Amorphous Twin Research Articles

P640: Molecular findings of a placental mass in association with neonatal mosaic trisomy 21: Teratoma vs monozygotic acardiac amorphous twin

P640: Molecular findings of a placental mass in association with neonatal mosaic trisomy 21: Teratoma vs monozygotic acardiac amorphous twin

Twin Reversed Arterial Perfusion Sequence.

Twin Reversed Arterial Perfusion Sequence.

Acardius-myelacephalus: management of a misdiagnosed case of twin reversed arterial perfusion sequence with tense polyhydramnios

Abstract Background: Twin reversed arterial perfusion (TRAP) sequence is the most severe form of twin to twin transfusion syndrome. Survival of the pump twin is threatened by extreme prematurity from polyhydramnios and cardiac failure, necessitating interventions. Rarely, interventions are indicated as a result of maternal life-threatening complications. The management of an acardiac-myelacephalus variant of TRAP sequence, complicated by severe maternal respiratory distress from tense polyhydramnios is presented in this report. Case presentation: A 29-year-old G3P2, Alive2 was referred to the Perinatal Unit on account of ultrasound diagnosed twin gestation with demise of one twin at an estimated gestational age (EGA) of 29 weeks. She was in severe respiratory distress with central cyanosis, and grossly distended abdomen. Ultrasonography revealed twin gestation with cardiac activity in only one twin and polyhydramnios. The second twin had no recognizable human body structure and retrograde umbilical arterial flow. TRAP sequence with tense polyhydramnios was diagnosed. The respiratory distress was relieved with serial reductive amniocentesis, and she was managed conservatively until an EGA of 34 weeks, when she delivered a live twin that weighed 2.05 kg, and an amorphous twin with a rudimentary limb that weighed 1.82 kg following spontaneous rupture of membranes. Monochorionic placentation was confirmed at delivery. The pump twin was discharged in a satisfactory state after a period of observation. Conclusion: TRAP sequence may be easily misdiagnosed due to its rarity, with adverse consequences. Accurate diagnosis of the condition, and the provision of basic facilities for in utero interventions when indicated are necessary for fetal salvage.

Prenatal diagnosis of an acardiac amorphous twin and the anomalous co-twin in a monoamniotic twin pregnancy

Prenatal diagnosis of an acardiac amorphous twin and the anomalous co-twin in a monoamniotic twin pregnancy

Nasal teratoma in a neonate associated with an acardiac amorphous twin

Nasopharyngeal teratomas are uncommon neoplasms found in neonates. A rare case of a teratoma arising from the nasal septum of a newborn associated with an acardiac amorphous twin is described. Antenatal ultrasonography suggested a fetal anomaly, for which a cesarean section was performed. Immediately after birth the tumor was excised, thereby eliminating life-threatening respiratory distress. The postoperative course was uneventful.

Acardiac amorphous twin with prune belly sequence in the co‐twin

We describe a twin with acardia acephalus or "Twin Reversed Arterial Perfusion Sequence" and prune belly sequence in the co-twin. In a former quite similar case a prune belly appearance of the co-twin of an acardiac fetus was found to be secondary to the ascites caused by cardiac failure. In the present case, we are dealing with the prune belly sequence as a separate condition, given the fact there were no signs of ascites or cardiac failure. We also found associated anomalies: agenesis of the left ureter and kidney, dysplastic right kidney and anal atresia. Urinary tract obstruction has never been described in the co-twin of an acardiac amorphous fetus.

Increased amniotic alphafetoprotein due to a haloacardium amorphous twin.

Clinical GeneticsVolume 21, Issue 6 p. 382-383 Increased amniotic alphafetoprotein due to a holoacardium amorphous twin A. P. Read, Corresponding Author A. P. Read University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandPhD Dept. of Medicul Genetics St. Mary's Hospital Manchester M13 OJH EnglandSearch for more papers by this authorDian Donnai, Dian Donnai University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandSearch for more papers by this authorJulia Tracey, Julia Tracey University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandSearch for more papers by this authorS. J. Fennell, S. J. Fennell University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandSearch for more papers by this author A. P. Read, Corresponding Author A. P. Read University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandPhD Dept. of Medicul Genetics St. Mary's Hospital Manchester M13 OJH EnglandSearch for more papers by this authorDian Donnai, Dian Donnai University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandSearch for more papers by this authorJulia Tracey, Julia Tracey University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandSearch for more papers by this authorS. J. Fennell, S. J. Fennell University of Manchester Department of Medical Genetics, St Mary's Hospital, Manchester, EnglandSearch for more papers by this author First published: June 1982 https://doi.org/10.1111/j.1399-0004.1982.tb01391.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume21, Issue6June 1982Pages 382-383 RelatedInformation

Increased amnionic fluid alpha‐fetoprotein due to a holoacardium amorphous twin

Amnionic fluid alpha-fetoprotein measurement was employed as a screening test for neural tube defects in a pregnancy only at risk due to advanced maternal age. The alpha-fetoprotein concentration was elevated more than 10 standard deviations above the mean and was found to be caused by a holoacardium amorphous twin. A normal female fetus was also present. Various causes of elevated alpha-fetoprotein concentration in amnionic fluid are discussed.

Retinal elements in an amorphous twin.

Retinal elements in an amorphous twin.