Prostaglandin E metabolite levels in umbilical cord plasma.
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Biomedical subjects
Publications and source records attributed to J H McCubbin.
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Human amniotic fluid has been separated into two fractions; one fraction inhibits prostaglandin biosynthesis and the other fraction is stimulatory. The activity of the stimulatory fraction increased with increasing gestational age and was greater still during labor. The activity of the inhibitory fraction decreased with increasing gestational age and was smaller still during labor. We speculate that these changes may play a significant role in parturition.
The possible relation between prostaglandin production and the sensitivity of pregnant women with pregnancy-induced hypertension to the pressor effects of angiotensin II was investigated. Plasma prostaglandin levels were determined in four groups of women before, during, and after intravenous infusion of angiotensin II. Concentrations of the stable metabolites of prostaglandin E2, prostaglandin F2 alpha, and prostaglandin I2 (prostacyclin) were quantified by specific radioimmunoassays in the plasma of nonpregnant women, women pregnant in the late third trimester, and women pregnant in the late third trimester with either pregnancy-induced or chronic hypertension. Plasma prostaglandin concentrations did not change significantly during angiotensin II infusion in any of the four groups of women. Levels of the prostacyclin metabolite, however, were significantly higher in the hypertensive pregnant women than in the normotensive pregnant women.
A prospective study comparing continuous intravenous magnesium sulfate to intramuscular magnesium sulfate was performed in 32 preeclamptic patients. Eighteen patients received the intramuscular regimen for mild and severe preeclampsia as recommended by Pritchard. The remaining 14 patients received an intravenous regimen consisting of a 4 gm loading dose administered over 15 minutes followed by a maintenance dose of either 1 gm/hr (n = 7) or 2 gm/hr (n = 7). All groups were similar regarding maternal age, height, weight, fetal gestational age, and laboratory findings. The intravenous regimen with a maintenance dose of 1 gm/hr produced serum magnesium levels that were much lower than those achieved with the intramuscular regimen. There was no significant difference after 3 hours of therapy between the mean magnesium levels achieved with the intramuscular regimen and the levels achieved with the intravenous regimen with a maintenance dose of 2 gm/hr. However, during the first 3 hours of therapy the intramuscular regimen for severe preeclampsia produced mean magnesium levels that were significantly higher than those levels obtained with the intravenous regimen with a maintenance dose of 2 gm/hr (p less than 0.001). Both methods were safe. However, the intravenous regimen with a maintenance dose of 1 gm/hr is inadequate in management of preeclamptic patients.
Infants of 72 recently managed women with eclampsia before delivery were studied. Infants with gestational age of 36 weeks or less (56%) were analyzed separately from those infants of more than 36 weeks' gestation (44%). In addition, premature infants of eclamptic mothers were compared with 40 premature infants whose mothers did not have any medical complications. Intrauterine growth retardation was symmetrical in all seven infants whose mothers had eclampsia prior to 32 weeks. All neurological abnormalities were associated with abruptio placentae or intrauterine growth retardation. Among the preterm infants of eclamptic mothers and those of normotensive mothers, there was no significant difference in any commonly acquired laboratory data. Neonatal complications in premature infants of eclamptic mothers were frequent. However, neonatal complications of the low-birth weight infants were strikingly similar regardless of the presence of eclampsia. It is possible that most neonatal complications are consequence of prematurity, instead of a sole consequence of eclampsia. Observations from follow-up data (up to 4 years of age) suggest normal growth and development for infants of mothers with uncomplicated eclampsia.
Although the recognition and treatment of preeclampsia theoretically should eliminate eclampsia, it has not disappeared and remains a substantial threat to maternal and fetal well-being. The therapy of choice for treatment and prevention of convulsions is magnesium sulfate (MgSO4 . 7H2O USP) and that for severe hypertension is intravenous hydralazine. Delivery of the fetus and placenta is recommended after the mother is stabilized from the effects of the convulsion(s). If the mother is to be transported before delivery, it is important that she receive an adequate dose of MgSO4.
Sixty-seven cases of eclampsia were managed between August 1977 and July 1980. Routinely acquired laboratory tests of these cases have been analyzed. In addition, the group of patients with eclampsia was compared with a group of 24 healthy pregnant women. There was no significant difference in platelet count, serum fibrinogen, and bilirubin values. The activated partial thromboplastin time was abnormal in 42% of patients with eclampsia. There was no clinical evidence of disseminated intravascular coagulation in any patient. Patients with eclampsia had abnormalities of lactic dehydrogenase, alkaline phosphatase, SGOT, uric acid, BUN, and creatinine. However, in any individual patients there was no single test of great clinical usefulness and no test predictive of maternal or fetal outcome. At present the authors recommend complete blood count (including blood smear and platelet count), clot observation, and serum creatinine tests. Liver function tests are reserved for the patient with upper abdominal pain. Additional tests are recommended if the diagnosis of eclampsia is questionable or if an additional disease process is suspected.
Plasma volume determinations for 9 women with severe chronic hypertension who delivered live-born infants with birth weights appropriate for gestational age (AGA) were compared with those for 7 women with chronic hypertension whose pregnancies ended in intrauterine fetal demise. Plasma volume determinations using Evans blue dye dilution technique were performed at 20 to 25 weeks' gestation (12 patients) and at 26 to 29 weeks' gestation (16 patients). In addition, plasma volume measurements were performed at 8 weeks post partum in 5 patients who had intrauterine fetal demise. Analysis of the clinical course, laboratory findings, and pregnancy outcome revealed that the degree of plasma volume expansion was the factor most significantly differing between the 2 groups of patients. The plasma volumes of 9 women who delivered AGA infants were comparable with those values previously reported for normal singleton pregnancy. In contrast, each patient with intrauterine fetal demise demonstrated failure in plasma volume expansion at 20 to 25 weeks' gestation when compared with her own postpartum value. In each of the 6 patients who had a second plasma volume determination at 26 to 29 weeks' gestation, there was a decrease (mean decrease, 13.5%) from the value at 20 to 25 weeks. Plasma volume determinations may be very helpful in making clinical decisions regarding women with severe hypertension. Plasma volume determination may be most helpful in identifying a subgroup of women who are at particular risk for having infants with intrauterine growth retardation and intrauterine fetal demise.
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Sixty-seven cases of eclampsia were managed from 1977 to 1980, for an incidence of 1 in 310 deliveries. Eighty-four percent of patients were nulliparous and 82% had received some prenatal care. Prior to convulsion, 14 patients (21%) had a diastolic blood pressure below 90 mmHg, 39% had no edema, and 21% had no proteinuria. Thirty-seven patients (55%) had their first convulsion in the hospital. Eight patients had convulsions while receiving magnesium sulfate therapy. Convulsions occurred post partum in 25 patients (37%). In 11 patients the onset of eclampsia occurrred 3 to 11 days after delivery. The total perinatal mortality was 8.6% for all cases of eclampsia. Excluding postpartum cases, perinatal mortality was 13.3%, but was only 5% for those fetuses alive on admission to the perinatal center. Abruptio placentae was present in 9 cases and accounted for 4 of the 6 perinatal deaths. The high incidence of eclampsia at the authors' center has not decreased over the past 20 years, but maternal mortality has been reduced from 2.1 to 0%. It was disturbing to find that management error played some role in the development of eclampsia in 50% of the cases. Significant errors--including ineffective magnesium sulfate therapy, failure to treat adequately prior to transport, and lack of communication with a perinatal center--are discussed.
Diagnosis of rubella during pregnancy is a challenge in a woman who is seronegative at the initial prenatal visit or in whom there has been no prior testing for rubella immunity. Detection of hemagglutination-inhibiting antibody is usually the best test. Diagnosis depends on a fourfold rise in antibody titer between paired acute and convalescent sera. In certain circumstances, it is necessary to ascertain complement-fixing antibody, fluorescent antibody or rubella-specific IgM.
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Thirty-four pregnant women with acute appendicitis presented at Parkland Memorial Hospital during a 15-year period. Abdominal pain, usually accompanied by nausea with or without vomiting, was the most common presenting symptom. Anorexia was less constant, and its occurrence decreased with advancing gestation. Physical findings usually included direct abdominal tenderness and, less often, rebound tenderness. Leukocytosis and/or a "left shift" were common laboratory findings, and the urinalysis was normal in most cases. Diagnosis was increasingly difficult as gestation progressed. This was reflected both by the increasing severity of the disease process found at surgery and by increasing fetal loss. If the diagnosis of appendicitis is suspected in the gravid patient, immediate surgical intervention is indicated to prevent the catastrophic complications associated with procrastination in diagnosis and treatment.
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