**3.1 Pathology of fetal weight develpoment**

In about 10% of monochorionic twins, there is an uneven distribution of placental tissue between the fetuses and therefore a pathological increase in the weight of one fetus from the second trimester of pregnancy.

### *3.1.1 Twin to twin transfusion syndrome (TTTS)*

In the placenta of monochorionic twins there are vessels - anastomoses on the surface of the placenta. Through these vessels there is an uneven distribution of blood between the two embryos, with one embryo receiving much more blood than the other. As a result, there is a difference in amniotic fluid, with the bigger fetus having increased amniotic fluid and the smaller fetus having very little fluid. TTTS observed only in monochorionic twin pregnancies due to the existence of vascular anastomoses and therefore common fetal circulation. In this syndrome there are intraplacental arteriovenous anastomoses (and more rarely arterial–arterial anastomoses without arteriovenous anastomosis), in which the blood deviates from one twin (donor) to another (recipient). Its incidence is 4 to 35% of monochorionic pregnancies and it shows high rates of perinatal mortality>50%. The diagnosis is ultrasound, usually between 16 and 26 weeks. 1 in 10 monochorionic twins will develop TTTS syndrome [34–40]. However, vascular anastomoses occur in>95% of monochorionic pregnancies. After some time, the twin recipient fetus shows great growth for gestational age (macrosomia, organomegaly), is profuse and hydropic and shows polycythemia, hypertension, congestive heart failure and hydramnios. The donor shows anemia and hypovolemia and, ultrasound, shows growth restriction and oligohydramnios. In TTTS, detected by some of the above characteristic manifestations from the first weeks of the second trimester, the perinatal mortality of both twins is almost 100%. Along with previous ultrasound findings, the hydropic placenta was described as the first manifestation of TTTS. The intense hydramnios of the recipient could be treated with drainage amniocentesis, which may result in>50% survival for both twins. Often, a drainage amniocentesis is sufficient but a repeat amniocentesis may be required. In recent years, with the help of embryoscopy, laser anatomy of the anastomoses is performed. The procedure involves a risk of miscarriage/premature birth at a rate of 10–15% within the next 6 weeks of surgery [34–38]. However, after this operation, an increased incidence of congenital heart disease was reported in both recipient and donor twins. Rarely, there may be similar development of twins and a normal amount of amniotic fluid in both sacs. Selective termination of a pregnancy is one of the possible "therapies." Ιnterventions (along with hydramnios drainage and photocoagulation of anastomoses) with a potentially increased risk of other pregnancies from possible embolism. It has been argued that the donor's death will stop the transfusion into the recipient while in the recipient killing there is a risk of increased resistance to the vascular network of the placenta, which will burden the already anemic donor. Dying of a fetus has the most serious risk of diffuse intravascular coagulation (usually after a few weeks). An extreme manifestation of TTTS is the presence of a normal anatomically

twin donor ("twin pump" [TP]) who usually has a large heart and signs of heart failure (resulting in mortality>50%) and "transfuses" blood (with arterial–arterial placental anastomosis). In a cardiac receptor twin (1% of monochorionic twin births) that does not have a direct vascular connection to the placenta (twin reversed arterial perfusion [TRAP]). The Acardiac twin (AT) recipient usually has other, very serious, anatomical abnormalities (Acardiac monster) (may be brainless or headless) while the normal fetus (if it survives) after birth usually has, remission of signs of heart failure. Transfusion from fetal donor to embryo recipient is done through anastomoses especially through arterial artery and less venous anastomoses in the placenta. The etiology of TRAP syndrome is reported to be either non-conformation of the fetal heart or reversal of blood flow leading to heart aplasia. In a continuing pregnancy, with TRAP, 1–2 times a week ultrasound monitoring of AT is recommended to look for hydrops. With the same frequency, Doppler should be performed in the DA to look for abnormalities of the umbilical artery, umbilical vein and venous pore. Given the increased risk of preterm birth, corticosteroids should be administered between 24 and 34 weeks of gestation (WG). As a prenatal treatment, amniotic fluid (due to coexistence and hydramnios) was removed in the past, the cardiac duct was removed by "caesarean section" (uterine cross-section) or alcohol was administered into the umbilical cord of the AT. Today, among other treatments (waiting or delivery), an attempt can be made to block the umbilical cord circulation of the cardiac twin (BUCCT). In particular, between 18 and 27 WG, BUCCT can be performed using laser, bipolar diathermy or the use of "radiofrequency ablation (RFA]), which are performed under local anesthesia and administration ofconscious sedation. Usually, under ultrasound control, a 2–3 mm fetoscope is inserted into the amniotic cavity (). An alternative but less common method is embryonic umbilical cord ligation [34–40]. Finally, there is a significant risk of structural abnormality in monochorionic twins, with 4% of cases the abnormality concerns only one of the two fetuses. TTTS syndrome is a complication that affects only monochorionic twins and is the most common cause of fetal loss and disability in monochorionic twins. It is characterized by a significant difference in amniotic fluid between the two embryos, increased amniotic fluid around the recipient fetus and minimal amniotic fluid around the donor fetus. The cause of the development of the syndrome is placental vascular anastomoses between the two fetuses. TTTS syndrome occurs in the early stages of pregnancy, when delivery is not an option because the fetuses are still very premature. Therefore, there is significant mortality and morbidity without therapeutic intervention, with possible miscarriage or fetal loss of one or both fetuses [34–40].

#### **3.2 Complications in dichorionic twins**

### *3.2.1 Intrauterine growth restriction (IUGR)*

In a 20% of dichorionic twins there is a significant difference in their development, with one of the fetuses not developing well. Probable cause is placental insufficiency in one of the two placentas. This probability is more common when the difference in the development of twins exceeds 18–20% [34–40].

#### *3.2.2 Structural anomaly*

The risk of structural abnormality does not increase in dichorionic twins. But since they are two babies, the chance of a structural abnormality in pregnancy, at least in one of the two babies, is twice as high as in a single pregnancy [34–40].
