Routine Neonatal Care: Neonatology DR - MHD Bonowara

Neonatology dr.
mhd bonowara
Routine neonatal care

Performed at delivery suite :
 Thermal Care : babies should delivered in a warm room ,rapidly dried with
warm towel and then covered with warm towel and a hat .
 Routine measure : measured within one hour of birth .
 Weight : ( term mean ~3.5kg ).
 Head circumference: ( mean ~ 35 ).
 Body length : (mean ~50 ).
 vitamin K : 1mg IM ( to avoid hemorrhagic disease of newborn).
 erythromycin ointment : - applied to both eyes for prophylaxis of
gonococcal ophthalmia neonatorum .
 Cord care : immediately after birth , clamp the cord with purpose made
device , keep the umbilicus clean & dry , antibiotic powder or spray are not
routinely required .
 Close observation of vital signs .
 Neonatal immunization : if mother hepatitis B surface antigen positive : HB
Ig and start hepatitis B vaccine series
Guthrie test : all infants should undergo a screening heel prick blood test
placed on specific card between day 3-10 , commonly screened disease include :
1) Congenital hypothyroidism ( ↑ TSH ).
2) Cystic fibrosis ( ↑ immune reactive trypsin ).
3) Phenylketonuria (↑phenylalanine ) .
4) Medium chain acetyl-CoA dehydrogenase deficiency .
5) Sickle cell disease .

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Neonatology dr.mhd bonowara
Newborn physical examination
i. Temperature : normal temperature :

 Oral = 36.6- 37.2 C
 Rectal = oral -0.5 C
 Axillary = oral + 0.5 C
ii. Respiration : normal RR in neoborn is 40-60 breath/min.
iii. Blood pressure : Normal bl.p at birth = 85/50 mmgh
Any patient with suspected heart disease, the bl.p
should be measured in the 4 extremities
iv. Pulse rate : normally 100-180 beat/min (usually 120-160)
i. Head circumference :
 by placing the measuring tape around the front of the head
above eye brow (ant. ) and occipital area (post).
 Value : reflects rate of brain growth ( maximum rate of brain
growth during first year ) .
 It should be measured 3 times & take the
highest reading
 OFC measurements during first 2 years :
 OFC at birth → ~ 35 cm
 1st 2 months → + 4 cm
 3rd & 4th months →+ 3cm
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 5th & 6th months →+2cm

 From 7th -12th →+ 1/2 for every month .
 At 1st year → 47 cm
 At 2nd year → 49 cm
ii. Length & height :
 length : measuring infant in supine position ( <2yrs )
 height : measuring child in standing position (usually >2)
 the average length at birth = ~ 50 cm .

 During first year :
 1st 3 months → +3 cm / month .
 Next 3 months → +2cm / month
 From 6-12 months → +1cm /month .
**After age of 1 year = age ( by years ) X 5 + 80

iii. weight : the average birth weight = 2.5- 4 kg
 below 2.5 kg = Low birth weight
 below 1.5 kg = very low birth weight (VLBW)
 below 1000 g = extremely low birth weight (ELBW )
 above 4 kg = high birth weight ( macrosomia )
 During 1st year :
 1st 4 months → 750g /month .
 Next 4 months → 500g / month
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 Last 4 months → 250g /month
**After 2nd year → weight = age ( by years) X 2 + 8
a) Skin : normally skin of newborn :

 Pink in colour
 Acrocyanosis may be present in first few hours after birth .
 Covered by greasy white substance ( vernix caseosa ) .
 Lacy red pattern ( mottling ) may be seen in healthy infants with cold
stress . D/D of mottled
 Dry peeling skin in postdate & post mature infants. skin :
 Some of benign cutaneous manifestation which 1/cold stress
usually resolve spontaneously : 2/hypovolemia

 Milia 3/sepsis
 Mongolian spots .
4/ down synd.
 Erythema toxicum
 Capillary haemangioma .
 Acne neonatorum .
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b) Head :
 Macrocephaly : ( OFC > 90th percentile ).
 Microcephaly : (OFC < 10th percentile ) .
 Ant . Fontanel :
 should be examined in semi-setting position.
 Ant. Fontanel close between ( 9-18 months )
 Normally less than 5cm in size = ( width + length/ 2 )
 Normally Diamond in shape .
 Should be at level ( not pulged / not depressed )
D/D of large Ant. Fontanel:

D/D of small Ant. Fontanel :
1) Down syndrome 2) Acondroplasia
1) Craniosynostosis .
3) Rickets 3) Hypothyroidism
2) Congenitalhyperthyroidism
4) Osteogenesis imperfecta 6) ↑ ICP
 Post. Fontanel : close at birth up to 2 months of age .

 3rd fontanel may be present in Down syndrome & preterm infant.
 Molding ( overlapping of skull sutures ) , most often seen with
prolonged vaginal delivery . normal shape regained within 1 week .
 Head swelling may be :
Capput succedanum cephalohaematoma
Diffuse soft tissue swelling Sub-periosteal hemorrhage
Diffuse & soft Localized & tense
Cross sutures Not cross sutures
Resolve within several days Usualy Resolve within 2-3 weeks
Not need further investigation May need ,to exclude fructures
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Not need medical intervension Rx complication ( anaemia / jaundice)

C) Eyes :
 red reflex positive bilateral by opthalmoscope .

 sclera may have normally bluish tint if infant is premature.
D) Nose :
 patency of bilateral nostrils must be checked .

 infants are obligate nose breathers ,therefore ,if they have
bilateral choanal atresia ,they will have cyanosis and severe
resp. distress.
 Nasal flaring is indicative of respiratory distress .
E) mouth : - soft and hard palate should be examined to exclude cleft palate.
- neonatal Benign lesion of the mouth :
 Ranula
 Epstein pearls
 Mucocele of salivary glands
 Natal teeth
Natal teeth : are usualy lower incisors , radiographs are need to differentiate
the two types because management of Each are different :
 Predecidous teeth : poorly formed and roots are absent.

Removal is necessary to avoid aspiration.
 True deciduous teeth : these teeth are true teeth that
erupt early , they should not be extracted.
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F) Ears :
 the normal position is determined by drawing imaginary horizontal

line from inner & outer canthi of the eye across the face , the helix of
the ear should be above the horizontal line .
 preauricular skin tags ( papillomas ) ,which are benign, are common .
 gross hearing can be assessed when infant blinks in response to loud
sounds .
G) Chest :
 the newborn’s thorax is nearly rounded. Gradually the transverse

diameter increases until the chest assumes the elliptical shape of the
adult at about 6 years of age .
 type of breathing is harsh vesicular ( expiration = inspiration ).
 A good place to listen is in the right & left axillae .
 The rhythm is irregular with apneic spells ( periodic breathing ).
H) Heart : normal heart rate ( 120-160 ) beat /min. awake , may drop to
(80 b/min) during sleep.
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i) Abdomen
 Abdomen is slightly distended .

 Visible peristalsis could be seen in thin newborns especially premature.
 The liver can be normally palpated 1-2cm below the costal margin.
 Normally the umbilicus has two arteries and one vein , the absence of
one artery could indicate renal or genetic problems .
 The cord should be translucent , a greenish yellow color suggests
meconium staining , usually 2ry to fetal distress .
J) Genitalia
 Normally , the ext. urethral meatus opens on tip of penis .

 The baby should not be circumcised before exclusion of any
penile abnormality .
 Infants will have well-developed scrotal rugae at term .
 A smooth scrotum suggest prematurity ( undescended testis).
 Labia majora at term are enlarged and cover completely labia

minora .
 vaginal discharge ( usually blood tinged ) may be present
due to withdrawal of maternal estrogen hormones .
 Term infant should pass meconium within 48 hours of birth ,

premature infants are usually delayed in passing meconium .
 Term infant pass urine within 24 h . ( Normal urine output =
1-3ml/kg / hour ) .
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infant feeding
is a learned skill for both mother & baby .
 Advantages :
1) ↓ maternal postpartum hemorrhage .
2) Mild maternal contraceptive effect . Types of breast milk :
3) ↓maternal breast cancer .
1st 5 day of life
4) ↑bonding between mother & baby .
5th – 21th day
5) Cheap .
6) ↓ GIT & respiratory infection. after day 21
 Contraindication :
a. +ve maternal HIV status .
b. Certain maternal medication (e.g. amiodarone )
c. Infantile galactosaemia or phenylketonuria .
d. Maternal herpes zoster over breast.
e. Primary lactose intolerance .
used to establish feed in preterm
 Types of feeding :
infants , but also useful if mother &
 Total : only breast feeding .
baby are separated for any reason ,
 Substitutional : Only breast feeding .
or if there are other maternal
 Complementary : Breast feeds are problems e.g. crackled nipple
Completed by bottle feeds .
Once expressed , can refrigerate
( breast feeding > bottle feeding )
and use within 24-48 hr , or freeze
Indicated when breast milk is not and use for up to 3 months.
Enough .
 Supplementary : bottle feeds more
than Breast milk feeds .
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 Types of formula milk :


Cow's milk formula is the most commonly used type. The milk has
been altered to resemble breast milk .
 :
Previously recommended for cow’s milk protein allergy or lactose
intolerance , but use not recommended now
 :
indicated in cow’s or soya milk protein allergy .

 exist for conditions such as preterm/LBW
infants, gastro-esophageal reflux (thickened with cornstarch) lactose

intolerance ( lactose milk free )& poor growth( high energy formula).
 Daily fluid requirement :
for full term baby .
 1st day : ( 75ml /kg )
 2nd&3rd day : ( 90ml /kg)
 4th day : ( 120ml/kg )
 5th day up to 1yr : ( 150ml /kg )
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Resuscitation of newborn
Definition : Steps to be done to optimize the airway , breathing & circulation of

newborn .

keep the infant warm ( resuscitation should be performed under radiant
warmer ).
Dry the newborn completely , remove wet towel and replace by dry one.
Do suction to mouth , oropharynx and nose respectively .
If infant with meconium staining → endotracheal suction .
Rapid evaluation of the infant by Apgar scoring at :
 minute = decide the need & method of resuscitation .
 5th minute = evaluate the adequacy of resuscitation & the need
for further efforts .
Pale / blue Pink with Pink

acrocyanosis
Absent <100 beat/min > 100 beat/min
No response Grimace Cry , cough
Flaccid limbs Some flexion Well flexion

Absent Slow irregular Normal & crying
 Interpretation of Apgar score :
a) Score > 7
 Indicate good general condition ( No asphyxia ).
So : - keep newborn warm .
- Give vit k (1mg ) Intramascular .
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- Dischare after complete examination

b) Score of 4 -6
 Indicate mild to moderate asphyxia .
So do : - gentle suction of air way .
- free O2 inhalation .
- tactile stimulation of breathing by slapping the soles

of the feet , rubbing sternum & back. .
 If no response : bag & mask

ventilation to expand the lung
using 100 % O2 at rate of 40-60
breath / minute .
c) Score < 4
 Indicate severe asphyxia .
So : - Endotracheal intubation and
bag ventilation with 100% O2
- check pulse :
if : HR < 80 b/min. not rising despite adequate vent. proceed to

cardiac
if : HR < 50 b/min. at 1 minute .
massage at
if : HR absent at birth . rate of
120/min
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chest compression
 the thumbs are placed on the lower third

of the sternum , between the xiphoid and
the line drawn between the nipples .
 the sternum is compressed a third of
anteroposterior diameter of the chest .
 Ratio of compression: lung inflation→3:1

rate of 90 compressions : 30 breaths/min
(120 events/min).
 Recheck heart rate every 30 seconds; stop
when heart rate >80 beats/min.
 if no improvement for 1-2 min.( HR<80 )
despite 100% O2 & cardiac massage →
insert umbilical venous catheter and give
resuscitation drugs .
 Resuscitation drugs :
Drugs should be given via an umbilical venous
catheter, or if not possible, via an intra-osseous
needle. Drugs given via a peripheral vein are unlikely to reach the heart.
Drugs Indication Dose /Route

Epinephrine Heart rate <80 beats/min in spite of 0.1-0.3ml /kg IV
adequate ventilation and external
cardiac compression . 1ml / kg by ETT
Naloxone Infants born to mothers who have
received opiate analgesia within a 0.1 mg/kg IV
few hours of delivery
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Na bicarbonate Severe Metabolic acidosis 2 ml/kg slow IV

Volume expander Blood loss ( hypovolemic shock ) Normal saline /
blood
10-20ml/kg
Dopamine Cardiogenic shock 5-20 µg/kg/min.
IVinfusion
Dextrose Hypoglycemia 2.5 ml/kg (250
mg/kg)
 If no improvement despite previous medications , you must check :

 head is not over flexed .
 endotracheal tube is patent & well placed .
 No air leak ( e.g. pneumothorax )
 the bag deliver 100% O2 .
 adequate cardiac massage .
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Perinatal asphyxia
definition : failure of newborn to establish spontaneous regular respiration
immediately after birth , leading to either death or survival with
permanent neurological damage .
 criteria for perinatal asphyxia :

1) Evidence of metabolic acidosis ( PH < 7) in fetal umbilical cord
arterial blood .
2) Apgar score <4 more than 5 minutes of life .
3) Onset of multi-organ failure involvement within 1st 3 days of life.
4) Neonatal neurological manifestation ( e.g. seizures , coma ) .
 Causes of perinatal asphyxia :
Intra uterine Intra-partum post natal

1) Maternal causes : - Prolonged labor . 1) Severe cyanotic
heart failure & - Obstructed labor . heart disaes .
hypotension . 2) Hge & anaemia
2) Decreased placental 3) shock
blood flow :
(e.g. abruptio placenta )
3) Impaired umbilical blood
flow e.g. cord compression.
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Clinical picture :- depend on severity & duration of asphyxia .

 Slow , weak , irregular heart beat on fetal monitor .
 scalp PH < 7.2
 action : - give mother high O2 concentration .
- prepare for immediate delivery .

 meconium staining of newborn .
 cyanosis & failure of spontaneous breathing .
 deceased level of consciousness & flaccidity .
 low Apgar score .
LATE MANIFESTATIONS OF PERINATAL ASPHYXIA
1. hypoxic ischemic encephalopathy (HIE)

Pathogenesis : Hypoxia → anaerobic glycolysis of brain cells → accumulation
of lactic acid & toxic metabolites → neuronal damage & VD →
brain edema → Ischemia → Encephalopathy .
Clinical presentation :
the severity of HIE correlates with the duration & severity of the asphyxia insult .
the main neurological signs evolved in 1st 72h of life best described by sarnat
clinical grading :
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Sign Stage 1 Stage 2 Stage 3

Consciousness Hyper alert lethargy Coma
Muscle tone Normal Hypotonic Flaccid
Tendon reflex Hyperactive Hyperactive Absent
Moro reflex Exaggerated weak Absent
Pupil dilated constricted Variable
Respiration Regular Periodic Apneic
Seizures No frequent Frequent
Outcome Good Variable Death or severe
neurological deficit .
Diagnosis :
 Cranial U/S , CT scan or MRI : for brain edema & injury

 EEG : low voltage EEG , if there is convulsion
 ABG : to confirm asphyxia .
2. Cardiac : myocardial necrosis , ventricular dysfunction & shock .
3. Respiratory : RDS , persistent pulmonary hypertension & pulmonary hge.
4. Renal : acute tubular or cortical necrosis & renal failure .
5. GIT : necrotizing enterocolitis & intestinal perforation .
6. Hepatic function : elevated liver enzymes & indirect bilirubin &

↓clotting factors .
7. Metabolic : lactic acidosis , hyponatremia ( SIADH) & hypoglycemia
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Management of perinatal asphyxia :
 the optimal management is prevention of risk factors .

 Immediate resuscitation of newborn .
 Incubator care , NICU admission & close observation .

 maintenance of oxygenation & ventilation .
 total parental nutrition for 72h. ( to avoid NEC ).
 maintain normal serum glucose level (~75-100).
 Volume expanders & inotropic ( dopamine infusion ) to
maintain mean arterial pressure > 40mmg .
 give IVF 2/3 maintenance ( to prevent heart , renal failure &
brain edema ).
 start breast milk feeding after 3 days ( 5cc /2hours ).
 symptomatic treatment ( e.g. convulsion ) .
 monitoring of :
o ABG
o cranial U/S & EEG
o hemoglobin
o body weight
o urea & electrolyte .
Prognosis : depends on sarnat clinical grading .
- sarnat grade 3 carries mortality rate of ~80% , the rest often have CP/MR
- sarnat grade 2 continuing > 5 days is a poor prognostic sign .

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Neonatal jaundice
Definition : yellowish discoloration of skin , sclera & mucous membrane due to
increased serum bilirubin level above normal level .
- Normal bilirubin level in neonate < 2mg /dl.
- Clinical jaundice in neonate appear when

serum bilirubin exceeds 5 mg /dl , versus
3mg/dl in adults .
- Over 50% of all newborn infants become

visibly jaundiced ( Physiological ) because of :
1) there is marked physiological release of
hemoglobin from the breakdown of red
cells because of the high Hemoglobin
concentration at birth.
2) the red cell life span of newborn infants
(70 days) , is markedly shorter than that
of adults (120 days) .
3) hepatic bilirubin metabolism is less
efficient in the first few days of life.
Neonatal jaundice is important as :
 unconjugated bilirubin can be deposited in the brain, particularly in

the basal ganglia, causing kernicterus.
 it may be a sign of another disorder, e.g. hemolytic anemia, infection,
metabolic disease , liver disease.
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Comparison between physiological & pathological jaundice :

Type Physiological Pathological
Onset 2nd day ( never 1st ) 1st day up to 1week .
Peak level of bilirubin
 Preterm < 15 mg /dl > 15 mg /dl
 Term < 12 mg /dl > 12mg /dl
General condition Completely well Generally Unwell
Type of bilirubin Always indirect Direct OR indirect
Direct bilirubin < 2 mg /dl > 2mg /dl
Rate of rise 1 – 3 mg /dl /day > 5mg / dl/ day
Incidence More common Less common
Diagnosis By exclusion of other causes Looking for the cause
(e.g. hemolysis )
Treatment Usually no treatment needed Usually need treatment.
UNCONJUGATED HYPERBILIRUBINEMIA
Considered if total bilirubin above normal & conjugated fraction < 15 % of total
bilirubin .
**Causes :
Hemolytic causes Non-hymolytic causes

A) patient with +ve coomb’s test : A) Extra-vascular Hge :
-Rh. incompatibility . – Cephalohematoma .
-ABO bl. group incompatibility . – Extensive bruising .
-Minor bl. group incompatibility. – Internal Hge ( IVH ) .
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B) patient with –ve Coomb’s test : B) Exaggerated entero-
- Spherocytosis. hepatic circulation e.g.
- Alpha-thalassemia. - cong. pyloric stenosis
- G6PD deficiency. - Intestinal obstruction
C) polycythemia .
Glucuronyle transferase enzyme may be :
 Absent : Criggler-Najjar syndrome type 1.
 Deficient : - Criggler – Najjar syndrome type 2 .

- Gilbert syndrome .
 Immature : physiologic jaundice .
 Under stimulated : hypothyroidism , hypoglycemia , hypoxia .
 Inhibited : breast milk jaundice , lucy-driscoll syndrome .
**Clinical picture :
- jaundice is evident on face with SBR ~ 5 mg/dl.
- On mid abdomen with level ~ 10 mg/dl .
- On soles of feet with level ~ 20mg /dl .
- Color of urine usually Normal .
- Color of stool may be Dark .
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** Rh-incompatibility :
- Occurs as a result of escape of small amout of Rh +ve fetal blood (usually at
delivery ) to the circulation of Rh –ve mother .
- this will result in sensitization of the Rh –ve mother & formation of
maternal anti-Rh antibodies (IgG ) .which cross the placenta and attack
fetal RBCs .
- the first baby usually escape hemolysis as sensitization usually occur near
time of delivery Except if the mother is already sensitized by Rh +ve blood
as in previous :
o abortion .
o blood transfusion .
o Ectopic pregnancy .
o amniocentesis .
Clinical picture :
According to severity , different presentations may occur :
Type Severe ( hydropes fetalis ) Moderate ( icterus Mild (hemolytic

gravis neonatorum ) anemia ).
Anemia Severe (intrauterine Less severe Mild
hemolysis ).
Peak of At birth . ( severe pallor ). At birth ( worsening Weeks after
st
anemia : rapidly during 1 birth
day
Hepato- Huge . ( extra-medullary Present ( less severe). Splenomegaly
splenomegally hematopoiesis. maybe present .
.
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Complication of Rh incompitabilty ( hydrops fetalis ):
1) Severe anemia .
2) anemic heart failure .
3) generalized edema with ascites & pleural effusion . ( edematous placenta ).
4) Still birth or death shorter after birth .
Investigation : cord blood sample should be taken immediately after birth for
any infant born to Rh-negative mother for :
 Blood group ( ABO & Rh factor )

 CBC : - hemoglobin : low
- reticulocyte count : high ( >6% ).
 SBR : increase unconjugated bilirubin .
 Direct coomb’s test : +ve
Prevention :
 Screening of all pregnant females for Rh group .

 anti D globulin injection for Rh –ve mother and Rh +ve fetus .
Treatment :
1) for Hydropes fetalis :

- Adequate resuscitation .
- Exchange transfusion with O –ve packed RBCs .
- Drugs : diuretic (pulmonary edema) , dopamine & digoxin .
- therapeutic thoracocentesis or paracentesis .
2) for indirect hyperbilirubinemia : phototherapy / exchange transfusion.
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**ABO incompatibility :
- Occurs usually when the mother blood group (O) and the baby is blood
group ( A or B ) ,
- The 1st baby can be affected as anti-A & anti-B antibodies are naturally
present .
- Most of anti-A & anti-B are of IgM type which can not cross the placenta .
but 10-15% of cases these antibodies are of IgG type which can cross
placenta .
Clinical picture : baby mildly pale (anemic ) & jaundiced .
Investigation :
- CBC : low hemoglobin .
- SBR : indirect hyperbilirubinemia .
- Direct coomb’s test : +ve
- Blood film : mild spherocytosis .
Treatment : Phototherapy / exchange transfusion .
**Other causes of indirect hyperbilirubinemia :
Type Criggler-Najjar Criggler-Najjar Gilbert

syndrome type 1 syndrome type 2 syndrome
Etiology Autosomal recessive Autosomal dominant. Autosomal
Absent glocoronyle- Partial deficiency of dominant .
transferase enzyme. Glucoronyle- deficient Z & Y
transferase enzyme. proteins ???
Clinical Very high level of Less than type 1 Mild hyper-
picture indirect bilirubin. bilirubinemia .
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Diagnosis -Enzyme assay in Genetic study . Genetic study .

liver biopsy.
-Absent conjugated-
bilirubin in
duodenum
Mangment -Exchange trans- Respond to Usually need no
fusion soon afterbirth. phenobarbitone treatment.
-Phototherapy .
-Liver transplant
(later on )
-Not respond to
phenobarbitone
** Physiological jaundice :
 Most common cause ( ~ 50% of full term infant ).
 Always indirect .
 No pallor , No Organomegally , No risk of kernicterus .
 Diagnosis by exclusion . Prolonged physiological jaundice :
 it caused by :
it is physiological jaundice persist
 Immaturity of liver enzyme .
>10 days in ( full term ) & >2 weeks
 Short life span of RBCs. (90 days)
in ( preterm ).
 reduced Z&Y proteins
during 1st week . Causes :
 breakdown of high hemoglobin 1) breast milk jaundice

formed intrauterine .
2) hypothyroidism. 3) UTI.
4) Intestinal obstruction 5) CHPS.

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Type Breast milk jaundice Breast feed jaundice .

Incidence 2-4% of jaundiced infants. 12% of jaundiced infants.
Onset Late onset (2nd week ) Early onset (1st week)
Causes Unkown etiology :but breast milk Insufficient breast milk
may contain: intake >> inadequate
 pregnandiol (inhibit GT quantities sufficient to
enzyme). make bowel movement
 Beta-glucoronidase (++ remove bilirubin from the
entero-hepatic body .
circulation ).
 Estridified free fatty
acid (compete with
bilirubin in GT enzyme
binding site
Diagnosis By exclusion ( normal The same .
investigation with high TSB ).
Treatment - Don’t advice mother to stop - No need for treatment .
breast feeding ,instead encourage - frequent breast feeding .
mother to ↑ frequency of feeding.
- Rarely lead to kernicterus.
- sun rays can be helpful .
**Investigation of indirect hyperbilirubinemia :
 Total serum bilirubin & direct fraction.

 CBC : - hemoglobin & hematocrit values .
- Reticulocyte count .
 Direct coomb’s test .
 Others : - septic screen .
- thyroid function test .
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**Treatment of indirect hyperbilirubinemia :
 Indication :
 bilirubin level on or above phototherapy line
 during waiting of exchange transfusion .
 Idea :
 Exposure to blue light with wave length
425-475nm convert insoluble unconjugated bilirubin to non-toxic,
soluble forms ( by photoisomerization ) excreted easly in urine & bile .
 Procedure :
1) baby is completely naked except eyes &
genitalia .
2) Continous monitoring of tempreture &
hydration state.
3) distant between baby and lamb 45-50 cm .
4) Change position with time ( or use multi-lamp machine ).
 Contraindication : Direct hyperbilirubinemia → Bronze baby syndrome.
 Complication :
i. Dermatitis ( skin rash , erythema )
ii. Dehydration
iii. Damage to exposed eye & genitalia .
iv. bronze baby syndrome .( if Direct hyperbilirubinemia ).
v. Hyperthermia .
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 Idea :
 Remove excess unconjugated lipid soluble bilirubin .
 Remove antibodies from the circulation.
 Correct anaemia .
 Indication :
 Bilirubin level on or above exchange line in bilirubin treatment chart.
 In Rh & ABO incompitability :
- Cord bilirubin >5mg/dl .
- Cord hemoglobin < 10g/dl.
- Rapid rise of bilirubin >0.5mg /dl / hour .
- Early sign of kernicterus or history of kernicterus in a sibling.
- bilirubin level exceeds :
 10mg /dl ( at 1st day).
 15mg /dl ( at 2nd day ).
 20mg /dl ( at any time ).
 Procedure :
 Blood used : O –ve , fresh , warm .
 Amount : double neonatal blood volume ( 80 x 2 ml/kg ).
 by umblical venous catheter ( UVC ) : small amount (10-20ml ) are
removed and replaced by equal amount of new blood .
 IV glucose & calcium gluconate are given at 100ml blood interval .
 Complication :
1) complication of UVC : sepsis , thrombosis , embolism .
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28
2) Heart failure : ( due to volume overload ).

3) Hazards of blood transfusion .
4) hypocalcemia , hypoglycemia & hyperkalemia .
Summary from toronto note
Timing of clinical jaundice :
In 1st day of life  Rh. Incompatibility ( most common).

 ABO incompitability .
In 2nd -3rd day  Physiological jaundice .
 Criggler Najjar syndrome .
After the 1st week  Breast milk jaundice .
 Hemolytic anaemia .
Persistent beyond 1st  Criggler najjar syndrome .
month  Prolonged physiological jaundice .
 Breast milk jaundice .
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29
Kernicterus
Definition : Yellowish staining of the cerebellar & cerebral
nuclei ( especially basal ganglia) due to
deposition of unconjugated bilirubin resulting
in neuronal necrosis .
Causes :-
A. Level of serum unconjugated bilirubin exceeds critical values :

 >10 mg/dl in 1st day .
 >15 mg/dl in 2nd day .
 > 25 mg/dl afterwards.
NB : kernicterus may occur at lower levels in presence of these risk factor :
1) Prematurity & LBW . 1) Drugs : ampicillin ,sulpha

2) Acidosis . & aspirine .
3) Sepsis . 2) Hypothermia
4) Hypoxia . 3) hypoalbuminemia .
5) Anemia .
6) hypoglycemia .
B. Duration of exposure to high bilirubin level ( the longer the duration the
more risk of kernicterus ) .
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30
Clinical picture : pass in 3 phases
 Early sings : poor suckling , lethargy , poor moro reflex

hypotonia , high bitched cry & emesis
 Late signs : Hypertonia & opisthotonus , fever , pulging of
ant.fontenel & seizures .
Infants with severe cases of kernicterus die in neonatal period.
- Survivors from phase 1 go into lucid interval for few months .

- There is apperant recovery or few symptoms .
 Picture of Cerebral Palsy ( Extra pyramidal type ).

 Association :
- Mental Retardation .
- Senserineural deafness .
- Squint & upward gaze palsy .
- Defective speech .
- Recurrent convulsion .
Management :
Prophylaxis : - Adequate treatment of indirect hyperbilirubinemia .
- Prevention of other risk factors : e.g. sepsis , hypoxia , acidosis
Treatment : - kernicterus not curable , only supportive treatment of CP .

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31
Conjugated hyperbilirubinemia
Definition : Rise of total serum bilirubin with the conjugation fraction >15% of
total OR ( >2mg /dl ).
Causes :
1) Defictive secretion of conjugated
bilirubin by hepatocytes :
a. genetic :
- Rotor & Dubin johnson syndrome .
- bile acid synthesis defects .
- Progresive familial intrahepatic cholestasis.
b. Acquired ( neonatal hepatitis ) due to :
 Infection :- TORCH
- Neonatal sepsis .
-Viral hepatitis
-Idiopathic neonatal heptitis.
 Metabolic : - alpha1-anti trypsin def.
- Galactosemia .
2) Defective excretion due to bile flow obstruction :

- Congenital exta & intra-hepatic biliary atresia .
- Inspissated bile syndrome ( Bile plug ).
- Choledochal cyst .
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32
Clinical features :
1) Color of sclera : greenish yellow .

2) Color of urine : Dark
3) color of stool : clay ( pale ).
4) possible associations :
 malabsorption & failure to thrive .
 hepatosplenomegaly .
 liver cell dysfunction .
 symptoms of underlying disease e.g. sepsis , TORCH
N:B :- NO risk of kernicterus in direct hyperbilirubinemia beacause it is

lipid insoluble ( Not pass blood brain barrier ).
Investigation :
1) liver function test .

2) liver Scan
3) liver biopsy .
4) Metabolic Screen .
5) septic screen .
6) TORCH screen .
Treatment :
 Treat the cause e.g. sepsis ( give antibiotic ) galactosemia ( lactose free milk)
 supportive : e.g. – fat soluble vitamins .
- liver transplant in advanced stage .
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33
Biliary Atresia
Causes :
 Congenital 20 %
 Aqcuired 80 %
Incidence :
- More common in female.

- More common in asian &
black race .
Clinical Picture :
1) Obstructive jaundice .
2) Dark urine & pale stool .
3) Hepatosplenomegaly ( later on ).
4) In approximately 10% of cases, anomalies associated with biliary atresia
include heart lesions, polysplenia, situs inversus, absent venae cavae, and a
preduodenal portal vein.
5) Later on : failure to thrive ( poor feeding & vomiting ) & bleeding tendency .
Types :
Limited to CBD Limited to hepatic ducts Atresia of Lt & Rt hepatic ducts
Type 1 Type 2 Type 3

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34
Investigation :
1) SBR : direct hyperbilirubinemia .

2) LFT : impaired.
3) Serum albumin : low .
4) PT / PTT : prolonged .
5) Ultra sound : exclude other anomaly e.g. Choledochal cyst . & type of
biliary atresia .
6) ERCP : diagnostic & therapeutic .
7) MRCP imaging : only diagnostic .
8) Liver biopsy : Diagnostic especially in intra-hepatic biliary atresia.
9) Chest X-ray : to exclude other associations e.g. situs inversus .
Treatment : Surgical : kasai operation (hepatoportoenterostomy).
 Done as early as possible before age of

2 months .
Complication of biliary
 Supportive treatment as: fat soluble vitamins
atresia :
& antibiotic before surgery .
1. Liver failure .
2. Bleeding .
3. Portal hypertension .
4. Ascites .
5. Failure to thrive .
6. Death may occur 2ry
to hepatic failure .
Liver transplant : if atresia is intrahepatic .

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35
Neonatal seizures
Definition : Paroxyamal alteration of neurological function including motor ,
Behavioral and/or autonomic function .
Onset of convulsion :
 1st 3 days of life : HIE , drug withdrawal , intra-cranial hge Or metabolic .
 After 3 days : intra-cranial hge , metabolic causes .
 After the 1st week : meningitis .
Causes :
i. CNS causes : ( commenest causes ~40% ) .
1) Hypoxic-ischemic-encephalopathy .
2) Intracranial hemorrhage . (especialy preterm ).
3) CNS infection e.g. meningitis , encephalitis , TORCH
4) Cerebral malformation .
5) Kernicterus .
6) Neurocautanous syndromes e.g. neurofibromatosis .
ii. Metabolic causes :
1) Hypoglycemia
2) Hypocalcemia
3) Hypomagnesemia
4) Hypo/hyper natremia .
5) Inborn irror of metabolism .
6) Pyridoxine deficiency ( vit B6 ) .
iii. Drug withdrawal : e.g. maternal opiates .
iv. Neonatal epileptic syndrome .
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36
Clinical Picture :
 Subtile seizures ) the commenest type ) : occur commenly in premature than

term infant . manifested as :
 Eye movement : blinking , nistagmus , or sustained eye opening .
 Repititive oral movements : suckling , chewing or lip smacking .
 Limb movements : pedaling , bicycling or boxing .
 Epileptic apnea .
 Tonic seizures :
- Sustained rigid posturing of the body .
- May be focal or generalized .
 Clonic seizures :
- Alternative contraction of flexor and extensor muscles
 Myoclonic seizures :
- Non rhythmic sudden fast shock like movement of limbs .
Investigation :
1) Check : blood glucose , Ca+ , Na+ , Mg+
2) Septic screen & TORCH screen .
3) Cranial U/S , CT-scan & MRI .
4) Metabolic screen : PH , plasma amonia … etc
5) Toxicology : in suspected cases .
6) Electroencephalogram ( EEG) .
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37
Treatment :
Step 1 :
 Stabilize the patient & put him in left lateral position .

 Secure airway , breathing & circulation .
Step 2 : Correct transient metabolic disturbances :
 Hypoglycemia : give dextrose 10% IV ( 2ml / kg ) .

 Hypocalcemia : give Ca gluconate 10% IV slowly ( 2 ml /kg ) .
 Hypomagnesemia : Mg sulphate 50% IM (0.2 ml /kg ).
Step 3 : Anticonvulsant drugs ( if seizure prolonged >5 minutes or recurent ).
-Loading dose = 20mg / kg slow IV.

Phenobarbitone
- maintanance dose = 3-8 mg/kg IV .
If no response
Maitanance & loading does as phenobarbitone .

Phenytoin
If no response
Midazolam or - 0.1 -0.3mg/kg IVI.
Diazepam
If no response
- 50mg IV
Pyridoxine
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38
Notes :
1) After controlling the attack , gradual withdrawal of anticonvulsants
in transient causes with low risk of recurrences .
2) febrile convulsion is not a cause of neonatal seizures .
3) jitteriness :
 Tremor like movement of limbs ( never affecting the face ).

 Precipitated by sensory stimuli & stopped by holding the limb.
 Not associated with EEG changes .
 May occur in normal infant , drug withdrawal , hypocalcemia
& hypoglycemia
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39
Neonatal Sepsis
Definition : Clinical syndrome characterized by systemic illness accompanied
by multiplication of bacteria with their toxins in blood .
Pathogenesis : neonatal sepsis can be classified into two syndromes based on

the age of presentation :
Type Early sepsis Late Sepsis

Onset 1st 5-7 days of life Afterward
Pattern -Intra partum (during delivery ). Acquired after birth .
- Vertical transmission .
Risk 1) Prematurity. 1) prematurity .
factors 2) PROM > 18 h. 2) Hospitalization.
3) Maternal fever/chorioamionitis 3) invasive procedures
4) Maternal infection e.g. UTI as ETT , UVC &
mechanical ventilation
Organism  Group B beta-hemolytic  Staphylococcus
streptococci aureus .
 E.coli  H.influenza
 Listeria monocytogenes .  Klebsiella .
Prominent Respiratory symptoms Meningitis

symptoms
Clinical picture :
Early manifestation : (Not specific )
 Respiratory distress & apneic attack .

 Lethargy & irritability .
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40
 Poor feeding & vomiting .

D/D of mottled skin
 Unstable temperature .
 Poor Moro & suckling reflexes . 1\ cold stress 3\ Down syn
 Skin manifestations : 2\ sepsis 4\ Shock .

 Jaundice .
 Mottled skin .
 Poor perfusion :-by applying pressure over sternum for 5 seconds
-Normally < 2 seconds .
 Petechial rash : pin point subcutanous heamorrhage.
 Sclerema : -skin become thick ,dry & hard in touch
-indicate irreversible condition .
Late manifestation : ( focal infection )
 Respiratory : pneumonia with respiratory distress .

 Neurologic : meningitis . manifested as :
 Seizures .
 Tense pulging fontanel.
 High pitched cry
 Hypotonia & hypo reflexia .
 Cardiac : -shock .
-heart failure(tachycardia ,tachypnea ,tender liver&cardiomegaly)
 Gastointestinal : -Vomiting & diarrhea .
- direct hyperbilirubinemia
- Necrotizing enterocolitis .
 Hematologic : pallor , purpura , DIC & bleeding tendency .
 Skin : scleroderma ( poor prognosis ) .
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41
Investigation :
1) CBC : leucopenia in severe sepsis ( less commonly leukocytosis ).

2) Inflammatory markers : ESR & CRP .
 Suprapubic urine culture
3) Complete septic screen :
 Lumbar puncture .
 Blood culture .
Treatment :
 Chest x ray .
 Supportive treatment :
 Swap from any opening .
 Incubator care in NICU.
 O2 inhalation & mechanical ventilation if needed .
 IV fluid & total parental nutrition in prolonged cases .
 Specific treatment : while waiting for culture results , empiric antibiotic
combination is given :
Early neonatal sepsis : Late neonatal sepsis
1st line : Ampicillin + gentamycin. Fluxacillin + gentamycin
2nd line :Ampicillin + 3rd g. cephalosporin 3rd generation cephalosporin
Notes :
 Ampicillin is drug of choice if group B beta hemolytic streptococci documented.

 Fluxacillin , cluxacillin or vancomycin + aminoglycoside such as gentamycin
best coverage for Staph.aureus.
 Third generation cephalosporin should be avoided as empirical therapy .
 3rd generation cephalosporin (ceftriaxone ) not use in neonate CNS damage.

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42
Congenital infection (Torch)

TORCH is an acronym that denotes a chronic non-bacterial perinatal infection ,
it stands for :
 Toxoplasmosis .
 Other infection : ( syphilis , hepatitis B , coxsackie virus , Epstein-barr ,
varicella zoster & human parvovirus ).
General features suggesting congenital
 Rubella
infection
 Cytomegalovirus .
 Herpes simplex virus .
 History suggestive of congenital
Infection :
1) Previous history of abortion ,
IUFD .
2) Maternal : skin rash, fever
Or genital vesicles during
Pregnancy .
 Congenital toxoplasmosis :
Special features • Retinopathy, an acute fundal chorioretinitis which

of sometimes interferes with vision
toxoplasmosis • Cerebral calcification
• Hydrocephalus.
• microphthalmia .
Diagnosis Serology ( Toxoplasma-specific IgM & persistent IgG )
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43
Isolation of organism in blood.

Cerebral imaging : diffuse calcification .
Treatment Triple therapy for 1 year :
 Pyrimethamine
 Sulphadiazine
 Folonic acid .
 Congenital rubella :
Special features  Cataract
of Rubella  CHD=patent ductus arteriosus & pulmonary stenosis
 Sensorineural deafness .
Diagnosis Serology : Rubella-specific IgM,
Treatment Prevention by MMR vaccine .
Symptomatic treatment ( No specific treatment of rubella ).
 Congenital CMV infection :

specific features  Sensorineural deafness .
of CMV  Epilepsy
 Cognitive impairment .
Diagnosis Serology : CMV-specific IgM,
Infant urine : CMV – culture
Brain imaging : periventricular calcification .
Treatment Symptomatic treatment .
Ganciclovir (Antiviral therapy ).
 Congenital HSV infection :
Specific features  Skin and mouth vesicles .
of HSV 2  Keratoconjunctivitis .
 Encephalitis .
Diagnosis Viral isolation & culture
Immunological assay to detect antigen in lesion scrapings.
Treatment Acyclovir & symptomatic treatment .
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44
Neonatal respiratory distress
Causes : can be classified to :-
Peripheral Central
CNS failure :
Pulmonary Extra-pulmonary 1/ sedation
I. Lung : I . Cardiac : 2/ perinatal asphyxia

 RDS - heart failure 3/ Intra-cranial hge.
 TTN - CHD
 Cong. Pneumonia II . hematologic :
 Cong. labor emphysema - polycythemia .
 Lung collapse ,hypoplasia - Severe anemia .
& cysts .
II. Airway : III . metabolic :
 Meconium aspiration - hypoglycemia .
Synd. – hypothermia .
 Obstruction as : - metabolic acidosis .
 Bilateral Choanal atresia.
 Vascular ring .
III. Pleura :
 Pneumothorax .
 Pleural effusion
 Diaphragmatic hernia .
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45
 Clinical picture :
 Tachypnea : Respiratory rate > 60 breath / min . ( in neonate )
 Recessions : intercostal , subcostal & suprasternal recessions .
 Cyanosis .
 Acting ala nasi .
 Grunting : is a physiologic response to end expiratory alveolar collapse.
Grades of respiratory distress :
 Grade 1 : tachypnea & acting alae nasi .

 Grade 2 : as 1 + intercostal & subcostal retractions .
 Grade 3 : as 1&2 + grunting .
 Grade 4 : as 1,2 & 3 +central cyanosis & disturbed consciousness .
Respiratory distress syndrome

( hyaline membrane disease )
 Definition : syndrome of respiratory distress occurs in newborn due to

surfactant deficiency .
 Causes of respiratory distress :
I. Prematurity : specially < 35 weeks .
II. Infant of diabetic mother :
Factors decrease RD
hyperglycemia reduce fetal cortisone
1\ maternal preeclampsia
which is essential for surfactant
production . 2\ antenatal steroids .
III. Caesarian section .
3\ IUGR .
IV. Perinatal asphyxia .
4\ PROM.
V. Other cause : male sex & 2nd twin .
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46
Pathophysiology :
 pneumocyte type II start producing surfactant at 21-24 weeks gestation
and mature after 35th weeks ( neer term ).
 Surfactant reduce surface tension within the alveoli , so it prevent the
alveolar collapse at the end of expiration .
 Low surfactant alveolar increased surface tension diffuse alveolar
collapse during expiration higher pressure is required to initiate lung
inflation increased work of breathing with impaired gas exchange
hypoxemia , hypercapnia & respiratory acidosis .
 Hypoxemia pulmonary vessels vasoconstriction alveolar hypo-
perfusion decreased surfactant production by pneumocyte type II
progressive collapse ( atelectasis ).
Clinical picture :
 Signs of respiratory distress develop within hours after birth .
 Diminished air entry by auscultation with fine basal crepitation.
Investigation :
 Chest X-ray :
 Diffuse reticulo-nodular infiltrates ( ground glass appearance ).
 Air bronchogram
 White lung ( opacification of both lungs ) in severe RDS
 Arterial blood gases :
 Hypoxemia in mild respiratory distress.
 hypoxemia , hypercapnia & respiratory acidosis in severe RDS
 complete septic screen :
 to rule out early onset sepsis .
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47
Prevention of RDS :
 Avoid risk factors :
- control maternal DM.
- avoid unnecessary C/S .
- avoid prematurity .
 Antenatal steroid therapy :
- Recommended for pregnant women <34 weeks gestation who at risk
for preterm delivery .
- Steroid enhance surfactant production .
- Dexamethasone 12mg IM ( 2 doses 24 hours apart ).
 Surfactant administration :
- Early postnatal surfactant administration by ETT (4ml /kg ).
- 2 doses : 1st dose given immediately after birth (as soon as possible )
2nd dose 12 hours after the 1st dose .
Complication of
Treatment : surfactant :
1/pneumothorax
a. NICU admission , incubator care & close observation .
2/ pulmonary hge.
b. Respiratory support : keep O2 sat >90% .
c. IV fluid & total parental nutrition in prolonged cases . 3/ bradycardia.
d. Symptomatic treatment for : acidosis & anemia . 4/ O2 desaturation.

e. Antibiotic : to rule out cong. Pneumonia .
5/ Sepsis .
f. Surfactant : 4ml /kg for 2-4 doses 8 hours apart .
Complication of RDS :
1/ intra ventricular hemorrhage .
2/ hypoxia & acidosis >>> cardiogenic shock . 3/ Patent ductus arteriosus .

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48
Comparison between TTN & MAS :
Definition Self limited respiratory Severe RD in post-term or full term

distress in full term baby . exposed to intrauterine asphyxia.
Patho- Delayed resorption of fetal Intra-uterine asphyxia →paralysis of
physiology fluids by pulmonary anal sphincter→ meconium stained
lymphatics liquor → meconium aspiration .
Risk factors a. Caesarian section. i. Post maturity .
b. Maternal smoking ii. Intrauterine hypoxia .
c. Maternal diabetes iii. IUGR.
d. Maternal excessive iv. Oligohydraminos.
analgesia . v. Abnormal fetal heart rate.
Clinical Mild respiratory distress Sever respiratory distress.

picture within few hours after birth Meconium staining of nail ,skin &
Resolve within 2-3 days . umbilicus
Chest x ray Hyperinflation of the lungs. Coarse irregular patchy infiltrate .
Prominent Perihilar streaks. Hyperinflation of lung field .
↑pulmonary vascular Flattened diaphragm .
markings . Pneumothorax may be present .
Mild cardiomegaly .
Treatment O2 support . Proper suction by ETT .
Antibiotic . NICU admission & O2 satmonitoring
NPO until RR<60cycle/min Cord ABG
O2 supply & mechanical ventilation
If needed .
Antibiotic
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49
Neonatal cyanosis
 bluish discoloration of skin & mucous membrane .
 cyanosis appear when reduced hemoglobin
>5g/dl in capillary blood .
 it can be peripheral ( not affecting tongue
frenulum ) or central ( affecting tongue
frenulum ).
Causes :
can be normal transiently but may indicate sepsis , shock or

temperature instability .
can be
Pulmonary : Hematological : Cardiac :
-Severe RD - Polycythemia - Cyanotic CHD
-Severe MAS - Methemoglobinemia

1/ TOF
-Congenital pneumonia.
2/ TGA
-Pneumothorax 3/ tricuspid
atresia
- diaphragmatic hernia .
4/total anomaly
Neurological causes : e.g. IVH , narcosis , myasthenia gravis .
of pulmonary
Sepsis . venous return.
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50
Congenital diaphragmatic hernea
developmental defect of diaphragm causing herniation of abdominal organs into

thorax . results in pulmonary hypoplasia on affected and
contralateral side
Clinical picture :
 May be asymptomatic .
 respiratory distress, cyanosis
 scaphoid abdomen and barrel-shaped chest
 affected side dull to percussion and breath
sounds absent. may hear bowel sounds instead.
 heart sounds shifted to contralateral side .
Diagnosis : Chest X-ray :
 portion of GI tract in thorax ( gas filled loops ) .

 displaced mediastinum to other side.
Types :
1/ bochdalek hernia ( > 90% ).
- Posterolateral mainly .
- On left side 80-85 % .
2/ Morgagni hernia : 3 / diaphragmatic eventration :
- Retrosternal mainly .
– on right side .
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51
management :
 Large NGT is passed and suction is applied to prevent distension of

the intra thoracic bowel.
 ETT inserted ( not use ambu-bag ).
 After stabilisation, the diaphragmatic hernia is repaired surgically
Complication of CDH :
 Pulmonary hypoplasia .
 Chest deformity : e.g pectus excavetum & scoliosis .
 GERD .
Choanal atresia
Congenital blochage of posterior nasal passage ( choana ) due to uni/bilateral
failure of recanalization of nasal fossae during fetal development .
Presentation :
 It can be unilateral or bilateral .
 Bilateral choanal atresia is a very serious life threatening condition
because neonates are obligate nasal breathing .
 Early diagnosis by failure to insert nasal catheter during routine neonatal
examination .
 Infants will present with cyanosis during feeding .
 The cyanosis may improve when the baby cries .
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52
Diagnosis :
 Diagnosis is confirmed by radiological

imaging as CT scan head .
Treatment :
 Surgery is the only definitive treatment .
CHARGE syndrome : is an acronym for the set of unusual congenital features

seen in a number of newborn children. The letters stand for :
 Coloboma of the eye .

 Heart deficit .
 Atresia of nasal choanae .
 Retardation of growth / development .
 Genital abnormalities
 Ear abnormalities & deafness .
Neonatal Apnea
Apnea : Cessation of breathing for more than 15-20 seconds (or less if associated
with bradycardia or cyanosis ) .
Causes :
I. Apnea of prematurity : combination of CNS prematurity and obstructive

apnea. resolves by 36 weeks GA ( diagnosis of exclusion )
II. Others as : sepsis , IVH , NEC , GERD , hypoxic injury, convulsions anemia ,
hypoglycemia , hypothermia & drugs ..
Mangment :O2 , CPAP ,mechanical ventilation , tactile stimulation & CNS stimulant.
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53
Infant of diabetic mother

 Neonate born to diabetic mother whether true or gestational diabetes .
 Commonly delivered preterm with high birth weight ( macrosomia ) .
**Common complication with IDM :
 Hypoglycemia : ( blood glucose <45mg /dl ).

 Found in 50% of IDM .
 Mechanism : maternal hyperglycemia → fetal hyperglycemia →fetal
hyperinsulinemia → after birth with cutting of cord and
interruption of glucose flow to fetus while hyperinsulinemia still
going on → hypoglycemia to the neonate .
 signs often non-specific as : lethargy, poor feeding, irritability,
tremors, apnea, cyanosis, seizures .
 onset during 1st 24 hours ( frequent monitoring of RBS in 1st 24h ).
 Hypocalcemia :
 Normal ca+ level 9 -11 mg /dl .( hypocalcemia <9mg/dl ).
 Found in 50 % of IDM .
 Unknow cause : but may be due to transient hypoparathyroidism .
 The serum ca+ levels are lowest at 24-72 h. of age .
 Manifested as jitterness & convulsion .
 Ca+ gluconate infusion is the management .
 Hypo-magnesemia :
 Serum magnesium level < 1.6 mg/dl .
 It is related to maternal hypomagnesemia & severity of maternal DM.
 ↓ mg+ is suspected when there is convulsion with normal ca+ level .
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54
 Hyperbilirubinemia :
 bilirubin production is apparently increased in the IDM 2ry to
prematurity , macrosomia , polycythemia .
 Also post natal hypoglycemia causes ↓ conjugation of indirect
bilirubin in liver .
 Respiratory distress : it may be due to :
 RDS ( hyaline membrane disease ) due to deficient lung maturation &
surfactant production ( ↑insulin →↓cortisone → ↓ surfactant ).
 Transient tachypnea of newborn : occur specially after elective C/S.
 Other cause : hypoglycemia , polycythemia & hypertrophic
cardiomyopathy .
 Cardiac problems :
 Cardiomegaly >30% of IDM .
 Heart failure ~ 5-10% of IDM .
 ventricular or atrial septal defect, TGA , truncus arteriosus, tricuspid
atresia & coarctation of the aorta are common in IDM .
 Macrosomia :
 Newborn with birth weight > 4 kg ( 4.5 kg in some sources ).
 Caused by maternal hyperglycemia →fatal hyperglycemia → fetal
hyperinsulinemia ( anabolic effect ) → ↑glycogenesis , lipogenesis
&protein synthesis → macrosomia .
D/D of macrosomic
 Macrosomia may lead to : baby :
 Birth injuries e.g. brachial plexus injury . 1/ Familial .
 Birth asphyxia : due to difficult prolonged
2/ IDM .
labour , head stuck.
3/ Beck with Widman
 Polycythemia : 2ry to ↑ fetal erythropoietin .
syndrome
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55
 Congenital Anomalies : 3 times more common in IDM .

 e.g. VSD , ASD & TGA
 renal agenesis
 small left colon syndrome .
 neural tube defect .
 lumbosacral agenesis .
** Investigation :
I. Frequent monitoring of blood glucose ( every 2 h in 1st day ).

II. Serum Ca+ should be obtained at 6 , 24 & 48 h of age .
III. Serum hematocrite should be checked at birth and 4 & 24 h of age.
IV. Serum bilirubin level if indicated by physical examination .
V. Echocardiography if cardiac anomalies is suspected .
** Management :
NICU admission & incubator care .

Treatment of hypoglycemia :
 Dextrose 10% ( 2 -4 ml /kg ) IV bolus.
 Followed by Dextrose 10% IV infusion .
 Repeat RBS / 2 hours .
 If blood glucose is controlled , gradual withdrawal of IV fluids and
advice oral feeding .
 use hydrocortisone & glucagon in poorly controlled cases .
 discharge if no hypoglycemia for 48 h with no other complications
Treat complication : - hypocalcemia → ca gluconate infusion .
- jaundice → phototherapy Or exchange transfusion.

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56
Necrotizing Enterocolitis
 intestinal inflammation associated with focal or diffuse

ulceration and necrosis .
 Affecting primarily terminal ileum and colon.
 affects 1-5% of preterm newborns admitted to NICU .
Pathophysiology : bowel ischemia → mucosal damage . entral feeding

provide substrate for bacterial growth → mucosal invasion → bowel necrosis ,
gangrene & perforation.
Risk factors :
1) Prematurity : ( week intestinal wall & week immunity ).

2) Enteral feeding with formula ( breast milk can be protective).
3) Sepsis .
4) Intestinal wall ischemia :
 Perinatal asphyxia
 Shock .
 Umbilical venous catheterization .
 PDA .
Clinical picture :
 presentation is usually within 1st 2 weeks of life .

 abdominal manifestation :
• distended abdomen
• increased amount of gastric
aspirate/vomitus with bile staining
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57
• frank or occult blood in stool

• feeding intolerance
• diminished bowel sounds
• signs of bowel perforation (sepsis, shock, peritonitis, DIC)
 Septic manifestations :
1) RD & apneic attack .
2) Lethargy .
3) Poor feeding .
4) Poor Moro & suckling reflexes .
5) Shock , DIC ( advanced stage ) .
Investigation :
 Abdominal X-ray :
 pneumonitis intestinalis ( intramural air, ) thickened bowel wall .
 free air under diaphragm .
 portal venous gas .
 CBC : ↓ or ↑ WBCs , low platelet .
 ABG : metabolic acidosis , hypoxia, hypercapnia.
 Complete Septic screen.
 Stool examination for occult blood .
Treatment :
1) NICU admission & incubator care .
2) NPO , NGT decompression, IVF & TPN for prolonged cases .
3) O2 support & mechanical ventilation if needed.
4) Stat broad spectrum antibiotic & consult pediatric surgeon .
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58
Prematurity
Baby born before completed 37 weeks gestation .
Causes :
1) Idiopathic in the most of cases .

2) Maternal causes : extreme of ages & chronic diseases .
3) Fetal factors : twins & congenital infections .
4) Obstetric factors : abnormal uterus / placenta & polyhydraminos .
Preterm infant has :
 Birth weight < 2.5 kg

 Birth length < 47 cm .
 OFC < 33 .
Physiological features of preterm :
 Activity : week activity , hypotonic

with frog like position .
 Crying : faint
 Breathing : need respiratory
support , apnea is common.
 Suckling & swallowing : weak &
not coordinated .
 Hearing : Startles to loud noise .
 Physiological jaundice : Delayed ( after 3rd day ) prolonged (for 2 weeks ) &
deeper ( up to 15 mg/dl ).
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59
Complication of prematurity :
System Complication Cause

 Heart failure PDA
 Hypotension Hypovolemia & H.F.
 RDS surfactant deficiency
 Aspiration syndrome -Loss of gag & cough reflex .
-Poor coordination between
suckling & swallowing &
breathing
 Pneumothorax Positive pressure ventilation
 Apnea of prematurity Immature resp. center
 NEC Weak intestinal mucosal barrier.
 GERD Weak cardiac sphincter.
Low gastric capacity .
Hyperactive pyloric muscle .
 Poor weight gain Poor suckling & swallowing .
 IVH Immature fragile blood vessels
 Kernicterus Immature BBB
 Retinopathy of Prolonged O2 therapy &
prematurity ventilation.
 Hypoxic ischemic Perinatal asphyxia.
encephalopathy
 Anemia Defect in iron store & frequent
sampling .
 Coagulopathy Defect in coagulation factors .
 Sepsis Low maternal antibodies .
Immature immune system .
 Dehaydration & Immaturity of kidney →↓ GFR .
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60
metabolic acidosis
 Hypothermia Lack of subcutaneous fat
Immature heat regulating center
 Hypoglycemia Poor glycogen storage .
Management :

 Induction of fetal lung maturity by parenteral steroid.
 Consider prenatal transfer to specialized center .

 place the baby under radiant warmer .
 dry the baby & do suction to oropharynx & nose .
 Apgar scoring & resuscitation if needed .
 Complete the examination .
 Give vit K (1mg IM ).
 NICU admission & incubator care .

Handling the infant is kept to a minimum and
done as gently, rapidly and efficiently as possible
 Temperature control :
 Preterm baby is in high risk for hypothermia .
 Place in plastic bag at birth to keep warm if extremely preterm
 It adjusted to keep body temp. around ( 36.5-37.2 OC ).
 Value : keep nursing the baby in neutral thermal environment
Neutral thermal environment : it is range of environmental

temperature in which O2 consumption is minimal & growth is maximum.
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61
 Humidity : kept around ( 40- 60% )

Value : reduce insensible water loss & prevent drying of resp. airway .
 Oxygen therapy :
Given in lowest concentration for shorter period with gradual withdrawal.
 Prevention of infection :
 All medical personnel must wash their hands before and after
examining the baby .
 Feeding :
 Oral feeding :
 Preterm infants at 34 week of gestation or more can often be fed by
bottle or at the breast. ( good suckling )
 Smaller or less vigorous infants should be fed by
gavage Through naso-gastric tube
 Use expressed breast milk not artificial formula
( to avoid NEC ).
 Intravenous fluid :
 In severe RD or intolerant to oral feeding .
 Start by 60-80 ml /kg / day ( dextrose 10% ) in 1st day .
 Gradual increase to reach 150ml /kg /day at 5th day using
( dextrose saline 10% ) .
 Total parental nutrition :
 when enteral feeding is impossible for prolonged periods, TPN may
provide sufficient fluid, calories, amino acids, electrolytes, and
vitamins to sustain the growth of ill infants .
 Start by 50Kcl / kg / day & increased slowly to 100Kcl/kg/day in
5-7days .
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62
management of some prematurity complications:

 surfactant administration through ETT .
 nasal CPAP ( continuous positive airway pressure ) . to avoid alveolar
collapse .
 caffeine ( CNS stimulant ) used for apnea of prematurity .

 50% of IVH occurs within 8 hours of birth ; 90% occurs by day 3
 incidence and severity inversely proportional to GA .
 risk factors include : prematurity , RDS, fluctuating cerebral blood
flow & coagulopathy
 clinical picture :
 many infants with IVH are asymptomatic
 subtle signs: apnea. bradycardia, changes in tone or activity,
altered level of consciousness
 catastrophic presentation : bulging fontanelle, drop in
hematocrit. acidosis, seizures, hypotension .
 Management :
 supportive care to maintain blood volume and acid-base status
 avoid fluctuations in blood pressure and cerebral blood flow
 follow-up with serial imaging .

 May be asymptomatic .
 May cause : Heart failure , bradycardia , apnea
 The pulses are ‘bounding’ from an increased pulse pressure .
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63
 the precordial impulse becomes prominent and a systolic murmur

may be audible.
 Echo-cardiogram is diagnostic .
 Management of PDA :
 Restrict IV fluid intake .
 Indomethacin ( prostaglandin synthetase inhibitor ).
 Surgical ligation if failed medical treatment .

 Interruption in the growth of developing retinal vessels.
 Pathophysiology :
 early vasoconstriction and obliteration of the capillary
bed →repair response → neovascularisation
 retinal detachment occurs in a small percentage
 Risk Factors :
 association with period of high oxygen concentrations is not clear
 extreme prematurity is the most significant risk factor.
 Clinical picture :
Criteria for incubator discharge
 No warning manifestation (
1. infant > 1750g with good
screening is needed ).
suckling & good oral feeding.
 Gradual occurring astigmatism ,
retinal detachment , amblyopia. 2. infant can maintain his
 Management : temperature outside the
 follow-up : eye examinations incubator .
for high risk babies . 3. No critical illness .

 laser photocoagulation .
4. Normal respiration .
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64
Intrauterine growth restriction

 SGA is birth weight < 10th centile for gestational age
 IUGR is failure of growth in-utero that may or may not result in SGA .
Types :
All growth parameters are Weight centile < length & head
symmetrical : weight ,OFC & circumference .
length<10th centile .
Fetus affected in early pregnancy ( 1st Usually because of IUGR due to insult in
trimester ). late pregnancy .
Due to : Due to :
 chromosomal anomalies  preeclampsia .
 constitutional (small  placental insufficiency .
parents ).  maternal mal-nutrition .
Bad prognosis Good prognosis .
Complication :
1) ↑ risk of fetal death & asphyxia .
2) Hypoglycemia ( due to ↓ glycogen storage ).
3) Hypothermia ( due to ↓ sub cutaneous fat ) .
4) Polycythemia ( 2ry to chronic intrauterine hypoxia ).
5) NEC ( chronic fetal bowel hypoxia ).
6) Coagulopathy ( bone marrow / hepatic compromise ).
7) Meconium aspiration syndrome ( 2ry to fetal hypoxia ).
Management :
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65
1) Routine post-natal care .

2) Clinical evaluation for features suggesting underling cause .
3) Particular attention to thermal care & blood glucose monitoring .
4) Close observation to vital signs .
5) Admission to NICU if birth weight < 1750g .
a. They are sucking all feeds 3-4 hourly .

b. Weight gain is satisfactory ( 20-30g /day ).
c. Body temperature is maintained at room temperature .
d. Mother is capable of caring for infant .
Post maturity
 Infant born after completed 42 weeks gestation .
 Causes are unknown in most cases .
 Significant ↑ perinatal mortality & morbidity :
 ↑risk of perinatal hypoxia due to placental insufficiency .
 Obstructed labor due to larger fetus .
 Meconium aspiration .
 Reduced skull molding .
 Clinical features include :
 Wrinkled dry skin .
 Over grown nails .
 Opened eye & a lot of hair on their head.
 Induction of labor is usually advised after 41 weeks .
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66
Birth injuries
Caput succedaneum -facial nerve -#clavicle -sternomastoid

-Cephalhematoma -Brachial plexus -#long bones muscle inj.
–Intracranial hge. -phrenic nerve inj. – visceral inj.
 Facial nerve injury :

 Peripheral facial nerve injury result in paralysis of whole face muscles
at same side .
 Manifested by :
 Absent nasolabial folds.
 Asymmetric cry .
 Deviation of mouth to healthy side .
 Inability to close the eye firmly .
 Treated by :
 Care of the eye with eye drop & ointment.
 Care of feeding .
 Physiotherapy .
 Fracture clavicle :
 It is commonest bone to be fractured in neonates .
 Manifedted by absent Moro reflex & pseudo paralysis on affected side.
 Chest X-ray is diagnostic .
 Treated by immobilization of arm ( figure 8 bandage ) .
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67
 Brachial plexus injury :
 Injury to upper nerve roots ( C5 –C6 ) → Erb’s palsy .
 Injury to lower nerve roots ( C7- C8 & T1 ) → klumpke’s palsy .
 Entire brachial plexus injury →whole limb flaccidity & loss of all
reflexes .
 If nerve root are intact , full recovery will occur in more than 90%
by 3 months .
 If No improvement within 3 movement , consult neurosurgery for
nerve grafting & neuroplasty .
Injury Erb’s palsy Klumpke’s palsy
Abnormality The arm is adducted , The arm supinated , elbow
pronated & internaly rotated. flexed & wrist extended .
( waiter’s tip posture ). ( claw hand posture )
Reflexes Absent Moro Absent grasp

Preserved grasp Preserved Moro .
Associations Phrenic nerve palsy Horner syndrome
(C3,C4&C5 ) in 75% of cases . ( if sympathetic fiber of T1
injured ).
Treatment -Partial intermittent -hand kept in neutral
immobilization to opposite position with pad of cotton in
position . in fist(hand writing position).
-Physiotherapy . -physiotherapy
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68
Primitive reflexes
 Cerebral cortex in newborn is not fully developed.
 subcortical centers ( spinal cord & brain stem ) mediate some primitive
reflexes .
 after time maturation of cerebral cortex occur with successive
disappearance of these reflexes .
 they appear prenatally at variable gestational ages and disappear post-
natally during 1st year of life as cerebral cortex matures .
 Significance of primitive reflexes :
1) Absence at time they should present signify damage to subcortical
concerned areas .
2) Persistent beyond time they should disappear signify failure of
development of cortical area which suppress the reflex .
I. Moro reflex :
Time Present at birth & disappear by 4-6 nonths .
Stimuli 1.sudden drop of the head from semisetting position .
2.making a loud noise near the ear .
3.sudden withdrawal of blankets from underneath the
infant.
Response  Extension of the trunk .
 Extension & abduction
then flexion & adduction
of upper limbs with little
share of lower limbs
( embracing movement ).
 Usually Followed with
loud cry.
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69
Value 1) Normal reflex in normal time → normal CNS .

2) persistent beyond 6 months → CP / mental retardation.
3) Absence :
 Bilateral :
 Premature < 28 weeks .
 CNS : depression by narcosis & ICH .
 Bilateral injury to brachial plexus or bilateral
#clavicle / humerus
 Unilateral :
 Erb’s palsy .
 # clavicle or humerus .
 Dislocated shoulder .
4) Sluggish :
 Sedation .
 Sepsis .
 Early kernicterus .
5) Exaggerated → CNS irritation as in late kernicterus .
I. Other important reflexes :
Reflex Method Response Time

Palmar Light touch to the Grasp response From birth up to
grasp
palm 2 months
Planter Light touch to the sole Grasp response From birth up to

grasp
10 months
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70
Suckling Stimulation of lips Suckling movement From birth up to

reflex
4months awake &
7months asleep
Rooting Finger stimulation Turning of mouth to From birth up to

reflex
near the angel of stimulus 4months awake &
mouth . 7months asleep .
Stepping The infant is held Walking movement From birth up to

reflex
upright with his soles 6 weeks
touching a flat surface
Placing The infant is held The baby will flex From birth to 6
reflex
upright with the sole then extend the leg weeks .
of one foot touching a to place it on upper
surface of table and surface of the table.
dorsum of other foot
touching the under
edge of the table
Glabellar Tapping fore head by Blinking From birth →

reflex
examiner finger persistent long
life
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71
Tonic neck While infant is supine Extebsion of upper From 1 month
reflex
the head is rapidly & lower limbs on →6 months
turned to one side side of turning &
flexion of the other
side .
Parachute Suspend the baby Extension of the From 9 months

reflex
from the trunk →then upper limbs → persist
sudden withdrawal . (protective reflexes).
Galant while newborn in Flexion of spine From birth up to

reflex
prone position toward the side of 4 months .
,stroking along the stimulus .
side of his spine .
_____________________________________________________________________________________
72
Hemorrhagic disease of newborn

 Hemorrhagic disorder in early neonatal period due to deficiency of Vit
K dependant clotting factors ( II , VII ,IX & X ).
 Affecting about 2% of neonates not given vit K at birth .
 Premature more reliable than full term .
 Breast feeder more reliable than formula feeder .
 Etiology :
** neonates at risk of vitamin K deficiency because :
 vitamin K poorly transferred across the placenta.
 insufficient bacterial colonization of colon at birth (synthesize vit K).
 dietary intake of vitamin K inadequate in breastfed infants.
 oozing from the umbilical stump, excessive bleeding from peripheral
venipuncture / IV sites, large caput succedaneum, cephalohematoma
(in absence of significant birth trauma), and prolonged bleeding
following circumcision .
 presents between the 2nd -7th day of life (may be early or late)
 Signs of anemia in severe hemorrhage ( pallor , tachycardia )
 Investigation :
1) PT & PTT are prolonged .
2) ↓ vitamin K dependant factors .
3) Normal bleeding time & platelet count.
 Treatment & prevention :
1) Vit K 1mg IM at birth ( as prevention ).
2) Vit K , fresh frozen plasma & blood transfusion in severe bleeding .
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73
Neonatal polycythemia
 Defined as arterial or venous packed cell volume ( hematocrit ) >65% .
 Etiology :
1) Placental insufficiency ( chronic intrauterine hypoxia ).
2) Delayed cord clamping .
3) Twin to twin transfusion syndrome .
4) Infant of diabetic mother .
5) Down syndrome & wilm’s tumor.
 may be asymptomatic ( only plethoric face ).
 Symptomatic :
 Poor feeding & Lethargy .
 Respiratory distress
 Necrotizing enterocolitis
 Treatment :
o Dilutional exchange transfusion with 20-30ml /kg of normal saline
over 30-60 minutes .
o Performed if symptomatic or asymptomatic with PCV >70% .
Physiological anemia of newborn
 Normal hemoglobin concentration at birth = 14-20g /dl .
 High HB volume at birth is due to intrauterine hypoxia→↑ erythropoietin.
 After birth HB ↓ to 10 -11g/dl because of : - No more hypoxia
- short life span of fetal RBCs.
 Anemia of prematurity occurs 6-12 weeks after preterm delivery and is
caused by shorter life span of pretem RBC,fast growth rate & ↓erythropiotin
_____________________________________________________________________________________
74
Sudden infant death syndrome (SIDS )

 is the sudden unexplained death of a child less than one year of age.
 Diagnosis requires that the death remains unexplained even after a
thorough autopsy and detailed death scene investigation.
 SIDS usually occurs during sleep , The exact cause of SIDS is unknown.
Risk factors :
a. Sleeping on the stomach or side.

b. Overheating.
c. exposure to cigarette smoke.
d. Accidental suffocation such as during bed
sharing or from soft objects may also play a role .
Prevention :
1) putting a child less than one year old on its back to sleep .
2) a relatively cool sleeping environment .
3) avoiding exposure to tobacco smoke.
4) Breastfeeding and immunization may also be preventive .
 Important definitions :
 Term baby : baby born btw 37 - 42 weeks gestation .
 Pre-term baby : baby born before completed 37 weeks gestation.
 Post-term baby : baby born after 42 weeks gestation .
 Still birth : baby died between 28 weeks gestation and birth.
 perinatal period : period btw 28 weeks gestation and 7th day after birth
 Neonatal period : from birth up to 28 days of life
 Early neonatal period : first 7 days of life
 Late neonatal period : from 8-28 day of life
_____________________________________________________________________________________
75

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Neonatology dr.

Routine neonatal care

1) Congenital hypothyroidism ( ↑ TSH ).

2) Cystic fibrosis ( ↑ immune reactive trypsin ).

4) Medium chain acetyl-CoA dehydrogenase deficiency .

5) Sickle cell disease .

Newborn physical examination

i. Temperature : normal temperature :

 5th & 6th months →+2cm

 the average length at birth = ~ 50 cm .

**After age of 1 year = age ( by years ) X 5 + 80

 Last 4 months → 250g /month

**After 2nd year → weight = age ( by years) X 2 + 8

a) Skin : normally skin of newborn :

 Some of benign cutaneous manifestation which 1/cold stress

usually resolve spontaneously : 2/hypovolemia

D/D of large Ant. Fontanel:

 Post. Fontanel : close at birth up to 2 months of age .

Not need medical intervension Rx complication ( anaemia / jaundice)

 red reflex positive bilateral by opthalmoscope .

 patency of bilateral nostrils must be checked .

- neonatal Benign lesion of the mouth :

the two types because management of Each are different :

 Predecidous teeth : poorly formed and roots are absent.

 the normal position is determined by drawing imaginary horizontal

 the newborn’s thorax is nearly rounded. Gradually the transverse

 Abdomen is slightly distended .

 Normally , the ext. urethral meatus opens on tip of penis .

 Labia majora at term are enlarged and cover completely labia

 Term infant should pass meconium within 48 hours of birth ,

 Types of formula milk :

indicated in cow’s or soya milk protein allergy .

infants, gastro-esophageal reflux (thickened with cornstarch) lactose

Definition : Steps to be done to optimize the airway , breathing & circulation of

Pale / blue Pink with Pink

Flaccid limbs Some flexion Well flexion

- Dischare after complete examination

- tactile stimulation of breathing by slapping the soles

 If no response : bag & mask

if : HR < 80 b/min. not rising despite adequate vent. proceed to

 the thumbs are placed on the lower third

 Ratio of compression: lung inflation→3:1

Drugs Indication Dose /Route

Na bicarbonate Severe Metabolic acidosis 2 ml/kg slow IV

 If no improvement despite previous medications , you must check :

definition : failure of newborn to establish spontaneous regular respiration

immediately after birth , leading to either death or survival with

permanent neurological damage .

 criteria for perinatal asphyxia :

Intra uterine Intra-partum post natal

Clinical picture :- depend on severity & duration of asphyxia .

- prepare for immediate delivery .

LATE MANIFESTATIONS OF PERINATAL ASPHYXIA

1. hypoxic ischemic encephalopathy (HIE)

brain edema → Ischemia → Encephalopathy .

Sign Stage 1 Stage 2 Stage 3

 Cranial U/S , CT scan or MRI : for brain edema & injury

2. Cardiac : myocardial necrosis , ventricular dysfunction & shock .

3. Respiratory : RDS , persistent pulmonary hypertension & pulmonary hge.