Clinical experience reported by candidates for the American Board of Obstetrics and Gynecology 1995 and 1997 oral examinations.

OBJECTIVE: The purpose of this study was to report the clinical experience collated from the 1995 and 1997 case list summary sheets of United States and Canadian active candidates who were completing the American Board of Obstetrics and Gynecology oral examination for the first time. STUDY DESIGN: Data from the case list summary sheets were entered into a computerized database and collated. Data from active candidates who had subspecialty training and from other international graduates were excluded. RESULTS: The difference in the ratio of men to women candidates between 1995 and 1997 was statistically significant (P =.02). Both years, 31% of the major operations were hysterectomies, of which 60% and 62.5%, respectively, were performed through an abdominal incision. The mean total cesarean delivery rate was 20.5% in 1995 and 19.7% in 1997. The ratio of primary to repeat cesarean deliveries was 2 to 1 in both years. The ratio of forceps to vacuum extraction deliveries was 3:7 in 1995 and 2:5 in 1997. CONCLUSION: This data set provides a national overview of the clinical experiences of a relatively homogeneous group of practicing obstetrician-gynecologists who have recently completed their training.

Workforce projections for subspecialists in obstetrics and gynecology.

OBJECTIVE: To project the future supply of practicing subspecialists in obstetrics and gynecology based on the most recent numbers of physicians entering fellowships. METHODS: A discrete actuarial model was developed, and supply projections were examined using 1999 subspecialty fellowship numbers from the American Board of Obstetrics and Gynecology. RESULTS: The numbers of obstetrician-gynecologists entering subspecialty fellowships in maternal-fetal medicine (MFM) and reproductive endocrinology-infertility (REI) declined sharply between 1994 and 1999. There was a slow increase in gynecologic oncology (GO) fellows. Projections show that the numbers of practicing MFM and GO subspecialists will double by 2020, but they will be serving a 20% larger female population in the United States. Numbers of practicing REI subspecialists will increase slowly. CONCLUSION: The number of fellows in GO continues to enlarge progressively though slightly, whereas those in MFM and REI have fallen sharply in recent years. Among four possible factors affecting growth or decline, the ones that seem most important are existing career opportunities for both generalist and subspecialist obstetrician-gynecologists and the length of subspecialty education.

A discriminant function for preeclampsia: case-control study of minor hemoglobins, red cell enzymes, and clinical laboratory values.

A case-control study was performed in eight pairs of women to determine whether preeclamptic women developed abnormalities in minor hemoglobins, glycolytic enzymes, or other blood components that might provide insight into the pathophysiology of preeclampsia, or that in combination might be used as a marker for the condition. These variables and standard clinical tests were analyzed as discriminators between preeclamptic and control women. The subjects were matched for age, ethnicity, parity, and gestational age. Blood samples were taken at the time of diagnosis of preeclampsia and at comparable gestational ages for matched normal controls. Variables differing significantly between groups included increases in uric acid (UA), low-density lipoproteins (LDL), phosphoglycerate kinase (PGK), and mean platelet volume (MPV), and decreases in glyceraldehyde phosphate dehydrogenase (G3PD) in preeclamptic women compared to normal controls. Discriminant analysis revealed the following function to separate the groups: 0.7764 (UA) + 0.8086 (PGK) -0.7032 (G3PD) + 0.1399 (LDL) -0.2386 (MPV). A discriminant score of > or = 275 indicated a > or = 90% probability of preeclampsia. The results are consistent with perturbations in red cell glycolysis in preeclampsia. Further prospective studies are warranted to test the efficacy of this discriminant function in predicting preeclampsia.

Angiotensin II metabolic clearance rate and pressor responses in nonpregnant and pregnant women.

OBJECTIVES: Normal pregnancy is associated with reduced pressor dose-responses to infused angiotensin II. We tested the hypotheses that alterations in the metabolic clearance rate and the half-life of angiotensin II account for reduced pressor dose-responses during gestation and that angiotensin II increases circulating levels of vasodilatory prostaglandins I2 and E2 relative to thromboxane A2. STUDY DESIGN: Eleven nonpregnant and 37 pregnant (30 +/- 0.3 weeks' gestation, mean +/- SE) women were infused with angiotensin II (3.11 to 22.36 ng/min.kg) for 15 minutes, and blood was obtained to evaluate steady-state immunoreactive plasma angiotensin II and eicosanoid concentrations. RESULTS: Angiotensin II pressor responses were dose dependent in all groups and reduced in pregnant women (p < 0.001). Basal immunoreactive plasma angiotensin II concentrations were 2.7-fold greater (p < 0.001) in pregnant versus nonpregnant women. Plasma levels reached steady state by 5 minutes of infusion, and at similar angiotensin II concentrations the increase in blood pressure was greater in nonpregnant versus pregnant women (p < 0.001). The angiotensin II metabolic clearance rate and half-life were similar in nonpregnant and pregnant women: metabolic clearance rate = 85 +/- 10 versus 68 +/- 3 ml/min.kg, respectively (p = 0.130), and half-life = 48 and 49 seconds, respectively. Plasma prostaglandin I2 (6-keto-prostaglandin F1 alpha) prostaglandin E2, and thromboxane B2 levels in pregnant women were unaffected by angiotensin II infusions. CONCLUSION: Neither changes in angiotensin II metabolism nor angiotensin II-induced increases in plasma levels of prostaglandin I2, prostaglandin E2, or the prostaglandin I2/thromboxane A2 ratio appear responsible for the decreased pressor response sensitivity to infused angiotensin II observed during normal human pregnancy.

Comparison of prophylactic angiotensin II versus ephedrine infusion for prevention of maternal hypotension during spinal anesthesia.

OBJECTIVE: Our purpose was to study the efficacy of ephedrine versus angiotensin II prophylactic infusions to counter maternal hypotension that occurs during spinal anesthesia at cesarean delivery. STUDY DESIGN: Healthy pregnant women undergoing elective repeat cesarean delivery at term with spinal anesthesia were randomized either to a control group (n = 10) or to one of two prophylactic infusion groups: angiotensin II (n = 10) or ephedrine (n = 10). Prophylactic infusions were titrated to a maternal diastolic blood pressure 0 to 10 mm Hg above baseline. Maternal and fetal blood samples for angiotensin II levels and acid-base status were obtained. Student's t test, chi 2, and analysis of variance were used. RESULTS: Mean arterial pressures were maintained after spinal anesthesia in the ephedrine and angiotensin II groups but decreased (p < 0.05) in the control group. Maternal angiotensin II levels rose with angiotensin II infusions but were unaltered in the other groups. Umbilical artery and vein angiotensin II levels were unaltered by angiotensin II infusions. Mean umbilical artery blood pH was lower (p < 0.05) in the ephedrine group than in the angiotensin II and control groups. CONCLUSIONS: In the healthy term fetus there is an advantage in using angiotensin II to maintain maternal blood pressure during regional anesthesia.

Management of eclampsia.

Mrs AB was admitted in the 34th week of pregnancy with eclampsia. Prompt parenteral (intravenous and intramuscular) administration of magnesium sulfate arrested the convulsions and prevented additional seizures. Because of a dangerously elevated blood pressure, intravenous hydralazine was administered to reduce the blood pressure. Unfortunately, the hydralazine was given more frequently than recommended, and the blood pressure was decreased rapidly and too far. This resulted in the development of a serious fetal bradycardia secondary to reduced uteroplacental perfusion. Fortunately, the blood pressure spontaneously recovered as did the fetus. Three hours after admission, Mrs AB was awake and alert. Her fetus had also recovered from the effects of the convulsions and the treatment with hydralazine. Mrs AB's laboratory values had all been reported by this time, and her intravenous intake and urinary output were well regulated. Importantly, because of the presence of significant hemoconcentration (hematocrit at 32 weeks' was 36 and at 34 weeks', 44), a careful search for pulmonary edema was made. Additionally, fluid administration was conservative in order not to produce pulmonary edema. At this point, an induction of labor was commenced. The induction of labor was rapidly successful, and Mrs AB delivered a small but vigorous male infant who subsequently did well. Mrs AB was monitored hourly for the first 12 hours postpartum to ensure adequate blood pressure control and to prevent pulmonary edema. Her subsequent puerperal course was without adverse incident. She diuresed massively, and her blood pressure rapidly returned to normal.

Control of vascular reactivity in pregnancy: the basis for therapeutic approaches to prevent pregnancy-induced hypertension.

The complete pathophysiology of pregnancy-induced hypertension may never be completely defined until the specific offending gene can be isolated. Until this has been accomplished, however, there seems to be hope that rational treatment regimens soon will be available to prevent or at least delay the onset of pregnancy-induced hypertension.

Mild pregnancy-induced hypertension at term.

It was elected to induce labor in Mrs AB after excluding any evidence of severe preeclampsia. Both the fetus and Mrs AB were evaluated. The history, physical examination, and laboratory results were all within normal limits for Mrs AB. Her fetus was appropriately grown for gestational age with an estimated fetal weight of 3,200 g. There was ample but not excessive amniotic fluid noted clinically and by sonography. An amniocentesis to document fetal lung maturation was not done. Two hours after commencing parenteral magnesium sulfate therapy, an oxytocin induction of labor was begun. Fetal well-being was assessed using continuous external electronic monitoring of the fetal heart rate and uterine contractions. Three hours after the induction was started, the cervix was completely effaced and 3 cm dilated. The fetal head was at O station. At this time, the fetal membranes were ruptured and clear amniotic fluid was noted. An internal uterine pressure catheter was inserted, and a fetal scalp electrode applied. The patient received 75 mg of meperidine and 25 mg of promethazine intramuscularly at this time. Five hours after commencing the induction of labor, both mother and fetus were tolerating the labor well. The cervix was 7 cm dilated, and the fetal head was at +2/+5 station. The oxytocin induction was discontinued and another 75 mg dose of meperidine was administered. Blood pressure readings between 150/100 mm Hg and 140/98 mm Hg were recorded throughout labor. Urine output exceeded 150 mL/h. The patient delivered a 3,070-g male infant approximately 9 hours after the start of the induction.(ABSTRACT TRUNCATED AT 250 WORDS)

Management of preeclampsia.

Mrs AB was admitted to the delivery unit during her 35th week of gestation because of severe preeclampsia. She had several laboratory features that suggested the true severity of her disease. The massive proteinuria identified her as having far advanced disease. This was confirmed by the presence of hemoconcentration, hemolysis, and a large number of abnormal laboratory values. Mrs AB's fetus was normally grown (absence of fetal growth retardation), and there was an adequate amniotic fluid volume. Despite these favorable features and the initial presence of long-term fetal heart rate variability, the fetus did not tolerate the induction of labor, and a cesarean delivery was performed. The anesthesia, surgery, and postpartum courses were uncomplicated. Moreover, blood pressure promptly returned to normal after the onset of a brisk diuresis.

Platelet-activating factor-acetylhydrolase activity in normotensive and hypertensive pregnancies.

OBJECTIVE: The purpose of our study was to evaluate the hypothesis that pregnancy is associated with decreased platelet-activating factor-acetylhydrolase activity in women with normotension, but not in women with hypertension. STUDY DESIGN: We evaluated plasma platelet-activating factor-acetylhydrolase activity in normal nonpregnant women (n = 10), normal pregnant women (n = 24), pregnant women with pregnancy-induced hypertension-preeclampsia (n = 7), and a group of men with normotension (n = 10). RESULTS: Platelet-activating factor-acetylhydrolase activity was lower at 32 weeks of gestation during normal pregnancies compared with nonpregnant controls (p < 0.001); however, in women with pregnancy-induced hypertension-preeclampsia, platelet-activating factor-acetylhydrolase activity was not decreased. Platelet-activating factor-acetylhydrolase activity in men was higher than in all women (p < 0.01). CONCLUSION: Pregnant women with normotension may be refractory to pressor agents such as angiotensin II in part because of the decrease in plasma platelet-activating factor-acetylhydrolase activity, which results in an increase in platelet-activating factor. In contrast, enzyme activity is not decreased in pregnant women with hypertension, who have increased sensitivity to various pressor agents.

Reliability of birth certificate reporting of congenital anomalies.

Birth certificates comprise an important source of data on the prevalence of genetic conditions and for monitoring possible teratogens in the population. Investigators have found wide variability (12 to 100%) in the accuracy of reporting. In a large public hospital, of those congenital anomalies detected at birth, only 5.4% were recorded on the birth certificate. This is one of the lowest rates ever reported. An underreporting correction factor may be applied if congenital anomalies are distributed randomly with respect to reporting status, and the rate of reporting is sufficient to comprise a valid sample for estimating a correction factor (that is, 20% or more reported). In this study, factors such as numbers or types of anomalies, race, infant birthweight, or estimated gestational age did not significantly influence the rate of birth certificate reporting. Thus, our data satisfied the first but not the second criterion for derivation of a correction factor. In conducting epidemiologic studies, birth certificate data should be used with: (1) great caution; (2) a system of validation with the medical record to estimate the degree of underreporting and to derive a correction factor; and (3) a priori knowledge that underreporting of congenital anomalies on this document is highly prevalent.

Infertility and endometriosis: comparison of pregnancy outcomes with laparotomy versus laparoscopic techniques.

OBJECTIVES: The null hypothesis of this retrospective literature analysis was that the superiority of laparoscopy over laparotomy to correct infertility resulting from tubal injury has not been proved because of the lack of well-designed comparative studies. The same was true for the correction of infertility caused by minimal and mild endometriosis. STUDY DESIGN: A retrospective review of the English-language literature since 1975 was made to ascertain whether laparoscopic surgical correction of infertility caused by tubal injury and endometriosis resulted in an increased pregnancy rate compared with laparotomy techniques. Complication rates associated with laparoscopy versus laparotomy were also compared. RESULTS: There were almost no adequate studies designed and executed to answer these questions based on criteria established by the United States Preventive Services Task Force. Furthermore, there was no evidence in the reported series that laparoscopic surgical procedures were superior to laparotomy in correcting infertility. The complication rates were similar. There was suggestive, but not yet proven, evidence that laparoscopic surgery with laser techniques may be superior to laparotomy in the management of infertility resulting from moderate and severe endometriosis. CONCLUSION: Although results and complications were similar, the cost in savings with respect to decreased hospital expenses and loss of work time favor the use of laparoscopy over laparotomy when results are similar and not associated with increased risk. What has not been established are costs and work-time losses for minilaparotomy compared with laparoscopy.

Low-dose aspirin. II. Relationship of angiotensin II pressor responses, circulating eicosanoids, and pregnancy outcome.

Forty pregnant women (28 to 32 weeks' gestation) were given low-dose aspirin therapy (81 mg/day) from the time of enrollment until delivery; circulating eicosanoid levels and angiotensin II pressor responses were measured before and after 1 week of aspirin therapy. Subsequent clinical outcome was correlated with these results. All women had significant reductions in serum and plasma thromboxane B2 levels with aspirin treatment (p less than 0.01). Eleven women who remained sensitive to the pressor effects of angiotensin II (effective pressor dose less than 10 ng/kg/min) after 1 week of low-dose aspirin treatment exhibited significant decreases (p less than 0.05) in plasma 6-keto-prostaglandin F1 alpha (264 +/- 119 vs 161 +/- 31 pg/ml, mean +/- SD) and prostaglandin E2 (476 +/- 174 vs 351 +/- 112 pg/ml) levels. In contrast, patients who were either nonsensitive (refractory) to angiotensin II (n = 18; greater than or equal to 10 ng/kg/min) before aspirin or became nonsensitive after aspirin administration (n = 11) had no change in either plasma 6-keto-prostaglandin F1 alpha or prostaglandin E2 concentrations. The occurrence of pregnancy-induced hypertension was 100% in the women who remained angiotensin II sensitive during aspirin therapy as compared with 36% and 39% in the other two groups (x2 = 16.14; p less than 0.001). Thus during low-dose aspirin therapy a failure to develop refractoriness to infused angiotensin II is associated with a nonselective inhibition of eicosanoids and the almost certain development of pregnancy-induced hypertension. These observations may reflect a basic defect in vascular adaptation to pregnancy.

Failure to recognize fetal alcohol syndrome in newborn infants.

A clinically distinct constellation of major and minor anomalies, termed the fetal alcohol syndrome, occurs among infants whose mothers abuse alcohol during pregnancy. In addition, significantly higher rates of pregnancy complications, including perinatal deaths and fetal growth retardation, occur among these women and their offspring. We studied the medical records of 40 infants born to 38 alcohol abusers and the frequency of characteristics associated with fetal alcohol syndrome. Physical examinations of 6 infants revealed primary features consistent with a diagnosis of fetal alcohol syndrome. Postnatal growth and development were very poor in 17 (50%) of 34 liveborn alcohol-exposed infants. The diagnosis of fetal alcohol syndrome did not appear in the medical records of any of these infants despite the fact that the mothers' obstetric records included a history of alcohol abuse during pregnancy. This finding emphasizes the importance of good communication between obstetric and pediatric medical staff at this hospital, particularly when providing care for pregnant women and newborn infants at high risk for complications due to maternal alcohol or other drug abuse.

Pathophysiology of preeclampsia.

In summary, the major pathophysiologic event that occurs in women with preeclampsia or pregnancy-induced hypertension is vasospasm. In turn, vasospasm leads to a wide range of dysfunction in many organ systems.

Alcohol abuse during pregnancy: changes in frequency in a large urban hospital.

The reported frequency of alcohol abuse during pregnancy was studied in a large urban public hospital in Dallas, Texas. During 1977-1980, 5602 pregnant women were surveyed and 0.7% (95% confidence interval 0.6-0.8%) reported abusing alcohol during pregnancy. In 1987, 1.4% (95% confidence interval 1.3-1.5%) of 1032 pregnant women, who were surveyed before delivery, reported alcohol abuse according to the same definition used 10 years earlier. The increase in the frequency of reported alcohol abuse during pregnancy between 1977-1980 and 1987 is statistically significant (P less than .05).

Low-dose aspirin. I. Effect on angiotensin II pressor responses and blood prostaglandin concentrations in pregnant women sensitive to angiotensin II.

Decreased incidence of proteinuric hypertension after low-dose aspirin therapy is hypothesized to be a consequence of selective thromboxane A2 inhibition and sparing of prostacyclin. This study was designed to ascertain if low-dose aspirin therapy (81 mg/day for 1 week) alters vascular refractoriness to angiotensin II and the prostacyclin/thromboxane A2 ratio in pregnant women sensitive to angiotensin II (n = 17). Low-dose aspirin increased the effective pressor dose of angiotensin II from 5.9 +/- 2.4 to 10.2 +/- 5.5 ng/kg/min (p less than 0.01, mean +/- SD). Platelet-derived serum thromboxane B2 (a metabolite of thromboxane A2), a measure of therapy compliance, decreased from 1804 +/- 1771 to 132 +/- 206 pg/ml (p less than 0.01). Plasma thromboxane B2 decreased from 130 +/- 107 to 19 +/- 12 pg/ml (p less than 0.01). Inhibition was not selective because 6-keto-prostaglandin F1 alpha (a metabolite of prostacyclin) also decreased from 243 +/- 90 to 163 +/- 90 pg/ml (p = 0.039) and prostaglandin E2 was reduced from 155 +/- 67 to 95 +/- 40 pg/ml (p = 0.014). Decreases in thromboxane B2, however, were significantly greater (75% +/- 19%) than decreases in 6-keto-prostaglandin F1 alpha (21% +/- 33%) or prostaglandin E2 (29% +/- 36%); thus the 6-keto-prostaglandin F1 alpha/thromboxane B2 ratio increased from 3.1 +/- 2.0 to 12.4 +/- 9.9 (p less than 0.01). Although low-dose aspirin increases the effective pressor dose of angiotensin II, it does not return to normal pregnancy values. This observation is consistent with the hypothesis that this represents only a partial selective prostaglandin inhibition.

Control of vascular reactivity in pregnancy.

Human pregnancy is characterized by a blunted pressor responsiveness to vasopressor substances. This was first reported by Dieckmann and Michel in 1937 in experiments in which they measured vascular reactivity to the pressor effects of a crude preparation of vasopressin. Recently, this has been reported to occur in response to epinephrine, norepinephrine (NE), and angiotensin II (AII). Gant and associates reported that the increasing vascular sensitivity to infused AII not only was characteristic of women who developed pregnancy-induced hypertension, but in fact preceded the development of pregnancy-induced hypertension. Although a variety of factors may mediate this blunted pressor responsiveness, the most likely candidate appears to be the localized production within endothelium and/or vascular smooth muscle of prostaglandins. Indeed, administration of indomethacin or aspirin results in an increased sensitivity to infused AII in normotensive previously AII-refractory women. Administration of the steroid hormone 5 alpha-dihydroprogesterone reverses this apparent prostaglandin-mediated response. In addition, administration of the phosphodiesterase inhibitor, theophylline, results in a restoration of vascular refractoriness to infused AII in women with pregnancy-induced hypertension or in women destined to develop pregnancy-induced hypertension. Although a variety of known and possibly unknown compounds might also effect the control of vascular reactivity during human pregnancy, the prostinoids appear to play a pivotal role in mediation of control of vascular reactivity during human pregnancy.