An In-Depth Examination of Umbilical Cord, Fetal Membranes and the Amniotic Fluid

The umbilical cord is typically attached to the center of the fetal surface of the placenta, but it can also be attached at other points such as the edge of the placenta or the membrane known as velamentous insertion. As the amniotic cavity expands, the amnion wraps around the umbilical cord to create an epithelial covering.

The umbilical cord is usually 1-2 cm in diameter and has a length of 30-90 cm (with an average length of 55 cm). Cords that are either too long or too short are rare occurrences. Long cords have a tendency to either prolapse or coil around the fetus. It is crucial to promptly recognize and address cord prolapse, as the cord can become compressed between the fetus and the mother's bony pelvis. This compression can result in fetal hypoxia or anoxia, which, if it lasts for more than 5 minutes, can cause mental retardation in the fetus.

The umbilical cord is composed of two arteries and one vein, surrounded by mucoid connective tissue known as Wharton's jelly. The umbilical vessels are longer than the cord itself, giving them a spiral and thickened appearance. These thickened areas can form knots, which are usually harmless. However, in 1% of births, true knots can form that may lead to fetal death due to lack of oxygen. Additionally, in 1/5 of births, the umbilical cord may coil around the fetus or the fetus's neck, posing a risk to the fetus.

In about one in 200 newborns, only one umbilical artery is present in the cord. This condition can be associated with fetal anomalies, particularly cardiovascular abnormalities. The absence of an artery is typically caused by the agenesis or degeneration of the vessel during early development.

The amnion, a membranous sac filled with fluid, surrounds the embryo and later the fetus. It is attached to the edges of the embryonic disc, with the junction located on the ventral surface after the embryo curls.

Amniotic fluid is secreted by amniotic cells, but most of it comes from the interstitial fluid of maternal tissue, diffusing along the amniochorionic membranes of the parietal decidua. As the pregnancy progresses, fluid also diffuses through the chorionic plate from the blood of the intervillous space of the placenta. Before the skin keratinizes, water and dissolved substances from the fetus pass into the amniotic cavity through the skin, making the amniotic fluid similar to fetal tissue fluid.

The fetal respiratory tract also secretes a portion of amniotic fluid, with a daily rate of 300-400 ml.

Starting from the 11th week, the fetus contributes to the accumulation of amniotic fluid by eliminating urine. In advanced pregnancy, around half a liter of urine is added per day.

The volume of amniotic fluid gradually increases, reaching 30 ml at 10 weeks, 350 ml at 20 weeks, and 700-1000 ml at 37 weeks.

The amniotic fluid undergoes changes every three hours. It passes through the amniochorionic membrane into the maternal tissue fluid and enters the uterine capillaries. Fluid exchange also occurs between the fetal blood and the amniotic fluid through the umbilical cord and the site where the amnion adheres to the chorionic plate on the fetal surface of the placenta. This ensures that the amniotic fluid is in balance with fetal circulation.

The fetus swallows the amniotic fluid, which is then absorbed by the fetal digestive and respiratory tract. In the later stages of pregnancy, the fetus can swallow up to 400 ml of amniotic fluid per day. The fluid enters the fetal bloodstream, and its metabolic byproducts cross the placental membrane and enter the intervillous space. Excess water from the fetal blood is excreted by the fetal kidneys and returned to the amniotic sac through the fetal urinary tract.

Oligohydramnios, a condition characterized by low levels of amniotic fluid (400 ml in the third trimester), is often caused by placental insufficiency and decreased fetal blood flow. Premature membrane rupture occurs in approximately 10% of pregnancies and is frequently a result of oligohydramnios. When there is renal agenesis or urinary tract obstruction, the amount of fetal urine secreted decreases, leading to oligohydramnios.

Polyhydramnios, a condition characterized by increased amounts of amniotic fluid (over 2000 ml), occurs when the fetus does not swallow the normal amount of amniotic fluid. Severe central nervous system abnormalities, such as meroanencephaly, are often associated with polyhydramnios. In other abnormalities, such as esophageal atresia, the fetus is unable to swallow the amniotic fluid, resulting in its accumulation. The amniotic fluid moves between maternal and fetal circulation, particularly through the placental membrane. The fluid swallowed by the fetus enters its gastrointestinal tract but can also enter the lungs and then reenter the maternal circulation through the placental membrane.

Amniotic fluid serves several important functions for the normal development of the fetus. It allows the embryo to move freely as it is suspended by the umbilical cord. The fluid promotes symmetrical growth of the embryo and acts as a barrier against infections. It also facilitates the development of the fetal lungs and gastrointestinal tract and prevents the amnion from adhering to the embryo. Additionally, the amniotic fluid protects the embryo from impacts and helps regulate fetal body temperature. It also allows the fetus to move freely, aiding in the development of its muscles.

However, approximately 10% of pregnancies experience premature rupture of the amniocorionic membranes. This is the most common cause of premature births and the main complication of oligohydramnios. When the amniotic fluid is absent, the fetus loses its protection against infections. The rupture of the amnion leads to various fetal anomalies that make up the amniotic band syndrome complex. These anomalies can range from digital or limb constrictions to major defects in the scalp, craniofacial, and visceral regions. The constriction caused by amniotic bands is likely responsible for these anomalies. The incidence of amniotic band syndrome (ABS) is approximately 1 in 2000 live births.

The yolk sac, which is connected to the midgut by a narrow yolk stalk, undergoes early development as described in previous chapters. During the fifth week, it becomes visible by ultrasound along with the amnion, allowing for early recognition and measurement of the embryo. However, by 20 weeks, the yolk sac is usually very small and not easily visible. Ultrasound can continue to detect the yolk sac until the end of the first trimester.

The yolk sac serves several functions. Firstly, it plays a role in transferring nutrients to the embryo during the second and third weeks of gestation. Additionally, vessel development initiates in the yolk sac wall from the third week and continues until liver hematopoiesis begins in the sixth week. In the fourth week, the dorsal part of the yolk sac becomes incorporated into the embryo as the primitive gut. The endoderm of the yolk sac gives rise to the epithelium of the trachea, bronchi, lungs, and digestive tract. Lastly, primordial germ cells appear in the yolk sac wall during the third week and later migrate to the developing gonads. These cells differentiate into germ cells, specifically spermatogonia in males and oogonia in females.

The yolk sac is initially found in the chorionic cavity between the amnion and the chorionic sac at ten weeks gestation. As the pregnancy progresses, it gradually shrinks and eventually disappears. However, in rare cases, it may persist throughout the pregnancy, appearing as a small structure near the umbilical cord insertion on the fetal surface of the placenta. This persistence does not have any clinical significance. The yolk stalk typically separates from the midgut by the end of the sixth week. Nevertheless, in about 2% of adults, the intraabdominal proximal part of the yolk stalk remains as a diverticulum known as Meckel's diverticulum.

Its early development has been described in previous chapters. During the second month, the extraembryonic umbilical portion of the allantois degenerates. Although the allantois is not functional in human embryos, it is important for the following reasons:

During the second month of development, the allantois undergoes degeneration in the extraembryonic umbilical portion. Although not functional in human embryos, the allantois plays an important role for several reasons. Firstly, blood formation begins in its wall during weeks 3-4. Additionally, its blood vessels transform into umbilical veins and arteries. Moreover, fluid from the amniotic cavity diffuses into the umbilical vessels and enters the fetal circulation through the transfer of maternal blood via the placental membrane. The intraembryonic portion of the allantois extends from the umbilicus to the urinary bladder, where it continues. As the bladder grows larger, the allantois regresses and forms a thickened tube known as the urachus. Following birth, the urachus transforms into a fibrous cord called the median umbilical ligament, which extends from the apex of the bladder to the umbilicus.

The arrangement of fetal membranes in twins can vary depending on the type of twins and when separation occurs in the case of monozygotic twins. Dizygotic twins, also known as fraternal twins, result from the fertilization of two different oocytes by two different spermatozoa. Each twin has a different genetic makeup and may or may not be of the same sex. They implant in the uterus and develop their own placenta, amnion, and chorion. The two placentas may fuse or be located very close together. In some cases, dizygotic twins may have red blood cells of two different types, indicating an exchange of red blood cells between the fused placentas.

Monozygotic twins, on the other hand, are identical twins formed from a single fertilized egg. They have the same genetic makeup and look identical as they grow. The division of the zygote at different stages of development determines the arrangement of their fetal membranes. If the separation occurs during cleavage, the monozygotic twins will implant separately and not share fetal membranes like dizygotic twins. If the division happens in the inner cell mass of the blastocyst, they will have the same chorion but separate amnions and placentas. And if the division occurs in the bilaminar germ disc, they will share the same amnion.

Due to the fusion of fetal membranes caused by the growth of the fetuses, it can be difficult to determine whether the membranous septum between twins consists of only amniotic membranes (indicating shared chorion) or fused chorions and amnions (indicating separate fetal membranes). The thickness and opacity of the septum distinguish between the two; amniotic membranes are thin and almost transparent, while chorionic membranes are thick and almost opaque.

In monochorionic twin placentas, the chorionic vessels can become connected, leading to various fetal complications.

Typically, monochorionic placentas are connected through anastomoses of the chorionic vessels, particularly the arteries, which usually do not cause significant issues. However, if one twin dies, the other may be affected by embolism, where small fragments of tissue from the deceased fetus enter the bloodstream and block blood vessels. If the blood pressure of one twin drops significantly, the other twin may experience cardiac arrest, as its heart must pump blood into both circulations.

Previously, the only solution for these situations was to wait until the healthy twin reached a viable size outside the uterus and then perform a cesarean section. However, recent advancements in surgical techniques now allow for the removal of the sick or deceased fetus, enabling the healthy twin to develop normally.

The influence of the Rh factor on pregnancy is significant. Rh factors are genetically determined surface molecules found on the plasma membranes of red blood cells. Most individuals have these molecules, making them Rh-positive (Rh+), while others do not, making them Rh-negative (Rh-). If an Rh-negative mother carries an Rh-positive fetus and fetal blood enters her circulation, she will develop antibodies against the fetal red blood cells. These antibodies are not produced during pregnancy but are induced by the fetus. However, if the same mother carries a second Rh-positive fetus, her anti-Rh antibodies can cross the placenta and destroy the fetal red blood cells, causing fetal and neonatal anemia. This condition is known as hemolytic disease of the newborn or fetal erythroblastosis. It is called erythroblastosis because the destruction of red blood cells stimulates the production of immature nucleated red cells called erythroblasts.

Hemolytic disease of the newborn can also lead to hydrops, which is the accumulation of water in the fetus and can be fatal. Additionally, the destruction of red blood cells results in the buildup of bilirubin, a degradation product of hemoglobin, in the fetal circulation. This bilirubin can reach the developing brain and cause cerebral impairment or even death. To prevent fetal erythroblastosis, Rh-negative blood can be transferred to the fetus in the uterus and to the newborn, reducing the number of cells for the maternal antibodies to destroy.

A more cost-effective preventive method involves administering anti-Rh antibodies to Rh-negative mothers immediately after the birth of each Rh-positive child. These antibodies destroy the Rh fetal red blood cells in the maternal circulation before they can stimulate the mother's immune system, thus preventing the production of anti-Rh antibodies by the mother.

References

1. Anatomia Omului, Volumul I: Embriologie; Semestrul I; Prof. univ. dr. med. Andrei Motoc; Editura „Victor Babeș”, Timișoara, 2018

2. Embriologie - Sinteze didactice; Romeo Chiriac, Anca Indrei ;Editura Fundatiei Chemarea, Iasi, 1997

3. Embriologie Umană; Lidia Chircor, Loredana Surdu;Editura Ex Ponto, Constanța, 2014

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