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Although maternal death remains rare in the United States, the rate has not decreased for 3 decades. The rate of severe maternal morbidity, a more prevalent problem, is also rising. Rise in maternal age, in rates of obesity, and in cesarean deliveries as well as more pregnant women with chronic medical conditions all contribute to maternal mortality and morbidity in the United States. We believe it is the responsibility of maternal-fetal medicine (MFM) subspecialists to lead a national effort to decrease maternal mortality and morbidity. In doing so, we hope to reestablish the vital role of MFM subspecialists to take the lead in the performance and coordination of care in complicated obstetrical cases. This article will summarize our initial recommendations to enhance MFM education and training, to establish national standards to improve maternal care and management, and to address critical research gaps in maternal medicine. [Copyright &y& Elsevier]

A review of pregnancy-associated thrombotic thrombocytopenic purpura (TTP) in 166 pregnancies was undertaken using 92 English-language publications from 1955 to 2006. Initial and recurrent TTP presents most often in the second trimester (55.5%) after 1-2 days of signs/symptoms; postpartum TTP usually occurs following term delivery. TTP with preeclampsia (n = 28) exhibits 2-4 times higher aspartate aminotransferase (AST) values and lower total lactate dehydrogenase (LDH) to AST ratios (LDH to AST ratio = 13:1), compared with TTP without preeclampsia (LDH to AST ratio = 29:1). Maternal mortality is higher with initial TTP (26% vs 10.7%), especially with concurrent preeclampsia (44.4% vs 21.8%, P < .02). Although maternal mortality with TTP has substantially declined when plasma therapy is utilized, delay of diagnosis and therapy for initial TTP confounded by preeclampsia/hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome remains a significant maternal-perinatal threat. Rapid and readily available laboratory testing to quickly diagnose TTP and HELLP syndrome/preeclampsia is desperately needed to improve care. [Copyright &y& Elsevier]

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=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. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this study was to determine the rate of uterine rupture and its complications as the result of trial of labor after previous cesarean delivery.Study Design: PubMed was searched from 1989 to 2001, with the terms "VBAC, uterine rupture," "trial of labor, uterine rupture," "cesarean delivery, uterine rupture," and "scarred uterus, rupture." For inclusion, reports had to contain data from at least 100 patients with trials of labor that included a description of adverse outcomes. Duplicate reporting from a single institution was excluded. Odds ratios and 95% CIs were calculated.Results: Seventy-two of the 361 articles (20%) that were identified met the inclusion criteria. A 6.2 per 1000 trial of labor rate of uterine rupture (total=880 uterine ruptures in 142,075 trials of labor) was determined. For every 1000 trials of labor the uterine rupture-related complication rate was 1.8 for packed red blood cell transfusion, 1.5 for pathologic fetal acidosis (cord pH<7.00), 0.9 for hysterectomy, 0.8 for genitourinary injury, 0.4 for perinatal death, and 0.02 for maternal death. The perinatal mortality rate was significantly lower among studies from the United States versus other countries (0.3 vs 0.6; odds ratio, 0.50; 95% CI, 0.26-0.94) and in series that exceeded 1000 patients (0.2 vs 1.7; odds ratio, 7.34; 95% CI, 3.94-13.69).Conclusion: Although relatively uncommon, uterine rupture is associated with several adverse outcomes, depending on the time of the publication and the site and size of the population that was studied. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this study was to establish whether ultrasound-estimated or dye-determined amniotic fluid distribution (upper compared with lower quadrant) is predictive of perinatal outcome.Study Design: Amniotic fluid distribution as measured by the amniotic fluid index, single deepest pocket, and dye-determined volumes was ascertained and correlated with intrapartum and neonatal outcomes.Results: Between January 1997 and January 2001, 135 women (70 upper-greater and 65 lower-greater) participated in this prospective observational study. The sum of the amniotic fluid index (P =.309), single deepest pocket (P =.168), and dye-determined amniotic fluid volume (P =.368) for the upper-greater compared with the lower-greater groups were similar. Decelerations in labor (P =.597), late decelerations (P =.999), cesarean deliveries for fetal distress (P =.413), and umbilical cord pH < 7.2 were similar (P =.647)Conclusion: Ultrasound-estimated and dye-determined amniotic fluid volumes are similar between upper-greater and lower-greater groups, and intrapartum/neonatal outcomes are not affected by the amniotic fluid distribution. [ABSTRACT FROM AUTHOR]

Investigates the utility of an admission battery of findings and laboratory data in the discrimination of patients with severe preeclampsia with or without hemolysis, elevated liver enzyme levels, and low platelet count syndrome at high risk for development of maternal morbidity. Relationship between laboratory values and maternal morbidity development.

Presents information on a study conducted to determine if the use of dexamethasone therapy in patients with postpartum hemolysis elevated liver enzymes and thrombocytopenia (HELLP) syndrome will produce specific and general therapeutic benefits. Details on the study design; Results of the study; Conclusions on the study.

Presents the reviewing of obstetric literature pertaining to delivery experience of patients with a prior low-segment vertical cesarean incision. What is the most important changes in operative obstetrics; How should a patient in such condition be managed; Information regarding instances of this nature.

Investigates the role of interpersonal injury in the pregnant trauma victim. Frequency of interpersonal violence in maternal injury; Inconstant relationship between Injury Severity Score and serious fetal injury or death; Need for emotional help and physical protection.

Background: There is a robust association between altered angiogenic factor concentrations, which includes placental growth factor and clinically recognized preeclampsia. Alterations in concentrations of angiogenic factors precede the clinical onset of preeclampsia by several weeks. The temporal relationship between the measured angiogenic factors and the time to delivery in women with suspected preeclampsia at <35 weeks gestation, however, remains to be clarified.Objective: The purposes of this study were to examine the relationship between placental growth factor and time to delivery in women at <35 weeks gestation with signs or symptoms of preeclampsia and to compare the performance of placental growth factor to other clinical markers for prediction of time to delivery in preeclampsia.Study Design: Women with signs or symptoms of preeclampsia between 20.0 and 35.0 weeks gestation were enrolled in a prospective, observational study at 24 centers. Blood was collected at presentation for placental growth factor, and subjects were evaluated and treated according to local protocols. Clinical outcomes were obtained, and all final diagnoses were adjudicated by an independent expert panel according to 2013 American College of Obstetricians and Gynecologists' Hypertension in Pregnancy criteria. Placental growth factor was measured retrospectively on the Alere, Inc, triage platform. A normal placental growth factor was defined as >100 pg/mL; the assay's limit of detection is 12 pg/mL. Two-by-2 tables were constructed for comparison of test outcomes that included negative predictive value; time-to-delivery was analyzed by survival curves and Cox regression.Results: Seven hundred fifty-three subjects were enrolled; 538 (71%) had a final diagnosis of preeclampsia; 542 (72%) delivered at <37 weeks gestation, and 358 (47%) delivered at <34 weeks gestation. Among the 279 women (37%) with a normal placental growth factor at presentation, the negative predictive value for preeclampsia delivered within 14 days or within 7 days was 90% and 93%, respectively. Compared with women with normal placental growth factor, women with placental growth factor ≤100 pg/mL have a hazard ratio of 7.17 (confidence interval, 5.08-10.13) in Cox regression for time to delivery after adjustment for both gestational age at enrollment and the final diagnosis of preeclampsia. The placental growth factor levels of normal (>100 pg/mL), low (12-100 pg/mL), and very low (<12 pg/mL) have well-separated distributions of time to delivery, with median values of 45, 10, and 2 days, respectively. Subjects with placental growth factor ≤100 pg/mL have a perinatal death rate of 5.7% and a small-for-gestational-age rate of 51.7%; subjects with placental growth factor >100 pg/mL have a perinatal death rate of 0% (no observations in this cohort) and an a small-for-gestational-age rate of 16.8%.Conclusion: In women with suspected preeclampsia at <35.0 weeks gestation, a low placental growth factor was correlated strongly with preterm delivery independent of a diagnosis of preeclampsia or gestational age at presentation, whereas a normal placental growth factor was associated with pregnancy prolongation, even in patients who ultimately had a final diagnosis of preeclampsia. This suggests that placental growth factor levels are superior to clinical markers in the prediction of adverse pregnancy in women with suspected preeclampsia. [ABSTRACT FROM AUTHOR]

Objective: Preeclampsia is a multisystem disorder recognized as hypertension with proteinuria developing >20 weeks' gestation. Preeclampsia is associated with chronic immune activation characterized by increased T and B lymphocytes, cytokines, and antibodies activating the angiotensin II type I receptor (AT1-AA). Hypertension in response to elevated interleukin (IL)-6 during pregnancy occurs with increased renin activity and AT1-AA, and reduced kidney function.Study Design: We aim to determine whether 17-alpha-hydroxyprogesterone caproate (17-OHPC), progesterone, improved inflammatory pathways during elevated IL-6 in pregnant rats. IL-6 (5 ng/d) was infused via miniosmotic pumps into normal pregnant (NP) rats beginning on day 14 of gestation and 17-OHPC (3.32 mg/kg) was diluted in normal saline and injected on day 18. Blood pressure (mean arterial pressure [MAP]) determination and serum collection were performed on day 19 of gestation.Results: MAP in NP was 100 ± 3 mm Hg, which increased with IL-6 to 112 ± 4 mm Hg (P < .05). Pregnant rats given 17-OHPC alone had a MAP of 99 ± 3 mm Hg and MAP increased to 103 ± 2 mm Hg in IL-6+17-OHPC. AT1-AA was 1.2 ± 0.5 bpm in NP rats, increased to 17 ± 9 bpm with IL-6 infusion but administration of 17-OHPC significantly blunted AT1-AA to 4 ± 0.8 bpm in NP+IL-6+17-OHPC. Total circulating nitrate/nitrite was significantly decreased and placental Ser(1177)-phosporylated-eNOS/eNOS was lowered with IL-6 infusion. Supplementation of 17-OHPC significantly improved placental Ser(1177)-phosporylated-eNOS/eNOS however, circulating nitrate/nitrite was unchanged with 17-OHPC supplementation.Conclusion: This study illustrates that 17-OHPC attenuated hypertension, decreased AT1-AA activity, and improved placental nitric oxide in response to elevated IL-6 during pregnancy and could lend hope to a new potential therapeutic for preeclampsia. [ABSTRACT FROM AUTHOR]

Objective: We sought to investigate the concurrence of posterior reversible encephalopathy syndrome (PRES) with eclampsia and to describe the obstetric, radiological, and critical care correlates. Study Design: This was a single-center, 2001-2010 retrospective cohort study of all patients with eclampsia who underwent neuroimaging via magnetic resonance imaging (MRI) or computerized tomography (CT) with or without contrast. Results: Forty-six of 47 of eclamptic patients (97.9%) revealed PRES on neuroimaging using 1 or more modalities: MRI without contrast, 41 (87.2%); MRI with contrast, 27 (57.4%); CT without contrast, 16 (34%); CT with contrast, 7 (14.8%); and/or magnetic resonance angiography/magnetic resonance venography, 2 (4.3%). PRES was identified within the parietal, occipital, frontal, temporal, and basal ganglia/brainstem/cerebellum areas of the brain. Eclampsia occurred antepartum in 23 patients and postpartum in 24 patients. Headache was the most common presenting symptom (87.2%) followed by altered mental status (51.1%), visual disturbances (34%), and nausea/vomiting (19.1%). Severe systolic hypertension was present in 22 patients (47%). Conclusion: The common finding of PRES in patients with eclampsia suggests that PRES is a core component of the pathogenesis of eclampsia. Therapy targeted at prevention or reversal of PRES pathogenesis may prevent or facilitate recovery from eclampsia. [Copyright &y& Elsevier]

Introduction: Administration of dexamethasone to the hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome patients (10 mg intravenously [IV] every 12 hours) shortens the disease course and reduces maternal morbidity in patients treated at the University of Mississippi Medical Center (UMMC), associated with this severe form of preeclampsia. However, the pathophysiological mechanisms involved with this intervention remain unclear. Objective: We sought to investigate the potential role of IV dexamethasone to restore the imbalance among antiangiogenic and inflammatory factors known to be significantly elevated in women with HELLP syndrome. Study Design: This was a single-center prospective study of women diagnosed with HELLP syndrome who were treated for IV dexamethasone at UMMC. Blood was drawn prior to dexamethasone administration and again 12 and 24 hours after the initial dexamethasone administration. Enzyme-linked immune assays were used to measure circulating inflammatory cytokines and antiangiogenic factors. A repeated-measures analysis of variance was used to analyze the data collected before, after, and during dexamethasone administration. Results: Seventeen women with HELLP syndrome were enrolled in this study. Dexamethasone significantly decreased evidence of hemolysis (P = .002) and liver enzymes (P = .003), and significantly increased platelets (P = .0001) within 24 hours of administration. Circulating interleukin-6 levels after 24 hours were decreased (P < .001); soluble fms-like tyrosine kinase-1 and soluble endoglin were also significantly decreased by 24 hours after dexamethasone administration (P < .002 and P < .004, respectively). There were no significant differences in circulating levels of placental growth factor (P = .886) due to dexamethasone administration. Angiotensin II receptor autoantibody levels were unchanged by dexamethasone administration. Conclusion: We conclude that 1 important mechanism of dexamethasone administration is to blunt the release of both antiangiogenic and inflammatory factors suggested to play role in the pathophysiology of HELLP syndrome. [Copyright &y& Elsevier]

Objective: We sought to determine the effect of an endothelin type A receptor antagonist (ETA) on uterine artery resistive index (UARI) and mean arterial pressure (MAP) in a placental ischemia rat model of preeclampsia produced by reduction in uterine perfusion pressure (RUPP).Study Design: UARI was assessed by Doppler velocimetry in RUPP and normal pregnant controls (NP) on gestational days (GD) 12, 15, and 18. UARI was also determined on GD 18 in NP and RUPP pregnant dams after pretreatment with ETA. MAP was recorded on GD 19.Results: The RUPP group had a higher MAP and UARI on GD 15 and 18 than the NP group. Pretreatment with ETA attenuated both the MAP and GD-18 UARI in the RUPP group without affecting these parameters in the NP group.Conclusion: The improvement in UARI could be one potential mechanism for the reduction in MAP in response to ETA in pregnant dams with ischemic placentas. [ABSTRACT FROM AUTHOR]

Objective: We sought to determine the effect of an endothelin type A receptor antagonist (ETA) on uterine artery resistive index (UARI) and mean arterial pressure (MAP) in a placental ischemia rat model of preeclampsia produced by reduction in uterine perfusion pressure (RUPP). Study Design: UARI was assessed by Doppler velocimetry in RUPP and normal pregnant controls (NP) on gestational days (GD) 12, 15, and 18. UARI was also determined on GD 18 in NP and RUPP pregnant dams after pretreatment with ETA. MAP was recorded on GD 19. Results: The RUPP group had a higher MAP and UARI on GD 15 and 18 than the NP group. Pretreatment with ETA attenuated both the MAP and GD-18 UARI in the RUPP group without affecting these parameters in the NP group. Conclusion: The improvement in UARI could be one potential mechanism for the reduction in MAP in response to ETA in pregnant dams with ischemic placentas. [ABSTRACT FROM AUTHOR]

Objective: Reduction in uteroplacental perfusion (RUPP) in pregnant rats is associated with hypertension, elevated cytokines, and activation of the endothelin (ET-1) system. Our objective was to determine whether the antiinflammatory properties of 17-alpha-hydroxyprogesterone caproate (17 OHP) reduce cytokine-stimulated vasoactive pathways that are associated with hypertension in response to placental ischemia. Study Design: Mean arterial pressure (MAP), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and renal ET-1 were measured in the following: pregnant controls, pregnant controls plus 17 OHP (6.6 mg/kg), RUPP rats, and RUPP rats plus 17 OHP. Results: MAP increased 29 mm Hg in RUPP rats compared with pregnant controls (P < .001), whereas in RUPP plus 17 OHP rats, MAP increased only 19 mm Hg (P < .05). TNF-α and IL-6 increased 2- to 3-fold, respectively, in response to placental ischemia but was normalized in RUPP rats treated with 17 OHP. ET-1 increased 3-fold in RUPP rats but was markedly less in RUPP plus 17 OHP rats. Conclusion: 17 OHP blunts hypertension associated with RUPP, possibly via suppression of cytokine-stimulated ET-1 activation. [Copyright &y& Elsevier]