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J E Dickinson

Publications and source records attributed to J E Dickinson.

14 recordsLinked to original sources
PubMed1995

Elevated mid-trimester hCG and maternal lupus anticoagulant.

An association is described between women with lupus anticoagulant and abnormal prenatal serum screening results. Three cases of positive second-trimester serum screening for Down syndrome, with karyotypically normal fetuses, in women demonstrated to have lupus anticoagulant are presented. Serum screening positivity was principally due to a disproportionately elevated maternal serum human chorionic gonadotrophin (hCG) level. In each case, early, severe intrauterine growth restriction was documented, with only one fetus surviving the neonatal period. As maternal lupus anticoagulant may have a profoundly adverse effect on the course of pregnancy, we suggest that an elevated hCG level on prenatal screening prompt consideration of maternal lupus anticoagulant testing if ultrasonography demonstrates an otherwise normal singleton gestation and the fetal karyotype is normal.

Adult↗
PubMed1995

Antenatal diagnosis and management of fetomaternal alloimmune thrombocytopenia.

Fetomaternal alloimmune thrombocytopenia (FMAT) arises from maternal-fetal platelet antigen incompatibility, which stimulates the production of maternal immunoglobulin G (IgG) platelet-specific antibody. Transplacental passage of this antibody results in fetal platelet destruction and consequent thrombocytopenia. Sequelae of thrombocytopenia may be observed in both the fetus and neonate with intracranial hemorrhage occurring in approximately 10 to 30% of affected infants. No antenatal universal screening test is currently available to detect the 50% of cases occurring in the first pregnancy. The recurrence rate in subsequent pregnancies is 75 to 85%, with a tendency to increasing disease severity. Paternal platelet genotyping is recommended to assist in risk counseling following an affected pregnancy. Prenatal therapeutic strategies are aimed at elevating the fetal platelet count in affected pregnancies and thus decreasing hemorrhagic sequelae. The most effective treatment regimen is uncertain, but encouraging results are reported with the use of maternal intravenous gamma globulin. We report our experience in the antenatal diagnosis and management of FMAT.

Adult↗
PubMed1995

Severe twin-twin transfusion syndrome: current management concepts.

The presence of functioning vascular anastomoses within the monochorionic placentation of a monozygotic twin pregnancy is responsible for the twin-twin transfusion syndrome. This is a heterogeneous disorder with a wide spectrum of severity. In the most severe form it results in the oligohydramnios-polyhydramnios sequence with a marked disparity in intertwin biometry and amniotic fluid volume. Without therapy, the perinatal mortality of severe twin-twin transfusion syndrome is 60-100%. Several therapeutic interventions have been attempted with therapeutic amniocentesis producing the most consistent improvement in fetal survival rates. The outcome of 10 cases of severe twin-twin transfusion syndrome, presenting as the oligohydramnios-polyhydramnios sequence, is presented. Gestational age at presentation ranged from 20-34 weeks. Three fetuses were hydropic at initial presentation and of these only 1 survived. All cases were treated with serial aggressive therapeutic amniocentesis, the number of procedures ranging from 1-9/patient. The volume of amniotic fluid removed ranged from 3,200-14,000 mL. Gestation was prolonged a mean of 46 days (range 1-106 days). The perinatal survival rate was 65% (13/20 infants). Preterm premature rupture of membranes and secondary preterm birth complicated 1 pregnancy treated with therapeutic amniocentesis. Short-term morbidity in the liveborn infants was predominantly secondary to prematurity and renal cortical necrosis. Severe twin-twin transfusion syndrome is the most common aetiology of the oligohydramnios-polyhydramnios sequence. Therapeutic amniocentesis offers an intervention that may reduce the high perinatal loss rate previously observed with this disorder.

Adult↗
PubMed1994

The ovine fetal sympathoadrenal response to the maternal administration of methamphetamine.

OBJECTIVE: We hypothesized that maternally administered methamphetamine would alter fetal sympathoadrenal activity. STUDY DESIGN: Six chronically catheterized near-term pregnant ewes received an intravenous bolus injection of methamphetamine (1.25 mg/kg). Maternal and fetal arterial blood gas values, glucose, insulin, lactate, and catecholamines were measured in the control period and at 15, 30, 60, 90, 120, and 180 minutes after methamphetamine. RESULTS: Fetal PO2 decreased from 21.4 +/- 1.9 mm Hg at control measurement to 15.3 +/- 3.3 mm Hg after 60 minutes (p < 0.05). Fetal pH declined from 7.35 +/- 0.014 at control to 7.29 +/- 0.024 after 180 minutes. Fetal plasma glucose rose from 15.3 +/- 2.4 mg/dl at control to peak at 51.2 +/- 6.8 mg/dl at 120 minutes. Insulin levels increased from a control of 40.5 +/- 8.06 to a peak of 128 +/- 46 microIU/ml at 180 minutes (p < 0.05). Lactate levels increased from a baseline of 33.5 +/- 2.0 mg/dl to 92.3 +/- 22.8 mg/dl at 180 minutes. Fetal catecholamines rose from a baseline of 153 +/- 20.2 pg/ml for epinephrine and 226 +/- 18.5 pg/ml for norepinephrine to maximum values of 518 +/- 87.3 and 661 +/- 59.3 pg/ml at 15 minutes (p < 0.05), declining thereafter. CONCLUSIONS: Maternal administration of methamphetamine is associated with a short-term increase in circulating fetal catecholamines followed by hyperglycemia, lactacidemia, and hyperinsulinemia. These findings suggest that the alteration of fetal sympathoadrenal activity may contribute to the various perinatal complications associated with methamphetamine use.

Animals↗
PubMed1992

The effect of fetal sepsis on umbilical cord blood gases.

The relationship between fetal sepsis and acid-base status is unknown. We hypothesized that in utero sepsis would result in fetal metabolic acidemia. In a retrospective study during a 38-month period, the acid-base status at birth of neonates with in utero sepsis, documented by positive blood cultures, was reviewed. Compared with term neonates, preterm neonates had a 22-fold increase in the risk of bacteremia at birth. In spite of this increased risk of sepsis, there was no significant alteration in arterial pH in preterm septic neonates when compared with preterm controls. Fetal sepsis at term was accompanied by a statistically significant reduction in arterial pH (7.21 +/- 0.07) compared with controls (7.26 +/- 0.06, p less than 0.05). When controlled for other variables, the decrease in arterial pH at term was correlated with an increased duration of labor (7.3 +/- 0.7 in controls vs 10.8 +/- 0.9 hours in neonates with sepsis, p less than 0.05). The classic predictors of chorioamnionitis were found to be poor prognostic indicators of fetal bacteremia. Fetal sepsis at term is associated with a deterioration in the fetal acid-base status and a prolongation of labor.

Acid-Base Equilibrium↗
PubMed1992

The effect of preterm birth on umbilical cord blood gases.

Apgar scores are used routinely to assess early neonatal status, but are less accurate in the preterm neonate because of developmental immaturity. Attention has been directed to umbilical cord gases as a method of neonatal evaluation. Using a retrospective chart review of all viable preterm births (24-36 weeks' gestation) between January 1986 and December 1989, we tabulated the umbilical cord gas indices of these infants. Fetuses with lethal congenital anomalies and those with abnormal heart rate tracings on admission were excluded from the data base, leaving 1872 infants. Cord arterial blood gas values were available for analysis in 74.4% of cases and cord venous gas values in 81.8%. The mean (+/- standard deviation [SD]) arterial and venous umbilical cord blood gas values for the preterm infants, were, respectively: pH, 7.26 +/- 0.08 and 7.33 +/- 0.07; oxygen pressure, 19.0 +/- 7.9 and 29.2 +/- 9.7 mmHg; carbon dioxide pressure, 53.0 +/- 10.0 and 43.4 +/- 8.3 mmHg; bicarbonate, 24.0 +/- 2.3 and 22.8 +/- 2.1 mEq/L; and base excess, -3.2 +/- 2.9 and -2.6 +/- 2.5 mEq/L. Acidemia was defined statistically as 2 SDs or more below the population mean. The incidence of 5-minute Apgar scores below 7 in the preterm infants was 8.5% and within this group, 17.8% were acidemic (arterial pH 7.10 or lower). More than 82% of neonates with 5-minute Apgar scores less than 7 had normal umbilical cord blood gases. There was no significant difference in umbilical arterial blood gas values between preterm infants and 1924 term deliveries at our institution between 1986-1988.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1991

The metabolic clearance rate of epinephrine in the fetus of the diabetic ewe.

Delayed organ maturation is a characteristic of the fetus of the diabetic mother with poor glucose control. We hypothesized that the ovine fetal catecholamine maturation sequence would be delayed in the fetus of the diabetic ewe. Twelve pregnant ewes were rendered glucose intolerant by the administration of streptozocin at 85 to 95 days' gestation. Maternal diabetic status was verified with fasting blood glucose assessments. The fetal metabolic clearance rate of epinephrine was determined at 126 to 140 days' gestation by the constant infusion of 0.1 micrograms epinephrine per kilogram estimated fetal weight per minute. Fetal arterial blood gas values, lactate, glucose, and insulin levels were measured before infusion; after 20, 30, and 40 minutes of epinephrine infusion; and 15, 30, and 60 minutes after cessation of infusion. Fetal plasma glucose rose significantly from a control level of 42.1 +/- 8.2 to 64.6 +/- 5.9 mg/dl during the epinephrine infusion (p less than 0.05). Fetal insulin levels increased from a baseline of 9.2 +/- 2.6 microIU/ml to 32.4 +/- 18.0 in the recovery period (p less than 0.05), and lactate levels similarly rose from 36.4 +/- 4.8 to 52.2 +/- 8.2 mg/dl (p less than 0.05). The plasma epinephrine production rates did not vary significantly between fetuses less than 135 and greater than 135 days' gestation (15.4 +/- 1.5 vs 13.9 +/- 2.0 ng/min, p greater than 0.5). The fetal metabolic clearance rate of epinephrine at early gestations (less than 135 days) was similar to that of the fetus of the nondiabetic ewe (35.3 +/- 3.4 vs 28.0 +/- 4.3 ml/min/kg, p greater than 0.2). However, at later gestations (greater than 135 days) the fetus of the diabetic ewe did not have the increase in the metabolic clearance rate previously published for the control fetus (32.0 +/- 4.6 vs 133.7 +/- 41.7 ml/min/kg, p less than 0.05). These data appear to indicate an absence in the maturation of the metabolic clearance rate of epinephrine in the fetus of the diabetic ewe. The observed alteration in the metabolic clearance rate of epinephrine of the fetus of the diabetic ewe could potentially impair the response to stress.

Animals↗
PubMed1991

Streptozocin-induced diabetes mellitus in the pregnant ewe.

To evaluate the effects of streptozocin on maternal pancreatic beta-cell function, we administered the agent to 14 pregnant ewes at 85 to 90 days' gestation on two occasions, 4 days apart. Intravenous glucose tolerance tests were performed before the initial administration, before the second dose, and 4 weeks after the final dose of streptozocin. There was a significant elevation in maternal fasting blood glucose (82 +/- 8.1 mg/dl before streptozocin and 102.6 +/- 6.8 mg/dl after streptozocin, p less than 0.05). Five late-gestation ewes were used as controls, and a significant elevation in fasting plasma glucose levels was found in the streptozocin-treated animals (71.4 +/- 7.1 mg/dl control vs 102.6 +/- 6.8 mg/dl after streptozocin, p less than 0.05). The glucose tolerance test curves showed a significant elevation 4 weeks after streptozocin compared with before streptozocin (p less than 0.05). The maternal insulin response to streptozocin demonstrated a loss of the second-phase insulin response to the glucose load after one dose of streptozocin and loss of the first phase after two doses. The fetuses of the streptozocin-treated ewes showed a significant elevation in plasma glucose level compared with that of controls (13.3 +/- 0.8 mg/dl, n = 5) vs 42.1 +/- 8.1 mg/dl, n = 10; p less than 0.05, control vs streptozocin, respectively). There was a consistent trend to fetal hyperinsulinemia in the fetuses of the streptozocin-treated ewes, although this did not achieve statistical significance (3.3 +/- 0.8 microIU/ml, n = 5 vs 9.6 +/- 2.5 microIU/ml, n = 10; p = 0.06, control vs streptozocin, respectively). The fetal insulin/glucose ratio was preserved in the streptozocin-treated ewes. Comparison of fetal weights between the control and diabetic ewes showed a significant increase in fetal weight in the fetuses of diabetic ewes (3280 +/- 46 gm in control fetuses vs 3710 +/- 54 gm in diabetic fetuses, p less than 0.05). The alterations in the maternal glucose and insulin response resulting from streptozocin-induced pancreatic beta-cell destruction combined with elevations in fetal glucose, insulin, and weight provides a large animal model suitable for investigation of gestational diabetes in pregnancy.

Animals↗
PubMed1990

Placental thromboxane and prostacyclin production in an ovine diabetic model.

We hypothesized that streptozocin-induced ovine diabetes would cause alterations in the placental production of thromboxane and prostacyclin. With a tissue incubation technique, we examined the placental production of thromboxane and prostacyclin in cotyledons from seven normal near-term ewes (127 +/- 3 days' gestation) and six streptozocin-induced diabetic ewes (125 +/- 3 days' gestation). Diabetic status was verified with serial fasting blood glucose assessments. Placental tissue was incubated in Dulbecco's modified Eagle's medium for 48 hours at 37 degrees C with 95% oxygen and 5% carbon dioxide. Samples were collected at 0, 1, 2, 4, 8, 20, 32, and 48 hours. Radioimmunoassay of the stable metabolites thromboxane B2 and 6-keto-prostaglandin F1 alpha were used to determine thromboxane and prostacyclin production, respectively. Placental thromboxane production was reduced in diabetic animals when compared with control animals (5.63 +/- 2.81 vs 7.32 +/- 1.37 pg/mg per hour, respectively; p less than 0.05). Prostacyclin production was also significantly reduced in the diabetic placentas compared with control placentas (11.44 +/- 4.06 vs 16.29 +/- 4.59 pg/mg per hour, respectively; p less than 0.05). We conclude that the ovine placenta produces thromboxane and prostacyclin. The ovine thromboxane production rate is comparable to that of the human placenta but the prostacyclin production rate is approximately two to three times higher. The observed decrease in the placental production of thromboxane and prostacyclin may reflect an adverse effect of hyperglycemia directly on eicosanoid production or indirectly through decreased placental cellular proliferation.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Oxytocin induced second trimester uterine rupture.

A case of oxytocin induced rupture of an unscarred uterus during the second trimester is presented. While rupture of the uterus by oxytocic agents in the second trimester has previously been documented, this case is unusual in that fetal parts were palpable through the cervical os, delaying diagnosis and definitive management. Digital palpation of fetal parts through the cervix does not preclude the diagnosis of fetal extrusion secondary to uterine rupture.

Adult↗