Multiple pregnancy: course and complications

The course of multiple pregnancies

In case of multiple pregnancies, the woman's demands are higher: the cardiovascular system, lungs, liver, kidneys and other organs function with great tension. Maternal morbidity and mortality in multiple pregnancy increases in 3-7 times compared with single-fetal; while the higher the order of multi-fetus, the higher the risk of maternal complications. Women who have combined somatic diseases note their aggravation in almost 100% of cases.

The frequency of gestosis in women with multiple pregnancies reaches 45%. In multiple pregnancy gestosis, as a rule, occurs earlier and proceeds more heavily than in single-pregnancy, which is explained by an increase in the volume of the placental mass ("hyperplacenta").

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

Anemia, whose frequency in pregnant women with twins reaches 50-100%, is considered an "ordinary" complication and is associated with an increase in intravascular volume. Since its main element is an increase in the volume of plasma (more so than in single-pregnancy), the end result is a decrease in hematocrit and hemoglobin, especially in the second trimester of pregnancy; The physiological anemia in multiple pregnancy is more pronounced. A significant increase in erythropoiesis during twin pregnancy may lead to a shortage of iron stores in some patients and may play the role of a trigger mechanism in the development of iron deficiency anemia. The best way to distinguish physiological hydremia from true iron deficiency anemia in twin pregnancy is to study blood smears.

The course of multiple pregnancies is often complicated by a delay in the growth of one of the fetuses, whose frequency is 10 times higher than that of single-pregnancy and is 34% and 23%, respectively, with mono- and bichorial twins. The dependence on the type of placentation on the growth rate of both fruits is more pronounced - 7.5% for monochorionic and 1.7% for bichorial double.

One of the most common complications of multiple pregnancy is premature birth, which is regarded as a consequence of overgrowing of the uterus. In this case, the more the number of bearing fruits, the more often the premature birth is observed. Thus, in the case of double genera, as a rule, occur in a period of 36-37 weeks, with a triple - 33.5 weeks, with quadruple - 31 weeks.

Complications of multiple pregnancies

Tactics of reference

In case of multiple pregnancy, it is possible to develop a number of complications that are not characteristic of single-pregnancy: feto-fetal hemotransfusion syndrome, reverse arterial perfusion, fetal death of one of the fetuses, congenital malformations of one of the fetuses, fused twins, chromosome pathology of one of the fetuses.

[1], [2], [3]

Feto-fetal blood transfusion syndrome

This syndrome was first described by Schatz in 1982, complicating the course of 5-25% of multiple-fruited single-egg pregnancies. Perinatal mortality with SFFG reaches 60-100%.

SFFG, the morphological substrate of which is anastomosing vessels between two fetal circulatory systems, a specific complication for monozygotic twins with a monochorionic type of placentation, observed in 63-74% of single-egg multiple pregnancy. The probability of anastomosis in monozygotic twins with a bichorial type of placentation is not greater than in dizygotic twins.

For SFFG are 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 cotyledon. The severity of SFFG (mild, moderate, severe) depends on the degree of redistribution of blood through these anastomoses.

The main triggering factor of the development of SFF is the pathology of placenta development of one of the fruits, which becomes, as it were, a donor. Increased peripheral resistance of placental blood flow leads to shunting of blood to another so-called fetus-recipient. Thus, the condition of the so-called donor fetus is disrupted as a result of hypovolemia due to loss of blood and hypoxia against placental insufficiency. The recipient fetus compensates for the increase in the volume of circulating blood by polyuria. In this case, an increase in colloidal osmotic pressure leads to an excessive intake of fluid from the maternal bed through the placenta. As a result, the condition of the recipient fetus is disrupted due to heart failure due to hypervolemia.

[4], [5], [6], [7], [8], [9], [10], [11], [12]

Diagnosis of feto-fetal blood transfusion

For many years, the diagnosis of SFFG was retrospectively in the neonatal period on the basis of the difference in hemoglobin concentration (50 g / L and more) in the peripheral blood of twins and the difference in body weight of newborns (20% or more). However, a significant difference in the concentration of hemoglobin and body weight of newborns is also characteristic for some bichorial twins, and in recent years these indicators have ceased to be considered as signs of feto-fetal blood transfusion syndrome.

Based on ultrasonic criteria, the stages of feto-fetal blood transfusion syndrome were developed, which are used in practice to determine the tactics of pregnancy management:

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

The presence of a large bladder in a fetus-recipient with polyuria on the background of pronounced polyhydramnios and the "absence" of a bladder in a donor fetus with anuria, which is characterized by a decrease in motor activity against a background of marked low blood pressure, are considered pathognomonic echographic signs of severe SFF.

[13], [14], [15], [16],