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).
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.
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.
