David Talbert

Colour Doppler energy insonation of placental vasculature in monochorionic twins: absent arterio‐arterial anastomoses in association with twin‐to‐twin transfusion syndrome

Objective To determine in vivo whether monochorionic pregnancies complicated by twin‐to‐twin transfusion syndrome are associated with absence of haemodynamically‐compensatory arterioarterial anastomoses.

Uterine artery blood flow response to correction of amniotic fluid volume

OBJECTIVE Our purpose was to investigate whether acute alterations of amniotic fluid volume affect uteroplacental perfusion. STUDY DESIGN Three groups of patients of comparable gestational age were studied in a fetal medicine referral unit: (1) eight pregnancies with severe polyhydramnios because of twin-twin transfusion syndrome undergoing therapeutic amnioreduction, (2) seven with severe oligohydramnios undergoing diagnostic amnioinfusion, and (3) six control women having invasive procedures of similar duration without manipulation of amniotic fluid volume. Color Doppler imaging was used to measure uterine artery impedance index values and quantitative blood flow before and within 15 minutes of the end of the procedure. RESULTS Quantitative flow measurements increased after amnioreduction (74% median increase of volume flow, range 22% to 329%, p < 0.01) and decreased after amnioinfusion (33% median decrease of volume flow, range 17% to 51%, p < 0.05). Impedance index values increased after amnioinfusion (25% median increase in pulsatility index, range 4% to 71%, p < 0.05) and did not alter with amnioreduction. There were no significant changes in the control group. CONCLUSION Acute changes in amniotic fluid volume alter uteroplacental perfusion. In twin-twin transfusion syndrome amelioration in uterine flow may improve fetal condition and explain in part the success of serial amnioreduction therapy.

Hydrostatic and osmotic pressure gradients produce manifestations of fetofetal transfusion syndrome in a computerized model of monochorial twin pregnancy.

OBJECTIVE In spite of recent advances in the assessment and treatment of fetofetal transfusion syndrome, its underlying mechanism remains controversial. We aimed to determine whether the clinical features of fetofetal transfusion syndrome could be explained by unidirectional or bidirectional intertwin transfusion along placental vascular anastomoses. STUDY DESIGN We constructed a dynamic computerized model of monochorial twin fetoplacental units on the basis of numerous interrelated hemodynamic, osmotic, and metabolic physiologic variables. The circulations were then linked by various combinations of direction and number of arteriovenous anastomoses. RESULTS With unidirectional anastomoses disease severity, characterized by disparity in blood solids, depended on donor arterial pressure but not on the number of anastomoses. In the chronic state water movement resulting from raised osmotic pressure in the recipient and reduction in the donor produced hydroosmotic pressure equilibrium, reducing anastomotic flow to near zero. Atrial natriuretic peptide-driven urine production was markedly increased in the recipient because of the raised vascular hydrostatic pressure component. With bidirectional anastomoses recirculation between twins reduced discordancy in colloids and hematocrit, and the clinical picture was determined by the degree of asymmetry in the number of connections. CONCLUSIONS Severe manifestations of fetofetal transfusion syndrome can be explained by unidirectional intertwin transfusion and lesser degrees by asymmetric bidirectional transfusion.

Low Amniotic Pressure in Oligohydramnios - Is This the Cause of Pulmonary Hypoplasia

The mechanism by which oligohydramnios produces lung hypoplasia is not understood. The current theory that extrinsic compression of the fetal thorax causes hypoplasia, either by inhibiting breathing movements or by squeezing out lung liquid, is not supported by observational or experimental data, or by our finding of decreased amniotic pressure around the fetus in oligohydramnios. We hypothesize that lung hypoplasia results from excess loss of lung liquid because of a reduction in amniotic pressure, and hence an increase in the alveolar-amniotic pressure gradient. The magnitude of this increased pressure gradient is calculated to exceed the small standing tracheal pressure; thus low amniotic pressure overcomes the normal laryngeal retentive mechanisms and allows a larger quantity of lung liquid to escape. In the prevention of pulmonary hypoplasia, a role is suggested for the instillation of artificial amniotic fluid to restore normal amniotic pressure.

Transmitted arterio-arterial anastomosis waveforms causing cyclically intermittent absent/reversed end-diastolic umbilical artery flow in monochorionic twins.

OBJECTIVES To characterize the phenomenon of retrograde transmission of arterio-arterial anastomosis (AAA) interference patterns on umbilical artery (UA) waveform by (a) documenting the periodicity, (b) correlation with in vivo and in vitro demonstration of AAAs and (c) reproducing these patterns by computer modelling. METHODS Monochorionic twins (MC) twins underwent placental and umbilical Doppler studies. AAAs were sought by pulse wave Doppler of their bi-directional interference pattern and confirmed by postnatal injection studies. The periodicity of transmitted patterns in the UA was determined. Determinants of the transmitted patterns were ascertained by computer modelling of physiological and fetal variables. RESULTS Among 83 prospectively studied MC twin pregnancies; a transmitted pattern was observed in 6 (7 per cent) patients for 15-114 days. This was found in 20 per cent (6/30) of smaller MC twins discordant for growth restriction but in no appropriately grown twins. It was only observed in association with AAAs validated both in vivo and in ex vivo. Computer modelling demonstrated that this pattern could be reproduced by summating end diastolic flow with a high pulsatility index in the UA in the presence of a large AAA. Consistent with this, MC twins with a transmitted pattern had larger AAAs (median diameter 4.3 mm interquartile range 4.1-5.2) compared to MC twins discordant for intrauterine growth restriction (2.1 mm interquartile range 1.5 to 2.8) (P<0.05) without a transmitted pattern. Perinatal mortality was similar in the fetuses with and without transmitted patterns (0/12 vs. 2/48 P=0.7).

Impaired Fetal Blood Gas Status in Polyhydramnios and Its Relation to Raised Amniotic Pressure

A substantial proportion of perinatal losses in polyhydramnios occur as unexplained normally formed stillbirths. In order to investigate the relationship between fetal condition and raised amniotic pressure (AP), fetal blood gas and acid-base status were determined together with AP in 22 pregnancies with polyhydramnios. At fetal blood sampling, 8 (36%) had a venous pH value and 16 (73%) a pO2 value below the reference range. Both fetal pH and pO2 were significantly negatively correlated with the degree of elevation in AP (y = 7.43 - 0.036x, r = 0.56, p = 0.006, where y = pH and x = AP z score, and y = -1.6 - 0.48x, r = 0.54, p = 0.01, where y = pO2 z score, respectively). Although some of these fetuses were hydropic, had congenital anomalies, or were from multiple pregnancies, univariate and multiple logistic regression analyses indicated that the above associations could not be accounted for by these potentially confounding variables. This work suggests that abnormal fetal blood gas status in human pregnancies with poly-hydramnios is associated with elevated AP.

Normal amniotic pressure throughout gestation

Objective To characterize amniotic pressure (AP) in pregnancies with normal amniotic fluid volume.

Changes in hemorheology with fetal intravascular transfusion

OBJECTIVE Our aim was to determine the changes in fetal hemorheologic parameters caused by fetal intravascular transfusion for alloimmune anemia. STUDY DESIGN Fetal blood samples were collected before and after 95 fetal transfusions in 31 women. Fetal hematocrit, whole-blood viscosity at a variety of shear rates, plasma viscosity, fetal fibrinogen, and fetal plasma proteins were measured. RESULTS Fetal whole-blood viscosity increased, sometimes massively, with transfusion. The rise in viscosity was principally dependent on the rise in hematocrit, with a linear rise in hematocrit producing a linear rise in the logarithm of whole-blood viscosity, but was also affected by the amount of adult plasma proteins present in the donor blood. CONCLUSIONS Rises in fetal whole-blood viscosity during transfusion can be minimized by using donor blood that has been serum depleted to a high hematocrit (> 90%) and by restricting the end hematocrit to 50% to 55%.

Pathophysiology of pressure changes during intrauterine transfusion.

Intraperitoneal and umbilical vein pressure readings were obtained during intrauterine transfusion in patients with Rh alloimmunization. In 15 nonacidotic fetuses, mean umbilical vein pressure before transfusion (4.5 mm Hg, SD = 2.3) increased by 4.6 mm Hg (delta umbilical vein pressure confidence intervals +2.8 to +6.4; p less than 0.0001) with transfusion. delta Umbilical vein pressure correlated positively with the increase in hematocrit level (r = 0.55; p less than 0.05) and negatively with gestational age (r = -0.58; p less than 0.05). Basal umbilical vein pressure was raised in the only acidotic fetus, whereas delta umbilical vein pressure was 0. Intraperitoneal pressure was recorded in 11 fetuses before and after transfusion, five of which were associated with fetal heart rate changes or preexisting ascites. Basal intraperitoneal pressure (2.5 mm Hg, confidence intervals 1.4 to 3.6) was significantly lower than basal umbilical vein pressure (confidence intervals, 3.2 to 5.8; p less than 0.02). In uncomplicated intraperitoneal transfusions, intraperitoneal pressure rose significantly (delta intraperitoneal pressure = +5.8; confidence intervals 2.9 to 8.8; p less than 0.005). In four transfusions associated with fetal bradycardia or tachycardia, delta intraperitoneal pressure (range, 16 to 26) was greater than in uncomplicated transfusions (range, 1 to 9). delta Intraperitoneal pressure was 0 in the fetus with ascites. These results implicate increases in umbilical vein pressure and intraperitoneal pressure in immediate complications of intrauterine transfusion, and support a role for intraperitoneal pressure monitoring during intraperitoneal transfusion.

When does death occur in an acardiac twin? Ultrasound diagnostic difficulties

Fetal acardia is a rare abnormality of multiple pregnancies, which is lethal for the affected fetus and can cause death in 50% of normal co-twins. Antenatal recognition with early ultrasound is essential to institute a prospective management to improve the outcome. Our communication outline the difficulties which may be encountered in ultrasound diagnosis. In particular the problem of distinguishing a fetal heart from large pulsating mediastinal vessels, which can be present in these fetuses, and the difficulty of diagnosing death in an acardiac fetus. Our report confirms that the co-twin remains at increased risk of sudden death, even without ultrasound evidence of cardiac failure or biochemical compromise. The finding in this fetus of intravascular fibrin deposits suggests the possibility of acute disseminated intravascular coagulation, not previously reported in association with an acardiac twin.