A 29-year-old primigravid woman at 30 weeks gestation comes to the office for evaluation of decreased fetal movement. The patient has had minimal fetal movement for the past few hours. She has had no vaginal bleeding or contractions. The patient has sickle cell disease and is taking low-dose aspirin. Her pregnancy is dated by a 10-week ultrasound, and she had a normal fetal anatomy ultrasound at 18 weeks gestation. At 24 weeks gestation, the patient had an abnormal glucose challenge test, but a normal glucose tolerance test. Blood pressure is 134/82 mm Hg and pulse is 90/min. BMI is 32 kg/m2. Fetal heart rate is 140/min. Fundal height is 26 cm. Ultrasound reveals a cephalic male fetus measuring at the 16th percentile and an amniotic fluid index of 4 cm (normal: >5 cm). Which of the following is the most likely cause of this patient's presentation?
Sickle cell disease in pregnancy | |
Prenatal care |
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Obstetric complications |
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Fetal complications |
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Patients with sickle cell disease are at risk for multiple obstetric complications (eg, preeclampsia, fetal growth restriction) due to vasoocclusion that can result in placental infarction, ischemia, and subsequent uteroplacental insufficiency.
Adequate uteroplacental blood flow is essential for normal fetal development. Uteroplacental insufficiency results in decreased fetal perfusion, which limits fetal oxygenation and nutrition. In response, the fetus has decreased fetal movement, slowed growth (with possible fetal growth restriction), and preferential shunting of blood flow from the kidneys to the brain, as evidenced by decreased urine production and resultant oligohydramnios (ie, amniotic fluid index ≤5 cm). Oligohydramnios can present with a uterine size-less-than-dates discrepancy (eg, fundal height 26 cm at 30 weeks gestation), as in this patient.
Due to the high risk of intrauterine fetal demise associated with uteroplacental insufficiency, management is with close antenatal surveillance (eg, serial growth ultrasound, umbilical artery Doppler ultrasound) for monitoring of fetal well-being and delivery planning.
(Choice A) Fetal congenital infections can cause decreased fetal movement and oligohydramnios; however, they typically present with additional ultrasound findings (eg, hydrops fetalis, microcephaly). This patient's 18-week fetal anatomy ultrasound was normal, making this diagnosis less likely.
(Choice B) Inaccurate pregnancy dating can cause a uterine size-dates discrepancy. However, first-trimester ultrasound is accurate within 7 days, making this an unlikely cause of this patient's presentation.
(Choice C) Maternal obesity increases the risk of obstetric complications (eg, gestational diabetes, fetal macrosomia) that can cause a uterine size-greater-than-dates discrepancy. However, maternal obesity does not typically cause oligohydramnios (as often evidenced by a uterine size-less-than-dates discrepancy).
(Choice D) Prepregnancy diabetes mellitus can cause chronic vascular disease leading to uteroplacental insufficiency, fetal growth restriction, and oligohydramnios. Gestational diabetes mellitus can cause fetal macrosomia and polyhydramnios (ie, amniotic fluid index ≥24 cm). However, pregnancy-induced hyperglycemia (eg, an abnormal glucose challenge test with a normal glucose tolerance test) does not cause significant changes.
Educational objective:
Maternal sickle cell disease causes vasoocclusion that can result in placental infarction, ischemia, and subsequent uteroplacental insufficiency. Uteroplacental insufficiency may present with decreased fetal movement and oligohydramnios (ie, amniotic fluid index ≤5 cm) due to decreased fetal perfusion.