Multiple pregnancies - Course and complications

The course of multiple pregnancy

In multiple pregnancies, increased demands are placed on the woman's body: the cardiovascular system, lungs, liver, kidneys and other organs function under great strain. Maternal morbidity and mortality in multiple pregnancies increases 3-7 times compared to singleton pregnancies; the higher the order of multiple pregnancies, the higher the risk of maternal complications. Women with combined somatic diseases experience their exacerbation in almost 100% of cases.

The incidence of gestosis in women with multiple pregnancies reaches 45%. In multiple pregnancies, gestosis usually occurs earlier and is more severe than in singleton pregnancies, which is explained by an increase in the volume of placental mass ("hyperplacentosis").

In a significant number of pregnant women with twins, hypertension and edema develop due to excessive intravascular volume expansion, and they are mistakenly classified as pregnant women with gestosis. In such cases, the glomerular filtration rate is increased, proteinuria is insignificant or absent, and a decrease in the hematocrit value over time indicates an increased blood plasma volume. In these pregnant women, significant improvement occurs with bed rest.

Anemia, the incidence of which in twin pregnancies reaches 50–100%, is considered a “common” complication and is associated with an increase in intravascular volume. Since its main element is an increase in plasma volume (to a greater extent than in singleton pregnancies), the end result is a decrease in hematocrit and hemoglobin levels, especially in the second trimester of pregnancy; physiological anemia is more pronounced in multiple pregnancies. A significant increase in erythropoiesis during twin pregnancies can lead to a deficiency of iron stores in some patients and play a role in the triggering mechanism in the development of iron deficiency anemia. The best way to distinguish physiological hydremia from true iron deficiency anemia in twin pregnancies is to examine blood smears.

The course of multiple pregnancy is often complicated by growth retardation of one of the fetuses, the frequency of which is 10 times higher than that of singleton pregnancy and is 34 and 23%, respectively, for mono- and dichorionic twins. The dependence of the frequency of growth retardation of both fetuses on the type of placentation is more pronounced - 7.5% for monochorionic and 1.7% for dichorionic twins.

One of the most common complications of multiple pregnancy is premature birth, which is considered a consequence of overstretching of the uterus. Moreover, the greater the number of fetuses being carried, the more often premature births are observed. Thus, with twins, birth usually occurs at 36-37 weeks, with triplets - 33.5 weeks, with quadruplets - 31 weeks.

Complications of multiple pregnancies

Tactics of management

In multiple pregnancies, a number of complications may develop that are not typical for singleton pregnancies: twin-to-twin hemotransfusion syndrome, reverse arterial perfusion, intrauterine death of one of the fetuses, congenital developmental anomalies of one of the fetuses, conjoined twins, chromosomal pathology of one of the fetuses.

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Feto-fetal transfusion syndrome

This syndrome was first described by Schatz in 1982 and complicates the course of 5–25% of multiple monozygotic pregnancies. Perinatal mortality in FFG reaches 60–100%.

SFFG, the morphological substrate of which is anastomosing vessels between two fetal circulatory systems, is a specific complication for monozygotic twins with a monochorionic type of placentation, observed in 63–74% of monozygotic multiple pregnancies. The probability of anastomoses in monozygotic twins with a dichorionic type of placentation is no greater than in dizygotic twins.

SFFH is characterized by arteriovenous anastomoses located not on the surface, but in the thickness of the placenta and almost always passing through the capillary bed of the cotyledon. The severity of SFFH (mild, moderate, severe) depends on the degree of blood redistribution through these anastomoses.

The main trigger for the development of SFFH is the pathology of the placenta of one of the fetuses, which becomes a donor. Increased peripheral resistance of the placental blood flow leads to shunting of blood to another, so-called recipient fetus. Thus, the condition of the so-called donor fetus is impaired as a result of hypovolemia due to blood loss and hypoxia against the background of placental insufficiency. The recipient fetus compensates for the increase in the volume of circulating blood with polyuria. In this case, an increase in colloid osmotic pressure leads to excessive fluid intake from the maternal bloodstream through the placenta. As a result, the condition of the recipient fetus is impaired due to cardiac insufficiency caused by hypervolemia.

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Diagnosis of feto-fetal blood transfusion

For many years, the diagnosis of FTTS was made retrospectively in the neonatal period based on the difference in hemoglobin concentration (50 g/L or more) in the peripheral blood of twins and the difference in the birth weight of newborns (20% or more). However, significant differences in hemoglobin concentration and birth weight are also characteristic of some dichorionic twins, and in recent years these indicators have ceased to be considered signs of twin-to-twin hemotransfusion syndrome.

Based on ultrasound criteria, stages of feto-fetal hemotransfusion syndrome were developed, which are used in practice to determine pregnancy management tactics:

• Stage I - the bladder of the donor fetus is determined;
• Stage II - the urinary bladder of the donor fetus is not determined, the state of blood flow (in the umbilical artery and/or venous duct) is not considered critical;
• Stage III - critical state of blood flow (in the umbilical artery and/or venous duct) in the donor and/or recipient;
• Stage IV - hydrops in the recipient fetus;
• Stage V - antenatal death of one or both fetuses.

Pathognomonic echographic signs of severe SFFH are considered to be the presence of a large bladder in the recipient fetus with polyuria against the background of severe polyhydramnios and the “absence” of a bladder in the donor fetus with anuria, which is characterized by decreased motor activity against the background of severe oligohydramnios.

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