Perinatology & Neonatology Flashcards
Early term
37 0/7 weeks of gestation through 38 6/7 weeks
Full term
39 0/7 weeks of gestation through 40 6/7 weeks
Late term
41 0/7 weeks of gestation through 41 6/7 weeks
Post term
42 0/7 weeks of gestation and beyond)
Perinatal Period:
After 28 weeks gestation up to 28 days following birth
Neonatal Period:
First 28 days (4 weeks) of life
Ductus venosus
O2 rich blood from maternal placenta enters
circulation (bypasses liver) via inferior vena cava
* Connects umbilical vein to
inferior vena cava
Ductus arteriosus
~90% of blood bypasses the pulmonary
vasculature directly to the aorta
* Connects the pulmonary
artery & aorta
Foramen ovale
O2 rich blood from the Right Atrium directly
to the Left Atrium (right-to-left shunting)
* Opening between the two atria of the fetal heart
Median closure time of ductus arteriosus
13.5 hours
Clamping the umbilical cord ___ preload to the left ventricle & ___ cardiac output = _____
↓; ↓ ; bradycardia
Delayed cord clamping =
After the lungs have aerated
- 30-60 seconds
- Cardiac output should not fall
- Delayed cord clamping should be performed in preterm & term newborns not requiring resuscitation at birth
Delayed umbilical cord clamping in term infants
↑ Hgb levels at birth
↑ iron stores during infancy
↑ neurodevelopment at 4 yo
Delayed umbilical cord clamping in pre-term infants
↓ need for blood transfusion
↓ intraventricular hemorrhage
↓ necrotizing enterocolitis
When to not delay cord clamp
- Resuscitation is required
- Placental circulation is disrupted by:
* Abruption
* Cord avulsion
* Bleeding placenta previa
* Vasa previa
Neonates are sensitive to
heat loss & retention
How do neonates thermoregulate at birth?
- Temperature has been tightly regulated for 9 months
- Now dependent mainly on metabolic heat from brown adipose tissue
Limited, esp. preterm
When is surfactant produced?
3rd trimester (28-40 weeks)
Surfactant
- Phospholipid & protein substance ↓ surface
tension at the liquid-air interface - Produced by Alveolar type II cells
- Without surfactant, ↑ pressure is required
to inflate & ventilate the lungs
–Without surfactant → alveoli collapse - Production minimally sufficient by 34 weeks gestation
Following birth, the neonate MUST transition from placental to pulmonary
gas exchange, meaning these things must occur:
- Pulmonary vascular resistance must ↓
- Pulmonary perfusion must ↑
- Fetal vascular shunts must close to separate systemic & pulmonic circulation
- Patent Ductus arteriosus & Foremen Ovale
At term, fetal lungs contain _____ of fluid
~90 mL (~3 1/8 oz)
How is the fluid from fetal lungs removed?
- Uterine contractions & vaginal birth
squeeze this from the lungs
~1/3 of fluid through nose & mouth - Fetal adrenaline stimulates pulmonary
epithelial cells to stop secreting & start
reabsorbing lung fluid via Na+ channel
activation
-Lung aeration changes the transpulmonary
pressure gradient & the remaining fluid is
reabsorbed via capillaries & lymphatics
T/F Pre-mature neonates &/or cesarean born do not experience the “vaginal squeeze” &
experience greater respiratory difficulty
T
Neonatal breathing begins within ____
seconds of birth & should be sustained
by ____ seconds
30; 90
Steps for newborn resuscitation
- Dry infant & place under radiant heat, monitor temp.
- Position infant to open airway, gentle suction of mouth/nose
- Assess respiratory effort (apneic v. gasping v. regular)
- Assess heart rate (>100 or <100 beats/min)
* ↓ HR is the MOST RELIABLE indicator for resuscitation - Gently stimulate (back rub, heel flick) if HR <100 or irregular respiration
- If stimulation fails within a few seconds begin bag & mask ventilation
* More to come in Pediatric Advanced Life Support
How many newborns need resuscitation?
~10% require active resuscitation & 1% need extensive care
The APGAR Score
- Time honored method in evaluating the
newborn infant at time of delivery - NOT predictive of long-term outcomes
- Description of the severity of perinatal
depression & the need for & response to
resuscitative efforts
APGAR Levels
Assessed at 1 & 5 minutes following birth
7-10 = stable infant
<7 = resuscitative measures continue &
scores assigned q 5 minutes until infant
stabilized
<7 after 3-4 intervals = consider ICU
Ophthalmia neonatorum
- Mucopurulent conjunctivitis of
newborns
12% of neonates
Gonococcal & Chlamydial
infections = MOST COMMON - 1% Silver Nitrate solution or
0.5% erythromycin ointment
First immunization a newborn will recieve
Routine immunization against
hepatitis B
Standard practice prior to d/c for all
medically stable newborns with
birthweights >2000 g
What if the mother is seropositive
for Hepatitis B surface antigen?
Neonate is also passively
immunized with Hep
B immune globulin
Vitamin K supplementation in newborns
- Single, IM dose of Vitamin K 0.5 - 1 mg given within 1 hour of birth
Prevents Vitamin K dependent hemorrhagic disease of the newborn
3 part newborn screening for rare disorders includes
- Blood sample (heel stick) collected on filter paper
- Pulse Oximetry
- Hearing Screen
60+ asymptomatic conditions including:
Phenylketonuria (PKU), galactosemia,
hemoglobinopathies, hypothyroidism, cystic fibrosis,
hearing,
Consequences for failure to screen for PKU
Phenylketonuria (PKU) → inability to break down the amino acid phenylalanine
Left untreated, PKU → brain damage or death
Consequences for failure to screen for galactosemia:
- Galactosemia → inability to digest galactose, a sugar found in milk
Builds up in the blood
Left untreated → seizures, sepsis, liver damage, or death
Consequences for failure to screen for hemoglobinopathies
- Hemoglobinopathies → Variety of inherited conditions affecting the number or
shape of RBCs.
Some cause life-threatening symptoms, while others do not cause medical
problems or even signs of the condition
Consequences for failure to screen for hypothyroidism
Hypothyroidism → thyroid gland does not produce enough thyroid hormone
(What does thyroid hormone do?)
Left untreated → sluggishness, slow growth, & learning delays
Consequences for failure to screen for Cystic fibrosis
- Cystic Fibrosis → an inherited disorder of the mucus glands
Causes excess, abnormally thick, sticky mucus production → variety of
health problems
Left untreated → serious lifelong morbidity & early mortality
Consequences for failure to screen for hearing loss
- Hearing loss can occur when outer ear,
middle ear, inner ear, or acoustic nerve do
not work appropriately - Left untreated, hearing loss affects
development of:
Speech
Language
Social skills
Why is there a loss of body weight occurs first
few postnatal days?
- Weight loss of 5-12% is normal
in first week after birth - Predominantly loss of
extracellular water - Inadequate nutritional intake
- Lag time for maternal breast milk
engorgemen
SGA
Small for gestational age or Intrauterine growth restriction (IUGR):
<10th percentile in weight
AGA
Appropriate for gestational age
LGA
Large for gestational age or fetal macrosomia
>90th percentile in weight
What does it mean when there is a symmmetric growth restriction?
- Weight, length, & head circumference
ALL ≤10th percentile - Symmetric implies an event in EARLY
pregnancy such as:
Chromosomal abnormalities
Drug or alcohol use
Congenital viral infections
What does it mean when there is an asymmetric growth restriction?
- ONLY WEIGHT ≤10th percentile
Asymmetric implies problem LATE in
pregnancy such as:
Pregnancy-induced hypertension
Preeclampsia
Placental insufficiency
Causes for LGA babies
- Infant of a diabetic mother (IDM)
- Normal variants:
Genetic predisposition
Male fetus
Post-dates gestation
Multiparity
Effects of LGA on the baby
Birth injury (fractures, shoulder dystocia, subdural hemorrhage)
Respiratory Distress Syndrome
Asphxia
Infants of diabetic mothers
In utero, ↑ flow of nutrients from
hyperglycemia
High glucose loads → fetal
pancreas secretes excessive
amounts of insulin to maintain
neonatal euglycemia
All LGA infants should be screened for
_____ while in the hospital
hypoglycemia
Normal-term infant blood glucose stabilizes at ___ mg/dL 3 hours after birth
50-80
If signs of hypoglycemia are present, they
are often relatively nonspecific & may be
subtle including
Lethargy
Poor feeding
Irritability
Tremulousness/jitteriness
Apnea
Seizures
T/F SGA (IUGR) infants can also have hypoglycemia
T
Different mechanism = ↓ glucose stores
Infant respiratory distress syndrome
- 1% of pregnancies in the US
50% of deliveries at 26-28 weeks
30% of deliveries at 30-31 weeks
More common in premature, Caucasian neonates (m/f)
Infant respiratory distress syndrome clinical presentation
Progressive, respiratory distress after birth
Tachypnea
Expiratory grunting
Subcostal & intercostal retractions
Cyanosis
Nasal flaring
Possible apnea &/or hypothermia
IRDS diagnosis
- CBC & Blood cultures
- Blood gases
- Pulse oximetry → should be 90-95%
- . CXR
- Echocardiogram
IRDS management
- Continuous positive airway pressure
(CPAP) if spontaneously breathing - Surfactant administration ↓
mortality rate by 50% - Tx other complications
(Eg. Pneumothorax) - Fluid & metabolic management to
↓ energy & O2 consumption - Possible empiric antibiotics
(ampicillin & gentamicin)
CXR findings for IRDS
- Bilateral, diffuse, reticular granular or ground-glass appearances
- Air bronchograms
* air-filled brochii on a background of airless lung - Poor lung expansion
Meconium composition
Sterile, thick, black-green (from bile),
& odorless material in the fetal intestine
Composed of debris
Desquamated cells from the intestine & skin
Gastrointestinal mucin & other intestinal secretions
Lanugo hair
Vernix caseosa
Amniotic fluid
Meconium aspiration syndrome epidemiology
0.1 - 0.4 of all births
2 - 10% with meconium-stained amniotic fluid
- Etiology (Theory)
Fetal distress → meconium passage in utero followed by aspiration
Meconium aspiration pathogenesis
- Aspirated during fetal gasping/initial
breaths after delivery. - Prolonged hypoxia stimulates fetal
breathing & gasping that can lead
to inhalation of amniotic in the
hypopharynx or trachea
Meconium aspiration clinical presentation
- Meconium-stained amniotic fluid (often can see staining under finger nails)
Similar to Respiratory distress syndrome
Cyanosis
End-expiratory grunting
Alar (nasal) flaring
Intercostal retractions
Tachypnea
↑ anteroposterior chest diameter
(“Barrel chest”) 2° air trapping
Auscultated rales & rhonchi
(in some cases)
MAS diagnosis
- ABGs
- Pulse Oximetry
- CBC c/ Diff
- Blood cultures
- CXR
- Echocardiogram
What would you see on a CXR for meconium aspiration?
Air space opacities “Fluffy infiltrates”
Echo findings for meconium aspiration
- Pulmonary consolidation with air
bronchograms - Pleural line anomalies & absence
of the A-line - Alveolar-interstitial syndrome or
B-lines in nonconsolidated regions
MAS management
Baby → NOT vigorous (depressed respiratory effort or poor muscle tone)
Baby to radiant warmer
Clear the secretions with a bulb syringe
Proceed with the normal steps of newborn resuscitation
Start positive pressure ventilation if, after these initial steps are taken, when
the baby is:
Not breathing OR
Heart rate is <100 bpm
MAS management
- Oxygen therapy with monitoring of blood gases
- May administer artificial surfactant
- CPAP or mechanical ventilation
- Administration of antibiotics may be considered for possible occurrence of
secondary bacterial pneumonia
Persistent pulmonary HTN of newborn (PPHN)
Failure to transition to normal circulation, aka persistent fetal circulation
PPHN epidemiology
0.4-6.8 per 1000 live births
- Etiology
Sustained ↑ pulmonary vascular resistance → pulmonary hypertension
Right to left shunting of desaturated blood through fetal pathways
Patent foramen ovale OR
Patent ductus arteriosus otherwise structurally normal heart
PPHN clinical presentation
Clinical Presentation
Respiratory distress, 1st 24 hrs
Tachypnea
Retractions
Grunting
Cyanosis
Management of PPHN
- Maintain normal body temperature
- Correction abnormal electrolytes &/or glucose
- Correct metabolic acidosis
- Maintain adequate systemic blood pressure
- ↓ pulmonary vascular resistance
- Ensuring O2 release to tissues
- Minimize barotrauma from ↑ O2 & high ventilator pressure settings
Transient tachypnea of the newborn (TTN) Epidemiology
~1% of newborns some general respiratory distress
33 - 50% have TTN
- Benign, self-limiting condition
- Delayed resorption/clearance of fetal alveolar fluid
- Often occurs in term or near-term infants (Esp. those not “vaginally squeezed”)
TTN clinical presentation
Signs of respiratory distress shortly after birth
Tachypnea
nasal flaring
grunting
Retractions
Hypoxia
↑ O2 requirement
Cyanosis (extreme cases)
CXR findings for TTN
↑ lung volume & flat diaphragm
Prominent vascular markings
(sunburst pattern) originating
from the hilum
Fluid in interlobar fissures
Alveolar edema (“Fluffy densities”)
When does physiologic jaundice of newborn occur?
Begins AFTER 24 hours of life!
Physiologic jaundice of newborn pathogenesis
Neonate → immature liver → impaired ability to conjugate bilirubin
Neonate gut is ____ so very little urobilin is created
sterile
Symptoms of Acute Bilirubin Encephalopathy
Sleepy
Hypotonia
High pitched cry
Retrocollis (arches neck & trunk)
Bicycling/twitching of the hands & feet
Death (respiratory failure or seizure)
Remove bilirubin from blood = _____
Prevent neurotoxicity (Kernicterus)
1st line treatment for physiologic jaundice of the newborn
Phototherapy
ABO & Rh hemolytic disease is caused by what combination of blood in the mother/baby?
Maternal type O blood
+
Baby type A or B
Treatment for breastfeeding failure jaundice
- Frequent feeds & adequate hydration
- Consider phototherapy
Depends on total serum bilirubin - Exchange transfusion, prn
SIDS defined
Unexplained death < 1 year of age
Leading cause of infant
mortality 1 to 12 mo
SIDS
Risk factors for SIDS
Sleeping position & Co-sleeping
Bottle feeding
Maternal smoking (pre & postnatal)
Infant overheating
Soft sleeping surface
Car seat napping (not car travel)
