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Mrs. JT is a 27 year old primigravida with an uncomplicated prenatal course, who came to the hospital yesterday afternoon with nausea, vomiting, swelling of her face and hands and a sense that something wasn’t right. She’s at 28 0/7 weeks gestational age, confirmed by 1st trimester ultrasound. Her prenatal course has been uneventful.
On arrival, her blood pressure was elevated to 200/120. She had visible periorbital edema and swelling of her hands and feet with 2+pitting edema. Her reflexes were brisk with one beat of clonus.
Her urine had 3+ protein. Electronic fetal monitoring showed a normal reactive fetus without decelerations and no contractions.
Based on this preliminary evaluation, she was diagnosed with severe pre-eclampsia. She received magnesium sulfate and intravenous hydralazine, with her BP falling to 146/96.
While 28 weeks gestation is a little earlier than what we usually see with pre-eclampsia, it is not rare for it to occur at this gestational age, or even earlier.
The presence of persistent hypertension, and significant proteinuria is the basis for the diagnosis of pre-eclampsia. The other two findings of edema and increased reflexes, while part of the classical description of pre-eclampsia, are not essential for the diagnosis.
Her pre-eclampsia can be categorized as severe at this point, based on the severity of the hypertension (greater than 160/110), although her subsequent laboratory tests will show additional evidence that confirms the severity of the disease.
We weren’t finished with our evaluation of her, but because of the very high (and dangerous) blood pressure and increased reflexes, we immediately loaded her with magnesium sulfate and also gave intravenous hydralazine. The magnesium sulfate was primarily to protect her against seizures, but it is true that magnesium sulfate also has some antihypertensive effects. In addition, we gave hydralazine to lower her blood pressure out of the dangerous range. Our intention was to lower the BP to approximately 140/90 and not to drop it to 110/70. An important physiologic aspect of pre-eclampsia is the peripheral vasospasm, which requires a certain amount of hypertension in order to continue to perfuse the tissues. Returning her to a normal blood pressure can jeopardize this perfusion.
It was important to evaluate the fetus. Some patients with severe pre-eclampsia will have compromised their fetus due to lack of satisfactory blood flow to the placenta, infarcts or abruptions. Further, even though the fetus was in good condition in this particular case, as soon as we start lowering her BP, the uterine perfusion may drop enough to create a fetal threat. Thus, the importance of continuing to monitor the fetus carefully.
Her initial laboratory tests were consistent with severe pre-eclampsia. Her liver enzymes SGOT and SGPT were mildly elevated due to swelling of the liver and microvascular spasm, with significant reduction in downstream perfusion. Her Hgb was 14.3, reflecting the intravascular fluid depletion and hemoconcentration that normally accompanies pre-eclampsia. Her platelets were normal at 220, although a drop in platelets commonly accompanies pre-eclampsia.
We scanned her abdomen, to check fetal presentation (cephalic), amniotic fluid volume (normal, although pre-eclampsia can be found with both polyhydramnios and oligohyramnios), and fetal anatomy. In this case, everything was normal.
We next considered ultimate disposition.
The only definitive treatment for pre-eclampsia is delivery. In this particular case, with the severity of the illness, it was important to take the necessary steps to get her delivered. However, because of her gestational age, early delivery poses a significant risk for the fetus. We compromised.
We started betamethasone to stimulate fetal pulmonary maturity. Betamethasone has its maximum beneficial effect after 48 hours, so if delivery could be safely postponed that long, the fetus would benefit. Further, if delivery could be postponed for a number of weeks, the fetus would be in even better condition. But this patient was sick enough with her pre-eclampsia that we believed it very unlikely we would be able to safely postpone delivery for a few weeks.
Her cervix was long, thick and closed, unfavorable for induction. While we could have opted for cesarean section, we chose a different approach. We started some intravaginal misoprostol to ripen her cervix for about 12 hours, and then started pitocin to induce labor. So long as the baby remains healthy, as evidenced by a normal fetal monitor tracing, and the mother remains stable (sick, but not worsening), then by the time we actually get her delivered, we will be approximately at 48 hours after initiating the betamethasone.
