment of dehydration are:
– prolonged capillary refill time
– abnormal skin turgor
– abnormal respiratory pattern

ESPGHAN/ESPID Guidelines, JPGN 2008

Items that reflect hydration
• Urine output
• General appearance
• Capillary refill (>3” = iv resuscitation!)
• Skin turgor
• Eyes
• Mucous membranes
• Tears
• Respiratory rate
• Heart rate
 Blood electrolytes?
• Electrolytes should be measured:
– In moderately dehydrated children whose history
and physical examination findings are inconsistent
with a straight diarrheal disease.
– in all severely dehydrated children.
– In all children starting intravenous (IV) therapy,
and during therapy, because hyper- or
hyponatremia will alter the rate at which IV
rehydration fluids will be given
 Indications for admission
• Shock
• Severe dehydration (>9% of body weight)
• Neurological abnormalities (lethargy, seizures, etc)
• Intractable or bilious vomiting
• ORS treatment failure
• Caregivers cannot provide adequate care at home
and/or there are social or logistical concerns
• Suspected surgical condition
 Oral rehydration
• First-line therapy for the management of
children with AGE
• When oral rehydration is not feasible, enteral
rehydration by the nasogastric route is as
effective if not better than IV rehydration.
• Enteral rehydration is associated with
significantly fewer major adverse events and a
shorter hospital stay compared with IV therapy
and is successful in most children.
• Children who are able to receive oral rehydration
therapy (ORT) should not be given IV fluids.
 Role of osmolality in ORS
• Lower osmolality increases water absorption
– (osmolar gradient)

• Hypertonic solutions (old WHO-ORS, Na+90 mmol/l)

may increase the risk of hypernatremia
• Current WHO (Na 75mmol/l) has a balanced
composition that is safe both for cholera and non-
cholera diarrhoea
 Composition of WHO ORS

grams/litre mmol/litre
Sodium chloride 2.6 Sodium 75
Glucose, anhydrous 13.5 Chloride 65
Potassium chloride 1.5 Glucose, anhydrous 75
Trisodium citrate Potassium 20
dihydrate 2.9 Citrate 10
Total Osmolarity 245
 Soft drinks
COCA- PEPSI- FANTA
Brand AQUARIUS GATORADE NESTEA SPRITE
COLA COLA ORANGE

Na (mEq/L) 13 23.5 10 6 5 8 6

Soft drinks are NOT recommended

for rehydration, specially in
K (mEq/L) 15 <1 3.37 1 0.9 1.2 3.4

infants or small children

Glucose
(mmol/L)
103.8 45 40.3 100.3 109 290.5 367.5

Osmolality
(mOsm/L)
406 330 326 509 571 703 859
 Alternatives to ORS?
• Home-made solutions?
– Risk of variable composition and osmolality
• Fruit juice?
– Benefit of potassium but content of fructose and
osmolality load
 Osmolality of fruit juices
Coconut water 300.4 ± 5.9
Peach 257.8 ± 14.3
Apple (natural) 258.4 ± 25.8
Apple (bottled) 773.4 ± 72.6
Orange (natural) 536.7 ± 32.5
Pear (natural) 302.1 ± 27.3
Pear (bottled) 449.5 ± 9.2
Pineapple (natural) 292.5 ± 54.0
Pineapple (bottled) 725.1 ± 42.3
Grape (bottled) 1087.9 ± 44.5
Fruit juice may affect duration of
diarrhea
N=90

S Valois et al Nutr J, 2005

 Rehydration stages

• Compensate for previous losses (Deficit):

– Calculate fluid deficit

• Compensate for on - going elevated losses

– Calculate 10ml/kg/liquid stool

• Compensate for basic needs (Maintenance):

– 100-150ml/kg/d
Reassess regularly!
 Fuid requirements

Previous losses
(rehydration)

Basic daily needs

Ongoing losses
(maintenance and
prevention of dehydration) First 10 kg 100 ml/kg
Second 10 kg 50 ml/kg
Subsequent kg 20 ml/kg
Normal losses
 ESPGHAN/ESPID guidelines on acute
diarrhoea
• Dehydration is the main clinical feature.
• Weight loss, prolonged capillary refill time, skin turgor, and
abnormal respiratory pattern are the best clinical signs.
• Microbiological investigations generally are not needed.
• Rehydration is the key treatment - apply as soon as possible.
• Low osmolality oral rehydration solution - offer ad libitum.
• Regular feeding should not be interrupted - carry on after
rehydration.
• Regular milk formulas are appropriate in the majority of
cases.
 ESPGHAN/ESPID Guidelines
• Drugs are generally not necessary.
• Selected probiotics may reduce the duration
and intensity of symptoms.
• Other drugs require further investigations.
• Antibiotic therapy is not needed in most cases
– May induce a carrier status (Salmonella).
– Antibiotic treatment mainly in shigellosis and in the
early stage of Campylobacter infection (Bacterial
aetiology).
 Pillars for treatment of acute
diarrhoea
• Oral rehydration solution over 3-4 h
• Rapid reintroduction of normal feeding thereafter.
• Breast-feeding should be continued as possible.
• Hypotonic solution is safe and effective
• Supplementation with oral rehydration solution.
• Lactose-free formulae unjustified in the majority.
– If diarrhea worsens check stool pH and/or reducing substances
– Lactose-free formula if stool is acid and >0.5% red substances.
• Do not dilute formula
• Provide additional ORS to compensate for ongoing losses
• Do not use unnecessary medication
Enteral vs parenteral rehydration – duration of diarrhoea

Enteral rehydration is as effective if not better

than IV rehydration.

Enteral rehydration by the oral or nasogastric

route is associated with significantly fewer
major adverse events and a shorter hospital
stay compared with IV therapy and is successful
in most children
 If iv fluids are necessary
• Check blood electrolytes
• Use isotonic saline solution (NaCl 0.9%) with
2.5% dextrose
• Possible alternative: half DD solution
• In case of hypernatremia, take additional care:
– Use 75% of calculated volume.
– Monitor serum Na+
– Aim at reducing Na + by 10mmol/l per day
 Instruct caregivers for:
• On- going vomiting despite small fluid sips,
especially if associated with abdominal distension
or pain
• Persisting fever after 24 hours of ORT
• Increasing lethargy and failure to feed
• Deteriorating hydration and failure to pass urine
• Presence of blood in the stools
• Diarrhoea persisting for more than 1 week.
 Oral rehydration

• May not reduce stool volume or duration of diarrhoea

• BUT saves lifes by preventing dehydration!
• Pro’s and Con’s of additional medication
– Cost
– Limited benefit
– Draw parents’ attention from the main intervention –
Rehydration!