Mechanisms of death in structurally normal stillbirths.

Autor: Pacora P; Perinatology Research Branch, NICHD/NIH/DHHS, Wayne State University/Hutzel Women's Hospital, 3990 John R, Box 4, Detroit, MI 48201, USA.; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA., Romero R; Perinatology Research Branch, NICHD/NIH/DHHS, Wayne State University/Hutzel Women's Hospital, 3990 John R, Box 4, Detroit, MI 48201, USA.; Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI, USA.; Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA.; Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA., Jaiman S; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA.; Department of Pathology, Wayne State University School of Medicine, Detroit, MI, USA., Erez O; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA.; Department of Obstetrics and Gynecology, Soroka University Medical Center, School of Medicine, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel., Bhatti G; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA., Panaitescu B; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA., Benshalom-Tirosh N; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA., Jung EJ; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA., Hsu CD; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA., Hassan SS; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA.; Department of Physiology, Wayne State University School of Medicine, Detroit, MI, USA., Yeo L; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA., Kadar N; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI, USA.; Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA.
Jazyk: angličtina
Zdroj: Journal of perinatal medicine [J Perinat Med] 2019 Feb 25; Vol. 47 (2), pp. 222-240.
DOI: 10.1515/jpm-2018-0216
Abstrakt: Objectives To investigate mechanisms of in utero death in normally formed fetuses by measuring amniotic fluid (AF) biomarkers for hypoxia (erythropoietin [EPO]), myocardial damage (cardiac troponin I [cTnI]) and brain injury (glial fibrillary acidic protein [GFAP]), correlated with risk factors for fetal death and placental histopathology. Methods This retrospective, observational cohort study included intrauterine deaths with transabdominal amniocentesis prior to induction of labor. Women with a normal pregnancy and an indicated amniocentesis at term were randomly selected as controls. AF was assayed for EPO, cTnI and GFAP using commercial immunoassays. Placental histopathology was reviewed, and CD15-immunohistochemistry was used. Analyte concentrations >90th centile for controls were considered "raised". Raised AF EPO, AF cTnI and AF GFAP concentrations were considered evidence of hypoxia, myocardial and brain injury, respectively. Results There were 60 cases and 60 controls. Hypoxia was present in 88% (53/60), myocardial damage in 70% (42/60) and brain injury in 45% (27/60) of fetal deaths. Hypoxic fetuses had evidence of myocardial injury, brain injury or both in 77% (41/53), 49% (26/53) and 13% (7/53) of cases, respectively. Histopathological evidence for placental dysfunction was found in 74% (43/58) of these cases. Conclusion Hypoxia, secondary to placental dysfunction, was found to be the mechanism of death in the majority of fetal deaths among structurally normal fetuses. Ninety-one percent of hypoxic fetal deaths sustained brain, myocardial or both brain and myocardial injuries in utero. Hypoxic myocardial injury was an attributable mechanism of death in 70% of the cases. Non-hypoxic cases may be caused by cardiac arrhythmia secondary to a cardiac conduction defect.
Databáze: MEDLINE