$244

601

SMFM Abstracts

THE EFFECTS OF VIAGRA O N FETAL OUTCOME IN NORMAL PREG- NANT RATS JERRIE REFUERZO 1, J O H N HOTRA 2, MORDECHAI HAL- LAK 3, IRINA BUHIMSCHI 1, YORAM SOROKIN 4, ROBERT SOKOLS; tWayne State University, Obstetrics a n d Gynecology, Detroit, MI; 2Wayne State University. Detroit, MI; 3Ben Gur ion University Soroka Medical Caenter, Beer Sheva, Israel; 4Wayne State University, Ob /Gyn /Ma te rna l Fetal Med, Detroit, MI; 5Wayne State University, Obstetrics/Gynecology, Detroit, MI

OBJECTIVE: Viagra (Sildenafil citrate) is a specific inhibi tor of type V phosphodies te rase that t h rough the act ion of cyclic guanos ine mono- phosphate (cGMP) may enhance pelvic blood flow. Conditions associated with vascular compromise inc luding p r e e d a m p s i a or growth restr ict ion might benefit f rom Viagra therapy. Our objective was to perforrn an initial assessment of the perinatal effects of Viagra in a normal non-hypertensive rat pregnancy model.

STUDY DESIGN: Four teen t imed-pregnant Long Evans rats were randomized (n = 7 per group) to receive either Viagra (45 mg /kg ) orally every twelve hours on gestational days (GDs) 18-20 or an equal volume of sterile water. Fetal pups were retrieved by cesarean section on GD 21. Sm-civabitity, congeni ta l anomalies , p u p weight, pup length a n d placenta l weight were evaluated. Statistical analysis using two-way ANCOVA was per formed for the effects of t reatment and gender, controlling for litter size and maternal weight on delivery.

RESULTS: There were no stillbirths or gross congeni ta l anomal ies between the study pups (n = 83) and controls (n = 80). The weights of the Viagra-exposed pups were 7% less than those of the controls (4.75 _+ 0.43 grams vs. 5.11 _+ 0.34, P = .0001). In addition, pup length was significantly less in the Viagra-exposed fetuses (40.9 _+ 1.6 mm vs. 41.4 _+ 1.l, P = .019). There was no be tween~roup difference in placental weight.

CONCLUSION: Viagra exposure in a normal rat model was not associated with any decrease in litter size, stiUbirth, gross congeni ta l anomal ies or dec rement in placental size, but was associated with decreased size of the offspring. Further studies in hypertensive and growth-restricted model systems are warranted.

603

December 2001 AmJ Obstet Gynecol

INTEGRATION OF PEDIATRIC CARDIOLOGY WITH PERINATAL OB- STETRICS: A MODEL FOR INCREASED DETECTION OF FETAL CARDIO- VASCULAR MALFORMATIONS BETTINA CUNEO 1, LETITIA CURRAN 2, JAMES KELLER 3, CALA HOLMGREN 4, HAIM ELRAD4; 1The University of Illinois School of Medicine, The Hear t Institute for Children, Oak Lawn, IL; -"Lutheran General Hospital, Obstetrics, Park Ridge, IL; 3Lutheran General Hospital, Obstetrics, Park Ridge, IL; 4Lutheran General Hospital, Obstetrics, Park Ridge, IL

OBJECTIVE: Traditionally, fetal congenital cardiovascular malformations (CCVM) are suspected dur ing obstetrical (OB) ultrasound, then referred to a pediatr ic cardiologist for an t epa r tum diagnosis and postnatal prognosis (referral model) . In an in tegra ted model of care, a pediatr ic cardiologist supelwises and instructs obstetrical sonographers in the perinatal uni t dur ing cardiac scanning of mothers at risk for fetal CCVM. We believe that an integrated care model improves the antenatal detection of CCVM.

STUDY DESIGN: OB ultrasounds with suspected CCNqVI at an academic tertiary care center using the referral model (period 1, 6/92-9/96) and the integrated model (period 2, 10/96-7/01) were reviewed. Fetal echocardio- grams were pe r fo rmed if CCVM was suspected (both periods) or with risk factors for CCVM (period 2). CCVM were diagnosed by abnormal 4 chambel, outflow tract or aort ic a rch views and conf i rmed by postnatal studies. Differences between nmdels in detect ion rate (percentage of total ultra- sounds), associated abnormalities and pregnancy outcomes were compared by Z2; test; gestational age was compared by t test.

RESULTS: There were 3500 ultrasounds dur ing period 1 with 37 supected and 28 tree CCVM, and 5133 ultrasounds with 89 suspected and 80 true CCVM in period 2, No differences were found in gestational age at diagnosis (25.1 +_ 5.1 vs. 24.2 +- 5.1), association with other anomalies or pregnancy outcome. CCVM detection rates nearly doubled between periods 1 and 2 from 8/1000 to 15.5/1000 respectively (P< .002). During period 2, 43% of femses with CCVM had no risk factors, and were recognized on routine OB ultrasound.

CONCLUSION: These results strongly suggest in tegra t ing pediatr ic cardiology and perinatal obstetrics as a model of care. We speculate the high detect ion rate of CCVM a m o n g low-risk fetuses in our study results f rom improved imaging and unders tanding of the fetal hear t which results from this association.

602 DOES FETAL ANEMIA INFLUENCE HEMATOLOGIC MARKERS USED TO TIME FETAL BRAIN INJURY?. CORTNEY KIRKENDALL l, MARISA ROMO I , JEFFREY PHELAN 1, GILBERT MARTIN2; 1Childbirth Injury Prevention Foundation, Pasadena, CA: 2Citrus Valley Medical Center, Neonatology, West Covina, CA

OBJECTIVE: To determine whether adjustment for fetal anemia alters the observed association between abnormal fetal hear t rate (FHR) t rac ing at presentat ion and hematologic markers in term infants who are subsequently found to be brain damaged.

STUDY DESIGN: Data from a cohort of 273 term brain damaged infants was evaluated. Nucleated red blood cells (NRBC), absolute NRBC (ANRBC), platelet counts (PC) [#/1000 mm3] , and hematocr i t (HCT) were taken from the first complete blood count aiter birth. Hematologic markers were termed abnm'mal for NRBC >20%, ANRBC >2000 cells, PC <150. FHR tracings were read by one reviewer (]PP) and categorized as either initially reactive (R) or nonreactive (NR) on presentation. Statistical analysis was done by ~2 analysis and Mantel-Haenszel.

RESULTS: The NR group was associated with increased rates of NRBC >20% (76% vs 11%; P = .01), PC <150 (35% vs 12%; P = .008), and anemia (22% vs 11%; P = .01). When stratified by anemia, anemia did no t appear to affect NRBC ->20% or ANRBC ->2000 cells. But, anemia may have an affect on the PC [anemia: 15/19 (79%) vs 12/25 (48%), OR 4.06, 95% CI 0.9 to 19.9; no anemia: 10/54 (19%) vs 55/184 (30%), O R 10.3, 95% CI 4.6 to 23.7; Mantel- Haenszel weighted OR 8.31, 95% CI 4.22 to 17.26].

CONCLUSION: In term infants who develop brain damage, NRBC and ANRBC counts continue to be linked to the FHR pattern but do not appear to be affected by fetal anemia. While a PC <150 may be affected by fetal anemia, the anemic populat ion was too small to determine a significant effect.

604 GASTROSCHISIS OUTCOMES AND SITE OF DELIVERY DREW RO- BILIO 1, LINDA GREVE 1, DENA TOWNER MD l, 1University of California, Davis, Obstetrics & Gynecology, Sacramento, C,A

OBJECTIVE: To determine the difference in major morbidity tbr infants with gastroschisis bo rn at a tertiary cm'e facility and those t ransported to such facility.

STUDY DESIGN: Using linked data from maternal and int~ant hospital discharge records, and f rom bir th a n d death certificates f rom acute care civilian hospitals in California from 1992-1997, we identified 515 inf~mts with gastroschisis repair at 34 weeks or greater. Infants were born either at a tertiary care facility capable of repairing the defect or were t ransported to one. ICD9 codes evaluated were length of stay (LOS), respiratory distress syndrome (RDS), meconium aspiration (MEC), sepsis, necrotizing enterocolitis (NEC), bowel atresia, delayed closure, major bowel surgery, and death. Statistical analysis was by logistic regression.

RESULTS: See Table. CONCLUSION: It is reassuring that major bowel morbidities, death, and

LOS were not different. RDS, meconium aspiration and sepsis did appear as complications more often in transported infants. This data again supports the recmrunendat ions for delivery of infants with gastroschisis at a tertiary care facility.

Table Results

I N B O R N O U T B O R N P O R (N = 413) (N = 102) VALUE (CI)

LOS (days) 40.4 (+ 2.18 SEM) 41.6 (_+ 4.74 SEM) .61 1.00 (0.99, 1.01) RDS 25 (6.05%) 15 (14.7%) .002 3.02 (1.48, 6.17) MEC 32 (7.75%) 22 (21.57%) .0002 2.66 (1.28, 5.56) Sepsis 28 (6.78%) 16 (15.69%) .009 2.67 (1.28, 5,56) NEC 8 (1.94%) 3 (2.94%) .90 1.10 (0.25, 4.89) Atresia 30 (7.26%) 9 (8.82%) .77 0.86 (0.32, 2.31) Delayed closure 115 (27.85%) 28 (27.45%) .85 1.05 (0.61, 1.81) Bowel surgery 52 (12.59%) 16 (15.69) .63 1.22 (0.54, 2.76) Death 11 (3.9%) 4 (5.4%) .52 1.40 (0.36, 4.96)