Pre-eclampsia is the consequence of an initial placental trigger, which initially has no adverse effect on the mother. As the preeclampstic process progresses, a maternal systemic inflammatory reaction results presenting the clinical signs and symptoms of the syndrome. Although pre-eclampsia is associated with a failure of the normal invasion of trophoblastic cells, leading to maladaptation of maternal spiral arterioles it can also be associated with hyper placentation disorders such as diabetes, hydatidiform mole, and multiple pregnancy.

The maternal arterioles are the source of blood supply to the fetus, and maladaptation of these vessels can interfere with normal villous development. In some cases, compensation can occur, but, in others, poor villous development results in placental insufficiency. Secondary damage, such as fibrin deposition and thrombosis, can then occur within the placenta. These features are found in cases of placental insufficiency whether preeclampsia is present or not. Not all women with the potential placental trigger develop pre-eclampsia; consequently the maternal response must be the decisive factor in development of systemic disease.

Although pre-eclampsia is considered primarily to be a vascular endothelial disorder, it presents as a multisystem disorder with various manifestations. This variation could be due to different vascular beds being affected to varying degrees, however research has shown that there is a differential maternal inflammatory response. The maternal syndrome of preeclampsia has previously been ascribed to generalized maternal endothelial cell dysfunction. Recent research is suggesting that the endothelial dysfunction is a part of a more generalized intravascular inflammatory reaction involving intravascular leukocytes as well as the clotting and complement systems [6] Pre-eclampsia may be a final common pathway response to inflammatory stimuli such as infection.

A possible interpretation of these observations suggests that the anti-inflammatory impact of dexamethasone may attenuate the inflammatory cascade involved in the pre-eclampstic process. Up to day 4, dexamethasone appears to moderate the progression of pre-eclampsia, reducing the blood pressure and leading to significant gain in gestational age. These finding begs the question - Would a repeat administration of dexamethasone in pre-eclampstic patients at day 3-4 gain a further reprieve from the pre-eclampstic process and consequently increase the gain in gestational age?

In a limited capacity other anti-inflammatory drugs such as aspirin given early in pregnancy have been associated with an attenuation of the pre-eclampstic process. Conversely nonsteroidal anti-inflammatory drugs have been linked with exacerbation of hypertension especially in the postpartum period.

The evaluation of the impact of antepartum administration of corticosteroids on the course of the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP) in pregnancies at 24 to 37 weeks' gestation has been initially attempted by Magann et al. A small prospective, randomized study was undertaken in 25 antepartum patients with atypical severe preeclampsia expressed as HELLP syndrome. Twelve pregnant women were randomized to receive double-dose dexamethasone (10 mg intravenously every 12 hours) until delivery, and 13 women were randomized to the control arm. Management and delivery decisions for all patients were based on a common protocol, with delivery undertaken for a deteriorating maternal or fetal condition.

In the corticosteroid-treated group the maternal platelet count significantly increased (p = 0.006), whereas lactic dehydrogenase and alanine aminotransferase significantly decreased over time (p = 0.03 and p = 0.005) in comparison to the 13 women who did not receive corticosteroids. Maternal urinary output after entry into the study was significantly increased within hours after steroid administration versus the control group (p = 0.0006). The study entry-to-delivery interval (41 ± 15 hours) was significantly longer in the group of steroid-treated women (p = 0.0068).

Stabilization and significant improvement in the laboratory and clinical parameters associated with HELLP syndrome occurred in women who received high-dose antenatal corticosteroids, as measured by maternal platelet count, urinary output, lactic dehydrogenase, alanine aminotransferase, and postponement of delivery. The findings of this investigation suggest that this therapeutic approach could enhances maternal-fetal care by postponing delivery of some previable fetuses, reduce the need for maternal transfusion of blood products, reduce neonatal morbidity or mortality from multiple systemic effects, and facilitate a safer transfer of the ill mother to a tertiary care site for optimal peripartal care.

With Regards,
Sara Giselle
Associate Managing Editor
Journal of Critical Care Obsestrics & Gynocology