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Volume 166 Number I, Part 2 552 MANAGEMENT OF PREMATURE RUPTURE OF MEMBRANES (PROM) : STATE OF THE ART, 1991, Uchenna Nwosu. M.D. Dept. of OB/GYN, East Tennessee State University College of Medicine, Johnson City, TN. 553 We surveyed all 1,041 members of the Society of Perinatal by signed questionnaire their current practice in the management of PROM at var- ious gestational periods, with regard to induction of labor, use of antibiotics, tocolytic agents and corticosteroids. We received 529 replies, 235 from regular and 294 from associate members.Analysis showed no difference in the practice of the two groups.With respect to labor induction the most controversial periods were 33-35 weeks with mature fetal lungs where 50\ will in- duce from 0-48 hours and 50\ will await spontaneous onset of labor, and 19-22 weeks where 48\ remained silent.Most responders do not use antibiotics at any time, and most of the antibiotic users do so for a limited period of time only, with ampicillin the overwhelming choice.Most responders do not use tocolytic agents at any time and most users do so therapeutically rather than preemptively, with MgS0 4 favored 2:1.Most responders do not use cortiosteroids to enhance fetal lung maturity at any period. This survey indicates need for a study of outcome of newborns induced with mature lungs 0-48 hours following PROM at 33-35 weeks, as compared with similar newborns delivered following spontaneous labor. PERINATAL OUTCOME IN DIABETIC PATIENTS WITH NEPHROPATHY AND RETINOPATHY VS. DIABETICS WITH ISOLATED PROLIFERATIVE RETINOPATHY. Jff.le GML Del Valle GO, Izquierdo LA, V M* ,Jones DK Gilson GJ, Chatteriee S, and Curet LB, Univ. New Mexico Med. Ctr., Albuquerque, NM An eight year review of pregnant diaQeticpatients with nephropathy and ret1nopathy vs those wlth -isolated retinopathy was completed. Out of 10 L POO admissions, patients with nephropathy' and retinopathy and 9 patients with isolated proliferative retinopathy were identified (incidence 0.13% and Patients wi th nephropathy and were older vs 2l.8+/-2.2gyears p:=. 005 ) , had higher incidence of chronic hypertension (86% vs 0% p=. 001) , lilid hilher incidence of cesarean section 86% vs 25% had earlier gestat onal age at delivery (34.4+/-2.6 vs wks p=.OllL and had lower neonatal birth weight: (2388+/-785 vs 3214+/-863 gm .p:=.01). Maternal age of onset of d18betes, gravidity, parity., Hgb AlC, AfGAR scores, and inciaence of congen1tal anomaly (12.5% in isolated retinopathy group) were not significantly different. This stUdy demonstrates that isolated proliferat1ve retinopathy may precede development of nePhropathr and chronic hyp!rtension and Is as soc ated with sign1ficantly better perinatal outcome. SPO Abstracts 425 554 EFFECT OF GENDER ON PERINATAL OUTCOME IN PREGNANCIES COMPLICATED BY DIABETES. 555 h.A. Bracero, and, S. Dept. of OB/GYN New York Medical College, Valhalla, New York Low birthweight female infants have been shown to have a higher survival rate than low birthweight males. This sex difference in mortality has been attributed to a higher inci- dence and severity of Respiratory Distress Syn- drome in male infants. The purpose of this study was to determine whether there is a sex difference in the morbidity and mortality of infants born to diabetic mothers. A review of 107 newborns from diabetic mothers was perform- ed. There were 63 males and 44 female infants. We looked at demographics, parity, White's cla- ssification, glycemic control, blood pressure, Hgb/Hct, mode of delivery, incidence of low birthweight & preterm deliveries and found no statistically significant difference between the groups. There was one female stillbirth as a result of an episode of ketoacidosis in the mother. There was more morbidity in the male group mainly as the result of hypoglycemia (23.8% of males VS 6.8% of females; Relative Risk=3.50; P value=.0208) and need to stay in the NICU 2 days (52.4% of males vs 29.5% of females; Relative Risk =1.78; P value=.0189). It appears that there is a disadvantage to being the male infant of a diabetic mother. OBSTRUCTIVE UROPATHY: A CAUSE OF REVERSIBLE HYPERTENSION IN PREGNANCY. A.J. Satin X , G.L. Seiken x , F.G. Cunningham. Dept. OB/GYN, Univ. Texas Southwestern Med. etr., Dallas, TX and Dept. Nephrology, Brooke Army Med. etr., San Antonio, lX. Hypertension with deterioration of renal function after mid- pregnancy often signifies preeclampsia and the need for del ivery. Over the past 12 years, we have encountered four pregnant women with reversible hypertension related to obstructive uropathy. These women presented between 24 and 35 weeks gestation with mean arterial pressure increased >20 ITIllHg above pregnancy basel ine accompanied by significantly increased serum creatinine (mean increase = 2. 5mg/dL). AL though pregnancy-i nduced hypertens ion was considered initially in all, there was no other evidence for preeclampsia. Ureteral obstruction was confirmed by ultrasound and was associated with congenital urinary anomalies in two, massive leiomyoma in one, and hydramnios in the other. Ret ief of obstruction by ureteral stent placement or decompression of arrnionic fluid volume resul ted in resoLution of hypertension and a fall in serum creatinine (mean decrease = 2.2mg/dl). Despite this, all four developed recurrent hypertension and/or renal insufficiency within 1 to 7 weeks, necessitating del ivery between 31 and 36 weeks gestation. Importantly, deLivery was deLayed more than 6 weeks in the 3 women in whom stents were placed. We can impl icate urinary obstruction as the cause of hypertension because blood pressure controL improved after rel ief of obstruction. In one early report (NEJM, 278:1133,1968) unilateral hydronephrosis was associated with renin mediated hypertension. Studies in men have implicated bilateral ureteral obstruction as a cause of hypertension secondary to sal t and water retention. Thus, urinary obstruction has been reported as a cause of reversible hypertension in nonpregnant patients, but to our knowledge, this is the first report of ureteral obstruct; on wi th revers i bLe hypertens i on secondary to the gravid uterus.

552 Management of Premature Rupture of Membranes (Prom) : State of the Art, 1991

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Page 1: 552 Management of Premature Rupture of Membranes (Prom) : State of the Art, 1991

Volume 166 Number I, Part 2

552 MANAGEMENT OF PREMATURE RUPTURE OF MEMBRANES (PROM) : STATE OF THE ART, 1991, Uchenna Nwosu. M.D. Dept. of OB/GYN, East Tennessee State University College of Medicine, Johnson City, TN.

553

We surveyed all 1,041 members of the Society of Perinatal ob~tetricians by signed questionnaire concern~ng their current practice in the management of PROM at var­ious gestational periods, with regard to induction of labor, use of antibiotics, tocolytic agents and corticosteroids. We received 529 replies, 235 from regular and 294 from associate members.Analysis showed no difference in the practice of the two groups.With respect to labor induction the most controversial periods were 33-35 weeks with mature fetal lungs where 50\ will in­duce from 0-48 hours and 50\ will await spontaneous onset of labor, and 19-22 weeks where 48\ remained silent.Most responders do not use antibiotics at any time, and most of the antibiotic users do so for a limited period of time only, with ampicillin the overwhelming choice.Most responders do not use tocolytic agents at any time and most users do so therapeutically rather than preemptively, with MgS04 favored 2:1.Most responders do not use cortiosteroids to enhance fetal lung maturity at any period. This survey indicates need for a study of outcome of newborns induced with mature lungs 0-48 hours following PROM at 33-35 weeks, as compared with similar newborns delivered following spontaneous labor.

PERINATAL OUTCOME IN DIABETIC PATIENTS WITH NEPHROPATHY AND RETINOPATHY VS. DIABETICS WITH ISOLATED PROLIFERATIVE RETINOPATHY. Jff.le GML Del Valle GO, Izquierdo LA, V M* ,Jones DK Gilson GJ, Chatteriee S, and Curet LB, Univ. New Mexico Med. Ctr., Albuquerque, NM

An eight year review of pregnant diaQeticpatients with nephropathy and ret1nopathy vs those wlth -isolated retinopathy was completed. Out of 10LPOO admissions, 1~ patients with bo~ nephropathy' and retinopathy and 9 patients with isolated proliferative retinopathy were identified (incidence 0.13% and ~.08% res~ctively). Patients wi th nephropathy and retino~thY were older (Z6.4~/-4.43 vs 2l.8+/-2.2gyears p:=. 005 ) , had higher incidence of chronic hypertension (86% vs 0% p=. 001) , lilid hilher incidence of cesarean section 86% vs 25% ~.Ol), had earlier gestat onal age at delivery (34.4+/-2.6 vs 36.8+/-2.~1 wks p=.OllL and had lower neonatal birth weight: (2388+/-785 vs 3214+/-863 gm .p:=.01). Maternal age of onset of d18betes, gravidity, parity., Hgb AlC, AfGAR scores, and inciaence of congen1tal anomaly (12.5% in isolated retinopathy group) were not significantly different. This stUdy demonstrates that isolated proliferat1ve retinopathy may precede development of nePhropathr and chronic hyp!rtension and Is as soc ated with sign1ficantly better perinatal outcome.

SPO Abstracts 425

554 EFFECT OF GENDER ON PERINATAL OUTCOME IN PREGNANCIES COMPLICATED BY DIABETES.

555

h.A. Bracero, and, S. Cassid~ Dept. of OB/GYN New York Medical College, Valhalla, New York

Low birthweight female infants have been shown to have a higher survival rate than low birthweight males. This sex difference in mortality has been attributed to a higher inci­dence and severity of Respiratory Distress Syn­drome in male infants. The purpose of this study was to determine whether there is a sex difference in the morbidity and mortality of infants born to diabetic mothers. A review of 107 newborns from diabetic mothers was perform­ed. There were 63 males and 44 female infants. We looked at demographics, parity, White's cla­ssification, glycemic control, blood pressure, Hgb/Hct, mode of delivery, incidence of low birthweight & preterm deliveries and found no statistically significant difference between the groups. There was one female stillbirth as a result of an episode of ketoacidosis in the mother. There was more morbidity in the male group mainly as the result of hypoglycemia (23.8% of males VS 6.8% of females; Relative Risk=3.50; P value=.0208) and need to stay in the NICU ~ 2 days (52.4% of males vs 29.5% of females; Relative Risk =1.78; P value=.0189). It appears that there is a disadvantage to being the male infant of a diabetic mother.

OBSTRUCTIVE UROPATHY: A CAUSE OF REVERSIBLE HYPERTENSION IN PREGNANCY. A.J. SatinX

, G.L. Seikenx, F.G. Cunningham. Dept. OB/GYN, Univ. Texas Southwestern Med. etr., Dallas, TX and Dept. Nephrology, Brooke Army Med. etr., San Antonio, lX.

Hypertension with deterioration of renal function after mid­pregnancy often signifies preeclampsia and the need for del ivery. Over the past 12 years, we have encountered four pregnant women with reversible hypertension related to obstructive uropathy. These women presented between 24 and 35 weeks gestation with mean arterial pressure increased >20 ITIllHg above pregnancy basel ine accompanied by significantly increased serum creatinine (mean increase = 2. 5mg/dL). AL though pregnancy-i nduced hypertens ion was considered initially in all, there was no other evidence for preeclampsia. Ureteral obstruction was confirmed by ultrasound and was associated with congenital urinary anomalies in two, massive leiomyoma in one, and hydramnios in the other. Ret ief of obstruction by ureteral stent placement or decompression of arrnionic fluid volume resul ted in resoLution of hypertension and a fall in serum creatinine (mean decrease = 2.2mg/dl). Despite this, all four developed recurrent hypertension and/or renal insufficiency within 1 to 7 weeks, necessitating del ivery between 31 and 36 weeks gestation. Importantly, deLivery was deLayed more than 6 weeks in the 3 women in whom stents were placed. We can impl icate urinary obstruction as the cause of hypertension because blood pressure controL improved after rel ief of obstruction. In one early report (NEJM, 278:1133,1968) unilateral hydronephrosis was associated with renin mediated hypertension. Studies in men have implicated bilateral ureteral obstruction as a cause of hypertension secondary to sal t and water retention. Thus, urinary obstruction has been reported as a cause of reversible hypertension in nonpregnant patients, but to our knowledge, this is the first report of ureteral obstruct; on wi th revers i bLe hypertens i on secondary to the gravid uterus.