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To study the effect of intrauterine growth retardation (IUGR) on fetal peripheral neuronal elements, we examined preputial skin tissues of ten growth-retarded neonates (mean gestational age 36 +/- 2.3 weeks) and six normal control neonates (mean gestational age 35 +/- 3.0 weeks) by transmission electron microscopy. The myelinated and unmyelinated nerve fibers of growth-retarded neonates contained significant ultrastructural alterations, consisting of 1) local aggregation of mitochondria, 2) loss of mitochondrial cristae, 3) the presence of large vacuoles within the axoplasm, and 4) myelinated fiber degeneration. The Schwann cells of these neonates exhibited accumulation of glycogen, disruption of cytoplasm, dilatation of rough endoplasmic reticulum, and extensive development of polyribosomes. None of the above changes were observed in the control infants, those appropriate for gestational age. We conclude that IUGR may cause significant ultrastructural changes in developing peripheral neuronal tissue.

Amniotic fluid spectrophotometric analysis for bilirubin (delta optical density [delta OD450], at 450 nm) is used to assess the severity of fetal involvement in isoimmunized pregnancies. Two patients presented with sickle cell anemia and hyperbilirubinemia who also were isoimmunized. The first patient had anti-kell and anti-e antibodies, whereas the second patient had anti-Lewisa and anti-Coltonb antibodies. Delta OD450 was elevated in both patients. The difficulty in interpretation of high delta OD450 in the presence of maternal hyperbilirubinemia is stressed. Sickle cell diseased patients are particularly prone to present with this problem. These patients always have hyperbilirubinemia and a relatively high incidence of irregular antibodies because of the numerous blood transfusions they receive. The management of these two patients is presented with suggestions for the use of alternative modalities of monitoring isoimmunized pregnancies in patients with hyperbilirubinemia.

The cardiovascular effects of ritodrine tocolytic therapy were assessed by noninvasive simultaneous recordings of indirect carotid pulse, electrocardiogram (ECG), phonocardiogram, and M-mode echocardiogram in 12 patients in preterm labor. The study was performed before and during infusion, and afterward when the patient was on oral drug therapy. Ritodrine therapy increased heart rate, left ventricular fractional shortening, pre-ejection period/left ventricular ejection time ratio, and cardiac index. A progressive rise in pulmonary capillary pressure was observed in all patients, exceeding 18 mmHg (the threshold for the development of pulmonary congestion) in six patients. Systolic arterial pressure, left ventricular end-diastolic dimension, and plasma protein oncotic pressure remained unchanged during therapy. Ritodrine therapy resulted in a significant drop in diastolic blood pressure and peripheral vascular resistance. This noninvasive means of measuring cardiovascular parameters, including pulmonary capillary pressure, may be useful in monitoring patients who develop significant cardiovascular side effects during tocolytic therapy.

Metastatic pheochromocytoma, a rare complication of pregnancy, was managed from 30 weeks' gestation until delivery three weeks later with a combination of alpha-adrenergic blockade (Minipres) beta-adrenergic blockade (Timolol), and dopamine synthesis inhibition (Demser). The biophysical parameters of fetal heart rate (FHR) baseline, variability, and reactivity, as well as fetal breathing movements, body movements, tone, and amniotic fluid volume were followed sequentially during this period. A 1450-g growth-retarded infant, who subsequently did well, was delivered by cesarean section; the mother received combined surgical and medical therapy for her metastatic disease in the postpartum period. The initial fetal biophysical alteration observed was a reduction in mean FHR baseline rate; further biophysical test abnormalities appeared only after overt fetal compromise was evident. Sequential multiple parameter biophysical testing in such circumstances appears to be a valid and valuable approach to antepartum management.

A retrospective search of the perinatal autopsy files at Magee-Womens Hospital of Pittsburgh from 1977 to 1979 disclosed 38 autopsies of preterm infants (gestational age 27 to 34 weeks) born to women with hypertensive disorders. Of these fetuses, 23 were chosen for the study of factors that lead to accelerated cerebral maturation in the preterm fetus. The sequential developmental changes of the individual fissures, sulci, and gyri of the cerebral hemispheres were used to assess gestational development of the brain. Seventeen infants showed accelerated cerebral maturation two weeks or more in advance of gestational age. Six infants showed gyral maturation appropriate for gestational age. Chronic maternal hypertension and fetal intrauterine growth retardation were found to be significant risk factors in accelerated intrauterine cerebral maturation. The chronicity of hypertension may be more important than its severity in accelerated fetal cerebral maturation.

Intermittent nipple stimulation has been proposed as a substitute for exogenous oxytocin infusion in the performance of contraction stress tests. To compare the uterine activity produced by these two methods, we studied a group of 45 term pregnant women undergoing indicated inductions of labor. Twenty-five patients had nipple stimulation and 20 patients received oxytocin infusions according to a study protocol. The two groups were similar in all obstetric parameters. Pre- and posttest uterine activity was measured by internal tocodynamometry and quantified in Montevideo units. A significant increase in uterine activity occurred in both groups (P less than .01). Regular uterine activity (three contractions in ten minutes) was achieved more rapidly (P less than .005), but at a lower level (P less than .001) in the nipple stimulation group. Pre- and posttest tonus did not change significantly in either group. In the nipple stimulation group, five patients (20%) did not achieve adequate contraction patterns after 15 stimulation-rest cycles (a total of 110 minutes) and three subjects (12%) experienced uterine hyperstimulation. These observations suggest that exogenous oxytocin and intermittent nipple stimulation may not have equivalent effects on uterine contractility. Therefore, it may not be justified to substitute one technique for the other or to use the same criteria for interpretation of contraction stress tests produced by both techniques.