AWASIR91

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Table of contents:
1- Neonatology 2
2- Malnutrition 25
3- Neuropediatrics 37
4- Hematology 46
5- Rheumatology 53
6- Exanthemas 59
7- Immunization 66

 Dr. Mousab Mohammed Ibrahim (Kibreet) (88)

 Dr. Emeirii Hatim Mustafa (88)

 Noora Abubaker Fadul (90)

 Maha Hussain (90)
 Asia Hassan (91)
 Hadeel Mohammed (91)
 Huda Faisal (91)
 Tasneem Ghazali (91)
 Ohayla Elfatih (91)
 Waad Taj (91)
 Waad Amir (91)
 Hajer Ismat (91)
 Dan Elrasheed (91)

1
PART 1: NEONATOLOGY
1. Important terms
2. Maternal diseases
3. Drugs
4. Congenital infections
5. Birth injuries
6. Neonatal care
7. New born resuscitation
8. Neonatal seizures
9. Respiratory distress in neonates
10. Other problems of prematurity
11. Neonatal infections
12. Neonatal jaundice
13. Primitive reflexes

1. Important terms:
- Embryo: < 9 weeks
- Foetus: 9 weeks - birth
- Still birth: born ≥ 24 weeks with no signs of life
- Prenatal mortality = Still birth + up to 1 week of delivery/ 1000 X live still births
- Neonatal mortality = Death in first 4 weeks of delivery/ 1000 X live births

o Pre-term: < 37 weeks

o Term: 37 - 41 weeks
o Post-term: > 42 weeks
o Low birth weight: < 2500g
o VLBW: < 1500g
o Extremely LBW: < 1000g
o Small for GA: BW < 10th centile
o Large for GA: BW > 90th centile

 Neonate: up to 28 days
 Infant: 1 - 12 months
 Toddler: 1 - 3 years
 Pre School: 3 - 5 years
 School: 5 - 12 years
، ‫إرا فعلت اليوم ها يتناسل غيرك عن فعله‬

.‫فسوف تفعل غذاً ها يعجز غيرك عن القيام به‬

2
 2. Maternal diseases:
- Most diseases affect foetus and neonate are:
1- DM. 2- Graves. 3- SLE.
4- AITP (auto immune thrombothytopenic purpura).

1) Problems related to diabetic mother:

1- Congenital malformations:
- Most common: Neural tube defects and cardiac malformations.
- Characteristics:
a- Caudal regression syndrome "sacral agenesis"
b- Hypo plastic left colon
- Control of DM decrease risk
N.B. Congenital malformation does not increase in Gestational DM
2- IUGR
3- Macrosomia:
- Shoulder dystocia
- Cephalo-pelvic disproportion
- Birth injuries

In neonate, increase insulin can cause:

1- Hypoglycaemia > (early feeding + close monitoring), Hypocalcaemia,

Hypomagnesaemia, Hyperbilirubinemia.
2- RDS (Insulin Anti cortisol)
3- Polycythaemia (Neonatal jaundice) -
4- Transient HoCM (hypertrophic obstructive cardiomyopathy) (resolves in few
weeks but may cause heart failure)
2) Graves:
- Antibodies cross the placenta
- Foetus> Tachycardia = CTG, goitre = US
- Neonates > irritability, weight loss, and tachycardia = Heart failure.... Diarrhoea
- Xerophthalmous
- May require Antithyroid
3) SLE
- Anti Ro/ Anti La
- Neonatal lupus syndrome (Self limiting rash +/- heart block

3
 4) AITP:
- Low platelets = increase intracranial haemorrhage
- If at delivery = petichea/severe Thrombocytopenia = I.V IGs
- If active bleeding = platelets.

3. Drugs:
Drug Effect
1- Warfarin 1. Cartilage (nasal Hypoplasia/Epiphyseal stippling)
2. Haemorrhage
2- Lithium Ebstein’s Anomaly
3- Phenytoin Hydantoid face (mid facial Hypoplasia)
4- Thalidomide Phocomelia (short limbs)

5- Tetracycline Enamel Hypoplasia

6- Diethylstilbestrol Vaginal/CX adenocarcinoma
(DES)
7- Alcohol 1-fetal alcohol syndrome
2-cardiac abnormalities
8- IV drugs Withdrawal ( jitteriness, seizures, yawing)
9- Smoking stillbirth/miscarriage , LBW, IUGR

Ebstein anomaly:

Rare heart defect in which the tricuspid valve doesn’t work properly, as a result blood
leaks back through the valve into the right atrium.

4
 Foetal alcohol syndrome:

1- Characteristic face
- Flat nasal bridge
- Maxillary Hypoplasia
- Absent philtrum
- Short thin upper lip
2- Growth abnormalities
3- Developmental delay
4- Cardiac abnormalities

Phocomelia

4. Congenital infections
Infection c/f Dx Tx
1- CMV Most common urine PCR for Gancyclovir,
90% Asymptomatic virus/culture Sedofovir, Foscarnet
5% Early symptoms IgG antibodies
Periventricular calcification. show previous
- Others: Hepatosplenomegaly, infection.
SN deafness, Microcephaly.
Primary infection is the most
serious
2- rubella - Earlier > Most dangerous IgM antibody
- Triad of: detection
1- Cataract
2- SN deafness

5
 3- CHD (e.g. PDA)
- Others: Blueberry muffins
spots, extra medullary
haematopoiesis
- After 4 months of gestation >
No infection
3-Toxoplasma - Triad of: IgM or IgG (later) Pyramethamine +
1- Diffuse calcification Sulfadiazine for 1 year
2- Chorioretinitis
3- Hydrocephalus
> Long term neurological
disability

4-varicella <20 wks ~Fetopathic VZ IG + IV acyclovir

(Embryopathic varicella) for the mother
- Zigzag scarring of skin, Limb
atrophy, digital dysplasia.
- Mortality 30%
- Rash, pnuomonitis, hepatitis.
- Very severe disease
5-Syphilis ≥ 2 years ~ Penicillin (mother 1
Hutchinson’s triad month or more before
1- H. teeth delivery)
2- interstitial keratitis
3- 8th SN deafness
- Other: rash on palm / sole
(early), bone deformity (saber
shin and saddle nose)

6
7
 5. Birth injuries
# Soft tissues:

1- Caput succedaneum:

- Oedema (diffuse) - abnormal skin over it - resolves in few days.

2- Cephalohematoma

3- Subperiosteal bleeding (usually involve parietal bone)

4- Subaponeurotic haemorrhage – shock, coagulopathy

Nerve injuries: (shoulder dystocia, breech)

1- Brachial plexus:

* Erb's: - confined (do not cross sutures).

- association: skull fractures #, I.C. haemorrhage.

- complications: neonatal jaundice Resolves in few weeks

2- Chignon: ventuse delivery

- In upper root of BP C5, C6

- Waiter's tip deformity

- Palm +ve grasp reflex

- Phrenic nerve palsy.

* Klumpek's:

- In lower root of BP C8, T1

- Claw Hand

- Small muscle wasting in hand

- -ve grasp reflex - Herne’s

3- Facial nerve injury: (forceps) Need methyl cellulose to protect the eyes

#Bones: Most common is the clavicle

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6. Neonatal care

9
 Guthrie
test

Neonatal
screening
Pass of
Apgar urine and
meconium

1- Erythromycin eye drops

Prevention of Gonococcal/Clamydial - Silver nitrate > against Gonococcalonly

conjunctivitis ..causes chemical conjunctivitis

2- Wash with Hexachlorophene

(in preterm > neurotoxic)

3- Vitamin K

4- Vaccination

5-Umblical cord care

6- Hearing test

10
 2- if not > renal agenesis or hypovolemia

Passage of meconium:

Passage of urine: - 80% in 1st 24h

- 25% in 1st 24h - 99% in 48h

- If not check the bladder: - If not > check for intestinal obstruction
or ano rectal anomalies
1- if palpable > obstruction

# Normal = 8 - 9 (1min - 5 min) # 4 - 7 (attention)# 0 - 3 (immediate resuscitation)

7. New born resuscitation:

▪ Observe for:

- Meconium - Pink colour

- Term
- Good muscle tone - If Yes >> Routine care
- Good cry - If No >> Provide warmth
Clear airway + O2 100%, check HR, Respiration.

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 HR<100>60 or apnea=positive
pressure ventilation

HR<60=ppv+ chest
compression

still<60=epinephrine

- N.B: most common cause => respiratory

- Aim of chest compression => provide blood to the heart not the brain like adults
- Chest compression = PPV 3:1
- In 1 minute: 90 chest compression: 30 breaths
- Site: lower 1/3 of the sternum just below an imaginary line between the nipples.
Thumb or two fingers method (less effective but easier)
- Diameter depress to 1/3 of anterior-posterior of the chest.
- Cause of respiratory depression = opioids by mother
- Give Naloxone (0.1 mg/kg/dose) “if RD continues despite resuscitation”
Hypoglycaemia: Glucose<45 mg/dL (2.6 mmol/L) need for neurological action (primary
fuel for the brain).

Risk
1. Mother DM
[Link] (<37 wk) i.e., glycogen in foetus is formed in the last month
3. SGA decreased stores / IUGR
4. LGA increased demands.
5. Illness / hypothermia increased demands.
6. Certain drugs.
Complain of neurological symptoms
+ sympathetic Sx( tremors, tachycardia, tachypnea)
Treatment Oral feeding
If comatose: IV 10% D (2 ml/khg )
If no response: increase the rate or the concentration central venues catheter to avoid skin
necrosis.
If you can't give 10% D or still no response gives glucagon + Hydrocortisone.
Whom to treat

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1- Symptomatic infants
2- Asymptomatic but 2 abnormal readings
3- Asymptomatic but 1 very low reading <1.6 mol/dL

Hypothermia:

- Normal temp : 36.5 - 37.5°C (axillary)

- 36 – 36.4 : cold stressors
- 32 -35.9° : moderate hypothermia.
- < 32° : severe hypothermia.
Or by touch:

- Cold trunk + cold extremities = severe hypothermia.

- Warm trunk + cold extremities = cold stress
Risk factors:

1. Pre maturity (low brown fat ) like SGA

2. Neurological problem, cardiac, respiratory no control
3. Large pores in the body (e.g. spina bifida)
4. Sedation.
N.B: Thermo-regulation in infants:
- Brown fat (barring). Brown fat doesn't form until late.
- Hypothalamic control to neither release nor epinephrine => vasoconstriction in
periphery & pulmonary. No shivering.
Treatment: Dryness, heater, O2 + glucose (burning; release heat).

N.B: losing of heat:

Abnormal neurological behaviour
1. Convection: air flow. caused by hypoxic ischemic brain
2. Conduction: direct contact.
3. Radiation: no direct contact. injury due to asphyxia.
4. Evaporation.
5. HIE (hypoxic ischemic
Is the single most important cause of
encephalopathy): prenatal mortality and morbidity

Causes

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 - Ante partum /peri partum / post partum
- Placenta: Abruption, excessive contraction, ruptured uterus
- Umbilical cord: Prolapsed or compression
- Blood: hypo or hypertension of the mother
- Fetal: e.g. IUGR
- Neonatal: kerinctrus, inborn error of metabolism

Classification of HIE

Feature G1mild G2 moderate G3 severe

Consciousness irritable Lethargic comatose

Tone Hypotonic Marked sever

seizures No Yes prolonged

suckling Poor unable(tube feed) unable to maintain resp.+/-MOF

Diagnosis: There is no clear diagnostic test for HIE

- Abnormal findings on the neurologic exam in the first few days after birth, is the
single most useful predictor that brain insult has occurred in the perinatal period
Essential criteria for diagnosis of HIE:
- Metabolic acidosis (cord pH <7 or base deficit of ≥12
- Early onset of encephalopathy
- Multisystem organ dysfunction
Characteristic MRI finding. Predominant pattern in preterm: Periventricular
leukomalacia (spastic diplegia)
In term babies: Parasagital cerebral injury (proximal quadraparesis)
Sequel:
- CP
- Neuronal damage: primary (immediate), secondary (respiratory failure)
Management:
- Supportive care, ABCD approach
- Prevent further brain damage

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Periventricular leukomalacia

‫ألاوكات كلها صباحات‬..‫في ألاصل‬

‫دعها فلط جشزق من داخلك‬

Neonatal HIE Parasagital brain injury

Child with HIE

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 8. Neonatal seizures:
Etiology Work up Treatment
At birth: First line: - Treat underlying
maternal anaesthesia injected into foetus 1. Pulse oximetry. cause
Day 1: 2. Glucose. -O2 then give glucose
1. Metabolic; hypoglycaemia/ 3. PCV. * seizure prophylaxis
hypocalcaemia 4. Serum Ca. (Ionized),Na, Mg. First line:
2. HIE => 6- 18h become more severe in 5. Arterial blood gases. - phenobarbitone 20-40
the next 24-48h. 6. LP, blood cultures. mg/kg then 5mg/kg
3. Birth trauma => 12h or more. primary 7. Cranial USS. 2nd line: phenytoin 10-
SAH, cerebral venues thrombosis 8. EEG. 20 mg/kg
4. CNS intrauterine infections & sepsis. Second line: 3rd line:
5- Drug withdrawal/ L.A. toxicity 1. MRI or CT. diazepam 0.3 mg/kg
24-72hrs: 2. Maternal & neonatal samples * prognosis depends
1- Cerebraldysgenesis. for drugs. on the cause
2- Vascular (infracts, haemorrhage). 3. Virology/Congenital
3- Intracranialhemorrhage. infection screen.
4- birth trauma +confusion 4. Serum ammonia & amino-
5- Tubulousclerosis. acids.
72hrs-1 week 5. Urine amino & organic acids.
1-. Cerebral malformation/infracts 6. Therapeutic trial of
2-. Familial neonatal seizures pyridoxine
3-. Hypoparathyroidism
4-. Kerinctrus

9. Respiratory distress in neonates:

Signs of respiratory Differentials

distress in neonate:
High respiratory rate I. RDS
Ressetion (sub/inter II. Pneumonia
costal/sternal) III. Pneumothorax
Cyanosis IV. Surgical
Grunting
V. cardiac

** IUGR is protective i.e. stress  ↑cortisol

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 RDS: Surfactant deficiency.

- Surfactant is produced by type 2 alveolar cell late ≥ 32 weeks.

Risk factors
-prematurity
Type 1 DM
-male
Diagnosis
--Confirmatory: CXR
- bilateral diffuse ground glass
appearance of lung
- airbronchogram
- atelectasis

Treatment
-O2 (best initial tx)
- [Link] by ET (best effective tx)
- Respiratory support (CPAP Or IPPV
- Fluids/Abx
- Monitor by  vital signs, ABG
Complications
1. PDA (HF+murmur+collapsing pulse)
2. Air leak (Pneumothorax, Pneumomediastainum, Emphysema)
3. chronic lung disease
4. Cerebral palsy
Prevention
prevent premature delivery
, if already occur
IV steroids for 48 hours Betamethasone (12 mg/24 hours X 2 doses) OR dexamethasone
(4 mg/12 hours X 4 doses)
Management of PDA: - Restriction of fluids + diuretics
- Indomethicin (medical) - Surgery
Management of chronic lung disease
Ventilation with low PO2 and high CO2 via tracheotomy by CPAP. Mechanical
ventilation if indicated only

17
steroids
give RSV prophylaxis
-improve lung function: bronchodilator, fluid restriction, diuretics, and steroids

10. Other problems of prematurity:

**Apnea of prematurity (immature resp center+ low HR)

DX of exclusion

(Apnea +high HR = subtle seizures)

Apnea: no breathing for ≥ 20 sec

TX: gentle stimulation, Xanthenes tx, CPAP if recurrent

**Retinopathy of prematurity:

- Due to oxygen therapy, damages growing retinal vessels>> blindness

- Laser therapy is sometimes needed, but it usually resolves alone.

** Jaundice of prematurity: - Premature liver - Self limiting

**NEC (necrotizing enterocolitis):

- Cow’s milk is a risk factor - Toxic child: distended shinny abdomen, central apnea,
bloody diarrhea, bilious vomiting

-Dx: Abdominal X ray

- Pneumonaleintestinalis

- Air in portal tract

-Air under diaphragm if perforated

- distended bowel loops

- Tx :

No entral feeding for 10 days (NPO, IV fluids, NGT)

IV broad spectrum Abx

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If perforation: surgery

- Complications:

Perforation>peritonitis, sepsis

Stricture> long term

Short bowel syndrome>malabsorption

Diaphragmatic hernia:

- Left sided in 85%

-resp. distress, failure to resuscitation (heart displacement to the right)

- Dx: CXR bowel in chest+ heart displacement

- Tx: first step NGT suction to decompress stomach

Then surgical repair

11. Neonatal infections:

Early < 72h (pneumonia and meningitis) Late > 72h
1- Group B strep (GBS) - Nasocomial
2- [Link] - [Link]
3- Listeria - If pneumonia ([Link], [Link])

~ Septic screen:
1- CBC > Neutropenia 2- CRP 3- Blood culture 4- Urine culture
5- CXR 6- LP 7- Throat, tracheal, skin, rectal swab
~ Mx: Benzyl penicillin (GBS) +Gentamycin ([Link]) + Ampicillin (Listeria)
Or ampicillin + gentamycin
- Prolong rupture of membranes > 18 h
Chorioamnionitis (fever, tender abdomen, foul smelling discharge)
- Preterm +ve GBS, in high vaginal swab
- Why preterm has increase risk?? IgG from mother cross placenta in the last month
of 3rd trimester.
- If mother increase R.F > take high vaginal swab
+ve GBS > Intrapartum Benzylpenicillin
Late onset > Vancomycin + Gentamycin

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Meningitis Conjunctivitis Meconium Transient tachypnea of
aspiration syndrome the newborn: TTN
- High mortality ▪ first 48 h: Sticky Meconium swolled bening self limiting RDS
- ttt: Penicillin / eyes > cleaning by with amniotic fluid of mature (&CS ) #1 / late
Ampicilin+ 3rd water or saline Post term, breech, premature
generation Discharge + redness fetal hypoxia
cephalosporin ( 14 - 21 > Staph or Strept - delayed clearance of lung
day) - ttt: topical Effect: liquids
- Sequele: abscess, antibiotics - Collapse > acute - appears shortly after birth
hydrocephalus, hearing airway obs. - resolve in 3 - 5 days
loss, - Purulent discharge (complete/partial) ▪ Clearance of lung by
Neurodevelopmental + injection of - Chemical Increase trans pul pressure
problems conjuctiva + swellen pneumonitis
* Ceftriaxone displace eyeled - RDS R.F:
Bilirubin > Jaundice - Air leak 1- C.S
* N.B sx not specific Gonococcal (most ~ ↑ 2ry pneumonia 2- Male
(eg; no stiffness) serious) - Persistent 3- Breech
> Bulging of fontanlle, - ttt: I.V 3rd pulmonary 4- Precipitus delivery
Lepithalamus :late generation hypertension of (extremly rapid labor)
cephalosporin newborn C/O:
- Dx: gram stain, - CXR: hyper - increase RR
▪CXR for pneumonia = culture inflation/ flattened - respiratory distress
RDS ▪ 7 - 14 days: diaphragm - increase AP of chest
- Chlamydia (most (barrel chest)
common) On examination:
- ttt: Oral - crackles
erythromycin for 2 - palpable liver and spleen
weeks
- Dx: Investigations:
immunoflurocent CXR: Gold standard >
stain Hyperinflation ( Perihilar
streaking , flat diaphragm)
No consolidation
Dx of exclusion
MX:
O2 / tmp.
Exclude sepsis
Feeding (avoid in RR
>60/min ie;aspiration
Prevention:
- CS at 39weeks
- ante natal steroid before
CS

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*** DDx of increase RR in
newborn: (TRACHEA) other causes of Persistent pulmonary
- TTN hypertension of newborn
- Respiratory infection
Birth asphexia, septicemia, RDS or a 1ry
- Aspiration disorder
- Congenital malformation
Cyanosis, HF , murmur are often
- Hyaline membrane
absent-
disease (RDS)
- Edema ttt: mechanical ventilation + circulatory
- Air lead. / Acidosis support

Vasodilators: inhaled NO , Sildenfi

(viagra)
if very severe: extra corpreal
membrane oxygenation in ECMO
(heart and lung bypass)

ً ً ً
.... ‫ سحصبح كمزا مشعا‬،‫سحصافح بيديك النجىم يىما‬

‫كاوم‬.... ‫فلاوم لطفا‬

21
 12. Neonatal jaundice:

Causes:

▪ 1st day: - Hemolysis: ABO incompatibility, G6PD, HS,Congenital infection (conjugated)

- Blood group
Rhesus: serious, 2nd child, Hepatosplenomegaly, Hydrops anemia
ABO : Commoner, 1est child may be affected, NO hepatosplenomedgaly

Rhesus: mother Rh -ve, fetus Rh +ve

ABO: mother O, fetus usually A
Dx: by coombs test

From 2nd - Physiological

day: - Breast milk jaundice
- B. feeding jaundice
- Infection (UTI)

☆Physiological jaundice:
Dx of exclusion
1-NEVER on day 1
2- Peak 3rd/4th day ( later in premature)
3- Not more than 12mg/dl
4- Early increase not more than 5mg/dl
5- Disappears in 7th day
Causes:
- Liver immaturity.
- decrease life span (80 days)
- increase RBC mass (hypoxic enviroment
Breast milk jaundice:
Breast milk contain inhibitors of conjugation
- increase enterohepatic circulation
- ttt: stop B.F for 1 - 2 days

VS
Breast feeding jaundice - ttt; fed the infant

Jaundice:Face (5mg/dl) > neck > upper chest (10mg/dl) > abd (12 mg/dl) > palm /
soles (15mg/dl)
Management:

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● If reach 16 mg/dl (lower in premature):-
 Phototherapy (blue/white light)

● If 20 mg/dl :-
>> Exchange transfusion > twice blood volume (2 X 85 X kg >> through umblical
Venous catheter

Side effects:

Phototheapy Exchange transfusion

- lethargy , retinal damage Blood  Infection, transfusion reaction,
- Nasal abs. by eye pads met.
- Mask cyanosis Catheter  Perforation, emboli
- Maculopapular rash Procedure hypotension, NEC, porto
- Increase insensible loss > dehydration splenic thrombosis
- Diarrhoea > dehydration

☆Kernicterous: Bilirubin encephalopathy:

- Unconjugated bilirubin > lipid soluble > crosses BBB

- Early > poor feeding/lethargy
- If severe  high pitch cry, Increase tone (opisthotonos), Convulsions, coma
- Deposition:In Basal ganglia/ hippocampus & Brain stem nuclei
☆ Polycythemia:
- HCT: > 65% - ttt: Portal exchange transfusion (replace blood by saline )
- Amount: blood volume (85) X HCT - desired HCT / observed HCT **Desired HCT
= 50%

▪ Un conjugated - Conjugated: (never physiological)

1- Breast milk 1- Neonatal hepatitis (viral, metabolic e.g.
2- Infection (blood, urine) cystic fibrosis, alfa 1 antitrypsin def. `most
3- Hypothyroidism in TFTs common genetic cause`)
4- Pyloric stenosis 2- TORCH > sepsis, hepatocellular damage
3- Biliary atresia/ Choledocal cyst ( U/S +
biopsy) ... ttt: surgery (kassi operation >
Porto entrostomy)

- Sequels:
Choreoatheliod CP

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SN deafness
Mental retardation
Enamel dysplasia

Keep smile

13. Neonatal reflexes:

▪ Moro: up to 4 months
- How: sudden drop of head/noise
>> Extension and abduction of upper limbs followed by flexion and adduction of Lower
limbs

- If absent bilaterally - If absent unilaterally

- CNS damage (HIE, Kernictrues, -Clavicle fracture
haemorrhage) - Shoulder dislocation
-Bilateral Erb’s - Erb’s
-Sepsis - Fracture humerous
-Septic arthritis

** SN deafness in
neonate:
- Kernictrues
- Rubella
- CMV
- Syphilis

..‫ وينطفئ ثماما حين جشعزه بأهه ال فائدة منك‬، ‫هذا العالم يبدأ منك حين ثنهض بهمة‬

24
Part 2: MALNUTRITION
1. Introduction 4. IDA
2. Marasmus 5. Management of malnutrition
3. Kwashicor 6. Rickets
Types of Nutrients

Type 1 Type 2
(Copper,Ca2+,I-,Fe2+ and vitamins) (essential aminoacids , Na+,K+ ‫الجدول‬
‫)الدوري‬
Functional Growth
+ve body stores Nobody stores
Signs of deficiency No signs of deficiency
↓ tissue concentration with deficiency No ↓ in tissue concentration with
deficiency (stable con.)
Variable in breast milk Stable in breast milk
Growth failure is not a feature Growth failure
Classification of PEM (protein energy malnutrition):

*Welcome Classification:

Class Weight (% of standard Oedema

forage)
Underweight 60-80 % No
Kwashiorkor 60-80 % Yes
Marasmus <60 % No
Mar. Kwash <60 % Yes

Advantage= Easy

Disadvantage= No acute/chronic, age-dependent

NB: Standard weight=50th percentile

months
NB: age in 1st year approx. =

In 2nd year= add 2.5kg

After 2 years= (Age “years” x2) +8

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Difference between wasting and stunting:

Weight/age Height/age Weight/height

Wasting - or ↓ - <5th percentile
Stunting ↓ ↓ -
* Water low classification= - Wt/Ht. - Not Age dependent

* Gomez= Researchers/ field work (weight/age)

* WHO= Age-dependent < ₋ 2 Z score :> malnutrition

- Low weight/age= under nutrition

- Low weight/height= wasting= acute malnutrition

- Low height/age= stunting= chronic malnutrition

Marasmus

Time: Early infancy

Diet: Deficiency in both proteins and carbohydrates
Causes:

- Primary (Nutritional): Failure of BF, feeding difficulties (e.g. CP, prematurity, cleft
palate)

- Secondary: Diarrhoea, malignancy, malabsorption, chronic disease etc.)

NB: Premature= feeding difficulty + rapid growth

Disease= Anorexia + ↑ catabolism + food intolerance

=Low (↓glycogen + diabetic pattern)

C/O:

1) Growth failure: Severe wasting, (↓weight/height), first failure to gain weight then
height then H.C

2) Loss of subcutaneous fat: First abdomen, then limbs, buttock, last: buccal pad of
fat. Gives wrinkled skin and old man face

3) Muscle wasting + Hypotonic: Scaphoid abdomen, stick like limb,

4) Psychological: Irritability, crying, little sleep

26
 Head is large, eyes starring and there are Lab:
mild hair changes BUT No dermatosis, no
-Proteins= (serum enzymes) = Normal
liver infiltration.
-Low urea (no [Link])

-Glucose=Low (↓glycogen + diabetic pattern)

Kwashiorkor:

Time: Weaning or post weaning (2-3years)

Diet: ↓ protein, normal carbohydrates
Causes: usually infections

1) Inadequate diet (↓ protein)

2) No synthesis of protein (liver diseases)

3) Loss of proteins (nephrotic syndrome, burns, haemorrhage etc.)

4) Malaria/ helminthic infections

5) Other causes

Features:

Constant features Usual features Occasional features

1-Growth failure 1-Hair changes: Sparse 1-Dermatosis (pathognomenic) :

2-Oedema (most (temple/occipital), thin, hyper/hypo pigmentation , desquamation,
constant). MildG. despigmented, easily ulceration, petichea due to low Zinc,
oedema (due to pluck able=loss of niacin, vitamin A, essential amino acids,
activation of RAA sys. sulphur containing amino adrenal gland abnormalities.
 due to hyovolemia, acids (cysteine, Weeping dermatitis resemble bruising
hypoprotinemia) methionine, pamtothenic 2-Hepatomegaly: Fatty infiltration. ↑free
3-Disturbed acid) and defect in FA
fat/muscle ration: Fat melanin and low synthesis,↑mobilization,↓oxidation,↓excre
is relatively present, pamtothenic acid) tion
muscle hypotonia and 2-GIT manifestations:
wasting Anorexia, Diarrhoea
4-Psychological: (lack of enzymes,
Apathetic, lacking infection, villous atrophy
interest (due to
aromatic AA deficiency

27
NB: Lack of dissaccridone= Fermentative diarrhoea (peri-anal excoriation)
Malabsorption of lipids= Defect in bile salt conjugation

Lab: 2 constant :-
 ↓Proteins  Fatty infiltration of liver
-↓ Proteins (including enzymes except liver enzymes ↑): only ↑ in gamma globulin
…..Reversed albumin: globulin ration
-↓ Urea -↓ Lipids
-↓ Carbohydrates + Diabetic pattern -↑ Na+, ↓K+, ↓ Total Mg2+( normal
(insulin deficiency and insensitivity) serum)
Poor prognostic features:
1) Hypoglycaemia, hypoprotinemia, 3) Liver size >6cm, jaundice,
hypoalbuminemia purpura
2) Sepsis 4) Vitamin A deficiency
Complications:
o Diarrhoea  dehydration, electrolytes dist.
o Infections (More in Kwash. , serious is Bronchopneumonia)
o Hypothermia (More in Mars.)
o Hypoglycaemia
 Mars.  Bleeding (purpura)
 Kwash.  Heart failure

Deficiencies:

B1 (Thiamine) Beriberi (HF, neuropathy)

B2 (Riboflavin) chelosis, angular stomatitis, glossitis

B3 Pellagra (Dermatitis<neck, face>, diarrhoea, dementia, death)
B6 Peripheral neuropathy
B12 Megaloblasticanaemia
Vit D Rickets
Vit C Scurvy (bleeding gums)
Zinc Dermatitis (acrodermatitisenteropathica)
IDA (iron deficiency anaemia)
- Cow’s milk “folic”=goat
- Affects: Cognition/ behaviour (may be irreversible if < 2 years)
- ↑Febrile convulsions, ↓ immunity

28
Vitamin A deficiency:

WHO classification of Vit A deficiency

class Ocular manifestation

XN Night blindness
X1A Conjunctival xerosis
X1B Bitot’s spots
X2 Corneal xerosis
X3A Corneal ulceration <1/3 of cornea
X3B Corneal ulceration >1/3 of cornea
XS Corneal scarring
XF Xerophthalmic fundus
Extra ocular:
Treatment schedule (orally):
 ↑ infections(esp; Measles) o <6 months: 50,000 IU Vit A (yellow pill)
 metaplasia O 6-12 months: 100,000 IU (blue pill)
o >12 months: 200,000 IU (red pill)
 UT= hematuria/pyuria
The dose is repeated in the next day, and after at
 Follicular hyperkeratosis
least 2 weeks (total of 3 doses). Prophylaxis= From 6
 Also ↑ I.C.P months, every 6months till 5 years

Dx: Plasma retinol, conj. Examination, vaginal scraping

NB: ↑ vitamin A= Teratogenicity/ Pseudotumourorcerebri

Management of malnutrition:
-MUAC (medium upper arm circumference) only valid from 6 months to 5 years.
Green(normal): >12,5cm
Yellow (MAM moderate acute malnutrition): 11-12.5cm
Red (SAM sever acute malnutrition): <11cm
*- 3SD: Severe wasting

29
Management of SAM:
If with:1) Medical complication (e.g. fever, pneumonia) 2)Grade 3 (+++) oedema (general
edema)
Next step is inpatient management.
If: 1)No medical complication 2) Grade 1 (dorsum of foot) or 2 (thigh)
Next step is appetite test by RUTF(ready to use therapeutic food): no water, no home
contamination
* Pass= eat >2/3, is an out patient * Fail: eat <2/3, treated as an in patient
Out pt Mx OF SAM: By RUTF. After 6-8 weeks will change to MAM
Mx of MAM: Supplementary feeding program (SFP) : 1- Food based 2- Non-
food based
IN Pt Mx of SAM: (10)
1. Treat/prevent hypoglycemia 7. Start cautious feeding
2. Treat/prevent hypothermia 8. Achieve catch-up growth
3. Treat/prevent dehydration 9. Provide sensory stimulation and
4. Correct electrolyte imbalance emotional support
5. Treat/prevent infection 10. Prepare for follow-up after recovery
6. Correct micronutrient deficiencies
1-Tx/prevention of hypoglycemia 2- Tx/prevention of hypothermia:

What is hypoglycemia?? What is hypothermia??

B.S < 54mg/dl = 3mmol/L Axillary temp <35 C
Tx : rectal temp < 35.5 c
- 1- If the child is conscious ,50ml Tx:
10 m% glucose or sucrose 1-Rewarm the child ( kangaroo technique,
oral/NGT heater, lamp ( net fluorescent) NOT hot
- If uncon.  IV 10% dextrose bottle
5ml/kg 2- feed straightway .F 75
3- Abx
- Then F.75 every ½ hour for 2 Monitor:
hours 1- Temp (first every ½ hour if heater ,
1- Abx if no heater used every 2 hours )
2- Blood glucose.
Monitor: PREVENTION :
1- Blood glucose , if < 3 repeat dose 1- Feeding 2hriy day + night :
2- Rectal temp ,if <35.5 , repeat hypoglycemia ,hypothermia
dextrose 2- Keep baby clothed.
3- LOC , i repeat dextrose 3- Keep baby dry
4- Avoid exposure (unnecessary ex.)
N.B :hypoglycemia often exists with hypothermia ( both are signs of infection)

30
Tx / prevent dehydration:
One indication for I.V fluids in malnutrition?? SHOCK
Fluid of dehydration in malnutrition: RESOMAL
Why not ORS?? In ORS, Na is high and K is low
Na K
ORS 90 20
RESOMAL 45 40
How to prepare ReSoMal:

1L O.R.S packet, 2L water, 50 g sugar, 40 ml electrolyte (K) / mineral solution (mg).

How to give ReSoMal:

-5-10 ml/kg / 1 hr for 4-10hrs (alternating with F-75) oral or NGT

SIGNS OF DEHYDRATION:

Reliable Not reliable

Hx of diarrhea Lethargy
-thirst Sunken eye
Recent sunken eye Skin turgor
Weak /absent radial pulse Dry membrane
absent urine flow
Monitor??Every ½ hour for 2hrs then hourly for 6-12hr

1-PR (low) 2-RR (low) 3- U.O.P (high)

If child develop increase RR, increase PR, puffy eyes + edema = stop fluids + reassess in
1 hour
To prevent after ReSoMal Tx:
After each loose stool: give 50-100 ml of ReSoMal
N.B: any child with watery diarrhea, assume dehydration.
How to treat septic shock??

- I.V fluids :
* 15 ml /kg / hr
Options; 5% D, 5% D+ ½ N.S, 5% D + R.L (ringer lactate)
- Broad spectrum Abx
N.B: achild is TX by those fluids but not improving or show signs of OHF what to do??

Slow blood transfusion 10 ml/kg over 3 hrs

31
4- Correct electrolyte imbalance:

Malnutrition: high Na, low K, low Mg

So we give extra k, Mg (electrolyte mineral solution)

How much?? 20 ml in 1L of food

5- Tx /prevent infection:

Usual signs of infection are not found (e.g. fever), so any child with malnutrition:

1 - Abx:

-Amoxicillin 15mg /kg 8hrly (no complication, oral) OR

-Ampicillin + gentamicin 50mg /kg 8hrly I.V /I.M (sever ill).

2- Measles vaccine if> 6months and not given.

Some add metronidazole 7.5mg /kg 8hrly

- If child is HIV +ve ,add cotimxazole

- If infection is identified specific Tx.

- If no improvement in 48 hrs, add chloramphrnicol

- If still anorexic after 5 days, continue for 10 days

- If still, reassess checking for infection sites, resistant organisms and you may try
Vit/mineral sup.

6- Correct Micronutrient DEFECIENCIES:

Vitamins, zinc, copper and iron

Vitamins: vit A at day 1 (same doses)

Folic acid (at day 1), Multivitamin complex

Iron: never in first week (increase infection), start after gaining wt (wk2) after
stabilization phase

32
 N.B: electrolyte / mineral solution contains: Zinc, copper, K, mg

7- START CAUTIOUS FEEDING:

By F-75 (milk based)

Components F-75 (100ml) contains:

-Calories 75 kcal

-Proteins 0.9 g

- Use day 1 wt to calculate how much to give

HOW TO GIVE:

Day 1-2 2 hrly 11ml/kg

Day 3-5 3hrly 16 ml/kg
Day 6-7 + 4 hrly 22ml /kg
How to give? by cup (no bottle)

NGT if: eat <80% (< 105ml/kg / day) or

Feeding problem (cleft palate)

Monitor:

1- Amount of food offered and left over

2- Diarrhea/ vomiting

3-Daily body wt

8- ACHIEVE CATCH -UP GROWTH (rehabilitation phase):

By F-100 or RUTF

Components: (100ml of F-100)

100 Kcal, 2.9gprotiens

Difference from F-75:

F75: high sugars, low vegetables, low milk, no creal flour in F-100

When to start F-100: significant rehabilitation, regaining of apitite , usually after one
week ,decreased edema .

33
Transition from F-75 to F-100 is gradual to avoid HF .

Transition: if the child eats < 50 % of the amount, back to F-75

You enter if he eats > 75% of F-100 or RUFT

-If during feeding HR increased by 25 and RR increase by 5 or more>>> lower the dose

-Aim of rehabilitation phase: rapid wt gain > 10 g /kg /day.

- Check if feeding target is met;

< 5-10 g/kg/day  look for infection

<5g/kg /day is poor need full assessment

10- PREPARE FOR FOLLOW UP AFTER RACOVERY:

Recovery: 90% wt for length (-1SD) CRITERIA FOR CURE by time:

1- 3-4 daysdisappearing of apathy and irritability
2- 10days skin lesions heal
3- 10 wkschild loss wt then gain wt 2.3kg
4- 3 Months Return to normal health
5- 5-albumin > [Link]

Some ER
SHOCK ANEMIA

The cause is either: Mild /moderate: iron in rehabilitation

- Dehydration or Septic shock for 2 months
Treatment: -If Hb< 4 or PCV <12% or 4-6 times
- Oxygen -I.V 10% D -Abx respiratory distress blood
 I.V fluids ( 15 mg /kg /hr over 1h) transfusion as above or packed cell
5%D + ½ NS / R.L (5-7), if he has signs of CHF (do not
If not all  R.L transfuse within 4 days)
-If child is improving (↓PR, ↓RR) : N.B : TB , if strongly suspected (Hx
-Repeat fluid dose of contact with TB pt ,poor growth
- Start ReSoMal( dehydration) despite good intake ,chronic cough
-If no improvement ,give maintenance fluid(4ml/kg/hr) ,chest infection not responding to
while waiting for Abx ),do:
- Fresh whole blood (10mg /kg over 3 hrs) -Monteux test
When to stop blood transfusion? - Chest x-ray.
- If transmission reaction occur ( fever , itchy rash, red If test is +ve or strong suspicious ,
urine, shock ,confusion) start anti-TB
-RR increase by 5,HR increase by 25

34
*RICKETS:

Definition: Defective mineralization of bone

Causes

Nutritional - Breast feed only after 6 months

(infantile) - No sun exposure
- Malabsorption
Impaired - CRF
metabolism - Chronic liver disease
- Anticonvulsants (e.g. phenytoin)
Others -Familial hypophosphatimicrickts (Vit D resistant rickets),no
phosphate : no mineralization . or Non familial, commonest
cause is Fanconi anemia
-Vit D dependent rickets:
Type 1: no 1α hydroxylase Type 2: unresponsive receptors.

C/O: General: - Failure to thrive - Short stature *Square box shape

* BONES:

- Head: ↑H.C, frontal + parietal bossing + flat occipital, large unclosed fontanels, cranio
tapes (earliest change)

N.B hydrocephalus, osteogenesis imperfecta: DDx for craniotapes just not all head
features

- Thorax: - Rachitic rosary (costochondral junction)

- Harrison sulcus (transverse)

- Longitudinal sulcus (pigeon chest)

- Extremities: bowing, #

- Pelvis: narrowing

- Muscles+pott-pelly abdomen: weakness + hypotoniaRepeated chest infection also

because of immunodeficiency

Delayed milestones

- Convulsions due to hypocalcaemia.

35
****Lab: Bone profile: ↓Ca+2 , ↓ PO₄ (in familial ↓↓↓), ALP: ↑, PTH: ↑ (except in
familial )

 ALP normal in hypoparathrodisim , it is zinc dependent so is not elevated

in malnutrition
Vit D:

25(OH) D3 (liver) 1,25 (OH) (Kidney)

Type 1 Dependent _ ↓
rickets

Nutritional ↓ ↓

Type 2 Dependent _ ↑
rickets

**Familial (x-linked dominant), males (short stature)

** Type 2 Dependent rickets (AR) (Alopecia)

Wrist x-ray in rickets:
Management:
1-Clubbing, fraying of
 Nutritional rickets:
metaphysis (broad)
1. Vit D Daily 3000-5000 (changes in x-ray 6-8 wks)
2. OR single dose (IM/oral) 600,000 2-↑ joint space
(changes in x-ray by 1 month)
3-#, deformities
3. Oral Ca+2
Monitor by ALP ↓/ Vit D level / x-ray: healing 4-Wide epiphysis plate.
Duration: 3 months When healing  lines of
 Hypophosphatimic oral PO₄ sup. calcification
 Vit D Dependent rickets Vit D
(in type 2 higher dose) , oral Ca
OR Ca infusion to bypass intestine for 1 year

‫ثلة منها إلى شأهك‬

ٍ ‫ ضعها ملء وجداهك وانهض على‬..‫يدبزألامز‬

36
 PART 3: NEUROPEDIATRICS
1. Seizures
2. Epilepsy
3. CP
4. Peripheral motor disorders
5. Peripheral nerve disorders
6. Muscular dystrophies
7. Floppy infant
8. Ataxis
9. Stroke
Seizures Causes:

1. Epilepsy (un provoked) 2. Non epileptic (provoked)

-Idiopathic (70% _ 80%) -Febrile convulsions

-Secondary( HIE ,congenital -Metabolic ( decreased glucose ,increased or decreased
malformation ) Na ,decreased Ca , decreased Mg )
-Neurocutanous syndrome -Infections (meningitis, encephalitis).
-Tumours. -Trauma
-Poisons , toxins
Febrile convulsion: Seizure + fever in the absence of intracranial infection cause rapid
increase in temp. (Viral infection) - Incidence: 3% - Age: 6 months _ 5 years

- Genetic predisposition 10%

Types:

Simple Complex

-Brief -Prolonged more than 15 mins

-Generalized tonic clonic -Focal
-Once/ day -More than one / day.
-No focal neurological deficit

*Increase likelihood of recurrence in the same illness:

1. Younger age. 3. Short period b/w illness will lead
2. Low temp. At the start. to convulsions
4. Family Hx.
-Risk of epilepsy: 1% as general population

But if complex: 4% _ 12%

37
Management:
-Rx of seizures: ABC + blood glucose
If more than 5 mins: rectal diazepam 0.5 mg/kg
Or buccal midazolam (same dose)
Then wait for 5 mins if not stop manage as status.
-Rx of fever: reduce clothes, fan, paracetamol, adequate fluid intake while looking for the
cause of fever.

*Admission, if:
1. First attack
2. In subsequent age less than 18 months (Complex seizure)
3. Social factors

N.B meningitis is not apparent in ages less than 18 months. (Start empirical antibiotics)
L.P is C.I if, 1. Unconscious 2. CV instability

Status: more than 30 mins or multiple without regaining consciousness.

Rx: ABC + blood glucose
1. If there is I.V access, apply I.V lorazepam 0.1 mg/kg or I.V diazepam 0.3 mg/kg.
-If there is no I.V access rectal diazepam 0.5 mg/kg or buccal midazolam 0.5 mg/kg.
Wait for 5 mins, if not stopped then
2. Repeat above drugs and wait for another 5 mins. if not stopped then
3. I.V infusion of phenytoin 18 mg/Kg with N.S 0.9%
-Or loading dose of phenoparb 20 mg/kg orally or by NGT.
N.B If on phenytoin don't give phenytoin
If not stopped
4. ICU : Intubation + general anaesthesia (thiopental 4mg/kg (I.U/ I.O))
Midazolam loading dose then 2 mg/kg/min maintenance dose.

Paroxysmal disorders (funny turns)

-there is broad D.D for children with paroxysmal disorders depending on thorough
history and examination+ investigations.

38
 Causes of funny turns

1-Reflex _ anoxic seizures Toddler + pain (head trauma) or fear / cold food / fever” 3fs”>>>>>
(Palloid B h attacks) become pale (a systole) + LOC (exaggerated vagal cardiac reflex).
2-Breath_ holding attacks Infant or toddler + crying (temper) = blue i.e.; holds his breath.
“cyanotic B.H.A”
3-Syncope. -
4-Benign paroxysmal Recurrent episodes of vertigo associated with nystagmus>>> viral
vertigo. labrynthitis
5-Basilar migraine. -
6-Others, fabricated, -
pseudo seizures, etc.
Childhood Epilepsy Some epilepsy syndromes:

WEST syndrome 4-6 months, infantile spasm on walking (salaam spasmflexion then
extension.)
EEG :hypsarrythmia“chaotic pattern”
Rx: ACTH.
If caused by [Link]>>vigabatran(visual field defect)
Complications: epilepsy , learning difficulty
N.B Infantile spasm +hypo arrhythmia =WEST syndrome
DDx : T.S
Hypoglycaemia.
LENNOX –GASTAUT Multiple seizures types “1-3 yrs”
syndrome (Atypical absence, tonic, a static “drop” attacks).
Neurodevelopment arrest or regression and behavioural disorders
JUVENILE At adolescence “ when absence end “
MYOCLONIC Throwing foods in the morning.
EPILEPSY Lifelong Tx, remission is unlikely. Learning is unimpaired
Anti-epileptic drugs:

First line: Sodium valporate, Carbamezapine.

Second line: Lamotrigine, Topiramate.

Cerebral palsy: Def.: Abnormal movement / posture caused by

non progr essive damage to the growing infant or
foetal brain (Damage before 2 yrs).

- Damage is non- progressive. But C/O Progressive. Incidence 2/1000 live births

39
 Causes:
1. Antenatal (80%) , congenital infections , [Link] , vascular problem, etc.
2. Natal (10%), HIE, Trauma.
3. Postnatal (10%), meningitis, encephalitis, hypoglycaemia, cardiopulmonary arrest,
haemorrhage, etc
C/O “clues”
1. Abnormal posture (limbs /trunk). 4. Persistent primitive reflexes.
2. Delayed motor milestones. 5. Gait problems when walking
3. Asymmetric hand function (less 6. Feeding difficulties (gagging ,
than 12 months) vomiting , in coordination)
Types:
1. Spastic 90%. 3. Ataxic 4%.
2. Dyskinetic 6%. 4. Mixed.(chorioathetoid)
spastic Dyskienetic ataxic
Damage :corticospinal pathways Old , kernicterus Genetic
*Hemiplegic: arms more than legs, sparing the face. now, HIE Damage:
Cause: neonatal stroke. Damage : basal cerebellum and
Arms: fist, flexed and pronated. ganglia its connections
Legs: tip toeing.
*Quadriplegic :
Cause: HIE
Most severe form and the most associated
with learning difficulties and epilepsy.
*Diplegic:
Cause: PVL (preterm)
N.B; Spasticity: crossing, tip toe gait.
*Problems of C.P or complications
1. Learning difficulties 5. Speech problems
2. Epilepsy 6. Feeding problem>> growth
3. Hearing loss failure.
4. Visual impairment , squint 7. Joint contractures.
Rx is multidisciplinary -Physiotherapist, orthopaedic surgeon, speech therapist, adequate
feeding, etc.

CP

40
 PERIPHERAL MOTOR DISORDERS:

- Degeneration of motor neurons in the anterior horn. (Fasciculation weakness)

**Spinal muscular atrophy SMA:

-AR “survival motor neuron (SMN) gene

Type 1 Type 2 Type 3

(Warding - Hoffman's ) (intermediate): (kugelberg-Welander):
C/o: sit but never walk Later in life (can walk).
-foetus with decreased movement independently
-At birth :arthrogryposis (deformity +
contracture of at least 2 joints) then LMN
features “remember tongue fasciculation’s”
-Never sit unaided , death by respiratory
failure at 12 month “diaphragm paralysis”
-Gold standard Dx is genetic study.
**Polio: Asymmetrical flaccid paralysis

Peripheral nerves (areflexia/ pescavus/ distal weakness):-

Hereditary motor sensory neuropathy (HMSN):

TYPE 1 (Charcot -Marie – Tooth disease)

-Peripheral muscular atrophy

N.B inverted wine bottle leg.

-AD. 1st decade: distal weakness/ wasting and pescavus.
DDx: F. Ataxia
-Normal life span. Nerves: enlarged “remyelination attempts”
Gold standard Dx: sural nerve biopsy. Biopsy: onion – skin.

41
 Fasciculation

Muscles: Muscular dystrophies:-

Duchene Becker's

X-linked recessive (dystrophin) Same but slower

C/o proximal weakness >>>waddling gait, gower sign. Dx: 11years “Duchene 4 to 5 yrs”
Age 4 - 5 years. Unambulant : 20s “Duchene 10 to 14 yrs”
Increased CPK. Death : late 40s “ Duchene late 20s”
At 10-14 yrs : not ambulant
Late 20s :death “respiratory failure , cardiomyopathy
DCM”
N.B Scoliosis is common.
Rx
1. Physiotherapy
2. Respiratory: NIV at night.
**Myotonia:-Delayed relaxation after sustained contraction.

42
**MyotoniaDystrophica: - AD (trineucleotide repeat) -Association: frontal
bladness, testicular atrophy, cataract, learning
difficulties and DM.

Death: cardiomyopathy.

Neuromuscular disease: illustrated

p.480

FLOPPY INFANT:

Rag – doll, head lag, slip through fingers

. Frog – like posture ( abduction of
LLs)
Causes:

Central 1. Cortex: HIE, [Link].

2. Genetics: Down’s, prder-willi.
3. Metabolic: hypothyroidsm, hypocalcaemia.
Peripheral 1. SMA
2. Myopathy
3. Myotonia
4. Congenital myasthenia

43
 ATAXIAS: Both are AR

1. [Link] 2. Ataxia telangectasia

Gene:frataxin DNA repair gene (ATM)

*Degeneration : -Infancy: oculomotor dyspraxia.
-Spinocerebellarataxia -4 yrs: telangectasia (eyes, shoulders, neck).
Corticospinalweakness + up going plantar -School age: ataxia.
reflex “sinopulmonary”
-[Link]areflexia (all reflexes) &wasting. -Associations >> IgA deficiency = infections.
-DCTLoss of vibration &proprioception. -Increase risk of ALL
-There is pescavus “high arch “so DDx is -Increase alpha fetoprotein
HMSN. Sensitivity of WBCs to radiation “remember
-Death 40 – 50 (HOCM, kyphosciliosis) Fanconi”

Other causes of ataxia:

 Infections: e.g. varicella

 Drugs: e.g. .phenytoin

 Posterior fossa neoplasm e.g. medulloblastoma

Telangectasia

Stroke: Causes:

1. Cardiac: cyanotic CHD

2. Heamatologic:SCD,anti-thrombin def
3. Post infective: varicella
4. Inflammatory:SLE
5. Metabolic\genetic :homocystinuria
6. Vascular malformations: moya-moya disease(abnormal vasculature).

Investigations: - MRI, MRA, carotid Doppler studies - Echo - Metabolic test.

44
 Child may need rehabilitation Aspirin prophylaxis.
Neural tube defects

-Failure of neural plate fusion to form neural tube in the first 28 days of life.

It include:

Anencephaly Encephalocele Spina bifida Meningiocele Myelomeningiocele

: occulta

Rx TOP Neurosurgery , Failure of fusion of Neurosurgery C/o

(termination but usually [Link] ASAP: Risk 1-LL paralysis (walking aid
of there is Skin : tuft of hair , of meningitis. , physiotherapy)
pregnancy). underlying birth mark , lipoma Good 2-Muscle imbalance :
Most severe: brain , sinus prognosis. dislocation ,
dead “still malformation Next step >>> U/S talipes(physiotherapy)
birth” or die or MRI 3-Loss of sensation (skin
shortly after WHY? To exclude care)
birth tethering of the 4-Neuropathic bladder
cord (intermittent
“diastomatomyelia” catheterization, oxybutinin be
If +ve ware of UTIs , RF ,
>>>neurosurgery. hydronehrosis)
5-Neuropathic bowel (
regular toileting , laxatives)
6-Scoliosis (surgery)
Hydrocephalus 80% due to
Arnold Chiari malformation
(shunt)
Most severe disease : above
L3

Hydrocephalus ‫الشيت‬ N.C syndromes illustrated page 489

‫ ال تعيش حياتل وأنت ترسن الحذود‬... ‫حتى تنجح‬

‫عش حياتل وأنت تتخطى مل الحذود‬

45
PART 4: HEMATOLOGY
1. Anemias
2. Sickle cell disease
3. Thalassemia
4. Anemia in newborn
5. Coagulation problems

Anemia: Main site of hemopoiesis in the fetus => liver.

Hb F Hb A Hb A2
Fetus 100% - -
At birth 75% 26% 1%
After one year - 97% 2%
*Differences b/w Hb F /Hb A: Hb F: higher affinity for [Link] curve: shifted
to the left.

At birth:

o Hb is very high (14-21g), gradually decrease over two months (10) => lowest
value .
o Blood volume: term 80 ml /kg , preterm 100 mg/kg
o WBCs = higher (10-25)
o PLTs = as adult.
o Iron, B12, folic acid => adequate stores in both term and preterm.
But in preterm: more ↓↓ and its lower (iron, folic acid).

*Diamond black fan anemia:

-Family hx =20% , Sporadic= 80%

-C/O: At birth (25%) , rest in 2-3 months.

Maybe associated with short stature, abnormal thumb .

-Gene RPS (ribosomal protein).

-Tx: Steroids. If unresponsive, monthly RBCs transfusion, stem cell transplantation.

*Transient erythroblastopenia:- No RBS gene - Resolves in few weeks.

- No family hx, no RPS, congenital anomalies.

46
 **Triggered by viral infection**

Increased RBCs destruction (hemolytic anemia) :-

↑Ritcs, ↑Bilirubin, ↑urobilinogen Hepatosplenomegaly.

Some points

*G6PD deficiency = most common enzymepathy.

= most common cause of severe neonatal jaundice requiring

transfusion.

- Hemolysis in G6PD deficiency => dark urine, fever.

Sickle cell disease:

Autosomal recessive inherited hemglobinopathy.

1- HbSS (SC anemia): no HbA

2- Hb SC: no HbA
3- Hb SB: Thalassemia no HbA
4- Hb SA (SC trait):40% of Hb is Hb S
Sickle cell crisis Dx Mx complications
1- vaso-occlusive 1-full blood Prophylactic : 1-Growth failure (delayed
crisis count 1- full immunization puberty).
2-hemolytic crisis 2-blood film 2-daily oral penicillin 2-HF --> anemia.
3-aplastic crisis 3-sickling 3-folic acid 3-Gall stones.
4- splenic solubility test 4-hydroxy urea 4-Renal impairment =>
sequestration crisis 4-Hb 5- Avoid precipitants (warm , exacerbate enuresis
electrophoresis. adequate hydration before (inability to concentrate
exercise urine).
Mx of acute crisis: 5- Leg ulcers. (Uncommon
1- hydration in children).
2-analgesia 6- Psychological problems.
3-oxygen 7-stroke
4-Abx
5- blood transfusion if needed

Indications of exchange transfusion:

- Sequestration crisis
- Acute chest syndrome
- Stroke , priapism

47
 # Thalassemia: Defects in production of the α or β chains of hemoglobin resulting
imbalance in globin chains leads to ineffective erythropoiesis and Hemolysis in the
spleen or BM

Types of Thalassemia:
 β.Thalassemia :-
-β- Thalassemia major => no Hb A
-β- Thalassemia trait (intermediate) => few Hb A , high Hb f .
β- Thalassemia major:
C\O:- severe anemia (Transfusion – dependent)
If no transfusion =>
- Extramedullary hemopoiesis(frontal bossing, maxillary overgrowth )
- Growth failure.
Mx:- Regular blood transfusion + iron chelation (oral \ SC desofrroxamine) **aim: Hb =
10 **
Complication of blood transfusion:-
1. Hemochromatosis (cardiomyopathy, 3. Infections (Hep B, C \ HIV \
growth failure …etc). malaria).
2. Abs formation (10%). 4. Venous access problems.
** Definitive => BM transplantation**
β- Thalassemia trait:
Sx: HbA= >90%
DDx: IDA. (Check ferritin)
N.B* Dis ↓ in MCV, MCH “very low”, RBCs may be even.
-Most important in DxHb A2.
 α.Thalassemia :-4 genes ,
All absentHb Part (hydropsfetalis)
3 absent Hb H (Moderate anemia)
2/1 absent α.Thalassemia trait (mild/no anemia)

**NB; β chain X  after 6 months, while α chain X at birth

** Perinatal diagnosis  chorionic villous sampling.

Thalassemic face

48
 Anemia in Newborn:- Causes

↓ Production congenital B19 infection, Diamond black fan

↑Destruction Immune / non immune(G6PD def., HS, α.Thalassemia )
Blood loss To mother (fetomaternalhemo.) / to twin (TTTTS) / at delivery
** ↑ Ritcs, normal Bilirubin
Anemia of prematurity ↓RBCs life span, inadequate erythropoiesis, ↓iron& folic acid,
frequent blood sampling
Bone marrow failure (A plastic anemia): **Pancytopenia

- Inherited: Fanconi, shawrman’s diamond - Idiopathic

- Acquired: Infections (hepatitis), Drugs (sulfa amide, chemotherapy), toxins
(benzene)
Fanconi anemia Shwachman Diamond Syndrome
(SDS)
AR (DNA repair gene) - AR.
C/O: - Association  Exocrine
 At birth: congenital anomalies (absent pancreatic abnormalities,
thumb),macropthalmia, Kidneys (horse-shoe, skeletal abnormalities, also
absent), skin (café aulait) increase risk of leukemia.
 5-6 years: Pancytopenia
Dx: Dx:
When exposed to damaging agent  ↑ chromosomal -prenatal Dx.
breakage of peripheral blood lymphocytes - Genetic study (SBDS).
Prenatal Dx, family screening
** ↑ risk of acute leukemia, other malignancies (e.g.
GI, gyne)
Mx:
B.M transplantation
Coagulation problems:

Inherited Acquired
Hemophilia -V k deficiency
-VWD -liver diseases
-ITB -DIC

PT = extrinsic pathway. APTT = intrinsic pathway. PT = not used now. (Platelet

function analyzer ). RiCoF “Ristocitin cofactor” = Vwf activity.(Vit D)

Ristocitin- induced platelet aggregation = abnormal in VWD.

49
Hemophilia VWD
- APTT. -AD
- X-linked / recessive. BT, APTT.
- A= factor VIII deficiency. -VwF: platelet aggregation, factor VIII
B= factor IX deficiency. carrying and protection.
C/O: Neonate  I.C hemorrhage, post- -Many subtypes:
circumcision/ venipuncture bleeding. # Subtype 1 = mild (commonest).
Toddlers when start to walk / crawl. ~ C/O :
*Severity: puberty/ adolescence:
- < 1% severespontaneous bleeding Skin bruising.
- 1-5% moderate bleed after Minor Mucosal bleeding (menorrhagia/ epistaxis).
injury. **N.B; Spontaneous bleeding not common.
- 5-40% mild after major injury. Tx :
Mx: -DDAVP  mild (subtype 1).
Very mild bleeding = DDAVP (desmopressin: Risk: hyponatremia (=seizure) especially if < 1
synthetic ADH). yr.
Others: factor VIII concentrate -F VIII concentrates (plasma – derived only).
How much? Not recombinant i.e.; do not containVwf.
If minor bleeding: till conc. reaches 30%. -replacement therapy.
If life- threatening: till “ “ 100%. Then Also avoid:
maintain 30-50% for 2 wks. -Aspirin
Severe hemophilia = F VIII prophylaxis. – NSAIDS.
(Risk of joint damage). -I.M injections.
also=
Hemophilia (including psychosociotherapy,
physiotherapy).
** avoid: I.M injection / NSAIDs- aspirin

Complications of Hemophilia:
• Joint bleeding
– Knees>elbows >ankles >shoulders – Leads to chronic synovitis
• Muscle bleeds
– Leads to fibrosis and atrophy – Can lead to compartment syndrome
• Pseudo tumors • Subdural hemorrhage
• Inhibitors • HIV/hepatitis C – 90% if Rx started before 1994

50
 Thrombocytopenia: Causes:

Destruction Immune: ITP , SLE

Non-immune: HUS , TTP , DIC , hypersplenism

↓ production Congenital :wiskott Aldrich , Bernard Soulier

Acquired: BM infiltration (leukemia, a plastic anemia) .

PLt: If 50 - 150.000 = mild (major surgery/trauma)

< 50 – 20 = moderate (moderate “surgery). < 20 = severe (risk of spontaneous

bleeding)

Bleeding: bruising, petichea, mucosal, GI , intracranial (rare)

*ITP (immune thrombocytopenic purpura):

- Commonest cause of thrombocytopenia in children. - IgG Abs against platelets.

# C\O:-
- Previously health child - 1-10 years - Sudden onset of generalized purpura and
petichea

- Profound thrombocytopenia - Bleeding from mucus membranes and gums.

#Dx: - by exclusion (ALL, SLE …etc)

N.B: you should examine the bone marrow if you want to give steroids, it will mask
ALL.

#Mx:- Self limiting in 6-8 wks.

No TX unless:

1. Severe bleeding (I.C, GI) . 2. If minor but affecting life

 Oral prednisolone or IVIG or IV anti D Avoid contact sport when platelets

are low.
**Chronic ITP = > 6 months Also no TX when: Same indications

Rituximab (monoclonal Abs against B lymphocytes).

51
- Splenectomy (non-responsive pt)

ITP

DIC: Sepsis, shock , major trauma , burns

Lab: PT, PTT.

- ↓PLTs, ↓fibrinogen. (Also ↓ protein C/S, ATIII).

- f. degradation products ,  D-Dimers
Mx:

- Ttt of underlying cause. - ATIII, protein C concentrates. (if

- F.F.B or cryoprecipitate needed)
- PLTs. (if needed)

‫كن راضيا وكأهك ثملك كل ش ئ‬

‫فما كحبه هللا لك ألطف مما جشاء‬

52
 PART 5: RHEUMATOLOGY
1) Juvenile idiopathic arthritis
2) SLE
3) Juvenile dermatomyocitis

◾Juvenile idiopathic arthritis:

The most common chronic rheumatological disease in children.

- Genetic susceptibility. - Environmental triggers.

◽C/O: ◽Criteria:
- Onset < 16 years.
- Morning stiffness (better during the day).
- Joint swelling ≥ 6 weeks.
- Arthritis or 2 of (joint pain / tenderness, - No other causes.

- ⬇ range of movement, worm).

◽Long term: Overgrowth:

- Discrepancy in length, genu valgus - Digits different in length.

- Wrist advance bone age

◾Types of JIA

- Systemic arthritis - Polyarthritis - Pauciarthritis or oligoarthritis

- Entheistis-related arthritis. - Psoriatic arthritis.

Pauciarticular Polyarticular
50%, Commonest. ≥5 joints (symmetrical)
<5 joints. Usually small joints.
Usually large ( knee, ankle, wrist) not hip F>M
F>M If RF +ve “early onset RA” (F adolescent 10-14
ANA +ve in 20% ( ⬆ risk of uveitis) years) worse prognosis than RF - ve.
Prognosis good. Cervical spine may be involved.
*N. B. If evolve to involved ≥5 joints after 6
months = extended Pauciarticular type.

53
 ◽Systemic onset JIV:

Fever, Hepatosplenomegaly, lymphadenopathy, salmon rash.

⬆ WBCs, ESR/CRP, Platelets, Anemia.

Worst type especially if Polyarticular.

▪ Other types:

Enthestitis- related arthritis Psoriasis related arthritis

Inflammation of tendon area e. g Achilles’ or Arthritis + psoriasis or

arthritis + ≥2 of : Arthritis + family Hx of psoriasis + dactilitis,
o 1. uveitis finger nail changes.
o [Link] pain
o [Link]
o 4. FamilyHx of HLA. B27 related
diseases (IBD, uveitis, and
spondyloarthritis).
o 5. HLA. B27
M>F
◾Complications:

- Chronic A. Uveitis. - Osteoporosis (nutrition, steroids,

⬇Wt bearing).
- Joint contracture = needs joint
replacement - Growth failure, delayed puberty.

- Amyleidosis.

◾Tx: Multi disciplinary: ❇ Drugs:

1st choice: NSAIDs (not aspirin)

Avoid steroids unless severe sys. Onset JIA or severe arthritis (unable to walk).

2 nd line: - Methotrexate (hepatotoxicity, B.M suppression)

- Sulfasalozine, hydroxychloroquine...etc

If failed = anti TNFα (inftiximab, etanarcept)

54
* N. B if you do arthrocentisis: WBCs 50,000 – 100,000, lymphocytes (no neutrophils)
 non suppurative

Remember: physiotherapy, ophthalmic follow u

◾SLE:
Criteria : MD SOAP N HAIR
M = Malar rash
D = discoid rash ( scaling)
S = serositis...
O = oral ulcer
A= +ve ANA
P = photosensitivity
N = neurological (seizure, psychosis)
H = hematology (+ve comb Anemia, Thrombocytopenia, lymphopenia).
A = arthritis≥2 peripheral joints.
I = immunology (anti ds-DNA, anti Smith Abs, false +ve tests for syphilis, anti
cardiolipin Abs= thrombaitis).
R = renal ( proteinuria, cellular casts)

Other manifestations:
Reynaud’s
Best for screening (highest sensitivity) = ANA
Specificity:
- Anti ds DNA. ⬆During active disease - Anti Smith Abs. Most specific
How to follow:
- Anti ds DNA. Best for follow up. - ESR = in RA, (CRP is normal).
- Complements: it is low first.
◾Tx:

55
 - Severe flares (nephritis, CNS, [Link]. etc). I. V cyclophosphamide.
- Maintenances + skin diseaseHydroxychloroquine (monitor eyes). - Steroids
as start

◾Neonatal lupus:
- Maternal Anti Ro. Anti LA, Abs.
- Rash, hepatitis, hematological reversible.
- Congenital Heart block Permanent.
TX: - Corticosteroids - [Link] - Cardiac pacing

Severe cardiomyopathy>>cardiac transplantation.

Neonatal lupus

◾Juvenile Dermatomyocitis:

- Most common idiopathic inflammatory myopathy in children.

- Auto immune capillary vasculopathy>> genetic susceptibility. - 4 _10 yrs. (F>M).

C/O:

- Symmetrical proximal weakness (Difficulty with stairs, getting up, +ve Gower's..
etc).

- May affect pharyngeal muscles =dysphagia. - May affect Resp. Muscles.

- Skin :

56
  Rash. (Face)

 Shawl’s sign.

 Gottrons papules.

 Heliotrope Rash.

 Periungualr erythema.

- Arthritis

Dx:

- No sys : inflammation ( just muscles), WBCs, ESR, CRP are normal

- EMG( electromyography changes) : myositis
- ⬆Muscle enzyme (AST, ALT, CPK, LDH, Aldolase).
- Biopsy : confirmatory
Mx:

- Steroids
- Skin: hydroxychloroquine , avoid sun(= SLE)
- #1 complication Calcinosis

Heliotrope rash

Gottrons papules

57
58
 ‫ال جسخسلم كلما جعثرت انهض وكلما اخطأت صحح وكلما فشلد حاول‬

‫وكلما اصزت الايام ان ثجعلك عابسا ابخسم رغما عنها‬

PART 6: EXANTHEMAS
A- Maculopapular rashes 6- Infectious mononucleosis
1- Measles B- Vesicular rash
2- Rubella 1- Varicella zoster
3- Fifth disease 2- Hand foot and mouth disease
4- Rorseola infantum 3- Kwasakis disease
5- Scarlet fever
______________________________________________________

Measles: Paramyxovirus * Infectivity: 4 days before- 4 days after the rash

C/O: High grade fever+3Cs (coryza, conjunctivitis, cough)

Koplik’s spot (oral mucosa) maculopapular rash (starts in the facebehind the
earsbody)

Season: late winter, spring

Complications:

1- Respiratory: pneumonia, otitis media (most common), and tracheitis

2- CNS:
A-encephalitis B-Sub acute sclerosing C-Febrile convulsions
pan encephalitis=SSPE
-7 days after starting illness -7 years after infection -
-15%=mortality -Dementia death
-40%of survivors=long term -very high measles Abs in
sequel(deafness, convulsions,) the serum/CSF

3- Others: appendicitis, hepatitis,

Long term:
- Diarrheadehydration
- PEM (protein energy malnutrition)
- Corneal cloudication
- Mouth ulcers

59
***Measles in special conditions (low CMI):

PEM: severe disease HIV: modified or absent +rash severe disease

Mx: - Antipyretics - Eye care=tetracycline ointment - Mouth care: salted water

- Nutrition + Vit. A - Ribavirin: immune compromised only

Rubella (German measles) Mild disease Risk= Congenital rubella syn.

C/O: prodrome: mild or no fever - Congenital rubella syndrome -

Arthritis in female usually -
Rash: maculopapular (face trunk) not
Myocarditis
itchy
Prevention: MMR
Disappears in 3-5 days (3 days measles)
Exanthemforscheiner spot in soft
palate

Dx: serology Most

characteristically= Sub occipital post
auricular lymphadenopathy

N.B: since fever is mild or absent the

rash is usually the first sign

Complications:

[Link] (Fifth disease)

- B19 disease As x Prodrome (wk.) slapped cheek

appearance

60
lace reticular rash in the
trunk+extrimities

Recurrence can occur; proactive

factors

Heat (sun exposure, hot path, emotional

upset

Complications:

- Arthritis (adults) - A plastic crises

1/chronic Hemolysis

2/immunodeficiency (can’t form Abs to clear infections) E.g. malignancy

- Non immune hydropsfetalis (vertical transmission); If affects pregnant women in the

first trimester

N.B: B19 affects eryothoblastoid cells (precursors of RBCs) (Bone marrow)

Roseola infantum (Exanthemsubitum)

- HHV 6, HHV 7 - Infant, high fever (but he is relatively well

- Fever disappears in 3or4 days

- Then rash appears in hours (rarely 24 hrs.)

- Starts from the trunkextremitiesneckface

N.B: miss diagnosed as drug allergy

Infant +fever=Abx, rash appears

Scarlet fever

61
Only rash covered by bacteria Group A streptococcus

C/O:Fever, exudative pharyngitis, tonsillitis - Abdominal pain, DDx for acute

appendicitis

- Maculopapular rash (goose like skin or sand paper) especially deep areas= antecubital
fossa, axilla, groin), areas of hyper pigmentation that doesn’t disappear by pressure

- White coated tongue then strawberry tongue

- Desquamation in 6 days sunburn like skin (esp. in fingers/ toes) +circumoral pallor.

TX: Penicillin

Complications:

1. RF 3. AGN
2. Peritonsillar abscess (hot potato 4. Retropharyngeal abscess
like voice)

Infectious mononucleosis (glandular fever) -EBV

Association with EBV (oncogenic) 1/Burkett’s lymphoma 2/Nasopharyngeal CA

Transmission: oral secretions (kissing disease)

C/O: fever, tonsillopharyngitis (may obstruct breathing)

62
 Lymphadenopathy (prominent cx) large Splenomegaly, hepatomegaly, rash

N.B: if treated with amoxicillinamoxicillin rash

Dx: Atypical lymphocytes (peripheral blood) Heterophil Abs +ve (monospot test is
+ve)

Serology: high EBV IgM, IgG

TX: supportive, avoid contact sporting (spleen rupture)

Vesicular rash

Varicella zoster (chicken pox)

Infectious: 2 Days before the rashuntil crusting of all lesions (5-7 days)

Rash: itchy, vesicular, starts in the trunk in different stages (macule, papule, pustule,
vesicle, crust) Goes in crop Sparing palms and soles

Complications:
1/2ry bacterial infection [Link], strep (most common complication)
-Mild or sever as toxic shock syndrome, necrotizing fasciitis
How to suspect? Recurrence of fever
2/CNS: encephalitis (better prognosis than HSV), cerebellitis
3/ in immune compromised: pneumonitis hemorrhagic vesicle, disseminated disease (may be
DIC)
4/Purpurafulminans=thrombocytopenia

TX: Supportive - Antiviral: IV acyclovir or oral Val

acyclovirImmunocompromized

Oral Val acyclovir=adults

VZIG  Immune compromised in contact with diseased

person

Severe disease:
adults+immunocompromised

Hand foot and mouth disease:

63
- Vesicles in these areas +buttocks

- Cause: coxackie virus, A16

Dorsum of the hands and feet, may affect palms and soles

Kawasaki disease( mucocutaneus LN disease)

- Vasculities - Target: 6months-4years (<5)

C/O: Fever >5 days + 4 of:

1/non purulent conj. Injection

2/mucus membranes (red, cracked lips, pharyngeal injection, strawberry tongue)

3/rash: polymorphous, no vesicles, no crust

4/cervical lymphadenopathy (1 L.N >1.5 cm)

5/extremities changes (palms soles edema, peeling (conuelsence), erythema

Lab: high WBCS/ESR/CRP/platelets (2nd wk.)

Complications: 1/ Coronary aneurysm (6wks) 2/ MI (thrombosis) 3/ Sudden death

TX: -IVIG (within 10 days) +high dose of aspirin until fever, inflammatory markers are
down

Then change to low dose aspirin (prevent thrombosis)

Echo: If +ve aneurysm= warfarin+ follow up

N.B: Aspirin is given for 6 wks. First high dose=anti-inflammatory. Then low dose=ant
platelet

If poor response to aspirin; infliximab or steroids

N.B: IVIG within 10 daysdecrease incidence of coronary aneurysm

64
‫فصبرا في مجال العلم صبرا فما هيل املنى سهل املزاد‬

‫‪65‬‬
 PART 7: IMMUNIZATION
Passive Active
- Natural: from the mother - Natural: post infection
- Acquired: Igs or antitoxins - Acquired:vaccination
- May be life long as in MMR & chicken pox
- EPI: Eradication of poliomyelitis, measles & Neonatal Tetanus
N. B.: 10 childhood infections + T. Toxoid
◾ Types of vaccines:
1. Live attenuated vaccine : most potent (BCG, OPV)
2. Killed vaccine
3. Recombinant vaccine : Hep B
4. Capsular polysaccharides vaccine : pneumococus&Hib
Contraindications to all vaccines:
1. Previous history of allergy (edema, breathing difficulties, shock)
2. Severe local reaction
3. Fever >40 c° or severe illness.
4. Within 6m of blood transfusion
For all live attenuated:
- Pregnancy - Immunocompromized with exception of MMR & varicella in child with HIV
infection
Schedule:

Day 0 - BCG(0.05)ml ,left upper third of forearm, intradermal

- OPV(zero dose (Sabin))2 drops oral
6 wks - OPV 1
- Pentavalent: 0.5 ml. IM. Left Anterolateral thigh
- Rota: 1ml oral. Live attenuated
- Pneumococcal vaccine: 0.5 ml IM/SC Right Anterolateral thigh. Capsular
conjugated to protein “Diphtheria Toxoid”
10 wks - OPV 2
- Rota
- Pentavalent
- Pneumococcal
14 wks - 0PV 3
- Pentavalent
- Pneumococcal
9 months - Measles : 0.5 ml. SC. Live attenuated
18 months - Measles

66
New: IPV “Salk” gives in 3 doses with Pentavalent

N.B. Pneumococcal vaccine:

- 13 valent “ immunization “
- 23 valent ( SCD, Splenectomy, Nephrotic syndrome, Immunocompromized,
cochlear implant, chronic diseases)
N.B

- MMR = Autism , IBD

- Rota = intesseception
- Pertussis = Encephalopathy
Measles = Thrombocytopenia
Side effects:

- All.: Mild local reaction ( redness, swelling), Mild symptoms (e.g. Fever)

- BCG: lymphadenitis, skin ulcer, scar, local abscess.

N. B. Mild disease, low grade fever, vomiting, mild diarrhea =not contraindications

N. B.

# Polysaccharides = B cells response > poor immunity less than 2 years, short term
immunity, Absence of Booster response when exposure.

VS

# conjugated polysaccharide = T cell response >⬆⬆⬆ level of functional Abs, long term
persistent IgG response, immunological memory.

Special contraindications:

- BCG : prematurity, skin infection

- DPT( Pertussis) : Encephalopathy within 7 days, seizure within 72 hours

- Measles: Thrombocytopenia purpura, neomycin allergy, Egg allergy (caution),

active TB.

Rota: gastroenteritis, hx of intusseption.

67
68