191 ANTENATAL MAGNESIUM SULFATE (MG SO4) EXPOSURE AND INCIDENCE OFPATENT DUCTUS ARTERIOSUS (PDA) IN EXTREMELY LOW BIRTH WEIGHT INFANTS(ELBW) VICTOR GONZALEZ-QUINTERO1, TERESA DEL MORAL2, NELSON CLAURE3,SILVIA VANBUSKIRK2, EDUARDO BANCALARI2, 1University of Miami, Obstetricsand Gynecology, Miami, Florida, 2University of Miami, Pediatrics, Miami,Florida, 3University of Miami, Neonatology, Miami, Florida

OBJECTIVE: Antenatal exposure to Mg SO4 either for tocolysis or seizureprophylaxis can have significant clinical effects in ELBW infants. Amongthese, it may adversely influence the closure of the ductus arteriosus.

The purpose of this study was to explore the relationship betweenantenatal exposure to Mg SO4 and the incidence of PDA in ELBW infants.

STUDY DESIGN: A total of 952 neonates with birth weight between 500-1000born at our institution between January 1996 and December 2003, and whosurvived more than 3 days were followed until death or discharge from thehospital. A research nurse prospectively collected Perinatal and hospital coursedata. The incidence of PDA was compared in infants exposed to Mg SO4 withthose not exposed, and between infants exposed to different maternal doses ofMg SO4. Indications for the administration of Mg SO4 to the mother werepreeclampsia and tocolysis.

RESULTS: The incidence of PDA was significantly higher in the group ofinfants exposed to Mg SO4 compared to non exposed (67% vs 60%, p =0.0178). When stratified by gestational age the differences were significant onlyin the group of infants with gestational age O26 weeks (58% vs 49%, p=0.0399). There was no relationship between prenatal exposure to Mg SO4 andthe duration of PDA. Logistic regression analysis to adjust for covariablesconfirmed the increased risk of PDA in infants exposed to Mg SO4 (OR 1.60,CI 1.18-2.16).

Furthermore the risk of PDA increased with higher doses of Mg SO4exposure (OR 1.24 CI 1.09-1.42 per 50g of Mg SO4).

CONCLUSION: In ELBW, infants antenatal exposure to Mg SO4 is associatewith a higher risk for PDA and this effect is dose related and more significantin the more mature infants (O26 weeks).

192 VERY LOW BIRTH WEIGHT NEONATES: DO OUTCOMES DIFFER IN MULTIPLECOMPARED TO SINGLETON GESTATIONS EDWARD HAYES (F)1, DAVID PAUL2,AMEN NESS1, VINCENZO BERGHELLA1, 1Thomas Jefferson University,Obstetrics and Gynecology, Philadelphia, Pennsylvania, 2Christiana CareHealth Services, Newark, Delaware

OBJECTIVE: To determine if outcomes of VLBW neonates differ in multipleversus singleton gestations.

STUDY DESIGN: A database of all neonates weighing less than 1500 gramsadmitted to a tertiary medical center from July 1993 until July 2004 wasreviewed. Through univariate analysis confounding variables were identifiedand then controlled for via logistic regression models.

RESULTS: 1779 VLBW infants, 475 multiple gestations (206! 1000, and 86! 750 grams) and 1304 singletons (578 ! 1000, and 262 ! 750 grams) wereidentified. The gestational age at delivery (28.2 G 2.9 vs. 28.0 G 2.9 weeks,P=.15) and birth weight (1039 G 277, vs. 1035 G 289grams, P=.80) were notsignificantly different between the two groups. Significant differences betweenthe two populations were Caucasian race (68% multiple vs. 43% singletongestations, P!.01), maternal age (28.7 G 5.7 vs. 26.1 G 6.5 years, P!0.01),birth at the facility (95% vs. 86%, P!0.01), antenatal steriods (74% vs. 58%,P!0.01), pre-eclampsia (14% vs. 24%, P!0.01), and pre-term labor (74% vs.62%, P!0.01). Correcting for these observations a comparative analysis wasformulated between the two groups (Table).

CONCLUSION: In contrast to prior reports, in this population, VLBWmultiple gestations have significantly higher morbidity and mortality thanweight matched singletons.

VLBW multiple gestations outcomes compared to singletons

OUTCOME WEIGHT ODDS RATIO (95%CI)

Death !1500 grams 1.3(.9-1.9)!1000 grams 1.5(.98-2.2)!750 grams 1.9(1.1-3.5)*

Severe IVH (grade 3-4) !1500 grams 1.2(.8-1.7)!1000 grams 1.1(.8-1.7)!750 grams 1.1(.60-2.1)

Death and/or Severe IVH !1500 grams 1.4(1.03-1.95)*!1000 grams 1.6(1.1-2.3)*!750 grams 2.3(1.3-4.2)*

NEC !1500 grams 1.1(.72-1.8)!1000 grams 0.99(.60-1.7)!750 grams 0.78(.30-2.1)

193 IS UMBILICAL ARTERIAL PH ASSOCIATED WITH NEONATALELECTROENCEPHALOGRAPHIC (EEG) ABNORMALITIES? WEN WEN1,CYNTHIA HOLCROFT2, CHRISTOPH LEHMANN3, ERNEST GRAHAM2, 1JohnsHopkins University, School of Medicine, Baltimore, Maryland, 2JohnsHopkins University, Gynecology and Obstetrics, Baltimore, Maryland,3Johns Hopkins University, Pediatrics, Baltimore, Maryland

OBJECTIVE: Although severe metabolic acidosis (umbilical arterial pH!7.0and base excess!�12 mmol/L) is associated with a significant increase inneonatal neurologic morbidity, up to half of infants have no identifiableneurologic morbidity at the time of discharge. Our objective was to determineif cord gas results correlate to EEG abnormalities. If so, this correlation mayidentify infants at increased risk of neurologic morbidity.

STUDY DESIGN: The study population consisted of infants who had both anEEG within the first week of life and an umbilical arterial gas. Databases at asingle university hospital were searched from 1/1/98 to 3/15/05. Infants withmajor anomalies were excluded. The neonates were divided into normal orabnormal groups based on their first EEG result. Logistic regression wasperformed using cord pH as an independent variable. The number of caseswith umbilical arterial pH!7.0 in each group was compared using Fisher’sexact test.

RESULTS: 28 neonates comprised the study population:15 with a normalfirst EEG and 13 with an abnormal EEG. Mean gestational age was 34.9 C/�6.2 vs 35.3 C/� 4.1 weeks with a range from 23.3-41.0 weeks. Mean birthweight was 2364 C/� 970 vs 2477 C/� 970 g with a range from 805–3710 g,(p=NS). Logistic regression showed an odds ratio of 0.1 (95% CI: 0.002–5.867) with lower cord pH́s more likely to be correlated with abnormal EEG’s.2/15 (13%) infants with normal EEG’s had a pH!7.0 compared to 3/13 (23%)infants with abnormal EEG’s, (p=0.64). Of the neonates with pH!7.0 andnormal EEG’s, one had seizure-like activity and one had no neurologicsequelae; of those with pH!7.0 and abnormal EEG’s, one had seizure-likeactivity, one had hypoxic-ischemic encephalopathy, and one had no neurologicsequelae at the time of discharge.

CONCLUSION: Abnormal neonatal EEG’s were not linked with metabolicacidosis at delivery in this cohort, however it is limited by small numbers.Further study will be helpful to elucidate whether or not neonatal EEG’s mayhelp predict poor neurologic outcome in the setting of perinatal metabolicacidosis.

194 PRE-INSULT BUT NOT POST-INSULT IMPLANTATION OF ENCAPSULATED GLIAL CELLLINE-DERIVED NEUROTROPHIC FACTOR-SECRETING CELLS PREVENTS LONG-LASTING LEARNING IMPAIRMENT AGAINST HYPOXIC-ISCHEMIC INJURY IN THENEONATAL RAT BRAIN SHINJI KATSURAGI1, TOMOAKI IKEDA1, ISAO DATE2,TETSURO SHINGO2, HITOSHI HAYASE2, KENICHI MISHIMA3, MASAHIKO HARADA3,NOBUAKI EGASHIRA4, KATSUNORI IWASAKI3, MICHIHIRO FUJIWARA3, TSUYOMUIKENOUE1, 1Miyazaki Medical College, University of Miyazaki, Obstetrics andGynecology, Kiyotake, Miyazaki, Japan, 2Okayama University GraduateSchool of Medicine and Dentistry, Neurological Surgery, Okayama, Japan,3Fukuoka University, Physiology and Pharmacology, Fukuoka, Japan,4Fukuoka University, Fukuoka, Japan

OBJECTIVE: We have shown that implantation of encapsulated glial cellline-derived neurotrophic factor (GDNF)-secreting cells into brain paren-chyma before hypoxic-ischemic (H/I) stress improves long-term learning andmemory impairment and prevents histological damage up to 18 weeks inneonatal rats. Here, we examine whether treatment given after H/I stress iseffective.

STUDY DESIGN: Baby hamster kidney (BHK) cells were transfected withexpression vector that either did (HI-GDNF group; n=10) or did not (HI-Control group; n=8) include human GDNF cDNA. BHK cells were encap-sulated in semi-permeable hollow fibers, and implanted into the left brainparenchyma of 9-day-old Wistar rats. Two days before implantation, the ratsreceived H/I stress, and their behavior was examined in several learning tasks:the 8-arm radial maze, choice reaction time, and water maze tasks, whichexamine short-term working memory, attention process, and long-term refer-ence memory, respectively. The rats were sacrificed 18 weeks after H/I insultfor evaluation of brain damage. Two additional control groups were used: thecontrol group (n=15) that did not undergo treatment, and the GDNF group(n=10) that underwent implantation of the GDNF capsule, but did notundergo H/I stress.

RESULTS: A decrease in cerebral hemisphere size was noted in both HI-Control and HI-GDNF groups, but the results were not significantly different.In both groups, performance in each of the three tasks was significantlyinferior to the control groups, but they were not significantly different fromeach other. All results for the GDNF group were similar to those for thecontrol group.

CONCLUSION: GDNF treatment before H/I stress was effective in reducingbrain damage and in inhibiting learning and memory impairment in neonatalrats. However, the same treatment after H/I insult was not effective.

S64 SMFM Abstracts