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Larsen B, Hwang J: Progesterone interactions with the cervix: translational implications for time period and preterm delivery, Infect Dis Obstet Gynecol 2011:353297, 2011. Ito A, Hiro D, Ojima Y, et al: Spontaneous manufacturing of interleukin-1-like factors from pregnant rabbit uterine cervix, Am J Obstet Gynecol 159:261�265, 1988. Ekerhovd E, Weijdegard B, Brannstrom M, et al: Nitric oxide induced cervical ripening in the human: involvement of cyclic guanosine monophosphate, prostaglandin F(2 alpha), and prostaglandin E(2), Am J Obstet Gynecol 186:745�750, 2002. Rizzo G, Capponi A, Vlachopoulou A, et al: Ultrasonographic assessment of the uterine cervix and interleukin-8 concentrations in cervical secretions predict intrauterine infection in sufferers with preterm labor and intact membranes, Ultrasound Obstet Gynecol 12(2):86�92, 1998. Hassan S, Romero R, Hendler I, et al: A sonographic short cervix as the only scientific manifestation of intra-amniotic an infection, J Perinat Med 34(1):13�19, 2006. Cervical perform and prematurity, Best Pract Res Clin Obstet Gynaecol 21:791�806, 2007. Diagnosis of placental abruption: relationship between medical and histopathological findings, Eur J Obstet Gynecol Reprod Biol 148(2):125�130, 2010. Arcuri F, Toti P, Buchwalder L, Casciaro A, et al: Mechanisms of leukocyte accumulation and activation in chorioamnionitis: interleukin 1 beta and tumor necrosis issue alpha enhance colony stimulating factor 2 expression in time period decidua, Reprod Sci 16(5):453�461, 2009. Rosen T, Schatz F, Kuczynski E, et al: Thrombinenhanced matrix metalloproteinase-1 expression: a mechanism linking placental abruption with premature rupture of the membranes, J Matern Fetal Neonatal Med 11(1):11�17, 2002. Oner C, Schatz F, Kizilay G, et al: Progestininflammatory cytokine interactions have an effect on matrix metalloproteinase-1 and -3 expression in time period decidual cells: implications for remedy of chorioamnionitis-induced preterm supply, J Clin Endocrinol Metab 93(1):252� 259, 2008. Krikun G, Schatz F, Mackman N, et al: Regulation of tissue issue gene expression in human endometrium by transcription factors Sp1 and Sp3, Mol Endocrinol 14:393�400, 2000. Schatz F, Krikun G, Runic R, et al: Implications of decidualization-associated protease expression in implantation and menstruation, Semin Reprod Endocrinol 17:3�12, 1999. Maymon E, Romero R, Pacora P, et al: Evidence for the participation of interstitial collagenase (matrix metalloproteinase 1) in preterm premature rupture of membranes, Am J Obstet Gynecol 183:914�920, 2000. Maymon E, Romero R, Pacora P, et al: Human neutrophil collagenase (matrix metalloproteinase 8) in parturition, premature rupture of the membranes, and intrauterine an infection, Am J Obstet Gynecol 183(1):94�99, 2000. Vadillo-Ortega F, Hernandez A, GonzalezAvila G, et al: Increased matrix metalloproteinase exercise and reduced tissue inhibitor of metalloproteinases-1 ranges in amniotic fluids from pregnancies complicated by untimely rupture of membranes, Am J Obstet Gynecol 174:1371�1376, 1996. Steffensen B, Chen Z, Pal S, et al: Fragmentation of fibronectin by inherent autolytic and matrix metalloproteinase activities, Matrix Biol 30(1):34�42, 2011. Chai M, Barker G, Menon R, et al: Increased oxidative stress in human fetal membranes overlying the cervix from term non-labouring and post labour deliveries, Placenta 33:604� 610, 2012. Romero R, Oyarzun E, Mazor M, et al: Metaanalysis of the relationship between asymptomatic bacteriuria and preterm delivery/low birth weight, Obstet Gynecol 73(4):576�582, 1989. Bejar R, Wozniak P, Allard M, et al: Antenatal origin of neurologic damage in newborn infants: I. Ronel D, Wiznitzer A, Sergienko R, et al: Trends, risk components and pregnancy consequence in girls with uterine rupture, Arch Gynecol Obstet 285(2):317�321, 2012. Torche F, Kleinhaus K: Prenatal stress, gestational age and secondary sex ratio: the sexspecific effects of publicity to a natural catastrophe in early pregnancy, Hum Reprod 27(2):558� 567, 2012. Fransson E, Ortenstrand A, Hjelmstedt A: Antenatal depressive signs and preterm delivery: a potential examine of a Swedish nationwide sample, Birth 38(1):10�16, 2011. Dunkel Schetter C, Tanner L: Anxiety, despair and stress in being pregnant: implications for moms, kids, analysis, and practice, Curr Opin Psychiatry 25(2):141�148, 2012. National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network, Am J Obstet Gynecol a hundred seventy five:1286�1292, 1996. Alder J, Fink N, Bitzer J, et al: Depression and nervousness during being pregnant: a threat factor for obstetric, fetal and neonatal end result A important review of the literature, J Matern Fetal Neonatal Med 20(3):189�209, 2007. Drugs with minimal or unknown human teratogenic impact, Obstet Gynecol 113:417�432, 2009. Vedhara K, Metcalfe C, Brant H, et al: Maternal temper and neuroendocrine programming: results of time of exposure and intercourse, J Neuroendocrinol 24(7):999�1011, 2012. Romero R, Mazor M, Gomez R: Cervix, incompetence and untimely labor, Fetus three:1, 1993. Microbial invasion of the amniotic cavity in sufferers with suspected cervical incompetence: prevalence and medical significance, Am J Obstet Gynecol 167:1086� 1091, 1992. Romero R, Espinoza J, Erez O, et al: the position of cervical cerclage in obstetric practice: can the affected person who may benefit from this process be identified Kyrgiou M, Koliopoulos G, Martin-Hirsch P, et al: Obstetric outcomes after conservative therapy for intraepithelial or early invasive cervical lesions: systematic review and metaanalysis, Lancet 367(9509):489�498, 2006. Noehr B, Jensen A, Frederiksen K, et al: Depth of cervical cone eliminated by loop electrosurgical excision procedure and subsequent threat of spontaneous preterm delivery, Obstet Gynecol 114(6):1232�1238, 2009. Shanbhag S, Clark H, Timmaraju V, et al: Pregnancy consequence after therapy for cervical intraepithelial neoplasia, Obstet Gynecol 114(4):727�735, 2009. MacDorman F, Kirmeyer S: Fetal and perinatal mortality, United States, 2005, Natl Vital Stat Rep 57(8):1�19, 2009. Fretts R: Stillbirth epidemiology, danger elements, and opportunities for stillbirth prevention, Clin Obstet Gynecol 53(3):588�596, 2010. Gordon A, Raynes-Greenow C, McGeechan K, et al: Stillbirth danger in a second pregnancy, Obstet Gynecol 119(3):509�517, 2012. Shalev E, Dan U, Yanai N, et al: Sonographyguided fetal blood sampling for pH and blood gases in premature fetuses with abnormal fetal coronary heart price traces, Acta Obstet Gynecol Scand 70(7�8):539�542, 1991. Jacobsson B, Hagberg G, Hagberg B, et al: Cerebral palsy in preterm infants: a populationbased case-control study of antenatal and intrapartal risk components, Acta Paediatr 91(8): 946�951, 2002. Malcus P, Svenningsen N, Westgren M: Reactivity of non-stress exams and its relationship to consequence in infants born previous to the thirty third week of gestation, Acta Obstet Gynecol Scand 65(8):835�838, 1986. Andreani M, Locatelli A, Assi F, et al: Predictors of umbilical artery acidosis in preterm supply, Am J Obstet Gynecol 197(3):303. The incidence of cerebral palsy in examined and untested perinates, Am J Obstet Gynecol 178(4):696�706, 1998. Rotmensch S, Lev S, Kovo M, et al: Effect of betamethasone administration on fetal heart 597. Gruslin A, Lemyre B: Pre-eclampsia: fetal assessment and neonatal outcomes, Best Pract Res Clin Obstet Gynaecol 25(4):491�507, 2011. Saleemuddin A, Tantbirojn P, Sirois K, et al: Obstetric and perinatal issues in placentas with fetal thrombotic vasculopathy, Pediatr Dev Pathol 13(6):459�464, 2010. Dolk H, Loane M, Garne E: the prevalence of congenital anomalies in Europe, Adv Exp Med Biol 686:349�364, 2010. A randomized trial of prenatal versus postnatal repair of myelomeningocele, N Engl J Med 364(11):993�1004, 2011. Deprest J, Jani J, Lewi L, et al: Fetoscopic surgery: encouraged by clinical experience and boosted by instrument innovation, Semin Fetal Neonatal Med 11(6):398�412, 2006. Gul A, Cebeci A, Aslan H, et al: Perinatal outcomes of dual pregnancies discordant for major fetal anomalies, Fetal Diagn Ther 20(4):244�248, 2005. Chitkara U, Wilkins I, Lynch L, et al: the role of sonography in assessing severity of fetal anemia in Rh- and Kell-isoimmunized pregnancies, Obstet Gynecol 71(3 Pt 1):393�398, 1988.

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Breysem L, Debeer A, Claus F, et al: Crosssectional research of tracheomegaly in children after fetal tracheal occlusion for extreme congenital diaphragmatic hernia, Radiology 257:226�232, 2010. Deprest J, Breysem L, Gratacos E, et al: Tracheal side effects following fetal endoscopic tracheal occlusion for severe congenital diaphragmatic hernia, Pediatr Radiol forty:670�673, 2010. Jani J, Valencia C, Cannie M, et al: Tracheal diameter at birth in extreme congenital diaphragmatic hernia treated by fetal endoscopic tracheal occlusion, Prenat Diagn 31:699�704, 2011. Fayoux P, Hosana G, Devisme L, et al: Neonatal tracheal changes following in utero fetoscopic balloon tracheal occlusion in extreme congenital diaphragmatic hernia, J Pediatr Surg 45:687� 692, 2010. McHugh K, Afaq A, Broderick N, et al: Tracheomegaly: a complication of fetal endoscopic tracheal occlusion within the treatment of congenital diaphragmatic hernia, Pediatr Radiol 40:674�680, 2010. Bush A: Congenital lung illness: a plea for clear thinking and clear nomenclature, Pediatr Pulmonol 32:328�337, 2001. Kotecha S, Barbato A, Bush A, et al: Antenatal and postnatal management of congenital cystic adenomatoid malformation, Paediatr Respir Rev thirteen:162�171, 2012. Langston C: New ideas in the pathology of congenital lung malformations, Semin Pediatr Surg 12:17�37, 2003. Desai S, Dusmet M, Ladas G, et al: Secondary vascular modifications in pulmonary sequestrations, Histopathology fifty seven:121�127, 2010. Tsao K, Hawgood S, Vu L, et al: Resolution of hydrops fetalis in congenital cystic adenomatoid malformation after prenatal steroid therapy, J Pediatr Surg 38:508�510, 2003. Bermudez C, Perez-Wulff J, Bufalino G, et al: Percutaneous ultrasound-guided sclerotherapy for complicated fetal intralobar bronchopulmonary sequestration, Ultrasound Obstet Gynecol 29:586�589, 2007. Oepkes D, Devlieger R, Lopriore E, et al: Successful ultrasound-guided laser remedy of fetal hydrops caused by pulmonary sequestration, Ultrasound Obstet Gynecol 29:457�459, 2007. Fortunato S, Lombardo S, Dantrell J, et al: Intrauterine laser ablation of a fetal cystic adenomatoid malformation with hydrops: the 290. Cavoretto P, Molina F, Poggi S, et al: Prenatal prognosis and outcome of echogenic fetal lung lesions, Ultrasound Obstet Gynecol 32:769�783, 2008. Bermudez C, Perez-Wulff J, Arcadipane M, et al: Percutaneous fetal sclerotherapy for congenital cystic adenomatoid malformation of the lung, Fetal Diagn Ther 24:237�240, 2008. Van Mieghem T, Lewi L, Van Schoubroeck D, et al: Prenatal therapy for primary fetal hydrothorax in a dichorionic twin being pregnant, Prenat Diagn 26:584�586, 2006. Picone O, Benachi A, Mandelbrot L, et al: Thoracoamniotic shunting for fetal pleural effusions with hydrops, Am J Obstet Gynecol 191:2047�2050, 2004. Nicolini U, Spelzini F: Invasive evaluation of fetal renal abnormalities: urinalysis, fetal blood sampling and biopsy, Prenat Diagn 21:964� 969, 2001. Welsh A, Agarwal S, Kumar S, et al: Fetal cystoscopy in the administration of fetal obstructive uropathy: expertise in a single European centre, Prenat Diagn 23:1033�1041, 2003. Ruano R: Fetal surgical procedure for extreme lower urinary tract obstruction, Prenat Diagn 31:667�674, 2011. Rychik J, Szwast A, Natarajan S, et al: Perinatal and early surgical outcome for the fetus with hypoplastic left heart syndrome: a 5-year single institutional experience, Ultrasound Obstet Gynecol 36:465�470, 2010. Arzt W, Tulzer G: Fetal surgical procedure for cardiac lesions, Prenat Diagn 31:695�698, 2011. Caldarelli M, Di Rocco C, La Marca F: Shunt problems within the first postoperative 12 months in children with meningomyelocele, Childs Nerv Syst 12:748�754, 1996. Blumenfeld Z, Siegler E, Bronshtein M: the early analysis of neural tube defects, Prenat Diagn 13:863�871, 1993. Ghi T, Pilu G, Falco P, et al: Prenatal prognosis of open and closed spina bifida, Ultrasound Obstet Gynecol 28:899�903, 2006. Lachmann R, Chaoui R, Moratalla J, et al: Posterior mind in fetuses with open spina bifida at eleven to thirteen weeks, Prenat Diagn 31:103�106, 2011. Kohl T, Hering R, Heep A, et al: Percutaneous fetoscopic patch protection of spina bifida aperta within the human: early medical experience and potential, Fetal Diagn Ther 21:185�193, 2006. Tadmor O, Bocker Y, Rabinowitz R, et al: Analysis of umbilical artery circulate parameters throughout fetal variable decelerations using computerized Doppler waveforms, Fetal Diagn Ther 14:2�10, 1999. Strauss A, Hasbargen U, Paek B, et al: Intrauterine fetal demise attributable to amniotic band syndrome after standard amniocentesis, Fetal Diagn Ther 15:4�7, 2000. In Van Vught J, Schulman L, editors: Fetal drugs, New York, 2006, M Dekker, pp 473�491. Arzt W, Wertaschnigg D, Veit I, et al: Intrauterine aortic valvuloplasty in fetuses with important aortic stenosis: experience and outcomes of 24 procedures, Ultrasound Obstet Gynecol 37:689� 695, 2011. Nicolini U, Poblete A, Boschetto C, et al: Complicated monochorionic twin pregnancies: experience with bipolar cord coagulation, Am J Obstet Gynecol 185:703�707, 2001. Immune globulins to stop alloimmunization to different purple cell antigens are unlikely to be developed by pharmacologic firms. Thus red cell alloimmunization in being pregnant is likely to proceed to complicate pregnancies for the foreseeable future. In most cases, the antigenic load of a putative antigen on the fetal erythrocytes and erythrocytic precursors is inadequate to stimulate the maternal immune system. However, in the case of a giant fetomaternal hemorrhage earlier than birth or at delivery, B lymphocyte clones that recognize the foreign pink cell antigen are established. The preliminary maternal production of IgM is short-lived and is adopted by a speedy change to an IgG response. A human antiglobulin titer can normally be detected by 5 to sixteen weeks after the sensitizing occasion. After the initial antigenic exposure, memory B lymphocytes await the appearance of pink cells containing the putative antigen 558 in a subsequent being pregnant. If stimulated by fetal erythrocytes, these B lymphocytes differentiate into plasma cells that may rapidly proliferate and produce IgG antibodies and an increase in the maternal titer. Maternal IgG crosses the placenta and attaches to fetal erythrocytes that have expressed the paternal antigen. These cells are then sequestered by macrophages within the fetal spleen, where they bear extravascular hemolysis, producing fetal anemia. Fetal sex could play a significant role within the fetal response to maternal antibodies. Ulm and associates2 reported that the chance for hydrops fetalis was increased 13-fold in RhD-positive male fetuses in contrast with their female counterparts; the adjusted odds ratio for perinatal mortality was three. Several necessary physiologic responses occur in fetuses on account of this anemia. An enhanced bone marrow manufacturing of reticulocytes is famous when the fetal hemoglobin deficit, compared with norms for gestational age, exceeds 2 g/dL, and erythroblasts from the fetal liver happen at a hemoglobin deficit of seven g/dL or larger. Hydrops fetalis, a set of fluid in a minimal of two serous compartments, typically heralds end-stage illness, and it occurs with hemoglobin deficits of 7 g/dL or higher. Reduced serum albumin ranges have been reported, presumably resulting from depressed synthesis by the fetal liver, which shifts to an erythropoietic operate. Iron overload secondary to ongoing hemolysis may contribute to free radical formation and endothelial cell dysfunction.

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This requires cautious sonographic evaluation of fetal anatomy (in particular, the presence of regular fetal kidneys), cardiac operate, and placental twine insertions for each fetuses. Although consideration ought to be given to the performance of amniocentesis to exclude chromosomal anomaly or infection, this process could intervene with subsequent management if fetoscopic laser remedy is a risk. Serial discount amniocenteses were suggested as a path to equilibrate amniotic fluid quantity throughout the dividing membrane and to cut back overall intrauterine stress. The examine was stopped early due to a significant advantage for those assigned to laser remedy. Compared with the group undergoing amniocenteses, the laser ablation group had significantly extended median gestational age at delivery (33 versus 29 weeks), significantly extra circumstances with at least one survivor at 6 months of age (76% versus 51%), and significantly fewer instances of major neurologic harm among surviving infants at 6 months of age (5% versus 10%). Whereas a straight fetoscope is used for posterior placental locations, fetoscopes with angled lenses or curved sheaths have been particularly developed for anterior placentas. It is important that all vascular communications that join the 2 fetal circulations be ablated, as a end result of this should forestall reverse fetal transfusion and scale back neurologic injury if one fetus dies. This selective strategy to laser ablation additionally includes leaving intact these vessels that drain an area of placenta both to and from one explicit fetus. Ablation of all placental anastomoses that connect the fetuses primarily makes the being pregnant dichorionic. Some technical refinements of the fetoscopic laser coagulation procedure are at present being investigated. Some authors have claimed that the sequence by which placental vessels are ablated could additionally be necessary for determining the speed of survival of the donor fetus. With the unique selective coagulation process, almost 30% of donor fetuses still died inside 4 weeks of the process. Another refinement, known as the Solomon approach, is to join the areas of ablated vessels on the placental floor by additional laser coagulation, to leave a coagulated line alongside the vascular equator of the placenta. The goal of this system is to further reduce the possibilities of lacking small residual anastomoses on the placental floor. Betamethasone administration is beneficial because of the excessive chance of early supply. Delivery ought to be based on traditional obstetric indications, although cesarean section is most likely going. Surviving infants are at elevated risk for long-term morbidity, including cardiomyopathy and periventricular leukomalacia, and due to this fact neonatal cranial imaging and follow-up echocardiography are really helpful. Perinatal end result after fetoscopic laser coagulation appears to rely upon operator experience, with the process in all probability having a steep learning curve. In a review of the nine largest collection of laser procedures, encompassing 1367 cases, total perinatal survival rate was 66% (range, 54% to 82%) with a minimal of one twin surviving in 72% of circumstances (range, 73% to 90%). In a review of 1367 laser procedures, a second laser process was carried out in only 4% of instances (range, 0% to 11%) and general survival of solely 50% is to be anticipated. Options for management embody preterm delivery, intrauterine fetal transfusion, selective fetocide, and repeat fetoscopic laser coagulation. Intrauterine fetal transfusion, whereas logical for the anemic fetus, has a risk for worsening polycythemia in the other fetus. Repeating the fetoscopic laser process can also be significantly difficult because of the conventional amniotic fluid volumes and the fairly doubtless tiny dimension of residual anastomoses. In a evaluate of 256 longterm survivors after laser remedy, adopted to 3 years of age at a single German middle, the incidence of severe neurologic impairment was 7%, and in a further 8% minor or moderate impairment was noted. The prognosis can be confirmed after sonographic identification of entangled umbilical cords. A, Color Doppler image of entangled umbilical cords, which is typical of monoamniotic twin pregnancy. B, Pulsed Doppler image of the identical affected person in which two separate heart rates are clearly visible inside the Doppler gate. C, Pathology image of the placenta from the same patient after supply, displaying each wire insertion websites in the placenta being shut together and with entangled umbilical cords. In the absence of non-reassuring fetal coronary heart fee test results, the timing and mode of delivery of monoamniotic twins are controversial. A report on 20 sets of monoamniotic twins discovered no fetal deaths after 32 weeks, suggesting that prophylactic early supply was not wanted. Although vaginal delivery of monoamniotic twins is clearly potential, the incidence of cesarean supply is excessive when fetal testing is non-reassuring. Whereas the majority of current research have suggested scheduled cesarean section, vaginal delivery may be acceptable if the fetal heart rates are repeatedly monitored and the mother has been informed that an emergent cesarean delivery may be needed. The incidence is estimated to occur in 1% of monozygotic twin pregnancies, with a start estimate of roughly 1 in 35,000 births. The situation happens due to early first-trimester circulatory failure of one fetus in a monochorionic twin pregnancy, together with the event of arterioarterial and venovenous anastomoses between the umbilical arteries of both fetuses. The donor, or "pump twin," offers circulation for itself and for the recipient (the "perfused twin") through a direct umbilical arterial�to�umbilical arterial anastomosis at the placental surface. There is reversal of blood move within the umbilical artery of the acardiac twin, with the artery bringing deoxygenated blood from the co-twin to the acardiac twin. This perfusion is normally uneven in the recipient twin, with relative hypoperfusion of the higher part of the physique, leading to important structural anomalies. A weird vary of anomalies could be seen within the acardiac twin, together with anencephaly, holoprosencephaly, absent limbs, absent lungs or heart, intestinal atresias, stomach wall defects, and absent liver, spleen, or kidneys. The acardiac fetus may be unrecognizable as a fetus or might have an abnormal-appearing head or trunk with no apparent coronary heart. Sonographic indicators of cardiac failure may be seen in the pump twin, including polyhydramnios, cardiomegaly, and tricuspid regurgitation. Doppler velocimetry of the umbilical cords demonstrating reversed path of circulate in the umbilical artery and vein could also be useful in confirming the prognosis. The pump twin is in danger for growth of hydrops or congestive cardiac failure. If features suggestive of impending cardiac failure are present at an early gestational age, consideration should be given to an invasive process to interrupt the vascular supply to the acardiac mass. Other sonographic options that help in making the diagnosis embrace bifid look of the first-trimester fetal pole, greater than three umbilical twine vessels, heads persistently on the same degree and physique aircraft, and failure of the fetuses to change position relative to one another over time. Thoracopagus, by which the 2 fetuses face one another, accounts for 75% of conjoined twins. The fetuses usually have frequent sternum, diaphragm, upper stomach wall, liver, pericardium, and gastrointestinal tract. Because 75% of thoracopagus twins have joined hearts, prognosis for surgical division is extraordinarily poor. Because joined hearts are uncommon in omphalopagus, twins on this subgroup have a much better surgical prognosis than twins with different types of thoracopagus. Pygopagus accounts for 20% of circumstances; the twins share a standard sacrum and face away from each other. There is 38 Multiple Gestation: Clinical Characteristics and Management 593 A single middle, 30 sets of twins were considered to have lethal situations, because it was not feasible to separate them. Five units of twins underwent surgical separation, and, in complete, six kids survived, giving an overall survival fee of only eight. When expectant management is selected, cesarean part (usually through a traditional incision) is the supply methodology of choice to decrease maternal and fetal trauma.

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The cutoff level and subsequent public policy was decided greater than 25 years ago and was based on a maternal age threat of 35 years at supply. The factors thought-about in In his initial description of the syndrome that bears his name, Langdon Down described skin so deficient in elasticity that it appeared to be too massive for the physique. The pores and skin and underlying lymphatic fluid within the fetal neck can now be seen with ultrasound at as early as 10 to 12 weeks of gestation. Eighty-two p.c of trisomy 21 fetuses have been recognized, for a screen-positive price of 8. Subsequent studies have demonstrated comparable Down syndrome detection charges, between 70% and 75% (Table 30-4). The success price for undertaking a measurement for these gestational ages is between 98% and one hundred pc. Either transabdominal or transvaginal scanning can be used; about 95% of circumstances can be imaged by the transabdominal route. The magnification have to be such that the fetus occupies a minimal of three fourths of the picture, and each increment in the distance between the calipers should be solely 0. Studies have demonstrated that ultrasound measurements can be correct to the nearest zero. Distinction could be completed by both ready for spontaneous fetal movement away from the amniotic membrane or by bouncing the fetus off the amnion by asking the mother to cough or by tapping on her stomach. The capacity to achieve a dependable measurement has been linked to the motivation of the sonographer. It is suggested that placement of the calipers somewhat than generation of the suitable picture accounts for a big a part of the variation between operators. Both confirmed that ongoing skilled evaluate of images is an inefficient and impractical strategy. Clear distinction between the amnion and the pores and skin edge is made by ready for fetal motion. Pregnancy-associated plasma protein A has been demonstrated to have a imply value of zero. In girls older than 35, 90% to 92% of trisomy 21 pregnancies can be recognized with a 16% to 22% false-positive price. Sonek and colleagues56 printed the primary large prospective trial of aneuploid threat analysis utilizing first-trimester ultrasound evaluation of the fetal nasal bone. Although these knowledge are promising, detection charges using this combined display screen can be expected to be significantly lower in an unselected population utilizing a similar 5% false-positive rate. Another potential ultrasound marker is tricuspid regurgitation decided by pulsed wave Doppler ultrasonography. When serum biochemical markers measured at 10 weeks have been also added, the modeled detection rate elevated to 92% with a 5% falsepositive price, or 84% with a 1% false-positive fee. Sixty-nine percent of trisomy 21 fetuses residing within the first trimester and 76% of those alive in the second trimester shall be born alive. Wapner and colleagues46 calculated that higher than 80% of screen-positive trisomy 21 pregnancies would be born alive. When the usual 1: 270 cutoff was used, roughly 25% of Down syndrome pregnancies amongst girls less than 35 years of age have been screen positive. The sensitivity of the triple screen for Down syndrome detection in girls younger than 35 years ranges between 57% and 67% if the false-positive rate is held constant at 5%. Because of the impact of maternal age on the risk analysis, screening ladies who shall be 35 years of age or extra will increase the sensitivity, using the same cutoffs, to approximately 87%, but with a false-positive fee of practically 25%. Other analytes or combinations of analytes have been tested to further increase sensitivity. With the addition of additional markers, the potential profit should be balanced in opposition to the cost. With each extra marker, costs to society can balloon into the hundreds of thousands because of the variety of pregnancies examined each year with solely a minimal enchancment in detection. The relative value worth of raising the sensitivity or decreasing the false-positive price a number of proportion factors is an ongoing debate. In those with a traditional ultrasound and amniocentesis, the danger for adverse consequence was 27% overall however various with the diploma of elevation. Data from Milunsky A, editor: Geneticdisordersandthefetus:diagnosis,prevention,andtreatment, ed three, Baltimore, 1992, Johns Hopkins University Press. To date, no administration protocol has been demonstrated to enhance consequence in these cases. Smith-Lemli-Opitz syndrome happens in roughly 1/60,000 pregnancies and is an autosomal recessive dysfunction ensuing from a defect in 3-hydroxysteroid-7-reductase, altering cholesterol synthesis and leading to low cholesterol levels and the accumulation of the cholesterol precursor 7-dehydrocholesterol in blood and amniotic fluid. Because cholesterol is a precursor of estriol, the defect ends in reduced or undetectable levels of estriol in maternal serum and amniotic fluid. Smith-Lemli-Opitz syndrome is characterized by low delivery weight, failure to thrive, and average to extreme psychological retardation. It is associated with a number of structural anomalies, including syndactyly of the second and third toes, microcephaly, ptosis, and a typical-appearing facies. Bradley and colleagues103 summarized findings in 33 ladies who delivered infants with Smith-Lemli-Opitz syndrome. Twenty-four of 26 ladies whose second-trimester estriol values have been obtained had ranges in less than the fifth percentile (<0. A threat evaluation based mostly on low maternal-serum unconjugated estriol levels, normally less than 30 Prenatal Diagnosis of Congenital Disorders 425 zero. This enzyme deficiency prevents removal of the sulfate molecule from fetal estrogen precursors, stopping conversion to estriol. The fetal phenotype depends on the extent of the deletion, with greater than 90% of circumstances presenting as X-linked ichthyosis. However, in about 5% of instances, there could be a deletion of contiguous genes inflicting psychological retardation. The deletion can, on occasion, extend to trigger Kallmann syndrome or chondrodysplasia punctata. The lack of estrogen biosynthesis could lead to delayed onset of labor, extended labor, or stillbirth. Prenatal prognosis for the deletion resulting in placental sulfatase deficiency and congenital ichthyosis can be carried out by figuring out the gene deletion by chromosomal microarray or fluorescence in situ hybridization. These embody a simian crease, a brief femur or humerus, clinodactyly, and excessive nuchal skin. Similarly, the in utero analysis of Down syndrome can be suspected when certain associated anomalies or bodily options are noted on an ultrasound examination. Certain of those anomalies, such as atrioventricular canal defect or duodenal atresia, strongly recommend the potential for Down syndrome and are unbiased indications for invasive testing. The ratio of the prevalence of those markers in Down syndrome fetuses to their prevalence in the regular population will result in a probability ratio that can be utilized to modify the a priori age or serum screening danger. A record of available markers and their chance ratios are seen in Box 30-1 and Table 30-7, respectively.

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Prenatal diagnosis is feasible in lots of circumstances and must be supplied to families with a previous affected baby. Cesarean delivery is controversial and should be reserved for obstetric indications. This risk have to be weighed in opposition to frequent antepartum, intrapartum, and postpartum hemorrhagic complications, particularly after delivery. Several other methods might reduce the chance of bleeding or could additionally be used to treat bleeding after delivery in ladies with Bernard-Soulier syndrome. These problems involve deficient or irregular platelet granules or their contents. Gray platelet syndrome is brought on by a deficiency of -granules in platelets and megakaryocytes. Characteristic gray-appearing platelets are observed on the peripheral smear or marrow aspirate after staining with Romanowsky solution. Good pregnancy outcomes have been reported for sufferers with gray platelet syndrome after platelet transfusion. A case of an uncomplicated pregnancy with out remedy was reported in a affected person with Chediak-Higashi syndrome. These patients are at lifelong risk for bleeding and sometimes require frequent platelet transfusions. Cordocentesis has been particularly risky in affected pregnancies and is finest averted. In instances of identified mutations, the fetal genotype could additionally be obtained from amniocytes or chorionic villi; chorionic villus sampling ought to be averted if the patient has antibodies. The major intrapartum treatment for Glanzmann thrombasthenia is platelet transfusion. If pooled platelets must be utilized in sensitized girls, immunosuppressive remedy could delay the life span and effectiveness of the platelets. Cesarean supply must be reserved for the similar old obstetric indications, including alloimmune thrombocytopenia. The condition often remits spontaneously, with or with out the use of immunosuppressive therapy. Rarely, a heterozygous lady has medical symptoms of bleeding, perhaps because of skewed inactivation of the X chromosome containing the traditional gene. Symptoms tend to be gentle, and critical hemorrhage during labor and delivery is uncommon. Vaginal delivery has not increased bleeding in affected male infants, and a trial of labor is an affordable possibility in such circumstances. Life-threatening umbilical wire stump hemorrhage has occurred in affected newborns. Dysfibrinogenemia has been weakly associated with hypercoagulability, quite than hypocoagulability. Successful pregnancies in ladies with hypofibrinogenemia have been reported with the utilization of fresh-frozen plasma or cryoprecipitate to maintain fibrinogen levels higher than 100 to 150 mg/dL. Boehlen F, Hohlfeld P, Extermann P, et al: Platelet rely at term being pregnant: a reappraisal of the edge, Obstet Gynecol 95:29�33, 2000. Mackman N: Role of tissue factor in hemostasis, thrombosis, and vascular development, Arterioscler Thromb Vasc Biol 24:1015�1022, 2004. Falati S, Liu Q, Gross P, et al: Accumulation of tissue issue into developing thrombi in vivo is dependent upon microparticle P-selectin glycoprotein ligand 1 and platelet P-selectin, J Exp Med 197:1585�1598, 2003. Ranby M, Brandstrom A: Biological control of tissue plasminogen activator-mediated fibrinolysis, Enzyme forty:130�143, 1988. Urano T, Ihara H, Takada Y, et al: the inhibition of human issue Xa by plasminogen activator inhibitor type 1 within the presence of calcium ion, and its enhancement by heparin and vitronectin, Biochem Biophys Acta 1298:199�208, 1996. Bergqvist A, Bergqvist D, Matzsch T, et al: Late symptoms after pregnancy-related deep vein thrombosis, Br J Obstet Gynaecol 97:338�341, 1990. Rosenkranz A, Hiden M, Leschnik B, et al: Calibrated automated thrombin technology in regular uncomplicated being pregnant, Thromb Haemost 99:331�337, 2008. Epiney M, Boehlen F, Boulvain M, et al: Ddimer levels during supply and the postpartum, J Thromb Haemost 3:268�271, 2005. Ferro D, Quintarelli C, Rasura M, et al: Lupus anticoagulant and the fibrinolytic system in younger sufferers with stroke, Stroke 24:368�370, 1993. Infante-Rivard C, David M, Gauthier R, et al: Lupus anticoagulants, anticardiolipin antibodies, and fetal loss: a case-control examine, N Engl J Med 325:1063�1066, 1991. Birkenfeld A, Mukaida T, Minichiello L, et al: Incidence of autoimmune antibodies in failed embryo switch cycles, Am J Reprod Immunol 31:65�68, 1994. Stern C, Chamley L, Norris H, et al: A randomized, double-blind, placebo-controlled trial of heparin and aspirin for girls with in vitro fertilization implantation failure and antiphospholipid or antinuclear antibodies, Fertil Steril 80:376�383, 2003. Oku K, Atsumi T, Bohgaki M, et al: Complement activation in patients with major antiphospholipid syndrome, Ann Rheum Dis sixty eight:1030�1035, 2009. Erkan D, Patel S, Nuzzo M, et al: Management of the controversial features of the antiphospholipid syndrome pregnancies: a guide for 70. Jaffe R: Investigation of irregular firsttrimester gestations by color Doppler imaging, J Clin Ultrasound 21:521�526, 1993. Vallance P, Collier J, Bhagat K: Infection, irritation, and infarction: does acute endothelial dysfunction provide a link Benirschke K, Kaufmann P: Pathology of the human placenta, ed 4, New York, 1999, Springer-Verlag. Isermann B, Sood R, Pawlinski R, et al: the thrombomodulin-protein C system is important for the maintenance of pregnancy, Nat Med 9:331�337, 2003. Sood R, Sholl L, Isermann B, et al: Maternal Par4 and platelets contribute to faulty placenta formation in mouse embryos missing thrombomodulin, Blood 112:585�591, 2008. Wu O, Robertson L, Twaddle S, et al: Screening for thrombophilia in high-risk situations: systematic evaluation and cost-effectiveness analysis. Currie L, Peek M, McNiven M, et al: Is there an increased maternal-infant prevalence of issue V Leiden in association with extreme preeclampsia Lin J, August P: Genetic thrombophilias and preeclampsia: a meta-analysis, Obstet Gynecol 105:182�192, 2005. Karakantza M, Androutsopoulos G, Mougiou A, et al: Inheritance and perinatal consequences of inherited thrombophilia in Greece, Int J Gynaecol Obstet one hundred:124�129, 2008. Martinelli P, Grandone E, Colaizzo D, et al: Familial thrombophilia and the incidence of fetal development restriction, Haematologica 86:428�431, 2001. Facco F, You W, Grobman W: Genetic thrombophilias and intrauterine progress restriction: a meta-analysis, Obstet Gynecol 113:1206� 1216, 2009. Dudding T, Heron J, Thakkinstian A, et al: Factor V Leiden is associated with preeclampsia however not with fetal development restriction: a genetic affiliation study and meta-analysis, J Thromb Haemost 6:1869�1875, 2008. Wiener-Megnagi Z, Ben-Shlomo I, Goldberg Y, et al: Resistance to activated protein C and the Leiden mutation: high prevalence in patients with abruptio placentae, Am J Obstet Gynecol 179:1565�1567, 1998. Alfirevic Z, Roberts D, Martlew V: How strong is the affiliation between maternal thrombophilia and adverse being pregnant end result Carp H, Salomon O, Seidman D, et al: Prevalence of genetic markers for thrombophilia in recurrent pregnancy loss, Hum Reprod 17:1633�1637, 2002. Jivraj S, Rai R, Underwood J, et al: Genetic thrombophilic mutations amongst couples with recurrent miscarriage, Hum Reprod 21:1161� 1165, 2006. Carraro P: Guidelines for the laboratory investigation of inherited thrombophilias: recommendations for the primary degree scientific laboratories, Clin Chem Lab Med forty one:382�391, 2003. Hellgren M: Hemostasis during normal pregnancy and puerperium, Semin Thromb Hemost 29:125�130, 2003. De Stefano V, Martinelli I, Rossi E, et al: the risk of recurrent venous thromboembolism in pregnancy and puerperium without antithrombotic prophylaxis, Br J Haematol one hundred thirty five:386�391, 2006.

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If aortic stenosis is severe-and particularly if it is symptomatic-the lady should be suggested against turning into pregnant. She must be advised that, if the aortic valve had to be replaced, pregnancy and labor would be tough and harmful because of the need for anticoagulant therapy after a mechanical prosthesis is implanted. Maternal mortality charges as excessive as 17% have been reported,45 although more recent knowledge have advised a considerably lower risk. However, these studies also emphasize the opposed effects of severe maternal aortic stenosis on fetal outcomes, including elevated charges of preterm supply and intrauterine progress restriction. Left ventricular failure may appear and should necessitate the use of diuretic brokers and digitalis. Rarely, even within the presence of extreme aortic stenosis, heart failure may have another cause. Vasodilators, helpful in patients with heart failure of other etiology, are harmful in patients with aortic stenosis, as a end result of the impeded left ventricle might not be succesful of fill the dilated peripheral vascular bed. It must be remembered that the lowered systemic vascular resistance of being pregnant adversely affects aortic stenosis. The obstructed left ventricle is limited in its capability to fill the dilated peripheral bed, a situation that can lead to syncope or more critical manifestations of limited, comparatively fastened cardiac output. The lesion is normally detected in early childhood and is prone to have been corrected before the childbearing age. The venous stress is regular, but there are putting a waves within the jugular venous pulse. The pulmonary valve closure sound is often too delicate to hear when pulmonary stenosis is extreme. Right ventricular enlargement and poststenotic dilation of the main and left pulmonary arteries are seen on the chest radiograph, which additionally might present slightly diminished peripheral pulmonary vasculature. Doppler echocardiography also permits calculation of the right ventricular stress and the systolic strain gradient throughout the valve. Pulmonic stenosis is generally well tolerated, and neither pregnancy nor labor poses a big menace. Extreme pulmonary stenosis (right ventricular systolic stress > systemic systolic pressure) is a contraindication to pregnancy until the lesion is sufficiently treated. Note the ventricular septal defect, the aorta (which overrides the defect), the pulmonary stenosis, and the best ventricular hypertrophy. Copyright � 1960 by the Commonwealth Fund of the President and Fellows of Harvard College. Moreover, the offspring of a mom with tetralogy of Fallot has a 2% to 13% chance of inheriting the condition. In the everyday case, proper and left ventricular systolic pressures are equal but the pulmonary artery stress is exceedingly low. Blood shunts from left to right by way of the ventricular septal defect because its flow to the lungs is impeded by pulmonary stenosis; this results in cyanosis. Patients are normally cyanotic and infrequently have vital clubbing of the fingers and toes. Ignoring this essential therapeutic principle leads to a microcytic anemia that further complicates being pregnant. The chest radiograph is characterised by a normal-size coronary heart and a concavity within the area the place the pulmonary artery should be. As in all malformations of this basic kind, the lung fields are oligemic, displaying small vessels throughout. Significant arrhythmia and conduction defects which will finally lead to the need for digital cardiac pacing or an implantable defibrillator may happen years after an apparently profitable operation. Other sequelae and residua include solely partial reduction of the right ventricular outflow obstruction and pulmonic regurgitation. This latter downside is often properly tolerated early however may result in rightsided heart failure, necessitating reoperation. In addition, women with repaired tetralogy of Fallot and vital pulmonic regurgitation have a higher threat of decompensation throughout being pregnant. The decreased systemic vascular resistance of being pregnant causes more blood to shunt from proper to left, leaving much less to circulate to the pulmonary circulation. The most dangerous instances for these ladies are late pregnancy and the early puerperium, because venous return is impeded by the large gravid uterus close to time period and by peripheral venous pooling after supply. Blood loss throughout labor could compromise venous return, and blood volume should be promptly and adequately restored. Because of the combined excessive maternal threat and high incidence of fetal loss, being pregnant is discouraged in girls with uncorrected tetralogy of Fallot. The prognosis is particularly bleak in girls with a historical past of repeated syncopal episodes, a hematocrit level higher than 60%, or a right ventricular systolic strain higher than 120 mm Hg. If a young woman with untreated tetralogy of Fallot requests pre-pregnancy counseling, she ought to be advised to endure surgical correction before being pregnant. Visible and palpable collateral arteries in the scapular space A late systolic murmur, usually loudest over the interscapular region � Femoral pulses that lag behind the carotid pulses and are of diminished amplitude � Notching of the inferior rib borders seen on the chest radiograph and ensuing from erosion by arterial collaterals that bridge the coarctation Electrocardiographic proof of extreme left ventricular hypertrophy strongly suggests related aortic stenosis. Whenever possible, the operation must be performed earlier than being pregnant; otherwise, the maternal mortality rate is roughly 3%. Coarctation is related to congenital berry aneurysm of the circle of Willis and hemorrhagic stroke. The threat of stroke could enhance throughout labor because of transient elevations in blood stress. Patients are in danger for aortic dissection and infective endocarditis involving an irregular aortic valve; these dangers increase throughout being pregnant. Although transvascular balloon dilation of aortic coarctation is a viable option for youngsters and infants with coarctation, its use in adults is controversial. Congenital heart disease occurred in 6% of the youngsters of mothers with Ebstein anomaly. Although these sufferers appear to do nicely during childhood and younger maturity, the lesion is associated with an unexpectedly excessive mortality rate. Survival to adulthood depends on a minimal of partial correction, which may have been furnished by surgical procedure or may be a half of the malformation. For instance, in D-type transposition of the good vessels, the aorta arises from the best ventricle, and the pulmonary artery from the left. Transposition of the good vessels is now treated by anastomosis of the aorta to the morphologic left ventricle, and of the pulmonary artery to the morphologic proper ventricle. Lesions similar to single ventricle may be palliated by the Fontan process, in which venous return is related directly to the pulmonary circulation, bypassing the best facet of the guts. The deformed tricuspid valve apparatus may be significantly incompetent or stenotic, depending on the placement of the anomalously placed cusps of the valve. The medical options are easily recognized by a heart specialist, and the echocardiogram is characteristic and dependable. This syndrome is frequently associated with anomalous atrioventricular conduction pathways and with the Wolff-Parkinson-White syndrome.

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Of the 947 instances of stillbirth within the second pregnancy, 20 instances occurred in girls with a history of stillbirth (stillbirth rate, 19. The adjusted threat for stillbirth was sixfold larger in girls with a prior stillbirth. Among low-risk women, who make up the overwhelming majority of pregnant ladies, historical past of stillbirth was associated with an increased stillbirth recurrence for all subtypes of stillbirth except late stillbirths after 28 weeks. A host of sociodemographic elements have been related to an increased risk for stillbirth. Having had a minimal of one stay delivery, regardless of whether or not the girl had a being pregnant loss at lower than 20 weeks, was somewhat protective. Although a quantity of threat components that were known at the time of pregnancy affirmation were related to stillbirth, they accounted for under a small quantity (19%) of the stillbirth risk. In developed nations, infection accounts for a larger share of preterm stillbirths than of time period stillbirths. Placental and fetal infections most likely originate from both ascending or hematogenous unfold. The most common is an ascending an infection from the vagina into the area between the maternal decidua and the maternal chorion. An immune response brings inflammatory cells into the chorioamnion (chorioamnionitis), the amniotic fluid (amnionitis), the umbilical cord (funisitis), or the fetus (usually pneumonitis). Maternal systemic infections can also unfold hematogenously and attain the fetus by way of the placental villi (villitis). Bacterial pathogens implicated in stillbirth include Escherichia coli, group B streptococci, Ureaplasma urealyticum, Mycoplasma hominus, Bacteroides species, Gardnerella, Mobiluncus species, and numerous enterococci, which produce ascending infection. Parvovirus results in the clinical manifestation of fifth illness (or erythema infectiosum) in children but may be asymptomatic in adults. When parvovirus is liable for stillbirth, the mechanism is most frequently destruction of erythropoietic tissue leading to extreme anemia and hydrops. In a cohort of 1018 girls with acute parvovirus B19 during pregnancy, fetal death occurred in 6. It is a known reason for fetal and placental harm, but its position in stillbirth remains unclear. Viruses for which vaccination is routine are hardly ever implicated in fetal death in developed nations. Recently, Ljungan virus, a picornavirus of bank voles, initially isolated in Sweden, has been reported to trigger stillbirth in each Denmark and the United States. In a prospective cohort research of 1948 ladies with hypertension throughout pregnancy, the stillbirth fee for ladies with isolated continual hypertension was comparatively low and much like the speed in the common population. The hyperlink between excessive fetal growth and stillbirth in all probability entails maternal hyperglycemia resulting in fetal hyperglycemia, which in turn triggers extra fetal insulin manufacturing to maintain fetal plasma glucose levels in the physiologic range. In the fetus, insulin stimulates fetal progress, which can lead to metabolic acidosis if excessive and if the placental oxygen provide is inadequate. Outcomes of pregnancies in kind 1 diabetic girls have improved over the past a long time due to tighter glycemic management. In a prospective examine evaluating 5000 kind 1 diabetics to nondiabetic controls, the speed of stillbirth was 1. Population-based studies confirm the elevated risks for stillbirth amongst diabetic ladies. Women with type 2 diabetes had been considerably older and more obese, and so they introduced later for care than ladies with type 1 diabetes. On the opposite hand, hypothyroidism, each overt and subclinical, is relatively common, occurring in about 2. There is a optimistic linear relationship between maternal creatinine levels and stillbirth rates. The role in stillbirth of heritable coagulopathies or thrombophilias that contain deficiencies or abnormalities in anticoagulant proteins or an increase in procoagulant proteins is unclear. The only exception will be the subset of stillbirths sophisticated by placental abruption or infarction, during which there was a rise in maternal thrombophilic defects. None of the other thrombophilias had been associated with individual or composite adverse outcomes. Thrombophilias are extraordinarily common in healthy ladies with normal pregnancy outcomes. Furthermore, therapy of women with thrombophilias in subsequent pregnancies has not been confirmed to enhance obstetric outcomes. However, three antibodies, anti-Rhesus (RhD), anti-Rhc, and anti-Kell, account for the majority of fetuses with extreme disease-that is, these requiring intrauterine transfusion for fetal anemia or resulting in hydropic stillbirth. The widespread forty five Stillbirth 723 use of RhD immune globulin has resulted in a substantial discount in the incidence of RhD alloimmunization in pregnancy. Therefore, maternal alloimmunization to non-RhD antigens continues to contribute to the prevalence of stillbirth. Fetal or neonatal alloimmune thrombocytopenia outcomes from maternal alloimmunization towards fetal platelet antigens inherited from the father (and absent on maternal platelets). When extreme, fetal alloimmune thrombocytopenia (platelet rely <50 � 109/L) results in intracranial hemorrhage and stillbirth. However, an elevated threat for opposed being pregnant outcomes, corresponding to spontaneous abortion, stillbirth, and fetal development restriction, happens in 15% to 20% of affected pregnancies. Structural Anomalies About 25% of stillborns have detectable structural anomalies as fetal causes of demise. Findings are variable and include amputations, constrictions, clefts, and deformations. Fetomaternal Hemorrhage Fetomaternal hemorrhage, the transplacental passage of fetal blood cells to the maternal circulation, has been attributed as the cause of about 4% of stillbirths. Acute fetomaternal hemorrhage leads to extreme fetal anemia, in the end resulting in cardiovascular decompensation, stroke, disseminated intravascular coagulation, and stillbirth. In distinction, continual bleeding is related to persistent hypoxia resulting in neurologic impairment or stillbirth. A massive fetomaternal hemorrhage will cause extreme fetal anemia and in some circumstances fetal death because of exsanguination. A transfusion of greater than 25% of fetal blood quantity (20 mL/kg or greater) has been related to excessive charges of stillbirth (26%) as well as with neonatal anemia requiring transfusion (21. Fetuses dying at earlier gestational ages are additionally extra severely progress restricted. It is a clue that should immediate evaluation for related circumstances, similar to preeclampsia or placental insufficiency, rather than being a analysis itself. Vasa previa happens when submembranous fetal vessels cross the endocervical os, and it might trigger stillbirth on account of rupture of fetal vessels during labor or rupture of membranes, resulting in fetal exsanguination. Fetal blood may move by way of the vagina rather than coming into the maternal circulation.

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In contrast, sufferers with collateral-dependent pulmonary blood move have severely hypoplastic or absent pulmonary arteries, an absent ductus arteriosus, and multiple aortopulmonary collaterals seen with shade flow imaging of the aortic arch. Patients with ductaldependent pulmonary blood circulate may undergo neonatal placement of an aortopulmonary shunt. Those patients with collateral-dependent pulmonary blood flow face a much more difficult course, requiring case-specific medical and surgical administration, and a a lot more guarded prognosis. The mixture of an augmented proper ventricular stroke volume and absent ductus arteriosus causes the department pulmonary arteries to dilate aneurysmally. With important stretch of the tricuspid valve annulus, tricuspid regurgitation may trigger proper atrial enlargement. In addition, elevated proper ventricular diastolic strain contributes to right atrial enlargement. Many infants with out respiratory compromise have a great long-term prognosis,221-223 albeit with multiple pulmonary valve replacements throughout a lifetime. Those infants with out respiratory compromise want detailed echocardiographic and medical analysis to determine the appropriate timing for surgical intervention. The pulmonary artery similarly arises completely or partly from the best ventricle. As with different cardiac lesions, pulmonary stenosis generally coexists with pulmonary artery hypoplasia, and aortic stenosis commonly coexists with aortic arch hypoplasia and coarctation of the aorta. Management and prognosis differ broadly, relying on details of the anatomy and pathophysiology. As a end result, systemic venous return passes from proper atrium to proper ventricle to aorta, and pulmonary venous return passes from left atrium to left ventricle to pulmonary artery. Instead, the pulmonary artery arises from the left ventricle and heads posteriorly, and the aorta arises from the proper ventricle and heads superiorly to give off the top and neck vessels earlier than becoming a member of the descending aorta at the isthmus. The ductus arteriosus ought to be evaluated with 2D imaging and colour or spectral Doppler for proof of ductal constriction. The systemic venous return passes from right atrium to left ventricle to pulmonary artery, and the pulmonary venous return passes from left atrium to right ventricle to aorta. Imaging of the outflow tracts demonstrates absence of crossing of one outflow over the other. The aortic valve, arising anterior to and leftward of the pulmonary valve, provides rise to the aorta, which heads superiorly. In distinction, the pulmonary valve, arising posterior to and rightward of the aortic valve, gives rise to the pulmonary artery, which heads posteriorly. Pulmonary stenosis or atresia is detectable with 2D and colour circulate imaging and may have an effect on the event of the primary and department pulmonary arteries. Finally, heart block could develop at any time prenatally or after start and could also be documented with 2D imaging, spectral Doppler, or M-mode analysis (see later discussion). Such associated abnormalities have an result on the prenatal and postnatal presentation, management, and prognosis. However, the presence of any related abnormalities might require neonatal or subsequent medical or surgical intervention. All patients require close clinical, echocardiographic, and electrocardiographic evaluation postnatally. Longterm prognosis varies widely, but, with out surgical procedure, all patients stay in danger for heart failure and arrhythmias because of their systemic right ventricle. The double-switch operation carries important danger up entrance but enables the left ventricle to turn into the systemic ventricle. Truncus arteriosus represents a posh conotruncal malformation wherein a single arterial trunk arises from the heart and offers rise to the systemic, pulmonary, and coronary circulations. Truncus arteriosus arises from irregular development of the truncal ridges and aortopulmonary septum and carries a powerful affiliation with DiGeorge syndrome. The pulmonary arteries arise from the truncal root either as a standard major pulmonary artery. The tricuspid valve, associated with the right ventricle, inserts extra apically onto the ventricular septum than does theright-sidedmitralvalve. In truncus arteriosus, blood from the pulmonary arteries is prograde from the truncal root. The single most important association with truncus arteriosus is DiGeorge syndrome. After supply, all sufferers require shut scientific and echocardiographic analysis, in addition to analysis for DiGeorge syndrome. Long-term prognosis is dependent upon the associated abnormalities and truncal valve perform but can be quite good if all goes properly. This section evaluations two of the commonest cardiac tumors seen within the fetus: rhabdomyoma and intrapericardial teratoma. Readers could seek the guidance of other sources for more detailed discussions of fetal cardiac tumors. By far the most typical fetal cardiac tumor,230,231 cardiac rhabdomyoma might occur as an isolated, single cardiac mass or, extra commonly, as a set of well-circumscribed tumors. In a considerable share of cases, cardiac rhabdomyomas occur as one manifestation of tuberous sclerosis. Most cardiac rhabdomyomas manifest as echogenic, homogeneous, well-circumscribed masses in or extending partially into the ventricular free wall or ventricular septum or both. Rarely, cardiac rhabdomyomas reside predominantly in the walls of the right or left atrium. The fetus with suspected cardiac rhabdomyomas ought to be evaluated thoroughly for tuberous sclerosis, presumably together with sonography, magnetic resonance imaging, or genetic testing. As a result, long-term prognosis, from a cardiovascular standpoint, is great if no vital rhythm, ventricular dysfunction, or hemodynamic obstruction manifests during the late fetal or neonatal intervals. Cardiac rhabdomyomas typically regress or stay steady in size postnatally,232,233 in contrast to different tumors, which may grow considerably after supply. The intrapericardial teratoma might be the second most typical major fetal cardiac tumor. Histologically, the intrapericardial teratoma represents a mixture of cystic areas, lined by varied types of epithelium, surrounded by stable areas composed of muscle, nerve, pancreas, cartilage, thyroid, or bone tissue. Intrapericardial teratomas typically come up from the ascending aorta and secrete fluid into the pericardial area. The analysis of intrapericardial teratoma may be suspected in the fetus with a pericardial effusion along side a heterogeneous, cystic mass with areas of calcification that arises from the ascending aorta. Affected fetuses require close observation and may profit from pericardiocentesis for progressive enlargement of the pericardial effusion and worsening tamponade. After supply, mass impact of the tumor could impede cardiac output or cause respiratory compromise by compressing the trachea or mainstem bronchi. Long-term prognosis after expeditious, early resection is superb, with little likelihood for recurrence.

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