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Cardiorespiratory system
Published in Helen Butler, Neel Sharma, Tiago Villanueva, Student Success in Anatomy - SBAs and EMQs, 2022
36 Which of the following statements regarding the anatomy of the foetal circulation is correct? The umbilical vein transports deoxygenated blood from the foetus to the placenta.At birth the umbilical vein fibrosis and its remnant is the ligamentum arteriosum, which attaches the umbilicus to the liver.The falciform ligament of the liver separates left and right lobes and is the remnant of the umbilical vein.The ductus venosus allows blood from the umbilical vein to bypass the foetal liver on its way to the inferior vena cava.The ligamentum teres is located on the underside of the liver and is the embryological remnant of the umbilical artery.
Umbilical artery doppler sonography for fetal surveillance: Principles and practice
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Dev Maulik, David Mundy, Timothy Bennett
Fetal surveillance should be multimodal including UA Doppler and full or modified biophysical profile. FHR pattern should also be used using the traditional NST or the computerized cardiotocography (cCTG). The frequency of these should be usually once a week. Daily fetal movement assessment by the mother may be added to this list. Many would also advise the incorporation of the ductus venosus Doppler.
Physiology of the Neonate
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The ductus venosus closes a few hours after birth, but the exact mechanism is unknown. With the closure of the shunts, the RV and the LV are in series, and the adult configuration of the circulation is complete.
The Green Placental Disk: Massive Placental Disk Bilirubin Deposition Due to Maternal Hyperbilirubinemia
Published in Fetal and Pediatric Pathology, 2023
Caitlin Hughes, Jiancong Liang
This case illustrates the microscopic changes of maternal hyperbilirubinemia in the placental disk during pregnancy. The placental disk had a green discoloration and microscopically showed bilirubin deposition within villous syncytiotrophoblasts and Hofbauer cells. Along with complications of prematurity including respiratory distress syndrome requiring bubble continuous positive airway pressure, the markedly jaundiced newborn was also diagnosed with hyperbilirubinemia with total bilirubin of 11.1 mg/dL and direct bilirubin of 2.4 mg/dL. AST and ALT were within normal limits. The newborn’s stools were pigmented and his GGT was elevated at 721 unit/L, making diagnoses of biliary atresia and progressive familial intrahepatic cholestasis, respectively, unlikely. Evaluation by pediatric hepatology favored patent ductus venosus as the cause of his hyperbilirubinemia but could not entirely rule out the effects of maternal liver disease during gestation. After a mildly delayed closure of the ductus venosus at 14 days of age, the hyperbilirubinemia resolved.
Fetal hydrops – a review and a clinical approach to identifying the cause
Published in Expert Opinion on Orphan Drugs, 2020
Esther Dempsey, Tessa Homfray, John M Simpson, Steve Jeffery, Sahar Mansour, Pia Ostergaard
In Noonan syndrome, approximately 50% of cases who present postnatally are found to have mutations in PTPN11 [135,136]. As we carry out increasing amounts of in-utero genetic sequencing, we may find that antenatal presentation correlates more strongly with a different Noonan-causing gene. It is reported that 59% of pregnancies affected by Noonan Syndrome show a consistent pattern of raised nuchal translucency, pleural effusions and nonimmune fetal hydrops, as well as polyhydramnios and cardiac defects [137]. Absence of the ductus venosus has also been observed in approximately 50% of cases [137,138]. It is thought that the lymphatic abnormalities in fetuses with Noonan syndrome result from a disturbance in lymphatic endothelial differentiation due to diminished expression of the lymphatic markers PROX1 and Podoplanin and an increase in the vascular markers VEGF-A and Neuopilin-1 [139]. The fetal hydrops in Noonan syndrome is likely due to lymphatic malformation rather than congenital heart disease.
TRAP Sequence in Monochorionic/Monoamniotic (MC/MA) Discordant Twins: Two Cases Treated with Fetoscopic Laser Surgery
Published in Fetal and Pediatric Pathology, 2018
Gabriele Tonni, Gianpaolo Grisolia, Paolo Zampriolo, Federico Prefumo, Anna Fichera, Paola Bonasoni, Mathilde Lefebvre, Suonavy Khung-Savatovsky, Fabien Guimiot, Jonathan Rosenblatt, Edward Araujo Júnior
In the placenta, the TRAP sequence is characterized by superficial vascular connections that exclude the deep villous placental circulation to the acardiac twin. These vascular anastomoses are among chorionic vessels and consist of wide artery–artery (A–A) and vein–vein (V–V) connections. In this kind of vascular organization, the normally formed co-twin, known as the pump twin, directly perfuses the acardiac twin through the umbilical artery (A–A connection) with subsequent reversed circulation. In normal condition, oxygenated blood from the placenta perfuses the fetus through the umbilical vein and then goes via the ductus venosus to the right atrium. In TRAP sequence, the blood from the artery of the pump twin perfuses directly the acardiac twin at the level of the internal iliac arteries. It is a mixture of blood that comes from oxygenated blood from the aortic arch and the desaturated blood from the fetal venous system (from the ductus arteriosus). Except from the head and the upper limbs that recieve highly oxygenated blood thanks to the right-left shunt of the foramen ovale, this mixed blood is adequately oxygenated for the rest of the body of the normal twin [31–33]. However, the pump twin may also have complications from this abnormal circulation, especially high-output cardiac failure leading to fetal hydrops. Moreover, the pump twin receives decreased oxygenated blood due to mixing of the deoxygenated umbilical vein blood from the reversed circulation of the acardiac twin. In fact, the mortality rate for the pump twin is high as 50%, which also involves the consequences of therapeutic treatments [34].