Screening and therapy for causes of immune fetal hydrops have decreased it's incidence, making nonimmune fetal hydrops and its causes more important. From 1/80 to 6/95, 105 cases of fetal hydrops were identified (23 weeks to term). In 79 (75%), the cause was identified. There were 16 cases of immune fetal hydrops, 7 (44%) died; 15 cases had atrial tachycardia, 2 (13%) died; 7 had structural heart disease, 6 (86%) died; 5 had renal/urolgoic disease, 3 (60%) died; 4 had cytomegalovirus, 2 (50%) died; 4 had chromosomal abnormalities (1 also had significant structural heart disease), 0 died; 3 had metabolic disease, 2 (67%) died; 3 had hepatitis, 2 (67%) died; 3 had syndromes, 3 (100%) died; 2 had cystic adenomatoid malformation, 1 died; 2 had twin-twin transfusion, 1 twin died; 2 had diaphragmatic hernia, 2 died. There was one case each of fetal-maternal transfusion [alive (A)]; sacrococcygial teratoma [died (D)]; osteogenesis imperfecta (A); pulmonary arteriosclerosis (D); cystic fibrosis (A); erythrophagacytic lymphohistiocytosis (D); streptococcal sepsis (D). Three cases had unknown viral infection, 1 died. There were 26 of unknown etiology, 12 (46%) died. Three cases were found to have nuclear inclusions consistent with parvovirus at autopsy. Only 1 had been tested for parvovirus. In 2 there was significant cardiac hypertrophy both echocardiographically and at autopsy. Conclusions: 1) Fetal hydrops due to structural heart disease has a high mortality (86%) whereas mortality due to supraventricular tachycardia is low (13%); 2) Parvovirus induced anemia can lead to heart failure but parvovirus also appears to directly effect cardiac cells and their function; 3) Cardiac hypertrophy on echocardiogram may indicate the presence of parvovirus infection; 4) Parvovirus was tested for in < 10% of the fetal hydrops cases.
|Original language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - Jan 1 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)