Neonatology

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                                     NEONATOLOGY 

                                                                                        By dr.  Adnan Al-Rikabi 

Definition of terms : 

1.  The normal human gestational period is 280 days or  40 weeks , calculated 

from the first day of the mother last menstrual cycle . 
a-  Preterm gestation refers to delivery at less than 37 wks gestation . 
b-  Term gestation refers to delivery at 38 to less than 42 wks gestation . 
c-  Post term gestation refers to delivery at or after 42 wks gestation . 

2.  The neonatal period is defined as the first 28 days ( 4 wks) of life for term 

infant , although , from a practical standpoint it is extended in the case of 
prematurely delivered infant. 

3.  Fetal and neonatal growth : 

a-  Fetal growth, the fetal growth rate is 5 g /day at 14-15 wks gestation, 10 

g/day at 20 wks and 30 g/day at 32-34 wks. The growth rate slows after 36 
wks gestation. 

b-  Neonatal growth : 

(1)-  after birth , there is a loss of weight due to a loss of extracellular 
water and suboptimal caloric intake . term infant lose 5% of their birth 
weight , preterm infants lose up to 15% of their  birth weight . 
(2)- term infant regain their birth weight by the end of the first week of life 
and thereafter gain 20-30 g/ day .   

Delivery room management of the newborn

A-  Goals .the goals of delivery room management are to assess and promptly 

attend the immediate needs (e.g oxygenations, ventilations ) and potential 
problems (e.g serious anomalies ) of the newborn . 

B-  Physical layout and equipment . the newborn resuscitation are should be in 

immediate proximity to the delivery room . it should have adequate lighting 
and space for personal and equipment for resuscitation, including a bed with 
a radiant warmer . 

C-  Preparation for delivery . 

1-  Obtaining perinatal information .the pediatrician must have specific 

information concerning the mother and the fetus to prepare for routine care 
of the mother and newborn as well as treatment of specific problems 
related to a particular delivery , 
a-  Obstetric history should include all information that may be pertinent 

to the immediate fetal conditions .the information is best obtained from 
the obstetrician and the medical chart and by direct communication 

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with parents .important issues are ( maternal age , medical and 
previous obstetric history , length of gestations , blood group 
incompatibilities , maternal infections , maternal drug use , ultrasound 
evaluations of fetal growth and amniotic fluid volume or congenital 
anomalies , signs of chorioamnionitis including prolonged rupture of 
fetal membrane ,maternal fever , and leukocytosis . 

b-  Labor history should include ( fetal heart tracing , duration of fetal 

membrane rupture , evaluation of amniotic fluid (color and quantity ), 
progress of labor and fetal blood PH. 

2-  Composition of the resuscitation team .personnel and their tasks vary with 

type of delivery that is anticipated .high risk deliveries include (maternal 
diabetic , RH and ABO incompatibility , preterm delivery at less than 38 
wks ,post term delivery at more than 42 wks , multiple gestations ,maternal 
bleeding , severe pre eclampsia ,IUGR, fetal anomalies , breech 
presentations , cesarean delivery , fetal distress .So high –risk team include  
a-  Team leader to direct resuscitation and direct and institute airway 

management . 

b-  One to assess heart rate and to initiate cardiac compression if needed . 
c-  One to assess with drying , suctioning , ventilation ,and prepare drugs 

for injection . 

d-  One to gain intravenous access and to administer drugs . 

3-  Equipment for resuscitation include : 

a-  Airway management (suction pump with regulator ,DeLee suction 

catheter , oral airway with deferent sizes ,endotracheal tubes , 
laryngoscope , suction catheter . 

b-  Ventilations and oxygenations ( oxygen source , mask of deferent sizes 

, bag with oxygen reservoir ) . 

c-  Intravenous access ( umbilical catheter 3.5 F and 5 F ,instruments for 

umbilical cut down , saline solution 0.9% . 

d-  Drugs like (epinephrine , plasma volume expander , sodium 

bicarbonate  or naloxone ) . 

D-  Assessment of the newborn and the  APGAR  score . The goal of the 

initial assessment is to determined the newborn state of oxygenation and 
ventilation. this is usually done by performing an abbreviated  APGAR  
evaluation. 

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TABLE .  APGAR  evaluation of the newborn  

Sign 

                                              Score  

                 0                                    1                                2 

Heart rate  

            Absent                         <100 beats/min               >100 beats/min 

Respiratory 
effort  

            Absent                         weak, irregular  

  strong , regular  

Muscle tone  

            Flaccid  

some flexion  

well flexed  

Response to 
catheter in 
nostril  

            No response                 grimace 

cough or sneeze 

Skin color  

Blue ,pale                    body pink 

entire body pink 

                                    Extremities blue                                                            

1-   The degree score was devised as a means of assessing the oxygenation , 

ventilation, and degree of asphyxia in a uniform manner that quickly 
communicates information to all people involved in the resuscitation of the 
newborn . 

The APGAR  evaluation is performed at one and five minutes after birth . 
Five signs – heart rate ,respiratory effort ,muscle tone ,reflex irritability 
and skin color __are examined and assigned a score of 0, 1, 2. The 
APGAR  score is obtained by adding all individual scores .  
a-  A score of 8-10 reflect good oxygenation and ventilation and indicates 

no need for vigorous resuscitation . 

b-  A score 5-7 indicate a need for stimulation and supplemental oxygen . 
c-  A score lees than  5 indicates a need for assisted ventilation and 

possible cardiac support . 

1-  The apgar score is a useful method of communicating the well-being of 

the newborn .however urgently needed resuscitation should not be delayed 
while a full examination Is performed . bradycardia or poor respiratory 
effort alone indicate a need for immediate resuscitation . 

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2-  The apgar score at five minute reflects the adequacy of resuscitation and 

the degree of perinatal asphyxia . 
 

E-  Resuscitation . the purpose of resuscitation is to re-oxygenate the CNS of 

the newborn by providing oxygen , establishing ventilation , and ensuring an 
adequate cardiac output  . although it may be difficult to differentiate 
primary apnea from secondary apnea , a quick assessment of the newborn 
skin color , respiratory activity , and heart rate should allow prompt 
institution of appropriate resuscitation . 

1-Routine procedures .the evaluation and procedures that constitute the 
resuscitation of the newborn are listed in the order in which they should be 
initiated . 

a-  Maintenance of body heat . the infant should be dried and provided 

with radiant heat to maintain body temperature . it is important to 
avoid hypothermia , which will increase the newborn oxygen 
consumption . 

b-  Establishment of an airway . immediately after delivery , the infant 

head should be placed in a neutral or slightly extended position and an 
airway established by clearing the mouth , nose and pharynx of thick 
secretion or meconium . deep and frequent oropharyngeal suctioning 
should be avoided because it will increase the vagal output causing 
apnea and bradycardia  . 

c-  Ventilation . the adequacy of air exchange in the newborn must be 

assessed . in the most cases , drying off, suctioning and tactile 
stimulation ( e. g. gentle flicking of the feet or rubbing of the back ) are 
adequate to induce effective spontaneous ventilation . 
(1) If ventilation is adequate , supplemental oxygen may be given to 

improve heart rate or skin color . 

(2)  If supplemental oxygen does not improve heart rate or skin color , 

or if ventilation is inadequate , mechanical ventilation should be 
initiated , using mask and bag ventilation . 
(a)  If spontaneous ventilation improves ,mechanical ventilation 

should be stopped and supplemental oxygen resumed . 

(b) If the response is poor or if airway obstruction occurs ,an 

endotracheal tube should  be inserted and mechanical 
ventilation continued . 

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d-   Circulation .  If mechanical ventilation does not improve the heart rate 

or skin color one of the following steps taken . 

(1)-    If heart rate is less than 60beats b/min or between 60 and 80 
beats / min         and not improving cardiac compression is initiated 
over the lower third of the sternum at a rate of 90 compression /min , 
the ratio of compression to ventilation is 3:1(90 compression , 30 
breath ) if heart rate not improve , epinephrine is administered via an 
umbilical venous catheter or endotracheal tube . 

(2)- If  heart rate is 80 beats /min or greater but there is poor perfusion 
or weak pulse , a plasma volume –expanding agent is administered at a 
dose of 15 ml / kg . 

d-  Drug support . the following drugs may be useful during resuscitation . 

(1) Sodium bicarbonate (2 mEq/kg ) should be reserved until it is 

clear that a metabolic acidosis exists . 

(2) Naloxone (0.1mg/kg) may be helpful for poor spontaneous 

respiratory effort secondary to maternal narcotic use during labor . 
Naloxone is contraindicated in an infant born to mother who is 
addicted to narcotics . 

(3) Dopamine (5-20 ug/kg/min) improve myocardial function . 

 
 
2-Special proplems requiring resuscitation: 

a-  Meconium aspiration syndrome . thick meconium is a serious 

concern because it may be aspirated and result in aspiration pneumonia 
, it imperative that the meconium be removed from the airway before 
any attempt is made to ventilate the infant . 

b-  Choanal atresia is a membrane or bony obstruction of the posterior 

nasal passage .  

c-  Progressive respiratory distress or cyanosis that occur in an infant 

despite appropriate resuscitation usually suggests an underlying 
disorder of the cardiopulmonary system , which require immediate 
investigation ( cyanotic heart disease , congenital or acquired disorders 
of the lung like diaphragmatic hernia or pneumothorax) . 
 

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Neonatal  examination  

Goals of neonatal examination : 

1-  Assess wellness of the newborn , screening for general abnormalities , birth 

trauma or acquired medical problems . 

2-  Assess the newborn for gestational age and appropriateness of size for 

gestational age . 

3-  When appropriate confirm infants normality to parents . 
4-  When appropriate demystify and reassure parents about common , benign 

variation in newborn physical examination or behavior . 

5-  Foster early infants –parent bonding and parental self-confidence . 

Physical examination : 

1-  general appearance  .important observation include body proportion , activity 

, quality of cry ,skin color , gross abnormalities ,unusual features and signs of 
respiratory distress , weight , length and head circumference measurement are 
obtained and recorded . 

2-  skin color may suggest cyanosis , pallor or jaundice . 

a-  normal peripheral vascular instability presentation include skin 

mottling . peri-oral cyanosis and cyanosis of the hand sand feet , with lips , 
mucous membrane , nail beds and tongue remaining pink . 

b-  cracking or desquamation of the skin is normal in the term and 

postmature infants . in the term infant fine downy hair known as lanugo 
covers the skin , particularly the shoulder and upper back . 

c-  jaundice  in the neonate is first visible on the face and as the serum 

bilirubin level rises it progress caudally to include the rest of the body and 
the sclera .natural sunlight should be used to inspect the skin for the extent 
of jaundice . 

d-  birth marks are common and visible at birth include flat vascular nevi 

(e.g.salmon patch nevus and port wine stains ) and Mongolian spots .raised 
vascular nevi usually become apparent several wks after birth ( e.g. 
capillary or strawberry hemangioma , cavernous hemangioma ) . 

e-  benign rashes are common : 

1-  comerythema toxi has a flea-bite appearance with scattered 

erythematous macules that may contain papulopustular centers filled 
with eosinophils . this rash typically changes distribution from day to 
day . 

2-  milia are transient fin , pinpoint, yellow-white papules caused by retain 

sebum that typically cover the bridge of the nose, chin,and cheeks . 

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3-  neonatal pustular melanosis consists of small vesiculopustules that 

are present at birth and rupture within a few days , leaving transient 
pigmented macules with scaly borders . 

          3-head and neck .the head and face frequently exhibit sequelae of the birth    

                   process including bruises and asymmetries . most resolve spontaneously         
.facial features should be carefully inspected for size , placement and symmetry .          

a-    .palpation of skull determines contour , extent of separation or over riding of 

sutures and the size of the fontanelles . 
1-  molding of the head shape into elongated or asymmetric contour occurs 

secondary to intrauterine pressure or forces during labor . 

2-  cephalhematoma and caput succedaneum .  

b-  eyes : dimming the room light cradling the occiput in the examiner hand to left 

the baby head off the mattress may stimulate the baby to open her or his eyes . 
1-  conjunctival or sclera hemorrhage resolve with time and usually benign . 
2-  the presence of a red reflex exclude the presence of lens opacities . 
3-  up to 3 months the eyes normally may appear to cross intermittently. 

c-  Ears patency of the canal should be determined . malformed or low set ears 

may be associated with auditory or renal abnormalities . 

d-  Nose newborns are nose breathers obstruction of the nasal passage reslt in 

respiratory distress . 

e-  Mouth . should be examined by inspection and palpation . common minor 

abnormalities include small, white epithelial pearls along the gum margins . 
small white cyst termed epistein pearls along the median raphe of the hard 
palate . palpation may reveal a submucosal bony cleft of palate . 

f-  Neck  must be hyperextended to inspect adequately for masses . congenital 

masses include goiter ,cystic hgroma , brachial cleft cysts and thyroglossal 
cysts . a webbing of the neck is seen in turner syndrome . 

4-chest : 

a-  Clavicles are palpated for signs of fractures  
b-  Respiratory rate and pattern and the presence of chest asymmetry , 

retraction granting and nasal flaring must be determined in some healthy 
infants , transient crackles may be auscultated during the first few hrs after birth 
, unaccompanied by signs of respiratory distress . a normal pattern of periodic 
breathing with pauses up to 10-15 seconds unaccompanied by bradycardia or 
change in the color and tone may be observed . 

c-  Cardiac location is screened by determined that the heart sound s are loudest in 

the left chest . soft systolic murmurs are commonly heard in the first 24 hours of 
life , probably because of closing ductus arteriosus or normal changes in the 
pulmonary vascular resistance . these murmur usually disappear within 48 hrs 
after birth. 

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5-abdomen is convex and moves prominently with respiration . 

a-  A normal liver edge may be palpated 1-2 cm below the right costal margin , 

and the tip of the normal spleen may be palpated ate the left costal margin . 

b-  Because the most common abdominal masses in the newborn involve the 

genitourinary tract , palpation of the kidneys is important . the kidney may 
be palpated in the fingertips pressing deeply onto the lower lateral aspect of 
the abdomen with opposite hand rested under the baby back at a level just 
superior th the iliac crest . 

6 - inguinal region and genitalia : 

a-  Femoral pulses must always be palpated because diminished pulse suggest 

coaractation of aorta . 

b-  Male genitalia examination should include location of the urethral meatus , 

palpation of the testes and a for bulge in the groin or scrotum suggesting 
hernia or hydrocele . 

c-  Female genitalia examination should a certain the presence of urethral and 

vaginal opening as well as a normal sized clitoris to exclude ambiguous 
genitalia , imperforated hymen and vaginal atresia . in normal infants a 
transient swelling of the labia minora or a vaginal discharge that is mucoid or 
bloody results from the influence of maternal hormones . 

d-  Anus is inspected for patency and placement . 
7-  Extremities temporary flexion contractures at the elbow , hips and knees are 

seen in the term newborn as a result of intrauterine pressure effects 
.approximately 5% of all newborn have more significant limb deformities 
either deformities caused by positional abnormalities and intrauterine posture 
or true malformation . 
a-  Developmental dysplasia of the hip (DDH) .occurs in 1 in 1000 live birth 

and is much more common in girls and breech delivery .. asymmetry in 
lower limb length , placement of the medial thigh and gluteal folds or 
degree of hip flexion should raise suspicion for unilateral hip dislocation . 
when the hips are flexed to 90 degrees the legs normally can be abducted 
fully to touch the examining table " telescoping " of the femoral head with 
subluxation ( barlow ) maneuver or a palpable " thump " with ortalani 
maneuver suggest dislocation . 

b-  Erbs and klumpke palsy as a result of trauma to the brachial plexus result 

in asymmetric or diminished arm movements . 

8-  Back .the spine is inspected and palpated for sinus tract or overlying lesions 

such as lipomas , hairy tufts , or hemangiomas ,any of which may be signs of a 
covert neural tube defect . 

9-  Neurological examination . overall state of consciousness and the ease with 

which the infant makes transition from waking to sleeping or fussing to 
calming as well as strength of cry should be noted .primitive primary reflexes , 
cranial nerves . 

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10- Gestational age . and appropriateness of size for gestational age . 

a-  Gestational age may be determined by assessing certain physical and 

neurological characteristic that evolve in a predictable and progressive 
fashion during the later part of gestation . finding are assigned numerical 
values when compared to standard rating scales and summed totals are 
correlated to specific gestational ages . 

b-  After determining gestational age , weight ,length , and head 

circumference values are plotted on graphs that classified newborns 
according to appropriateness of size for gestational age . 

CARE  OF  THE  NEWBORN . 

A-  Fluid and electrolyte requirements . 

Water represents 94% of the fetal weight at three months of gestation. At term 
,water content has decline to 80% of the birth weight of the newborn. 

1-  Fluid loss and replacement : 

a-  Fluid loss. 

(1) During the first week of life , the extracellular fluid space contracts 

,resulting in large reduction in body water . This water loos is 
responsible for 5% of the weight loss observed in term infants .the 
preterm infant may loss up to 10-15% of his birth weight . 

(2) Water loss through evaporation from the skin and from expired air 

is referred to as insensible water loss. Water loss through the urine 
and stool is referred as sensible water loss .stool accounts for a 
very small amount of sensible water loss . 

b-  Fluid replacement , is based on fluid loss and calculated as the sum of 

insensible and sensible water loss. Initial parenteral fluid replacement 
should be accomplished with a 10% of dextrose solution . 
Fluid intake in term infants is usually begun at 60-70 ml/kg on day one 
and increased to 100-120 ml/kg by days  2-3.smaller , more premature 
infants may need to start with 70-80 ml /kg on day one and advance 
gradually to 150 ml/kg .day . 
 

c-  Fluid balance is monitored by examining : 

(1)-  urine output . 
(2)-  change in body weight . 
(3)-  serum sodium concentration . 
(4)-  urine specific gravity . 

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2-  Electrolyte loss and replacement : 

a-  Sodium , potassium and chloride , are the principle salts that are lost 

through the urine and should be replaced accordingly .assuming an 
adequate urine output , replacement is begun 24 hrs after birth at the 
following rates: 
(1)- sodium 1-3 mEq/kg/day . 
(2)- potassium 1-2 mEq /kg/day . 
(3)- chloride   1-3 mEq /kg /day . 

                   b- Calcium .a decrease in serum calcium concentration frequently occurs                                                         

                          during the first week of life . serum calcium concentration below 7                           

                          mg/dl or below 3-3.5 mg/dl(ionized )bare considered hypocalcemia . 

                        (1)- early neonatal hypocalemia . nearly all infants experience small 
decline in tatal serum calcium during the first few days of life owing to intrauterine 
parathyroid hormone suppression . early neonatal hypocalcemia rarely requires 
treatment except in preterm , infant of diabetic mother and asphyxiated infants . 

                       (2)- late neonatal hypocalcemia (non physiological )is seen at the end of   

                            the first week of life , may be due to : 

                              (a)- increased phosphate ingestion , as occur in infant whon are fed        

                                     cows  milk .  

                              (b)- hypomagnesemia . 

                              ( c)- hypoparathyroidisim . 

                        (3)- therapy usually consists of calcium replacement with calcium     

                                 gluconate and treatment of underling cause of hypocalcemia . 

                ( c )- other required mineral as phosphorus , magnesium , iron and trace    

                         Metals . 

b-  Nutritional consideration . the composition of the nutritional solution 

and the route of delivery depend on the gestational age , general 
medical condition and possible special nutritional need of the newborn  
a- Enteric nutrition . 

(1)- Route of feeding : 
       (a)-the term infant can be breast- fed or bottle fed on demand 
as long as attention is paid to intake and fluid balance . 

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       (b)- the otherwise healthy preterm infant who is between 34-
38-wks should be fed every 3 hrs by breast bottle or gavage depend 
on the infant strength and alertness . 
        ( c)- the preterm infant who is less than34 wks does not have a 
well coordinated suck and swallow reflex , and therefore should be 
fed via a feeding tube . the feeding may be gastric bolus every 2-3 
hrs except in infant weighting less than 1000 g . 
        (d)- continuous gastric or transpyloric feeding is employed in 
the infant who weight less than 1000 g , because this infant has a 
limited gastric volume and may experience intermittent 
hypoglycemia and hypoxia when given bolus feedings .so trophic 
feeding can be given at 10-20 ml/kg/day and the volume increased 
accordingly .intravenous fluid are needed until feeding provide 
approximately 120/kg/day . 
       (e)- continuous transpyloric feeding should be considered for 
the infant who require an endotracheal tube and mechanical 
ventilation to prevent gastric reflex and aspiration . 
(2)- feeding solution .  
       The composition of the feeding solution depends on the 
presence or absence of special protein , carbohydrate , or fat 
requirements or intolerance which in turn depend on gestational 
age , gastrointestinal motility status , and the possibility of 
intestinal enzyme deficiencies or other metabolic disorders . 
 (a)- term infant who do not have complicating metabolic problem : 
       All of the water  calorie , protein , and vitamin requirement of 
the normal term infant are met by human milk or 20 kcal/oz cows 
milk based formula . 
The specific nutritional need of these infant for normal growth are 
as follow: 
(!) the normal term infant needs 100- 120 kcal/kg /day to meet 
basal and growth requirement . 
(!!) the infant also needs 2-3g/kg/day of protein for cellular growth 
which represent approximately 10% of total daily calorie intake . 
(!!!) in addition ,40% of the daily calorie requirement should be 
derived from carbohydrates with remainder provided by dietary fat. 
(b)- preterm infant :have decreased gastric  motility and intestinal 
lactase activity as well as increased calcium and phosphorus 
requirement ,among other nutritional problems. The initial feeding 
solution should be a dilute whey –based formula or human milk as 
positive nitrogen balance is achieved , the infant may be advanced 
to a formula that is high in calcium ,phosphorus and protein , or to 
supplemented human milk .a 24kcal/oz formula is reserved for 
infants whose water intake must be restricted and infants who can 
not tolerate adequate feeding volumes . 

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( c)- infant with special metabolic needs . special formula solutions 
are available for infant with selected intestinal enzyme deficiencies 
( sucrase – isomaltase deficiencies ) or metabolic diseases (PKU) . 

 
(3)- Vitamins and mineral . commercially available formula now are 
fortified with vitamins ,minerals, and trace elements .therefore formula 
fed term infants do not routinely require vitamins or mineral addition . 
        (a)- special vitamins need . 
               (i) infants who are fed human milk may receive a multiple –     
vitamins supplement containing vit. A,D and C . 
               (ii) Owing to small body store and inadequate feeding 
volumes , preterm infants should routinely receive a multiple –vitamin 
supplement containing a the fat soluble vitamins ( A and D ) and the 
water –soluble vitamins (B and C ). In addition , the preterm infant 
who is less than 36 wks and should receive vitamin  E to prevent 
hemolytic anemia . 
       (b)- special mineral and trace element needs : 
              (i) Iron .all infant require iron supplementation ,which may be 
obtained via iron –fortified formula or through a separate supplement . 
iron supplement may be delayed in the preterm infant until enteric 
feeding are tolerated . because of the increased bioavailability of iron 
in human milk ,iron supplementation in term breast –fed infants may 
wait the introduction of iron –fortified cereal at 4-6 months of age . 
Folic acid also needed to be added for DNA and produce new cells . 
       ( ii) fluoride .supplementation probably should not be given to 
infant younger than 6 months of age , even when otherwise indicated , 
because the danger of fluorosis . 
       ( iii) calcium and phosphorus . the needs of the growing term 
infant are met by either commercial formula or human milk . owing to 
rapid bone growth , the calcium and  of phosphorus requirements of 
the preterm infants are greater and necessitate special fortified formula 
or supplementation if fed human milk . 

  b. Total parenteral nutrition . 

                        preterm and other sick infants may required total parenteral nutrition 
because of gastrointestinal disorders ( e.g. neonatal necrotizing enterocolitis ) as well 
as nongastrointestinal disorders ( e.g.respiratory diseases , sepsis ) an intravenous 
solution of dextrose , aminoacid , fat , vitamins ,and mineral can be administered by 
either peripheral or central venous access . appropriately used ,total parentral nutrition 
can provide adequate calories and protein to support the basal need and growth of the 
sick infants . 

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C  - Principles of drug therapy in neonate  . 

    
  The administration and dosing of drug a are different in neonates 
.disregarding this fact may result in toxicity or nontherapeutic use of drugs 
.after administration of a drug , the effect and disposition depend on a number 
of the following factors : 
1-  Route of administration, determines the peak drug level , how quickly the 

peak level is reached ,and how long the peak drug level is sustained . 

2-  Solubility and PH  determine the compatibility of drugs, tissue penetration 

and excretion rate . 

3-  Protein binding .the plasma total protein and albumin level of the new born 

are lower than the adult levels . 
a-  At similar total drug concentration , there will be , a larger unbound 

drugs fraction for drugs with strong protein binding in the newborn 
compared to the adult .because unbound fractionis the active ftaction in 
the blood , lower total drug concentrations are needed to achieve a 
therapeutic effect in the newborn . 

b-  Drug competition for albumin binding sites in the infant with 

hyperbilirubinemia also poses a problem . if all the albumin binding 
sites are occupied with bilirubin , there will be a larger free fraction of 
drug in the blood . conversely , if the drug displaces bilirubin or is 
already occupying the binding site, the increase in free bilirubin may 
increase the risk of kernicterus . 

4-  Metabolism of the drugs by the liver : often is suboptimal because of low 

levels of glucuronyl transferase . this often result in increase in plasma 
drug level and excretion of unchanged drug compared to the adult. 

5-  Excretion of drugs by the kidney : often is impaired owing to low renal 

blood flow , low glomerular filtiration rate ,and immature tubular function  
 
Gestational age assessment : 
    
 Estimation of gestational age can be based on : 

  Menstrual period . 
  Date of conception . 
  Fetal ultrasonography . 
  Physical and neuromuscular criteria after birth ( ballard score ). 

The ballard score is based on the neonate physical and 
neuromuscular maturity and can be used up to 4 days after 
birth .the neuromuscular component are more consistent over 
time because the physical component mature quickly after 
birth . however , the neuromuscular component can be affected 
by illness and drugs. 

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The physical and neuromuscular score are added to calculate 
gestational age . 
Physical criteria include ( increasing firmness of the pina of the 
ear ,size of the breast tissue , lanugo hair , creases of planter 
surface and genitalia ) . 
Neurological criteria include ( posture , squire window , arm 
recoil ,popliteal angle , scarf signs and heal to ear ) . 
 

Birth trauma  

Birth injury refers to avoidable and unavoidable injury to the fetus during the birth . 

Caput succedaneum 

is a diffuse edematous often dark swelling of the soft tissue of 

the scalp that extended across the midline and suture line ,and seen after prolong labor 
in fullterm and premature infants . 

Cephalhematoma  

 is a subperiosteal hemorrhage that does  not cross the suture lines 

and may associated with skull fractures . with time may organized and calcified , also 
may cause jaundice , both caput and cephalhematoma not need treatment . 

Retinal and subconjuctiveal hemorrhage   

are common and not need treatment . 

Brachial plexus   

may result from excessive traction on the neck producing paresis or 

complete paralysis .the  simplest one Erb- duchenne  paralysis involve the fifth and 
sixth cervical nerves .the usual picture is is painless adduction , internal rotation of the 
arm and moro reflex absent on affected side and the hand grasp is intact . Klumpke 
paralysis is caused by injury to the seventh and eight cervical nerve and the first 
thoracic nerve , if the sympathetic nerve are injured an epsilateral Horner syndrome ( 
ptosis ,miosis ) treatment of brachial injury is supportive and include positioning to 
avoid contracture , active and passive exercise may be needed and nerve graft in 
persist defect . 

Facial nerve injury may be the result of compression of the seventh between the 
facial bone and the mother pelvic bone or the physician forceps .this peripheral injury 
is characterized by asymmetric crying face and the affected side is flaccid , the eye 
does not close , the nasolabial fold is absent and the side of the mouth is dropped at 
rest . if there is a central injury to the facial nerve , only the lower two third of the face 
( not the forehead ) are involved . 

skull fractures  are rare are usually linear and require no treatment other than 
observation for very rare delayed complications like leptomeningeal cyst .depressed 
fractures may need elevation . 

clavicle fracture is the most common fractures and usually is unilateral of course in 
macrosomic infants after shoulder dystocia .decreased the movement and moro reflex 

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on the affected side . the prognosis is excellent and  many infants require no 
treatment. 

Extremity fractures are less commonly than clavicle and involve humerus more than 
the femur .the treatment involve immobilization and triangular splint pandage for the 
humerus and traction suspension for the legs for femoral fractures . 

Visceral trauma to the liver and spleen or adrenal gland occurs in macrosomoc 
infants and in extremely premature infants with or without breech or vaginal 
delivery.rupture of the liver with subcapsular hematoma formation may lead to 
anemia and shock and DIC . infants with anemia and shock who are suspected to have 
intraventricular hemorrhage but with normal head ultrasound examination should be 
evaluated for hepatic or splenic rupture .infants with severe adrenal gland 
hemorrhage may exhibit a flank mass , jaundice and hematuria with or without shock . 

Certain procedures that can be done to the newborn : 

1-  Metabolic screen . before discharge a blood sample should be obtained from 

every neonate for presence of congenital hypothyroidismand  phenylketonuria. 
In certain states screening also performed for other inborn error of metabolism 
like ( galactosemia , cystic fibrosis . sickle cell anemia , maple syrup urine 
disease homocystinuria , histidinemia ) . 

2-  Every newborn should receive a single dose of 0.5 -1 mg of natural vitamin K 

within one hour of birth . 

3-  Prophylaxis of gonococcal ophthalmia either a 1% silver nitrate or 0,5 

erythromycin . 

4-  Newborn circumcision has potential medical benefits and advantage with 

disadvantage . benefit and risk should be carefully explained to the parents  
a-  Benefits : 

  Prevent inflammation of glans and prepuce  . 
  Decrease the incidence of penile cancer at adult . 
  Reduce urinary tract infection . 

b-  Risk :  

  Local infection . 
  Bleeding . 
  Pain . 

5-  All newborn should be vaccinated with first dose of hepatitis vaccine .and if 

the mother is hepatitis B surface antigen –positive should also receive a dose 
of hepatitis B immunoglobulin as soon as possible after birth . 
 

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Problems in bonding between the sick infant and his parents : 

Bonding :the process of psychological attachment of the parents to the newborn .the 
following procedures are recommended to minimized the physical separation of the 
infant from the parents and to encourage the formation of a strong bond . 

1-  Whenever possible , the mother should be transported to a tertiary care center 

before delivery . 

2-  When the infant is transported to another hospital , the father should travel 

immediately to the referral center so that he may keep close contact with the 
infant and bring photographs and information back to the mother . 

3-  Visitation should be available 24 hrs a day . 
4-  A strong line of communication be established between the medical staff          

( i.e .physician, nurse , social workers ) and the parents . 

5-  The parents should encourage to keep in contact by telephone when visitation 

is difficult . 

6-  The parents suold be prepared regarding what to expect during their first visit 

to the nursery ,and they should be made aware of any sudden change in the 
infant condition . 

7-  Information should conveyed in a positive and truthful manner . 
8-  Psychological evaluation and support should be made available to parents who 

are having a particularly difficult time coping with their sick infant or the 
intensive care unit setting . parents groups often are helpful . 

9-  Plans for discharge should be made in advance and should include the parents 

.having the parent stay overnight in the hospital before discharge can 
significantly help them adapt to new roles that they will perform after they 
leave the hospital . any current or future medical problems and follow-up 
plans should be explained to the parents . 

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 Prematurity : 

Live infants delivered before 37 wks from the last day  of the last menstrual period . 

Low birth weight ( weight  2.5 kg or less ) due to prematurity or to poor intrauterine 
growth or both . 

Prematurity and IUGR are associated with increased neonatal morbidity and mortality  

Very low birth weight infants weigh less than 1.5 kg .and predominantly premature . 

Causes of prematurity  

  Fetal like ( multiple gestation , fetal distress , ). 
  Placental  ( placenta previa , placental dysfunction ). 
  Uterine  ( bicornuate uterus ) . 
  Maternal ( heart diseases , D .M . ,renal disease , maternal infection ). 
  Others like premature rupture of membrane ,trauma , polyhydramios . 

A premature infant may show these signs soon after birth : 

  Trouble breathing . 
  Low weight . 
  Low body fat . 
  Inability to maintain a constant body temperature . 
  Less activity than normal . 
  Movement and coordination problems . 

Complication of prematurity : 

  Brain hemorrhage . 
  Pulmonary hemorrhage . 
  Hypoglycemia . 
  Infection . 
  Anemia . 
  Patent ductus arteriosus . 
  Respiratory distress syndrome . 

Long term outlook for premature infants include : 

  Hearing and speech problems  . 
  Vision loss or blindness . 
  Learning disability  . 
  Physical disability . 
  Delayed growth and poor coordination . 

 
that interfere with the circulation and efficiency of the placenta , with 
the development or growth of the fetus or with the general health and 
nutrition of the mother  . 
 

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Intrauterine growth restriction and small for gestational age : 
 

IUGR represent a deviation from expected growth pattern . the decreased fetal growth 
associated withIUGR is adaptation to unfavorable intrauterine conditions that result in 
permanent alteration in metabolism , growth and development . 

SGA describes an infant who birth weight is statistically less than 10

th

 percentile or 

two standard deviation below the mean birth weight for gestational age . 

Causes of IUGR and SGA : 

1-  Maternal causes ( genetic short stature, infections , young age , 

smoking , poor nutrition black race , chronic diseases like diabetes) 

2-  Fetal congenital infection , defect in metabolism , multiple 

gestation , chromosomal abnormalities ) . 

3-  Maternal medication ( antimetabollites , lead mercury , narcotics 

steroid , warfarin ). 

4-  Placental and uterine ( abruption placentae , abnormal implantation 

At birth infants who are mildly to moderately SGA appear smaller than normal with 
decreased subcutaneous fat . 

More severely affected may present with a wasted appearance with asymmetrical 
findings including larger head for size of the body (central nervous system sparing ) 
widened anterior fontanelles , small abdomen thin arms and legs decreased 
subcutaneous fat dry skin and meconium stained umbilical cord . 

Physical examination should detail the presence of dysmorphic features like 
abnormal extremities and hepatosplenomegaly . jaundice , skin rash and cataract that 
may suggest the presence of congenital infection or metabolic defect . 

Infants with severe IUGR or SGA may have problems at birth include respiratory 
acidosis ,metabolic acidosis , asphyxia , hypotension , hypoglycemia , polycythemia , 
meconium aspiration syndrome . 

Management of IUGR and SGA infants is usually symptomatic and supportive . the 
diagnosis evaluation at birth should be directed the cause if possible . the mortality 
rate are 5-20 times those of infants who are appropriate for gestational age . postnatal 
growth and development depend on part on the etiology , the postnatal nutritional 
intake and the social environment .infants who have IUGR and SGA secondary to 
congenital infection , chromosomal abnormalities or constitutional syndromes remain 
small throughout life . infants who have growth inhibited late in gestation because of 
uterine constraints , placental insufficiency , or poor nutrition have cutch up growth 
and approach their inherited growth and development potential under optimal 
environmental conditions .  

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Post –term infants : 

 Post term infants are those born after 42 completed weeks of gestation regardless the 
birth weight . 

Clinical features may involve skin desquamation , long nail abundant hair ,pale skin 
alert face , and loose skin meconium stained nails and umbilical cord . 

Complication include ( perinatal depression . meconium aspiration . persistent 
pulmonary hypertension , hypoglycemia , hypocalcemia , and polycythemia . 

Large –for- gestational – age infants: 

Infants with birth weight >the 90

th

 percentile for gestational age are called large for 

gestational age . neonatal mortality rate decrease with increasing birth weight until 
approximately 4kg after which they increased . maternal diabetes , obesity and large 
parental size are predisposing factors .infant have a higher incidence of birth trauma 
like ( brachial plexus injuries, fractured clavicle cephalhematoma ) 

Increased risk of hypoglycemia and polycythemia , congenital anomalies , 

Multiple gestation : 

   Multiple gestation always should be seen as a high risk event owing to its increased 
association with intra uterine accidents , growth abnormalities , prematurity and 
problems at the time of delivery like abnormal position and asphyxia . 

1-Incidence . approximately 1-1.3% of all live birth are the result of twin gestation . 
the true incidence of twin gestation is probably is slightly higher . the monozygotic 
twining rate is 3.5-4 in live births or 35-40 %of all twin who are born . 

1-  Etiology : 

a-monozygotic twin : maybe viewed as a teratogenic event because 
it occurs more frequently with increasing maternal age 
.isassociated with more congenital malformation and can be caused 
by teratogen . a problem of a symmetry in the developing embryo 

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may result in conjoined twins .the incidence of monozygotic twins 
is unaffected by racial and familial factors . 

      b-dizygotic twinning :is caused by double ovulation , which may                 
be related to elevated gonadotropin .twin not of the same sex are 
dizygotic . in twin of the same sex , zygosity should be determined and 
recorded at birth through carefull examination of placenta . 
c. incidence increase due to treatment of infertility with overian 
stimulant and in vitro fertilization . 
2-  Prenatal problems :  

a-  Death : may be occur because of cord accidents and twin to 

twin transfusion , which may lead to the death of one fetus , 
with thromboplastin release and subsequent DIC  in the second 
twin . 

b-  Growth disturbances are the rule : 

(1)-  IUGR  there is a decrease potential for growth in twin 
fetus compared to a single fetus ., probably owing to the 
limitation of placental area for nutrient transfer . 
(2)- twin to twin transfusion , resulting in a large polycythemic 
twin and a small anemic twin . 

                               c- the incidence of congenital malformation is doubled . 

c-  Increased spontaneous apportion . 
d-  Preterm delivery is the most common complication of multiple 

gestation it occurs in up to 50% of twin pregnancies , the 
incidence is even higher in triplet and quadruplet pregnancy . 

e-  Maternal complications include  

  Pregnancy induced hypertension . 
  Polyhydramnios . 
  Hyperemesis and nausea . 
  Anemia . 

3-  Postnatal problems include : 

1.  Prematurity and its complications. 
2.  Growth retardation. 
3.  Perinatal asphyxia .especially of the second twin because the 

placenta may be separated after birthof the first twin . and in 
instances of malpresentation or vasa previa may result in long 
term morbidity and mortality . 

4-  Management is aimed at : 

a-  Identifying multiple gestation as early as possible . 
b-  Managing other medical problems . 
c-  Controlling preterm labor . 
d-  Identifying ideal route of delivery . 
e-  Avoiding asphyxia in the second twin 

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       Maternal diseases affecting the newborn  

1-  Idiopathic thrombocytopenia ITP :  ITP is immune process in which 

antibodies are directed against platelets that cross the placenta and cause 
thrombocytopenia in the fetus and newborn , that increase the risk of 
intracranial hemorrhage .close maternal and fetal management is vital . infants 
with hemorrhage may need platelets transfusion or intravenous 
immunoglobulin .the condition usually resolve within 4-6 wks . 

2-  Systemic lupus erythematosus SLE : immune abnormalities in SLE can lead 

to the production of antibodies that can cross the placenta and injure fetal 
tissues and the most serious problems in fetus is damage to the cardiac 
conducting system which result in congenital heart block . neonatal lupus may 
occur and is characterized by skin lesion thrombocyropenia , autoimmune 
hemolysis and hepatic involvement . the mortality rate is about 2o% and most 
surviving infants require pacing . 

3-  Neonatal hyperthyroidism :  is due to the transplacental passage of thyroid –

stimulating antibodies , hyperthyroidism can appear rapidly within the 12 to 
48 hrs . symptoms may include IUGR prematurity , goiter exophthalmos , 
stare , craniosynostosis . flushing, congestive heart failure tachycardia 
,arrhythmia , hypertension , hypoglycemia , thrombocytopenia and 
hepatosplenomegaly .treatment include propylthiouracil , iodine drops and 
propranolol .the condition usually resolve in 2-4 months . 

4-  Antiphospholipid syndrome: is associated with throbophilia and recurrent 

pregnancy loss . antiphspholipid antibodies are found in 2-5% of the general 
healthy population . obstetric complications arise from the prothrombotic 
effects of theantiphospholipid  antibodies on the placental function . 
vasculopathy ,infarction, and thrombosis have been identified  in the mothers 
with antiphospholipid syndrome that manifested by fetal growth impairment , 
placental insufficiency , maternal preeclampsia and premature birth . 

5-  Diabetes mellitus : 

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RESPIRATORY   TRACT   DISORDERS  

Respiratory disorders are the most frequent cause of admission for neonatal intensive 
care in both term and preterm infants . signs and symptoms of respiratory distress 
include  cyanosis , grunting , nasal flaring retraction, tachypnea , decreased breath 
sounds with or without rales and pallor . 

The first breath : 

Initiation of the first breath is caused by a decline in Pao2  and PH  and a rise in Paco2 
as a result of interruption of the placental circulation , a redistribution of cardiac 
output , a decrease in body temperature and various tactile and sensory inputs . 

Hyaline membrane disease (respiratory distress syndrome of newborn ) 

Is a respiratory disorder that primarily affects preterm infants who are born before the 
biochemical maturation of their lungs .  

Biochemical development : the most important prenatalevent is the production of 
surfactant by type II alveolar cells . 

The major function of surfactant is to decrease alveolar surface tension and 
increasing lung compliance . surfactant prevent alveolar collapse at the end of 
expiration and allows for opening of the alveoli at a low intra-thoracic pressure . the 
ratio of lecithin to sphingomyelin in the aminiotic fluid is areflection of the amount of 
intrapulmonary surfactant and lung maturity .an L/S ratio of 2:1 or greater usually 
indicates biochemical lung maturity . 

Surfactant increase by ( steroid administration , prolonged membrane rupture 
,preeclampsia , placental insufficiency , thyroide hormone , theophyline ). 

Surfactant decreased by ( maternal diabetes , acute asphyxia ) . 

1-  Pathophysiology . the lungs are poorly compliant owing to deficiency of 

surfactant resulting in classic complex of progressive atelectasis , 
intrapulmonary shunting , hypoxemia ,and cyanosis .the hyaline membrane 
that forms and lines the alevioli is composed of protein and sloughed 

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epithelium – the result of oxygen exposure , alveolar capillary leakage and the 
forces generated by the mechanical ventilation of these infants . 

2-  Clinical features:   affected infants characteristically present with tachypnea , 

grunting , nasal flaring , chest retraction ,and cyanosis , in first three hours of 
life . there is decrease air entry on auscultation .apnea and irregular respiration 
are ominous sign requiring immediate action .respiratory failure may occur in  
severe course  

3-  Clinical course : the natural course is a progressive worsening over the first 

48- 72 hrs of life . 
(a)  After the initial insult to the airway lining , the epithelium is repopulated 

with type II alveolar cells . 

(b) Subsequently , there is increase production and release of surfactant , so 

that there are sufficient quantities in the air spaces by 72 hrs of life .this 
result in improvement in lung compliance and resolution of the respiratory 
distress . 

4-  Diagnosis :is confirmed by a chest radiograph that reveals a uniform ground-

glass pattern and an air bronchogram  that is consistent with a deffuse 
atelectasis , clinical manifestation and gas analysis . 
RDS should be differentiated from ( early onset sepsis , pneumonia , cyanotic 
heart diseases , aspiration syndromes , spontaneous pneumothorax , transient 
tachypenia of newborn .) . 

5-  Therapy and prognosis : 

a-  Conventional therapy for the affected premature infant include supportive 

care as well as the administration of oxygen . it also necessary to increase 
the main airway pressure by use of continuous positive airway pressure , 
intermittent assisted ventilation , or a high frequency oscillation . outcome 
with conventional therapy is good . 

b-  Exogenous surfactant replacement therapy with artificial or bovine 

surfactant has become an important  intervention for those infants with 
severe surfactant deficiency . alveolar opening and improvement in 
oxygenation and ventilation occur almost immediately . 

6-  Prevention . when amniotic fluid assessment reveals fetal lung immaturity 

and preterm delivery can not be prevented , administration of corticosteroid to 
the mother 48 hrs before delivery can induce or accelerate the production of 
fetal lung surfactant . 

7-  Complications :common complications and associated findings include 

pneumothorax , patent ductus arteriosus , intraventricular hemorrhage , 
necrotizing enterocolitis , bronchopulmonary dysplasia and retinopathy of 
prematurity . 
 

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Transient tachypnea of newborn : 

      Is thought to result from decreased lymphatic absorption of fetal lung fluid 
It most commonly occurs in the infant born near term by cesarean section 
,without preceding labor ( the catecholamine surge associated with labor and 
delivery which is thought to enhance pulmonary lymphatic drainage does not 
occur in this setting ) 
(1)- 

clinical features

 . the tachypnea is quiet or mild and usually not associated                  

       with retraction . the infant appears comfortable and rarely cyanotic . 
(2

)- diagnosis :

 is based on the delivery and chest radiograph ,which  

       characterized by fluid in the major fissure , prominent vascular marking ,  
       increased interstitial markings and hyperinflation . auscultation may  
       reveal rales . 
(3)- 

therapy

 is supportive . the tachypnea resolves in a few days .low doses of  

       supplemental oxygen may be required . 
 
persistent of the fetal circulation( persistent pulmonary hypertension ). 
 
Usually a disease of term infants who are experience acute or chronic in utero 
hypoxia .it is seen frequently in infant with meconium aspiration syndrome . 
(1) Pathophysiology . the primary abnormality is a failure of the pulmonary 

vascular resistance to fall with postnatal lung expansion and oxygenation . 
(a)  Normally at birth the systemic vascular resistance rises as a result of 

cessation of blood flow through the placenta , and pulmonary vascular 
resistance falls with the first breath . 

(b) With persistence of the fetal circulation , the pulmonary vascular 

resistant continues to be high and may in fact be higher than the 
systemic resistance .this result in shunting of the deoxygenated blood 
which is returning to the right side of the heart away from the lungs. 
The right to left shunt can occur at both the atrial level(foramen of 
ovale ) and through the ductus arteriosus .because the lung are 
bypassed the blood is not oxygenated and hypoxemia ensues.  

(2)  Clinical features . these infants have rapidly progressive cyanosis 

associated with mild to severe respiratory distress . there is a varied 
response to oxygen administration depending on the size of the shunt . 

(3) Diagnosis : 

(a)  The diagnosis is suggested by a history of perinatal asphyxia and 

clinical cyanosis at birth combined with a negative cardiovascular 
examination and negative chest radiograph , although parenchymal 
disease may coexist ( MAS,RDS ) . 

(b) Echocardiography should be used to establish the diagnosis and should 

demonstrate : 
(!)   the absence of cyanotic heart disease . 
(!!)  an increased pulmonary vascular resistance . 

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(!!!) the presence of right to left shunt at the foramen of ovale ductus    
        arteriosus , or both . 

(4) Therapy : include supplemental oxygen , mechanical ventilation , 

hyperventilation ,support of systemic blood pressure and administration of 
sodium bicarbonate and pulmonary vasodilators . 

(5) Prognosis : the overall mortality rate associated with this disease is high 

.extra-corporeal membrane oxygenation may improve the outcome . 

 Apnea  

    Apnea is cessation of breathing for longer than 20 seconds . apnea often occurs in 
preterm infants ( apnea of prematurity ) and reflect immaturity of the respiratory 
control mechanism in the brain stem . 

(1)- clinical features ,bradycardia ( HR less than 80beats/min  ) often associated with 
apnea .apnea of prematurity is characterized by  periodic breathing and intermittent 
hypoxia , which further diminish respiratory derive . 

(2)- diagnosis . of apnea of prematurity is made after excluding other reason for the 
apnea like : 

  Respiratory ( pneumonia , airway obstruction, hypoxia , pneumothorax ). 
  CNS ( intracranial hemorrhage , seizure , drugs ,hypoxic injury ). 
  Infections ( sepsis , meningitis ). 
  Metabolic ( hypoglycemia , hypocalcemia , decrease or increase sodium , 

hypothermia ). 

  Cardiovascular ( heart failure , hypotension , ). 
  Gasrtointestinal ( necrotizing enterocolitis , ). 

   (3)- therapy : therapy of apnea of prematurity include one of ht efollowing : 

            a-  tactile stimulation  

b--maintain body temperature . 

c-  supplemental oxygen . 
d-  administration of respiratory stimulant ( theophyline , caffeine ) 
e-  use continuous positive air way or intermittent assisted ventilation ) . 
f-  treatment of underling cause . 

prognosis : apnea of prematurity dose not alter prognosis unlees it severe , 
recurrent and refractory to therapy ). 

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Choanal  atresia 

: is a unilateral or bilateral obstructionof the posterior 

nasal airway by a membrane or bony septum .this life threatening anomaly 
result from failure of the bucconasal mucosa to rupture . 

Clinical features : because most newborn are obligate nose breathers , 
bilateral atresia usually presents in the delivery room as airway obstruction , 
apnea and cyanosis .distressed neonate then cry which relieve the cyanosis . 
unilateral obstruction may be asymptomatic . 

Diagnosis : is confirmed either by inability to pass a suction catheter through 
the nostril into the oropharynx or by radiography using radioopaque dye to 
show the area of nasal obstruction . 

Therapy : emergency management consists of establishing an airway either 
with an oral airway or by endotracheal intubation . definitive therapy is 
surgical reconstruction performing in neonatal period .  

Diaphragmatic hernia : 

Diaphragmatic hernia is a displacement of the abdominal content into the 
thoracic cavity through a defect in the diaphragm . 

Types : 

(a)  hernias through the foramen of bochdalek are by far the most commonly 

seen diaphragmatic hernia . the defect , which almost always is on the left 
occurs in the posteriolateral portion of the diaphragm . it results from 
failure of the pleuroperitoneal canal to close , which normally occurs 
between 6-8 wks gestation.  

(b) Herians through the foramen of morgagni are somewhat rare , the hernia 

usually on the right .frequently the hernia contain only omentum and the 
affected newborn is asymptomatic . 
 
Pathophysiology : ipsilateral pulmonary hypoplasia results from 
compression of the affected lung by the displaced gastrointestinal organs   
a shift of the mediastinal structures resulting in compression of the 
contralateral lung may cause hypoplasia of the lung to a lesser degree . 
 
Diagnosis : is confirmed by a chest radiograph demonstrating air-filled 
bowel in the hemithorax . 
 
Therapy : includes intubation , vigorous oxygenation and mechanical 
ventilation , decompression of the intestinal tract with  a nasogastric tube , 

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correction of metabolic acidosis , and surgical removal of the abdominal 
contents from the thorax with repair of the hernia . 
(a)  Mask and bag ventilation should be avoided or minimized because it 

results in distension of the bowel and further compromises the 
pulmonary function of the affected newborn . 

(b) Pulmonary hypertension frequently complicates the preoperative and 

postoperative course . 

(c)  Extracorporeal membrane oxygenation may be helpful in selected 

infants . 
Prognosis : survival rates depend on the degree of the lung hypoplasia 
and the presence of other anomalies ,symptoms before 24 hrs of age , 
herniation to the contralateral lung and need for ECMO . with 
conventional therapy , survival rates are approximately 67% , however 
the use of extracorporeal membrane oxygenation may improve 
survival . 
 

Meconium aspiration syndrome (MAS) 
 

   MAS is a multiorgan disorder with perinatal asphyxia as the 
underlying cause . it is most commonly occurs in post term infants and 
in infants who are small for gestational age due to intrauterine growth 
retardation . both have placental insufficiency as a common for fetal 
hypoxia . 
(1) Pathophysiology . the fetal hypoxia triggers via a vagal reflex , 

the passage of thick meconium into the amniotic fluid  .the 
contaminated amniotic fluid is swallowed into the oropharynx and 
aspirated at birth with the initiation of breathing . with severe fetal 
asphyxia and acidosis , the meconium may be aspirated prenatally 
because of fetal gasping .other organ affected by the perinatal 
hypoxia include the brain ,heart gastrointestinal tract and kidneys . 

(2) Diagnosis : is established by the presence of mecomium in the 

tracheal or amniotic fluid combined with symptoms of respiratory 
distress and a chest radiograph that reveals a pattern of diffuse 
infiltrate with hyperinflation . 

(3) Therapy : because most episodes of aspiration occur with the 

initiation of respiration , the most effective therapy is prevention . 
this consist of removal of the meconium before the initiation of 
ventilation . the meconium is removed from the infant airway as 
follows: 
  The oropharynx is suctioned before both delivery of the thorax 

and initiation of breathing  ,and again when the infant is on the 
warmer bed . 

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  The vocal cords are visualized using a laryngoscope , and a 

large endotracheal tube or DeLee  catheter is inserted . 

  Direct wall-unit suction is applied to the tube or catheter as it is 

removed . this procedure is repeated if significant meconium is 
removed . only after the trachea is cleared of any meconium 
should spontaneous or artificial ventilation be initiated . 

  If aspiration has occurred and the infant is in distress , therapy 

consists of administration of oxygen and mechanical 
ventilation . 

  Persistent pulmonary hypertension also may coexist and should 

be vigorously treated . 
 
 

Pneumothorax : 

     Pneumothorax is presence of free air in the pleural space . the air often is under 
pressure and in this setting is referred to as tension pneumothorax . 

(1) Incidence and etiology . asymptomatic , spontaneous pneumothorax occurs in 

1-2% of otherwise healthy newborn at birth . symptomatic pneumothorax 
more commonly occurs in the infant who is receiving mechanical ventilation 
or who has underling lung disease ( RDS, MAS) . 

(2) Clinical manifestations . symptoms and signs include cyanosis , tachypnea 

,and elevation of the affected hemithorax . auscultation reveals diminished 
breath sounds on the affected side . 

(3) Diagnosis : 

(a)  The diagnosis made by a chest radiograph that demonstrate a dense 

partially collapsed lung surrounded by a large area of radiolucent air 
within the hemithotax . depending on the degree of tension and lung 
compliance , the mediastinal structures are shifted toward the opposite side 
of the chest . 

(b) Transillumination of the thorax may aid in the diagnosis of the 

pneumothrax in the emergencies , positive evidence is the transmission of 
light through the affected side . 

(4) Therapy :varies with the severity of the symptoms . 

(a)  If no other lung disease exists and there is minimal respiratory distress , 

supplemental 100% oxygen ( nitrogen wash out technique ) for several 
hours usually is sufficient . 

(b) If a significant degree of tension , respiratory distress ,or some other lung 

disease exist the air should be evacuated by aspiration with a syringe and 
needle or by a chest tube if a continuous air leak exists .  

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Digestive system disorders  

Neonatal necrotizing enterocolitis ( NEC ) : refers to a spectrum of varying degrees of 
acute intestinal necrosis usually following injury of the bowel with secondary 
invasion and devitalization of the bowel wall . 

1-  Incidence . this is a serious and common problem affecting 1-5% of all 

newborn admitted to the intensive care units . affected infants most commonly 
are premature near 90%  , asphyxiated and suffering from other medical 
problems . necrotizing enterocolitis rarely observed in a healthy term infants 
and less common in in infants fed human milk  . 

2-  Etiology and pathogenesis :  

(a)  Bowel ischemia secondary to preceding perinatal asphyxia generally is 

regarded as the cause of bowel wall injury . the introduction of formula or 
human milk then provides the substrate for bacterial overgrowth . bacterial 
invasion of thr bowel wall often with gas production ( pneumatosis 
intestinalis ), leads to tissues necrosis and perforation . 

(b) Other predisposing factors includes : 

(1) Systemic hypotension . 
(2) Patent ductus arteriosus . 
(3) Placement of au umbilical artery catheter . 
(4) Exchange transfusion . 
(5) Previous treatment with systemic antibiotics . 
(6) Use of hyperosmolar formula . 
(7) Rapid advancement of the feeding volume . 

3-  Clinical features and diagnosis : signs and symptoms are usually are noted 

during the first 2 wks of life , shortly after enteric feeding has begun : 

  Gastric residuum which often is bile stain . 
  Abdominal distension . 
  Blood in stool . 
  Lethargy and apnea . 
  Poor perfusion with hypotension or shock . 
  Abdominal wall discoloration . 
  Unstable temperature and metabolic acidosis . 

4-  Laboratory findings :  

(1) Suggestive on blood film leukocytosis , neutropenia or thrombocytopenia. 
(2) Suggestive findings on abdominal radiography include : 

(a)  Dilated thickened bowel loops . 
(b) Pneumatosis intestinalis which usually starts in the right lower part . 
(c)  Perforation , with free abdominal air and portal vein air . 

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5--Clinical course :two distinct clinical patters are noted : 

a-  Most infants follow a course characterized by feeding intolerance , 

abdominal distension occult blood in the stool , and dilated bpwel loops on 
radiography . these finding improve rapidly with therapy . 

b-  The other group of infants has severe progressive symptoms including 

groos blood in the stool , extreme abdominal tenderness , hypotension 
disseminated intravascular coagulation and sepsis . peumatosis intestinalis 
and perforation frequently occur in this setting . 

6-  Therapy : 

a-  Treatment should begin with discontinuation of enteric feeding , gastric 

drainage and administration of intravenous fluid . 

b-  Once culture have been taken ,systemic antibiotics ( e.g. ampicillin 

,gentamicin ) shloud be given .also any accompanying disorders (e.g. DIC) 
should be treated . 

c-  Surgical resection of the necrotic bowel segment is indicated for infants 

who have a progressive downhill course and for those in whom intestinal 
perforation has occurred . 

7-  Prognosis : the mortality rate associated with necrotizing enterocolitis which 

is highest in the most premature infants is approximately 30% .later 
complications may include intestinal strictures and short bowel syndrome .. 
 

 
Anemia of the newborn  
 

     Neonatal hemoglobin concentration at birth about 16.5-18 g/dl. After birth 
hemoglobin decline to 11-12 g/dl at 3-6 months at term . premature infant has 
a lower hemoglobin concentration to achieves a nadir at 1-2 months after birth 
.fetal hemoglobin represent 60- 90 %of hemoglobin at term birth and the level 
decline to adult level by 4 months of age . for term infant blood volume is 70-
90 ml/kg and a preterm infant ,blood volume is 90-100 ml/kg . 
The physiological anemia noted at 2-3 months of age in term infant and at 1-2 
months of age in preterm infants , is a normal process that does not result in 
signs of illness and does not require any treatment . it is a physiological 
condition believed to be related to several factors including increased tissue 
oxygenation experience at birth , shortened RBC  life span and low 
erythropoietin levels . 
Etiology : symptomatic anemia in the newborn period may be caused by 
decreased RBC  production ,increased RBC destruction or blood loss .. 
 
 
 
 

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Hemolytic disease of the newborn ( erythroblastosis fetalis ) . 
     
    Result from blood group incompatibility between the mother and the fetus . 
hemolysis occurs when maternal antibodies to a particular blood group antigen 
cross the placenta and bind to fetal red blood cells , which are then destroyed 
in the spleen . 
ABO blood group incompatibility : with neonatal hemolysis develops only if 
the mother has IgG antibodies from a previous exposure to A or B antigens 
.these IgG  antibodies cross the placenta by active transport and affect the 
fetus or newborn . sensitization of the mother to fetal antigens may have 
occurred by previous transfusion or by condition of pregnancy that result in 
transfer of fetal erythrocyte into maternal circulation such as first trimester 
abortion , ectobic pregnancy amniocentesis , or normal pregnancy . 
ABO incompatibility with sensitization usually does not cause fetal disease 
other than mild anemia . it may produce hemolytic disease of newborn , 
however which is manifested as significant anemia and jaundice . because 
many mother who have blood group O have antibodies to A and B before 
pregnancy , the first born infant of A or B type may be affected . in contrast to 
RH  disease , ABO  hemolytic disease dose not become mre severe with 
subsequent pregnancies .hemolysis with ABO  incompatibility is a less severe 
than hemolysis in RH-sensitized pregnancy , either because the anti A or anti 
B antibody may bind to non erythrocytic cells that contain A or B antigen or 
because fetal erythrocyte have a fewer A or B antigenic determinants than they 
have RH sites . with declining incidence of RH hemolytic disease , ABO 
incompatibility has become the most common cause of neonatal jaundice 
requiring therapy . 
 
Erythroblastosis  fetalis : 
       
 Erythroblastosis fetalis classically is caused by Rh blood groip 
incompatibility . most RH negative mother have no anti-Rh antibodies at the 
time of their first pregnancy . in most Rh-sensitized cases ,the D antigen of the 
fetus sensitized the Rh negative mother resulting in IgG antibody production 
during the first pregnancy . because most mothers are not sensitized to Rh 
antigen at the start of pregnancy . Rh erythroblastosis fetalis is uaually a 
disease of second and subsequent pregnancies .the first affected pregnancy 
results in an antibody response in the mother which may be detected during 
antenatal screening with coombs test and determined to be ant-D antibody . 
The first affected newborn may show no serious fetal disease and may 
manifest hemolytic disease of the newborn only by development of anemia 
and jaundice . subsequent pregnancies result in an increasing severity of 
response because of an earlier onset of hemolysis in utero . fetal anemia , heart 
failure elevated venous pressure , portal vein obstruction and 

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hypoalbuminemia result in fetal hydrops, which is characterized by ascites , 
pleural and pericardial effusion and anasarca .the risk of fetal death is high . 
If the fetus near term can be delivered and treated in neonatal intensive care 
unit . if the fetus less than 33 wks and immature lung intrauterine transfusion 
O-negative blood into  the umbilical vein is indicated and may have to be 
repeated until pulmonary maturity is reached  
 
Prevention : of sensitization of the mother carrying an Rh –positive fetus is 
possible by treating the mother during gestation ( more than 28 wks 
gestational age and within 72 hrs after birth with anti-Rh-positive immune 
globulin . the dose (300ug) is base on the ability of this amount ao antiRh- 
positive antibody to bind all the possible fetal Rh positive erythrocytes 
entering the maternal circulation during the fetal –to-maternal transfusion at 
birth ( approximately 30 ml).   
Diagnosis and management : 
Hemolysis in utero result in hydrops with ( ansarca ,heart failure,and 
pulmonary odema that result in asphyxia , hepatosplenomegaly ,pallor and 
become jaundice within 24 hrs after birth . patients with ABO incompatibility 
often are asymptomatic and show no physical signs at birth , mild anemia with 
jaundice develops during the first 24-72 hrs of life . 
Newborn with acute blood loss due to( feto-maternal hemorrhage , placenta 
previa ,or internal hemorrhage ) is characterized by pallor , diminished 
peripheral pulses ,and shock but no hepatosplenomegaly . 
Newborn with chronic blood loss caused by ( chronic fetal-maternal 
hemorrhage , twin to twin transfusion ) present with marked pallor , heart 
failure hepatosplenomegaly with or without hydrops with low HB at birth and 
decreased serum iron store . shock is more typical in patient with internal 
hemorrhage whereas in hemolytic diseases heart failure may br seen with 
severe anemia . 
Laboratory evaluation : 
A complete blood count , blood smear , reticulocyte count , blood type and 
direct coombs test (to determined the presence of antibody coated RBCs) 
should be performed in the initial evaluation of all infants with hemolysis . 
RBC enzymes , hemoglobin electrophoresis and RBC membrane tests . 
The diagnosis of fetal- maternal hemorrhage is confirmed by the Kleihauer –
Betke acid elusion test . 
Internal hemorrhage or when nonimmune hemolysis is suspected ,ultrasound 
of liver brain spleen or adrenal gland may be indicated . 
The treatment of symptomatic neonatal anemia is transfusion of cross 
matched packed RBCs .if immune hemolysis is present ,the cells to be 
transfused must be cross matched against maternal and neonatal plasma . 
Acute volume loss may need non blood products such as saline if blood not 
available . 
To correct anemia 10-15 ml/kg of packed RBCs can be given   

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Neonatal hyperbilirubinemia  

 
      Neonatal hyperbilirubinemia is a condition characterized by an excessive 
concentration of bilirubin in the blood .there are two types of neonatal 
hyperbilirubinemia ( unconjugated ) which can be physiological or pathologic 
in origin and (conjugated ) which always stems from pathologic cause . both 
types may lead to jaundice . neurotoxic concentration of unconjugated 
bilirubin can cause kernicterus . 
 
1-  Normal bilirubin metabolism : bilirubin is a bile pigment formed from the 

degradation of heme  that is mainly derived from red blood cell destruction 
75% but also from ineffective red blood cell production 25% . 

Bilirubin is poroduced by the catabolism of hemoglobin in the reticuloendotheelial 
system . the tetrapyrole ring of the heme is cleaved by heme oxygenase to form 
equivalent quantities of biliverdin and carbine monoxide . biliverdin is converted to 
bilirubin by bilivedin reductase . one gram of hemoglobin produce 35 mg of bilirubin 
compared with adult newborn have two to three fold greater rate of bilirubin 
production (6-10 mg/kg/day vs.3mg/kg/day ) this increased production is caused in 
part by increased RBC mass and short half life of erythrocyte 70-90 days compared to 
120 days in adult .Bilirubin produced after hemoglobin catabolism is lipid soluble and 
unconjugated and react as un indirect reagent in the van den bergh test .indirect –
reacting unconjugated bilirubin is toxic to the central nervous system and is insoluble 
in water ,limiting its excretion . unconjugated bilirubin binds to albumin on specific 
bilirubin binding sites , one gram of albumin binds 8.5 mg of bilirubin in the newborn 
.if the binding sites become saturated or if a competitive compound binds at the site  
displacing bound protein , free bilirubin becomes available to enter the central 
nervous system .organic acids and and drugs like sulfisoxazole can displace bilirubin 
from its binding sites on albumin .Bilirubin dissociates from albumin at the 
hepatocyte and become bound to a cytoplamic liver protein Y ligandin . hepatic 
conjugation result in the production of bilirubin diglucuronide , which is water suloble 
and capable of biliary and renal excretion . the enzyme glucuronosyl transferase 
represents the rate – limiting step off bilirubin conjugation . the concentration of 
ligandin and glucuronosyl transferase are lower in newborn particularly in premature 
than in older children .Conjugated bilirubin gives a direct reaction in the van den 
bergh test . most conjugated bilirubin is excreted through the bile into the small bowel 
and eliminated in the stool .some bilirubin may undergo hydrolysis back to the 
unconjugated fraction by intestinal glucuronidase , however and may be reabsorbed 
(enterohepatic recirculation ) . in addition , bacteria in the neonatal intestine covert 
bilirubin to urobilinogen and stercobilinogen which are excreted in urine and stool 
and usually limit bilirubin reabsorbtion . delayed passage of meconium which contain 
bilirubin , also may contribute to the enterohepatic recirculation of bilirubin .maternal 
indirect hyperbiliruninemia also may increase fetal bilirubin level . 

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Physiological jaundice : 

    Physiological jaundice is a common cause of hyperbilirubinemia among newborn it 
is a diagnosis of exclusion made after careful evaluation has ruled out more serious 
causes of jaundice such as hemolysis , infection and metabolic diseases . 

Physiological jaundice as opposed to pathological jaundice is characterized by : 

(1) Clinical jaundice appearing after first day . 
(2) An increase in the total serum bilirubin concentration of less than 5mg/dl/day  
(3) A total serm bilirubin concentration of less than 13 mg/dl in term and less than 

15mg/dl in preterm and direct bilirubin of less than 1.5-2 mg/dl . 

(4) Persistence of clinical jaundice for less than one week . 

Pathological jaundice : 

Jaundice and underling hyperbilirubinemia are considered pathological if the time of 
appearance ,duration ,or pattern varies rom that of physiological jaundice .the greatest 
risk associated with indirect hyperbilirubinemia is the development of bilirubin 
induced neurological toxicity which typically occurs with high indirect bilirubin 
levels , the development of kernicterus depends on : 

1-  Level of indirect bilirubin . 
2-  Duration of exposure to bilirubin elevation . 
3-  The cause of jaundice . 

The infants well-being . 

specific causes of nonphysiological indirect hyperbilirubinemia include : 

(i) – hemolytic diseases of immune etiology .(fetomaternal blood group 
incompatibilities RH  and ABO as well as non immune like spherocytosis , 
hemoglobenopathies red blood cell enzyme deficiency . 

(ii)- extravascular blood loss and accumulation ( cephalhematoma ) .   

(iii)- increased enterohepatic circulation due to intestinal obstruction . 

(iv)- breast feeding associated with poor intake . 

( v)- disorder of bilirubin metabolism like Gilpert syndrome and Crigler-Najjar                   
syndrome.    

(vi) – metabolic disorder like hypothyroidism   . 

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Jaundice associated with breast –feeding : 

Significant elevation in indirect bilirubin (breast milk jaundice ) develops in term 
infants after the seven day with maximum concentration as high as 10-30 mg/dl 
reached during the 2

nd

 -3

rd

 wk .and may persist for 3-10 wk at a lower level if the 

breast feeding discontinued for one or two days the serum level fall rapidly. although 
uncommon kernicterus can occur .the cause of breast milk jaundice is unclear but may 
be due to glucuronidase in some breast milk . 

The late jaundice associated with breast feeding should be distinguished from early 
onset known as breast feeding jaundice which occur in the 1

st

 wk and may be a result 

of decreased milk intake or dehydration . 

Crigler –najjar syndrome : 

     Is a serious rare autosomal recessive , permanent deficiency of 
glucuronosyltransferase that result in severe indirect jaundice . type ll respond to 
enzyme induction by Phenobarbital producing elevted enzyme and reduce bilirubin 
.type l does not respond to Phenobarbital and manifest as persist indirect jaundice 
often leeding to kirnicterus in absence of hemolysis . 

Gilbert disease : is caused by a mutation of the promoter region of 
glucuronosyltransferase and result in mild indirect jaundice and usually occur after 
puberty  and not need treatment . 

Causes of jaundice in the first wks ( physiological jaundice , ABO and Rh –
incompatibility , concealed hemorrhage , congenital infection , sepsis ,breast feeding 
jaundice , Crigler –Najjar syndrome ,urinary tract infection , polycythemia ) . 

Causes of jaundice after first wks ( beast milk jaundice , septicemia , bile duct atresia , 
hepatitis , galactosemia , hypothyroidisim , CF ,inborn error of metabolism ) . 

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Kernicterus ; 

  Kernicterus is a severe neurological condition associated with very high levels of 
unconjucated bilirubin in the blood . kernicterus is characterized by yellow staining of 
the basal ganglia and hippocampus ,which is accompanied by wide spread of cerebral 
dysfunction . 

(a)  Causes . kernicterus occurs when free bilirubin crosses the blood brain barrier 

and enter the brain cell . 
(i)- normally unconjugated bilirubin is bound tightly to albumin which prevent 
bilirubin from crossing the blood brain barrier .free bilirubin exists when ths 
amount of unconjugated bilirubin exeeds the binding capacity of albumin. 
(ii)- bilirubin also may enter the brain at a low concentration owing toe 
displacement from the albumin binding site by another compound ( e.g. sulfa 
drugs). Which lead to increased free bilirubin concentration or because of 
disruption of the blood brain barrier by sepsis , asphyxia , acidosis , or 
infusion of hyperosmolar solutions . 

(b) Kernicterus causes a complex of neurologic symptoms including the earliest 

clinical manifestation as lethargy ,hypotonia , irritability poor moro response 
and poor feeding . later signs include bulging fontanelle , opisthotonic 
posturing , pulmonary hemorrhage ,fever and seizure . 
Infants with severe cases of kernicterus die in the neonatal period , survived 
infants may developed nerve deafness . choreosthetoid cerebral palsy , mental 
retardation and discoloration  of the teeth . 
Kernicterus can be prevented by avoiding high indirect bilirubin levels and 
avoiding condition and drugs that may displace bilirubin from albumin . 
Early signs occasionally may be reversed by immediately exchange 
transfusion . 

Treatment of jaundice : 

Regardless the cause the goal of therapy is to prevent neurotoxicity related to indirect 
–reacting bilirubin . 

(1)--Phototherapy : is an effective and safe method for reducing indirect bilirubin 
particularly when initiated before serum bilirubin increased to levels associated with 
kernicterus . in term infants phototherapy is begun when indirect levels are between 
16- 18 mg/dl . in premature infants when bilirubin is at lower levels . blue and white 
lights are effective in reducing bilirubin levels . 

Phototherapy causes a photochemical reaction producing the reversible , more water 
soluble isomers of indirect bilirubin this isomr can be excreted bypassing the liver 
conjugation system or excreted in urine . 

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Because phototherapy may require 6-12 hrs to have a measurable  effect it must be 
started at bilirubin level below those indicated for exchange transfusion . the 
therapeutic effect of phototherapy depend on : 

  Light energy and effective wavelength 425-to475 nm wavelength . 
  The distance between the light and infant 15-20 cm . 
  The surface area of exposed skin . 
  Rate of hemolysis and metabolisim and excretion of bilirubin . 

Complications of phototherapy include : 

  Increased insensible water loss and dehydration  . 
  Macular –papular skin rash . 
  Lethargy and masking of cyanosis . 
  Nasal obstruction by eye pads and potential retinal damage . 
  Loose stool . 
  Bronze baby syndrome in infants with direct jaundice . 

(2)- intravenous immunoglobulin in jaundice caused by isoimmune hemolyric disease 
and can be used if phototherapy not effective and bilirubin approaching exchange 
level . 

(3)- metalloporphyrins a single i.m dose on the first day of life may reduce the need 
for subsequent phototherapy . the proposed mechanism is competitive enzymatic 
inhibition of the rate – limiting conversion of heme protein to biliverdin . 

(4)- exchange transfusion : is used principally in hemolytic disease or when the 
bilirubin concentration is very high . this procedure directly remove the bilirubin from 
the intravascular space . unbound antibodies that initiate the hemolytic process and 
affected red blood cell also are removed beside correction of anemia  .  

Exchange transfusion usually is performed when the serum bilirubin concentration is 
20 mg/dl or more . the specific bilirubin concentration that requires treatment varies 
with gestational age , the cause of jaundice and the presence of medical complications 
(e.g. sepsis , acidosis ). 

As the rule of thumb alevel of 20 mg/dl for bilirubinnis te exchange number for 
infantwith hemolysis who weigh more than 2000g .asymptomatic infant with 
physiological or breast milk jaundice may not require exchange transfusion unless 
indirect bilirubin level exceed 25 mg/dl .the exchangeable level of bilirubin for other 
infants may be estimated by calculating 10% of birth weight in grams , so the level in 
an infants weighing 1500g would be 15mgdl . 

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The exchange transfusion is usually performed umbilical catheter in vein to a distance 
no greater than 7 cm in a full term .the exchange should be carried out over 45-60 
min.with aspiration of 20 ml of infant blood alternating with infusion of 20 ml of 
donor blood , 5-10 ml may be indicated in sick or premature infants . 

1-  Rh hemolytic disease of the newborn need O Rh negative RBCs do not have 

major blood group antigen so they are not memolysed by maternal antibodies 
that may still be present in the infants circulation .if RBC are made available 
before delivery of the sensitized infant the RBCs must be O Rh negative and 
cross matched against the mother . if the  RBCs are sourced after delivery the 
RBCs  must be cross matched against infant . 

2-  ABO incompatibility : use group O , Rh specific RBCs . these RBCs 

contained low levels of antibodies and lack antigens that could trigger any 
circulating maternal antibodies in th newborn .                                                                                                                              
Estimated double volume to be exchange : 
Term/preterm=85ml x 2 x weight(kg)= 170 ml x weight (kg) . 
 

The infants stomach should be emptied before transfusion to prevent aspiration and 
body temperature should be maintained and vital signs monitored . 

After exchange transfusion the bilirubin level must be determined at frequent intervals 
every 4-8 hrs because bilirubin may rebound within hrs as a result of continued 
hemolysis and redistribution of bilirubin from tissue store . 

Acute complications include ( transient bradicardia , cyanosis ., transient vasospasim , 
thrombosis , apnea , infections necrotizing enterocolitis , vessel perforation or 
hemorrhage , metabolic instability ). 

Late complications ( late anemia GVH  reaction , inspissated bile syndrome , portal 
vein thrombosis ) . 

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Conjugated or direct hyperbilirubinemia  

Direct jaundice defined as direct bilirubin level > 2mgdl or > 20% of the total 
bilirubin is never physiological . direct bilirubin is not neurotoxic to the infant but 
signifies a serious underling disorder involving cholestasis or hepatocellular injury . 

Causes of direct jaundice : 

1-  TORCH  infection ( toxoplasmosis ,rubella,cytomegalovirus ,herpes simplex) 
2-  Metabolic disorders ( e.g. galactosemia ). 
3-  Bacterial sepsis . 
4-  Obstructive jaundice ( e.g. biliary atresia ) . 
5-  Prolonged administration of intravenous protein solution . 
6-  Neonatal hepatitis , alpha one antitrypsin deficiency , cystic fibrosis . 
7-  Inspissated bile from prolonged hemolysis . 

diagnosis : is based on conjugated fraction of the bilirubin level and ( liver enzymes 
,bacterial and viral culture , metabolic screen , hepatic ultrasound sweet chloride and 
possible liver biopsy ) .                                                                                                 
therapy : is directed to the underlying cause of direct jaundice . 

Hydrops fetalis :  

I s a condition that develops I utero , usually as a result of chronic anemia due to 
hemolytic disease ,although many etiologies exist and its chief features include 
anemia or anasarca and hypoptoteinemia with heart failure . 

1-  Etiology : 
a-  Severe chronic anemia due to ( isoimmunizationdue to Rh and ABO 

incompatibility ) ,homozygous alph thalasemia , twin to twin transfusion . 

b-  Cardiac ( structural defect , paroxysmal aterial tachycardia ) . 
c-  Hypoproteinnemia . 
d-  Intrauterine infection including syphilis , toxoplasmosis  and CMV ) . 
e-  Chromosomal disorders ( e.g. turner syndrome ) . 
2-  Pathophysiology : 

The exact pathophysiology is unknown , but the central factor in the 
development of the hydrops fetalis appears to be severe chronic anemia with 
loss of oxygen-carrying capacity , leading to hypoxia and acidosis . a 
controlling factor is hypoproteinemia , which together with anemia causes the 
development of congestive heart failure , edema , pleural effusion and ascites 
.all of these problems contribute to the respiratory distress seen at birth . 

3-  Clinical features : 

a-  Signs and symptoms include ( congestive heart failre,pallor, pleural 

effusion.periphral edema and hepatosplenomegaly ). 

b-  Laboratory findings include ( anemia,hypoprotenemia,hypoxia.acodosis ) . 

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4-  Therapy : is aimed at correcting the anemia and treating the cogntive heart 

failure and respiratory distress .in addition appropriate treatment should be 
provided for associated etiologies .idiopathic causes of hydrops are associated 
with a high mortality rate . 
 
 
Polycythemia : 
        
    Polycythemia occurs in 2-5% of all newborn and is defined as a hematocrit 
of 65% or greater when a freely following blood sample is taken from a large 
vein . hyperviscosity of the blood almost always exists in associated with 
polycythemia . 
a-  Etiology. Polycythemia has been associated with the following conditions 

: 
1-  Fetoplacental transfusion associated with birth asphyxia or delayed 

cord clamping . 

2-  Twin to twin transfusion . 
3-  Chronic intrauterine hypoxia secondary to placental insufficiency (e.g. 

pregnancy induced hypertension with fetal growth retardation or 
increased fetal metabolism ( e.g. with maternal diabetes ) . 

4-  Endocrine disorder ( e.g. hyperthyroidism ) . 
5-  Genetic disorder ( e.g. down syndrome , Beckwith –Wiedeman syn.) . 

b-  Pathophysiology : 

1-  Many of the problems associated with polycythemia were originally 

thought to be caused by organ ischemia and hypoxia secondary to an 
increase in blood viscosity . it is now known that most of the blood 
flow reduction is the result of an increased oxygen content in the 
arterial blood .this reciprocal relationship of decreased blood flow and 
increased arterial oxygen content result in a normal or increased 
delivery of oxygen to most organs . 

2-  Therefore , most of the problems associated with polycythemia are 

more likely the result of the perinatal events ( i.e. acute or chronic 
hypoxia ) that also are responsible for the development of the 
polycythemia , rather than any flow disturbance attributable to the 
polycythemia itself . 

c-  Clinical features :  

1-  Symptoms and signs include : 

a-  Tachypnea and cyanosis and feeding intolerance  . 
b-  Jitterness and seizure . 
c-  Renal dysfunction . 
d-  Hypoglycemia ,thrombocythemia  . 
e-  Necrotizing enterocolitis . 

2-  Complications .polycythemia is associated with an abnormal long term 

neurologic outcome . 

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d-  Therapy : generally is supportive .reduction of the hematocrit by partial 

exchange transfusion may be helpful in alleviating distress , renal 
dysfunction and hypoglycemia , but may increase the risk of necrotizing 
enterocolitis . 
The equation used in partial exchange is : 
        Volume of exchange (ml) = blood volume x ( observed – desired 
hematocrit ) /observed hematocrit . 
The desired hematocrit is 50% and the blood . 

Hemorrhagic disease of the newborn  

    Have the most profound deficiency of  vitamin K-dependent factors ( VII,X,V and 
II )  and these factors decline further after birth , because breast milk is a poor source 
of vit. K , breastfed infants are at increased risk for hemorrhage that usually occurs 
between day three and seven of life . bleeding usually ensues from the umbilical cord 
, circumcision site ,intestine , scalp , mucosa , and skin but internal hemorrhage places 
the infant at risk for fatal complications such as intracranial hemorrhage . 

Hemorrhage on the first day of life resulting from the deficiency of the vitamin K 
dependent factors often is associated with administration to the mother of drugs that 
affect vitamin K metabolism in the infant . this early pattern of hemorrhage has been 
seen withmaternal warfarin and antibiotics ( e.g.isoniazid or rifampicin ) therapy and 
in infants of mothers receiving Phenobarbital and phenytoin . bleeding also may occur 
1to 3 months after birth particularly among breastfed infant  .vitaminK deficiency in 
breastfed infant also should raise suspicion about the possibility of vitamin K 
malabsorption resulting from cystic fibrosis , biliary atresia , hepatitis or antibiotics 
suppression of the colonic bacteria that produce vitamin K . 

Levels of PIVKA ( protein induced by vitamin K absence ) increased in vitamin K 
deficiency and are helpful diagnostic marker, vitamin K  administration rapidly  
correct the coagulation defects ( normalizes prothrombin time which is depend on 
vitamin K ) and reducing PIVKA to undetectable levels .the bleeding time which 
reflect platelet function and number is a normal during newborn period . 

Prevention and treatment : 

     Bleeding associated with vitamin K deficiency may be prevented by administration 
of vitamin K to all infants at birth . before routine administration of vtamin K 1-2% of 
all newborn have hemorrhagic disease of newborn . 

One intramuscular dose ( 1 mg) of vitamin K  prevents bleeding . 

Treatment of bleeding resulting from vitamin K deficiency involves intravenous 
administration of 1-5 mg of vitamin  K . if severe life threatening hemorrhage is 
present fresh frozen plasma also should be given . unusually high doses of vitamin K 
may be needed for hepatic disease and for maternal warfarin or anticovulsant therapy .  

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Neurological disorders 

Hypoxic –ischemic encephalopathy (HIE ) : 

        Condition known to reduced uteroplacental blood flow or to interfere with 
spontaneous active respiration after complete birth lead to perinatal hypoxia , to lactic 
acidosis and if severe enough to reduce cardiac output or cause cardiac arrest to 
ischemia . the combination of the reduced availability of oxygen for the brain 
resulting from hypoxia and the diminished or absent blood flow to the brain resulting 
from ischemia leads to reduced glucose for metabolism and to accumulation of lactate 
that produces local tissue acidosis . after reperfusion hypoxic-ischemic injury also 
may be complicated by cell necrosis and vascular endothelial edema , reducing blood 
flow distal to the involved vessels .typically hypoxic –ischemic encephalopathy in the 
term infant is characterized by cerebral edema , cortical necrosis , and involvement of 
basal ganglia  , whereas in the preterm it characterized by periventricular 
leukomalacia . both lesions may result in cortical atrophy , mental retardation and 
spastic quadriplegia or diplegia . 

Perinatal risk factors  and conditions  associated with birth asphyxia : ( extremes in 
maternal age i.e.<20 yrs or > 35 yrs , placental abruption or previa , preeclampsia , 
preterm gestation , meconium stain ameniotic fluid feat bradycardia , malpresentation 
, multiple gestation and maternal diabetes ). 

Postnatal symptoms of asphyxia : 

a-  Brain : 

1-  Mild asphyxia .the infants initially well be depressed . this followed by a 

period of hyperalertness which resolves within 1 or 2 days . there are no 
focal signs and the prognosis is excellent for a normal outcome . 

2-  Moderate asphyxia . the infants will be very depressed . this is followed by 

a prolonged period of hyperalertness and hyperreflexia . generalized 
seizure often occur hours after the episode of asphyxia but are controlled 
easily , resolving in a few days regardless the therapy . the prognosis is 
variable , negative result on EEG are predictive of normal outcome . 

3-  Severe asphyxia .is associated with coma , intractable seizure , cerebral 

edema and intracranial hemorrhage . the infant becomes progressively 
more depressed over the first 1-3 days , as rhe cerebral edema develops 
and death may occurs during this period . survival usually is associated 
with a poor long term outcome .also the prognosis depend on other organ 
injury and low apgar score especially if the score remains low by 20 min . 

b-  Heart . severe or prolonged episodes of asphyxia may result in hypoxic –

cardiomyopathy . signs and symptoms include hypotension, poor myocardial 
contractility , cardiomegaly and congestive heart failure . 

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c-  Lung . respiratory distress and a need for oxygen can occur owing to a delay 

fall in pulmonary vascular resistance . 

d-  Kidney . depressed renal blood flow during the aspyxial events causes acute 

tubular necrosis . this is usually self limiting . 

e-  GIT is associated with poor GIT motility or ileus . the hypoxia also predispose 

to secondary bacterial invasion and to the development NEC . 

f-  Blood . hypoxia depressed bone marrow function and initiates intravascular 

coagulopathy which result in thrombocytopenia prolonged PT and PTT and 
clinical evidence of bleeding . 
 
Diagnosis : MRI is the preferred imaging modality in neonates with HIE . CT  
scan are helpful in identified focal hemorrhage lesion ,diffuse cortical injury 
later on and damage to basal ganglia .ultrasonography it is the initial preferred 
modality in preterm infant not in term .EEG may help to determined which 
infants are at highest risk for long term brain injury . 
 
Therapy : 
1-  General principles . the primary objective in treating perinatal asphyxia is 

to restore oxygen supply to the body tissues , especially the brain . this 
require ventilation with oxygen and ensuring adequate cardiac output . the 
secondary objective is to evaluate the degree of hypoxic injury and to plan 
treatment . whole body hypothermia or selective reduce mortality or major 
neurodevelopmental impairment in term infants with HIE .phenobarbital is 
the drug of choice for seizure . phenytoin and lorazepam may be needed 
for refractory  seizures . monitoring of blood pressure, hemodynamic 
status , acid –base balance , hypoglycemia and possible infection is vital . 

2-  Specific therapy . specific delivery room resuscitation procedures . 

And anticipate the conditions associated with asphyxia and treat if present. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

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Intracranial hemorrhage : 
 
1-  Subarachnoid hemorrhage:  may occur after a normal or traumatic 

delivery . bleeding is self limited and symptoms like irritability and 
seizure resolves in a few days .the infant may be asymptomatic . 

2-  Subdural hemorrhage: also is seen with birth trauma . a significant 

amount of blood can accumulate and cause focal neurological deficits 
owing to pressure exerted on the brain . however drainage is necessary 
only if symptoms are severe or do not resolve . 

3-  Intraventricular hemorrhage : is seen almost exclusively in preterm 

infant and is the result of bleeding of the germinal matrix , frequently 
after asphyxial insult .the hemorrhage occur in the first three days of 
life . the clinical manifestation of IVH include seizures, apnea , 
bradycardia , lethargy ,coma , hypotension , metabolic acidosis , 
anemia not corrected by blood transfusion , bulging fontanelle and 
cutaneous mottling . 
Infants with small hemorrhage (grade 1 or 2 ) are asymptomatic , 
infants with larger hemorrhage ( grade 4) often have catastrophic event 
that rapidly progress to shock and coma . 
The diagnosis of IVH is confirmed and the severity graded by 
ultrasound or CT examination through the anterior fontanelle : 

  Grade 1 IVH is confined to the germinal matrix . 
  Grade 2 blood noted in ventricle without ventricular dilation . 
  Grade  3 extension of grade 2 with ventricular dilation . 
  Grade 4 blood in dilated ventricle and in cerebral cortex . 

       Grade 4 hemorrhage has a poor prognosis as does the development of 
periventricular , small echolucent cystic lesion with or without porencephalic cysts 
and posthemorrahgic hydrocephalus . the cysts may correspond to the development of 
periventricular leukomalacia which may be a precursor to cerebral palsy . 

      Treatment :  treatment of acute hemorrhage involves standard supportive care 
including ventilation for apnea and blood transfusion for shock . post hemorrhagic 
hydrocephalus may be managed with serial daily lumber puncture ,external 
ventrculostomy tube or a permanent ventricular –peritoneal shunt .implantation of the 
shunt often is delayed because of the high protein content of the hemorrhagic 
ventricular fluid . 

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Neonatal seizures : 

Are not uncommon in the neonatal period subtle seizures which manifest as rhythmic 
eye deviation or blinking lip smacking tongue thrusting , fluctuation of vital signs or 
apnea are the most common form followed by generalized tonic , multifocal clonic , 
focal clonic and myoclonic seizures . 

Seizures may be difficult to differentiate from benign jitteriness or from 
tremulousness  in infants of diabetes mother , in infants with narcotic withdrawal .in 
contrast to seizures , jitteriness and tremors are sensory dependent elicited by stimuli 
and interrupted by holding the extremity . seizure activity becomes manifested as 
coarse , fast and slow clonic activity , whereas jitteriness is characterized by fine rapid 
movement . seizures may be associated with abnormal eye movement .  

Etiology : 

1-  Asphyxia . 
2-  Brain anomalies . 
3-  Intracranial hemorrhage  
4-  Systemic metabolic disorders ( hypoglycemia , hyponatremia ,hypernatremia , 

hypocalcemia ,hyperammonemia ) and inborn error of amino acid and organic 
acid metabolism . 

5-  Meningitis and encephalitis . 
6-  Pyridoxine deficiency . 

Diagnosis : the following evaluation should be made in effort to pin point the cause of 
the seizure activity : 

1-  Neurological examination . 
2-  EEG . 
3-  Ultrasound and CT scanning  
4-  Screening for metabolic disorders involving ( glucose , calcium , or sodium ) 

for inborn error of metabolism ( amino acid s or organic acid . 

5-  Lumbar puncture and evaluation of the SCF for sepsis . 

Treatment : 

      The treatment of neonatal seizures may be specific such as treatment of meningitis 
or the correction of hypoglycemia , hypocalcemia , hypomagnesemia , hyponatremia 
or vitamin B6 deficiency or dependency . in the absence of identifiable cause , therapy 
shloud involve anticonvulsant agent such as ( 20-40 mg/kg of phenobarbital )  (10-20 
mg/kg of phenytion ) or ( 0.1-0.3 mg/kg of diazepam ) followed by one of the two 
longer acting drugs . the long term outcome for neonatal seizure usually is related to 
the underlying cause and to the primary pathology such as hypoxic- ischemic 
encephalopathy , meningitis , drug withdrawal , stroke or hemorrhage . 

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Neonatal hypoglycemia : 

   Neonatal hypoglycemia is defined as a plasma glucose concentration less than 35 
mg/dl during the first 24 hrs and lees than 45 mg/dl thereafter . hypoglycemia is very 
common in infants of diabetes mother as well as in infants who are born after various 
perinatal complication , including prematurity , IUGR , and asphyxia . 

1-  Pathogenesis . the pathogenesis varies depending on the clinical setting and 

the associated conditions affecting the infants . 
a-  Maternal diabetes , the hypoglycemia in infants of diabetes is the result of 

a hyperinsulinemia state that persist after the umbilical cord is cut and the 
maternal supply of glucose is interrupted . 

b-  Prematurity . preterm infants become hypoglycemia owing to diminished 

glycogen store and to immaturity of gluconeogenic enzymes . 

c-  Growth retardation . growth retarded infants frequently are depleted of 

hepatic glycogen and quickly become hypoglycemic . 

d-  Perinatal asphyxia . forces the fetus to use anaerobic metabolism , which 

quickly depletes stored glycogen and result in hypoglycemia. 

e-  Cold stress . increased oxygen  consumption as well as glucose 

consumption . it also may increase free acids and result in hypoglycemia . 

f-  Sepsis. May cause hypoglycemia , although hyperglycemia also is 

observed which presumably is caused by insulin insensitivity . 

g-  Beckwith-Wiedmann syndrome . is characterized by hypoglycemia , 

visceromegaly , macroglossia and omphalocele . hyperinsulinemia 
secondary to pancreatic islet cell hyperplasia is responsible for 
hypoglycemia . 

h-  Nesidioblastosis and pancreatic islet cell adenoma are associated with 

hyperinsulinemia and hypoglycemia . 

i-  Metabolic disorder such as galactosemia and panhypopituitarism . 

Clinical features : 

         Infants with hypoglycemia are not always symptomatic . however the following 
symptoms may occur ( hypotonia or jitteriness , apnea or tachypnea, cyanosis 
,hypothermia , poor feeding  and seizures . 

Therapy : 

a-  Primary therapy is intravenous glucose . the glucose infusion may be required 

for several days until the basal insulin secretion rate decreases , glycogen 
stores are replenished or gluconeogenesis improves . bolus infusion of 
hypertonic glucose should be avoided because they may result in a rebound 
hypoglycemia .intravenous glucose should be administered as a constant 

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infusion begun at a rate of 6-8mg/kg/min .this may be increased to a rate of up 
to 20mg/kg/min ( a central venous access should be used for infusion given at 
a rate above 15 mg/kg/min . 
A small ( 0.5-1.0 g/kg ) bolus may be used for extreme hypoglycemia or if 
severe symptoms related to hypoglycemia . this shloud always be followed by 
a constant infusion . 

b-  Hypoglycemia that is secondary to hyperinsulinemia and resistant to 

intravenous glucose should be treated with corticosteroid or diazoxide . if drug 
treatment fails partial pancreatectomy should be performed . these more 
aggressive forms of therapy rarely are necessary except for hypoglycemia that 
associated with Beckwith-Wiedmann syndrome , nesidioblastosis , or islet cell 
adenoma . 

Infant of diabetic mother  

Women with diabetes in pregnancy are at increased risk for adverse pregnancy 
outcome . adequate glycemic control before and during pregnancy is crucial to 
improving outcome . 

The effect of diabetes on the fetus depend in part on severity of the diabetes state , age 
of onset of diabetes , duration of treatment with insulin and presence of vascular 
disease .poorly control maternal diabetes leads to maternal and fetal hyperglycemia 
that stimulates the fetal pancreas , resulting in hyperplasia of the islets of Langehans 
.fetal hyperinsulinemia results in increased fat and protein synthesis and fetal 
macrosomia except brain and ossification centers  . 

Hypoglycemia develops in about 25-50% of of infants of diabetic mother and 15-25% 
of infants of mothers with gestational diabetes . infants should initiate feeding within 
1 hour after birth and a screen glucose test should be performed within 30 mint. Of 
the first fed. In asymptomatic infants treatment indicated if plasma glucose less than 
30mg/dl . in symptomatic infants the treatment indicated if plasma glucose less than 
40% . treatment of hypoglycemia as mention above . 

Neonatal problems of diabetic mother : 

1-  Birth asphyxia and birth trauma due to macrosomia  . 
2-  Hypoglycemia , hypocalcemia , hypomagnecia . 
3-  Polycythemia and indirect jaundice . 
4-  Congenital anomalies is increased 3-folds like congenital heart disease . 
5-  Neurological disorders like neural tube defect and holoprosencephaly . 
6-  Renal disorders likes renal agenesis ,double ureter , renal vein thrombosis . 

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7-  Respiratory likes RDS due low surfactant synthesis  and TTN . 
8-  Preterm labor is common and the result of fetal distress or a planed early 

delivery . 
 
Prognosis : 
The neonatal mortality rate is > 5 times that of infants of non diabetic mother 
.the subsequent incidence of diabetes mellitus in infants of diabetic mother is a 
higher than that in general population . 
The key to optimal outcome is consistent euglycemia in the mother . 
 
 
 
 

Neonatal hypocalcemia : 

Hypocalcemia is a common in sick and premature newborn . total serum 
calcium levels less than 6 mg/dl and ionized calcium levels of lees than 3 to 
3.5 mg/dl are considered hypocalcemia . 
Early onset neonatal hypocalcemia occurs in the first 3 days of life and is 
often asymptomatic and can result from transient hypoparathyroidism or 
congenital absence of the parathyroid gland and DiGeorge syndrome . 
Hypomagnesemia ( < 1.5 mg/dl ) may be seen with hypocacemia that may 
need to treat both conditions . 
Late onset neonatal hypocalcemia or neonatal tetany often is the result of 
high phosphate containing milk or the inability to excrete the usual 
phosphorus in commercial infant formula . vitamin D deficiency and 
malabsorption also can be associated with late onset hypocalcemia . 
The clinical manifestations of hypocalcemia include ( apnea , muscle 
twitching seizures , laryngospasm . 
Chevostek sign and Trousseau sign can be see more with late onset 
hypocalcemia . 
Neonatal hypocalcemia may be prevented by administration of IV or oral 
supplement at a rate of 25 to 75 mg /kg /day . 
Early asymptomatic hypocalcemai of preterm infants and infants of diabetic 
mother often resolved spontaneously . 
Symptomatic hypocalcemia should be treated with 2- 4 ml /kg of 10% calcium 
gluconate given intravenously and slowely over 10 to 15 minutes followed by 
a continous infusion of 75 mg/kg/day of elemental calcium . 
If hypomagnesemia is associated with hypocalcemia , 50% magnesium sulfate 
0.1 ml/kg should be given by IM and repeated every 8 to 12 hrs . 
The treatment of late hypocalcemia include immediate management as in early 
hypocalcemia plus the initiation of feeding with low phosphate formula .  

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Infection 

   Infection continues to be a major cause of neonatal mortality and morbidity despite 
advance in therapy . although perinatally acquired bacterial infections are the most 
common infections that are acquired in utero remain important source of long term 
disability . 

General consideration : 

a-  Predisposing factors . the newborn is particularly susceptible to infection 

owing to immaturity of immune system mechanism including  

  Neutrophil chemotaxis . 
  Neurtophil phagocytosis . 
  Bacterial activity . 
  Humeral components. 

b-  Timing and route of infection . the causative organism and abnormalities 

associated with neonatal infection vary with time and route of infection . 
1-  Organisim responsible for transplacental infections before birth are ( CMV 

, HIV , Rubella virus , toxoplasma gondi , echovirus and listeria 
monocytogenes ) .and can cause abnormalities associated with infection 
acquired in the first trimester ( congenital malformation , IUGR , 
microcephaly , hydrocephalus and still birth ) and also can cause 
abnormalities with infection acquired later in pregnancy ( microcephaly , 
hydropes fetalis , DIC , anemia , IVH , hepatosplenomegaly , jaundice , 
skin and eye lesions beside still birth ) . 

2-  Perinatal infection include infections acquired through the fetal membrane 

ascending infections acquired after rupture of membrane and infection 
acquired via the birth canal . common causative organisims are ( Group B 
Beta-hemolytic streptococcus , E-coli . Klebsiella species , streptococcus 
pneumoniae Herpes simplex virus, Chlamydia trochomatis , neisseria 
gonorrhoeae , neisseria meningitidis ) .and can cause the following 
abnormalities ( respiratory distress , temperature instability , septic shock , 
neuropenia , thrombocytopenia , meningitis ) . 

3-  Postnatal infections most often are required as a result of nosocomial or 

community exposure . hospitalized newborns who are premature or require 
instrumentation are particularly susceptible . common causative organisms 
are ( staphylococcus aureus , staphylococcus epidermidis , pseudomonas 
aeruginosa , candida albicans , E –coli , klebsiella,clostridia, 
enterococcus)and associated abnormalities are ( respiratory distress , 
feeding intolerance , apnea, anemia shock , DIC , hypoglycemia and 
temperature instability )  

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2-  Bacterial infection and neonatal sepsis . bacterial infection most frequently 

are acquired via the birth canal or nosocomialy . the infection almost always is 
bacteremic and associated with systemic symptoms – a condition referred to as 
neonatal infection . 
a-  Incidence . neonatal sepsis is common in premature infants . about 1-4% 

of these infants have at least one episode of sepsis during their 
hospitalization . sepsis in term infants are rare , occurring in less than 1% . 

b-  Risk factors for early neonatal sepsis include : 

1-  Premature labor . 
2-  Low birth weight . 
3-  Prolonged rupture of the fetal membrane . 
4-  Chorioamnionitis . 
5-  Maternal fever . 

c-  Etiology . . the most common causative organisims include : 

1-  Gram-positive cocci especially group B Beta –hemolytic streptococci , 

but also staphylococcus aureus and staphylococcus epidermidis . 

2-  Gram- negative rods especially E-coli and klebsiella pneumoniae . 
3-  Gram-positive rods like listeria monocytogenes . 

d-  features : 

1-  Signs and symptoms of bacterial infections include : 

  Unexplained respiratory distress . 
  Unexplained feeding intolerance . 
  Temperature instability . 
  Hypoglycemia and hyperglycemia . 
  Apnea , lethargy or irritability . 

2-  Laboratory findings include : 

a-  Abnormal white blood cell count ,including neutropenia or un 

elevated ratio of immature to total neutrophil suggest sepsis . 

b-  Prolonged of  PT and PTT . 
c-  Tracheal aspirate , gastric aspirate for neutrophil count , gram stain 

and culture . 

d-  Blood culture . 
e-  A lumber puncture . 
f-  Urine for general exam and culture . 
g-  Chest radiograph , 
h-  Arterial blood gas analysis . 

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  Therapy :  

1-Empiric antibiotics therapy should begin after the diagnostic work up and consist of 
a broad –spectrum penicillin ( usually ampicillin ) and un aminoglycoside ( usually 
gentamicin ) . once culture data available . therapy should be tailored to the specific 
organism . 

2-The initial choice of antibiotics for nosocomial infection depend on nursery . 
community and individual patient exposure information. 

3-The duration of therapy usually is 7-10 days except for invasive infections ( e.g. 
meningitis , osteomyelitis ) which require longer course of antibiotics therapy  

4-Other complication can be treated accordingly for example treatment of shock with 
fluid and vasopressor .  

1-  Monitoring serum drug level . 

Persistent signs of infections despite antibacterial treatment suggest 
candidal or viral sepsis .                        
 
 

Best  regard  

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