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Online ISSN (İngilizce)
1305-3124

Basılı ISSN (Türkçe)
1300-5251

Online ISSN (Türkçe)
1305-3132

Kuruluş
1993

Editör
Cihat Şen

Yardımcı Editörler
Murat Yayla, Oluş Api

Ductus venosus in the management of multiple pregnancies

Alexandra Matias, Nuno Montenegro

Künye

Ductus venosus in the management of multiple pregnancies. Perinatoloji Dergisi 2005;13(2):s47-50

Yazar Bilgileri

Alexandra Matias,
Nuno Montenegro

  1. Department of Obstetrics and Gynecology, S. João Hospital, Medicine Faculty of Porto- Porto PR
Yazışma Adresi

Alexandra Matias, Department of Obstetrics and Gynecology, S. João Hospital, Medicine Faculty of Porto- Porto PR,

Yayın Geçmişi

Yayınlanma Tarihi: 01 Nisan 2005

Çıkar Çakışması

Çıkar çakışması bulunmadığı belirtilmiştir.

Giriş

While accounting for only 2.5% of the population, twins are responsible for 12.6% of the perinatal mortality. Inthe particular case of monochorionic twinning the fetal loss rate is even more relevant and there is an increasedrisk of adverse perinatal outcome. Therefore targeted surveillance of monochorionic twins at earlier stages ofgestation could anticipate and provide timely management of the pregnancies at risk of one of the most devastating type-specific complications: twin-to-twin transfusion syndrome (TTTS).
Twin-to-twin transfusion syndrome (TTTS) is the most common complication of monochorionic twin pregnancies, affecting approximately 10% of all such pregnancies (Cincotta and Fisk, 1997). With an estimated18.000 monochorionic births per year in the United States, roughly 2000 of these patients will be affected with TTTS. By way of intertwin vascular connections, blood is transfused from the donor, who becomes growth-restricted and develops oligohydramnios, to the recipient, who develops circulatory overload andresponds with polyuria resulting in polyhydramnios. Ultimately this reflects a circulatory imbalance.
The consensus is that monochorionic monoamniotic placentas and 95-98% of monochorionic diamniotic placentas have anastomoses. A paucity of vascular anastomoses, especiallly if the overall flow is unidirectional,increases the risk for the development of TTTS due to uncompensated arteriovenous flow from recipient todonor (Bajoria et al, 1995). Certain vascular patterns may be more common in monochorionic twins developing TTTS but other factors including discordant/asymmetrical chorion development must also be considered.

√ Nuchal Tanslucency

Data gathered from the literature show that increased nuchal translucency thickness (NT) at 10-14 weeks ofgestation was found twice as much as in monochorionic than in singleton pregnancies, and the likelihood ratioof developing twin-to-twin transfusion syndrome in those twins with increased NT was 3.5 (Sebire et al, 1997,2000). Considering that monochorionic pregnancies do not show a higher prevalence of chromosomal abnor-malities, the higher prevalence of increased NT in those twins could be ascribed to cardiac dysfunction. Withadvancing gestation, this transient heart failure eventually resolves with increased diuresis and ventricular compliance.
It would clearly be a major advance if the sequence of events could be anticipated as early as the first trimesterof pregnancy based on indirect signs of haemodynamic compromise (Matias et al, 2000, 2005). But can the characteristic circulatory imbalance of TTTS, fully expressed later in pregnancy, disclose indirectsigns of cardiac dysfunction in early stages of gestation? √

Ductus Venosus Flowmetry

Ductus venosus (DV) is a fetal structure shunting the blood from the umbilical vein to the inferior vena cavaand foramen ovale, bypassing the hepatic circulation (Montenegro et al, 1997a). This structure enables thewell-oxygenated blood originating from the placenta to course almost directly to the left atrium, and thence tothe left ventricle and ascending aorta, favouring flow to the fetal brain and trunk.
Alterations in the fetal venous return blood flow have been described during the second and third trimesters ofpregnancy in association with hemodynamic deterioration, namely in cases of absent or reversed end-diastolic(ARED) flow in the umbilical artery (UA), end-stage fetal hypoxia or increased right ventricular afterload(Kiserud et al, 1994), or in the presence of cardiac anomalies (Kiserud et al, 1993). It is well recognised, however, that in most forms of major structural heart defect, fetal well-being is not markedly affected and overtevidence of cardiac dysfunction is not a usual finding. In hearts with markedly impaired diastolic function, atrial contraction occurs against increased impedance to forward flow. The proportion of blood ejected retrogradely into the great veins is greater than when ventricular filling is unimpaired and this explains the transient flow reversal in the ductus venosus that constitutes the negative A-wave.
The introduction of transvaginal Colour Doppler ultrasound has allowed venous return assessment in early latefirst- and second-trimesters of human pregnancy. Vascular haemodynamics studies from our group in fetuseswith increased NT at 10-14 weeks demonstrated that abnormal flow in DV was more frequently recorded infetuses with chromosomopathies (Montenegro et al, 1997b, Matias et al, 1998), with or without cardiac defects(Areias et al, 1998, Matias et al, 1999), probably related to heart strain. These findings are in good agreementwith the overt haemodynamic alterations found in TTTS later in pregnancy (Matias et al, 2000, 2005).Therefore, strong evidence suggests that increased NT along with abnormal flow in the DV, even in the presence of a normal karyotype, may be early signs of cardiac impairment or defect (Montenegro et al, 1997b,Matias et al, 1998, 1999) (Figures 1 and 2).
During a four-year period 55 monochorionic diamniotic pregnancies were identified in our Ultrasound Unitduring routine ultrasonographic assessment at 11-14 weeks of gestation. Nuchal translucency and Dopplerblood flow waveforms in the DV were recorded in both twins between 11-14 weeks of gestation. TTTS wasrecorded in those fetuses which combined increased NT and abnormal flow in the DV. Until now, in all caseswith both discrepant NT and abnormal blood flow in the DV, TTTS eventually developed. Whenever NTs werediscrepant but with normal flow in the DV, no cases of TTTS were found (Figures 1 and 2).
Acute polyhydramnios/oligohydramnios sequence in the second trimester of pregnancy occurred in four out of 55 cases of monochorionic twin pregnancies. Three cases shared two characteristics: increased NT thickness inat least one of the fetuses and abnormal DV flow. In the fourth case, though NTs were similar, there wasabnormal flow in the ductus venosus of one fetus. In the other 15 cases, in which one of the fetuses presented increased NT thickness but normal flow in the DV, no signs of TTTS were recorded throughout pregnancy.The remaining cases with normal NT and normal findings in the DV were uneventful. In one case, NTs werediscrepant and DV flow was abnormal in one of the fetuses, but only growth discordance >20% was detected atbirth.
It is widely accepted that alterations in cardiac hemodynamics leading to cardiac failure are accuratelydescribed by alterations in venous blood flow waveform patterns: the abnormal pulsatility pattern consists ofincreased velocity of blood flow away from the heart during atrial contraction and has been reported in thefetus with heart failure (Montenegro et al, 1997b, Matias et al, 1998, 1999). Further transmission of the venouspulsations into the portal and umbilical circulations correlates with increasing cardiac compromise. The moststriking feature is the reduced or reversed velocity during atrial contraction in the DV. In fetuses with congenital heart defects, growth restriction and TTTS as well as in our series this particular haemodynamicalteration seems to reflect impaired cardiac performance and appears as a sign of ominous prognosis.
Hecher and coworkers (1995 a, b) found highly pulsatile venous waveforms in the recipient with fully established TTTS. Umbilical vein pulsations correlated to atrial contraction and absent or reversed flow duringatrial contraction in the DV are signs of congestive heart failure due to hypervolemia and increased preloadfrom placental vascular anastomotic transfusion. Zosmer et al proposed that cardiac dysfunction may beinduced in utero by sustained strain upon the heart by TTTS, predominantly affecting the right ventricle, and, in fact, some surviving twins of TTTS show a persistent right ventricular tract obstruction (functional pulmonary stenosis) and pulmonary hypertension in the neonatal period, which may be aggravated by systolicright ventricular dysfunction. Diastolic abnormalities were also described in the right ventricle, with abnormalfilling patterns, prolonged isovolumic relaxation time and abnormal flow patterns in the inferior vena cava andductus venosus.
Our results are in good agreement with the evidence that increased NT thickness along with abnormal flow inthe DV, even in the presence of a normal karyotype, may be early signs of cardiac impairment or defect.Following the same rationale, the underlying haemodynamic changes associated with TTTS may manifest asincreased NT thickness in the recipient between 10 and 14 weeks of gestation (Matias et al, 2000, 2005) as aconsequence of heart failure due to hypervolemia. With advancing gestation, this transient heart failure mayresolve due to increased diuresis and ventricular compliance. This is not surprising with the sphincter-like ductus venosus being known as a crucial distributor of well-oxygenated umbilical venous blood to the coronaryand cerebral circulations. In fact, DV appreciation as a regulatory shunt can add valuable information to fetalvenous haemodynamic evaluation. Blood flow in the ductus venosus is characterised by high velocity duringventricular systole (S-wave) and diastole (D-wave) and the presence of forward flow throughout the cardiaccycle. Only in the presence of cardiac failure, with or without cardiac defects, when end-diastolic pressurebecomes elevated, does atrial systole produce large atrial pressure waves and cause reversal in the atrial waveform of ductus venosus(5,7,9). The issue of safety at such a vulnerable gestational period as the first trimester of pregnancy should be mentioned. The Pulsed Doppler mode has the highest energy output, but combining it with much lower energyoutput modes, such as Colour Doppler and Power Doppler, the identification of vascular structures is easier andthe time of fetal exposure to the ultrasound beam will be shorter. As bone ossification is incipient at this stageof pregnancy, the danger of aggressive thermal effects is reduced.
Until now we could only been able to diagnose TTTS in monochorionic pregnancies when fully established by identifying the disparity in fetal size and amniotic fluid volume between donor and recipient. Howeverobstetrical management might be more efficacious if TTTS could be screened in earlier stages of pregnancy. It may well be that the combination of discrepant NT and abnormal venous return at 11-14 weeks of gestationin monochorionic twins represents the warning sign predictive of the subsequent development of TTTS. The usefulness of both first trimester clues should be further investigated in a large multicenter collaborative study.Only then, assessment of both NT and DV flow would turn out to be clinically significant and motivate theultrasonographer to undertake a closer surveillance of these twins highly prone to develop TTTS. Therefore,positive screening could facilitate timely therapeutic strategies and thus improve outcome of these high riskpregnancies.

Acknowledgments:We are indebted to Dr. Matos Cruz and Alexandra Cadilhe (S. Marcos Hospital, Braga) forreferring some of the monochorionic twin pregnancies for assessment at 11-14 weeks. Cases 48, 49 and 50were a courtesy of Dr. Maria Augusta Rebordão from Garcia d´Orta Hospital (Almada). Case 50 was kindlygranted by Dr. Carlinda Cruz and Dulcínea Ramada from Vila da Feira Hospital
Anahtar Kelimeler

 

 

Kaynaklar

1. Cincotta RB, Fisk N. Current thoughts on twin-twin transfusion syndrome. Clin Obstet Gynecol 1997; 40 (2): 290-302
2. Bajoria R, Wigglesworth J, Fisk NM. Angioarchitecture of monochorionic placentas in relation to twin-twin transfusion syndrome. Am J Obstet Gynecol 1995; 172: 856-63 
​3. Sebire NJ, D’Ercole C, Hughes K, Carvalho M, Nicolaides KH. Increased nuchal translucency thickness at 10-14 weeks of gestation as a predictor of severe twin-to-twin transfusion syndrome. Ultrasound Obstet Gynecol 1997; 10: 86-9 
4. Sebire NJ, Souka A, Skenton H, Geerts L, Nicolaides KH. Early prediction of severe twin-to-twin transfusion syndrome. Hum Reprod 2000; 15: 2008-10 
5. Matias A, Montenegro N, Areias J.C. Anticipating twin-twin transfusion syndrome in monochorionic twin pregnancy. Is there a role for nuchal translucency and ductus venosus blood flow evaluation at 11-14 weeks? Twin Res 2000, 3: 65-70 
6. Matias A, Ramalho C, Montenegro N. Search for hemodynamic compromise at 11-14 weeks in monochorionic twin pregnancy: is abnormal flow in the ductus venosus predictive of twin-twin transfusion syndrome? J Perinatol 2005 (in publication)
7. Montenegro N, Matias A, Areias JC, Barros H. Ductus venosus revisited: a Doppler blood flow evaluation in the first trimester of pregnancy. Ultrasound Med Biol 1997a; 23: 171-6
8. Kiserud T, Eik-Nes SH, Blaas HG, Hellevik LR, Simensen B. Ductus venosus blood velocity and the umbilical circulation in the seriously growth retarded fetus. Ultrasound Obstet Gynecol 1994; 4: 109-14
9. Kiserud T, Eik-Nes SH, Hellevik LR, Blaas HG. Ductus venosus blood velocity changes in fetal cardiac diseases. J Matern Fetal Invest 1993; 3: 15-20 
10. Montenegro N, Matias A, Areias JC, Castedo S, Barros H. Increased nuchal translucency: possible involvement of early cardiac failure. Ultrasound Obstet Gynecol 1997b; 10: 265-8 
11. Matias A, Montenegro N, Areias JC, Brandão O. Anomalous venous return associated with major chromosomopathies in the late first trimester of pregnancy. Ultrasound Obstet Gynecol 1998a; 11: 209-13
12. Matias A, Gomes C, Flack N, Montenegro N, Nicolaides K.H. Screening for chromosomal defects at 11-14 weeks: the role of ductus venosus blood flow. Ultrasound Obstet Gynecol 1998b; 12: 380-384 
13. Areias JC, Matias A, Montenegro N, Brandão O. Early antenatal diagnosis of cardiac defects using transvaginal Doppler ultrasound: new perspectives? Fetal Diagn Ther 1998; 13: 111-4 
14. Matias A, Huggon I, Areias J.C, Montenegro N, Nicolaides KH. Cardiac defects in chromosomally normal fetuses with abnormal ductus venosus blood flow at 10-14 weeks. Ultrasound Obstet Gynecol 1999; 14: 307-310 
15. Hecher K, Campbell S, Doyle P, Harrington K, Nicolaides K (1995a). Assessment of fetal compromise by Doppler ultrasound investigation of the fetal circulation. Arterial, intracardiac and venous blood flow velocity studies. Circulation 1995; 91: 129-38 
16. Hecher K, Ville Y, Snijders R, Nicolaides KH. Doppler studies of the fetal circulation in twin-to-twin transfusion syndrome. Ultrasound Obstet Gynecol 1995b; 5: 318-24 
17. Zosmer N, Bajoria R, Weiner E, Rigby M, Vaughan J, Fisk N. Clinical and ecographic features of in utero cardiac dysfunction in the recipient twin-to-twin transfusion syndrome. Br Heart J 1994; 72: 74-79
Dosya / Açıklama
Figure 1.
A monochorionic biamniotic twin pregnancy was established at 12 weeks of gestation (case 3). Doppler bloodflow waveforms in both fetuses were obtained in the umbilical vein (UV) and ductus venosus (DV) in the same scan. Anuchal translucency (NT) discrepancy was noted (NT=3.7/1.0 mm). The fetus with increased nuchal translucency shows aninverted A-wave in the DV and dicrote pulsatility in the UV. TTTS developed at 17 weeks and the patient was referred forlaser ablation of anastomosis (with permission from Twin Research).
Figure 2.
A monochorionic biamniotic twin pregnancy was established at 12 weeks of gestation (case 1). Doppler bloodflow waveforms in both fetuses were obtained in the ductus venosus (DV). A discrete nuchal translucency (NT) discrepancywas noted (NT=3.3/3.7 mm). The fetus with the highest nuchal translucency shows an inverted A-wave in the DV and laterdeveloped signs of TTTS at 18 weeks of gestation.