Faculty Bibliography

The objective of this study was to determine whether vacuum extraction is associated with umbilical cord blood acid-base changes when used electively or in the presence of suspected fetal distress. Data from 1,428 patients from a previously published randomized trial of intrapartum electronic fetal heart rate monitoring versus intermittent auscultation were analyzed to identify differences in umbilical cord blood acid-base measurements associated with the elective use of vacuum extraction (patients with duration of second stage of labor 60 min or less) and also in the presence of suspected fetal distress during the second stage of labor. When used electively, vacuum extraction was associated with lower pH (in both umbilical cord artery and vein), lower venous base excess, and higher venous carbon dioxide tension (PCO2), as compared to normal spontaneous vaginal delivery. After correcting for duration of second stage of labor, elective vacuum delivery was significantly associated only with a decrease in cord venous pH and increase in venous PCO2. However, these cord blood acid-base changes were not accompanied by any differences in perinatal morbidity and mortality or in the number of neonates born with acidemia (cord arterial pH < 7.15 or < 7.10). In cases of suspected fetal distress, the use of vacuum extraction was not associated with any detectable cord blood acid-base changes as compared to normal spontaneous vaginal delivery. These data support the continued use of vacuum extraction, especially in cases of suspected fetal distress during the second stage of labor

OBJECTIVE:Our purpose was to establish the sensitivity and specificity of various ultrasonographic markers of trisomy 21 in the second trimester of pregnancy on the basis of literature review and to generate tables that would allow adjusting the risk for trisomy 21, and therefore the need for genetic amniocentesis, depending on the presence or absence of these markers. STUDY DESIGN/METHODS:A computer search was performed of the English literature, including the years 1983 through 1993, of studies that used second-trimester ultrasonography to detect fetuses with trisomy 21. After statistical analysis of the reported studies was performed, the average sensitivity and specificity of the following ultrasonographic markers were determined: structural malformations, short femur, short humerus, combination of short femur and short humerus, pyelectasis, nuchal fold thickening, echogenic bowel, and short ear length. After the average sensitivity and specificity of these ultrasonographic markers were established, appropriate tables were generated by Bayes' theorem to adjust the risk for trisomy 21 in the second trimester depending on the presence or absence of these markers. Statistical analyses were performed with the statistical package Excel on a personal computer. RESULTS:The average detection rate (sensitivity) of structural fetal malformations was 28%, short femur 31%, short humerus 33%, short femur and humerus 32%, nuchal fold thickening 32%, echogenic bowel 7%, and short ear length 71%. The nuchal fold thickening had the highest specificity (99.5%). Isolated pyelectasis was not associated with an increased risk for trisomy 21. However the risk was increased when pyelectasis was associated with other markers. In the presence of normal ultrasonographic results, the negative prediction can be combined with maternal age-related or biochemical prediction of trisomy 21 to help in the informed consent process in counseling women about the benefits and harms of genetic amniocentesis. Genetic amniocentesis should be considered in women of any age when second-trimester ultrasonography reveals the presence of one or more of the following: fetal structural malformations, short femur (determined by biparietal diameter-to-femur length ratio), combination of short femur and humerus, abnormal (> or = 6 mm) nuchal fold thickening, echogenic bowel, or short ear length. CONCLUSION/CONCLUSIONS:In experienced hands second-trimester ultrasonography may be used to adjust the priori risk of both high and low-risk women for trisomy 21 and therefore the need for genetic amniocentesis.

Fetal heart rate monitoring, uterine contraction monitoring, and amnioinfusion are procedures used commonly during labor that have also improved our understanding of intrapartum physiology, although there are limitations to the ability of these procedures to improve pregnancy outcome. The current status of intrapartum fetal heart rate monitoring, uterine contraction monitoring, and amnioinfusion is reviewed.

OBJECTIVE:This study was designed to evaluate the significance of gender differences for commonly used biometric parameters obtained ultrasonographically from second-trimester euploid fetuses. STUDY DESIGN/METHODS:Gender-specific linear regression equations were developed for gestational age dependent and independent biometry from second-trimester ultrasonographically normal singleton euploid fetuses by use of biparietal diameters and femur and humerus lengths. Regression lines for male fetuses were compared with those for females by determining overlap of 95% confidence intervals at specific points. RESULTS:A total of 288 male fetuses (mean gestational age 16.7 +/- 1.0 weeks) and 251 female fetuses (mean gestational age 16.8 +/- 1.2 weeks) (not significant) were evaluated. Small statistically significant gender differences in fetal biometry were identified. The largest gender difference for gestational age-dependent parameters was a biparietal diameter difference of 1.15 mm at 21 weeks. The largest gender difference for gestational age-independent parameters was a femur length difference of 1.7 mm at a biparietal diameter of 50 mm. CONCLUSION/CONCLUSIONS:Statistically, but not clinically, significant gender differences of small magnitude exist for second-trimester fetal biometry, suggesting that gender-specific nomograms may be of limited value.

This study tests the hypothesis that histologic placental lesions were significantly related to incidence of early or late germinal matrix/intraventricular hemorrhage (GM/IVH) in infants of less than 32 weeks' gestation independent of maternal or neonatal factors. Maternal and neonatal charts of 406 singleton liveborn nonanomalous infants born at less than 32 weeks' gestation were studied retrospectively for principal indication for delivery, delivery mode, timing of antenatal steroid treatment, diagnosis of labor and augmentation, tocolysis, fetal presentation, and umbilical arterial and venous blood gas values. Extracted from neonatal charts were gestational age, growth measurements, initial hematocrit and white blood cell count, administration of surfactant, and in the first 3 days of life, the use of pressor agents and volume expansion, lowest blood pressure, and data pertinent to respiratory function. Placental histologic examination was reviewed for various lesions, including histologic acute inflammation (graded on a scale of 0 to 4). GM/IVH (grades 1 to 4) diagnosed ultrasonographically less than 72 hours after birth was 'early.' GM/IVH diagnosed after 72 hours of life was defined as 'late.' Of the 406 patients, 44 (10.8%) had early GM/IVH; 21 (4.9%) had late GM/IVH. Stepwise logistic regression selected five factors independently related to increased early GM/IVH risk: Histologic acute inflammation (p < 0.002); gestational age in days (p = 0.053); antenatal steroid treatment less than 48 hours before birth (p < 0.035); volume expansion in the neonate (p < 0.30), and magnesium sulfate tocolysis (p < 0.025). Stepwise regression analysis considering the grade of GM/IVH changed the order of variables, with gestational age and use of pressor therapy being more strongly related to higher grade of GM/IVH than amnion inflammation. Delivery mode, presentation, principal indication for delivery, presence/augmentation of labor, mean biophysical profile scores, mean umbilical arterial and venous blood gas values, and surfactant therapy were not related to early GM/IVH in univariate or multivariate analyses. Neonatal factors associated (p < 0.05) with amnion inflammation were volume expansion at delivery and in the first 3 days of life, low mean systolic pressure, low mean oxygen pressure, low initial hematocrit and cord pH, and increased initial WBC and toxic granulations of neutrophils. Only gestational age, and no maternal or placental factors, was significantly related to late GM/IVH. Infants who have placentas with acute amnion inflammation and receive volume expansion, born to mothers who receive less than 48 hour's exposure to antenatal steroids and are selected to receive magnesium sulfate tocolysis, have increased incidence of early but not late GM/IVH. Amnion inflammation is significantly related to early GM/IVH and with early neonatal abnormalities in oxygenation, perfusion, and effective blood volume. Intra-amniotic infection leads to advanced preterm labor, which is unresponsive to tocolysis because of the inflammation. Intra-amniotic inflammation may sensitize the fetus to postpartum stresses or initiate early GM/IVH in utero via cytokine effects on cardiovascular instability

OBJECTIVE: Our purpose was to compare the incidence and interrelationships of uteroplacental vasculopathy and chronic inflammatory and placental vasoocclusive lesions in preeclampsia and spontaneous delivery before 32 weeks' gestation. STUDY DESIGN: Review of singleton live-born nonanomalous infants born at 22 to 32 weeks' gestation identified 76 cases of preeclampsia and 353 cases of spontaneous prematurity (spontaneous premature membrane rupture [n = 192], preterm labor, intact membranes [n = 161]). Histologic lesions were considered as belonging to one of five major pathophysiologic groups: (1) uteroplacental vascular lesions and related villous lesions, (2) chronic inflammatory lesions, (3) coagulation-related lesions, (4) acute inflammatory lesions, and (5) unclassified lesions. Contingency table analyses considered p < 0.05 significant. Factor analysis extracted combinations of related variables. RESULTS: More frequent in preeclampsia versus spontaneous prematurity were chronic uteroplacental vasculitis (29% vs 20%, p < 0.05), chronic villitis (20% vs 3%, p < 0.001), avascular villi (39% vs 16%, p < 0.001), and 'hemorrhagic endovasculitis' (9% vs 2.5%, p < 0.03). In the preeclampsia cases factor analysis extracted 13 categories of related lesions. Four categories contained uteroplacental vascular lesions. Five categories included lesions related to chronic inflammation, and eight included lesions related to coagulation. Four categories loaded lesions from one major pathophysiologic group only. Three categories loaded lesions from all three pathophysiologic groups. Unclassified lesions loaded into two factor categories that were unrelated to the other lesions. CONCLUSIONS: Chronic inflammatory and placental vasoocclusive lesions are more common in preterm preeclampsia than in spontaneous prematurity. Immunopathologic processes and coagulation may be involved in the pathophysiologic mechanisms of preterm preeclampsia independent of uteroplacental vascular pathologic features

OBJECTIVE: Our purpose was to study the incidence and location of histologic evidence of intrauterine bleeding in preterm and term placentas. STUDY DESIGN: A total of 462 consecutive placentas delivered at < 32 weeks' gestation, from which cases of placenta previa, stillbirth, and multiple gestation were excluded, were compared with 108 consecutive term placentas (with similar exclusion criteria) in regard to the presence of hemosiderin in decidua of basal plate or placental membranes. Of the 462 preterm cases, 448 charts made specific reference to the presence or absence of vaginal bleeding. Bloody show alone was not considered bleeding. The blinded scoring of lesions (including acute ascending infection, uteroplacental vascular pathologic processes and related ischemic damage, chronic inflammation, and coagulation related lesions) was analyzed by contingency tables (p < 0.05 significant). RESULTS: A total of 196 of 462 (43%) preterm placentas had any decidual hemosiderin compared with one of 108 (0.8%) at term (p < 0.00001). Among the preterm cases, hemosiderin was significantly more common in preeclampsia (45/76, 60%) and in cases clinically diagnosed as nonhypertensive abruptio placentae (21/33, 64%) than in premature membrane rupture (72/192, 37.5%) and preterm labor (58/161, 36%, p < 0.003). The incidence of placental lesions in preterm cases with extraplacental membrane hemosiderin was not different than it was in cases without hemosiderin. Placental lesions related to basal-plate decidual hemosiderin in the preterm cases were villous infarct (p < 0.0001), uteroplacental vessels with absence of physiologic change (p < 0.003) and increased numbers of circulating nucleated erythrocytes (p < 0.0007), uteroplacental thrombosis (p < 0.0001), and villous fibrosis (p < 0.0001) and hypovascularity (p < 0.0001). Among the preterm cases, 23 of 48 (48%) with first-trimester bleeding, 33 of 66 (50%) with second-trimester bleeding, and 31 of 64 (48%) with multiple episodes of bleeding had decidual hemosiderin (p < 0.0001). A clinical history of gestational bleeding was significantly less common in cases of preterm preeclampsia with histologic evidence of bleeding (four of 73, 5.5%) than in nonhypertensive abruptio placentae (18/31, 58%), premature rupture of membranes (52/183, 28%), or preterm labor (31/161, 19%, p < 0.0001). Hemosiderin was not related to clinical bleeding < 72 hours of delivery (p > 0.20). CONCLUSIONS: Decidual bleeding is common in all clinical types of preterm birth and is most common in preterm preeclampsia and nonhypertensive abruption placentae. A clinical history of bleeding is not correlated with the presence of decidual hemosiderin. Bleeding in the basal plate is related to histologic evidence of chronic uteroplacental vascular pathologic processes, which in cases of spontaneous prematurity (premature rupture of membranes, preterm labor, nonhypertensive abruptio placentae) may be associated with decidual bleeding which occasionally may be clinically manifested as gestational bleeding

OBJECTIVE: Our purpose was to test the hypothesis that placental histologic lesions reflect abnormal placental respiratory function in preterm gestations. STUDY DESIGN: A retrospective study of preterm deliveries from 22 to 32 weeks revealed 431 patients with umbilical venous or arterial blood gas values. Excluded were stillbirth, multiple gestations, placenta previa, maternal medical diseases, and fetal anomalies. Charts were reviewed for principal indication of delivery, diagnosis of labor, and mode of delivery. Blood gases were studied within 10 minutes of delivery on a model 178 automatic pH analyzer (Corning Med, Boston). Placental data included uteroplacental vascular lesions and related villous lesions, lesions of acute inflammation, chronic inflammation, and coagulation. Contingency tables and analysis of variance considered p < 0.05 as significant. RESULTS: Mean +/- SD umbilical vein pH was 7.36 +/- 0.07 (range 6.94 to 7.56) and umbilical artery pH was 7.30 +/- 0.08 (range 6.83 to 7.55). Increasing severity of uteroplacental thrombosis, villous lesions reflective of uteroplacental vascular pathologic mechanisms, avascular villi, histologic evidence of abruptio placentae, chronic villitis, and increased circulating erythrocytes were associated with decrease in umbilical vein and artery pH, increase in umbilical vein and artery PCO2, and decrease in umbilical vein and artery PO2. Histologic evidence of acute infection and villous edema were associated with a higher pH and PO2 and a lower PCO2 in both umbilical vein and artery. Umbilical vein or artery base excess was not related to placental lesions. Labor was not related to blood gas values in this data set, although a subset of cases of extremely preterm premature rupture of membranes and preterm labor who labored and were delivered by cesarean section had significantly poorer umbilical venous and fetal arterial blood gas values (all p < 0.005). Lesions related to poorer blood gas values were significantly more frequent in preterm preeclampsia and nonhypertensive abruptio placentae than in premature rupture of membranes or preterm labor. CONCLUSIONS: Changes in umbilical vein and artery pH, PO2, and PCO2 are significantly related to lesions of uteroplacental vascular pathologic mechanisms and intraplacental thrombosis. Placental lesions may be associated with chronic fetal distress by altering fetal oxygen availability and acid-base status. Placental immaturity resulting from prematurity may be associated with inefficient placental respiratory function and an increased likelihood of cesarean delivery in cases of premature rupture of membranes or preterm labor. Altered fetal acid-base balance plus excess numbers of circulating nucleated erythrocytes suggests that placental respiratory function is functionally abnormal when these lesions are present and leads to fetal tissue hypoxia