NEONATOLOGY
Classification of newborn
infants on the basis of risk
Well High-
Sick
infants risk
infants
infants
To decide which group an infant falls into:
History Examination
Who is a well infant?
A well infant has all of the following features:
Normal history of pregnancy, delivery and
post delivery period.
Born at term.
Weight appropriate for gestational age.
Vital signs are normal.
Infant appears normal on examination.
Well infants only require routine level 1 care
in a clinic or at home
What is a high-risk infant?
Appear clinically well on examination.
Has a greater chance than most infants
of developing a clinical problem.
(e.g. hypothermia, hypoglycemia, apnea,
infection….etc.).
High risk newborns
Infants who should be under close observation by
experienced Physicians and Nurses.
High Risk Pregnancies
Factors exist that increase frequency of:
Abortion and fetal death,
Premature delivery,
Malformations,
Mental retardation or
Other handicapping conditions.
Etiology of high risk newborns:
(A) Demographic & social factors:
Maternal age < 16 years > 40 years.
Poverty.
Emotional or physical stress.
(B) Medical History of mothers:
Diabetes mellitus (DM).
Hypertension.
Asymptomatic bacteruria.
Collagen disease.
(c) Previous pregnancies:
Neonatal deaths.
Prematurity.
Intrauterine growth retardation.
Congenital Malformations.
Neonatal jaundice.
(D) Present pregnancy:
Vaginal bleeding.
Multiple pregnancies.
Premature rupture of membranes > 18 hrs.
Short inter-pregnancy time.
Poly or oligohydramnios.
Pre-eclampsia.
Inadequate prenatal care.
(E) Labor & Delivery:
Premature labor < 37 wks.
Postdate delivery >42 wks.
Breech presentation.
Meconium stained amniotic fluid.
Cesarean section.
Forceps delivery.
(F) Neonate:
Apgar score <4 at 1 min.
Birth weight < 2.5 kg or >4 kg.
Gestational age < 37 wks, > 42 wks.
Congenital malformations.
Definition:
Newborn infant born before 37 weeks
gestation.
Causative factors of preterm birth:
Maternal
1) Incompetent cervix.
2) Pre-eclampsia.
3) Antepartum hemorrhage.
4) Severe maternal illnesses e.g. heart disease.
5) Polyhydramnios.
6) Premature rupture of membranes.
Fetal :
Fetal developmental anomalies.
Multiple pregnancies.
Unknown.
Anatomic and physiologic features
of preterm infants
General characters of preterm infants:
Weight less than 2500 gm ( LBW).
Length related to maturity than is weight.
Head circumference exceeds that of the chest.
“Lanugo”especially if less than 30 week’s
gestation.
Nails are soft but not necessarily short.
Skin is shiny, unwrinkled and has a darker
pink color than at term .
Labia minora are protuberant and gaping,
Testes are usually incompletely descended.
Creases on the soles of the feet are almost
absent except for a single one anteriorly.
Ears are floppy and lacking formed cartilage.
Breast: The palpable nodule at the nipple is absent
before 34 weeks.
Skull is soft and easily indented around the
fontanels before 36 weeks.
Muscular activity is less .
Eyes remain closed for most of the time
Cry, if present, is weak,
Movement of the body and limbs tends to be in little
bursts of activity and is often jerky and frog-like.
Posture is less flexed than at term.
Essential issues regarding
premature baby
Temperature control in preterm infants
Heat production is low and
Heat loss is high.
Why Heat loss in preterm is high ?
Because:
1) Surface area is large in proportion to the body’s
weight.
2) Subcutaneous fat is little.
3) Brown fat that is a source of heat production in
normal term babies is deficient.
4) Thermostatic mechanism is poor.
5) Heat production by shivering or muscle activity is
minimal.
Blood and circulation
• Capillary walls …….. week
• Clotting factors …….. reduced lead to
greater tendency to bleed.
• Hemoglobin is as high as in a term infant .
Respiration
• Nasal airway is narrow and easily obstructed.
• Respiratory passages are narrow giving greater
resistance to air flow.
• Thoracic cage is soft, so that it is sucked in by
negative pressure during inspiration.
• Cough reflex is poorly developed.
Respiration
• Gaseous exchange is relatively inefficient as
pulmonary surfactant is diminished causing
collapse of the alveoli.
• Respiratory centers are not fully developed
resulting in an unstable respiratory system with
periods of apnea.
Digestion
• Suckling and swallowing is not well developed.
32-34 weeks becomes sufficiently coordinated to begin
to feed from the breast.
36-37 weeks becomes fully effective.
• Function of digestion matures early.
Sugar is well tolerated protein is less so and fat is least
well tolerated.
• liver function Immaturity is seen mainly as a reduced
ability to conjugate bilirubin resulting in increased
physiological jaundice in pre-term infants.
Renal function
• Able to excrete urea and water
adequately even in very premature baby
• Unable to excrete big fluid loads and
edema may result.
• Less able to retain sodium than in mature
babies.
Resistance to infection
• Limited passive immunity
• Ability to produce antibodies is poorly
developed.
Common disorders of preterm infants
1- Respiratory problems: respiratory distress
syndrome and apneic attacks.
2- Alimentary tract problems: abdominal distension,
regurgitation of gastric contents.
3- Hyperbilirubinemia.
4- Hypothermia.
5- Hypoglycemia.
6- Hypocalcaemia.
7- Anemia.
8- Edema.
9- Circulatory instability.
10- Infection.
11- Cerebral anoxia .
Management of the preterm infant
Care in the delivery room
• Same measures of ordinary care given to term babies.
• Preterm baby must be handled very gently and placed in
a pre-warmed towel under a source of radiant heat.
• Prompt resuscitation with endotracheal intubation and
ventilation is advisable for most preterm babies of less
than 32 weeks gestation to provide maximal initial
expansion of the alveoli and thus reduce the severity of
any subsequent respiratory distress syndrome.
• The baby should be transferred in a transport incubator
at 34-35 ºC or in a warmed cot to the neonatal unit.
Subsequent care of preterm infant
1- Maintenance of body temperature and oxygen
supply: incubator .
2- Humidity: about 50-60%. Humidity helps to:
- reduce heat loss,
- avoid drying of respiratory tract and
- helps thinning of viscid secretion.
3- Precautions against cross infection
a- Nurse or medical attendant should be clear of
infection.
b- Meticulous hand washing before and after
handling babies .
c- Meticulous sterilization of the incubator and
other equipment and fluids used for every
baby.
d- Avoidance of air contamination and
overcrowding.
4- Observation and recording of changes
skin color, type and rate of respiration, heart
rate, body temperature and any abnormal
movements.
5- Feeding of preterm infants: may be
-parenteral or
-enteral
Discharge criteria of preterm babies from
the neonatal unit
1- Post conceptual age of about 36 weeks.
2- Current weight of 1800gm or more with an
average of weight gain of 15-30 gm/day.
3- Stable temperature in an open crib.
4- Taking all nutrition by nipple (bottle or
breast).
5- No recent apnea or bradycardia.
6- No need for parenteral drugs or oxygen.
Birth weight is two SD below mean or less than the
10th percentile of weight for gestational age
normal and SGA twins
Associated factors
Fetal: chromosomal disorders (e.g. trisomies).
chronic fetal infection (cytomegalovirus,
rubella, syphilis).
Placental: decreased placental weight, cellularity,
surface area, placental infarction, separation or
infection.
Maternal: toxemia, hypertension, renal disease,
malnutrition or hypoxemia (cyanotic heart or
pulmonary disease).
Problems encountered in SGA or
IUGR
1- Perinatal asphyxia.
2- Hypoglycemia.
3- Hypothermia.
4- Polycythemia.
5- Pulmonary hemorrhage.
6- Meconium aspiration
Management
- Obstetrical monitoring and
- care of the above problems.
Large For Gestational Age
macrosomic baby
• Birth weight is two SD above mean or more than
the 90th percentile of weight for gestational age
Etiology
• Maternal diabetes
• obesity
Risks of macrosomic baby
• High incidence of birth injuries as brachial
plexus, cephalohematoma or fractured clavicle.
• High incidence of congenital malformation.
• Management
Blood sugar monitoring for IDM
I- Choanal atresia
A congenital blockage of the posterior nares caused by
persistence of a bony septum or a soft tissue membrane.
It presents by respiratory distress due to upper airway
obstruction.
Diagnosis
It is confirmed by inability to pass a
catheter into the nasopharynx through
the nostril (unilateral or bilateral).
Treatment
Cases with bilateral atresia require
oral airway and surgical correction.
II- CLEFT LIP AND CLEFT PALATE
These are the most common
congenital anomalies of head and
neck.
Cleft lip: a defect in the upper lip.
Cleft palate: it is a defect in the
palate (hard and soft palate) leads to
feeding difficulties, nasal
regurgitation, recurrent chest and ear
infections.
Management
Provision of adequate nutrition and
prevention of aspiration and infection.
Closure of a cleft lip is usually performed
at 1-3 months of age and of cleft palate at
6-12 months.
III- TRACHEOESOPHAGEAL FISTULA (TOF)
It usually occurs in an isolated form. Oesophageal
atresia with distal TOF represents 84% of cases,
whereas other subtypes are less common.
Clinical picture and diagnosis
It should be suspected in cases with polyhydramnios.
Affected infants have a lot of mucus with cough and
chocking during feeding.
Diagnosis is rapidly confirmed by failure to pass a
nasogastric tube beyond the proximal esophagus.
Plain x ray shows coiled catheter in the proximal
oesophagus.
DIAGNOSIS
Attempt to pass catheter into stomach. Cannot pass more
than 10-15 cm.
Management
1-Tracheoesophageal fistula is a
surgical emergency and surgical
repair is indicated.
2- Supportive measures.
Patient should be placed at 30º upright
position.
Contents from upper oesphageal pouch
should be drained.
V- Imperforate anus ± fistula
• Two lesions, low or high . Treatment and
prognosis are different in these two lesions.
Treatment
Imperforate anus should be surgically
corrected. Temporary colostomy is performed
in all neonates with high imperforate anus
with or without fistula. Later complete surgical
correction is performed.
V- Meningeomyelocele
It is evident at birth as a skin defect over the
back bordered laterally by unfused neural
arches of the vertebrae. The defect is usually
covered by a transparent membrane which
may have neural tissue attached to its inner
surface. The membrane bulges and forms a
large sac.
Varying degrees of motor and sensory deficits are
noted below the level of the lesion.
Examination of the skull is important as many
cases are associated with hydrocephalus which
will need shunt operation.
Treatment: consists of prompt surgical
closure of the skin defect, preferably within 48 hours
after birth, to prevent ascending meningeal infection.
Definition: mechanical and hypoxic-
ischemic injury occurring during labor.
Predisposing factors
1- Macrosomia.
2- Prematurity.
3- Cephalopelvic disproportion.
4- Dystocia.
5- Prolonged labor.
6- Abnormal presentation .
7- Instrumentation e.g. ventose and
forceps delivery.
8- Multiple births.
I- HEAD INJURIES
1- Caput succedaneum
Area of edema over the presenting part of the
scalp during vertex delivery.
Clinical manifestations:
Soft swelling which may extend across the
suture lines (external to periosteum).
Differential diagnosis:
Occasionally caput succedaneum may be
difficult to distinguish from a cephalheinatoma
Treatment:
Usually no treatment is required.
Prognosis:
Usually resolves within several days.
B) Cephalhematoma:
A subperiosteal collection of blood overlying a cranial
bone.
Aetiology:
Rupture of blood vessels that traverse from skull
periosteum secondary to prolonged or difficult labor and
mechanical trauma caused by forceps or ventose
Clinical manifestations:
•Bleeding is limited by suture line.
• Overlying scalp is not discolored.
• Swelling may be delayed for hours or days after
birth.
• Resolves within 2 weeks to 3 months.
Treatment:
• No treatment for uncomplicated cephalhematoma.
• Significant hyperbilirubinemia may result
necessitating phototherapy or even exchange
tranfusion according to level of bilirubin.
C.) Intracranial hemorrhage:
Occurs in 20% - 40% of infants with birth weights
under 1500 gm. It is less common among more
mature newborns.
Bleeding can occur in:
a. Epidural, subdural or subarachnoid space.
b. Parenchma of the cerebrum or cerebellum .
c. Ventricles.
Clinical presentation:
1-A silent presentation may occur in up to 50% of
cases.
2-Signs of blood loss: Shock, pallor, respiratory
distress, DIC, jaundice.
3-Signs of neurologic dysfunction:
• Bulging anterior fontanelle.
• Hypotonia, weakness, seizures.
• Temperature instability.
• Apnea.
Diagnosis:
• Cranial U/ S
• CT Scan
Management:
• Avoid unnecessary manipulations of
infant.
• Administer volume expander slowly:
albumin, plasma and blood.
• Vitamin K .coagulation defects.
• Treat seizure and hyperbilirubinaerma if
present.
Apnea
Apnea: means cessation of breathing
Significant apnea: means cessation
of breathing for longer than 20 sec,
or any duration if accompanied by
cyanosis and bradycardia.
Apnea is a common problem in
preterm infants that may be due to
idiopathic apnea of prematurity or
an associated illness
Causes of significant neonatal apnea:
1- Idiopathic apnea of prematurity
2- Central nervous system: e.g. intraventricular hemorrhage,
drugs, seizures, hypoxic injury.
3- Respiratory: e.g. pneumonia, obstructive airway lesions,
atelectasis, severe hyaline membrane disease,
pneumothorax, hypoxia.
4- Infectious: e.g. sepsis, meningitis.
5- Gastrointestinal e.g. esophagitis, intestinal perforation.
6- Cardiovascular: e.g. hypotension, hypertension, anemia,
hypovolemia.
7- Metabolic: e.g. hypoglycemia, hypocalcemia hypothermia.
9 - Others: e.g. immaturity of respiratory center, extreme
prematurity.
• Idiopathic apnea of prematurity:
It occurs in the absence of identifiable
predisposing diseases.
• Classification:
a- Obstructive apnea is characterized by absent
airflow but persistent chest wall motion.
b-Central apnea is characterized by decreased
central stimulation to respiratory muscles with
decreased air way airflow and chest wall
motion.
c- Mixed etiology the most common pattern of
idiopathic apnea in preterm neonates. It
involves obstructive apnea preceding or
following central apnea.
Clinical manifestations
• The incidence of idiopathic apnea of prematurity
varies inversely with gestational age.
• The onset of idiopathic apnea occurs on the 2nd
– 7th day of life. It is rare on the 1st day of life.
• Apnea immediately after birth signifies another
illness but not idiopathic.
• The onset of apnea in a previously well
premature neonate after the 2nd week of life or
in a term infant at any time is a critical event
that needs immediate investigations.
Treatment:
- Treatment of the cause
- Infants at risk for apnea should be monitored with apnea monitor.
- Gentle cutaneous stimulation is often adequate therapy for
neonatal infants with mild and intermittent episodes.
- Infants with recurrent and prolonged apnea require immediate bag
and mask ventilation.
- Oxygen should be administered carefully to treat hypoxia.
- Recurrent apnea of prematurity not due to precipitating identifiable
cause may be treated with theophylline or caffeine.
- Oxygen therapy by high-flow nasal cannula or assisted ventilation
by nasal continuous positive airway pressure are effective
therapies for mixed or obstructive apnea.
Central cyanosis
Causes:
A- Respiratory insufficiency : may be due to:
1- Pulmonary conditions: such as:
- Upper airway obstruction by choanal atresia.
- Lower airway diseases as respiratory distress syndrome,
transient tachypnea, meconium aspiration, pneumonia,
pneumothorax, congenital diaphragmatic hernia, pulmonary
hypoplasia.
2- CNS depression :as a result of drugs, intracranial
hemorrhage, or anoxia; respiration tend to be irregular and
weak and are often slow.
B- Congenital cyanotic heart
disease: may be due to:
- Transposition of great vessels
- Pulmonary atresia.
- Tetralogy of Fallot (presenting at a later age)
C- Methemoglobinemia
- Congenital.
- Acquired (e.g., nitrates, nitrites toxicity).
N.B: Episodes of cyanosis may also be the initial sign of
hypoglycemia, bacteremia, meningitis, shock, or
pulmonary hypertension.
Respiratory failure is the inability of the
respiratory system to provide exchange of
oxygen and carbon dioxide between air and
blood, resulting in an impaired supply of
oxygen and excretion of carbon dioxide to
meet the body’s demands.
Causes and clinical manifestations of respiratory distress
and failure in newborn infants
Type Manifestations Causes
Central failure o Apnea o Narcosis
o Slow, irregular, gasping o Prenatal or perinatal
respiratory efforts anoxia
o Cyanosis o Intracranial hemorrhage or
trauma
o CNS anomalies
Peripheral o Rapid respiratory rate o Pulmonary
failure o Intercostal retraction - Primary atelectasis
o Subcostal retraction - Hyaline membrane disease
o Xiphoid retraction - Pneumonia
o Expiratory grunt - Lung cysts
o Frothing at lips - Emphysema
o Cyanosis - Pneumothorax
- Meconium aspiration
syndrome
o Extra pulmonary
- Diaphragmatic hernia
- Bilteral choanal atresia
- Congestive heart failure
I- Respiratory distress syndrome (RDS) of the newborn
(Hyaline membrane disease)
To maintain alveolar stability, surfactant reduces
the surface tension and prevents collapse of small
air spaces at end of expiration. The primary cause
of respiratory distress syndrome (hyaline
membrane disease) is inadequate pulmonary
surfactant with consequent diffuse alveolar
atelectasis, edema, and cell injury.
Risk factors
1- Infant of diabetic mother.
2- Pre mature infants.
3- Cesarean section delivery.
4- Multi fetal pregnancies.
5- Asphyxia.
6- A history of prior affected infants.
Clinical manifestations
• Signs of respiratory distress appear within minutes or
few hours of birth (tachypnea, grunting, intercostal and
subcostal retractions, nasal flaring and cyanosis).
• Breath sounds may be normal or diminished.
• Fine rales may be heard especially over the lung bases.
Roentgenogram of the chest
It reveals fine reticular granularity of the lung
parenchyma and air bronchograms.
II- Meconium aspiration syndrome (MAS)
Fetal distress and hypoxia can lead to meconium
aspiration by the fetus in utero or by the newborn
during labor. Aspirated meconium can cause airway
obstruction, an intense inflammatory reaction and
respiratory distress.
Risk factors
1- Post-term pregnancy.
2- Abnormal fetal heart rate.
3- Maternal hypertension, diabetes mellitus.
4- Maternal pre-eclampsia.
5- Maternal respiratory or cardiovascular disease.
Clinical picture
• Respiratory distress occurs at or few hours after birth.
Skin and umbilical cord may be stained with
meconium.
• There are manifestations of airway obstruction with
difficult expiration.
• Pneumothorax and pneumonia are common
complications.
Roentgenogram of the chest
It shows hyperinflated lung with bilateral
patchy opacity, pneumothorax may be
identified.
Treatment
Chest physiotherapy and suctioning of the
oropharynx and trachea in delivery room may
be useful to help removal of meconium from
the airways in infants who develop
respiratory symptoms.
III- Pneumonia
Types
Congenital pneumonia: early onset of respiratory
distress within 3-6 hours is observed. Clinical findings
may be similar to hyaline membrane disease. There may
be temperature instability and apneic spells.
Acquired pneumonia: late onset of respiratory distress
(at any time of neonatal period) commonly follows
aspiration, mechanical ventilation or septicemia.
Aspiration pneumonia: may occur due to aspiration of
amniotic fluid or milk. Predisposing conditions as
tracheoesophageal fistula and gastro-esophageal reflux
should be considered and excluded.
Clinical picture
Bad general condition, respiratory distress and
fine crepitations over the chest.
Roentgenogram of the chest
It reveals bilateral patchy opacities or lobar
opacity commonly in the right upper lobe
(aspiration pneumonia).
Screening for sepsis: is useful for diagnosis.
Management of respiratory distress of the newborn
Babies with respiratory distress should be admitted
to neonatal intensive care unit where facilities for
investigations and respiratory support are
available.
1- Investigations
Chest x ray: to distinguish different pulmonary
causes.
Blood gases: to detect metabolic acidosis and
respiratory failure.
Hb level and hematocrite: to detect anemia and
polycythemia.
Laboratory indicators for sepsis.
2- Respiratory monitoring
a- Clinical monitoring: by assessment of degree of
respiratory distress.
b- Arterial oxygen saturation monitoring: by use of pulse
oximeter to assess degree of hypoxemia.
c- Arterial blood gases: it is the most sensitive and reliable
method for state of oxygenation and acid-base
balance.
3- Respiratory support
The principal goal is to ensure adequate oxygenation and
ventilation.
a- Chest physiotherapy and suctioning: the aim is to
mobilize secretions, clear the alveoli and airways and to
improve ventilation.
b- Oxygen therapy: it is indicated in all cases of
respiratory distress to correct hypoxemia and relieve
cyanosis. Oxygen preferably warmed and humidified,
given by head box to keep arterial levels between 55-70
mmHg and >90% saturation.
c- Assisted ventilation: it is indicated in cases with
persistent hypoxemia (PaO2≤50mmHg), hypercarbia
(PaCO2 60 mmHg) and pH<7.2.
4- Specific treatment
• Surfactant replacement therapy (delivered through
endotracheal tube) for cases with hyaline membrane
disease.
• Specific antibiotics for cases with pneumonia to
eradicate infection.
• Fluid therapy aiming at adequate hydration and tissue
perfusion.
• Naloxone as an antidote is given to patients with CNS
depression due to maternal morphine overdose.