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1
Question:

A male newborn infant born at 39 weeks gestation is evaluated in the newborn nursery.  The mother is a 24-year-old primigravida whose pregnancy was complicated by preeclampsia with severe features.  Magnesium sulfate was initiated for seizure prophylaxis and induction of labor started, but an emergency cesarean delivery was performed due to uncontrollable maternal hypertension and nonreassuring fetal heart rate status.  Apgar scores were 8 and 8 at 1 minute and 5 minutes, respectively, for poor tone.  On examination, the infant's weight is 2.3 kg (5 lb 1 oz), placing him in the 3rd percentile; height is 46 cm (18 in), placing him in the 5th percentile; and head circumference is 33 cm (13 in), placing him in the 10th percentile.  There is a paucity of subcutaneous fat and areas of skin peeling on the soles and trunk of the infant.  The remainder of the physical examination is unremarkable.  This infant is at risk for which of the following complications?

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Explanation:

Fetal growth restriction

Symmetric

Asymmetric

Definition

  • Estimated fetal weight <10th percentile or birth weight <3rd percentile for gestational age

Onset

  • 1st trimester
  • 2nd/3rd trimester

Etiology

  • Chromosomal abnormalities
  • Congenital infection
  • Uteroplacental insufficiency
  • Maternal malnutrition

Clinical
features

  • Global growth lag
  • "Head-sparing" growth lag

Management

  • Monitor/treat complications (eg, hypoglycemia, hypothermia, polycythemia)
  • Hypoglycemia: frequent screening and frequent feedings
  • Hypothermia: skin to skin with mother, examinations in incubator
  • Polycythemia and hypocalcemia: screen if symptoms develop (eg, poor feeding, vomiting, jitteriness)

This infant has fetal growth restriction (FGR), which is defined as an estimated fetal weight <10th percentile or a birth weight <3rd percentile for gestational age.

FGR occurs from a variety of etiologies, including maternal, placental, or fetal factors.  Maternal factors include malnutrition (eg, hyperemesis gravidarum), substance use, and conditions leading to vasculopathies (eg, preeclampsia, pregestational diabetes).  Fetal conditions include chromosomal aneuploidies and congenital infections.

Most cases of FGR are a result of uteroplacental insufficiency, which is impaired blood flow to the fetus with subsequent decreased oxygen and nutrient delivery.  Fetuses adapt to a hypoxic, nutrient-depleted in utero environment by shunting blood from nonvital organs (eg, liver, subcutaneous fat) to preserve blood flow to vital organs (eg, brain), which can lead to the following complications at birth:

  • Polycythemia:  chronic hypoxia induces increased erythropoietin and red blood cell expansion

  • Hypoglycemia:  chronic nutrient deprivation results in lower plasma glucose and insulin concentrations, leading to decreased liver and muscle glycogen stores (Choice A)

  • Hypothermia:  shunting blood to vital organs causes a decrease in subcutaneous fat and increased heat loss (Choice B)

  • Hypocalcemia:  placental dysfunction decreases calcium transfer to the fetus

  • Perinatal asphyxia and meconium aspiration:  growth-restricted infants have a difficult respiratory transition following birth and may experience hypoxic events leading to organ damage; placental dysfunction can cause intrauterine stress during labor and increase the likelihood of meconium-stained fluid

(Choice C)  Magnesium freely crosses the placenta; therefore, the fetus's serum concentration equals the mother's serum concentration.  Infants born to mothers receiving magnesium sulfate for either seizure prevention or fetal neuroprotection have hypermagnesemia at birth, resulting in respiratory depression and hypotonia.

(Choice E)  Infants born to mothers with preeclampsia are at risk of thrombocytopenia due to decreased platelet production, which typically normalizes by 7 to 10 days of life.

Educational objective:
Fetal growth restriction is defined as an estimated fetal weight <10th percentile or a birth weight <3rd percentile for gestational age.  The fetal adaptation to uteroplacental insufficiency places infants at risk for complications at birth, including polycythemia, hypoglycemia, hypothermia, and hypocalcemia.