Biomedical subjects

Asli Umur

Publications and source records attributed to Asli Umur.

7 recordsLinked to original sources

PubMed2005

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.

Abnormalities, Severe Teratoid↗

PubMed2004

Modeling a hydropic recipient twin in twin-twin transfusion syndrome.

We developed a mathematical model of twin-twin transfusion syndrome (TTTS) that includes a hydropic recipient twin, adding interstitial and intracellular fluid compartments, fetal congestive cardiac failure, and the dynamics of renin-angiotensin system (RAS) mediators to our previous TTTS model. Ten differential equations for each twin, coupled by the net fetofetal transfusion of blood and blood components, i.e., colloids, osmoles, and RAS mediators, describe the development of fetal arterial and venous blood volumes, blood osmolality and colloid osmotic pressure (COP), interstitial fluid volume and COP, intracellular fluid volume, amniotic fluid volume and osmolality, and RAS mediator concentration. We included varying placental anastomoses, placental sharing, and amnionicity. The 20 differential equations were solved numerically from 0 to 40 wk with a 0.6-s time step. Consistent with clinical experience, model predictions are as follows. Unidirectional arteriovenous anastomoses and arteriovenous anastomoses inadequately compensated by oppositely directed anastomoses cause severe TTTS that includes a hydropic recipient. Adequately compensated arteriovenous anastomoses simulated TTTS without hydrops. The probability that oppositely directed anastomoses prevent onset of a hydropic recipient after TTTS onset, i.e., the largest interval between onset of TTTS and onset of hydrops in the recipient, was best for a venovenous anastomosis, closely followed by an arterioarterial and finally an oppositely directed arteriovenous anastomosis. Hydropic recipients have decreased amniotic fluid volume. Unequal placental sharing and amnionicity modify hydrops onset. In conclusion, our model simulates a sequence of events that results in a hydropic recipient twin in severe TTTS. The model may allow an assessment of the efficacy of current therapeutic interventions for TTTS cases that include a hydropic recipient twin.

Adult↗

PubMed2004

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.

Biophysics↗

PubMed2004

Modelling the influence of amnionicity on the severity of twin-twin transfusion syndrome in monochorionic twin pregnancies.

Clinical treatment for diamniotic-monochorionic twin-twin transfusion syndrome (TTTS) may include conversion of diamniotic pregnancies to a monoamniotic-monochorionic state by disrupting the amnion septum. We sought to test the underlying hypothesis, i.e. that a monoamniotic state reduces the severity of TTTS. With use of our previously developed mathematical model of two equal fetoplacental circulatory units connected by various sizes and types of placental anastomoses, we compared the haemodynamic and amniotic fluid dynamics of monoamniotic and diamniotic twins that develop TTTS. We used three anastomotic patterns that produce severe, moderate or mild forms of TTTS, respectively, in our diamniotic-monochorionic twin model. Monoamnionicity was modelled by adding the two amniotic fluid volumes and using the volume-averaged amniotic fluid osmolality. The results were as follows: for severe TTTS, small differences develop between diamniotic and monoamniotic donor twins in fetal urine production, swallowed volume, blood volume, blood pressures, net fetofetal transfusion, and blood and amniotic fluid osmolality. However, the circulatory imbalance between the monoamniotic twins deteriorates similar to that of diamniotic twins. The pathophysiological differences tend to disappear for milder TTTS. In conclusion, our model suggests that the uncommon finding of TTTS in monoamniotic twins is not due to the presence of a single amniotic sac. Rather, clinically significant differences in anastomotic patterns and the delayed or lack of identification of manifestations in monoamniotic twins account for the reduced rate of TTTS diagnosis. Based on these results we expect the clinical disruption of the amnion septum in diamniotic-monochorionic TTTS pregnancies to have only minimal benefits.

Amnion↗

PubMed2003

Monoamniotic-versus diamniotic-monochorionic twin placentas: anastomoses and twin-twin transfusion syndrome.

OBJECTIVE: The purpose of this study was to compare monoamniotic-monochorionic and diamniotic-monochorionic twin placentas and to estimate the incidence of twin-twin transfusion syndrome in monoamniotic-monochorionic twin pregnancies. STUDY DESIGN: We analyzed the angioarchitecture and cord insertion distance in 24 monoamniotic-monochorionic and 200 diamniotic-monochorionic placentas. RESULTS: Compared with diamniotic-monochorionic placentas, monoamniotic-monochorionic placentas had significantly more arterioarterial anastomoses (20/20 vs 159/200, respectively; P=.013), significantly less opposite arteriovenous anastomoses (10/20 vs 165/200, respectively; P=.002), similar venovenous anastomoses (6/20 vs 46/200, respectively; P=.323), and arteriovenous anastomoses (20/20 vs 187/200 respectively; P=.279) and significantly shorter umbilical cord distances (median [+/-SD], 5.0+/-6.9 cm vs 17.5+/-6.8 cm; P<.001). CONCLUSION: Monoamniotic-monochorionic and diamniotic-monochorionic placentas have different anastomotic patterns. The (virtually) 100% incidence of arterioarterial anastomoses in monoamniotic-monochorionic placentas explains the reason that twin-twin transfusion syndrome rarely occurs in monoamniotic-monochorionic twin pregnancies and predicts that twin-twin transfusion syndrome manifestations are approximately 5 times less often recognized in monoamniotic-monochorionic pregnancies than in diamniotic-monochorionic pregnancies.

Amnion↗

PubMed2002

Does amniotic fluid volume affect fetofetal transfusion in monochorionic twin pregnancies? Modelling two possible mechanisms.

Clinical evidence suggests that increased amniotic fluid volume due to polyhydramnios increases placental vascular resistance. We have sought to model the possible effects of an increased amniotic fluid volume on the net fetofetal transfusion in monochorionic twin pregnancies. We wanted to compare these effects with the results of previous simulations, which aimed to explain why the twin-twin transfusion syndrome (TTTS) placentas more often include bidirectional arteriovenous (AV) rather than AV plus arterioarterial (AA) anastomoses. We extended our mathematical model of TTTS by simulating two different mechanisms that increase the placental vascular resistance as a consequence of polyhydramnios. First, there is an increase in the placental capillary resistance and hence in deep AV and opposite AV (denoted as VA) resistances due to polyhydramnios. Second, there is an increase in the resistance of chorionic veins due to polyhydramnios, assuming that these veins act as Starling resistors. We then simulated the effects of polyhydramnios on different placental anastomotic patterns. The results were as follows. In the first mechanism (polyhydramnios affects AV-VA resistances), an increased amniotic fluid volume hardly affected bidirectional AV, but slightly decreased fetofetal transfusion in AV plus AA anastomoses. However, for these effects to change the natural development of the pregnancy, polyhydramnios needed to persist for approximately 4 weeks, and by comparing the effects of polyhydramnios with the effects of amnioreduction, amnioreduction was more beneficial for normalizing the donor amniotic fluid volume. Therefore, these beneficial effects due to polyhydramnios have no practical clinical significance. In the second mechanism (Starling resistor for chorionic veins), polyhydramnios slightly increased fetofetal transfusion and hence slightly increased TTTS severity in bidirectional AV and AV plus VV, but did not affect AV plus AA anastomoses. In conclusion, we hypothesize that the simulated effects of polyhydramnios are not the primary cause of the fact that TTTS placentas more often include bidirectional AV than AV plus AA anastomoses. Rather, the more likely explanation is the previously identified larger range of AA than VA anastomotic diameters that adequately compensate for the effects of the AV.

Amniotic Fluid↗

PubMedDate not supplied

Discordant fetal growth patterns in monochorionic twin pregnancies described by simple algebraic relations.

OBJECTIVE: To test whether twin-twin transfusion syndrome (TTTS) and non-TTTS cases that were suspect but not confirmatory for developing the syndrome (non-TTTS-with-symptoms) have discordant fetal growth patterns that correlate with our previously derived algebraic relations. METHODS: In 25 monochorionic twin pregnancies, fetal growth was determined by standard ultrasonography. The difference between estimated fetal weights (dEFW) as well as the difference divided by the average of the two weights, the difference average ratio (DAR), were fitted to the predicted trends of discordant fetal growth for TTTS and non-TTTS pregnancies. The best fits were compared with the clinical data. RESULTS: Out of 13 TTTS cases, dEFW analysis correctly correlated with 8 (62%) and DAR analysis correctly with 10 (77%). Out of 12 non-TTTS-with-symptoms cases, dEFW analysis correctly correlated with 7 (58%) and DAR analysis correctly with 9 (75%). If TTTS correlated best, dEFW analysis was correct in 8/12 (67%), and DAR analysis in 10/11 (91%) cases. If non-TTTS correlated best, dEFW analysis was correct in 7/9 (78%), and DAR analysis in 9/12 (75%). The likelihood ratios of TTTS and non-TTTS were 1.9 and 0.26, respectively, with dEFW analysis, and 9.2 and 0.31 with DAR analysis. CONCLUSION: The simple algebraic relations derived to identify trends of fetal discordant growth show evidence that clinical TTTS and non-TTTS manifestations are quantifiable. The relations may contribute to future risk stratification in monochorionic twin pregnancies, e.g., by prospectively distinguishing between cases that will develop TTTS and those that will not, despite presenting with symptoms.

Chorion↗