Beta agonist therapy of fetal complete heart block

Beta agonist therapy of fetal complete heart block

426 SPOAbstracts J a n u a r y 1995 A m J Obstet Gynecol 609 INTRAMUSCULAR DIGOXIN FOR FETAL SUPRAVENTRICULAR TACIIYCARDIA W I T H HYDROPS FETALIS...

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426

SPOAbstracts

J a n u a r y 1995 A m J Obstet Gynecol

609

INTRAMUSCULAR DIGOXIN FOR FETAL SUPRAVENTRICULAR TACIIYCARDIA W I T H HYDROPS FETALIS. B.V. parilla, M.L. Socol, J.F. StrasburgeP, Departments of Obstetrics and Pediatrics, Noflhwestern University Medical School, Chicago, 11. OBJECTIVE: Maternally administered digoxin for the treatment of fetal supraventrieular tachycardia (SVT) complicated by hydroids fctalls may be ineffective secondary to poor transplacental drug transfer. We hypothesized that direct fetal intramuscular administration of digoxin would result in more rapid cardioversion of fetal SVT. STUDY DESIGN: Response to treatment for maternal intravenous administration of disoxin (MW) versus a combination of fetal intramuscular digoxin (FIM) and M W was compared in eight hydropic fetuses during 9 suec.essful pharmacologic conversions. MIV was administered using standard loading and maintenance protocols. FIM was administered at a dose of 88 /~g/kg q12-24h, to a maximum of 3 injections. Time to onset of the first two hours of sinus rhythm (TO2°), time to onset >90% sinus rhythm (TO>90%), and time to resolution of hydropa retails (HF) were noted. RESULTS: Mean SVT rate was 257 +36 bcata/min and mean gestational age was 29 5:4.8 wks. SVT mechanism was related to accessory connection in all eases. For MIV only (Group 1, n=3), TO2* was 145+ 114h, TO >90% was 176:1:55h, and HF resolved in 30 days (range 19-52). For MIV patients who failed treatment and subsequently underwent FIM (Group 2, n=2), TO2* was 203+180h, T O > 9 0 % was 313+270h, and HF resolved in 56 days (range 52-450). Once FIM was begun in these 2 patients, TO2* and TO > 90 % were 17+7h and 60:1:13h respectively. When compared to Groups I and 2, initial combined FIM and MIV therapy (Group 3, n=4) resulted in a TO2 ° o f 5 . 5 + 4 h (p <0.008), TO >90% of 22+14h (p<0.014), and resolution of HF in 24 days (range 2-48),(p<.00g). CONCLUSION: Direct fetal intramuscular injection ofdigoxin shortened the time to initial conversion of SVT, subsequent control of SVT, and resolution of HF. Therefore, it shou!d be the primary management for fetuses with SVT and hydrops.

611 BETA AGONIST THERAPY OF FETAL COMPLETE HEART BLOCK. JY Hare, JC Huhta x, S. Weil-Chalkerx, N. Staufferx, BF Cuneo x, M. Respondek x, A. Ludomirsky. MFM and Perinatal Cardiology Sections, Dept. OB/GYN, Pennsylvania Hospital, Philadelphia, PA. OBJECTIVE: To determine if transplacental beta agonist therapy can increase the heart rate in fetuses with in utero congenital heart block (CHB). STUDY DESIGN: Seven fetuses (GA 25-32 wks) were diagnosed with CHB by fetal echocardiography (FE) using 2-D, M-Mode, and Doppler techniques. Two were SSA/SSB positive on steroid therapy with normal anatomy and five had complex congenital heart disease (CHD). Hydrops was present in 6/7. All were treated with beta agonist therapy (6terbulaline and 1-fenoterol 5mg IX) q 6 hours). Weekly ultrasound and FE evaluated the heart rate, degree of hydrops, and venous Doppler. RESULTS: Fetal heart rate increased immediately in 6/7 (p<0.05) from 56 to 87 (mean 30 BPM), and hydrops improved in 4/6. Six of seven had atrial umbilical venous pulsations. CONCLUSIONS: Beta agonist therapy increased ventricular rate in fetuses with complete heart block and may improve hydrops. The use of beta agonist therapy in the prehydropic fetus with atrial venous pulsations may be useful in the management of fetal congenital heart block.

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UMBILICAL VENOUS PRESSURE AND SEVERE, EARLY ONSET GROWTH RESTRICTION. C. Weiner. Dept. Ob/Gyn, Univ. of la. College Med., Iowa City, IA. OBJECTIVE: To determine the effect of severe, early onset growth restriction (IUGR) on the umbilical venous pressure (UVP). It has been suggested (Am J Obstet Gynacol 1994; 170:487) that the UVP reflects to a significant degree placental resistance to blood flow. This conclusion was based on 20 growth deficient fetuses whose UVPs were widely scattered, did not significantly differ from control, and were unrelated to either fetal size or blood gas measurements. METHODS: 39 fetuses Underwent cordocentesis during an evaluation of severe, early onset IUGR (diagnosed <32w or symmetrical IUGR at any gestation). Each fetus had an AC <2.5 percentile and a SEFW <10 percentile. IUGR was confirmed at delivery. Based on laboratory findings, 7 had aneuploidy, 4 viral infection, 7 misc. causes and 23, by exclusion, UP dysfunction. RESULTS: The mean GA was 31.4w (range 23-38w), Hct 40% (1956), WBC 5.1 (1-9.8), platelets 194 (35-326), UVpH 7.38 (7.27-7.45) and UA RI .74 (,46-1.0). The UVP of 3 fell outside the 95% C.I. for GA-2 with aneuploidy (a 1:7 translocation with a normal UA RI and a trisomy 21 mosaic), and 1 with UP dysfunction. Regardless of IUGR etiology, the UVP rose with advancing gestation as previously reported. There was a weak relationship between UVP and the UA RI (but not pH or PO2) independent of gestation (r2=.08, p<0.05). CONCLUSIONS: These findings indicate that placental resistance has little clinically relevant impact on the UVP. Coupled with prior obaervationa of the UVP in fetueea with treatable heart failure, an elevated UVP in the absence of an anatomic L-~R ahunt or an obstructive leeion usually indicates myocardial dysfunction.

612 VESICO-AMNIOTIC SHUNTS ARE EFFECTIVE EVEN IN FETUSES WITH POOR PROGNOSIS BY URINE ELECTROLYTES ~ Harp., JE Tolosa, D Coplan x. MFM Section, Dept. OB/GYN, Pennsylvania Hospital, and Dept. of Urology, Children's Hospital of Philadelphia, Philadelphia, PA. OBJECTIVE: To evaluate if bladder shunts/taps prevent lethal hin 8 hypoplasia in fetuses with obstructive uropathy and ofigohydramnios, its complications and neonatal outcome. STUDY DESIGN: From 1987-1993 10 fetuses between 19 and 30 weeks were diagnosed with severe obstructive uropathy by level II ultrasound. Karyotype and urine electrolytes were obtained in all patients. If oligohydramnios (<2cm) was present a bladder shunt or serial taps with amnioinfusion was offered. Detailed neonatal and long term follow-up was obtained. RESULTS: In 3 fetuses normal amniotic fluid was present and only serial ultlasound was used for follow-up. One of the 3 had poor prognosis by electrolytes (PPE), was dialysed, and received a kidney transplant at 17 mos of age. Seven fetuses had oligohydramnios; 6/7 had PPE and 217 ultrasound evidence of kidney dysplasia. Two patients who had serial bladder taps and amnioinfusion (delivered at 31 and 37 wks) had non-lethal pulmonary hypoplasia. Another with a 47XY karyotype (intervention was declined) was delivered at 33 wks; he died early in the neonatal period of Potter's syndrome. Four received vesico-amniotic shunts between 22-24 wks. The first, dehvered at 37 wks. is alive and well. The second, delivered at 37 wks, needed cutaneous ureterostomies at birth and a nephrectomy at 3 yrs. This fetus, as well as the third (46XX karyotype, delivered at 36 wks) needed postnatal laparotomy to retrieve a migrated pigtail catheter. The fourth was delivered at 33 wks but died of multisystem failure at 2 yrs of age. CONCLUSIONS: Bladder shunt/taps with reversal of oligoliydraminos prevent lethal lung hypoplasia even if there is a prenatal prognosis of poor renal function. If renal insufficiency then occurs, postnatal dialysis and renal transplant may benefit fetuses.