NEWBORN DISORDERS
____
1. SMALL FOR GESTATIONAL AGE (SGA) NEWBORN
 Birth weight is below the 10th percentile on an
intrauterine growth curve for that age.
 May be preterm, term or postterm.
 Experienced intrauterine growth restriction
(IUGR) or failed to grow at expected rate in
utero.
 A growth curve, as seen in the photo, estimates
expected weight for every week of gestation.
 Born less than 37 weeks, born between 37 to 42
weeks, born beyond 42 weeks.
 SGA newborns are small for their age because
either….. These have several causes.
ETIOLOGY:
1. Nutrition during pregnancy, adolescent
pregnancy
 Plays a major role in fetal growth. PA have
higher incidence of SGAs because they need
to meet their own nutritional and growth
needs first. In effect, needs of growing fetus is
compromised.
2. Placental anomaly
 This is the most common cause of IUGR.
Either did not obtain sufficient nutrients
from mother’s uterus or insufficient at
transporting nutrients to the fetus.
3. Women with systemic diseases, diabetes
mellitus, pregnancy-induced hypertension
 These diseases cause decreased blood flow to
placenta.
4. Maternal lifestyle, smoking, narcotics
 Some studies show that women who smoke
heavily or use narcotics tend to have SGA
newborns.
5. Intrauterine infection, chromosomal
abnormality
 In this case, the placental supply of
nutrients is sufficient, but fetus cannot use
them because the infection or abnormality.
ASSESSMENT:
1. PRENATAL
 Fundic height less than expected.
 Sonogram reveals small fetal size.
 Poor biophysical profile results.
2. APPEARANCE
 Wasted, decreased anthropometrics.
 Poor skin turgor.
 Large head
 Widely separated skull sutures.
 Dull and lusterless hair.
 Sunken abdomen.
 Dry and yellow cord.
3. LABORATORY FINDINGS
 High hematocrit.
 Polycythemia.
 Hypoglycemia.
 Assess need for CS delivery, especially poor
placental function.
 Since age is advanced than weight, this
neonate may have better-developed
neurologic responses, sole creases, and ear
cartilage than expected for a baby of that
weight.
 Less plasma than RBC due to lack of fluid
in utero, fetal anoxia stimulates RBC and
causes blood viscosity putting extra work on
heart, below 45 mg/dL and may need IV
glucose.
2. LARGE FOR GESTATIONAL AGE (LGA)
NEWBORN
 Birth weight is above the 90th percentile on
an intrauterine growth chart for that
gestational age.
 Appears deceptively healthy but with
immature development.
ETIOLOGY:
1. Overproduction of growth hormone in
utero, mothers with diabetes mellitus or
who are obese.
 LGA often happens to women with
diabetes mellitus or obese. Fetuses of
these women have been subjected to
macrosomia
3. PREMATURITY
2. Multiparous women
 With each succeeding pregnancy,
babies tend to grow larger.
3. Conditions such as transposition of the
great vessels, Beckwith syndrome, and
omphalocele.
 A congenital CV disorder, a rare
condition characterized by overgrowth,
and a GI abnormality where internal
organs usually intestines stick outside
of the belly.
ASSESSMENT:
1. PRENATAL
 Uterus unusually large for gestation age.
 Sonogram reveals a big baby for age.
 Non-stress test to assess placental
function and amniocentesis to
check lung maturity can be done.
Detected during labor too, CS to
prevent shoulder dystocia.
2. APPEARANCE
 Immature reflexes.
 Low scores on gestational examinations.
 Extensive bruising or birth injury.
 Prominent caput succedaneum,
cephalhematoma, or molding.
 Same care with a preterm.
3. CARDIOVASCULAR DYSFUNCTION
 Hyperbilirubinemia.
 Tachycardia.
 Cyanosis.
 Absorption of blood from bruising,
extra load of heart, transposition of
great vessels associated with
macrosomia.
4. HYPOGLYCEMIA
 Require large nutritional stores to
sustain weight. If mother has DM,
high glucose caused high insulin in
utero and still high 24 hours after
birth so can cause rebound
hypoglycemia.
 Born after 20 weeks and before the end of
37 weeks gestation.
 Weighs less than 2500 grams.
 Low birth weight
1500 to 2500 grams
 Very low birth weight
1000 to 1500 grams
 Extremely low birth weight
500 to 1000 grams
 Exact cause is rarely known.
 Infant mortality could be reduced
dramatically if causes of preterm birth
could be discovered and corrected and all
pregnancies brought to term.

 Preterm babies must be differentiated
from SGA babies as they result from
differing situations and will cause different
problems in adjusting to extrauterine life.
 Not all SGAs are PTs, and likewise, not all
PTs are SGAs.
 Always consider the basis, FT at 37 to 42
AOG must be within 2.5 to 3.5 kg.
ASSESSMENT FINDINGS
Respiratory System
 Insufficient surfactant, apneic episodes,
tachypnea, nasal flaring, retractions,
grunting, seesaw pattern of breathing,
cyanosis.
 Lung maturity is achieved later in IUL,
normal L:S ratio at 2:1
Thermoregulation
 Body temperature fluctuates easily due to
lesser fat and muscles.
 T is difficult to regulate
Nutritional Status
 Poor sucking, swallowing, gag, and cough.
 Risk of aspiration
Skin
 Lack of fat, reddened, translucent.
 As compared to a full term newborn
with a well-moistened, beautiful skin
Cardiovascular System
 Petechiae due to fragile capillaries and
increased prothrombin time, increased
bleeding time.
 Risk of bleeding

Neuromuscular System
 Poor muscle tone, weak reflexes, weak and
feeble cry.
 Immature neuromuscular system
POTENTIAL COMPLICATIONS
A. Anemia of Prematurity.
 A normochronic, normocytic
hypoproliferative anemia in preterm
newborns due to decrease in
erythropoietin.
 Normal cells, but few in number. Bone
marrow does not increase production until
32 weeks AOG. Looks pale, lethargic,
anorectic.
B. Kernicterus.
 Destruction of brain cells by invasion of
indirect bilirubin.
 May occur as low as 12 mg/dL in preterms,
20 mg/dL in full terms. Phototherapy or
DVET can be done.
C. Persistent Patent Ductus Arteriosus.
 Non-closure of ductus arteriosus due to
difficulty of blood flow from pulmonary
artery to aorta caused by lack of lung
surfactant.
 Leads to PAH. Indomethacin or ibuprofen
to close DA.
D. Periventricular or Intraventricular
Hemorrhage.
 Bleeding within and around the ventricles
due to fragile capillaries and immature
cerebral vascular development.
 Hydrocephalus may occur, and prognosis
is guarded.
E. Respiratory Distress Syndrome.
 A breathing disorder in preterm newborns
due to lack of lung surfactant.
 May cause atelectasis.
F. Retinopathy of Prematurity.
 A blinding disease caused by abnormal
development of retina in premature
newborns.
 Caused by oxygen therapy in preterms
experiencing RDS, which damages retina
as a SE so weaning is necessary.
G. Necrotizing Enterocolitis.
 Bacterial infection and inflammation of
intestines among premature newborns.
 Occurs in 3 to 4 days after birth, usually
on NPO and ventilator.
4. POSTMATURITY
 An infant who stays in utero past 42 weeks
is at special risk, because a placenta
appears to be timed to last effectively for
40 weeks.
ASSESSMENT:
 Less amniotic fluid and meconium-stained
at birth.
 Vernix and lanugo. completely disappeared
 Dry, cracked, leather-like skin.
 Depleted subcutaneous fat.
 Hard nails extending beyond fingertips.
 Signs of birth injury or poor tolerance of
birth process.
 All these findings are associated with a poorly
functioning placenta and fetal distress.
 The skin and nail characteristics on the photo
are common among postmature newborns.
CONSIDERATIONS:
1. Monitor for any difficulty establishing
respirations.
 Especially if meconium aspiration
occurred.
2. Establish nutrition as hypoglycemia may
occur.
 Since fetus used its glycogen stores
in the last weeks of intrauterine
life.
3. Regulate temperature as fats have been
used in utero as well.
 Prevent further complications
related to hypothermia such as
 hypoglycemia, acidosis, and
respiratory distress.
5. RESPIRATORY DISTRESS SYNDROME (RDS)
 Pathologic feature is hyaline-like or
fibrous membrane formed from an exudate
of an infant’s blood that begins to line the
terminal bronchioles, alveolar ducts, and
alveoli.
 Cause is a low level or absence of
surfactant, the phospholipid that lines the
alveoli and reduces surface tension to keep
it from collapsing on expiration.
 Most often occurs in preterm infants, but
also among neonates:
1. of diabetic mothers
2. born by cesarean birth
3. with meconium aspiration
 This membrane prevents exchange of O2 and
CO2 at the alveolar–capillary membrane.
 Surfactant does not form until 34th week AOG.
PATHOPHYSIOLOGY
1. Collapse will:
 Require forceful inspirations,
hypoinflation occurs and pulmonary
resistance increases, blood shunts through
FO and DA, lungs are poorly perfused, poor
oxygen exchange leads to tissue hypoxia
and releases lactic acid – acidosis
 Form hyaline membrane on alveolar
surface, increases CO2 – acidosis
2. Acidosis will cause pulmonary
vasoconstriction – RDS, lung injury, BPD
ASSESSMENT
AT BIRTH:
 Nasal flaring, Tachypnea, Retractions, Low
body temperature, Cyanotic mucus
membranes.
 Most infants who develop RDS have
difficulty initiating respirations at birth.
WITHIN SEVERAL HOURS:
 Expiratory grunting, Cyanotic body, PO2
and O2 saturation fall, Fine rales,
Diminished breath sounds.
 Even with an attempt at better oxygen
exchange, however, if the child still cannot
tolerate and the disease progresses
AS DISTRESS INCREASES:
 Seesaw respirations, Heart failure, Pale
gray skin, Periods of apnea, Bradycardia,
Pneumothorax.
 There is progressive deterioration
DIAGNOSTIC AND LABORATORY FINDINGS:
 Chest radiograph reveals diffuse pattern of
radiopaque areas with haziness, Blood gas
shows respiratory acidosis.
 Poor gas exchange.
THERAPETIC MANAGEMENT:
1. Surfactant Replacement.
 Synthetic S through ET at birth.
2. Oxygen Administration.
 CPAP or PEEP exert pressure on
alveoli at end of E to prevent
collapse, complication of O2 to
premature is retinopathy.
3. Ventilation.
 I < E (1:2) and it’s difficult to deliver
O2 to stiff, noncompliant lung at this
usual ratio, forcing air at high
pressure and rapid rate can cause
pneumothorax so Vs can either be
reversed I:E of 2:1 or high-frequency,
oscillatory, and jet ventilators which
maintain airway pressure in an
 intermittent oscillate or jet of air at
400 to 600 times per minute.
4. Administer muscle relaxant,
pancuronium IV.
 Increase pulmonary blood flow.
5. Some are maintained on extracorporeal
membrane oxygenation (ECMO).
 Like open-heart surgery where blood
removed from venous catheter to RA,
then to machine which pumps and
oxygenates blood allowing heart and
lungs to rest, then back to aortic arch
through carotid artery.
6. Keep warm.
 Prevent acidosis, reduces O2
demand.
7. IV hydration and nutrition.
 Newborn too exhausted to suck.
PREVENTION:
1. Tocolytic, terbutaline.
 Prevent premature birth.
2. Dexamethasone to mother at 6 mg IM/IV
Q12 for 4 doses.
 L:S must be 2:1, steroids quicken
formation of L so surfactant matures.
6. TRANSIENT TACHYPNEA OF THE NEWBORN
(TTN)
NORMAL PHYSIOLOGY:
1. At birth, a newborn may have up to 80
breaths per minute when crying caused by
retained lung fluid.
2. Within 1 hour, however, this rapid rate
slows between 30 and 60 breaths per
minute.
In about 10 in 1000 live births, respiratory rate
remains high between 80 and 120 breaths per
minute, termed as transient tachypnea of the
newborn which may occur within 36 to 72 hours
after birth.
 Transient tachypnea may reflect a slight
decrease in mature surfactant but is a direct
result of retained lung fluid.
 Retained lung fluid limits the amount of
alveolar surface that is available for oxygen
exchange.
 It peaks approximately 36 hours and then
begins to fade. Typically, by 72 hours of life, it
spontaneously fades as the lung fluid is
absorbed and respiratory activity becomes
effective.
OCCURS OFTEN AMONG NEONATES:
 Born by cesarean birth.
 Whose mothers received extensive fluid
administration during labor.
 Who are preterm.
ASSESSMENT:
 Mild retractions but not marked cyanosis.
 Mild hypoxia and hypercapnia
 Difficult feeding
 Chest radiograph will reveal some fluid in
the central lung, but aeration is overall,
adequate.
 The infant does not appear to be in a great
deal of distress, aside from the tiring effort
of breathing so rapidly.
 O2 may be necessary, assist with feeding,
close observation and watch carefully to
be certain the increased effort is not tiring,
and watch for signs of more serious
disorders.
7. MECONIUM ASPIRATION SYNDROME
A newborn may aspirate meconium either in utero
or with first breath at birth.
 Meconium is present as early as 10 weeks
AOG.
 Greenish to greenish black in AF.
 Release of meconium into amniotic fluid is
caused by:
1. Relaxation of rectal sphincter
 Hypoxia causes vagal stimulation,
relaxing rectal sphincter.
2. Pressure on buttocks
 Babies born breech have more
pressure on buttocks during labor
and delivery.
Causes severe respiratory distress in 3 ways:
1. Inflammation of bronchioles because it is a
foreign substance.
2. Block small bronchioles by mechanical
plugging.
 3. Decrease in surfactant production through
lung trauma.
 Hypoxemia, carbon dioxide retention, and
intrapulmonary and extrapulmonary
shunting occur.
 A secondary infection of injured tissue
may lead to pneumonia.
ASSESSMENT
At Birth:
 Apgar score is low
 Tachypnea
 Retractions
 Cyanosis
After Initiation of Respirations:
 Still with tachypnea
 Coarse bronchial sounds
 Retractions
 Barrel chest
 Blood gases reveal poor gas exchange
 Chest radiograph shows bilateral coarse
infiltrates, hyperaeration
 Diaphragm pushed downward by the over-
expanded lungs
 Difficulty establishing respirations at
birth.
THERAPEUTIC MANAGEMENT:
PRIOR TO BIRTH:
1. Amnioinfusion to dilute amount of
meconium in amniotic fluid.
 Reduce risk of aspiration.
2. Some infants scheduled to be born by
cesarean birth.
 If deeply meconium-stained during
labor.
DURING OR AFTER BIRTH:
3. Suction, oxygen administration, and
assisted ventilation.
 At perineum if meconium-stained AF
to prevent aspiration and intubate
for severe staining and no oxygen
yet, then oxygen, then maintain
ventilation.
4. May start antibiotic therapy and
administer surfactant.
 For pneumonia and lung compliance.
5. Maintain temperature-neutral
environment.
 To prevent increasing O2 demand.
6. Perform chest physiotherapy.
 Removal of remnants of meconium
from lungs
7. Some maintained on ECMO.
 Ensure adequate oxygenation.
8. SUDDEN INFANT DEATH SYNDROME (SIDS)
 A sudden unexplained death in infancy who
die quietly while asleep at a peak age of 2 to
4 months.
 Autopsy often reveals petechiae in the lungs
and mild inflammation and congestion in
the respiratory tract.
 Well-nourished, no sound so
laryngospasm, blood-flecked sputum
or vomitus in mouth.
It tends to occur at a higher-than-usual rate in
infants:
1. of adolescent mothers.
2. of closely spaced pregnancies.
3. who are underweight and preterm.
4. with bronchopulmonary dysplasia.
5. born twins.
6. of Native-American and Alaskan parents.
7. who are economically disadvantaged.
8. of narcotic-dependent mothers.
 SIDS may be because of prolonged,
unexplained apnea. Although its exact
cause is unknown.
Recommendations to decrease incidence of
SIDS:
1. Positioning infant to sleep on back.
2. Offering pacifiers while asleep.
3. Putting on a fan in infant’s room to keep air
moving.
4. Using an apnea monitor while sleeping.
 According to the American Academy of
Pediatrics, compliance to the following
recommendations caused a decline in the
incidence of SIDS by 50%.
9. HEMOLYTIC DISEASES OF THE NEWBORN
 An Abnormal RBC destruction in the
newborn caused by mother’s build-up of
antibodies.
 Leads to severe anemia and
hyperbilirubinemia.
 Hemolytic means destruction of RBCs, but RBC
destruction is a normal physiologic process.
1. Newborn – fetal RBCs only last for 90 days
2. Adult – every 120 days
 During these days, normal RBC breakdown
occurs, but if there is abnormal destruction, that
is when hemolysis occurs.
Newborn Hemolytic Diseases:
1. RH INCOMPATIBILITY
 If mother’s blood type is Rh (D)
negative and fetal blood type is Rh
positive, which contains the D
antigen, the introduction of fetal
blood causes sensitization to occur,
where woman begins to form
antibodies against the D antigen.
 Mommy Rh (-) and baby Rh (+).
When Sensitization Can Occur:
1. During pregnancy, an occasional
placental villi break and a drop or two
of fetal blood does enter the maternal
circulation.
 Theoretically, there is no direct
connection between fetal and
maternal circulation, so no fetal
blood cells should enter the
maternal circulation….. Few
antibodies form this way, however.
2. First 72 hours after birth when there
is an active exchange of fetal and
maternal blood as placental villi
loosen.
 The second case is the most
common form when sensitization
occurs in the….. After several years,
when the woman becomes
pregnant for the second time, there
is already a high level of antibody
D circulating in the woman’s blood
which was formed after the first
pregnancy’s sensitization. This will
now destroy the new fetal red
blood cells if the new fetus is Rh
positive again. In this case,
subsequent pregnancies are most
often affected.
ASSESSMENT:
COOMB’S TEST
1. Indirect. Rising anti-Rh titer or rising level
of antibodies in a woman during pregnancy.
2. Direct. Detecting antibodies on fetal
erythrocytes in cord blood or at birth.
 May or may not appear pale.
 Accelerated production of RBCs during the
last few months in utero compensates to
some degree for the destruction.
 Progressive jaundice within 24 hours of
life, seen more among breast-fed
newborns due to pregnanediol.
 Hemolytic process is at work for both Rh
and ABO while P is a breakdown product
of progesterone, interfere with IB to DB,
excreted in breast milk 24 to 48 hours
after birth.
 Liver or spleen may be enlarged.
 Attempt to destroy damaged RBCs.
 Extreme edema.
 RBC decreases, blood may be hypotonic to
interstitial, fluid shift from lower to higher
isotonic pressure by osmosis, causing
extreme edema.
 Heart failure from severe anemia.
 Heart has to beat fast to push dilute blood
forward
 Hydrops fetalis is old term for the
appearance of a severely involved infant at
birth. Hydrops is edema and fetalis is
lethal state.
MANAGEMENT:
1. Intrauterine transfusion to combat red cell
destruction.
2. Preterm labor may be induced to remove the
fetus from the destructive maternal
environment.
3. Administering phenobarbital to women
during the last weeks of pregnancy to reduce
symptoms in newborns as it speeds liver
maturity to better convert indirect to direct
bilirubin, but carries risk of fetal sedation.
4. Administering Rho(D) immune globulin,
RhoGAM IM/IV, at least one dose between 26
to 28 weeks AOG and an additional dose
within 72 hours after delivery.
2. ABO INCOMPATIBILITY
 Hemolysis occurs mostly when mother is
blood type O and fetus is either A, B, or AB.
 Antibodies to A and B blood types are
present from birth in newborns whose red
cells lack these antigens.
 Infant is not born anemic as RBC
destruction begins at birth and may
continue up to 2 weeks, jaundice and
pallor occurs within 24 hours.
 Mommy is O and fetus is A (most
common), B (most serious), or AB.
 Blood and antibodies are exchanged
during mixing of maternal and fetal blood
as placenta is loosened, reaction is less
severe than Rh, first born is affected.
 These ABs are large IgM class and does not
cross placenta, breastfed babies show
more jaundice than bottle-fed due to
pregnanediol.
THERAPEUTIC MANAGEMENT OF HEMOLYTIC
DISEASES
1. Initiation of Early Feeding
 Bilirubin removed into feces so early
feeding stimulates bowel peristalsis.
2. Phototherapy
 Light activates liver to convert IB to DB.
3. Exchange Transfusion
 Alternating hypovolemia and
hypervolemia, 1 to 3 hours procedure.
10. NECROTIZING ENTEROCOLITIS (NEC)
 The infant’s bowel develops necrotic
patches from ischemia of intestinal blood
vessels from hypoxia.
 Develops in about 5% of all infants in
intensive care units, with average onset of
about 4 days.
 Escherichia coli or Klebsiella
pneumoniae, interferes with digestion
and leads to a paralytic ileus.
 Highest in preterms, with gastric tubes and
ventilators.
ASSESSMENT:
 Distended and tense abdomen.
 Stomach does not fully empty, may aspirate
undigested milk.
 Stool may be positive for occult blood.
 Periods of apnea may begin or increase in
number.
 Lowered blood pressure.
 Inability to stabilize temperature.
 Abdominal x-ray films show picture of air
invading intestinal wall, air in abdominal
cavity if with perforation.
 Abdominal girth measurements increase
every 4 to 8 hours.
 Lower incidence in breastfed, intestinal
organisms grow more profusely with cow’s
milk and lacks antibodies, response to foreign
protein in cow’s milk starts the necrotic
process.
THERAPEUTIC MANAGEMENT:
 1. Start with IV or total parenteral nutrition
to rest GI tract.
2. An antibiotic may be given to limit
secondary infection.
3. Perform surgery to remove area of
necrosis in the bowel.
11. NEWBORNS FROM DIABETIC MOTHERS
ASSESSMENT:
 Greater chance congenital anomaly such as
cardiac anomaly.
 Caudal regression syndrome, hypoplasia of
the lower extremities.
 Typically longer and weighs more than
other babies, macrosomia.
 Cushingoid appearance.
 Often immature, may have signs of
respiratory distress.
 Lethargic or limp in the first days.
 Loses great portion of weight in the first
few days of life because of loss of extra fluid
from utero.
Hyperglycemia in utero:
1. Is teratogenic to a rapidly growing fetus.
2. Stimulates high fetal insulin secretion causing
overstimulation of GH and extra fat deposits.
3. Interferes with cortisol and blocks formation
of lecithin so lack of surfactant causes
immaturity.
COMPLICATIONS AND MANAGEMENT:
Greater chance of birth injury, especially
shoulder and neck injury.
 Cesarean birth to avoid cephalopelvic
disproportion (CPD).
Severe hypoglycemia, less 45 mg/dL.
 Feed early with formula or continuous
infusion of glucose.
Hyperbilirubinemia.
 Since immature, cannot effectively clear
bilirubin from their system so need to start
phototherapy.
Hypocalcemia.
 Due to low parathyroid hormones from
excessive renal losses of magnesium, can
give IV calcium gluconate.
12. NEWBORNS FROM DRUG-DEPENDENT
MOTHERS
 Infants of drug-dependent women tend to
be small for gestational age (SGA).
 Will show withdrawal symptoms upon
birth but onset and duration varies among
different substances, maybe in 24 to 48
hours up to 10 days.
MANAGEMENT:
1. Keep newborn in an environment free
from excessive stimuli.
2. Maintain fluid and electrolyte balance is
essential. If with vomiting or diarrhea,
intravenous administration may be
indicated.
3. Start drugs used to counteract withdrawal
symptoms such as paregoric,
phenobarbital, methadone,
chlorpromazine (Thorazine), and
diazepam (Valium).
4. Avoid breastfed to prevent passing
narcotics in breast milk to the child.
FETAL ALCOHOL EXPOSURE
 Alcohol crosses placenta in the same
concentration as is present in the maternal
bloodstream, this results in fetal alcohol
exposure and fetal alcohol syndrome.
 The syndrome appears in about 2 per
1000 newborns and is often more difficult
to document than recreational drug
exposure.
 Alcohol has an unknown safe threshold of
ingestion during pregnancy and may cause
deteriorating impact on the placenta and
teratogenic effects to newborn.
CHARACTERISTICS:
 Prenatal and postnatal growth restriction.
 Central nervous system involvement such
as cognitive challenge, microcephaly, and
cerebral palsy.
 Distinctive facial feature of a short
palpebral fissure and thin upper lip.
 During the neonatal period, an infant may
be tremulous, fidgety, irritable,
demonstrate weak sucking reflex, and have
sleep disturbances.
 Behavior problems such as hyperactivity
may occur in school-age.

 Parents must prepare for long-term care.