301 A NEW OBSERVATION – CHRONIC VILLITIS IN UNTREATED NEONATALALLOIMMUNE THROMBOCYTOPENIA (NAIT): AN ETIOLOGY FOR SEVERE EARLYINTRAUTERINE GROWTH RESTRICTION (IUGR) AND THE EFFECT OF INTRAVENOUSIMMUNOGLOBULIN (IVIG) THERAPY JANYNE ALTHAUS1, EDWARD WEIR2,FREDERIC ASKIN2, THOMAS KICKLER2, KARIN BLAKEMORE1, 1Johns HopkinsUniversity, OB/GYN, Baltimore, Maryland, 2Johns Hopkins University,Pathology, Baltimore, Maryland

OBJECTIVE: To examine placental histopathology in IVIG-treated anduntreated NAIT pregnancies and correlate pathological findings with clinicaloutcomes.

STUDY DESIGN: Placentas of 14 NAIT-affected pregnancies were identifiedfrom 8 women. Data concerning maternal antepartum treatment with IVIG(1 g/kg weekly) vs no treatment, and fetal/neonatal outcomes including IUGR,intrauterine fetal demise (IUFD), and intracranial hemorrhage (ICH) wereabstracted from the medical records. Placental H&E sections were read andgraded (mild, moderate, severe) by two pathologists blinded to the clinical data.Histopathology and clinical outcomes were compared between IVIG and noIVIG treatment groups using c2. One subject, not treated until after an ICH wasdiagnosed at 21 weeks, was excluded from the analysis. P ! .05 was consideredsignificant.

RESULTS: Five of 6 untreated pregnancies demonstrated pathologicalchanges in the placenta including chronic villitis, advanced villus maturation,and increased syncytial knots (Table). IUGR and IUFD occurred as frequentlyas ICH in this group, with one subject presenting with her 3rd pregnancy affectedby severe early IUGR. Seven pregnancies were treated with IVIG beginning at12 ( n = 6) or 17 (n = 1) weeks. None of the 7 IVIG-treated pregnancies showedchronic villitis or any histologic findings described as severe. IUGR, IUFD orICH did not occur in the IVIG-treated group.

CONCLUSION: Chronic villitis is frequently manifest in NAIT, with IVIGalleviating this inflammatory immunologic response. NAIT should be reconsid-ered as a multifaceted disease process with adverse consequences that extendbeyond thrombocytopenia and include IUGR and IUFD. We suspect a moreuniversal role for the maternal antibody in NAIT, such as fetal endothelial celldamage.

Outcomes by IVIG status

� IVIG + IVIG P value

Chronic villitis 5 (83.3%) 0 .005Other histopath 5 (83.3%) 3 (42.9%) .266ICH 1 (16.7%) 0 .46IUGR 2 (33.3%) 0 .56

S90 SMFM Abstracts

299 PERIPARTUM VENOUS THROMBOEMBOLISM IN THE UNITED STATES 2000-2001:INCIDENCE, MORTALITY AND RISK FACTORS ANDRA JAMES1, LEO BRANCAZIO1,MARGARET JAMISON1, EVAN MYERS1, 1Duke University, Obstetrics andGynecology, Durham, North Carolina

OBJECTIVE: The purpose of this study was to determine the incidence,mortality and risk factors for peripartum venous thromboembolism (VTE) in theUnited States.

STUDY DESIGN: The Nationwide Inpatient Sample (NIS), from the Health-care Cost and Utilization Project of the Agency for Healthcare Research andQuality (AHRQ), for 2000-2001 was queried for all pregnancy-related dis-charges. The records were classified as antepartum, delivery-related or post-partum. Venous thromboembolism (VTE) was defined as deep vein thrombosis(DVT), pulmonary embolus (PE) or both. Counts, rates and standard errorswere calculated using methods accounting for the survey design. Odds ratioswith 95% confidence intervals were estimated from logistic regression models.

RESULTS: There were 14,334 records with a diagnosis of VTE, or 1.72 eventsper 1000 deliveries. 6% were antepartum, 44% delivery-related and 50%postpartum. 79% had a diagnosis of DVT and 21% a diagnosis of PE orboth. There were 89 deaths, or 1.1 per 100,000 deliveries. Women 35 years orolder had 2.11 events per 1000 deliveries. Black women had 2.64. Risk factorswith odds ratios greater than 2 are listed in the table below.

CONCLUSION: Women 35 years or older, black women and women withcertain risk factors were more likely to experience peripartum VTE.

Risk factors for peripartum VTE

Risk factor Odds ratio Confidence interval

Heart disease 7.1 6.2, 8.3Thrombophilia 27.9 22.6, 34.3Sickle cell disease 6.7 4.4, 10.1Lupus 8.7 5.8, 13.0Obesity 4.4 3.4, 5.7Anemia 2.6 2.2, 2.9Hyperemesis 2.5 2.0, 3.2Fluid and electrolyte imbalance 4.9 4.1, 5.9Antepartum hemorrhage 2.3 1.8, 2.8Postpartum infection 4.1 2.9, 5.7Transfusion 7.6 6.2, 9.4Cesarean delivery 2.1 1.8, 2.4

300 MIDTRIMESTER DILATION AND EVACUATION DOES NOT INCREASE THE RISK FORSUBSEQUENT PREGNANCY COMPLICATIONS JENNIFER JACKSON1, HOLLY CASELE2,1Northwestern Feinberg School of Medicine, Obstetrics and Gynecology,Chicago, Illinois, 2Northwestern University, Maternal Fetal Medicine,Evanston, Illinois

OBJECTIVE: To evaluate subsequent pregnancy outcome in women who havehad a mid-trimester termination (12-24 weeks) by laminaria dilation andevacuation (D&E) compared to the outcome in women who did not.

STUDY DESIGN: Medical records for 317 women who underwent a D&Ebetween 1995 and 2003 at our hospitals were reviewed. Subsequent pregnancieswere identified and were matched 1:2 with controls who were women with viablepregnancies and no history of second trimester D&E. Controls were matched formaternal age, date of subsequent pregnancy, parity and delivery hospital.Statistical analysis was performed with chi square and paired t-test asappropriate and a P value ! .05 was considered significant.

RESULTS: Eighty-seven viable subsequent pregnancies were identified inwomen with a history of midtrimester D&E. Although women with a prior D&Edelivered almost 1 week earlier than controls (38.9 weeks vs 39.5 weeks,P = .013), there was no significant difference in preterm delivery !37 weeksor !34 weeks, abnormal placentation, infant weights, need for cerclage andoverall pregnancy complications.

CONCLUSION: Midtrimester termination by D&E does not increase theincidence of subsequent pregnancy complications as compared to a matchedcontrol cohort.

IUFD 3 (50%) 0 .07

302 MATERNAL HYDRONEPHROSIS IN PREGNANCY: POOR CORRELATION WITHCLINICAL SYMPTOMS WILLIAM WATSON1, BRIAN BROST1, 1Mayo Clinic, MaternalFetal Medicine, Rochester, Minnesota

OBJECTIVE: The objective of this study was to investigate the incidence,timing, and severity of maternal hydronephrosis during pregnancy, and tocorrelate these findings with maternal symptoms of flank pain.

STUDY DESIGN: Eighty one subjects were prospectively studied longitudinallyduring pregnancy. We included consecutive patients with a singleton pregnancy.Gravidas with chronic medical illness, recurrent UTI or pyelonephritis, orhistory of renal stones were excluded. Real time ultrasound of the maternalkidneys was done serially, in the first, second and third trimesters, as well aspostpartum. Each subject was questioned about presence and severity of flankpain prior to the ultrasound. Scans were perfomed by a registered diagnosticmedical sonographer, and all images were reviewed by one of the authors. Allpatients had 4 ultrasound studies performed.

RESULTS: Seventeen of 81 patients (21%) were observed to have some degreeof hydronephrosis, 14 on the right side and 3 bilateral. No cases of hydro-nephrosis were observed during the first trimester. Four of 81 had hydro-nephrosis initially noted during the second trimester; most cases were observedonly during the third trimester. Nine patients reported significant flank pain;three of these had hydronephrosis. There was no observed correlation betweenflank pain and the development of hydronephrosis. Chi square = .282, P= .60;RR= 1.88 (0.54-6.15). There was no correlation between maternal symptomsand severity of hydronephrosis. Two patients developed severe hydronephrosis,with a mean renal pelvis diameter >7 cm, and both had no flank pain. At postpartum sonography, all cases of hydronephrosis had resolved.

CONCLUSION: Hydronephrosis is common during pregnancy, and it hasa poor correlation with maternal symptoms. This may have implications forureteral stent placement during pregnancy.

Correlation of hydronephrosis with flank pain: Clinical results

Hydronephrosis + Hydronephrosis �

Flank pain 3 6No flank pain 14 58