NEWBORN/NICU REVIEW
THE NORMAL NEWBORN INFANT
Delivery Room Management
1.
The cold stressed newborn rapidly depletes essential stores of fat and
glycogen. The newborn is prone to heat loss (conductive, convective and
evaporative) because of high surface area-body mass ratio. Heat loss in the
delivery room can be reduced by the use of radiant warmers, drying and
swaddling.
2.
Radiant warmers allow the infant to use calories for growth rather than for
heat maintenance. Skin temperature is best measured with the skin probe
over the EPIGASTRUM. If the probe loses contact with the skin, the
warmer produces excessive heat. There is insufficient heat production if
the infant or probe is covered by a blanket, placed over the liver, or the
skin set point is below the neutral thermal point (the temperature is which
the least amount of calories is required for thermoregulation).
3.
The Apgar score components: heart rate, respiratory effort, tone, reflex
and color.
4.
The significance of the ONE and FIVE minute Apgar scores
a.
b.
c.
d.
e.
The 1 minute Apgar is not predictive of later neurologic problems.
A five minute Apgar of less than 6 is associated with later evidence
of neurological injury. The 10, 15, and 20 minute Apgar are the
most reliable predictors of outcome especially for IVH and
respiratory distress.
An Apgar score of 3 or less prolonged for more than 5 minutes is
regarded as asphyxia. HOWEVER a low Apgar score in a preterm
or SGA infant (6 or 7) is considered normal (they all have low tone
by definition).
Low Apgar may present in non-asphyxiated infants with
depression
to maternal medications, trauma, metabolic or
infectious disease, CNS, cardiac or pulmonary malformations.
A preterm infant usually has an Apgar score of <7 due to decreased
tone impaired reflex irritability and irregular respiratory drive.
A preterm Apgar of 6 is equivalent to a full term Apgar of 9-10.
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5.
THE NORMAL NEWBORN CAN FIXATE (but vision is about 20/4000)
Fetal Assessment
1.
The non-stress test monitors fetal heart rate reactivity in response to fetal
activity, particularly intact fetal brainstem function. Over a 20 minute
period, a reactive non-stress test shows at least two accelerations of the
fetal heart (fifteen beats/min above baseline lasting at least fifteen
seconds. The stress test is used to evaluate uteroplacental insufficiency.
An adequate stress test has at least 3 contractions lasting at least 40-60
seconds during a 10-minute time period. If contractions do not occur then
the mother is instructed to stimulate her nipples or given oxytocin. No
decals should occur.
2.
The biophysical profile used by OBs to evaluate fetal well-being prior to
birth includes: gross body movements, fetal tone, fetal breathing
movements, reactive nonstress test, and qualitative amniotic fluid volume.
US is used. 8-10 is considered normal. 4-6 indicates possible fetal
compromise and 0-2 predicts high perinatal mortality.
3.
Fetal dysrhythmias
a.
Normal fetal heart rate is 120-160 bpm.
b.
Decelerations

Early decels are related to the onset of a contraction. The
fetal head is compressed which leads to increased
intracranial pressure => a vagal response => decrease in
FHR. It is usually of no consequence.

Late decels occur after the contraction. It indicates
uteroplacental insufficiency and fetal distress.
Management includes changing mother’s position,
applying oxygen to the mother, stopping oxytocin if
uterine hyperstimulation is suspected, or starting a
tocolytic to stop contractions.

Variable decels can occur before, during or after a
contraction. This is secondary to cord compression. It
may indicate fetal distress when prolonged and
associated with bradycardia. Changing the position of the
mother may help.
Transition
1.
2.
Physical and behavioral characteristics of the preterm, full term and postterm infants. See new Ballard chart attached.
Preterm is defined as <37 weeks gestation. Full term is defined as 37-41
6/7 weeks gestation. Post-term is defined as >42 weeks gestation.
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3.
SGA is defined as a weight less than the 10th percentile or 2 SD below the
mean weight for gestational age. SGA is seen in infants of mothers with
hypertension, pre-eclampsia or tobacco use, as well as TORCH infections.
4.
AGA is defined as weight in the 10th to 90th percentile.
5.
LGA is defined as weight greater than the 90th percentile or 2 SD above
the mean weight for gestational age. LGA is seen in infants of diabetic
mothers, in Beckwith syndrome, and in hydrops fetalis.
6.
Remember, when using the growth curves, plot anthromorphic measures
against gestational age.
Routine Care
1.
Hemorrhagic Disease of the Newborn
a.
Occurs in 1 of every 200-400 neonates not given Vitamin K
prophylaxis.
b.
Vitamin K is necessary for the function of factors II, VII, IX, X
and proteins C and S.
c.
The platelet count is normal but the PT is prolonged in
disproportion to the PTT. It usually presents within the first 48
hours with bleeding and bruising (skin, GI tract, head bleed).
d.
HDN is related to decreased placental transfer of maternal Vitamin
K. It can also be related to breast feeding since there is less
Vitamin K in breast milk vs. cow’s milk.
e.
Treatment: 10 cc/kg of FFP and Vitamin K 1 mg IV.
f.
Maternal drugs which predispose to HDN: phenytoin, primodone
(similar to phenobarb), methsuximide (anti-epileptic), and
Phenobarbital. Drug exposed infants usually present within the
first 24 hours of life => if mom is on any of these drugs, she
should receive Vitamin K 24 hours PTD and the baby should
receive Vitamin K at birth and again 24 hours later.
g.
Delayed hemorrhagic disease of the newborn can occur at 4-12
weeks of age. Risk factors include: treatment with antibiotics
(which decreased Vitamin K absorption), infants with a
malabsorption (liver dx, CF), and breast fed infants who did not
receive Vitamin K prophylaxis.
2.
Ophthalmia Neonatorum
a.
Definition: Inflammation of the conjunctiva within the first month
of life.
b.
Causes: chemical conjunctivitis, bacterial (Neisseria gonorrhea,
Chlamydia trachomatis, Staphylococci, Pneumococci,
Streptococci, E. Coli and other GNRs), and herpes virus.
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c.
Treatments:
1.
N. Gonorrhea – conjunctivitis with chemosis, purulent
exudates and lid edema starting 1-4 days after birth.
There may also be clouding or perforation of the cornea.
Complications: scalp infections, anorectal infection,
sepsis, arthritis, and meningitis. Treatment includes
cefotaxime or ceftriaxone for 7 days if the infection is
local. With disseminated disease, treatment extends to 1014 days.

In a mom with untreated GC, the infant
should receive one dose of abx as well as
topical prophylaxis.

Prophylaxis of ocular gonorrheal infection
should include silver nitrate solution in
single dose ampules or single-use tubes of
ophthalmic ointment containing
erythromycin or tetracycline.
2.
C. Trachomatis is the MOST COMMON cause of
infectious conjunctivitis. It usually presents 5-14 days
after birth with minimal swelling and rare corneal
involvement. Diagnosis is by DFA, ELISA, or DNA
probes. REMEMBER silver nitrate is not adequate
prophylaxis for neonatal chlamydial conjunctivitis.
Treatment should include 14 days of crythromycin. This
can eradicate the organism from the upper respiratory
tract and limit the risk of Chlamydial pneumonia.
3.
Caloric requirements per kilogram for adequate growth is greater in
preterm infants. Preterm infants also have a greater daily fluid requirement
per kilogram of body weight than full term infants. Remember that
insensible loss is increased with prematurity, phototherapy, and the use of
radiant warmers.
4.
Most newborns urinate within the first 12 hours of life. 93% urinate by 24
hours, 99% by 48 hours. If a newborn doesn’t urinate within 24 hours,
consider the Crede’s maneuver to compress the bladder or catheterization.
A workup including serum electrolytes and a U/S should be performed.
THE MOST LILKELY EXPLANATION IS AN UNDOCUMENTED
VOID IN THE DELIVERY ROOM. Other causes include: UPJ (the most
common cause of hydronephrosis), hypovolemia, neurogenic bladder, and
posterior urethral valves. (males only)
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5.
Preterm infants have a lower hematocrit than full term infants. The normal
hematocrit for a newborn infant is 56%(51 +/- 4.5). The H/H of a full term
newborn is fairly stable for weeks 1-3. After that, the Hgb falls about 1
mg/del per week until the nadir is reached at 7-9 weeks. Also, the timing
of the physiologic anemia in the full term infant differs from the preterm
infant.
a. The Hgb nadir occurs earlier in the preterm
infant because of 1) decreased RBC survival,
2) more rapid rate of growth and 3) Vitamin E
deficiency which causes shorter RBC survival.
b. Term nadir (Hgb=9.5-11) at 8-12 weeks
c. Premature nadir of 1200-1500 grams (Hgb=810) at 5-10 weeks
d. Premature nadir of <1200 grams (Hgb=6.5-9) at
4-8 weeks
***Remember, capillary samples have slightly
higher results for the H/H compared with venous
samples, sometimes up to 20%!***
6.
Blood pressure values vary directly with gestational age, postnatal age of
the infant, and birth weight.
7.
Bilirubin Metabolism & Jaundice
a.
Bilirubin metabolism
1.
The heme ring is oxidized in the RES to biliverdin by
heme oxygenase. This reaction releases CO and iron.
Biliverdin is then reduced to bilirubin by the enzyme
biliverdin reductase.
2.
Bilirubin is transported to liver cells bound to albumin.
Conjugation occurs in the liver by uridine diphospate
glucuronyl transferase. Deficiencies of this enzyme lead
to Crigler-Naijar Syndrome and Gilbert’s Syndrome and
cause hyperbilirubinemia in the newborn.
3.
Excretion of conjugated bilirubin takes place in the GI
tract and to some extent in the urine. Abnormalities that
decrease stooling frequency such as Hirschsprung’s
disease lead to unconjugated hyperbilirubinemia.
b.
Physiologic Jaundice
1.
Full term infant bilirubin peak at 6-8 mg/dl by 3 days of
age….a rise to 12 is still considered physiologic.
2.
Preterm infant bilirubin peak at 10-12 mg/dl on the 5th
day of life with a rise up to 15 mg/dl still considered
physiologic.
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3.
4.
c.
8.
Guidelines for the Use of Phototherapy (see handout).
Physiologic Jaundice is due to:
a. Increased RBC volume/kilogram and decreased
RBC survival
b. Increased ineffective erythropoiesis and
increased turnover of non-hemoglobin heme
proteins.
c. High levels of intestinal beta-glucuronidase
causing increased enterohepatic circulation.
d. Immature conjugation due to decreased
UDPG-T activity in the liver.
Nonphysiologic Jaundice
1.
Any onset of jaundice before 24 hours of age
2.
Any elevation requiring phototherapy
3.
A rate of rise greater than 0.5 mg/dl/hour
4.
Jaundice persisting after 8 days in the term infant and 14
days in the preterm infant
5.
The differential diagnosis of negative Coom’s and direct
hyperbilirubinemia includes: 1) hepatitis 2) biliary
obstruction 3) sepsis 4) galactosemia 5) alpha-1
antitrypsis deficiency 6) cystic fibrosis 7)
hyperalimentation 8) syphilis 9) hemochromatosis
Causes of decreased serum thyroxine concentration in term and preterm
infants include:
a.
Hypothyroxinemia of prematurity is immaturity of the
hypothalamic portion of the hypothalamic pituitary thyroid axis.
Lack of TRH leads to decreased TSH and T4.
b.
Sick euthyroid syndrome – nonthyroidal illness increases reverse
triiodothyronine. Deiodination of T4 produces T3 and rT3. In sick
preterm infants, the predominant triiodothyronine is rT3, the
inactive metabolite of thyroid hormone, which explains the low
thyroid hormone activity.
c.
In preterm infants, there is an obtunded surge of thyroid hormone
activity (compared with full term infants). It spontaneously
resolves in 4-8 weeks.
d.
Excessive topical application of iodine containing antiseptics is
also a potential cause of iodine induced transient
hypothyroxinemia.
e.
The use of thyroid hormone replacement therapy in premature
infants is controversial.
6
9.
PKU screening: the utility and limitations
a.
Newborn screening of PKU relies on the detection of elevated
levels of blood phenylalanine. Prenatally, fetal phenylalanine
crosses the placenta and is metabolized by the mother =>a
newborn with PKU will not initially have hyperphenylalaninemia.
b.
Phenylalanine levels begin to rise only after feeding has been
established and may not be detectable in the first 24 hours=>with
infants discharged within the first 24 hours, follow up within 2-3
days including repeat NBS is necessary.
10.
The recommended methods of umbilical cord care include local
application of triple dye or antimicrobial agents.
11.
Most infants stool within 48 hours. The delayed or absent passage of
meconium is associated with colonic obstruction due to meconium plug
syndrome, Hirshsprung disease, and imperforate anus. It is also due to
ileal atresia, malrotation, or maternal use of magnesium sulfate.
12.
Bilious vomiting is a common finding in infants with small bowel
obstruction.
13.
Bottle fed vs. breastfed infants=>differences in stooling and frequency
a.
Breastfed infants have stools that are more yellow and seedy.
b.
Breastfed infants stool more often than bottle fed infants.
14.
The rapid assessment of whole blood glucose concentrations (glucose
oxidase test strips) may yield falsely high or low values.
a.
Falsely elevated results can be due to high levels of fructose or
galactose or a sample contaminated with glucose containing
solution.
b.
Falsely decreased results usually occur due to shortened retention
time on the test strip.
15.
Remember, there should be close follow-up with any newborn discharged
early.
a.
Early hospital discharge is defined as the discharge of a newborn
earlier than 48 hours following vaginal delivery and 96 hours
following cesarean delivery. (at Duke it is 72 hours – could not
find info on this).
b.
The most common reason for readmission is hyerbilirubinemia
since peak serum bilirubin is not reached until DOL 3.
c.
The age of the infant at the time of newborn screening is also
critical.
d.
Many congenital heart defects (esp. ductal dependent lesions) may
not be detected clinically during the first 24 hours of life.
e.
With the exception of late onset meningitis, most newborns with
bacterial sepsis are symptomatic within 8 hours after birth when
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f.
g.
respiratory symptoms predominate. (Risk factors for sepsis
include: low birth weight, prolonged rupture of membranes, and
chorioamnionitis).
A newborn should not be discharged until two feeds have been
taken with coordinated suck and swallow and at least one stool has
passed.
All infants discharged early should have follow up within 72
hours.
16.
Home birth is associated with many clinical problems, especially Vitamin
K deficiency.
a.
Vitamin K IM given in the hospital helps prevent hemorrhagic
disease of the newborn (see above for further information).
b.
Classic Vitamin K deficiency can present with melena, large
cephalohematoma, intracranial hemorrhage, and bleeding from the
umbilical stump, injection sites, and after circumcision.
c.
Bleeding is most often seen during the second to seventh days of
life in healthy breastfed infants. Formula fed infants receive
enough vitamin K in their formula so this is rarely seen.
d.
Early Vitamin K deficiency within the first 24 hours is usually
related to maternal medication, most often anticonvulsants. Late
Vitamin K deficiency (2-8 weeks) is linked with compromised
supply of Vitamin K, as seen in diarrhea, cystic fibrosis, hepatitis,
and celiac disease.
17.
Understand the use of otoacoustic emission (OAE) devices for neonatal
hearing screens. This is used as a screening tool and can detect hearing
loss down to 30-40 dB. OAE’s originate from the hair cells in the cochlea
and travel through the middle ear to the external auditory canal where they
are detected by little microphones. Otitis media and congenital
abnormalities of the ear can incorrectly identify cochlear dysfunction so a
failed OAE must be followed by a BAER.
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THE ABNORMAL INFANT
General
1.
2.
Management of neonatal abstinence syndrome
a.
Classic presentation: SGA, irritable, inconsolable, generalized
hypertonia, posturng tremors, exaggerated startle responses, skin
excoriations, high-pitched cry, and uncoordinated suck and
swallow.
b.
With maternal opiate use, oral paregoric represents the most
physiologic treatment for the infant. It is administered every four
hours with a total daily dose of 0.8 to 2.0 ml/kg. Once stable, the
dose is tapered by 10% every 24 hours. It is discontinued at a dose
0.5 ml/kg….monitor for rebound symptoms!
c.
Manifestation of drug withdraw in the neonate can be remembered
by WITHDRAWAL:
W
wakefulness
I
irritability
T
tremulousness, temperature variation, tachypnea
H
hyperactivity, high pitched persistent cry, hyperacusis,
hyperreflexia, hypertonus
D
diarrhea, diaphoresis, disorganized suck
R
rub marks, respiratory distress, rhinorrhea
A
apneic attacks, autonomic dysfunction
W
weight loss or failure to gain weight
A
alkalosis (respiratory)
L
lacrimation
Know the differential diagnosis of lethargy and coma in a neonateinfection, asphyxia, hypoglycemia, hypercarbia, sedation from maternal
analgesia, or anesthesia, cerebral defects, inborn errors of metabolism, any
severe disease.
Resuscitation
1.
A newborn has established regular respirations by 1 minute of age.
2.
A newborn infant with a one minute Apgar of less than 3 requires positive
pressure ventilation. Remember, the initial lung inflation requires
increased pressure for the first breath.
3.
If meconium is present in the amniotic fluid, the mouth and hypopharynx
need to be suctioned. Suctioning should take place before the delivery of
the body. And, in addition to nasopharyngeal suctioning, the larynx needs
to be visualized and the trachea suctioned if thick or particulate meconium
is present in the amniotic fluid.
4.
If the infant’s heart rate does not increase above 80 beats per minute after
effective ventilation with oxygen has been established, external cardiac
massage is needed.
9
5.
Continued poor perfusion with pallor, cool extremities, and poor capillary
refill is often due to hypovolemia. The metabolic effects include:
metabolic acidosis, hypoxia, anaerobic glycolysis and hypoglycemia,
hypocalcemia, and production of lactic acid with an increased anion gap.
Very-Low Birth-Weight Infants
1.
VLBW infants may not achieve an Apgar >6 because of neurological
immaturity such as hypotonia and blunted response to noxious stimuli.
2.
Initial care includes monitoring of blood glucose and arterial oxygen
concentrations as well as maintenance of a thermoneutral environment
3.
Prognostic factors for VLBW infants:
a.
The most important determinant of neurodevelopmental outcome
in VLBW infants is length of gestation.
b.
Birth weight has also been associated with mental retardation and
CP.
c.
More recently, one third of the decline in mortality has been
attributed to better obstetric and delivery care => e.g.
administration of corticosteroids to improve fetal pulmonary
immaturity.
d.
Female gender is associated with a slightly lower risk of neonatal
morbidity and mortality.
e.
Maternal education and socioeconomic status may affect long-term
developmental outcome of VLBW infants.
Conditions & Diseases
1.
Asphyxia is the most frequent cause of neonatal seizure in the full-term
infant. Neonatal seizures secondary to asphyxia characteristically occur
within 24 hours of birth. Perinatal asphyxia is a frequent complication of
interuterine growth retardation.
2.
Polycythemia
a.
b.
c.
d.
e.
f.
A venous Hct over 65% or an arterial Hct over 63%.
The incidence increases with infants who are SGA or post dates.
Causes include: delayed cord clamping, cord stripping, holding the
baby below mom, maternal to fetal transfusion, twin-twin
transfusion, infants of diabetic mothers, placental insufficiency,
maternal use of propranolol, congenital adrenal hyperplasia,
trisomy 21, 13 or 18 and dehydration.
Clinical symptoms: poor feeding, lethargy, hypotonia, apnea,
seizure, cyanosis, tachypnea, CHF, hematuria, proteinuria,
thrombocytopenia, jaundice, and persistent hypoglycemia.
Newborns with polycythemia are at risk for hypoglycemia and
hyperbilirubinemia.
Treatment for symptomatic polycythemia is a partial exchange
transfusion. Asymptomatic infants with Hct=65-70 can receive
IVF followed by a repeat Hct in 4-6 hours.
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3.
Intracranial hemorrhage in the neonate
a.
In the term infant, the most common location is subarachnoid and
it is associated with trauma or asphyxia, as well as prolonged
second stage of labor, precipitous delivery, and forceps delivery.
b.
Presentation of subarachnoid hemorrhage: apnea, episodes of
cyanosis, persistent resting sinus bradycardia and seizures.
c.
Presentation of subdural hemorrhage: macrocephaly, frontal
bossing, bulging fontanelle, seizures, and anemia.
d.
Presentation of IVH: shock, metabolic acidosis, mottling, anemia,
coma, bulging fontanelle, and apnea, often in the 2nd or 3rd day of
life.
e.
Opisthotonos is rare but can be seen in subarachnoid, subdural and
IV hemorrhages.
f.
Diagnosis

Ultrasound is used to detect germinal matrix and
ventricular hemorrhages in the preterm infant.

CT scan is indicated in term infants when hemorrhage is
suspected (U/S doesn’t visualize the periphery or posterior
fossa well.)

Nontraumatic LP may show elevated protein and many
RBCs in a subarachnoid hemorrhage.
4.
SGA infants have higher neonatal mortality and are prone to fasting
hypoglycemia, polycythemia, and temperature instability.
5.
Normal arterial blood gas values for a newborn infants: PO=60-90
mmHg, PCO2=35-45 mmHg.
6.
Neonatal pneumonia can mimic idiopathic respiratory distress syndrome
a.
b.
7.
Abnormalities in WBC are useful in distinguishing GBS
pneumonia vs. RDS=>neutropenia is often seen in early
GBS….but the I:T ratio > 0.2. In RDS the I:T ratio is <0.2.
With RDS, the effects of surfactant administration include
decreasing pulmonary vascular resistance, increasing left to right
shunting across the ductus arteriosus, and potential development of
hemorrhagic pulmonary edema. Surfactant can reduce lung injury
and decrease the incidence of pneumothorax and pulmonary air
leads. Surfactant has also been shown to decrease the occurrence
of BPD, IVH, and ROP.
Neonatal thyrotoxicosis
a.
Graves disease complicates 1 in 1000 pregnancies. It is the most
common cause of neonatal thyrotoxicosis. Graves is an
autoimmune disorder that results in the production of antibodies
again thyroid antigens, most often the TSH receptor antibody.
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b.
c.
d.
e.
Thyroid stimulating immunoglobins readily cross the placenta and
cause neonatal thyrotoxicosis.
Clinical findings of fetal hyperthyroidism usually occur during the
2nd half of pregnancy. Thyrotoxicosis leads to tachycardia,
craniosynostosis, frontal bossing, and mental retardation.
Premature infants may have microcephaly, IUGR, irritability,
tachycardia, goiter, CHF, vomiting and diarrhea, FTT despite
hyperphagia, hypertension, and exophthalmos.
Lab findings include increased thyroxine and free T4 with
suppressed TSH.
Treatment is usually supportive…the length of the disease usually
last 2-3 months. In severe cases, PTU or methimazole may be
given to the infant. Propranolol is often used to control
tachycardia.
8.
Peripheral cyanosis is a common finding in healthy full-term infants.
9.
Persistent fetal circulation without Meconium aspiration is often difficult
to distinguish from cyanotic heart disease.
a.
b.
c.
10.
Cyanotic heart diseases without murmurs include transposition of
the great arteries and pulmonary atresia. No murmur is present but
there may be an abnormal 2nd heart sound and precordial impulse.
With persistent pulmonary hypertension (aka persistent fetal
circulation), there is cyanosis without evidence of a heart murmur.
PPHN occurs due to asphyxia, meconium aspiration, and sepsis.
With PPHN, if there is significant shunting of pulmonary arterial
blood into the descending aorta across a PDA, there may be
differential cyanosis of the feet with lower sats noted in feet vs. the
right hand. This helps differentiate PPHN from cyanotic heart
disease.
The typical presentation of a neonate with persistent pulmonary
hypertension after meconium aspiration includes:
a.
Full term or post dates.
b.
Prenatal history includes: fetal distress, low Apgar, amnionitis, and
oligohdamnios (if there is pulmonary hypoplasia).
c.
Usually presents from birth to the first 6 hours.
d.
Neonatal history includes: tachypnea, cyanosis, minimal
retractions, Meconium stained umbilical cord and fingernails, and
failure to suction below vocal cords.
e.
CXR may be normal or show Meconium induced pneumothorax,
pneumomediastinum, atelectasis, or marked hyperinflation.
f.
Labs may show polycythemia.
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11.
The full-term infant who has severe respiratory failure at birth that does
not respond to intubation and assisted ventilation most likely has persistent
pulmonary hypertension (PPHN). Evaluation/Management includes:
a.
Echocardiogram to rule out congenital heart disease.
b.
Initiate nitric oxide administration to vasodilate the pulmonary
vasculature. Adverse effects include: 1) methemoglobinema, 2)
nitric dioxide exposure and 3) platelet dysfunction.
c.
Bicarbonate administration to induce metabolic alkalosis. This
attenuates the hypoxic pulmonary vasoconstriction and improves
oxygenation.
d.
High frequency oscillation to minimize lung injury when
conventional ventilation fails to promote adequate gas exchange or
if the required PIP setting too high.
e.
Supportive measures: sedation, muscle paralysis, blood
replacement, maintenance of fluid/electrolyte balance.
f.
ECMO if the above fail.
**With assisted ventilation, pulmonary air leaks are common in
newborns**
12.
In suspected sepsis, particularly after premature prolonged rupture of
membranes, ampicillin and gentamicin are the most appropriate antibiotics
in the immediate newborn period.
a.
Most likely organisms include: GBS, E. Coli, Listeria
monocytogenes, H. Influenzae, and enterococci.
b.
Ampicillin covers gram positive organisms and gentamicin covers
gram negative organisms.
c.
There is an associated risk of sepsis with the use of umbilical
arterial catheters.
13.
Congenital Syphilis
a.
Major factors contribute to the occurrence of congenital syphilis
1.
No prenatal care
2.
Negative serologic test in the first trimester but the test
not repeated later in pregnancy…a question may state the
nontreponemal test was negative but the infant has classic
signs and symptoms of syphilis.
3.
Negative serologic test at delivery in a mom with syphilis
who has not yet converted.
4.
Lab error.
5.
Delay in treatment of a mom with syphilis.
b.
All pregnant women should be tested at the first prenatal visit and
again at 28 weeks.
c.
False positives of the non-treponemal test include: viral
exanthems, vaccinations, hepatitis, mononucleosis, IV drug use,
mycoplasma, TB and autoimmune diseases such as SLE or RA,
pregnancy.
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d.
e.
Signs and symptoms
1.
Persistent rhinitis, snuffles, rash, hepatosplenomegaly,
lymphadenopathy, anemia, DIC, jaundice, chorioretinitis,
osteochrondritis, peritonitis, IUGR, FTT
2.
THE MOST COMMON RASH: diffuse, copper-colored,
maculopapular, rash involving the hands and feet. Diffuse
vesicobullous lesions are less common but very
characteristic when seen. Raised, flat, moist, wart like
lesions (condyloma lata) in the anorectal region, nares, and
angles of the mouth may also be present.
Treatment of the infant
1.
Who should be treated: 1) Mother treated during last month
of pregnancy, 2) Mother treated with another antibiotic
besides Penicillin, 3) Mother’s titer did not drop fourfold,
4) symptomatic baby (snuffles, radiographic findings on
long bones, hemolytic anemia, thrombocytopenia)
regardless of mother’s treatment, 5) CSF suggests
infection.
2.
Treatment includes Penicillin for 10-14 days. If there is a
suspicion of disease but no proof, the infant may receive a
one-time dose of Penicillin IM.
14.
Congenital Toxoplasmosis
a.
Incidence: 0.1/1000
b.
The later in pregnancy the maternal infection occurs, the higher the
risk of vertical transmission to the infant. HOWEVER, the severity
of the disease is inversely proportional to the gestational age (most
fetuses infected during the first trimester die in utero or during the
neonatal period).
c.
The majority of infants (70-90%) with congenital toxoplasmosis
are asymptomatic in the neonatal period.
d.
Signs at birth include: a maculopapular rash, generalized
lymphadenopathy, hepatomegaly, splenomegaly, jaundice and
thrombocytopenia. Mirocephaly, chorioretinitis, and seizures can
develop.
e.
Treatment: pyrimethamine and sulfadiazine (or clindamycin if the
infant does not tolerate sulfadiazine).
15.
Necrotizing enterocolitis
a.
The presentation is more common in neonates convalescing from
the NICU than infants undergoing intensive care. Most infants are
not ventilated or on CPAP. NEC is more common in African
Americans. NEC usually presents within the first week of life or 37 days after initiating enteral feeding. Presentation includes
abdominal distention, ileus, increased gastric aspirates, labile
temperature, A & Bs, and bloody stools.
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b.
c.
d.
The age of onset is inversely related to the gestational age at birth.

An infant < 30 weeks gestation => 20 do at presentation

An infant 31-33 weeks gestation => 14 do at presentation

An infant > 34 weeks gestation => 5do at presentation
The radiographic finding of pneumatosis intestinalis is the
hallmark of NEC. Bowel wall thickening and the presence of
intraperitoneal fluid may also be seen. Linear or cresenteric
distribution of gas in the bowel wall in specific for NEC.
Intestinal stricture formation, esp. in the large intestine, is a late
complication of NEC.
16.
Small bowel obstruction vs. large bowel obstruction:
a.
Duodenal obstruction presents with vomiting (often bilious).
Abdominal distention is usually not a prominent feature.
Polyhydramnios may be present. Differential diagnosis includes:
duodenal atresia, annular pancreas, and malrotation with or without
midgut volvulus. The classic x-ray finding is the double bubble
(duodenal obstruction).
b.
Distal intestinal obstruction presents with a distended abdomen,
failure to pass meconium, and vomiting bilious material.
Differential diagnosis includes: ileal atresia, meconium ileus,
colonic atresia, meconium plug, and Hirshsprung’s disease.
17.
Meconium ilueus
a.
The 3rd most common etiology for small bowel obstruction.
b.
After the first few days of life, the infant has abdominal distention,
bilious vomiting, and respiratory distress.
c.
Differential diagnosis: Meconium plug syndrome, ileal atresia,
colonic atresia, intestinal pseudo-obstruction, Hirschsprung’s
disease
d.
Strongly associated with cystic fibrosis
e.
The radiograph can be diagnostic. There is a ground glass
appearance with dilation of the proximal small intestine and the
sentinel loop of small intestine. Minimal air fluid levels may be
visualized. A barium enema will show microcolon of the unused
large intestine.
f.
Treatment includes gastrografin or N-acetyl-cysteine enemas.
Surgery is rarely needed.
18.
Esophageal atresia with tracheoesophageal fistula
a.
Symptoms include copious oral secretions with episodes of coking,
coughing, and cyanosis within hours of birth.
b.
Diagnosis can be confirmed by placing a suction catheter in the
esophagus and doing plain AP and lateral radiographs.
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19.
Infant of a Diabetic Mother
a.
The pathogenesis of hypoglycemia is due to increased pancreatic
insulin secretion.

Maternal hyperglycemia is paralleled by fetal
hyperglycemia => this leads to pancreatic beta cell
hypertrophy and hyperplasia => resulting in increased
insulin secretion.

After delivery, the transfer of glucose from mother to
infant is interrupted. The hyperinsulinemic infant becomes
hypoglycemic.
b.
An infant of a diabetic mother is at risk for hypoglycemia,
hypocalcemia, polycythemia, jaundice, caudal regression
syndrome, macrosomia, visceralomegaly, and neonatal small left
colon syndrome.
c.
Management includes frequent accuchecks and glucose containing
IVF until the hypoglycemia resolves.
20.
Effects of drugs given to mom during labor and the effects on the fetus
a.
Beta adrenergic tocolytics can cause pulmonary edema and
hypotension in the mother.
b.
Prostaglandin synthetase inhibitors (e.g. indomethacin)

Effects on the mother include a coagulopathy due to
increased bleeding time.

In the newborn, there could be premature closure of the
PDA.
c.
Magnesium sulfate

Respiratory arrest can be seen in the mother.

There may be respiratory depression or hypotonia in the
newborn.
d.
Opiates can lead to apnea and hypotension in the newborn.
21.
Association of maternal use of drugs and any fetal effects.
a.
Alcohol: Fetal alcohol syndrome => growth retardation, neurologic
abnormalities, cardiac defects, craniofacial dysmorphology, renal
anomalies, and impairment in mental and motor function.
Spontaneous abortions and alcohol withdrawal syndrome can
occur.
b.
Marijuana: May impair fetal growth and cause acute
nonlymphoblastic leukemia.
c.
Tobacco: dose related risk of low birth weight, decreased placental
blood flow, decreased fetal breathing movements, stillbirth,
neonatal death and SIDS.
d.
Opiates: May cause respiratory depression and withdrawal
syndrome.
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e.
f.
g.
Amphetamines: with abuse, it causes increased incidence of
preterm labor, placental abruption, fetal distress, postpartum
hemorrhage, IUGR, feeding difficulties, drowsiness, and lassitude.
Barbituates: Limb anomalies, nail hypoplasia, low nasal bridge,
hypertelorism, and short nose (similar effects to hydantoin, and
anticonvulsant.
Cocaine: cardiac anomalies, skull defects, GU abnormalities, prune
belly syndrome, intestinal atresias, cerebral infarctions, NEC
retinal disgenesis and retinal coloboma. NO DYSMORPHIC
FACIAL FEATURES!! Infants have 3-7 times higher risk of
SIDS.
22.
Recognize that intrapartum asphyxiation can cause injury to multiple
organ systems (eg. kidney, lung, intestine, liver, brain, heart)
23.
Understand the risk of sepsis from the use of an umbilical arterial catheter.
Sterile technique should be used and the catheter should not be advanced
once placed.
24.
Recognize that perinatal infection with cytomegalovirus may be acquired
in utero, during delivery, or in the neonatal period (eg. breast milk, blood
transfusion. The period of greatest fetal risk and neurologic impairment is
the first 22 weeks gestation. 1-2% of babies are born with CMV and 10%
are symptomatic. Symptomatic infant morality rate is 20-30%. More
common with maternal primary infection.
25.
Recognize the signs and symptoms of symptomatic congenital
cytomegalovirus disease. Subclinical disease is 10 times more likely than
clinical illness. Low birth weight and SGA. Classic disease-rare. IUGR,
hepatosplenomegaly w/jaundice, abnormal LFT’s, thrombocytopenia w/ or
w/o purpura, microcephaly, intracerebral calcifications, chorioretinitis,
progressive sensorineural hearing loss (10-20%), hemolytic anemia,
pneumoitis. By 2yo, asymptomatic infants may develop hearing loss and
ocular abnormalities.
17