Acardiac Twin Pregnancies Research Articles

Twin Reversed Arterial Perfusion Sequence.

Twin Reversed Arterial Perfusion Sequence.

Acardiac twin pregnancies part VI: Why does acardiac twinning occur only in the first trimester?

BackgroundClinical observation suggests that acardiac twinning occurs only in the first trimester. In part, this contradicts our previous analysis (part IV) of Benirschke's concept that unequal embryonic splitting causes unequal embryo/fetal blood volumes and pressures. Our aim is to explain why acardiac onset is restricted to the first trimester.MethodsWe applied the vascular resistance scheme of two fetuses connected by arterio‐arterial (AA) and veno‐venous (VV) anastomoses, the small VV resistance approximated as zero. The smaller twin has volume fraction α < 1 of the assumed normal larger twin, and has only access to fraction X < 1 of its placenta; the larger twin's larger mean arterial pressure accesses the remaining fraction. Before 13 weeks, embryos have a much smaller vascular resistance than placentas. After 13 weeks, when maternal blood provides oxygen, smaller twins can increase their vascular volume by hypoxemia‐mediated neovascularization. Estimated AA radii at 40 weeks, , are 0.5–1.3 mm.ResultsEmbryos with α < 0.33 unlikely survive 13 weeks and acardiac twinning occurs under appropriate conditions (AA‐VV, small placenta). Acardiac body perfusion occurs because of a much smaller vascular resistance than the placenta. When α > 0.33 and =1.3 mm, modeled survival is >32 weeks.ConclusionBefore 13 weeks, embryos with α < 0.33 cannot survive and may result in the onset of acardia. Beyond 13 weeks, fetuses with α ≥ 0.33 survive because is too small for acardiac onset. Following fetal demise, exsanguination from the live twin increases its blood volume and, we assumed also, its vascular resistance. Perfusion then occurs through the lower resistance placenta.

Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios?

BackgroundAcardiac twinning is a complication of monochorionic twin pregnancies. From literature reports, 30 of 41 relatively large acardiac twins with renal tissue produced polyhydramnios within their amniotic compartment. We aim to investigate the underlying mechanisms that cause excess amniotic fluid using an established model of fetal fluid dynamics.MethodsWe assumed that acardiac onset is before 13 weeks, acardiacs with renal tissue have normal kidney function and produce urine flow from 11 weeks on, and acardiac urine production requires a pressure of half the pump twin's mean arterial pressure. We apply a resistance network with the pump twin's arterio‐venous pressure as source, pump umbilical arteries, placenta, placental arterio‐arterial (AA) anastomoses and acardiac resistances. Acardiac amniotic fluid dynamics excluded acardiac lung fluid secretion, swallowing and the relatively small intramembranous flow.ResultsIn small acardiacs with sufficient urine production, polyhydramnios will occur due to the lack of amniotic fluid resorption. Urine production is dependent upon having sufficient mean arterial pressure, which requires nearly a two‐fold larger resistance within the acardiac as compared to the placental AA resistance. Subphysiologic arterial pressure may result in renal dysgenesis.ConclusionOur findings suggest the potential for prediction of which clinical acardiac cases may or may not develop polyhydramnios based upon noninvasive assessments of renal tissue, blood flow and urine production. This information would be of great value in determining early obstetric interventions as opposed to conservative management. These findings may also contribute to an improved knowledge of the fascinating pathophysiology that surrounds acardiac twinning.

Akardiyak İkiz: İki Farklı Olgu İki Farklı Prognoz

A-cardiac twin pregnancy is a rare complication occurs in 1,46 %of all monochorionic twin pregnancies. The fetus whose heart and upper body haven’t been developed and the rest of the body has its blood supply from a branch of the umbilical artery can be considered a healthy fetus? . Usually the complication can be diagnosed in the end of 1st trimester and if the anastomosis of circulation isn’t separated on time, the mortality rate for the healthy fetus who has the blood pumper role will be 55 %. So the obstetric problems such as preterm delivery increase. The death for the fetus who has no heart is certain. Therefore, stopping the blood circulation of the fetus with cardiac abnormality is the main approach to prevent problems such as the lose of the healthy fetus and preterm delivery. We aim to discuss the clinical management of two cases which have been diagnosed with TRAP Twin Reversed Arterial Transfusion in their 11th week of gestation and have had totally different prognosis

Successful treatment of very PPROM caused by bipolar cord coagulation in acardiac twin

The authors report management of a woman with an acardiac twin pregnancy complicated by preterm premature rupture of the membrane (PPROM) for more than two months after intrauterine treatment with bipolar cord coagulation at 24 weeks of gestation.

Acardiac twin pregnancies part IV: Acardiac onset from unequal embryonic splitting simulated by a fetoplacental resistance model.

Benirschke postulated that acardiac twinning occurs when markedly unequal embryonic splitting combines with arterioarterial (AA) and venovenous placental anastomoses. We tested this hypothesis by model simulations and by comparison of outcomes with 18 "pseudo-" (twin fetus with beating heart but otherwise with clear signs of an acardiac) and 3 "normal" acardiac cases. The smaller/larger cell volume ratio at embryonic splitting becomes the smaller/larger embryonic/fetal blood volume ratio (a). From a, we derived nonpulsating blood pressures using normal values (larger twin) and normal values at an appropriate earlier gestational age (smaller twin). These unequal pressure sources were used in a linear resistance fetoplacental network to calculate umbilical venous diameter ratios. Acardiac onset occurs when the smaller twin has 50% left of its normal, singleton placenta. Comparison with clinical cases approximated a by crown-rump-length-ratio to the 3rd power. Input parameters are a and the AA-radius at 40 weeks. Acardiacs can be small or large, can occur early or late, earlier at smaller a and larger AA, with larger umbilical venous diameter ratios at smaller a and smaller AA. Comparison with the 21 clinical cases was good, except for 2. Our analysis supports Benirschke's hypothesis. The smaller twin has to share its placental perfusion with the larger twin, which is a novel finding. The AA size is essential for the future of both fetuses but complicates easy understanding of (pseudo-)acardiac clinical presentations. Late acardiac onset occurs infrequently. Using nonpulsating circulations may have caused our extensive predictions of late onset. An improved model requires including hypoxemia in the smaller twin from chronic placental hypoperfusion. Birth Defects Research 109:211-223, 2017. © 2016 Wiley Periodicals, Inc.

Acardiac Acephalus Twin Pregnancy with Poor Prenatal Outcomes: A Case Report

Introduction: Acardiac twin refers to a monochorionic pregnancy in which there is a twin with absent or nonfunctioning heart and a normal co-twin. This was a very rare disorder of monozygotic twin pregnancy. The aim of this report was to introduce a case of acardiac acephalus twin pregnancy. Case Presentation: A 32- year- old woman (G3 P2 L2) referred to the hospital because of a decrease in fetal movement at 32 weeks of gestation. Ultrasonography showed a dead fetus. Her earlier sonography showed the possibility of acardiac twin pregnancy, but she did not have any appropriate or special prenatal care for this problem. After delivery, there was a normal dead fetus without any gross abnormality and another acardiac fetus. Conclusions: Early diagnosis of acardiac twin pregnancy and appropriate prenatal care are of prime importance for appropriate intervention and best fetal outcomes.

Acardiac twin pregnancies part III: Model simulations.

Acardiac monochorionic twins lack cardiac function but grow by passive perfusion of the pump twin's deoxygenated arterial blood through placental arterioarterial (AA) and venovenous (VV) anastomoses and by hypoxia-mediated neovascularization. Pump twins therefore must continuously increase their cardiac output which may cause heart failure. Our aims were: to adapt our twin-twin transfusion syndrome model for acardiac twin pregnancies, to simulate pump and acardiac twin development, and to examine the model for early prognostic markers of pump twin survival. We used an infinite acardiac placental resistance, based on placental dye injection studies and simulations, suggesting the AA-Acardiac-VV series resistance determines the pump twin's excess cardiac output. Pump and acardiac development were expressed by the pump's excess cardiac output versus its normal value, represented by pump/acardiac umbilical venous diameter (UVD) ratios. UVD ratios distinguish between AA-VV anastomoses that do and do not cause hydropic pump twins. Pump twins can handle relative larger acardiac perfusion at later than earlier gestation. Both VV and acardiac resistances are significantly smaller than the AA resistance, based on respectively clinical data and acardiac blood volumetric growth. Our simulations support clinical results which show that UVD ratios aid in the prediction of pump twin risk. The AA anastomosis controls the future of both the pump and the acardiac. Correlation between acardiac size and pump twin risk is secondary to the AA size but remains clinically usable. These factors may aid in the development of methods for pump twin prognosis and the promotion of selective clinical interventions.Birth Defects Research (Part A), 2016.© 2016 Wiley Periodicals, Inc. Birth Defects Research (Part A) 106:1008-1015, 2016. © 2016 Wiley Periodicals, Inc.

Akardiyak ikiz gebelikte intrafetal lazer tedavisi: Olgu sunumu

Akardiyak ikiz gebelikte intrafetal lazer tedavisi: Olgu sunumu

Acardiac twin pregnancy: successful intrauterine ablative treatment with alcohol at 14 weeks of gestation

Twin reversed arterial perfusion (TRAP) sequence is a serious condition of monochorionic twin pregnancy, occurring in approximately one in 35,000 cases. First trimester treatment of TRAP sequence is controversial with higher incidence of procedure related complications. Present case demonstrates a TRAP sequence that was managed by intrauterine treatment with one ml 100% pure alcohol injection into the abdominal part of the umbilical artery and obliteration of the acardiac twin at 14 weeks of gestation. Antenatal follow-up was uneventful and elective cesarean section was performed at 39 weeks’ gestation. Postnatal outcome of the pump twin was excellentat 30 months after birth. Early second trimester elective ablation by alcohol injection can be an inexpensive, alternative, and reasonable minimal invasive treatment option to prevent fetal loss of pump twin before mid and late second trimester in perinatology centers where intrafetal cord occlusive methods are not available.

Akardiyak ikiz gebelikte intrafetal lazer tedavisi: Olgu sunumu

Akardiyak ikiz gebelikte intrafetal lazer tedavisi: Olgu sunumu

Hypothesis acardiac twin pregnancies: Pathophysiology‐based hypotheses suggest risk prediction by pump/acardiac umbilical venous diameter ratios

A total of 75% of monozygotic twins share 1 monochorionic placenta where placental anastomoses cause several serious complications, for example, acardiac twinning. Acardiac twins lack cardiac function but grow by perfusion of arterial blood from the pump twin. This rare pregnancy has 50% natural pump twin mortality but accurate risk prediction is currently impossible. Recent guidelines suggest prophylactic surgery before 18 weeks, suggesting 50% unnecessary interventions. We hypothesize that (1) adverse pump twin outcome relates to easy-to-measure pump/acardiac umbilical venous diameter (UVD) ratios, representing acardiac perfusion by the pump's excess cardiac output. This hypothesis suggests that (2) UVD-ratios are large, mildly varying in cases without complications but small and decreasing when complications develop, thus predicting that (3) UVD-ratios may allow risk prediction of pump twins. In this exploratory clinical pilot, we tested whether UVD-ratio measurements support these predictions. We included 7 uncomplicated (expectant management), 3 elective surgical, and 17 complicated cases (pump decompensation, emergency intervention/delivery or demise). Nine UVD-ratios were measured sonographycally and 18 by pathology. Uncomplicated cases have larger, two serial measurements showing mildly varying UVD-ratios; elective surgical cases show larger UVD-ratios; complicated cases have smaller, two serial measurements showing decreasing UVD-ratios. There were no false-positives, no false-negatives and noncrossing linear trendlines of uncomplicated and complicated cohorts. Our data provide first evidence that UVD-ratios allow risk prediction of pump twins. More early uncomplicated and late complicated cases are needed, for example, in a prospective trial, before the separation between uncomplicated and complicated cohorts is accurate enough to support a well-founded decision on (early) intervention.

A case of acardiac twin pregnancy with fetus survival after successful radiofrequency ablation of umbilical cord

Acardiac twin is a rare anomaly that occurs 1% in monochorionic twins and 1 in 35,000 pregnancies overall. Acardiac twin, also known as twin-reversed arterial perfusion (TRAP) sequence, involves a “pump” or donor twin perfusing a recipient or “acardiac” twin through vascular (usually arterial–arterial and venous–venous) anastomoses. Perinatal mortality rate for the pump twin has been reported to be 50~75%, mainly as a result of polyhydramnios, preterm labor, and congestive heart failure. Therefore, occlusion of the circulation to the acardiac twin has been recommended to improve perinatal outcome of the pump twin. Radiofrequency ablation of the acardiac twin effectively protects the pump twin from high-output cardiac failure and death. We report our experience in the treatment of patients with TRAP sequence using radio frequency ablation to stop perfusion to the acardiac twin.

Twin Reversed Arterial Perfusion Syndrome: the Role of Ultrasound in Diagnosis and Management

Acardiac twin pregnancies are a rare but severe complication of monochorionic twinning. This complication occurs in 1% of monozygotic twin pregnancies or 1 in 35 000 births. The anomaly arises due to superficial artery-to-artery placental anastomoses leading to reversed perfusion from the donor or pump twin to the acardiac twin. It is postulated that as a consequence of the hypoxic environment within the recipient fetus there is secondary atrophy of the heart and other organs. The acardiac twin has no chance of survival and it is kept alive by its structurally normal twin. The presence of the acardiac twin can adversely affect outcome in a number of ways. First, a growing parasitic mass can increase the cardiovascular demands on the pump twin leading to congestive heart failure and polyhydramnios. The continued growth of the acardiac twin can increase the intrauterine volume and this increased uterine mass effect may lead to preterm delivery. Finally, blood returning from the acardiac twin to the pump twin is deoxygenated which may lead to chronic hypoxia and growth restriction in the donor fetus. The perinatal mortality rate for the pump twin is approximately 50%. The twin reverse arterial perfusion sequence can be quite variable in its presentation and outcome. The role of ultrasonography is central to making the initial diagnosis, determining the prognosis, optimizing the time of intervention and follow up of treatment.

Modeling Acardiac Twin Pregnancies

Acardiac twin pregnancies are a rare but severe complication of monochorionic twinning, where the acardiac twin lacks cardiac function but nevertheless grows during pregnancy because it is perfused by the pump twin through a set of placental arterioarterial and venovenous anastomoses. Because the acardiac twin's body is only perfused by the pump twin's arterial blood, acardiac twins have reduced blood oxygen saturation (SO(2)) levels. Furthermore, the pump twin has reduced blood oxygen saturation because the anastomoses merge the blood of the two twins. We suggested that angiogenesis from hypoxia mediated neovascularization increases the capillary density in the acardiac twin and causes a continuously decreasing vascular resistance of the acardiac body. The pump twin therefore has a continuously increasing cardiac output and decreasing oxygen saturation, which may cause a vicious circle of increasing levels of pump twin complications, often leading to intrauterine fetal death. Our aim in this article was twofold. First, to summarize our previous modeling work of acardiac twin pregnancies, and add an estimate of the capillary density in mammals at different levels of SO(2) from a literature search on angiogenesis related to SO(2), Hypoxia Inducible Factor, and Vascular Endothelial Growth Factor. Second, to speculate that combination of these efforts and our most recent model of monochorionic twin pregnancies and twin-twin transfusion syndrome may result in an improved computational model for acardiac twin pregnancies, aimed at identifying early clinical prognostic markers for pump twin complications.

Successful Intrauterine Treatment with Alcohol Ablation in a Case of Acardiac Twin Pregnancy

Acardiac twinning is a rare obstetric condition unique to monochorionic twin gestation and the pump twin has high perinatal mortality. We report an acardiac twin pregnancy, in which the pump twin presented with intrauterine growth restriction and oligohydramnios, and grossly hydropic acardiac fetus measured 12 x 14 x 18 cm, and with no cardiac activity at 27 weeks of gestation. We treated the acardiac fetus with 1 ml alcohol ablation in utero, and delivered a live male baby weighing 1750 g at 36 weeks' gestation.

Increasing cardiac output and decreasing oxygenation sequence in pump twins of acardiac twin pregnancies

An acardiac twin pregnancy is a rare but serious complication of monochorionic twinning and consists of an acardiac twin and a pump twin. The acardiac twin is a severely malformed fetus that lacks most organs, particularly a heart, but grows during pregnancy because it is perfused by the developmentally normal pump twin via a set of arterioarterial and venovenous placental anastomoses. Pump twins die intrauterine or neonatally in about 50% of the cases. Because the effects of an acardiac mass on the pump twin's development are incompletely known, methods for outcome prognosis are currently not available. We sought to derive simple relations for the pump twin's excess cardiac output and decreased oxygenation and to use available clinical cases for a preliminary test of the model. As a method, we used a theoretical flow model to represent the fetoplacental circulation of an acardiac twin pregnancy and estimated blood deoxygenation and reoxygenation following perfusion of the two bodies and placentas, respectively. The results show the pump twin's excess cardiac output and decrease of venous oxygen saturation to depend on the ratio of pump twin to acardiac twin umbilical blood flow, whose ratio can be measured by ultrasonography. The clinical cases show a decreasing umbilical flow ratio with gestation. In conclusion, prospective serial study is necessary to test whether measurement of umbilical flow ratios allows monitoring the pump twin's pathophysiologic development, possibly resulting in a guideline for prognosis of pump twin survival.

Haemodynamic resistance model of monochorionic twin pregnancies complicated by acardiac twinning

An acardiac twin is a severely malformed monochorionic twin fetus that lacks most organs, particularly a heart. It grows during pregnancy, because it is perfused by its developmentally normal co-twin (called the pump twin) via a set of placental arterioarterial and venovenous anastomoses. The pump twin dies intrauterine or neonatally in about 50% of the cases due to congestive heart failure, polyhydramnios and prematurity. Because the pathophysiology of this pregnancy is currently incompletely understood, we modified our previous haemodynamic model of monochorionic twins connected by placental vascular anastomoses to include the analysis of acardiac twin pregnancies. We incorporated the fetoplacental circulation as a resistance circuit and used the fetal umbilical flow that perfuses the body to define fetal growth, rather than the placental flow as done previously. Using this modified model, we predicted that the pump twin has excess blood volume and increased mean arterial blood pressure compared to those in the acardiac twin. Placental perfusion of the acardiac twin is significantly reduced compared to normal, as a consequence of an increased venous pressure, possibly implying reduced acardiac placental growth. In conclusion, the haemodynamic analysis may contribute to an increased knowledge of the pathophysiologic consequences of an acardiac body mass for the pump twin.

The management of acardiac twins: a conservative approach

Objective Optimal management of acardiac twin pregnancies is controversial. Data suggest a 50% mortality rate in the “pump” twin when the pregnancy is managed expectantly. Because of increased antenatal diagnosis, outcomes in expectantly managed cases may be better than reported. Our objective was to determine the outcome of expectantly managed acardiac twin pregnancies. Study design All cases of antenatally diagnosed acardiac twins delivered in our community between 1994 and 2001 were ascertained. All were managed expectantly. Perinatal outcome of pump twins was the primary outcome variable. Results Ten cases were identified. Nine women were delivered of healthy pump twins. There was one neonatal death. The mean gestational age at delivery was 34.2 weeks. The mean weights of the pump and acardiac twins were 2279 g and 1372 g, respectively. Conclusion Neonatal mortality of pump twins in antenatally diagnosed acardiac twin pregnancies may be considerably less than reported. Expectant management with close antepartum surveillance deserves consideration.

Acardiac twin: a misdiagnosed, mismanaged case

Acardiac twins are usually diagnosed during the antenatal period and almost invariably cause complications to the other fetus. In this case, an acardiac twin pregnancy was misdiagnosed antenatally as a degenerated myoma but ended with delivery of a healthy baby.