Brad Thigpen

Stroke and severe preeclampsia and eclampsia: a paradigm shift focusing on systolic blood pressure.

OBJECTIVE: To identify important clinical correlates of stroke in patients with preeclampsia and eclampsia. METHODS: The case histories of 28 patients who sustained a stroke in association with severe preeclampsia and eclampsia were scrutinized with particular attention to blood pressures. RESULTS: Stroke occurred antepartum in 12 patients, postpartum in 16. Stroke was classified as hemorrhagic-arterial in 25 of 27 patients (92.6%) and thrombotic-arterial in 2 others. Multiple sites were involved in 37% without distinct pattern. In the 24 patients being treated immediately before stroke, systolic pressure was 160 mm Hg or greater in 23 (95.8%) and more than 155 mm Hg in 100%. In contrast, only 3 of 24 patients (12.5%) exhibited prestroke diastolic pressures of 110 mm Hg or greater, only 5 of 28 reached 105 mm Hg, and only 6 (25%) exceeded a mean arterial pressure of 130 mm Hg before stroke. Only 3 patients received prestroke antihypertensives. Twelve patients sustained a stroke while receiving magnesium sulfate infusion; 8 had eclampsia. Although all blood pressure means after stroke were significantly higher than prestroke, only 5 patients exhibited more than 110 mm Hg diastolic pressures. In 18 of 28 patients, hemolysis, elevated liver enzymes, low platelets syndrome did not significantly alter blood pressures compared with non–hemolysis, elevated liver enzymes, low platelets. Mean systolic and diastolic changes from pregnancy baseline to prestroke values were 64.4 and 30.6 mm Hg, respectively. Maternal mortality was 53.6%; only 3 patients escaped permanent significant morbidity. CONCLUSION: In contrast to severe systolic hypertension, severe diastolic hypertension does not develop before stroke in most patients with severe preeclampsia and eclampsia. A paradigm shift is needed toward considering antihypertensive therapy for severely preeclamptic and eclamptic patients when systolic blood pressure reaches or exceeds 155–160 mm Hg. LEVEL OF EVIDENCE: III

Maternal benefit of high-dose intravenous corticosteroid therapy for HELLP syndrome

OBJECTIVE We compared maternal outcomes for patients with HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome treated with or without high-dose corticosteroids to ameliorate maternal disease. STUDY DESIGN An analysis of data for patients with HELLP syndrome (platelets, <or=100,000/microL; lactate dehydrogenase level, >or=600 IU/L; aspartate aminotransferase and/or alanine aminotransferase level, >or=70 IU/L) who were treated during the 7-year epochs before and after the clinical trials in 1992 and 1993 demonstrated maternal benefit with high-dose dexamethasone. RESULTS Corticosteroid use increased from 16% (39/246 patients) for fetal indication from 1985 to 1991 to 90% (205/228 patients) for maternal-fetal indications from 1994 to 2000. Significantly reduced composite maternal disease from 1994 to 2000 was evidenced by improvements in laboratory parameters, disease progression to class 1 HELLP syndrome, the degree of hypertension, the need for antihypertensive therapy, the use of transfusion, and the presence of maternal morbidity (P<.05). Indices of postpartum recovery also were shortened significantly (P<.001). CONCLUSION Routine early initiation of high-dose intravenous corticosteroids for patients with HELLP syndrome significantly lessened maternal disease, reduced maternal morbidity, and expedited recovery.

Obstetric implications of antepartum corticosteroid therapy for HELLP syndrome

OBJECTIVE: We reviewed the impact of intravenous high-dose corticosteroid administration for preterm hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome on vaginal delivery rate and degree of clinically significant thrombocytopenia. METHODS: Retrospective analysis of 1991–2000 HELLP syndrome (platelets < 100,000/uL, lactate dehydrogenase > 600 IU/L, aspartate aminotransferase and/or alanine aminotransferase > 70 IU/L) data focusing on labor inductions for gestations of less than 34 weeks and increase in platelet count sufficient to permit regional anesthetic techniques. RESULTS: Antepartum high-dose corticosteroid use increased from 32% (1991–1995) to 67% (1996–2000) for 350 patients studied (n = 199, < 34 weeks; n = 151, > 34 weeks). Corresponding vaginal delivery rates were 32% for gestations of less than 30 weeks, 61% at 30–31 weeks, and 62% at 32–33 weeks. Similarly, 27% of patients with a platelet count of less than 75,000/uL and 52% with a platelet count of less than 100,000/uL who received high-dose corticosteroids during the study interval subsequently achieved a 100,000/uL threshold in time to perform regional anesthesia for delivery. CONCLUSION: Administration of intravenous high-dose corticosteroids for preterm HELLP syndrome increases probability of successful labor induction and candidacy for regional anesthesia. LEVEL OF EVIDENCE: II-3

Reduced placental perfusion causes an increase in maternal serum leptin

OBJECTIVE We tested the hypothesis that the inadequately perfused placenta increases production of leptin, which can be detected in maternal serum. STUDY DESIGN Sprague-Dawley rats (n=13), on day 14 of gestation, had placement of clips on the aorta and the ovarian arteries providing 35 per cent occlusion of the vessels. Eight rats had sham surgery and 14 rats served as non-surgical controls. All animals were sacrificed on day 19 of gestation. Maternal serum was obtained, and pups and placentae were weighed. RESULTS Both placental weights and pup weights were reduced due to reduced uterine perfusion and were negatively correlated with maternal serum leptin (P=0.018 and 0.028, respectively). Maternal serum leptin was increased in the treatment group (2.21 ng/ml+/-64 ng/ml) compared to controls (1.66 ng/ml+/-38 ng/ml) (P=0.031). CONCLUSIONS Our findings suggest that reduced placental perfusion results in an increase in maternal serum leptin. Further investigation is needed to determine if maternal serum leptin may be useful in identifying pregnancies with uteroplacental insufficiency.