A 17-year-old girl, gravida 1 para 0, at 37 weeks gestation comes to the emergency department with headache, blurry vision, and fatigue. The patient has not had a prenatal visit for the past month due to final exams in school. She has no chronic medical conditions, and her only medication has been a daily prenatal vitamin. Blood pressure is 190/96 mm Hg and pulse is 106/min. Urinalysis shows 4+ protein. Physical examination shows increased ankle clonus but no neurologic deficits. Laboratory results are as follows: The patient is admitted to labor and delivery for induction of labor and undergoes a spontaneous vaginal delivery of a male infant. Which of the following complications is most likely present in the neonate?

Question

A 17-year-old girl, gravida 1 para 0, at 37 weeks gestation comes to the emergency department with headache, blurry vision, and fatigue.  The patient has not had a prenatal visit for the past month due to final exams in school.  She has no chronic medical conditions, and her only medication has been a daily prenatal vitamin.  Blood pressure is 190/96 mm Hg and pulse is 106/min.  Urinalysis shows 4+ protein.  Physical examination shows increased ankle clonus but no neurologic deficits.  Laboratory results are as follows:  The patient is admitted to labor and delivery for induction of labor and undergoes a spontaneous vaginal delivery of a male infant.  Which of the following complications is most likely present in the neonate?

Quizplus · Accepted Answer

11ec25c8_da6d_f9b9_bc81_35518b0b1f75_MD0003_00 This pregnant patient with severe-range hypertension (systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥110 mm Hg) and proteinuria has preeclampsia with severe features, which likely occurs due to abnormal placental development. Under normal conditions, early cytotrophoblast invasion remodels the uterine spiral arteries into high-flow, low-resistance vessels that increase oxygen and nutrient delivery to the growing fetus and placenta. In contrast, abnormal cytotrophoblast invasion in preeclampsia results in low-flow, high-resistance vessels that cause decreased placental perfusion. abnormal cytotrophoblast invasion During the first and second trimesters, the decreased placental perfusion is often subtle and not clinically noticeable because the placenta can keep up with the metabolic demands of the fetus. However, during the third trimester, there is rapid fetal growth (~0.2 kg [0.4 lb]/week), and the chronically under-perfused placenta cannot provide adequate oxygen to the fetus. In patients with preeclampsia, this uteroplacental insufficiency often coincides with the onset of wide-spread maternal vasoconstriction, which can manifest as hypertension and signs of end-organ damage, such as headache, proteinuria, thrombocytopenia, and hemolysis (eg, anemia, elevated lactate dehydrogenase). The addition of vasoconstriction on the already under-perfused placenta culminates in substantially decreased fetal oxygenation and nutrient supply. Over the course of several weeks (as in this patient with no prenatal care in a month), fetal growth can rapidly decrease, resulting in a small-for-gestational-age infant (potentially 1-2 lb less than average birth weight). (Choice A) Neonatal hypoxic brain injury can occur with severe, acute decreases in placental perfusion or fetal oxygenation (eg, severe placental abruption, shoulder dystocia) because the fetus has no time to adapt to lower oxygen levels. Because preeclampsia causes chronically low uteroplacental perfusion, over time the fetus adapts by preferentially shunting oxygenated blood from the body to the brain, thereby sparing brain injury. placental abruption (Choices B and D) Intraventricular hemorrhage and neonatal respiratory distress syndrome are complications of prematurity (ie, <37 weeks gestation). Preeclampsia is not an independent risk factor for either. (Choice C) Kernicterus, the neurologic sequelae of neonatal hyperbilirubinemia, most commonly is caused by neonatal hemolysis (eg, ABO or Rh[D] incompatibility). Preeclampsia can cause hemolysis and hyperbilirubinemia in the mother, but there is minimal transplacental bilirubin transfer to the fetus. (Choice F) Preeclampsia causes maternal platelet consumption and thrombocytopenia. It does not cause neonatal thrombocytopenia, which typically occurs due to immune-mediated thrombocytopenia. Educational objective: Preeclampsia with severe features increases the risk of fetal growth restriction (ie, small-for-gestational-age infant) due to uteroplacental insufficiency. References: Impact of fetal growth on pregnancy outcomes in women with severe preeclampsia. (http://www.ncbi.nlm.nih.gov/pubmed/28501274) Association of chronic hypertension with birth of small-for-gestational-age neonate. (http://www.ncbi.nlm.nih.gov/pubmed/28636133)

A 17-Year-Old Girl, Gravida 1 Para 0, at 37 Weeks