Fifty pregnancies complicated by fetal ascites and generalized edema are reviewed and their prenatal findings, obstetric management, and fetal outcome are discussed. From the myriad of maternal, fetal, and placental problems which are known to cause nonimmune hydrops fetalis, many different causes of the disorder could be identified in 84% of all patients studied by extensive prenatal and postnatal workup. Therefore, in only 16% of the cases was the nonimmune hydrops fetalis labeled "idiopathic." The most common demonstrable causes of the disorder in this series were cardiac anomalies, followed by chromosomal disorders, congenital malformations, alpha-thalassemia, and the twin-twin transfusion syndrome. A systematic approach to the prenatal diagnostic workup of nonimmune hydrops fetalis is outlined, starting with the least invasive techniques (ultrasound, echocardiography, complete blood count, Kleihauer-Betke analysis, TORCH testing, and so forth) followed by more invasive techniques (amniocentesis and fetoscopy). Although the detection and prognostic evaluation of nonimmune hydrops fetalis are greatly improved by applying these techniques, the overall prognosis for most fetuses with nonimmune hydrops fetalis is still very poor, and only a few conditions causing the disorder, such as prenatally detected cardiac arrhythmias or selected cases of urinary tract obstruction, are amenable to treatment in utero.
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http://dx.doi.org/10.1016/0002-9378(84)90453-8 | DOI Listing |
Eur J Obstet Gynecol Reprod Biol
January 2025
Department of Obstetrics and Gynecology, Ministry of Health, Ankara Bilkent City Hospital, Ankara, Turkey; University of Health Sciences, Ankara Bilkent City Hospital, Ankara, Turkey.
Placental mesenchymal dysplasia (PMD) is a rare placental pathology that sonographically mimics gestational trophoblastic diseases. However, mesenchymal dysplasia can be distinguished from other conditions by the presence of villous edema and the absence of trophoblastic proliferation in the placental tissue. This pathology has been demonstrated to be associated with fetal growth restriction, Beckwith-Wiedemann syndrome, some chromosomal abnormalities and intrauterine fetal demise.
View Article and Find Full Text PDFAsian J Transfus Sci
September 2022
Department of Obstetrics and Gynecology, Faculty of Medicine Padjajaran University, Hasan Sadikin General Hospital, Bandung, Indonesia.
Anti-M antibody is one of the causes of severe fetal anemia and intrauterine death despite its relatively low frequency. A G3P2 26-year-old pregnant woman referred to our hospital at 29 weeks gestational age (WGA) with fetal hydrops. Her second pregnancy results in intrauterine fetal death at 35 WGA due to fetal hydrops.
View Article and Find Full Text PDFPrenatally diagnosed intracranial hemorrhage in the fetus is associated with a wide range of neonatal disorders, from completely uncomplicated physiological development to severe neurological impairment or death. The incidence is 0.6-1/1,000 births.
View Article and Find Full Text PDFTaiwan J Obstet Gynecol
January 2025
Department of Obstetrics and Gynecology, MacKay Memorial Hospital, Taipei, Taiwan; Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan; School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan; Institute of Clinical and Community Health Nursing, National Yang Ming Chiao Tung University, Taipei, Taiwan; Department of Obstetrics and Gynecology, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan; Department of Medical Laboratory Science and Biotechnology, College of Medical and Health Science, Asia University, Taichung, Taiwan. Electronic address:
JIMD Rep
January 2025
The Morris Kahn Laboratory of Human Genetics, Faculty of Health Sciences Ben Gurion University Beer-Sheva Israel.
The tightly-regulated spatial and temporal distribution of zinc ion concentrations within cellular compartments is controlled by two groups of Zn transporters: the 14-member ZIP/SLC39 family, facilitating Zn influx into the cytoplasm from the extracellular space or intracellular organelles; and the 10-member ZnT/SLC30 family, mobilizing Zn in the opposite direction. Genetic aberrations in most zinc transporters cause human syndromes. Notably, previous studies demonstrated osteopenia and male-specific cardiac death in mice lacking the ZnT5/ zinc transporter, and suggested association of two homozygous frameshift variants with perinatal mortality in humans, due to hydrops fetalis and hypertrophic cardiomyopathy.
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