Placental Structure, Circulation, and Function
The placenta has a pancake-like appearance, with 2 sides:
- Basal plate (maternal side):
- Divided into lobes
- Separated by septa
- Chorionic plate (fetal side):
- Contains branching chorionic villi, providing a massive surface for exchange
- Umbilical cord emerges from the fetal side of the placenta.
- Basal plate (maternal side):
- Membranes (by delivery they have fused into a single membrane):
- Umbilical cord:
- 2 arteries: carry deoxygenated fetal blood to the placenta
- 1 vein: carries oxygenated blood back to the fetus
- Chorionic villi provide a large surface area for maternal–fetal exchange.
- Spiral arteries (maternal) fill the intervillous spaces in the decidua basalis layer of the endometrium:
- Bring in oxygenated blood for fetus
- These spiral arteries “rupture” and become large spaces called lacunae, which:
- Are extremely low-resistance areas
- Do not have the ability to regulate blood flow through the organ
- 2 umbilical arteries bring deoxygenated blood from fetus to placental chorionic villi
- Gas and molecule exchange occurs between the fetal blood in the chorionic villi and the maternal blood in the lacunae, across the placental barrier (see below for layers).
- 1 umbilical vein transports oxygenated blood back to the fetus.
- Maternal veins take deoxygenated blood back to the maternal circulation.
- Maternal and fetal blood never come into direct contact.
- Fetal hemoglobin has ↑ affinity for oxygen compared to maternal hemoglobin → causes O2 to move from maternal RBCs to fetal RBCs.
The placental barrier is a selectively permeable membrane separating the maternal and fetal blood. The barrier is comprised of the following layers:
- Maternal lacunae containing free-flowing maternal blood
- Cytotrophoblast (later fuses with the syncytiotrophoblast)
- Basal lamina of trophoblast (later fuses with that of villi)
- Extraembryonic mesenchyme
- Basal lamina of the vessels endothelial cells in the tertiary chorionic villi
- Fetal vascular endothelial cells
Functions of the placenta
The table lists the many critical functions of the placenta for the fetus.
|Primary functions||Important details|
|Waste product removal|
|Immune system rejection||Creation of an immunologically privileged site|
Steps in placental development:
- Implantation begins 7–9 days after fertilization.
- Fetal cells involved in placental formation:
- Cytotrophoblast: the outer layer of cells of the blastocyst
- Outer layer of cells of the blastocyst in contact with the uterine wall
- Invade uterine wall
- Have lost their outer membranes and are simply “nuclei” floating in cytoplasm, eating their way into the uterine wall
- Trophoblastic villi begin to form from invaginations of cytotrophoblast into the space created by the syncytiotrophoblast.
- On the maternal side, lacunae are created from ruptured maternal blood vessels in the decidua basalis layer of the endometrium:
- Engulfed by syncytiotrophoblast
- Fill the spaces surrounding the chorionic villi with maternal blood
- The trophoblastic villi begin creating a branching tree-like structure for nutrient and gas exchange:
- Primary chorionic villi: form from the invagination of cytotrophoblast cells into the maternal lacunae
- Extraembryonic mesenchyme invades the core of primary villi, creating secondary villi.
- Blood vessels differentiate within the secondary villi, creating tertiary villi.
- These vessels ultimately connect to fetal umbilical vessels, later forming the umbilical cord.
- Villi become increasingly more concentrated opposite to the endometrial cavity, forming the chorion frondosum.
The umbilical cord connects the fetus to the placenta. The cord contains 2 arteries and 1 vein and extends from the fetal umbilicus to the fetal surface of the placenta.
Umbilical cord structure
- Contains 2 arteries and 1 vein
- Vessels are surrounded by a protective substance called Wharton’s jelly.
- Counted by sonographic evaluation, with the 3 vessels seen in the 1st trimester
- Coiling: The vein and arteries spiral around each other.
- Blood flow:
- Umbilical vein supplies oxygenated blood to the fetus.
- Umbilical arteries take deoxygenated blood away from the fetus.
- Cord length:
- Average: 40–70 cm
- Depends on amniotic fluid volume and fetal mobility.
- Insertion into the placenta:
- Normal: central insertion
- Eccentric, marginal: the cord inserts on the edge of the placenta.
- Velamentous: occurs when the last portion of the umbilical cord lacks the protective Wharton’s jelly, leaving the umbilical vessels exposed
- Clinical relevance of abnormal insertion: may increase the risk of complications during labor and/or delivery, like umbilical cord rupture and/or antenatal hemorrhage
The amniotic cavity is a fluid-filled cavity that encases the developing embryo/fetus; the fluid is called amniotic fluid.
- Development: the amniotic cavity appears on day 8 of gestation as amniotic fluid collects between cells of the epiblast and trophoblast.
- An avascular, tough but pliable membrane
- 1 of the 2 primary fetal membranes (along with the chorion; these 2 layers ultimately fuse together)
- Develops from a layer of epiblast cells (in the bilaminar embryonic disc)
- Functions of the amnion:
- Involved in solute and water transport required for amniotic fluid homeostasis
- Produces bioactive compounds
- Amniotic fluid:
- Liquid that surrounds the embryo and fetus during its development
- As the fetus grows, it “creates” amniotic fluid via urination, and continually “recycles” the fluid by swallowing it.
- Congenital defects in swallowing and/or the renal/urinary system can lead to abnormalities in amniotic fluid volume.
- Functions of the amniotic cavity:
- Protects fetus against trauma
- Protects umbilical cord against compression
- Nutrient reservoir for the fetus
- Provides adequate space for normal fetal growth and development (especially the limbs and lungs)
Placenta and Childbirth
- The delivery of the placenta constitutes the 3rd stage of labor.
- As the newborn is delivered, the uterine cavity undergoes contraction, causing separation of the placenta.
- As separation begins, a hematoma is formed between the uterine decidua and the placenta → detaches it from the uterine wall
- Once completely loose, the placenta is removed through the birth canal, which can occur via:
- Passive management: Natural uterine contractions expel the placenta.
- Active management: provider applies gentle downward traction on the clamped umbilical cord while providing countertraction with firm suprapubic pressure:
- Avoid downward fundal pressure during placental delivery, which can lead to uterine inversions.
- Gentle downward traction prevents tearing of the umbilical cord.
- Active management is usually recommended to reduce hemorrhage risk.
- Signs the placenta is ready to deliver:
- Lengthening of the umbilical cord
- Gush of blood
- Uterus becomes more globular.
- Placenta previa: abnormal attachment of the placenta in the lower uterine segment, which can obstruct (partially or completely) the internal cervical os. Maternal and fetal hemorrhage can result from cervical dilation. Placenta previa classically presents as painless bright red vaginal bleeding and is diagnosed by ultrasonography. Patients are treated with pelvic rest (avoiding digital exams and intercourse) and are delivered via C-section prior to the onset of labor (or emergently if there is clinical bleeding).
- Vasa previa: situation in which the vessels of the umbilical cord traverse the internal cervical os. Often these vessels are not surrounded by the protective Wharton’s jelly (velamentous cord insertion) and can rupture easily, leading to maternal and fetal hemorrhage. Vasa previa is diagnosed with ultrasonography. The potential for vasa previa (and/or placenta previa) is the primary reason why it is imperative to know the location of the placenta prior to performing a digital cervical exam. These infants must be delivered via C-section prior to the onset of labor.
- Placenta accreta, placenta increta, and placenta percreta: abnormal implantation of the placenta into the uterine wall. In placenta accreta, villi invade to the myometrium. In placenta increta, villi penetrate deeper into the myometrium. In placenta percreta, villi reach the uterine serosa and/or invade other organs. These conditions are diagnosed by ultrasonography. Women with these conditions are delivered via planned C-section, often with concurrent hysterectomy (especially in cases of increta and percreta because full removal of the placenta, and thus cessation of hemorrhage, may be impossible).
- Placental abruption: premature separation (partial or complete) of the placenta from the uterine wall before delivery of the infant. Abruption is primarily a clinical diagnosis based on a presentation with painful contractions with or without bleeding (look for a history of trauma or other risk factors) with characteristic findings on fetal monitoring and tocometry. Large abruptions may be seen on ultrasonography, but smaller ones frequently are not. Management depends on the gestational age and size of abruption; significant abruptions require immediate delivery.
- Hydatidiform moles: spectrum of placental disorders resulting from abnormal placental trophoblastic growth. Hydatidiform moles range from benign molar pregnancies to neoplastic conditions discovered postpartum, such as choriocarcinoma. Diagnosis is confirmed by high serum β-hCG levels and characteristic ultrasound findings. Management is primarily through dilation and curettage and/or with methotrexate.
- Polyhydramnios: excess amniotic fluid, diagnosed on ultrasonography. Polyhydramnios may lead to an increased risk of preterm labor, premature rupture of membranes, umbilical cord prolapse (when membranes rupture), placental abruption, and fetal malpresentation (e.g., breech). Most mild cases are idiopathic or associated with maternal diabetes; however, other causes may include obstruction in the fetal GI tract (e.g., esophageal atresia), neuromuscular disorders that affect swallowing, aneuploidy, or high cardiac output states (e.g., arteriovenous shunting).
- Oligohydramnios: low levels of amniotic fluid, diagnosed on ultrasonography. Causes of oligohydramnios include uteroplacental insufficiency (e.g., preeclampsia), medications (e.g., ACEis), placental thrombosis, fetal growth restriction, and congenital anomalies associated with urine production. Many cases are due to poor circulation through the placenta, which increases the risk of poor fetal lung, brain, and musculoskeletal development, preterm birth, and other pregnancy complications.
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