438
SPO Abstracts
Jan lIary 1992 Am J Obstet Gynecol
623 GRAY SCALE AND COLOR DOPPLER ULTRASONOGRAPHY IN THE DETERMINATION OF AMNIOTIC FLUID INDEX G Colmorgen. C Foster,X A Janneman,x A Sciscione,x P Shlossman, R Gormanx Medical center of Delaware, Newark, DE Concern that space occupied by the umbilical cord could be included inappropriately in measurements for amniotic fluid index (AFI) in pregnancies complicated by oligohydramnios led to an investigation comparing measurement of AFI by gray scale as opposed to color Doppler. Two hundred thirty-one patients (of whom 24 had oligohydramnios) were entered into the study. The general group of patients, as well as the sub-group with oligohydramnios, was found to have statistically lower AFI when measured by color Doppler than with gray scale alone (P
624 PRENATAL ULTRASOUND FINDINGS IN ASPHYXIATING THORACIC DYSTROPHY (ATD). O. Khawli, R. Morcos~ M. Makii~ Dept. Ob/Gyn, St. Elizabeth Hospital Medical Center, Youngstown, OH Two cases of ATD (Jeune Syndrome) were diagnosed prenatally. Case #1: 30 year old G2 P1 has a child with Jeune Syndrome, referred because of a short femur at 36 weeks. The femur & humerus were 5th percentile for gestational age. The thorax was bell shaped & on real time exams two weeks apart the fetus was in the same position, flat on the back with both thighs & knees flexed. The diagnosis of Jeune Syndrome was confirmed at delivery. Case #2: 34 year old G1 with negative family history, referred at 23 weeks because of short femur by ultrasound. At 16 wks, femur was at the 90th percentile. At 23 wks, femur was ~ 5th percentile & thorax was at 97th percentile. At 27 & 34 weeks, the femur & humerus were 5th percentile (Rhizomelic Dwarfism). The thoracic circumference, which was) 50th percentile at 27 wks, fell below 5th percentile at 34 weeks. Diagnosis of Jeune Syndrome was suspected & confirmed after birth. CONCLUSION: Prenatal diagnosis of Jeune Syndrome can be made by ultrasound based on the short femur length & a small thorax.
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625 ANTENATAL SONOGRAPHIC DIAGNOSIS OF DANDY· WALKER MALFORMATION IN THE LATE FIRST TRIMESTER. J N Boualico pO, D. HuH, M.D.x, B. Penny, R.D.M.S.x, L. Miller, R.D.M.S!, University of Medicine and Dentistry of New Jersey· School 01 Osteopathic Medicine, Departments of Ob/Gyn and Pathology, Stratford, NJ The Dandy-Walker Malformation (DWM), characterized by complete or partial absence of the cerebellar vermis, cystic dilatation of the fourth ventricle and frequently hydrocephalus has been detected in-utero, but often after fetal viability. DWM is thought to originate in the 6th or 7th week of embryonic development but most case reports to date describe antenatal diagnosis at gestations averaging about 24 wks. Early prenatal diagnosis allows more time for thorough fetal anatomic evaluation and chromosome studies, thus increasing management options. We recently detected a cystic dilatation in the posterior fossa of a fetus at 12.5 wks. gestation (by LMP and crown rump length) along with probable cerebellar maldevelopment, using transvaginal sonography (TVS). Repeat TVS at 13.5 wks revealed dilatation of the fourth ventricle which appeared to communicate through the absent vermis with a posterior fossa cyst. Transabdominal CVS revealed a normal karyotype and no other anomalies were noted. The patient elected termination of pregnancy at 18 wks. via prostaglandin induction of labor. Evaluation by a fetal pathologist confirmed the DWM with a cystically enlarged fourth ventricle, absent cerebellar vermis and elevation of the tentorium and torcula. A 4mm round midline occipital defect was also found along with mandibular hypoplasia, cleft palate and limb contractu res. Thus it becomes apparent that TVS may allow the antenatal diagnosis of DWM as early as 13 wks though problems remain regarding the prediction of its natural history in-utero as well as prognostication for postnatal life.
627 EFFH:T CF IJ:W J:XH: ASPIRIN CN M'ill'Rii'IL AN)
FEIN, FllW futer- JVC RJrlarrl,X J.M. R3arcE~ Fetal W2lfare W:aratory, st. ~'s H::q:ri.tal, Im:b1, U.K. PrEe:::1.aq:s:ia is as=iata:1 with J:Ed.ud uI:erq:llacmtal an:! UTbilical blax1 flo.v. 'liE:in::rms3:1 platelet activity an:! J:Ed.ud placmtal flo.v t:h3.t in this c:l:irortEr nay te clE to t:hmIb:l>are N. iON dB2 aEpirin (liA) lEs l::EEn sh:w1 to :re:ll:E tiE ID:::id:n:E an:! SS'va'ity of prEB::laJIEia bj inhibit::irg platelet t:hmIb:l>are ('IXA2), a p:lta1t inhibitor of vascilar STCOI:h IllECle ortIactim am platelet ~m Wlilst relatiU21y ~ ~lin pr:u:lcticn. 'llus it nay te eYfEd:a:l t:h3.t liA w:JiLd :irrpro.e blax1 flo.v resistan::E in:li02S frun tiE uI:erq:llacmtal am urbilical c:ira.llatirrs. As r:mt of a ran:bnisaJ. pl.cntn =trollEd sb.rly eJal\.13.tin:j tiE role of ID"I (7:ngs/cl3.y) frun 24 v..cEks in high risk ratialts r:twler strrlies W2rE r:erfCltlTErl in ratialts at 24-25, 27-28, 32-34 am 3&-37 VEI[CIT'{ W'\VERR1).
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I€sults
UterqJlacmtal (RI) liTbilical (S;tJ) Pl.cntn (ED) Aspirin (ED) Pla:E:o Aspirin W:Eks (rF26) (rF26) (rF26) (rF26) 24-25 0.68 (0.08) 0.67 (0.05) 4.08 (1.2) 4.09(0.9) 27-28 0.62 (0.09) 0.57 (0.09) 3.72 (1.5) 3.32(0.8) 32-34 0.61 (0.08) 0.55 (0.1) 3.07 (0.8) 3.06(0.8) 3&-37 0.53 (0.07) 0.52 (0.1) 2.57 (0.4) 2.64(0.5) Alt:l"r.uJh clinical tErefit WlS SEB'l in tiE aEpirin ~, m differaXES in resistan::E in:li02S W2rE SEB'l J:::eb...e31 tiE 2 CJ!:ClP3 ~ m significant vas:xlilatory effEct of lo.v dB2 aEpirin