Topic 1: Acute gastroenteritis
Causes of acute gastroenteritis in children:






Viruses (70%) -> rotavirus, norovirus, enteric adenovirus,
calicivirus, astrovirus, enterovirus
Bacteria (20%) -> Campylobacter jejuni, non-typhoid
salmonella, EPEC, shigella, Yersinia enterocolitica, shiga
toxin producing E.coli, salmonella typhi, vibrio cholera.
Protozoa (10%) -> Cryptosporidium, giardia lamblia,
entamoeba histolytica
Helminths -> strongyloides stercoralis
Villus -> absorption
Crypts -> secretion
Acute gastroenteritis -> decrease in the consistency of
stools ± an increase in the frequency of evacuations
(typically ≥ 3 in 24 hours) ± fever or vomiting
in the first months of life, a change in stool consistency is
generally more indicative of diarrhea than simply an increase
in the number of stools because:
🍼 Normal Infant Stool Patterns Vary Widely



Breastfed infants may pass multiple loose stools per day
— sometimes with every feeding — and that's normal.
Formula-fed infants tend to have fewer stools, often more
formed.
Some healthy infants may go several days without
stooling.
So, frequency alone isn't diagnostic.
✅ What Indicates Diarrhea in Infants:




A sudden change from a baby’s usual stool pattern
toward looser, more watery stools.
Increased fluidity (more than just being soft — truly
watery or mucousy).
Explosive stools, or stools that soak through the diaper
more than usual.
Sometimes accompanied by other signs: fever, vomiting,
poor feeding, dehydration signs.

Acute diarrhea typically lasts less than 7 days (chronic >
14 days)
Key facts:





Second leading cause of death in children under
five (525,000) each year.
Globally 1.7 billion episodes diarrheal every year
leading cause of malnutrition in children under five
years old
It is both preventable and treatable
Peak incidence is between 6-11 months:



Age of complementary feeding
Related to developmental age (mouthing)
Declining maternal antibodies
Complications of diarrhea:






Dehydration leading to shock
Electrolytes imbalance
Metabolic acidosis
Convulsions (brain edema)
Malnutrition if chronic or recurrent
Sepsis and DIC
Assessment of dehydration:
ORS osmolarity:
Na+1
Cl-1
Glucose
K+1
Citrate or (HCO3-1 -> 30 mM)
Total
90 mM
80 mM
110 mM
20 mM
10 mM
310 mM
Give:



75ml/kg in 3-4 hours
Regular food
100 ml after each loose stool
Nutritional management
Who needs workup for diarrhea?
Most children with acute gastroenteritis do not require
diagnostic workup except:





very young children
underlying chronic conditions (e.g. cancer, inflammatory
bowel diseases, immune deficiency disorders, diabetes
mellitus)
very sick
febrile invasive diarrhea or bloody diarrhea with or
without fever
known travel to high-risk areas or during disease
outbreak.
Indications for hospital admissions:








Shock
Moderate-to-severe dehydration in young children
Neurological abnormalities (lethargy, seizures, etc.)
Intractable vomiting
Failure of oral rehydration
Suspected surgical conditions
Electrolyte and/or acid/base imbalance
Unmet conditions for safe follow-up and home
management.
Diarrhea management:



Oral rehydration solution (first line for mild/moderate)
Feeding
Additional therapies -> Probiotics – Antibiotics – Antidiarrheal drugs – Antispasmodics
Prevention of acute gastroenteritis:




Wash hands thoroughly before and after eating or when
preparing the meals
Make sure that the tools used for eating and preparing
the meals are clean
Cover our food or put them in the fridge to prevent any
contamination
Rotavirus vaccines
Topic 2: Chronic diarrhea
Chronic diarrhea is a decrease of the consistency ±
🔹 Abdominal distension ->Possible causes:
increase of frequency ± volume of stools lasting longer
than two weeks, where the change in stool consistency
is more important than stool frequency



Pathogenesis of diarrhea:





Osmotic
Secretory
Inflammatory
Dysmotility
Factitial
Malabsorption syndromes (e.g., celiac disease, lactose
intolerance)
Protein-energy malnutrition
Ascites in liver disease or protein-losing enteropathy

A distended abdomen in a child with diarrhea could
suggest intestinal dysfunction or low protein levels.
🔹 Tenderess -> Palpating the abdomen for tenderness or
guarding helps rule out:
Chronic diarrhea evaluation:





Chronic diarrhea usually starts gradually (insidiously) and
is often not associated with fever, unlike acute infectious
diarrhea. This suggests non-infectious causes like
malabsorption, food intolerance, or inflammatory
conditions
If the small intestine is involved -> Stool tends to be
large volume, watery, and foul-smelling (offensive).
Usually no blood present. Causes may include celiac
disease, lactose intolerance, giardiasis, or other
malabsorptive disorders
If the colon is affected:
o Diarrhea tends to be smaller in volume but may
be more frequent.
o Blood or mucus is often present → suggests
dysentery or colonic inflammation.
o Possible causes: inflammatory bowel disease,
infections, or allergic colitis.
Dietetic history (formula, gluten, soy, eggs etc..)
Drugs (antibiotics, laxatives, colchicine, propranolol etc..)


Inflammatory conditions (e.g., IBD, infections)
Complications like mesenteric adenitis, enterocolitis,
etc.
🔹 Perianal area -> Examining the perianal region helps
detect:



Perianal dermatitis, often due to stool acidity or
infection
Fissures, fistulas, tags, which are seen in Crohn's disease
Signs of abuse or trauma, if suspected
🔹 Oral lesion -> Seen in some chronic GI and systemic
diseases:


Aphthous ulcers → can be a sign of Crohn’s disease or
celiac disease
Glossitis, angular cheilitis → due to vitamin deficiencies
(e.g., B12, iron)
🔹 Other organs affected (e.g., skin, respiratory…)
History
Age
Family history
Growth
Associated symptoms
Dietary history
Stool characteristics ->
undigested food, blood,
steatorrhea, offensive smell
Physical examination
Weight and height for age
Abdominal distention
Tenderness
Perianal area
Oral lesions
Other organs affected
(respiratory, skin)
Dermatitis herpetiformis
(small clusters of itchy
bumps)
🔹 Weight and height for age -> Why important? Chronic
diarrhea often leads to malnutrition, which can show as:



Weight loss
Growth faltering or stunting
Tracking growth over time helps assess severity and
chronicity of illness.
Chronic diarrhea may be part of a systemic condition:



Skin: Rashes, dermatitis herpetiformis (in celiac),
acrodermatitis enteropathica, eczema (in food allergies)
Respiratory: Suggests cystic fibrosis, which affects both
lungs and pancreas
Eyes, joints, etc.: May point toward autoimmune or
inflammatory conditions (like IBD)
Acrodermatitis (Enteropathica)
The pictures show symmetrical
erythematous, scaly plaques around the
mouth, buttocks, and limbs.
This is classic for Acrodermatitis
Enteropathica, a condition due to zinc
deficiency, often seen in:
o
o
o
Malabsorption
Chronic diarrhea
Genetic defects in zinc transport
Causes of chronic diarrhea for children:
Birth – 1 month:
DH (Dermatitis Herpetiformis)


Seen in celiac disease, particularly in older children
and adults.
Skin lesions are symmetrical, itchy, and typically
located on elbows, knees, and buttocks
Older children:
Gluten ingestion → production of IgA antibodies against
tissue transglutaminase (tTG). These antibodies cross-react
with epidermal transglutaminase (eTG) in the skin. IgA gets
deposited in the dermal papillae → inflammation →
blistering and itching
Chronic diarrhea investigations:
1.
Red flags:





Poor weight gain, weight loss or FTT
Night stool
Acid stools with burning sensation and redness
Presence of blood and mucus
Associated symptoms of systemic disease, rash,
fever, arthritis etc..
Feces
2.
Blood tests
Celiac disease:

Age of onset
Usually manifests in infants or young children after the
introduction of gluten-containing foods. Can appear at any
age, but often between 6 months to 2 years when cereals are
introduced.
3.

Implicated food
Gluten-containing grains: Wheat, barley, rye. Oats are
controversial; some patients tolerate oats, others do not.

Pathology
Characteristic changes in the small intestinal mucosa:
Imaging
o
o
o

4.


An immune-mediated reaction (IgE or non-IgE) to
proteins found in cow’s milk.
Most common food allergy in infants and young
children.
Different from lactose intolerance (which is non-immune
and enzyme deficiency)
Presentation
o
o
o
o
Endoscopy & Pathology
Cow’s milk protein allergy:

Villus atrophy (flattening of the villi → decreased
absorption surface).
Crypt hyperplasia (increased depth of intestinal
crypts).
Increased intraepithelial lymphocytes (IELs) (immune
cells infiltrate mucosa).

Abdominal distension (bloating).
Chronic diarrhea.
Failure to thrive (FTT) or poor growth.
Other symptoms may include abdominal pain,
anemia, fatigue.
Screening:
Tissue transglutaminase IgA antibody (tTG-IgA). Total
serum IgA to rule out IgA deficiency.

GFD (Gluten-Free Diet)
The cornerstone of treatment is a lifelong gluten-free
diet. Complete avoidance of wheat, barley, and rye
gluten-containing foods.

Associations:
Type 1 diabetes, thyroid disorders, and dermatitis
herpetiformis.
Cystsic fibrosis:
1. Neonatal Period: Meconium Ileus

Many CF infants present early with intestinal
obstruction called meconium ileus, caused by thick,
sticky meconium blocking the intestines.
2. Respiratory Symptoms

Recurrent or persistent cough, often accompanied
by wheeze due to chronic lung infections and mucus
plugging.
3. Malabsorption


Pancreatic enzyme insufficiency leads to
malabsorption of nutrients.
Results in large, pale, bulky, and foul-smelling
stools.
Toddlers diarrhea (chronic non specific diarrhea):
4. Failure to Thrive (FTT)

Due to malabsorption and increased energy needs
from chronic illness.
5. Rectal Prolapse







Most common cause between two and four years of age
Intermittent and self limited
No pain, no distension, no vomiting
No effect on weight and on nutrition
Large consumption of juices
Undigested food particles
Occurs due to frequent coughing and malnutrition.
6. Heat Stroke (Rare)

CF patients can develop heat stroke because of
abnormal salt loss in sweat.
7. Sweat Chloride Concentration

Elevated sweat chloride (>60 mmol/L) is a diagnostic
hallmark of CF.
8. Common Pathogens
Treatment of chronic diarrhea:

Chronic lung infections with Staphylococcus aureus
and Pseudomonas aeruginosa are typical.
9. Management



Physiotherapy: Chest physiotherapy to clear mucus
from lungs.
Enzyme Replacement: Pancreatic enzyme
supplements to aid digestion.
Increased Fluid and Salt Intake: Especially important
in hot weather to prevent dehydration and heat
stroke.



Supportive : Dehydration, Electrolyte imbalance, Nutrients
Empirical: Antidiarrheal drugs
Curative: Antibiotics, pancreatic enzymes, dietary
Topic 3: Neonatal jaundice

Jaundice is yellowish discoloration of the skin ± conjunctiva
caused by bilirubin deposition.
Hyperbilirubinemia is a state of excessive amount of bile
pigment bilirubin in the body visibly manifested as jaundice
(TSB > 1 mg/dL [17.1 µmol/L])
Significant neonatal hyperbilirubinemia in infants ≥35 weeks
gestational age is defined as: TSB >95 percentile on the hourspecific Bhutani nomogram
Severe neonatal hyperbilirubinemia: TSB > 25 mg/dL [428
µmol/L] -> Associated with BIND (Bilirubin - Induced
Neurologic Dysfunction)
BIND -> spectrum of neurologic problems caused by elevated
levels of unconjugated bilirubin in the brain. This condition
occurs when bilirubin crosses the blood-brain barrier and
accumulates in brain tissues, particularly the basal ganglia,
leading to neurotoxicity.
Clinical Spectrum of BIND:
Acute Bilirubin Encephalopathy (ABE) – early, potentially
reversible phase:
Kernicterus – chronic, irreversible neurologic damage. Longterm effects:









Cerebral palsy (especially athetoid type)
Hearing loss (sensorineural)
Gaze abnormalities
Intellectual disability
Dental enamel hypoplasia
85 % of infants > 35 weeks have visible jaundice due to
hyperbilirubinemia in the first week after birth.
Nearly all preterm have hyperbilirubiemia
10% of term. require intervention
25% of late preterm require intervention

Bilirubin source:
80 – 90 % = Hb degradation
10 – 20 % = Hemoproteins (Catalases +cytochrome
oxidase) degradation in liver
Bilirubin metabolism -> retriculoendothelial system
(monocytes and macrophages) in the spleen, liver and
bone marrow.
🚫 Unconjugated bilirubin, even when elevated, still doesn’t
show up in urine
Bilirubin is transported
to the liver through
carrier proteins organic
anion transporter
protein OATP-2
Breast milk jaundice:
prolonged unconjugated hyperbilirubinemia that occurs in
healthy, breastfed infants, usually after the first week of life.
It’s benign, self-limited.


Unconjugated bilirubin in plasma is bound reversible to
albumin. Can be displaced by free fatty acids and drugs
(valium, ceftriaxone, sulfa drugs)
Unconjugated bilirubin is:
1. Not soluble in water because it's lipid-soluble, UB
cannot be excreted directly by the kidneys or into bile.
2. Potentially toxic especially in newborns, high levels of
unconjugated bilirubin can cross the immature bloodbrain barrier, leading to BIND or kernicterus.
3. Made soluble and less toxic by albumin binding. In
the bloodstream, UB is tightly but reversibly bound to
albumin, which prevents it from entering tissues and
keeps it less toxic and transportable to the liver for
conjugation
Breastfeeding jaundice:
Why Unconjugated Bilirubin Is Not Found in Urine?


UB is bound to albumin in the blood
Albumin is a large protein that is not filtered by the
glomerulus in the kidney
This is why no bilirubin in urine is a hallmark of unconjugated
hyperbilirubinemia.
High UGB -> can exaggerate physiologic jaundice. Weight loss
more than 8 % of birth weight (day 3-4). Associated with
increased Na+ serum and dehydration and fever.
🔹 Normal Serum UB Levels:


< 1.5 mg/dL is the typical upper limit
At this level, most bilirubin in blood is:
o Unconjugated
o Bound to albumin
o Not dangerous under normal conditions
🔹 Exception – When You Might See Bilirubin in Urine:

Conjugated bilirubin is water-soluble and can
appear in urine if:
o Liver disease (e.g., hepatitis impairs
excretion)
o Biliary obstruction (e.g., gallstones block
bile flow)
May need phototherapy. No water or dextrose
supplementation.
Bilirubin is excreted actively into bile canaliculus by MRP – 2
(multi resistant associated protein 2) enhanced by
phenobarbital. Dubin – Johnson syndrome -> Abnormal
MRP2 -> Conjugated bilirubin increases in blood.
Pattern:
o
o
3-4 days term, 5- 7 days preterm
Disappears by 4-5 days term, 7-9 preterm
The baby is well
Bilirubin rise trend:
o
o
Increase < 0.2 mg/dL/h and < 5 mg/dL/day
Mean peak according to race (<15)
Maybe exaggerated when:
Obstruction of GI (delayed meconium, or fasting) -> more
time for conjugated bilirubin to be deconjugated by beta
glucuronidase in the intestinal mucosa. The UCB gets
reabsorbed and enters the entero – hepatic circulation.
Bilirubin measurement:

Transcutaneous bilirubinometer

TSB
o
o
o
o
o
o
o
o
o
o
Breast feeding
Male sex
Cephal hematoma
Cutaneous bruising
Polycythemia
Weight loss/ caloric deprivation
Dehydration
Maternal DM
Trisomy
Drug (K3, novobiocin, oxytocin)
Types of neonatal jaundice:
1. Physiologic
Mechanism:
o
o
o
o
Increased RBC + ineffective erythropoiesis
Shortened RBC lifespan
Immature hepatic uptake and conjugation
Increased EHC (increased intestinal glucoronidase)
Prolonged jaundice (persists after 2 weeks (term) , 3 weeks
(preterm) -> evaluate):
2. Breast feeding jaundice
After birth:
3. Breast – milk jaundice
4. Pathologic
Medical emergency
Causes of high UGB causing jaundice:

Increased production:
o Hemolysis (ABO or RH incompatibility, Inherited
spherocytosis, G6PD)
o Sepsis
o RBC breakdown (polycythemia, cephalohematoma)
o Ineffective erythropoiesis
o Galactosemia
Post-discharge follow – up:

ABO incompatibility:


o Early onset (within 24 h after birth)
o Baby blood A/B, mother bood is O
o Direct combs test positive
o Blood smear shows increased spherocytes
o Can be controlled with phototherapy
Decreased clearance / excretion:
o Inherited (galactosemia, crigler najjar, gilbert, OATP
polymorphism)
o Congenital hypothyroidism
Increased EHC
o NPO
o Obstruction

Infants discharged before 72 hours of life should be seen
within 2 days of discharge
Infants with significant risk factors for development of
severe hyperbilirubinemia should be seen within 1 day
Therapeutic options:



Phototherapy for neonates with mild jaundice
Exchange transfusion for severe cases
Iv immune globulin
How to recognize pathologic jaundice?
1.
Jaundice appearing in the first 24 hours of life
is always pathologic until proven otherwise. early
bilirubin values have high sensitivity and specificity for
predicting severe hyperbilirubinemia later on:
2.
3.
4.
Rapidly rising TSB (> 5 mg/dL per day
> 0.2 mg/dl/hour
TSB high risk zone (> 75th)
Persists after two weeks
High conjugated bilirubin (physiologic is UGB)
5.
Assess risk factors
Topic 4: Liver disease