September Board Review - LSU School of Medicine

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Transcript September Board Review - LSU School of Medicine

September Board Review
Fetus and Newborn
CARE OF THE WELL NEWBORN
Prenatal Visit
• Most important focus: begin a positive
relationship with the parents!!
• History
– Mother’s medical and pregnancy history
• Depression
• Medications
• Use of tobacco/ other substances
– Maternal and paternal family history
– Social History
• Support system
Prenatal Visit
• Feeding plan
– BF (encourage!!)
• Anticipatory guidance
• Routine office procedures
Antenatal US Findings
• Choroid plexus cysts
– Seen commonly prior to 24 wga
– If not associated with other anomalies, unlikely to be
of any significance
– No need for follow-up
• Echogenic intracardiac focus
– Bright spot near the papillary muscle of left ventricle
– May be associated with Trisomy 21
– Is a normal finding in most cases
Antenatal US Findings
• Echogenic bowel
– ?Marker for:
•
•
•
•
Aneuploidy
CF
Congenital Infections
Rare intestinal d/o
– Most infants normal
• Mild enlargement/ asymmetry of the cerebral
ventricles
– Cranial US after delivery appropriate
Antenatal US Findings
• Hydronephrosis
– If pelvic dilatation >4mm in second trimester, or
>7mm in the third trimester postnatal US
– If caliectasis (dilation of the calyces) seen, do US
even if hydronephrosis doesn’t meet size
requirements
– VCUG
Delivery
• 10% of infants require some form of
resuscitation
– 20% of those infants require aggressive
intervention
• Most infants establish regular respirations at 1
min of age
Delivery
• Minimize heat loss!
– At risk due to large area-to-body mass ratio
– Cold stress depletion of fat and glycogen
– Healthy infants:
• Dry
• Swaddle with dry linen
• Skin-to-skin contact with Mom
– Sick Infants
• Radiant warmer
Question #1
• A 37 wga M was born via C-section for failure to
progress. His Apgars were 9 and 9 at 1 and 5 minutes.
The significance of his one and five minute Apgar
scores is:
– A. He tolerated the delivery process well, but his transition
has not been successful
– B. He did not tolerate the delivery process well, but his
transition has been successful
– C. He tolerated the delivery process well, and his transition
has been successful
– D. He did not tolerate the delivery process well, and his
transition has not been successful
– E. He is alive
Apgar Scoring
Sign
0
1
2
Heart Rate
Absent
Over 100 bpm
Color
Blue/pale
Under 100
bpm
Pink body,
blue ext
Respiratory
Effort
Muscle Tone
Absent
Slow
(irregular)
Some flexion
of ext
Good crying
Reflex
Irritability
No response
Limp
Grimace
All pink
Active motion
Cough or
sneeze
After Delivery
• Frequent VS in the first hours after birth
– Frequent BPs not necessary
• Identify infants at risk for specific problems:
– Infection
– Hypoglycemia
– HIV
– Hepatitis B
– Effects from maternal medications
• Vitamin K and erythromycin
After Delivery
• First Feedings
– Formula should be avoided in absence of medical
indication
– Sterile water/ glucose water should be avoided
First Exam
• Estimated gestational age
– Definitions
• Preterm: <37 wga
• Term: Between 37 and 41 6/7 wga
• Postterm: >42 wga
• Growth Parameters (plot them!)
– Birthweight <10th percentile: SGA
•
•
•
•
•
Problematic transition
Poor feeding
Hypothermia
Hypovolemia
Hypoglycemia
First Exam
• Growth Parameters (con’t)
– Birthweight >90th percentile: LGA
• Hypoglycemia
• Birth Trauma
– Clavicular fracture
– Scalp hematoma
– Brachial plexus injury
– IUGR: baby that does not follow the expected
prenatal growth pattern
– Low birth weight: <2500g
First Exam
• Weight loss
– Healthy infants may loose 2-3% of BW for the first
2-3 postnatal days
– When BF is optimal, weight loss begins to plateau
after 48-72h
– Weight loss >7-8% should be evaluated
Question #2
• All of the following are physical characteristics
of a post-term infant EXCEPT:
– A. Dry/peeling skin
– B. Sparse hair
– C. Decreased subcutaneous tissue
– D. Wrinkled skin
– E. Abundant vernix
First Exam
• Consider doing at bedside with parents present
– Can assess the quality of the infant-parent interaction
• Confirm EGA
– Preterm Infants
•
•
•
•
•
Abundant vernix
Decreased subcutaneous fat
Pink, thin skin
Decreased tone
Immature reflexes
First Exam
• Confirm EGA (con’t)
– Term Infant
• Pink and chubby
• Alert, able to fixate visually
• Normal muscle tone and reflexes
– Post-term Infant
• Decreased subcutaneous tissue
• Dry or peeling skin
• Wrinkled skin or sparse hair
First Exam
• Important components of the PE:
– Red Reflex
– Palate
– Calm assessment of:
•
•
•
•
Heart
Lungs
Abdomen
Hips
Question #3
• All of the following are issues encountered by
near-term infants (35-37 6/7 wga) EXCEPT:
– A. Hypothermia
– B. Decreased daily fluid requirement
– C. Breastfeeding problems
– D. Increased insensible water loss
– E. Increased rate of readmission
Care of Near-Term Infants
• Near-Term Infants at risk for:
–
–
–
–
–
Hypothermia
Hypoglycemia
Jaundice/ kernicterus
Breastfeeding problems/ dehydration
Increased rate of readmission
• Greater daily fluid and calorie/kg requirement
• Increased insensible water losses
– Prematurity
– Radiant warmer
– Phototherapy
Care of Near-Term Infants
Breastfeeding
• Recommend human milk for all infants except
where contraindicated
Breastfeeding
• Educate and support both parents
• Put healthy infants skin-to-skin until first feeding
accomplished
• Avoid procedures that may interfere
• Avoid glucose water or formula supplements
• Avoid pacifiers during initiation
• Feed on infant demand (at least 8-12 times/d)
• Formal evaluation twice daily while in the
hospital
Breastfeeding
• Close f/u after hospital d/c
• Encourage exclusive BF for 6 months
• Have mother and infant sleep in close
proximity
• Should either Mom or baby need
hospitalization, make every effort to maintain
BF or provide human milk for the infant
Routine Screening and Testing
• Blood glucose
– Infants at risk for hypoglycemia
•
•
•
•
•
IDM
LBW (<2500g)
SGA or LGA
Hypothermia
Signs of hypoglycemia or sepsis
• Hearing screening
– OAE
– BAER
Routine Screening and Testing
• Newborn metabolic/genetic screening
• Hepatitis B prevention
– Vaccination for everyone!
– HBIG (in addition to vaccine) to infants born to
mothers HbSAg+
• Syphilis
– More info to come later!
Routine Screening and Testing
• Group B Strep
– All women should be screened at 35-37 wks
– Prophylaxis indicated with:
•
•
•
•
Previous infant with invasive GBS
GBS bacteruria during the current pregnancy
Positive GBS screen during the current pregnancy
Unknown GBS status AND:
– Gestation <37 wks
– ROM> 18h
– Intrapartum fever >38.0
Fig 3.5. Empiric management of a neonate whose mother received intrapartum antimicrobial prophylaxis
(IAP) for prevention of early-onset group B streptococcal (GBS) diseasea or suspected chorioamnionitis.
Red Book Online Visual Library, 2009. Image FIGURE3E. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Question #4
• You are examining a 24h old female in the room with Mom
and Dad. When you begin to examine her hips, Mom
mentions that her first child had a hip problem that
required a harness. On your exam, both the Barlow and
Ortolani are negative. She asks if any testing will need to
be done for this baby to make sure her hips are normal.
Your answer is:
– A. No, since her physical exam is normal, no further testing is
needed
– B. You will see her weekly for the next 4-6 weeks to check her
hips, and if her exam becomes abnormal x-rays will be done
– C. Yes, you will do pelvic x-rays before the infant is discharged
– D. No, there is no significance in the positive family history
– E. Yes, a screening hip US will be done at 4-6 wks of age
Common Problems
• Hyperbilirubinemia
• Developmental dysplasia of the hip
– Positive Barlow or Ortolani Ortho referral
– Equivocal signs re-examine in 2 weeks and refer
if signs persist
– Those with risk factors: Hip US at 4-6wks
• Breech presentation
• Positive FHx
Common Problems
• Delayed voiding or stooling
Anticipatory Guidance
• Back to sleep
– “Tummy time” as much as possible while baby is
awake to help with positional plagiocephaly
• Car seat
– Appropriate fit and position in the car
– Hands-on teaching
– Car seat testing for infants <37 wks
• Umbilical cord care
– Dry cord care
Discharge
• Normal discharge criteria
– 48h after a vaginal delivery and 72-96h after CS
– Medical readiness:
•
•
•
•
•
•
•
Stable VS x12h
Normal PE, well-appearing
Voided and stooled
Feeding well
Completed all screening tests
Appropriate F/U scheduled
Parent education completed and competency demonstrated
Early Discharge
• Criteria for early discharge (<48h)
– After vaginal delivery only
– Antepartum, delivery, and postpartum course
uncomplicated for mother and baby
– Term baby, appropriate for gestational age
– Evaluation for jaundice completed
– Prompt outpatient F/U arranged
Early Discharge
• Benefits
– Improved bonding and attachment
– Minimization of iatrogenic risks
• Complications
– Delayed detection of treatable medical conditions
– Hyperbilirubinemia
– Poor feeding/ early termination of BF
– Hospital readmission
First Outpatient Visit
• Several days (not 2 weeks) after D/C
• Weight?
– Should not have lost more than 7-8% of BW
• Feeding?
– Volume/duration, frequency, spit-ups?
• Voiding?
– 6-8 voids
– Yellow, seedy stools daily
• Sleeping?
– Back to sleep
• Concerns?
NEWBORN RESUSCITATION
Newborn Resuscitation
• Achieving a stable airway, ventilation, and
oxygenation are the first and most important
steps
Airway, Ventilation, Oxygenation
• A normal newborn infant has established
regular respirations by 1 minute of age
• Bag-valve-mask ventilation can be difficult due
to poor lung compliance and fluid-filled alveoli
– Increased positive pressure is necessary
(especially for the first breath)
• Recent recommendations are to use 100%
oxygen during PPV, monitor arterial sats, and
decrease concentration as soon as possible
Question #5
• You are attending the birth of a 36 WGA male, who was
just delivered via C-section. After being warmed with
blankets and stimulated, you notice his color is blue
and he is not taking effective respirations. You begin
positive pressure ventilation via bag-mask with 21% O2,
and ask for a pulse ox reading. After getting good chest
rise and hearing adequate breath sounds throughout,
the pulse ox reads SaO2 89% and HR of 45.
• Of the following, the next BEST step in resuscitation is:
A.
B.
C.
D.
E.
Intubate immediately and begin mechanical ventilation
Give Epinephrine
Chest compressions
Intubate immediately and give surfactant via ETT
Give Dopamine
External Cardiac Massage
• Adequate ventilation is usually sufficient to
reverse bradycardia
• Compressions should be initiated if the
infant’s heart rate remains less than 60
beats/min
– Should be directed above the xiphoid process
– Depress chest 1/3 AP diameter
– Recommended ratio is 3 compressions to 1
ventilation at a rate of 100 compressions per
minute
External Cardiac Massage
• Encircle the infant’s chest with 2 hands and
depress the sternum with both thumbs
Metabolic Consequences
• Endothelial cell damage → release of von
Willebrand factor and tissue thromboplastin →
activates a procoagulant state →microthrombosis
and tissue ischemia
• Free radical release
• Arachindonic acid cascade activation
• Excessive neurotransmitter release
• Mitochondrial damage
• Neutrophil activation
• Cell apoptosis
• Inflammatory cascades
Question #6
• The use of hypothermia is recommended as
effective treatment for asphyxia-related brain
injuries.
A. True
B. False
Return of Circulation
• Management of multiorgan dysfunction
• Maintain adequate blood pressure, cerebral
perfusion pressure and cardiac function
• Closely monitor body temperature
– Avoid hyper- or hypothermia
– Minimize heat loss by wrapping the baby
Meconium Aspiration
• 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
VERY-LOW-BIRTH WEIGHT INFANT
Resuscitation
Check to ensure all necessary equipment
is available:
-Warmer
-Blankets
-Suction
-Laryngoscope
-ETT (appropriate size)
<28 weeks (<1000 g): 2.5 mm
28-34 wks(1000-2000 grams): 3.0 mm
34-38 weeks (2000-3000 grams): 3.5 mm
>38 weeks (>3000 grams): 3.5 to 4.0 mm
-UVC/UAC supplies
-Meds for resuscitation
-Oxygen
-Pulse ox
Thermoneutral Environment
• Core body temp decreases rapidly from
heat loss after delivery
• Hypothermia is assoc. with adverse
outcomes
– Goal is to keep body temp 97.7 to 98.6°F
• Keep delivery room 77 to 80.6°F
• Place infant on radiant warmer
• Wrap in prewarmed blankets
• Place baby in polyethylene bag
immediately after delivery before
drying
APGAR Scores
• Difficult in VLBW infant
• Tone and reflexes are
diminished
• Often cannot achieve
an Apgar greater than 6
because of neurologic
immaturity
– Hypotonia
– Blunted response to
noxious stimuli
Question #7
• A 28 WGA male infant was just delivered via Csection. He weights 1000g. He is intubated in the
delivery room due to respiratory distress, and has
UAC and UVCs placed. He is stabilized, and upon
arrival to NICU, his nurse asks if you want to start
IVFs.
• Of the following, the MOST appropriate initial
solution for parenteral administration is:
A.
B.
C.
D.
E.
5% dextrose
5% dextrose and 0.2% sodium chloride
10% dextrose
10% dextrose and 0.2% sodium chloride
0.9% sodium chloride
Blood Glucose
• Obtain blood glucose measurement as part of
initial assessment
• Preterm infants have low endogenous glycogen
and fat stores and a relatively limited capacity for
gluconeogenesis
– Require a continuous infusion of glucose to prevent
hypoglycemia
– Initial requirement is 4 to 6 mg/kg/min (GIR)
– Provided as 10% dextrose at a rate of 80 to 120
ml/kg/day
– BG should be >50 in first 24 hours, and >50 to 60
thereafter
Blood Glucose
• At 1 week after birth total fluid is 130 to 170
ml/kg/day
• GIR of 8 mg/kg/min provides adequate
carbohydrate nutrition while maintaining
appropriate blood glucose in a baby not being
fed
• Some develop hyperglycemia on lower
glucose infusion rates and require lower
concentrations of dextrose (7.5 or 5%)
Nutrition
• VLBW infants develop significant protein deficits
in first week
– Start TPN with at least 1.5 g/kg/d of amino acids
– 40 cal/kg from carbohydrate and fat
• Early feeds with human milk have shown to
improve survival
–
–
–
–
Promote intestinal growth
Reduce risk for late-onset sepsis and NEC
Improve neurodevelopmental outcome
Requires nutrient fortification
Respiratory Distress
• RDS caused by lung immaturity and surfactant
deficiency is common in VLBW
• Pulse ox and arterial blood gas analysis can
minimize episodes of hyperoxia and
hypocarbia
• Give supplemental oxygen to keep PaO2
between 50 and 70 mmHg and sats between
85-95%
• CPAP and intubation with surfactant
administration when appropriate → as soon
as possible
Sepsis
• Unless there is a clear noninfectious cause for the
preterm delivery, the infant should be evaluated
for infection and treated with abx
• CBC, blood cx, and CRP
• Broad-spectrum abx: Amp and Gent
– To cover most common pathogen:
• GBS, Listeria, E. coli
– Infants who’s mom’s received abx have a greater risk
of infection with gram-negatives
• If suspect HSV (vesicular rash, thrombocytopenia,
seizures)
– CSF and surface cultures, PCR
– Start Acyclovir
Question #8
• You are seeing a 2 ½ month-old female in clinic for a
well-check. The patient is an ex-premie born at 27
weeks and had a NICU course complicated by NEC
requiring surgery to remove part of her small intestine.
Since discharge from the NICU, she has been doing
well, tolerating feedings and gaining weight. Her mom
asks you about her development and if she will be
normal.
• Of the following, which is NOT a factor associated with
high risk for adverse neurodevelopmental outcome:
A.
B.
C.
D.
E.
Female sex
Gestational age less than 28 weeks
NEC
Need for surgery
Cerebral white matter injury
Neurodevelopmental Outcome
• 15 to 20% of VLBW infants develop an
intracranial hemorrhage
– Grade I IVH (subependymal or periventricular
hemorrhage) → do not have a significantly
increased risk of adverse neurodev. Outcome
– Grade II IVH (bleeding into the ventricle without
dilatation) → a small increase in adverse
neurodev. outcome (academics, memory,
executive function)
Neurodevelopmental Outcome
– Grade III IVH (bleeding into ventricle with
dilatation) → 30% have neurodev. Impairment
– Grade IV IVH (intraventricular and
intraparenchymal bleeding) → 90% have
neurocognitive or motor impairment
Neurodevelopmental Outcome
• Highest risk for adverse outcomes:
– Male
– <28 weeks
– BPD
– Cerebral white matter injury
– Late onset sepsis
– NEC
– Need for surgery
– Poor weight gain or head growth
NEONATAL JAUNDICE
Bilirubin Metabolism
• Conjugation reaction is
catalyzed by UGT-1A1
– Then excreted into bile and
the gut
• In the newborn, much of
the conjugated bili in the
intestine is hydrolyzed
back to unconjugated bili
– Then reabsorbed into the
blood stream by
enterohepatic circulation
Breastfeeding and Jaundice
• A strong association between breastfeeding and
hyperbili
• Breastfeeding jaundice
– In the first 2 to 4 postnatal days
– Related to increase in enterohepatic circulation stimulated
by fewer calories received until milk “comes in”
• Human milk jaundice syndrome
– Appears later (onset at 4 to 7 days)
• Gilbert syndrome
– Increased incidence in prolonged hyperbilirubinemia
beyond 2 to 3 weeks
Pathologic Causes of Jaundice
ABO Hemolytic Disease
• Baby = A or B
• Mom = O
• 1/3 of these infants have
a positive Coombs or DAT
test
• Twice as likely to have
moderate
hyperbilirubinemia, but
sever jaundice is
uncommon
• Common in the first 24
hours
G-6PD Deficiency
• Most common and clinically significant red cell
enzyme defect
• 11 to 13% of African-American newborns
• 30% of infants with kernicterus found to be
deficient
• Gene is on X chromosome
– Hemizygous males = full enzyme deficiency
– Heterozygous females = also at risk
Question #9
• You get a call from the newborn nursery that a
baby has just been delivered. The infant is a
healthy 37 WGA African-American male, and
mom plans to breastfeed.
• Of the following, which is associated with
DECREASED risk of significant jaundice:
A.
B.
C.
D.
E.
His brother received phototherapy as an infant
African-American race
He has a cephalohematoma on physical exam
Gestational age of 37 weeks
Male sex
Question #10
• You are about to discharge a 48 hour old full-term
male infant born via uncomplicated vaginal
delivery. At 40 hours old, his total serum bilirubin
was 9 mg/dl. On physical exam he is jaundiced in
the face. He is successfully breastfeeding, and he
has the same blood type as mom.
• Of the following, the next BEST step in managing
is jaundice is:
A. Schedule follow-up for 1 week
B. Obtain CBC with retic
C. Schedule follow-up appointment within 48 hours
D. Start phototherapy
E. Repeat total serum bilirubin
Follow-up
• The AAP now recommends that any infant
discharged at less than 72 hours of age should
be seen within 2 days of discharge
– Most infants delivered vaginally leave the hospital
before 48 hours, so bilirubin peaks after discharge
(peak = 3 to 5 days)
• It is essential that total serum bilirubin values
be interpreted in terms of the infant’s age in
hours not days
When to Seek a Cause
• Cause is often apparent from history and
physical
• If total bili is above 95th percentile or rising
rapidly and crossing percentiles
– Blood type and Coombs
– CBC, retic
– Direct bili
– Consider G-6PD
• If elevated direct bili → UA, urine cx, evaluate
for sepsis
Visual Assessment of Jaundice
• Visual diagnosis is
unreliable, especially in
dark skinned infants
• The difference b/w a TSB
of 5 and 8 cannot be
detected with the eye,
but represents a
difference b/w the 50th
and 90th percentile
• Some experts
recommend screening all
newborns with a TSB or
TcB
Question # 11
• You see a 4-day-old (96 hours) female in clinic for
follow-up of hyperbilirubinemia. She was born at
36 WGA and has been breastfeeding well. Both of
her older sisters required phototherapy as
infants. You repeat total serum bilirubin today
and the value is 16 mg/dl.
• Of the following, the next BEST step is:
A.
B.
C.
D.
E.
Admit to the hospital for exchange transfusion
Instruct mom to breastfeed every 4 to 6 hours
Start Phenobarbital
Admit to the hospital for phototherapy
Start home phototherapy
Treatment
• 1) Exchange transfusion to remove bili
mechanically
• 2) Phototherapy to convert bili to products
that can bypass the liver’s conjugating system
and then be excreted in bile or urine
• 3) Pharmacologic agents
Phototherapy
•Photons are absorbed by
bili in the skin
•Undergoes photochemical
reaction to form excretable
isomers
•Most effective light is in
the blue-green spectrum
•When applied
appropriately, expect a 30
to 40% decrease in bili in
the first 24 hours (most
significant decline happens
in 4 to 6 hours)
•Home phototherapy
should not be used in
infants with risk factors
Pharmacologic Therapy
• Phenobarbital
• Ursodeoxycholic acid
• Tin mesoporphorin
NEWBORN RESPIRATORY
DISORDERS
Presentation of Respiratory Distress
• Tachypnea
– RR>60
• Grunting
– Produces elevated transpulmonary pressures maintenance of FRC
– Seen in disease states where alveoli are prone to collapse (RDS)
• Nasal flaring
– Reduction in nasal resistance reduction in total lung resistance
• Retractions (intercostal, subcostal, suprasternal)
– Become more apparent as the lung becomes less compliant (RDS)
• Central cyanosis
– Advanced sign of respiratory distress
– Less clinically apparent when the patient is anemic
Assessment
• First thing’s first: ABCs!!
– Stabilize per NRP
• Physical Exam
– Temperature instability infection
– Tachycardia infection, hypovolemia
– Scaphoid abdomen CDH
– Asymmetric chest wall movement tension PTX
– Asymmetric breath sounds PTX
– Stridor UA obstruction
Assessment
• Initial labs/ radiology
– CXR
– Glucose
– ABG
– CBC with diff
– BCx
Assessment
• History
– Maternal
• DM?
• Medications?
– Pregnancy
• Polyhydramnios?
– TEF
• Oligohydramnios?
– Pulmonary hypoplasia
• Triple Screen
– Genetic defects
• Prenatal US
• BPP (fetal heart rate, muscle tone, movement, breathing, and
amniotic fluid index)
Assessment
• History (con’t)
– Labor and delivery
• Fetal monitoring?
• Complications?
– Placenta previa/ abruption
• Presence of meconium?
– History of presentation
• Initial respiratory distress that improves with minimal
intervention TTN
• Gradual deterioration PNA, RDS, sepsis
Differential Diagnosis
• Pulmonary causes
– RFLLS (TTN)
– RDS
– Meconium aspiration
syndrome
– PNA
• Non-pulmonary causes
–
–
–
–
Cardiac disease
Infection
Metabolic d/o
CNS d/o
Question #12
• A 3260g term male infant was born via spontaneous vaginal
delivery. There was an prolapsed umbilical cord during
delivery, but the infant emerged vigorous and pink.
Maternal history was negative with the exception of some
analgesia needed during labor. You were called right after
the infant arrived in the nursery, because he was
tachypenic with some nasal flaring and retractions. All the
following details of the history are consistent with diagnosis
of transient tachypnea of the newborn (or RFLLS) EXCEPT:
–
–
–
–
–
A. Male infant
B. Vaginal delivery
C. Umbilical cord prolapse
D. Maternal analgesia during labor
E. Respiratory distress presenting immediately after birth
TTN (RFLLS)
• Pathophysiology:
– Transient pulmonary edema resulting from
delayed clearance of fetal lung fluid
• During pregnancy, lung epithelium primarily a secretory
membrane
• 2-3 days prior to onset of labor, epithelium becomes an
absorbing membrane
• 40% of lung fluid is absorbed before a spontaneous
vaginal delivery
• Rest of fluid must clear within hours of birth for
successful transition to occur
TTN (RFLLS)
• Risk factors
– Male sex
– C-section delivery
– Perinatal asphyxia
– Umbilcial cord prolapse
– Maternal complications
• Asthma
• Diabetes
• Need for analgesia/ anesthesia during labor
TTN (RFLLS)
• Occurs in 3.6-5.7 per 1000 term infants and 10
per 1000 preterm infants
• Presentation (immedately after birth)
– Tachypnea
– Grunting
– Nasal flaring
TTN (RFLLS)
• Diagnosis
– Resolution of Sx 1-5d
after minimal therapeutic
Intervention
– CXR
• Prominent perihilar
streaking
• Increased interstitial
markings
• Fluid in the interlobar
fissures
TTN (RFLLS)
• Treatment
– Supportive
• Oxygen (at times, high concentrations)
• CPAP
– Helps with the absorption of the fluid
• (Rarely) mechanical ventilation
• Prognosis
– Benign and self-limited disease
– No long-term sequelae
Question #13
• A 30 wga male is born via SVD. Immediately after
birth, he has signs of respiratory distress. CXR
shows diffuse microatelectasis, diminished lung
volume, and air bronchograms. The underlying
pathophysiology of this infant’s illness is:
–
–
–
–
–
A. Meconium aspiration
B. GBS infection
C. Retained fetal lung fluid
D. Surfactant deficiency
E. Airway hyperreactivity
Respiratory Distress Syndrome (RDS)
• Pathophysiology
– Surfactant deficiency
• Mixture of lipids and proteins
• Produced by type II pneumocytes
• Absence increased surface tension and alveolar collapse
• Risk Factors
– Prematurity!!!
• 60% of babies born at <28wks
• 30% of babies born at <30wks
• <5% of term babies
RDS
• Risk Factors (con’t)
– Male sex
– Maternal gestational diabetes
– Perinatal asphyxia
– Hypothermia
– Multiple gestations
RDS
• CXR
– Diffuse microatelectasis
”ground glass”
appearance
– Overall diminished lung
volume
– Air bronchograms
RDS
• Treatment
– Antenatal
• Administration of corticosteroids to women at risk for
preterm labor before 34 wga
– Reduces risk of RDS by accelerating fetal lung maturation
– Postnatal
• Surfactant replacement
– Intubation surfactant administration immediate
extubation becoming more popular
• Nasal CPAP or mechanical ventilation
RDS
• Complications (associated with Rx for RDS)
– Bronchopulmonary dysplasia (BPD)
• Supplemental oxygen needed at 36 wks corrected
gestational age
• Results from high levels of oxygen administration and
mechanical ventilation
Question #14
• A 41 wga F is transferred to the NICU 12h after delivery for
worsening respiratory distress. Pregnancy and delivery
were unremarkable, except for moderately meconiumstained amniotic fluid. She decompensates and requires
intubation and mechanical ventilation after her arrival to
the NICU. You suspect meconium aspiration syndrome
(MAS). All of the following have been proven efficacious
interventions for MAS EXCEPT:
–
–
–
–
–
A. Amnioinfusion
B. Inhaled NO
C. ECMO
D. Surfactant therapy
E. Mechanical ventilation
Meconium Aspiration Syndrome (MAS)
• Definition
– Respiratory distress in an infant born through
meconium-stained amniotic fluid whose symptoms
cannot be otherwise explained
• 13% of deliveries with meconium-stained fluid
– 4-5% develop MAS
• Pathophysiology
– Increased fetal stress relaxation of the anal
sphincter passage of meconium in utero
– Chronic fetal hypoxia and acidosis gasping
aspiration of meconium severe MAS
MAS
• Pathophysiology (con’t)
– Severe MAS remodeling and thickening of the
pulmonary vessels pulmonary vascular
hyperreactivity, vasoconstriction, and HTN
– Meconium also directly toxic to the lungs (bile
salts and pancreatic enzymes)
• Causes chemical pneumonitis
• Inactivates surfactant
• Activates complement
– Thick meconium itself causes airway obstruction
MAS
• Presentation
– First 12h after birth
– Varying degrees of respiratory distress
– Barrel chests, crackles and rhonchi on exam
MAS
• Patchy atelectasis
– Complete airway obst
• Overinflation
– Air trapping with partial
airway obst
• Widespread involvement
• Most severe cases
white out
• Extreme overinflation
air leaks
Treatment
• Good oxygenation
– Hypoxemia increased pulmonary vascular
resistance worsening of PHTN
• Surfactant replacement
• Inhaled NO
• High frequency ventilation
– No RCT have compared conventional to HFOV
• ECMO
– For pts who fail iNO therapy
– Survival rate of 93-100%
Question #15
• An 39 wga F is transferred to the
NICU at 6h of age after a
prolonged apneic episode. She
was also noted to be lethargic
and feeding poorly. Her PE is
significant for some crackles at
the RUL. Pulses are 2+
throughout and CRT< 2sec. CXR
obtained on admit is shown.
Appropriate treatment for this
illness would include:
– A. Supportive care
– B. Surfactant administration
– C. Intubation and suctioning of the
trachea
– D. IV Ampicillin and Gentamicin
– E. ECMO
Pneumonia
• Most common infection in the neonate
• May develop:
– Antenatally:
•
•
•
•
•
•
Rubella
HSV
CMV
Adenovirus
Toxoplasma
Varicella
Pneumonia
• May develop (con’t):
– Perinatally
•
•
•
•
GBS
E.Coli
Klebsiella
Chlamydia trachomatis
– Post-natally
• RSV
• Gram-positive bacteria
• Gram-negative bacteria
Pneumonia
• Presentation
– Signs typically present at birth
•
•
•
•
•
•
Respiratory distress
Lethargy
Poor feeding
Jaundice
Apnea
Temperature instability
Pneumonia
• CXR
– Appearance depends on
the cause:
• In utero infection
bilateral “white out”
• GBS PNA can be
indistinguishable from
RDS or RFLLS
– Pleural effusion
– Mild cardiac
enlargement
Pneumonia
• Additional work-up
– CBC with diff
– BCx
• Before ABx therapy started
• Treatment
– Antibiotics
• Ampicillin and Gentamicin
– Supportive therapy
• Oxygen
• Mechanical ventilation
• Vasopressor support
NEONATAL INFECTIONS
Toxoplasma Gondii
• Oocytes shed in cat feces
• In Mom
– Mono-like illness
– LAD
• Transmission:
– Early in pregnancy: lower chance of fetal infection
but consequences of infection are more severe
– Later in pregnancy: greater chance of fetal
infection but with less severe sequelae
Toxoplasma Gondii
• Presentation (vast majority asymptomatic in
the newborn period)
– Microcephaly
– Hydrocephaly
– Chorioretinitis
– Diffuse cerebral calicifications
– Jaundice
– HSM
Image 139_28. Toxoplasma gondii Infections (Toxoplasmosis) A white male neonate with congenital
toxoplasmosis with petchiae, hepatosplenomegaly, and micropenis.
Red Book Online Visual Library, 2009. Image 139_28. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 139_04. Toxoplasma gondii Infections (Toxoplasmosis) T gondii retinitis. Note well-defined areas of
choroidoretinitis with pigmentation and irregular scarring.
Red Book Online Visual Library, 2009. Image 139_04. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 139_27. Toxoplasma gondii Infections (Toxoplasmosis) A CT scan of an infant with congenital
toxoplasmosis demonstrating multiple intracranial calcifications.
Red Book Online Visual Library, 2009. Image 139_27. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Toxoplasma Gondii
• Diagnosis
– Toxoplasma IgM (IgG)
• Treatment
– Pyrimethamine
– Sulfadiazine
– Leucovorin
Rubella
• Person-to-person transmission by droplets
• In Mom
–
–
–
–
Posterior auricular LAD
Rash
Low-grade fever
Polyarthralgia/ arthritis
• Fetal transmission
– 1st trimester: high likelihood of infection (90%) with
serious sequalae
– 3rd trimester: infection risk 60-100% but nonteratogenic
Rubella
• Presentation
– Thrombocytopenic purpura (“blueberry muffin” lesions)
– Radiolucencies in the metaphyseal long bones
– Congenital heart disease
• PDA +/-PPS or ASD/VSD
– Sensorineural deafness
– Cataracts/ glaucoma
•
Diagnosis
–
•
Rubella IgM (acute and convolescent IgG)
Treatment
–
Supportive
Image 115_14. Rubella Newborn with congenital rubella rash.
Red Book Online Visual Library, 2009. Image 115_14. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 115_16. Rubella This photograph shows the cataracts in an infant's eyes due to Congenital Rubella
Syndrome. Rubella is a viral disease that can affect susceptible persons of any age. Although generally a mild
rash, if contracted in early pregnancy, there can be a high rate of fetal wastage or birth defects, known as
Congenital Rubella Syndrome (CRS).
Red Book Online Visual Library, 2009. Image 115_16. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 115_08. Rubella Radiolucent changes in the metaphyses of the long bones of the upper extremity of an
infant with congenital rubella.
Red Book Online Visual Library, 2009. Image 115_08. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
CMV
• Transmission through contact with infected
blood, urine, respiratory secretions
• In Mom
– Mono-like illness
• Fever, malaise, mild hepatitis
• Fetal transmission
– In utero (most severe)
– During delivery
– Neonatal period (breastmilk, blood transfusion)
CMV
• Presentation (cytomegalic inclusion disease)
– IUGR
– HSM/ jaunice
– Thrombocytopenia
– “Blueberry muffin” rash
– Microcephaly
– Chorioretinitis
– Sensorineural hearing loss
– Periventricular cerebral calcifications
Image 039_22. Cytomegalovirus Infection This is the same infant as in image 039_21.
Red Book Online Visual Library, 2009. Image 039_22. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 039_33. Cytomegalovirus Infection Cytomegalovirus infection with periventricular calcification
Red Book Online Visual Library, 2009. Image 039_33. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
CMV
• Diagnosis
– Urine culture in the first 3-4 wks of life
• Treatment
– Supportive
Herpes Simplex Virus
• Transmission usually from intrapartum contact
– If Mom has active lesions or symptoms/ signs of
prodrome C/S recommended
– Fetal transmission risk high among women who
get their first episode of HSV at the time of
delivery
• Low risk among women with recurrent herpes
HSV
• Presentation (1-2 weeks of life)
– 40 % SEM (skin, eye, mucosa)
• Macular lesions that quickly vesicular on a red base
• Lesions occur at sites of trauma
– Fetal scalp monitor sites
– Eye margins
– On the presenting body part
– 35% CNS
• Encephalitis
• Focal neurologic signs
• Seizures
– 25% Disseminated
Image 060_34. Herpes Simplex Neonatal herpes simplex infection with disseminated vesicular lesions.
Red Book Online Visual Library, 2009. Image 060_34. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 060_40. Herpes Simplex Neonatal herpes skin lesions of the head and face. This is the same patient as
shown in image 060_39.
Red Book Online Visual Library, 2009. Image 060_39. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
HSV
• Diagnosis
– HSV DFA or PCR
• Treatment
– IV Acyclovir
Syphilis
• Presentation
– HSM/ jaundice
– Rhinitis (“Snuffles”)
– Pseudoparalysis of an extremitiy
– Uveitis/ chorioretinitis
– Skin rash
• Vesicular or vesiculobullous lesions superficial
desquamation
– Hutchinson teeth
Image 128_42. Syphilis The face of a newborn infant displaying pathologic morphology indicative of
"Congenital Syphilis" with striking mucous membrane involvement.
Red Book Online Visual Library, 2009. Image 128_42. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 128_11. Syphilis Newborn with congenital syphilis with cutaneous ulceration (luetic gumma). These
lesions are highly infectious.
Red Book Online Visual Library, 2009. Image 128_11. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 128_18. Syphilis Hutchinson's teeth, a late manifestation of congenital syphilis. Changes occur in
secondary dentition. The central incisors are smaller than normal and have sloping sides.
Red Book Online Visual Library, 2009. Image 128_18. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Image 128_50. Syphilis This is the same child depicted in Image 128_10 of the collection. The mother of this
six month infant was not screened for syphilis during pregnancy or at delivery due to a series of medical
errors. The x-ray displays the characteristic "celery stalking" and widening of the metaphases in long bones
found in untreated congenital syphilis.
Red Book Online Visual Library, 2009. Image 128_50. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
Fig 3.6. Algorithm for evaluation and treatment of infants born to mothers with reactive serologic tests for
syphilis.
Red Book Online Visual Library, 2009. Image FIGURE3F. Available at:
http://aapredbook.aappublications.org/visual.
Copyright ©2009 American Academy of Pediatrics
TERATOGENS/MATERNAL DRUGS
“Fetal Anticonvulsant Syndrome”
• Phenytoin
– a broad, low nasal
bridge
– epicanthal folds
– wide-spaced eyes
(hypertelorism)
– cardiovascular
abnormalities
– distal digital hypoplasia
(fetal hydantoin
syndrome)
“Fetal Anticonvulsant Syndrome”
• Valproic Acid
– increased risk for neural
tube defects as well as
cardiac, limb, and renal
anomalies, and a
characteristic facies (fetal
valproate syndrome)
• Phenobarbital and
carbamazepine also are
associated with increased
risks for malformations
and dysmorphic features
following prenatal
exposure
Valproate
Syndrome
Isotretinoin
• “Accutane embryopathy”
• Affects the craniofacial, CV,
and CNS
– Microtia , depressed nasal
bridge, ocular hypertelorism,
cleft palate, macrocephaly
– Truncus arteriosus
• 35% risk in infants of women
who take isotretinoin beyond
15 days after conception
• Maternal use prior to
conception does not appear
to be an increased risk for
anomalies
Labor Drugs
• Terbutaline – tachycardia, hyperglycemia →
hyperinsulinemia
• Indomethacin – premature closure of the
ductus, oligohydramnios
• Magnesium – reduced heart rate, hypotonia,
apnea, feeding intolerance, hypermagnesemia
• Opioid analgesic- decreased heart rate, poor
suck and feeding (can be reversed with
naloxone)
Lithium
• *Ebstein anomaly, ASD
• Thyroid function disturbances
• Take precautions with breastfeeding
Coumadin
• “Fetal Warfarin Syndrome”
– Hypoplastic nose
– Depressed nasal bridge
– Stippling of vertebrae
• Frequently have upper airway obstruction
• Most affected children do well
• The stippling is incorporated into calcifying
cartilage and is no appears on radiographs
after age 1
Fetal Alcohol Syndrome
•
•
•
•
short palpebral fissures
thin vermilion border of the upper lip
smooth philtrum
evidence of pre- or postnatal growth
restriction (height or weight <10th percentile)
• abnormal brain growth (head circumference
<10th percentile) or brain development
(structural brain anomalies).
Fetal Alcohol Syndrome
Infants also can be unusually hirsute (ethnicity always must be considered when
judging hirsutism), and this feature typically dissipates over the first 6 postnatal
months
Fetal Alcohol Syndrome
• Although there is no well-characterized
neonatal alcohol withdrawal syndrome, the
physician should be alert to signs of drug
withdrawal when FASD is suspected due to the
frequent concomitant use of alcohol and
drugs
• FAS is a frequently documented cause of
mental retardation
Marijuana
• Not known to be associated with an increased
incidence of birth defects, dysmorphic
features, or developmental delay in exposed
offspring, although further study is needed in
this regard
• Prenatally exposed newborns may have
tremulousness, increased irritability, and
abnormal visual response to light stimulus
Tobacco
• Associations between maternal cigarette smoking
and miscarriage, fetal growth restriction, preterm
birth, and low birth weight
• A statistically significant increase in cleft lip +/cleft palate was shown in at least one study
• *Increased risk for sudden infant death syndrome
among exposed children
• Multiple studies examining the association
between in utero cigarette smoke exposure
(without postnatal environmental tobacco smoke
exposure) and childhood respiratory disorders
demonstrate a significantly increased prevalence
of physician-diagnosed asthma and wheezing.
Opiates
• Places the newborn at risk for neonatal opiate
withdrawal syndrome, often referred to as
neonatal abstinence syndrome (NAS)
• May not become apparent until 5 days after birth
• For methadone-treated mothers, a higher daily
methadone dose may be associated with a
greater likelihood of the newborn experiencing
NAS
Amphetamines
• *No amphetamine withdrawal syndrome has
been described
• No pattern of fetal anomalies attributable to
maternal amphetamine ingestion
• Direct effects are:
1)Fetal growth restriction (due to vascular effects on
the uteroplacental vasculature)
2) Neonatal agitation, irritability, and hypersensitivity
to environmental stimuli
3) Potential developmental and cognitive impairment
in early childhood
Cocaine
• Associated with vascular disruptive events in
the embryo/fetus due to its potent
vasoconstrictive and hypertensive effects
• Such events include cerebral infarction,
urogenital anomalies, and limb reduction
defects
• Placental abruption appears to be increased in
cocaine-exposed pregnancies