Transition out of the Perinatal Period Flashcards
Perinatal catecholamine surge
At birth, there is a massige surge in epinephrine and norepinephrine in the infant, which lasts for approximately four hours
This facilitates the increased cardiac output and myocardial contractility, increased pulmonary surfactant production, and promotes reabsorption of fluid in the lungs. Heart rate is usually ~160 bpm and drops to ~130 bpm 1 hour after birth.
It also enhances gluconeogenesis and lipolysis, mobilizing fuel for breathing and feeding.
Changing flow through the ductus arteriosus after birth
As pulmonary vascular resistance declines, the right-to-left shunt through the ductus arteriosus becomes bidirectional, then left-to-right.
A combination of increased oxygenation and diminished signaling from placental PGE2 are responsible for the ductus’ closure in the weeks following birth.
The ductus is at risk of premature closure if NSAIDs are used after 33 weeks EGA, as it will shut down placental PGE2 production.
Misoprostol vs dinoprostone vs dinoprost
Misoprostol: PGE1
Dinoprostone: PGE2
Dinoprost: PGF2a
Respiratory syndromes that may prevent proper cardiovascular transition in neonates
- Meconium aspiration
- Amniotic fluid aspiration
- Respiratory distress syndrome of the newborn (surfactant deficiency)
- Pneumonia or other lung infections
- Congenital hypoplastic lungs (as in diaphragmatic hernia or oligohydramnios)
Premature closure of the ductus arteriosus leads to a syndrome of. . .
. . . pulmonary hypertension with cyanosis and respiratory distress
This usually presents shortly after birth in a case where the mother has used NSAIDs during the third trimester (after EGA 33)
Transient tachypnea of the newborn
- Onset at birth, mild course, lasts 48-72 hours and resolves spontaneously
- Baby will be tachypneic and grunting (to raise EEP)
- Diagnose with CXR (shows hyperextended, wet lungs)
- Treat w/ positive pressure ventilation
- Thought to be due to delayed reabsorption of pulmonary fluid and consequentially low pulmonary compliance. Mechanistically, low catecholamine surge at birth has been implicated.
- Risk factors: Cesarean section, Excess maternal analgesia, birth asphyxia, excessive maternal fluid administration, breech delivery, delayed cord clamping, fetal polycythemia
While functional ductus arteriosus closure occurs in virtually 100% of infants by ___, permanent anatomic ductus arteriosus closure may occur ____.
While functional ductus arteriosus closure occurs in virtually 100% of infants by 4 days, permanent anatomic ductus arteriosus closure may occur months later or not at all.
Transitional cardiac abnormalities in infants from GDM pregnancies
Presumably due to the cardiac growth-stimulating effects of insulin
- Asymptomatic cardiomyopathy
- Hypertrophic subaortic stenosis
Transitional cardiac abnormalities in infants born to mothers with anti-Ro or Anti-La
5% risk of congenital heart block due to deposition of transplacentally acquired antibody
Neonatal Grave’s disease
- Heart failure
- Goiter
- Tachycardia
- Low weight
- Failure to thrive
- Proptosis
Ritodrine neonatal cardiac effects
Associated with neonatal interventricular septal hypertrophy
Respiratory rate in healthy newborns
Newborns are typically born with tachypnea which stays relatively constant for 6 hours, then regresses to what we expect for an infant.
Apnea of the neonate (differential)
- Sepsis
- Intracranial hemorrhage
- Hypocalcemia
- Hypoglycemia
- Seizure
- Maternal myasthenia gravis
- Maternal drugs (especially narcotics, benzodiazepines, magnesium sulfate)
Pulse oximetry in a newborn
Usually does not reach 90% until ~9 minutes after birth
Neonatal dependence upon gluconeogenesis and glycogenolysis
During the first few days, only ~20-50% of the glucose utilized for energy comes from milk. All the rest is produced by hepatic metabolism.
Fat metabolism and ketone metabolism are also highly active during this time as suppleental energy sources.
Etiologies of transient neonatal hypoglycemia
- Fetal: IUGR (low glycogen stores), LGA (unknown etiology), erythroblastosis fetalis-associated hyperinsulinemia, infection, hyperviscosity syndrome
- Maternal: GDM, excessive intrapartum parenteral glucose administration, beta-sympathomimetic tocolytics, oral hypoglycemics
Symptoms of neonatal hypoglycemia
- Jiteriness
- Irritability
- Lethargy
- Cyanosis
- Apnea
- Seizures
- Poor feeding
- Unexplained respiratory distress
- Abnormal cry
Defining hypoglycemia in neonates
Neonates have much lower physiologic blood sugars than children or adults, with sugars of ~35mg/dL being relatively normal.
That said, most clinicians would define neonatal hypoglycemia as plasma sugar < 40 mg/dL with symptoms at any postnatal age
Fetal calcium regulation
In the fetus, PTH and calcitriol are low, but calcitonin is high, favoring calcum deposition into bones.
Shift in calcium homeostasis in the neonate
During the fetal period, calcitonin is the predominant hormone and PTH levels are very low.
Following delivery, calcium levels begin to drop over time, stimulating PTH and calcitriol. This begins bone resorption, sensitizes the gut to absorb calcium, and causes reabsorption of calcium at the nephron.
Calcium levels stabilize around 8 mg/dL by 48 hours and gradually rise to reference range over the next several weeks.
Neonatal hypocalcemia
May be asymptomatic or may present similarly to hypoglycemia (jitteriness, poor feeding, seizures, cyanosis) along with increased tone.
Usually between 24-48 hours age.
Natal transfusion
At the time of birth, the placenta delivers an effective transfusion to the infant due to contraction of the uterine wall.
This is an important determinant of blood and plasma volume within the first few postnatal days.
This amounts to a rise of about 1-2g/dL Hgb
Effects of delaying cord clamping by 3 minutes and holding the baby below the level of the introitus
These would increase the amount of blood transfused from the placenta into the neonate, potentially by up to 50%.
This may result in polycythemia and subsequent hyperbilirubinemia
Etiologies of neonatal polycythemia
- Excessive placental transfusion
- Twin-twin transfusion syndrome
- Gestational diabetes mellitus
- Fetal hypoxia (may be due to placental insufficiency, toxemia, postmaturity syndrome, maternal smoking)
- Thyrotoxicosis
- Congenital adrenal hyperplasia
- Down syndrome
Definition of polycythemia in a newborn
Venous hematocrit > 65%
Symptoms of polycythemia in the newborn
- Plethora
- Irritability
- Poor feeding
- Seizures
- Apnea
- Abnormal cry
- Respiratory distress
- Hypoglycemia
- Necotizing enterocolitis
- Oliguria with hematuria
Definition of neonatal anemia
Hematocrit of <42% immediately after birth
Whether delayed cord clamping transfuses the infant, or drains blood from the infant, depends entirely upon. . .
. . . gravity