1

1
st Concised Scientific Letters
(CSL)
1/11/2020

Antiepileptic
Drugs: Uses &
Doses

2

By / Proff. Emad Hammad El. Dally
Prof of Neuropediatric
Assiut University
3
*Golden Rules for childhood epi-
lepsy
1. Epilepsy is a clinical diagnosis ,EEG is a
confirmatory test .
2. The cornerstone for diagnosis of epilep-
sy is EEG video monitoring.
3. Before starting treatment of epileptic
child, you should exclude syndromes that
mimic epilepsy as (breath holding at-
tacks,syncope, cataplexy,Mastarbation
spasm…..etc)
4. Duration of treatment of epilepsy is min-
imal 2 years free from fits.
5. Follow up EEG is not indicated except
for special cases.
6. EEG could be normal in a well known
epileptic patient and 7-8 % of normal pop-
ulation had an abnormal EEG.
7. Monotheropy is better than polytherapy
-Indictions Electroencephalogra-
phy(E.E.G)
E.E.G has the following advantages in the
diagnosis of epilepsy:
1) E.E.G with hyperventilation is highly
diagnostic for
absence attacks & other epilepsies.
2) E.E.G showing hypsarrythmic pattern is
diagnostic for
infantile spasms.
3) E.E.G is important in diagnosis of myoc-
lonic epilepsy.
4) E.E.G is important for classification of
epilepsy and
epileptic syndromes.
5) E.E.G may direct the attention for brain
focal lesion, which
needs further imaging studies.
6) E.E.G gives an idea about the maturation
of brain in
neonatal, infancy and childhood periods.
- Indictions CT. and MRI:
They are not indicated in every child with
convulsions, it is
indicated for the child with recurrent sei-
zures under several
circumstances:
1. The presence of an abnormal neurologi-
cal examination.
2. The presence of dysmorphic features.
3. The presence of skin lesions suggesting
neurocutaneous
syndromes.
4. Intractable epilepsy.
5. The presence of focal E.E.G slowing or
E.E.G
lateralization.
6. Post-traumatic seizures.
7. Post-asphyxial seizures in neonates.
8. On planning for surgical treatment of
epilepsy.
*Individual antiepileptic drugs:-
1-Carbamazpine (Tegretol ,Tegral , car-
bapex):-
- Used in partial epilepsy mainely but
could be used in G.T.C.
- It aggrevates absence, myoclonic and
infantile spasm.
- Dose: 10 mg/kg/day → gradual increase
up to 30 mg/kg/day 3
times/day.
2- Oxcarbazepine: (Trileptal&Oxaleptal):-
α ketosubstituted analogue with the same
spectrum of
carbamazpine and lower side effects.Its
dose is 10-30 mg/kg/day.
3- Phenytoin (Epanutin,Ipantin):-
- Used in acute seizures of any type I.V.
and in G.T.C. as a long
term therapy it is the drug of choice in
infancy and neonates.
- It aggrevates absence, myoclonic and
infantile spasm.
- I.V. Loading (20 mg/kg) after 12 hours →
4
5-10 mg/kg/day which
is the oral form.
4-Phenobarbital : (sominalleta):-
- Used in G.T.C. and simple partial.
- It is the drug of choice in neonates and
infants
- Dose:- - Neonate (20-mg/kg) → 5-10
mg/kg/d.
- Children (10 mg/kg) → 3-5 mg/kg/d.
5-Diazepam : (Valium,Valpam ,Neural ):-
- In acute seizures.
- I.V. or rectal (0.3 – 0.5 mg/kg/dose )
6- Clonazepam : (Rivotril , Aptryl &Amo-
tril).
-Used in Absence, myoclonic, inf. Spasms,
atonic, partial and as an
add on therapy in G.T.C.
-Dose: 0.05 mg/kg/day and increase by
0.01 mg /kg/week until
response or reach 0.25 mg/kg/day
7- Ethosuximide: (Ethoxa & Zarontin):-
- The drug of choice in absence epilepsy.
- It aggrevates G.T.C.
- Dose :-20-40mg/ kg/day.
8- Midazolam: (Dormicum): -
In acute seizures: 0.1-0.2 mg/kg/dose.
9- Valproic acid:-
(Depakine,Dekadel,Convulex,Valopnex,-
Vedge)
- G.T.C., absence, myoclonic, partial and
atonic.
Dose : start with 15-20 mg/kg/day divided
into two doses and increase
gradually untill response. The range of
dose is 20-60 mg/kg/day.
10-Lamotrigine: (Lamictal,lamotrine,Larogen&Leptrogine):
- Used in partial. Could be used as an add on therapy in uncontrolled fits of any type.
- Dose: See table

11-Topiramate: (Topamax ,Topiramate,Delpirmate):-

- G.T.C., absence, myoclonic, partial and atonic.
-Dose :3-9 mg/ kg / day

12-Vigabatrin (Sabril):-
- The drug of choice in infantile spasms.
- Add on therapy in uncontrolled convulsions.
- Dose: start with 30 mg/kg/day and increase gradually (30-100 mg/kg/day).

13- Levetiracetam ( Tiratam, Sycocetam, Kepra)

- It has broad spectrum antiepileptic activity like valproate.
- Dose 30-60 mg/ kg/ day.

5
2
nd Concised Scientific Letters
(CSL)
1/12/2020

When to Sus-
pect a Genetic
Syndrome

6

By / Dr.Klaled Hashim Mohmoud
Lecturer of Pediatric
Assiut University
7
A genetic syndrome is a clinical situation
that combines major and minor malforma-
tions, anomalies of growth and of psycho-
motor development.
Although many genetic conditions are
individually rare, they are common in ag-
gregate and place a great burden on af-
fected patients and the medical system.
Congenital malformations (many of
which are related to genetic disturbances)
occur in approximately 5 percent of live-
born infants; a much higher proportion of
conceptions are affected by genetic anom-
alies. In one study, an estimated 79 of
1,000 live-born infants were found to have
a genetic syndrome and/or congenital
malformation by 25 years of age.
Prompt recognition of features suggestive of
genetic conditions can improve the selection of
appropriate, cost-effective diagnostic tests, the
performance of well-informed genetic coun-
seling related to issues such as prognosis and
future family planning and timely referral to
subspecialists.
General themes that can alert pediatricians
to the presence of genetic syndromes in-
clude dysmorphic features that are evident
on physical examination; multiple anoma-
lies in one patient; unexplained neurocog-
nitive impairment; and a family history that
is suggestive of a hereditary disease.
Taking an accurate three-generation family
history is important when a genetic syn-
drome is suspected.
Important elements include the age and
sex of family members; when family mem-
bers were affected by disease or when
they died; the ethnic background; and if
there is consanguinity.
Every effort should be made to obtain • Loose or stiff joints
complete information about the gestation • Unusually tall or short stature
leading to the birth of the affected child . • Webbed fingers or toes
• Excessive skin
Events surrounding the birth of the child • Unusual birthmarks
may be critical: antepartum status, length • Increased or decreased sweating
of labor, mode of delivery, baby’s condition • Unusual body odor
at birth, measurements.Finally, information • Abnormal hand creases
is obtained about the child’s course since
infancy along the lines of a standard pedi-
atric history, but with a few special empha-
ses:general health, growth, developmental
progress, behavior, special testing or ther-
apy.

The physical examination is of enormous

importance: the basic techniques of phys-
ical diagnosis are used, but the examina-
tion is fine tuned to promote detection of
many subtle physical clues that might oth-
erwise be overlooked. Selected measure-
ments of physical features can be extreme-
ly useful in confirming a clinical impression
of abnormality.

The following list includes some features

that might suggest the child has a genetic
diso der. However, some of these charac-
teristics are commonly found in people
without a disorder:
• Ear abnormalities
• Unusually shaped eyes
• Different colored eyes
• Facial features that are unusual or differ-
ent from
other family members
• Brittle or sparse hair
• Excessive body hair
• White patches of hair
• Large or small tongue
• Misshapen teeth
• Missing or extra teeth

8
3 rd Concised Scientific
Letters
(CSL)
1/1/2021

Notes to
remember in
DKA

9

By / Prof. Azza Ahmed El-Tayeb
Prof of pediatric
Assiut University
10
* History:
1- Thirst
2- Toilet
3- Tired
4- Thinner
5- Test
*Laboratory investigation:
1- RBS is more than 200 mg >(11.1 mmol)
You can use glucometer while awaiting the
result of serum
blood glucose.
2- Urine ketones (moderate to large ketonemia)
or ketonemia
if bedside test available equal or more than 3
mmol
*Assessment:
1- Airway.
2- Vital signs.
3- Level of consciousness.
4- Degree of dehydration.
a- 5 % dehydration
- CRT more than 2s.
- Poor skin turgor.
- Tachypnea.
b- 10 % dehydration
- Weak rapid pulse.
- Non palpable peripheral pulsation.
- Cold mottled extremities.
- Oliguria.
- Hypotension.
5- Weight of patient.
6- Collect urine in sterile urine bag (no
need for cauterization unless critically ill).
*Lab assessments:
1. RBS.
2. Serum electrolytes .
- NA
-K
- Chloride
- If available: Ca, Mg and phosphorus.
* Calculate:- 7- Required glucose reduction 2-5 mmol
1- Calculate anion:- (35-90 mg).
- Na-(HCO3+CLV. 8- Rapid reduction more than 100mg pet
- Normally 12 mmol/L hour can reduce
insulin rate only if Improved acidosis,
2- Calculate corrected sodium:- 9- Consider adding glucose 5 percent if
- Actual sodium +2(glucose – 100) /100. blood glucose decline
to 250 to 300 mg or even before if there is
3- Calculate effective asmolarity:- rapid reduction
- 2(Na}+ glucose/t8. of glucose more than 100mg per hour to
- Normally 275- 295 mosm per kg water. avoid brain edema.
10-You may increase glucose cone to 10 or
*Goals of therapy:- even 12.5 percent.
1- Correct dehydration. 11-If blood glucose less than 100 mg give
2- Reverse ketosis. bolus of glucose 10
3- Correct acidosis. percent 2mI per kg.
4- Return glucose & asmolarity to near normal
levels.
5- Identify and treat precipitating factors.
6- Avoid DKA complications.

* Fluid therapy:-
Very important to start with fluid before insu-
lin to restore tissue perfusion, improve renal
blood flow, correct acidosis and hyperglycemia.

* Insulin therapy:-
1- Should start at least one hour after
fluids .
2- No direct bolus insulin IV in pediatrics.
3- Risk of hypovolemia, brain edema, hy-
pokalemia.
4- 50 units of regular insulin added to 50
ml normal saline by
infusion or syringe pump at a rate 0.05 to
0.1 units per kg .
5- In 30 kilo child insulin infusion rate is
about £.5 to 3mL per hour.
6- Start with lower rate esp in young child ,
recent onset and
pts with rapid declinig glucose.

11
4 th Concised Scientific
Letters
(CSL)
1/2/2021

Cow milk
allergy

12
 * Overview:
Milk allergy is an abnormal response by
the body’s immune system to milk and
products containing milk. It’s one of the
most common food allergies in children.
Cow’s milk is the usual cause of milk
allergy, but milk from sheep, goats, buffalo
and other mammals also
can cause a reaction.

Avoiding milk and milk products is the

primary treatment for milk
allergy. Fortunately, most children outgrow
milk allergy. Those who
don’t outgrow it may need to continue to
avoid milk products.

* Symptoms:
Milk allergy symptoms, which differ from per-
son to person, occur
a few minutes to a few hours after milk or eats
milk products.

By / Dr. Amir Mohammed * Symptoms in infants with immedi-

Abo El Gheet ate-onset reactions to cow’s milk
Lecturer of pediatric
Assiut University Cutaneous
 Pruritus without skin lesions
 Urticaria
 Angio-oedema
 Atopic eczema exacerbation

Gastrointestinal
 Vomiting
 Diarrhoea
 Bloody stools
 Gastro-oesophageal reflux
 Abdominal pain

Respiratory
A. Upper respiratory
 Rhinitis
 Nasal congestion

13
B. Lower respiratory
 Wheeze
 Cough
 Stridor
 Difficulty breathing

Cardiovascular
 Hypotension/shock
 Prostration

General
 Anaphylaxis
 Irritability
 Failure to thrive

* Common gastrointestinal symptoms in cow’s milk allergy (Delayed onset)

Vomiting/posseting
Irritability (colic)
Dysphagia
Diarrhea
Constipation

*Some symptoms and signs related to CMPA

14
Figure (1): Algorithm for the diagnosis and management of cow’s milk pro-
tein allergy (CMPA) in exclusively breast-fed infants. eHF, extensively hydro-
lysed formula.

Figure( 2) Algorithm for the diagnosis and management of cow’s milk pro-
tein allergy (CMPA) in formula-fed infants.

15
5 th Concised Scientific
Letters
(CSL)

1/3/2021

Primary
Immunodefi-
ciency

16

By / Dr. Naglaa Samy Osman
Lecturer of pediatric
Assiut University
17
Primary Immunodeficiency )PID) are a
group of more than 400 genetic defects, in
which part of the body’s immune system
is missing or functions improperly. They
cause increased susceptibility to a wide
range of infections, affecting the skin, the
ears, the lungs, the intestines and other
parts of the body.
Some disorders present at birth or in early
childhood, the disorders can affect anyone,
regardless of age or gender. Children
with PID live their entire lives more susce
tible to infections, enduring recurrent
health problems and often developing se-
rious and debilitating illnesses. Fortunately,
with proper medical care, many patients
live full and independent lives.
Is it just an infection?
You should be suspicious if the child has an
infection that is…
 Severe - requires hospitalization or intrav
nous antibiotics.
 Persistent - won’t completely clear up or
clears very slowly.
 Unusual - caused by an uncommon orgaism.
 Recurrent - keeps coming back.
 Runs in the Family (previous sibling deaths).
The characteristic clinical presentation of PID
involves frequent and often severe pulmonary
tract infections (recurrent bronchitis and/
or pneumonia). Other frequently described
symptoms of a PID are intestinal infections.
Chronic diarrhea, especially when it is caused
by unusual bacteria (e.g., Yersinia or Campylo-
bacter), fungi (e.g., Cryptosporidium), or even
common infections such as persistent rotavirus
or Salmonella, accompanied by the presence of
failure to thrive should trigger an immunologic
workup for PID in infants or young children.
Warning signs for Pediatric Immuno-  Third step
deficiency  Candida skin test.
1. Four or more new ear infections within 1  CD markers by flow cytometry (CD3- CD4-
year. CD8- CD19- CD16/56).
2. Two or more serious sinus infections within  DHR 123.
1 year.
3. Two or more months on antibiotics with  Forth step
little effect.  Complement assay (CH50- C3- C4 +/- AH50).
4. Two or more pneumonias within 1 year.  Enzymes and Cytokine assay.
5. Failure of an infant to gain weight or grow  Genetic testing.
normally.
6. Recurrent, deep skin or organ abscesses.
7. Persistent thrush in mouth or fungal infec-
tion on skin.
8. Need for intravenous antibiotics to clear
infections.
9. Two or more deep-seated infections includ-
ing
septicemia.
10.A family history of Primary immunodefi-
ciency.
Ten warning clinical signs for PIDs developed
by the Jeffrey Modell Foundation Medical Ad-
visory Board. (Lehman H, Hernandez-Trujillo
V, Ballow M. Diagnosing primary immunodef-
ciency: a practical approach for the nonimmu-
nologist).

Steps for Diagnosis of PID in a sus-

pected child

 First step
 History, physical examination, and anthropome
ric
measurements.
 CBC with differential count.
 Immunoglobulin assay IgA-IgG-IgM-IgE (co
relate to age).

 Second step
 Specific antibody response (against Tetanus,
Diphtheria).
 Response to pneumococcal vaccine (pre and
post).
 IgG subclass analysis

18
6 th Concised Scientific
Letters
(CSL)

1/4/2021

Drugs And Breast

Feeding

19

By / Proff. Emad Hammad El. Dally
& Dr.Moh.Kalaf & Dr.Nancy Alaa
Assiut University
20
A-GALACTAGOGUES
TYPES:
1-Antipsychotic drugs can increase pitu-
itary prolactin secretion and breast milk
production through dopamine antagnism,
2-Gastrointestinal motility drugs metoclo-
pramide and domperidone
B-Lactation suppression
• Nicotine
• Alcohol
• Sedating Antihistamines (eg. Di-
phenhydrarnine)
• Estrogen containing oral contracep-
tives
• Progesterone contraceptives (if
started early
• postpartum before milk supply es-
tablished)
• Bromocriptine (Parlodel)
WHO classification of drugs during
breastfeeding (2002)
1. Compatible with breastfeeding
2. Compatible with breastfeeding (oc-
casional mild side effects} Monitor infant
for side effects
3. Avoid if possible, {significant side
effects} Monitor infant for side-effects
4. Avoid if possible. {May inhibit lacta-
tion}. Monitor for amount of milk
5. Contraindicated {dangerous side
effects}
Best choice of drugs during breast-
feeding
• Medications Contraindicated in
Breast Feeding
• Antineoplastics
• Immune suppressants
• Ergot alkaloids
• Gold
• lodine/Radiocontrast media
• Lithium carbonate
• Certain antibiotics
• Social drugs and drugs of abuse
• Antibiotics
• Penicillins and cephalosporins are com-
patible with breast feeding
 Monitor infant for diarrhea (change in
gut flora)
• Quinolones have not been rated by AAP
• Trimethoprim-sulfamethoxazole (Bac-
trim) is compatible with breast feeding
 Not recommended in infants < 2 month
• Analgesics
- Acetaminophen is compatible with
breast feeding
- Nonsteroidal antiinflammatory drugs
 ibuprofen is preferred
 Naprosyn, sulindac, piroxicam should
be avoided
- Narcotic/Opiates
 morphine, oxycodone, and hydroco-
done are compatible with breast feeding
 Meperidine (Demerol) should be avoid-
ed
 Codiene is highly contraindicated
• Antidepressants
Tricyclic antidepressants
• little or no effect on breast feeding infant
• AAP lists as possible concern with expo-
sure long-term
Selective serotonin reuptake inhibi-
tors (SSRIs)
• generally Istst choice
• Paroxetine (Paxil) or Sertraline (Zoloft)
preferred to Fluoxetine (Prozac)
Serotonin Norepinephrine Reuptake
Inhibitors (SNRIs)
• Venlafaxine (Effexor)
N.B.Take dose at bedtime to limit exposure to
infant
21
• Antiepileptic Drugs
Phenytoin, Carbamazepine, and
Valproic acid are compatible with
breast feeding
• Caution in use due to risk for hepato-
toxicity (Valproate)
Lamotrigine , Phenobarbital are com-
patible with breast feeding
• not preferred due to slow metabolism in
the infant
resulting in sedation
Levetiracetam and Topiramate com-
patible with breastfeeding
AEDs contraindicated during lacta-
tion.
Ethosuximide should be used only when there
are no alternatives and after informed consent
of the mother . Lastly, zonisamide and the con-
tinuous use of diazepam or clonazepam should
be avoided
Antihistamines
• All sedating antihistamines have the
possibility of causing sedation in the infant
• Sedating antihistamines (esp. with de-
congestant) can decrease milk supply
• Nonsedating antihistamines are compat-
ible with breast feeding
• Loratadine preferred
Blood Pressure Medications
• Diuretics are compatible with breast
feeding
– Avoid high doses
• Beta blockers are compatible with breast
feeding
– Propranolol, metoprolol, and labetalol pre-
ferred
– Atenolol, nadolol, and sotalol can lead to SE
(hypotension, bradycardia, tachypnea)
• Calcium channel blockers (CCBs) are compatible
with breast feeding
– Nifedipine (Procardia) is preferred
- ACE inhibitors and ARBs must use with caution

Before Prescribing Drug Therapy in the Lactating Woman

 Is drug therapy really necessary?
 The safest drug should be chosen.
 If there is a possibility that a drug may present a risk to the infant, then consider measuring
blood levels
 Drug exposure in the infant may be limited by timing of medication and breastfeeding

22
7 th Concised Scientific
Letters
(CSL)

1/5/2021

Neonatal
Hyperbilirubinemia

23

By / Prof. Nafisa Hassan Refat
Prof of pediatric
Assiut University
24
*INTRODUCTION
Neonatal jaundice (NJ) refers to yellow dis-
coloration of the skin and sclera of newborn
babies. It is generally considered a benign self-
limiting condition, affecting more than 60% of
healthy term and 80% of preterm infants. How-
ever, in some cases, severe neonatal hyperbili-
rubinemia (SNH) can lead to irreversible brain
damage and kernicterus. Surviving infants
may acquire long-term neuro-developmental
sequelae such as cerebral palsy, sensorineural
hearing loss, intellectual difficulties or gross
developmental delays.
Q1) What are the features of physio-
logic hyperbilirubinemia?
In full term healthy infants, jaundice becomes
visible on the 2nd- 3rd day, usually peaking at
2nd- 4th day at 5-6 mg/dL, usually disappear at
6th-8th day, however it may last up to the 14th
day with maximum total serum bilirubin (TSB)
of <12mg/dL. In preterm infants, physiologic
jaundice is more severe with TSB reaching 12
mg/dL at 5th day of life.
Q2)What are the features of non
physiologic hyperbilirubinemia?
a) Clinical jaundice in the first 24 hrs of
life.
b) TSB concentration increasing by more
than 0.2mg/dl/hr or5mg/dL/day.
c) TSB concentration exceeding the 95th
percentile for age in hours.
d) Direct serum bilirubin exceeding 2 mg/
dL.
e) Clinical jaundice persisting after 8 days
in full term and more than 14 days in preterm.
f) Signs of underlying illness in any infant.
Q3) How can severe hyperbilirubin-
emia be prevented among newborns?
1- During pregnancy: All pregnant women
should be tested for ABO and Rh
(D) blood types.
2- Parental education: Expecting mothers
should be offered information about neonatal
jaundice.
3- Following delivery: Support breast
feeding, breastfed infants should not be supple-
mented with water or dextrose.
Q4) How to monitor and assess for
jaundice?
A) Clinically: The assessment of jaundice
must be performed in a well-lit room or, pref-
erably, in daylight at a window.
B) Anticipatory lab work on infant’s cord
blood or blood: If a mother has not had prena-
tal blood grouping or is Rh- or blood group O,
a direct (Coombs’ test), blood type, and Rh (D)
on the infant’s blood are strongly recommend-
ed.
C) Estimation of bilirubin level either by
skin (TcB) or total serum bilirubin (TSB):
1- Transcutaneous bilirubinometry (TcB)
TcB decreases the number of invasive blood
tests. It is used to screen for unconjugated
hyperbilirubinemia. TcB is NOT recommended
during or after phototherapy and following an
exchange transfusion.
3- Total serum bilirubin measurement:
TSB should ALWAYS be measured IF baby is
visibly jaundiced at less than 24 hours of age
Therapeutic interventions should always be
based on a TSB level.
Q 5) What are the most important
risk factors for developing severe
hyperbilirubinemia?
• Jaundice observed in the first 24 hours
• Blood group incompatibility with positive
direct antiglobulin test
25
• Known hemolytic disease (e.g., G6PD
deficiency),
• Preterm and late preterm (Gestational
age 35–36 weeks)
• Previous sibling received phototherapy
• Cephalohematoma or significant bruis-
ing
• Suboptimal exclusive breastfeeding with
excessive weight loss
Q6) What are the investigations re-
quired for a case with neonatal jaun-
dice?
1. TSB, Blood group and RH of mother
and baby, Full blood count (FBC) with reticu-
locyte count in all cases.
2. Direct antiglobulin test (DAT)(Coombs
test) to identify blood group alloimmunization.
3. G6PD and albumin especially in near
exchange level.
4. In prolonged jaundice, Liver function
tests, thyroid function tests, urine microscopy
and culture.
5. Test for red cell membrane disorders,
e.g. hereditary spherocytosis or elliptocytosis.
6. If infection is suspected, C-reactive
protein, Blood culture, urine–microscopy and
culture
7. Investigate for congenital infections if
there are other indications.
8. Investigate for inborn errors of metabo-
lism if baby looks unwell and jaundice is se-
vere, e.g. galactosemia.
9. Liver function tests (LFT) as liver en-
zymes may be increased, e.g. in congenital
infections, inborn errors of metabolism. If
conjugated bilirubin is elevated, evaluation for
the causes of cholestasis is required.
Q7) What are the different modalities of treatment for a case of neonatal jaun-
dice?

-If the TSB is at a level at which exchange transfusion is recommended or if the TSB level is 25 mg/
dL or higher at any time, it is a medical emergency and the infant should be admitted immediately
for intensive phototherapy.
-In infants with isoimmune hemolytic disease and TSB level rising inspite of intensive phototherapy
or within 2-3 mg/dL of exchange level, administer
intravenous immunoglobulin 0.5–1 g/kg over 2 h, and repeat in 12 h if necessary.
-Intravenous fluids are NOT necessary for term or near-term infants receiving phototherapy unless
there is evidence of dehydration not corrected by adequate oral intake.

Q8) When is exchange transfusion indicated? Where and how is it done? What
is needed post exchange?
-The aim of an exchange transfusion is to rapidly reduce the TSB by removing small aliquots of
blood from the baby and replacing it with donor blood components, thus removing bilirubin, anti-
bodies and correcting anemia.
-Phototherapy especially intensive for a high risk baby can decrease the need for an exchange trans-
fusion.
-Indications: •TSB continues to rise despite intense phototherapy.
•Baby showing signs of acute bilirubin encephalopathy.
- Post exchange transfusion :•Continue intensive phototherapy
• Measure TSB within 2 hours of exchange transfusion.

26
Q9) What are the guidelines for management of hyperbilirubinemia in preterms?

Q 10) When and how to give intravenous immunoglobulin(IVIG)?

In isoimmune hemolytic disease, administration of intravenous immunoglobulin (0.5- 1 g/kg over 2
hours) is recommended if the TSB is rising despite intensive phototherapy or the TSB level is within
2 to 3 mg/dL of the exchange level. If necessary, this dose can be repeated in 12 hours.

Q11) Is there any role for other medicines in the treatment of neonatal hyper-
bilirubinemia?
There is NO role for the use of the following medications to treat neonatal hyperbilirubinemia (phe-
nobarbitone, Agar, Clofibrate, albumin, charcoal, metalloporphyrins)

Q 12) How to follow up the baby with severe hyperbilirubinemia after dis-
charge?
-Infants requiring exchange transfusion or those who exhibit neurological abnormalities should be
referred to a neurological follow-up programs and must have a hearing screen. Infants with isoim-
munization are at risk for severe anemia after several weeks; it is suggested that a repeat hemoglobin
measurement be performed at two weeks of age.

27
8 th Concised Scientific
Letters
(CSL)

1/6/2021

The emergence of
antibiotic
resistance:
Myths and Facts in
Clinical Practice

28

By / Dr. Rania Saad Mahmoud
Clinical Pharmacist at
clinical nutrition unit
Assiut University
29
* Overview:
Antibiotic resistance is one of the biggest global
public health challenges of our time. The an-
tibiotic resistance crisis has been attributed to
the overuse and misuse of these medications, as
well as a lack of new drug development by the
pharmaceutical industry due to reduced eco-
nomic incentives and challenging regulatory
requirements.
There has been a dramatic rapid global spread
of multi- and pan-resistant bacteria (also
known as “superbugs”) mostly due to the
production of extended-spectrum β-lactamas-
es (ESBL) and carbapenemases, those cause
infections that are not treatable with existing
antibiotics. Currently, 700,000 people die each
year from resistant infections.
That number is set to rise to ten million by
2050 if no action is taken. Far from being
someone else‟s problem, the release of a World
Health Organization (WHO) multi-country
survey describes public awareness around anti-
biotic resistance and highlights common mis-
conceptions that are driving the current crisis.
Here are six of them.
* Myth 1 - Antibiotic resistance
means my body has become resistant
to a particular antibiotic.
The WHO reports that 76% of people surveyed
said antibiotic resistance is what happens when
the body becomes resistant to antibiotics, when
in fact it is the bacteria that becomes resistant
and spreads illness.
* Myth 2: Only people who use antibi-
otics regularly are at a risk for anti-
biotic resistance.
Forty-four percent of people thought this was
true, but in actuality, as the WHO points out,
anyone can get an infection that‟s resistant to
antibiotics.
* Myth 3: Resistance only happens
from repeated courses.
Antibiotic resistance can occur whenever you
take an antibiotic, whether it is a single course
or multiple repeat courses. The more courses
you take; the more resistance can occur. But
that doesn‟t mean it doesn‟t occur with a
single course. On top of that, a single course
of antibiotics can lead to life-threatening un-
wanted side effects and potentially catastrophic
changes to the normal bacteria that live in our
guts. The imbalance can allow dangerous bac-
teria like Clostridium difficile to predominate
and cause severe diarrheal illness.
* Myth 4: Superbugs are a good thing.
„Bugs‟ is a simple term used to describe bacte-
ria; superbugs are a term often used to describe
resistant bacteria. They are certainly not super
as in „super good‟; quite the opposite – they
are super bad. They are particularly dangerous
as they are resistant to antibiotics, which means
that the drugs we usually use to get rid of them
are not effective.
* Myth 5: Antibiotics treat all types
of infection.
Antibiotics are only suitable for treating bacte-
rial infections. Other infections, such as those
caused by viruses or fungi, will not respond to
treatment with antibiotics. This is why your GP
will not prescribe antibiotics for most coughs
and colds, the flu, athletes foot, thrush or a
range of other infections.
* Myth 6: If one antibiotic doesn’t work,
there will be another one that does.
Unfortunately, there are a growing number of mul-
tidrug-resistant strains of bacteria that are resistant
to many antibiotics.
30
Antibiotic resistance is one of the biggest global
public health challenges of our time. The an-
tibiotic resistance crisis has been attributed to
the overuse and misuse of these medications,
as well as a lack of new drug development In
some cases, there is no treatment at all.
For extended-spectrum β-lactamase and
AmpC producers, carbapenems are the drugs
of choice, but alternatives are needed because
the rate of carbapenem resistance is rising.
Potential active drugs include classic and newer
βlactam–β-lactamase inhibitor combinations,
cephamycins, aminoglycosides, tigecycline,
fosfomycin, and, rarely, fluoroquinolones or
trimethoprim-sulfamethoxazole. These drugs
might be considered in some specific situa-
tions. AmpC producers are resistant to cepha-
mycins, but cefepime is an option.
In the case of carbapenemase-producing
Enterobacteriaceae (CPE), only some “sec-
ond-line” drugs, such as polymyxins, tigecy-
cline, aminoglycosides, and fosfomycin, may
be active; double carbapenems can also be
considered in specific situations. Combination
therapy is associated with better outcomes for
high-risk patients, such as those in septic shock
or with pneumonia.
Ceftazidime-avibactam was recently approved
and is active against KPC and OXA-48 pro-
ducers; the available experience is scarce but
promising, although development of resistance
is a concern. New drugs active against some
CPE isolates are in different stages of devel-
opment, including meropenem-vaborbactam,
imipenem-relebactam, and aztreonamavibac-
tam. Overall, therapy of multidrug-resistant
infections must be individualized according to
the susceptibility profile, type, and severity of
infection and the features of the patient.
9 th Concised Scientific
Letters
(CSL)

1/8/2021

Glucose-6-phosphate
dehydrogenase
deficiency (G6PDD)

31

By / Dr. Mostafa Embaby
Associate Professor of Pediatrics
Assiut University
32
Overview:
• Glucose-6-phosphate dehydro-
genase (G6PD) is the first enzyme in the
pentose phosphate pathway of glucose.
metabolism.
• Deficiency diminishes the reductive
energy of the red cell and may result in
hemolysis, the severity of which depends
on the quantity and type of G6PD and the
nature of the hemolytic agent.
Classification:
The World Health Organization (WHO)
classifies G6PD variants into five classes
according to their enzyme activities and
clinical manifestations:
• Class I: Severely deficient; related to
chronic non-spherocytic hemolytic anemia.
• Class II: Severely deficient with
1–10% residual activity; it is associated
with acute hemolytic anemia.
• Class III: Moderately deficient with
10–60% residual activity
• Class IV: Normal activity (in the
range 60–150%)
• Class V: Increased activity (more
than 150%)
Pathogenesis
• Red cell G6PD activity falls rapidly and
prematurely as red cells age.
• Decreased glucose metabolism.
• Diminished NADPH/NADP and GSH/
GSSG ratios.
• Impaired elimination of oxidants (e.g.,
H2O2).
• Oxidation of hemoglobin and of sulfhy-
dryl groups in the membrane.
• Red cell integrity impaired, especially on
exposure to oxidant drugs, oxidant re-
sponse to infection and chemicals.
• Oxidized hemoglobin precipitates to
form Heinz bodies which are plucked out
of the red cell leading to hemolysis and
“bite cell” and “blister cell” morphology.
Clinical Manifestations of G6PD defi-
ciency
1. Acute hemolytic anemia
a. induced by oxidative drugs
b. Favism
c. Infection-induced hemolysis
2. Chronic non spherocytic hemolytic ane-
mia
3. Neonatal jaundice
1. Drug-induced hemolysis
a. Typically in African-Americans but also
in Mediterranean and other types.
b. List of drugs (see Table); occasionally
need additional stress of infection or the
neonatal state.
c. Acute self-limiting hemolytic anemia
with hemoglobinuria.
d. Heinz bodies in circulating red cells.
e. Blister cells, fragmented cells, and
spherocytes.
f. Reticulocytosis.
g. Hemoglobin normal between episodes.
2.Favism
a. Acute life-threatening hemolysis, often
leading to acute renal failure, caused by in-
gestion of fava beans especially fresh fava
beans and that’s why the highest incidence
rate of favism is at the time of harvest.
Clinical symptoms of favism are pallor,
jaundice, hematuria, and acute hemolytic
anemia occurs 24-48 h after consumption
of fava beans, suddenly
b. Associated with Mediterranean andCan-
ton varieties.
c. Blood transfusion required.
3.Infection-Induced Hemolytic Ane-
mia
Infection is perhaps the most usual cause of hemo-
lysis in children with G6PD deficiency. The most
common agents are hepatitis viruses A and B, cy-
tomegalovirus, and conditions such as pneumonia
and typhoid fever are all notable causes.
33
4. Chronic non spherocytic hemolytic
anemia (CNSHA)
a. Occurs mainly with sporadic inheritance.
b. Clinical picture:
i. Chronic non-spherocytic anemia variable but
can be severe with transfusion dependence.
ii. Reticulocytosis.
iii. Intense neonatal presentation.
iv. Shortened red cell survival.
v. Increased autohemolysis with only partial
correction by glucose.
vi. Slight jaundice.
vii. Mild splenomegaly.
5. Neonatal jaundice
a. Usually associated with Mediterranean and
Canton varieties but can occur with all vari-
ants.
b. Infants may present with pallor, jaundice
(can be severe and produce kernicterus), and
dark urine.
c.The excessive jaundice resulting in kernicter-
us is not only due to hemolysis but may be due
to reduced glucuronidation of bilirubin caused
by defective G6PD activity in the hepatocytes.
diminished bilirubin conjugation would be the
main cause of hyperbilirubinemia in G6PD-de-
ficient newborn infants.
d. Profile of serum bilirubin in newborns with
G6PD-deficiency showed that the amount of
total and unconjugated bilirubin is high and
conjugated bilirubin is low.
Diagnosis
The diagnosis is generally suspected when
patients from certain ethnic groups develop
anemia, jaundice and symptoms of hemolysis
after challenges from any of the above causes,
especially when there is a positive family histo-
ry.
Generally, tests will include:
• Complete blood count and reticulocyte
count; in active G6PD deficiency, Heinz bodies
can be seen in red blood cells on a blood film;
• Liver enzymes (to exclude other causes
of jaundice);
• Lactate dehydrogenase (elevated in he-
molysis and a marker of hemolytic severity)
• Haptoglobin (decreased in hemolysis);
• A “direct antiglobulin test” (Coombs’
test) – this should be negative, as hemolysis in
G6PD is not immune-mediated;
• When there are sufficient grounds to
suspect G6PD, a direct test for G6PD is the
“Beutler fluorescent spot test”, which has large-
ly replaced an older test (the Motulsky dye-de-
colouration test).
• Other possibilities are direct DNA test-
ing and/or sequencing of the G6PD gene.
• Testing during and for many weeks after
a hemolytic episode will lead to false negative
results as the G6PD deficient RBC will have
been excreted and the young RBC (reticu-
locytes)will not yet be G6PD deficient. False
negative results will also be likely following
any blood transfusions. For this reason, many
hospitals wait for 3 months after a hemolytic
episode before testing for G6PD deficiency.
• Females should have their G6PD ac-
tivity measured by quantitative assay to avoid
being misclassified by screening tests
3. Indication for transfusion of
packed red blood cell in children
presenting with acute hemolytic ane-
mia:
a. Hemoglobin (Hb) level below 7 g/dl.
b. Persistent hemoglobinuria and Hb below 9
g/dl.
4. CNSHA:
a. In patients with severe chronic anemia:
transfuse red blood cells to maintain Hb level
8_10 g/dl and iron chelation, when needed.
b. Splenectomy has only occasionally amelio-
rated severe anemia in this disease. Indications
for splenectomy are as follows:
i. Hypersplenism.
ii. Severe chronic anemia.
iii. Splenomegaly causing physical impediment.
c. Genetic counseling and prenatal diagnosis
for severe CNSHA if the mother is a heterozy-
gote.

Treatment
1. Avoidance of agents that are dele-
terious in G6PD deficiency. (For a con-
sistent, up-to-date list of drug susceptibilities
visit: www.favism.org.)

2. Education of families and patients

in recognition of food prohibition
(fava beans), drug avoidance, heightened
vigilance during infection and the symptoms
and signs of hemolytic crisis (orange/dark
urine, lethargy, fatigue, jaundice).

34
10 th Concised Scientific
Letters
(CSL)

1/10/2021

Approach for
management of
the child with
hematuria

35

By / Dr. Mahmoud Abd-Elfattah
Ahmed
Assistant lecturer of pediatrics
Assiut University
36
* Definition:
• 5 RBCs\ hpf on a cenrifuged urine spec-
imen.
• Growth hematuria( visible to naked eye)
it is either:
 Originate from glomerulus: if brown,
“cola colored” or smoky, change RBCS mor-
phology, may contain RBCs cast , proteinuria ˃
100mg\dl, may clinically associated with edema
, hypertension , renal insufficiency . as in trau-
ma,tumor,urolithasis,meatal stenosis,UTI, etc
…
 Originate from lower urinary tract:
where urine is red or pink color, normal RBCs
morphology, may contain clots & minimal pro-
teinuria on dipstick < 100 mg\dl.
• Microscopic hematuria (detected only
by dipstick or microscopy) if 5 RBC\ on urine
specimen in the sediment from 10ml centri-
fuged freshly voided urine but no discolored
urine.
 Incidence: 0.5-2 % among school aged
children.
 Evaluation of patients with hematuria :-
 History: very helpful to detect underly-
ing causes of hematuria.
1. History of recent upper respiratory ,
skin, or gastrointestinal infection:
It suggests acute glomerulonephritis, hemolyt-
ic-uremic syndrome, or HSP nephritis.
2. Rash and joint complaints: they point
toward HSP nephritis or SLE nephritis.
3. Frequency, dysuria, and unexplained
fever: they suggest a urinary tract infection.
4. Renal colic: it suggests nephrolithiasis &
crystaluria.
5. Headache, visual changes, epistaxis, or
congestive heart failure: they suggest hyperten-
sion.
6. History of trauma: child abuse must al-
ways be suspected in a child with unexplained
bruising and hematuria.
7. Recurrent episodes of gross hema-
turia: they suggest IgA nephropathy, Al-
port syndrome, thin glomerular basement
membrane disease, hypercalcuria, or uro-
lithiasis.
8. Family history of similar condition:
Hereditary glomerular disease includes he-
reditary nephritis (Alport syndrome), thin
glomerular basement membrane disease,
SLE nephritis & IgA nephrobathy. Other re-
nal disorders with ahereditary component
include polycystic kidney disease, urolithia-
sis and sickle cell disease \ trait.
 If NO consider extra glomerular he-
maturia , so do the following investigation
in stepwise order:
Step 1: urine analysis & culture, sensitivity.
Step 2: urine calcium \ creatinine, sickle
preparation, renal \ bladder ultrasound.
Step 3: urine analysis (siblings & parents) ,
serum electrolytes , Cr , Ca .
-If crystalluria , urolithiasis , ornephrocal-
cinosis:24 hour urine for Ca , Cr, uric acid
,oxalate.
-If hydronephrosis \ pyelocaliectasis :
crystalogram ± renal scan.

 Physical examination: Indication of renal biopsy in achild

1. Hypertension, body edema, hepatospleno-
megaly, or signs of congestive heart failure: they
suggest acute glomerulonephritis.
2. Flank mass: it may signal hydronephrosis
(obstructive uropathy), cystic disease, renal vein
thrombosis, or tumors (as wilms tumor).
3. Several malformation syndromes asso-
ciated with renal disease: they include VATER
syndrome (vertebral body anomalies, anal atresia,
trachea-esophageal fistula and renal dysplasia).
4. Hematuria associated with neurologic or
cutaneous abnormalities: renal cystic disease or tu-
mors associated with several syndromes, including
tuberous sclerosis, von Hippel-Lindau syndrome
and Zellweger (cerebrohepatorenal) syndrome.
5. Anatomic abnormalities of the external
genitalia: they may be associated with renal disease.
with hematuria:-
 Asymptomatic hematuria for more than 1
year.
 Hematuria with positive family history.
 Hematuria + moderate to severe protein-
uria, hypertension or elevated BUN, serum Cr for
2-3 weeks.
 Deafness.
 Positive serology for hepatitis B or SLE.
 Distinguishing features of glomer-
ular and non- glomerular hematuria:
See Table below

 Laboratory and radiologic eval-

uation of patients with glomerular or
extraglomerular hematuria:
If Cola\ brown urine? , proteinuria˃30 mg \ dl,
RBCcasts?, Acute nephritic syndrome?
 If yes consider glomerular hematuria , so
do the following investigation in stepwise order:
CBC with differential, Electrolytes , calcium , BUN\
Cr, serum protein\ albumin , cholesterol , C3\C4,
ASO\anti-DNase B , ANA , antineutrophil anti-
body , throat \ skin culture ( if indicated) , 24 hour
urine total protein , Cr clearance.

37
38
11 th Concised Scientific
Letters
(CSL)

1/12/2021

How to deal with

a case of
recurrent
pneumonia
in a child

39

By / Dr. Mohamed Sayed
Lecturer of Pediatric Pulmonology
Assiut University
40
Recurrent pneumonia is defined as two epi-
sodes of pneumonia in one year or three epi-
sodes during any time frame, with intercritical
radiographic normality.
Three groups of children are considered on the
basis of their personal and family history and
clinical findings:
1) Otherwise, healthy children who do not
need further investigations.
2) Those with risk factors for respiratory infec-
tions for whom a wait-and-see approach can be
recommended; risk factors include prematuri-
ty, atopy, indoor and outdoor pollution.
3) Those in whom further investigations are
mandatory.
When evaluating a child with recurrent LRTIs,
the first step is to distinguish otherwise healthy
subjects from those with an underlying chronic
disease that require further investigations.
Table 1 shows the clinical characteristics of a patient’s medical history that
should be assessed.

What remains is a ‘grey area’ represented by children with early respiratory symptoms, an occa-
sional need for hospitalization, and short periods of well-being between episodes, without any
focal involvement. In this case, the presence of the risk factors mentioned above (i.e. prematu-
rity, atopy, passive smoking, exposure to indoor and/or outdoor pollution) may justify a wait-
and-see approach for 6-12 months.

If the number and the characteristics of the LRTIs do not change during the follow-up period
despite the elimination of avoidable risk factors, further investigations should be made.

41
Figure 1 summarizes the investigations required in relation to clinical histry.

42
Figure 2 shows the investigations recommended in children with recurrent
LRTI and a suspected underlying disease.

43