Abortion: is there a rational precept?
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Biomedical subjects
Publications and source records attributed to D P Cruikshank.
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Most pregnancies with severe twin-twin transfusion syndrome before 27 weeks' gestation result in perinatal death. Previous attempts at therapy have been generally unsatisfactory and rarely successful. We have developed a technique for intrauterine ablation of the vascular communications between the fetoplacental circulations with a fetoscopically directed neodymium:YAG laser. The operation was performed on three women at risk for pregnancy loss from acute hydramnios at 18.5, 22, and 22.5 weeks' gestation. The first two procedures were uneventful, but the third was complicated by a placental vessel perforation. The first two patients delivered at 27 and 34 weeks after premature rupture of membranes and spontaneous labor, whereas the third woman developed severe preeclampsia at 29 weeks which necessitated delivery. Four of the six infants survived. Clinical and ultrasonographic evidence, as well as pathologic examination of the placentas, suggested that stabilization or resolution of the syndrome was due to photocoagulation of the vascular communications. This initial experience suggests that fetoscopic laser occlusion of placental vessels is feasible and superior to previous therapies because it treats the underlying pathophysiology directly.
Two cases occurred of colon carcinoma complicating pregnancy. Both patients presented with occult blood in the stool and iron deficiency anemia; that makes their cases different from the 20 previously reported ones of colon carcinoma above the peritoneal reflection associated with pregnancy. These cases illustrate the importance of a rectal examination and stool guiaic test in evaluating iron deficiency anemia in pregnancy.
A secundigravida developed culture-proved Listeria monocytogenes sepsis with signs and symptoms of chorioamnionitis at 13 weeks' gestation. Pregnancy termination was refused, and she was treated with intravenous ampicillin and gentamicin followed by oral trimethoprim/sulfamethoxazol. Fifteen days after initiation of therapy, an amniotic fluid culture was negative, although uterine tenderness persisted for 7 weeks. A healthy, culture-negative infant was delivered at term.
A prospective study of 53 nulliparous teenagers was conducted to determine differences in erythrocyte and plasma magnesium concentrations between subjects who had normal full-term deliveries (normal pregnant group) and those who developed pregnancy-induced hypertension. Magnesium content of monthly blood samples was determined by atomic absorption spectrophotometry. Socioeconomic data and information on use of supplements, medicines, tobacco, and alcohol were obtained by interview and medical chart review. Erythrocyte magnesium levels in both groups remained stable during pregnancy, whereas plasma magnesium showed a slight decline (P less than .08). Plasma and erythrocyte magnesium did not differ significantly between the normal pregnant (N = 30) and pregnancy-induced hypertension (N = 12) groups. Overall, mean arterial pressure was not significantly related to plasma or erythrocyte magnesium values. Within the pregnancy-induced hypertension group, there was a slight (P less than .05) inverse relationship between mean arterial pressure and plasma magnesium. The two groups were similar for socioeconomic characteristics, gynecologic age, previous use of oral contraceptives, and use of tobacco and magnesium-containing supplements. Pregnancy-induced hypertension subjects reported more alcohol use than did normal pregnant subjects (P less than .02). In conclusion, there was no evidence of magnesium depletion among teens who developed pregnancy-induced hypertension, by measurement of erythrocyte or plasma magnesium.
Fifty-four cases in which surgical intervention during pregnancy was required for definitive therapy of adnexal masses were reviewed. The calculated incidence of adnexal masses that required surgical intervention during pregnancy in our primary population (patients who were not referred for evaluation of an already identified mass) was one case per 1300 live births. A malignant tumor was found in 5.9% of the pregnant patients who underwent exploratory celiotomy for therapy of an adnexal mass. Those pregnant women who underwent emergency celiotomy because of hemorrhage or torsion as a complication of an adnexal mass spontaneously aborted or underwent premature delivery more frequently than those patients who underwent elective celiotomy for removal of the mass (p less than 0.001). On the basis of this review, we recommend that pregnant women with persistent adnexal masses undergo elective extirpation of the mass in the second trimester of pregnancy.
Ehlers-Danlos syndrome (EDS) is a rare connective tissue disorder known to be associated with complications during pregnancy. Recently, the syndrome has been subdivided into a number of types with different clinical manifestations. We report a maternal death with type IV, and review the literature for obstetric complications of the syndrome by type. A very high risk of maternal death with type IV is identified. Recommendations for managing pregnancies complicated by EDS are given.
Term fetal deaths occurring in Virginia in 1983 were reviewed to determine potential preventability. During this period, 52 (48%) of 108 such deaths were judged preventable. The leading cause of preventable antepartum death was maternal hypertension, followed by diabetes, inadequate fetal surveillance, and postterm pregnancy. The major cause of intrapartum fetal death was long delay between the onset of obvious fetal compromise and delivery. The incidence of preventable term stillbirth seemed inversely proportional to hospital size.
In order to differentiate pregnancy-induced hypertension from chronic systemic hypertension, we measured left ventricular mass for comparison in each trimester of pregnancy in 11 normotensive patients and 14 patients with chronic hypertension and in the third trimester in 10 patients with pregnancy-induced hypertension. The mean left ventricular mass was comparably increased above normal in the patients with chronic hypertension in all three trimesters. In the third trimester in the normotensive women, left ventricular mass (147 +/- 12 gm) was similar to that of the group with pregnancy-induced hypertension (157 +/- 16 gm), whereas the group with chronic hypertension had an elevated left ventricular mass (238 +/- 39 gm) (p less than 0.01). However, three patients with chronic hypertension developed superimposed pregnancy-induced hypertension. We concluded that an elevated left ventricular mass during pregnancy is consistent with underlying chronic hypertension but does not rule out superimposed pregnancy-induced hypertension. A normal left ventricular mass in the third trimester of a hypertensive pregnancy is most consistent with pregnancy-induced hypertension.
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Previous studies have characterized the pharmacology of propylthiouracil (PTU) in normal and hyperthyroid subjects, but there is little information available regarding PTU pharmacokinetics in pregnant hyperthyroid women. We investigated the serum PTU response to an oral dose of PTU in six hyperthyroid pregnant women both ante- and postpartum. The serum PTU profile during the third trimester of pregnancy was qualitatively similar to that in nonpregnant subjects, but serum PTU concentrations were consistently lower in the late third trimester compared with postpartum values. Cord serum PTU concentrations were consistently higher than simultaneously obtained maternal serum PTU concentrations, suggesting slower PTU clearance in the fetus. There was a significant inverse correlation (r = -0.92; P = 0.026) between the maternal serum PTU area under the curve in the third trimester and the cord serum free T4 index.
To determine the clinical usefulness of plasma volume determinations, we measured plasma volume serially throughout pregnancy with the use of the Evans blue dye-dilution technique in 20 subjects with normal pregnancies. In comparison, four preeclamptic subjects were studied. In preeclamptic subjects compared to normal subjects, plasma volume was reduced (1763 +/- 216 versus 2345 +/- 198 ml/m2, p less than 0.001). Two normotensive subjects who subsequently developed preeclampsia had reduced plasma volumes prior to the onset of hypertension as compared to volumes in those who remained normotensive (1918 +/- 86 versus 2345 +/- 198 ml/m2, p less than 0.01). Those subjects who were delivered of infants who were small for gestational age had significantly reduced plasma volumes compared to volumes of those who were delivered of infants who were appropriate for gestational age (1950 +/- 333 versus 2237 +/- 259 ml/m2, p less than 0.05), but this was true only among gravid women with pregnancies complicated by preeclampsia. We conclude that failure of plasma volume expansion is associated with the development of preeclampsia and also intrauterine fetal growth retardation in preeclamptic subjects.
Twenty-nine preterm patients with premature rupture of the membranes who were not in labor and who did not have clinical chorioamnionitis underwent successful amniocenteses. Nine fluids were positive for bacteria. Subsequent clinical chorioamnionitis and shorter latency periods were more common in these 9 patients than in the 20 with sterile amniotic fluid. Positive fluids were more likely to be obtained from patients tapped within 48 hours of membrane rupture. In most patients with heavy bacterial growth, clinically apparent infection and/or labor soon supervened.
Maternal, fetal, and neonatal results and complications were analyzed after 923 genetic amniocenteses. Maternal age of 35 years and beyond was associated with a 2.0% risk of fetal trisomy 21 and a 3.0% risk of all major chromosome abnormalities. Comparable rates for women aged 40 and beyond were 4.8% and 7.2%. Neural tube defects were detected in 0.15% of procedures done for maternal age and 3.4% of those done for a previous involved child. The risk of spontaneous abortion as a result of amniocentesis was 0.2% to 1.4%. Mahogany or green fluid was associated with a 29% rate of fetal loss. Unexplained midtrimester elevations of maternal serum alpha-fetoprotein were associated with a 38% risk of a subsequent low-birth weight infant. The only neonatal complication associated with amniocentesis was an apparent marked increase in the incidence of lower-extremity orthopedic abnormalities.
Peripheral blood levels of the minerals and hormones involved in calcium homeostasis were measured in insulin-dependent diabetic patients at delivery, and in umbilical arterial and venous blood. The minerals were also measured in neonatal blood at 24 hours of age. Insulin-dependent diabetic patients at delivery have depressed serum levels of parathyroid hormone, although serum total and ionized calcium levels are not different from those of nondiabetic patients. Fetuses of diabetic mothers are hypocalcemic and have reduced parathyroid hormone levels. Infants of diabetic mothers demonstrate early neonatal hypocalcemia. No differences between diabetic and control patients could be demonstrated in terms of calcitonin or phosphorus levels, in either mother, fetus, or neonate.
At 28 weeks' gestation a patient developed polyhydramnios associated with a large fetal renal cyst demonstrated by ultrasound. Drainage of the cyst was performed, resulting in the disappearance of polyhydramnios. The pregnancy progressed normally to term and resulted in the delivery of a healthy infant.
Serial maternal and cord blood determinations of the ions and hormones involved in calcium homeostasis were made in pre-eclamptic women treated with intravenous magnesium sulfate. A 4 gm loading dose followed by 1 to 2 gm/hr caused maternal serum magnesium concentrations to rise 150%, to levels of 3.3 to 4.5 mEq/L, and ionized calcium levels to fall 16%, to 1.89 mEq/L. The hypocalcemia etly altering calcitonin. Changes in total calcium paralleled those of ionized calcium; phosphorus levels were not affected by magnesium infusion. At the time of delivery the offspring of these women were hypermagnesemic and relatively hypocalcemic, although less so than their mothers. Fetal ionized calcium levels, although lower with magnesium treatment than in control subjects, were within the lower limits of the normal range, which perhaps explains why the fetus did not respond with increased PTH or decreased calcitonin output. These results indicate that the principal maternal response to magnesium-induced hypocalcemia involves increased parathyroid hormone secretion which tends to preserve maternal calcium homeostasis, while the fetus is partially protected from hypermagnesemia and hypocalcemia by the placenta.