based on 2

1. Fetus and Newborn Infant
♦Normal Newborn Infants
o Delivery room management
 Know that a newborn infant who is cold stressed rapidly depletes essential stores of fat
and glycogen
 Know that heat loss in the delivery room can be reduced by use of radiant warmer,
drying and swaddling
 Recognize the hazards and benefits associated with the use of radiant warmers for
neonates
• Benefits: decrease heat loss
• Hazards: increase water loss
 Know that a normal newborn infant can fixate
 Know the components of the Apgar score
• Activity
• Pulse
• Grimace (reflex irritability)
• Appearance (skin color)
• Respiration
 Know the significance of the one and five minute Apgar scores
• One minute Apgar score indicates the infant’s intrauterine environment and
tolerance of the delivery process
• Five minute Apgar score reflects the success of the infant’s transition
• Infants with a 5-minute score of 7 or less are at risk for suboptimal transition and
may require closer observation
• Infants with a 5-minute of 3 or less need very careful monitoring and observation,
likely the NICU
• Ability of an infant to maintain temp, HR, RR generally indicate a successful
transition
o Fetal Assessment
 Know that the nonstress test monitors fetal heart rate reactivity in response to fetal
activity
• This tests the fetal autonomic nervous system integrity
• The nonstress test is the initial eval done to look for fetal HR, short and long term
fetal HR variability, and reactivity to any fetal movement
 Recognize that the stress test is used to evaluate uteroplacental insufficiency
• Measures fetal HR response to uterine contractions, and is therefore able to
assess uteroplacental sufficiency and tolerance of labor
 Understand the significance and plan the management of dysrhythmias
• Arrhythmias are detected in about 1% of all fetuses and may be quite benign;
when they are sustained they are categorized as brady or tachycardic as follows
• BRADYCARDIC:
∗ Complete heart block
 One etiology of these is due to exposure to maternal antibodies
(SS-B/La antigens) and seen most commonly in maternal
autoimmune disorders like SLE
• TACHYCARDIC:

2. ∗ Atrial tachys: a. flutter, a. fib, SVT
∗ Persistent tachycardia can cause myopathy that might lead to heart failure
and to nonimmune hydrops
∗ When tx is required for control it can often be administered to the mother
and then it is transferred across the placenta and txe the fetus
∗ Preferred over preterm delivery or umbilical artery catheterization
o Maternal screening
o Transition
 Recognize the need to plot anthropomorphic measurements against the gestational age
on a graph
• Helps to assess whether the baby is outside the 95% range (either small or large),
and this can help guide further workup/management/treatment
 Know the physical and behavioral characteristics of the preterm infant
• Physical: thin, moist, transparent skin, flattened thin ears without cartilage or
recoil, small phallus and empty scrotum (if male)
• Behavioral: low muscle tone, relative inactivity, absence of flexed posture,
random, purposeless flailing of extremities in response to tactile stimulation
 Distinguish between small for gestational age and preterm gestation in low birth weight
infants
• SGA means that they are underweight for their gestational age;
∗ Term SGA infants have a greater risk for neurodevelopmental disability in
preschool years and beyond than compared with term appropriately
grown infant peers; risk is predicted by serial neurodevelopmental testing,
and is better predictive in the preschool age than earlier (i.e. better
predictive based on outcomes from age 3-5)
• Preterm infants can be AGA but LBW – meaning that if their weight is adjusted for
their GA it will be appropriate, but their actual birth weight is still considered low
• LBW = any baby born weighing <2500g
• SGA = any baby who is below the 10th percentile for their GA
 Know the physical and behavioral characteristics of a full term infant
• Physical: pink and chubby
• Behavioral: alert, able to fixate visually, normal muscle tone and reflexes
 Know the physical and behavioral characteristics of a post-term infant
• Physical: decreased subQ tissue, dry and peeling skin, wrinkled skin and sparse
hair
o Routine care
 Plan appropriate evaluation of an infant with physiologic breast hypertrophy
• Not necessary
 Recognize that maternal exposure to drugs that may affect coagulation and can result in
early hemorrhagic disease of the newborn
• Drugs that affect it are certain anticonvulsants, antibiotics and anticoagulants
taken during pregnancy
• Usually due to causing a vit K deficiency in the baby
• Can manifest as cephalohematoma, often accompanied by bleeding at unusual
sites
• All babies should get Vit K at birth
 Recognize the caloric requirement per kg for adequate growth is greater for preterm

3. infants than for full term infants
 Recognize that preterm infants have a greater daily fluid requirement per kg of body
weight than term infants
 Recognize that insensible water loss is increased by prematurity and use of radiant
warmers
 Recognize that the rapid assessment of whole blood glucose concentrations may yield
falsely high or low values
• Can be due to methodologic errors/incorrect technique, etc
 Know the normal range of the hct for newborn infants
• Term newborn has Hct of about 61%; hgb is about 19.3
 Recognize that preterm infants have lower hct than term infants
• Begin with lower baseline hct and hgb and also lower Fe stores
 Distinguish between the timing of physiologic anemia of the term and preterm infant
• Term infants have their nadir at about 8-12 weeks of age
• Preterm infants have their nadir between 3-8 weeks of age
 Recognize the presenting signs and sx of congenital syphilis
• Congenital syphilis is contracted by transplacental transmission of the spirochetes
and can occur at any stage of pregnancy, more commonly when the mother has a
primary or secondary infection rather than latent infection
• Early congenital syphilis:
∗ Liver manifestations: HSM, jaundice, elevated LFTs, bile stasis
∗ Hematologic: LAD, Coombs negative hemolytic anemia, TCP due to
platelet consumption in the spleen
∗ Mucous membrane involvement: mucous patches, rhinitis (“snuffles”),
condylomatous lesions
∗ Musculoskeletal disease: osteochondritis, pseudoparalysis of Parrot (won’t
move a limb due to pain), periostitis
∗ CNS abnormalities, FTT, choreoretinitis, pancreatitis and renal disease are
also possible
∗ Per a question critique, important to know that early physical signs of
congenital syphilis are hydrops fetalis, IUGR, HSM, hemolytic anemia,
jaundice, maculopapular rash, and radiographic findings of lines of
arrested growth, metaphyseal destruction, periosteal changes (periostitis)
• Late manifestations of congenital syphilis: prominence of forehead (“Olympian
brow”), anterior tibial bowing (“saber shins”), scaphoid scapulae, Hutchinson
teeth (peg shaped upper incisors), mulberry molars, saddle nose (due to the
rhinitis), rhagades (linear scars from prior mucocutaneous fissures), neurologic
abnormalities, interstitial keratitis, eight nerve deafness, Clutton joint (painless
arthritis of the knee)
 Know the utility and limitations of PKU testing
• Is able to screen for elevated phenylalanine levels but does not distinguish
between those babies who just don’t yet have matured metabolizing enzymes
and those with true PKU
• Will need to have a repeat screening test or blood to be sent for amino acid
quantification; amino acid analysis allows a geneticist to determine of it is true
PKU, hyperphenylalaninemia, and newborn immaturity
• Note: in the child with true PKU, tyrosine becomes and essential amino acid
 Understand the use of OAE devices for neonatal hearing screening

4. • OAE (evoked otoacoustic emissions)
∗ Measures tiny sounds generated in the cochlea that can be measured in
the external auditory canal after acoustic stimulation
∗ Two kinds: transient evoked OAE and distortion product OAE
∗ Requires a quiet environment and a still, quiet infant for best results
 Know the recommended methods of umbilical cord care
• Goal of care = maintaining hygiene, avoiding infection, promoting cord separation
• ”Dry cord care” is okay in developed countries and it just calls for drying the
stump after the baby is bathed with water and gentle soap
• There is a trend toward reduced infections with application to triple antibiotic
ointment; use of alcohol may delay cord separation but can allay familial concerns
• Lots of folk remedies – if they aren’t doing harm, don’t worry about it
 Recognize that delayed or absent passage of meconium is associated with colonic
obstruction (e.g. meconium plug syndrome, Hirschsprung, imperf anus)
• Meconium plug syndrome
∗ Typically an isolated phenomenon, not associated with anatomic
obstruction
∗ May be associated with maternal mag sulfate tx for
preeclampsia/eclampsia
∗ Plain radiographs show nonspecific findings
∗ Contrast enema will illuminate the plugs AND facilitates their elimination
∗ Colonic motility is usually normal after evacuation of the plug
• Hirschsprung disease: congenital absence of ganglion cells
∗ 95% of those affected fail to pass meconium in the first 24 hours
∗ a contrast enema may show a transition zone in the rectosigmoid colon
∗ if being considered then a diagnostic rectal bx should be performed
• Imperforate anus occurs in about 1 in 4000-5000 births and may be seen in
conjunction with other anomalies (VACTERL syndrome)
• Plan of care for delayed stooling should be a repeat exam of the abd and rectum,
assessing for adequacy of feeding, if no stool for 48 hours then a barium enema,
surgical consult for rectal bx, observing for signs of intestinal obstruction,
hydration and feeding until a dx is established
 Know the difference between bottle fed infants and breast fed infants as related to stool
frequency and frequency of feeding
•
 Know that a newborn infants who does not void by 24h of age warrants eval
 Plan the eval of an anuric infant
• Repeat exam of the abd and genitalia
• Assess for adequacy if feeding
• Cath baby to see if urine present
• Obtain UA
• Check BUN and Cre
• Order renal US
• If starts to void spontaneously and is observed to have no further problem than
no more w/u is required
• If continues not to void a urology referral may be needed
 Know that blood pressure varies directly with gestational age

5. •As a rule for preterm infants, know that their MAP should not be less than their
corrected GA in weeks
 Recognize the bilious vomiting is a common finding in infants with SBO
• Bilious vomiting in a neonate is unusual and it should be considered a medical
emergency
• About 20% of neonates with bilious vomiting have a condition that requires
surgical intervention; most life threatening condition is midgut rotation with
volvulus
• Other conditions include duodenal atresia, annular pancreas, jejunal atresia, ileal
atresia, colonic atresia, meconium ileus, Hirschprung dz
 Understand bilirubin synthesis, transport and metabolism
• Produced from the catabolism of heme in the reticuloendothelial
systemunconjugated bilirubin enters the circulation reversibly but tightly
bound to albuminB-A complex enters the liver and the hepatocytes and is
enzymatically combined with glucuronic acid; the conjugation reaction is
catalyzed by UGTthe mono and diglucuronides are excreted into the bile and
gutin newborns much of the conjugated bili in the gut gets hydrolyzed back to
unconjugated biliunconjugated bili is reabsorbed into the bloodstream vie the
enterohepatic circulationadds to the bili load already in the live
• The enterohepatic circulation is an important part of neonatal jaundice; in adults
the bacteria on the colon rapidly reduce the conjugated bilirubin and little
enterohepatic circulation occurs
 Distinguish between physiologic jaundice in a full term infant and physiologic jaundice in
a preterm infant
• Preterm infants are at a much higher risk of complications due to jaundice and
there is a lower threshold for starting tx of the hyperbilirubinemia
o Discharge plans
 Know the qualifications for consideration of early discharge on a newborn infant
• Most infants are ready for discharge 48 hours after vaginal delivery and 72-96
hours after cesarean delivery
• Infant is medically ready for discharge when vitals have been stable for 12 hours,
appears healthy and has normal results on physical exam, has stooled and voided,
is feeding well, has completed all screening tests, has appropriate follow up
planned. Additionally, need to have completed parent education and competency
must be demonstrated
• Early discharge is discharge prior to 48 hours
∗ Should only occur after vaginal delivery
∗ When antepartum, delivery and postpartum courses are uncomplicated
for both mother and baby
∗ When baby is term and AGA
∗ When baby has been evaluated for jaundice
 Know the benefits and complications of early discharge of a newborn infant
• Benefits: can improve bonding and attachment while minimizing iatrogenic risks
• Complications: delayed detection of treatable medical conditions, hyperbili, poor
feeding, early termination of breastfeeding, hospital readmission
o Home births
♦Abnormal newborn infants
o General

6.  Know the management of any neonatal abstinence syndrome
• Early discharge is not an option for any baby with prenatal drug exposure
• Cocaine and amphetamines don’t have a true NAs associated with them, but the
effects of the drug exposure can be damaging nonetheless, especially
CNS/neurotransmitter problems
• Alcohol and barbiturates have similar NAS sx of hyperactivity, irritability, crying,
hyperphagia but poorly controlled sucking and oral feeding, altered sleep wake
periods, tremors, diaphoresis, seizures
∗ Tx = controlled, thermoneutral environment, minimal stimulation, and
using phenobarb for pharmacologic management. Phenobarb dose is
titrated to effect
∗ The phenobarb is then tapered over 4-6 weeks
• Opioid NAS includes hyperirritability, tremors, jitteriness, hypertonia, GI distress
(loose stools, emesis, feeding probs), and autonomic sx like yawning, lip
smacking, persistent sucking, mottling, fever. May have seizures
∗ Tx = methadone or oral morphine
∗ Note that sx may not be evident for up to 5 days, and can be longer if the
exposure was to methadone
 Formulate a ddx of lethargy and coma in a neonate
• Can be associated with sepsis and asphyxia, inborn error of metabolism
o Resuscitation
 Know that a normal newborn infant has established regular respirations by 1 minute of
age
 Recognize that an infant who has a slow heart rate and impaired ventilatory effort
requires immediate PPV
 Recognize the need to establish airway before applying PPV
 Know that initial lung inflation may require increased pressure for the first breath
 Recognize that, in addition to nasopharyngeal suctioning, a newborn infant’s larynx
needs to be visualized and the trachea suctioned if thick or particulate meconium is
present in the amniotic fluid and the infant is not vigorous
• Suctioning does not need to be done in a vigorous infant; but if the infant is not
vigorous then tracheal suctioning needs to be done before additional
resuscitative efforts. If mec is recovered then sxning should be repeated until
little additional mec is aspirated or the HR is no longer stable
 Recognize that if mec is present in the amniotic fluid the mouth and hypopharynx of the
infant need to be suctioned
• Only need to do deep sxning as above
 Recognize when during resuscitation external cardiac massage needs to be initiated in a
newborn infant (e.g. if the HR does not increase above 60 BPM after effective ventilation
with oxygen has been established)
 Know the proper technique for external cardiac massage of a newborn
• Compressions should be directed above the xyphoid process and the chest
depressed to 1/3 the A-P diameter
• Recommended ratio of three compressions to one ventilation at a rate of 100
compressions / minute
• The rescucitator should encircle the baby’s entire chest with the hands and
depress the chest with the thumbs, compressing the entire thorax
circumferentially

7. • Minimize interruptions and allow full chest recoil between compressions
Recognize the metabolic consequences of continued poor perfusion in a newborn infant
• Low cardiac output results in endothelial cell damage with resultant activation of
the coagulation cascade into a procoagulant state
• Subsequent microthrombosis and tissue ischemia result in free radical release,
excessive neurotransmitter release, mitochondrial damage, neutrophil activation,
nitric oxide induced cell apoptosis, activation of additional inflammatory cascades
and cell necrosis all contributing to diffuse tissue damage
o VLBW infant
 Recognize that VLBW infants often cannot achieve and Apgar score greater than 6
because they are neurologically immature
• Have diminished tone and reflexes, the HR, RR and color are also interrelated and
affected by the infant’s clinical status
 Recognize that initial care of a VLBW infant includes administration of a parenteral
glucose soln
• Have low endogenous fat and glycogen stores and limited capacity for
gluconeogenesis and so they need continuous infusion of glucose to prevent
hypoglycemia
• Initially need to 4-6mg/kg/min of dextrose soln (D10); then eventually need
higher rates
 Recognize the initial care of a VLBW infant includes maintenance of a thermoneutral
environment
• Immature skin with minimal keratininzation as well as immature kidneys led to
increased water losses, so a humidified incubator is best
 Recognize the initial care of a VLBW infant includes monitoring of blood glucose and
arterial oxygen concentrations
• Goal PaO2 is 50-70 (SaO2 of 85-95%)
• Blood glucose concentrations need to be greater than 50n the first 24 hours after
birth, and greater than 50-60 thereafter
 Recognize the initial care of a VLBW infant includes evaluation for sepsis if appropriate
• Unless there is clear noninfectious cause for the preterm delivery can be
identified then workup for sepsis and prophylactic treatment needs to be
undertaken
• Initial lab eval should include a CBC, blood culture and CRP
• Initial abx should be ampicillin and gentamicin
• Usual suspects for infection are GBS, listeria and gram negatives like e. coli; (if
mom was txed with abx there is a greater chance of a gram negative infection)
 Understand the prognostic factors for VLBW infants
• Highest risk for neurodevelopmental problems in those who are
∗ Male
∗ GA under 28 weeks
∗ BPD
∗ CP
∗ Cerebral white matter injury
∗ Late onset sepsis or NC and need for surgery
• Other risk factors are persistent poor weight gain or head growth after 36 weeks
postmenstrual age

8. • The degree of immaturity is the principal determinant for prognosticating the
outcome of VLBW infants; the degree of illness experienced in the NICU also
contributes to survival prognostication and acute and long term morbidity
o Conditions, diseases
 Know that HIE is the most common cause of seizure in a full term infant
• Accounts for about 67% of early neonatal seizures
• Other causes: intracranial hemorrhage, CVA or hemorrhagic infarct; intracranial
malformation; transient hypoglycemia or hypocalcemia; drug withdrawal; inborn
errors of metabolism
 Recognize that neonatal seizures secondary to HIE characteristically occur within 24
hours after birth
• If the seizure onset is beyond the first 24 hours need to broaden the differential
and also consider infection (meningitis, encephalitis)
 Recognize the majority of full term newborn infants who have neonatal seizures
secondary to asphyxia do not manifest long term neurodevelopmental sequelae
• Motor abnormalities may be found on exam in a slight majority (53%) of
newborns having an sz for any cause, few have CP
• Severe impairment in neurodevelopmental outcomes occurs in fewer than 50% of
newborns who had sz due to asphyxia; Mild to moderate neurodevelopmental
impairment in cognitive and motor function is about 33%
• Early predictors of outcome for such children may be determined by evaluating
the worst EEG finding, the follow up 1-week EEG, and findings on cranial MRI
 Recognize that intrapartum asphyxiation can cause injury to multiple organ systems
• CV: systemic hypotension, pulm htn, dilated cardiomyopathy, myocardial
ischemia
• Pulm: respiratory distress, surfactant depletion/disruption with capillary-alveolar
leak, hypoxic respiratory failure with pulm htn, apnea
• Renal: oliguria, ATN, renal failure
• GI: impaired gastric motility, GI hemorrhage, NEC (even in term infants), ischemic
hepatitis, hepatopathy
• Hematopoietic: anemia, TCP, coagulopathy
• Metabolic: academia, hypoglycemia, hypocalcemia, hypomagnesemia
• CNS: HIE, apnea, irritability, jitterniess, abnormaities in neuromuscular tone,
seizure, coma
 Recognize that newborn infants with polycythemia are at risk for hypoglycemia and
hyperbilirubinemia, and manage appropriately
• When a baby is discovered to have polycythemia they need to be screened for
hypoglycemia and hyperbilirubinemia
• If the hypoglycemia does not improve with IV glucose then need to consider
exchange transfusion with IV NS (reduces the RBC mass and helps with circulatory
flow in the microcirculation)
 Know that the treatment for symptomatic polycythemia is partial exchange transfusion
 Plan the management of a patient with hyperbilirubinemia
•
 Understand the strategies for prevention of severe hyperbilirubinemia in newborn
infants (e.g. increased breastfeeding, screening prior to discharge)
•
 Plan the evaluation and management of a neonate with intracranial hemorrhage

9. • Requires stabilization of the airway, control of respiratory function, support of
circulation (PRBC transfusion), correction of acidosis and hyperglycemia; can start
anticonvulsant tx of they have seizures (phenobarbital); bedside cranial U/S is
best imaging; also need to investigate for underlying causes like a coagulopathy
or sepsis
• Avoid hyercarbia, hyopxia and hypotension
 Recognize the clinical and lab findings associated with intracranial hemorrhage in a
neonate
• Acidosis (metabolic, due to tissue damage and hypovolemic shock),
hyperglycemia (due to acute stress), anemia (acute decrease in HCT into the
brain), TCP (consumptive), hyponatremia (SIADH)
 Recognize the SGA infants have a higher neonatal mortality rate than AGA infants
 Recognize that SGA infants are prone to fasting hypoglycemia, polycythemia, and
temperature instability, and manage appropriately
• Need glucose infusions, might need NG/OG feeding tubes due to likely feeding
probs
• Keep them in thermoneutral environment
 Know that perinatal asphyxia is a frequent complication of IUGR
• Poor tolerance of labor and asphyxia are more common
 Know the normal arterial blood gas values for a newborn infant (pO2 60 to 90mmHg,
pCO2 35 to 45 mmHG)
•
 Understand the effects of surfactant administration in and infant with RDS
• Clinically will have less work of breathing, improved oxygenation and ventilation,
reduction in assisted ventilation (decreased FiO2), decreased mean airway
pressure (reduction in needed inspiratory pressure), improved pulmonary
compliance (improved changes in lung volume per unit of inspiratory pressure)
• On x-rays the degree of lung aeration improves as the microatelectasis is
overcome, lung volumes also improve
• On lab the academia improves
 Recognize that pulmonary air leaks are common in newborn infants who are treated with
assisted ventilation
• Grunting respirations are a clinical sign
 Recognize that neonatal pneumonia can mimic RDS
• RDS is due to surfactant deficiency and characteristically affects newborns born
under 32 weeks GA
• In term and late preterm infants who have respiratory dustress, need to look for
other causes, including infection, aspiration, cardiac disease, congenital
anomalies
• Congenital pneumonia can cause resp distress and would be seen in babies of
moms with chorio, prolonged rupture of membranes, GBS carriers
• Would see tachypnea, tachycardia, need for supplemental O2, temp instability,
poor feeding
• Radiographically will resemble RDS with air bronchograms, diffusely hazy lung
fields, low lung volumes
 Identify and manage transient tachypnea of the newborn
• Dx is based on clinical and radiographic findings
∗ Frequently a dx of exclusion and need to r/o other conditions like RDS,

10. pneumonia and pneumothorax
∗ Usually presents within a few hours after birth with tachypnea,
retractions, grunting and occasionally with need for supplemental O2
∗ Tachypnea resolves by 72 hours by can last longer
∗ If grunting and other signs of distress persist then may need more
workup/intervention
∗ Barrel shaped chest due to hyperinflation and might be able to feel the
liver and spleen due to the hyperinflation pushing them down
∗ Crackles may be present
∗ BP usually normal
∗ Radiographic findings: prominent perihilar vascular markings due to
engorged periarteriolar lymphatics, edema of the interlobar septae, fluid
in the fissures, possibly hyperinflation, fluid in the costophrenic angles,
widening of intercostal spaces
• Management: “rue of two hours” to determine of it is due to transtion or possibly
other respiratory problems.
∗ if no improvement in the degree of distress than get a CXR; if desats on
room air an ABG might be helpfulif the CXR is abnormal, baby is
worsening clinically, requires >40% O2 to maintain sats, or no
improvement after 2 hours of feasible interventions then need to consider
transfer to higher level of care
∗ if tachypnea associated with increased WOB then need to keep baby NPO,
start IVFs
∗ if the increased WOB persists beyond two hours with the tachypnea then
need to worry about other possible etiologies; majority of cases of TTN
have resolution of the tachypnea by 48 hours of age
∗ preferably give O2 supplementation by hood
∗ cannot have a definitive dx of TTN until the tachypnea resolves; babies
should not be discharged until have a resp rate <60 for more than 12
hours
 Know that peripheral cyanosis is a common finding in healthy full term newborn infants
 Know that it is difficult to distinguish between persistent pulmonary hypertension
without meconium aspiration and cyanotic congenital heart disease
• Persistent pulmonary hypertension of the newborn is also referred to as
“persistence of fetal circulation”
∗ Called this b/c there remains a persistent right to left shunt via the PDA;
usually due to increased pulmonary vascular resistance cause by one of
many problems. The pulm vascular resistance may be higher than
systemic vascular resistance and so deoxygenated blood from the right
ventricle traverses the PDA and enters the aorta rather than traveling vie
the pulmonary artery to the lungs
• Signs include grunting, tachypnea and respiratory distress and failure; precordial
lift due to increased work of the RV; lower O2 sat in the lower body than the
upper body
• Causes of increased pulmonary vascular resistance include pneumonia, lung
collapse, pulmonary hypoplasia
 Recognize the clinical presentation of a neonate with persistent pulmonary hypertension
following mec aspiration

11. • As above, including the differences in oxygenation of upper and lower extremities
• Also have CXR findings of MAS: hyperinflated lung fields, patchy infitrates, varying
degrees of atelectasis and hyperaeration
 Know the appropriate abx treatment for suspected sepsis in the immediate newborn
period
• Ampicillin and gentamicin
 Know the significance for infection of prolonged premature rupture of the membranes
• Two maternal coditions increase the risk of early onset neonatal sepsis in the face
of PROM
∗ Choriomanionitis
 Risk for fetal infection that may not be treated fully with maternal
abx; hence the baby might have partially treated bacteremia, pna,
or meningitis and require treatment for presumed sepsis
∗ GBS colonization
 Infants born before 36 weeks gestation are more susceptible to
GBS infection especially in the face of PROM or chorioamnionitis; a
sepsis eval and empiric abx tx is recommended for the preterm
infant following PROM
 Understand the risk of sepsis from the use of intravascular catheters
• UAC and UVC lines- get colonized with commensal staph within 24 hours of
insertion; need to be removed by day 10-14, preferably by day 7
 Recognize the perinatal infection with CMV may be acquired in utero, during delivery, or
in the neonatal period (e.g. breast milk, blood transfusion)
• If a primary CMV infection during pregnancy the risk of transmission from mother
to fetus is about 50%; if mother infected before pregnancy then risk of
transmission is 0.5-2%
• If term infant acquires during delivery or from breastfeeding, there is no apparent
disease, but there can be illnesses associated with this kind of transmission for
the preterm infant
• Can be transmitted via transfusion of whole blood; it resides in the white cell
fraction
 Recognize the si and sx of symptomatic congenital CMV disease
• Blueberry muffin baby, due to extramedullary hematopoiesis
• Petechiae, purpura, HSM, jaundice, SGA, microcephaly
• They get biliary obstruction due to the extramedullary hematopoiesis, leading to
hepatomegaly, hepatitis, and elevated d. bili
• Neurologic features occur in about 2/3 of symptomatic newborns; includes
seizures, ocular abnormalities (notable chorioretinitis), hypotonia, poor suck
 Recognize the clinical manifestations of congenital CMV infection including hearing loss
and MR
 Recognize that the majority of infants with congenital toxoplasmosis are asymptomatic in
the neonatal period
 Plan the eval of a full term infant who has severe respiratory failure at birth that does not
respond to intubation and assisted ventilation
 Know the usual presentation of necrotizing enterocolitis, and plan initial management
 Know that radiographic findings of pneumointestinalis is the hallmark of NEC
 Recognize that intestinal stricture formation is a late complication of NEC
 Recognize the clinical si and sx of congenital bowel obstruction

12.  Know the tx of abd distention caused by congenital bowel obstruction
 Recognize the si and sx of esophageal atresia with tracheoesophageal fistula
 Know how to evaluate an infant with TE fistula
 Recognize that an infant of a diabetic mother is at risk for hypoglycemia, hypocalcemia,
polycythemia, and neonatal small left colon syndrome
 Understand the pathogenesis of hypoglycemia in an infant with a diabetic mother
 Understand the management of a newborn whose mother has DM1
 Understand the effects of drugs given to the mother during labor (e.g. opiates, beta
andrenergic tocolytic agents) on the fetus/neonate
 Know the association between maternal use of alcohol and any fetal abnormalities
and/or neonatal abstinence syndrome
 Know the association between maternal use of marijuana and any fetal abnormalities
and/or neonatal abstinence syndrome
 Know the association between maternal use of tobacco and any fetal abnormalities and/
or neonatal abstinence syndrome
 Know the association between maternal use of opiates and any fetal abnormalities
and/or neonatal abstinence syndrome
 Know the association between maternal use of amphetamines and any fetal
abnormalities and/or neonatal abstinence syndrome
 Know the association between maternal use of barbiturates and any fetal abnormalities
and/or neonatal abstinence syndrome
 Know the association between maternal use of cocaine and any fetal abnormalities and/
or neonatal abstinence syndrome