UMBILICAL PRESSURE MEASUREMENT IN THE EVALUATION OF NONIMMUNE HYDROPS-FETALIS

被引:25
作者
WEINER, CP
机构
[1] Fetal Diagnosis and Treatment Unit, Division of Maternal-Fetal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
关键词
PREGNANCY; NONIMMUNE HYDROPS-FETALIS; FETAL THERAPY; CORDOCENTESIS; UMBILICAL VENOUS PRESSURE;
D O I
10.1016/S0002-9378(12)90827-3
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
OBJECTIVE: Nonimmune hydrops fetalis continues to have a perinatal mortality rate > 50%. Although many abnormalities are associated with nonimmune hydrops fetalis, the direct mechanism by which the hydrops occurs is often obscure, even after delivery. There are at least three possible mechanisms for hydrops: heart failure (whether primary or a secondary effect of obstructed venous return), lymphatic malformation, and liver or peritoneal disease. The development of safe access to the fetal circulation by cordocentesis allows for the measurement of the umbilical venous pressure, which is closely related to the fetal central venous pressure. The premise that nonimmune hydrops fetalis of cardiac origin could be distinguished from that of noncardiac origin was examined by measuring the umbilical venous pressure. STUDY DESIGN: Umbilical venous pressure was measured during indicated diagnostic cordocentesis in three groups of fetuses: 20 with nonimmune hydrops fetalis, four with a cardiac malformation but without nonimmune hydrops fetalis, and eight with immune hydrops (fetal hemolytic disease). In 16 of 20 fetuses with nonimmune hydrops fetalis the serum total protein and albumin concentrations were also measured. RESULTS: Presumed inadequate cardiac output, as indicated by an elevated umbilical venous pressure, was the mechanism of nonimmune hydrops fetalis in 13 of 20 (65%). The pathologic condition included arrhythmia, cardiothoracic abnormalities, severe polycythemia and hyperviscosity, viral infection, and severe anemia. Successful antenatal treatment normalized the umbilical venous pressure. Nonimmune hydrops fetalis secondary to noncardiac mechanisms did not progress in severity and was not amenable to antenatal therapy. Hypoproteinemia and hypoalbuminemia were found in only six of 16 cases and were similarly distributed between cardiac and noncardiac mechanisms. CONCLUSIONS: This is the first report where the measurement of umbilical venous pressure was applied to the evaluation of nonimmune hydrops fetalis. Cardiac dysfunction was the most common mechanism causing hydrops. The finding of a normal umbilical venous pressure greatly reduces the likelihood that the heart is the cause of the hydrops, even when there is a coexistent heart malformation. This immediate information allows the practitioner either to focus on therapeutic interventions that might lower the umbilical venous pressure or to look for noncardiac causes for the hydrops.
引用
收藏
页码:817 / 823
页数:7
相关论文
共 28 条
[1]  
BENDER MD, 1986, GASTROINTESTINAL DIS, P1582
[2]  
CHIBA Y, 1990, Fetal Diagnosis and Therapy, V5, P175
[3]  
FADEL HE, 1988, OBSTET GYNECOL, V71, P1003
[4]   HYDROPS FETALIS - SONOGRAPHIC EVALUATION AND CLINICAL IMPLICATIONS [J].
FLEISCHER, AC ;
KILLAM, AP ;
BOEHM, FH ;
HUTCHISON, AA ;
JONES, TB ;
SHAFF, MI ;
BARRETT, JM ;
LINDSEY, AM ;
JAMES, AE .
RADIOLOGY, 1981, 141 (01) :163-168
[5]   PRENATAL-DIAGNOSIS OF ATRIOVENTRICULAR-CANAL MALFORMATIONS WITH UP-TO-DATE ECHOCARDIOGRAPHIC TECHNOLOGY - REPORT OF 14 CASES [J].
GEMBRUCH, U ;
KNOPFLE, G ;
CHATTERJEE, M ;
BALD, R ;
REDEL, DA ;
FODISCH, HJ ;
HANSMANN, M .
AMERICAN HEART JOURNAL, 1991, 121 (05) :1489-1497
[6]  
HOLZGREVE W, 1985, SEMIN PERINATOL, V9, P52
[7]   ELECTROPHYSIOLOGICAL PRINCIPLES AND FETAL ANTIARRHYTHMIC THERAPY [J].
KLEINMAN, CS ;
COPEL, JA .
ULTRASOUND IN OBSTETRICS & GYNECOLOGY, 1991, 1 (04) :286-297
[8]  
LINGMAN G, 1989, Fetal Therapy, V4, P120
[9]   Investigations into a possible immunological origin of idiopathic non-immune hydrops fetalis and initial results of prophylactic immune treatment of subsequent pregnancies [J].
Mallmann, Peter ;
Gembruch, Ulrich ;
Mallmann, Rolf ;
Hansmann, Manfred .
ACTA OBSTETRICIA ET GYNECOLOGICA SCANDINAVICA, 1991, 70 (01) :35-40
[10]  
MCFADDEN D E, 1989, Pediatric Pathology, V9, P11