The placenta, cord, and membranes are the building blocks of human pregnancy. Vast changes take place throughout pregnancy that can be followed sonographically. The placenta provides the essential connection between the mother and developing fetus. Many clinical problems are attributed to the placenta, even though they cannot always be explained after pathologic placental examination.

A thorough understanding of the anatomy of the normal placenta and its variations, as well as the pathologic conditions that are known to occur, is necessary to correctly interpret the sonographic appearance. Placental location with respect to the internal cervical os and the maternal urinary bladder will be reviewed, especially in light of the increasing cesarean delivery rate and abnormal placentation. The umbilical cord and membranes share similar developmental origins, which will be considered. Intrauterine membranes can be delineated with sonography in patients who have bleeding episodes and in uncomplicated pregnancies. Their assessment is clinically important in multifetal pregnancies.

This chapter examines the embryology of the placenta, cord, and membranes. Normal and abnormal processes of placentation and umbilical cord development will be reviewed. Pertinent clinical aspects are highlighted.

Decidual Change

The endometrium undergoes changes in preparation for embryo implantation known as the decidual reaction or decidualization, where secretory endometrium is transformed into decidua.^1,2 This change is prompted by estrogen, progesterone, and other factors secreted by the invading blastocyst.² There are 3 parts of the decidua: (1) decidua basalis, the modified portion of decidua directly beneath the implantation site; (2) decidua capsularis, the portion overlying the blastocyst; and (3) decidua parietalis, the portion covering the remainder of the endometrium (Figure 7-1). Initially, there is a gap between the decidua capsularis and decidua parietalis since the gestational sac does not fill the entire uterus.² The intradecidual sign describes the early sonographic appearance of the gestational sac that does not deform or displace the central uterine cavity (Figure 7-2A). As the gestational sac continues to grow into the central uterine cavity, the double decidual sac sign is seen (Figure 7-2B) with the echogenic decidua capsularis and peripheral decidua parietalis.³

Fertilization and Implantation

Fertilization of the ovum usually occurs in the ampulla of the fallopian tube, and the compact ball of cells or morula, containing an inner cell mass and an outer cell mass, reaches the uterine cavity 3 days after fertilization (Figure 7-3). The morula is converted to a blastocyst as fluid enters from the uterine cavity, and the blastocytic cavity is divided into 2 parts. The outer cell layer proliferates to form the trophoblast or embryonic portion of the placenta, and the inner cell mass forms the embryo.^2,4,5

The trophoblast proliferates once the blastocyst attaches to the endometrial tissues at about 6 days after fertilization and differentiates into an inner layer (cytotrophoblast) and outer layer (syncytiotrophoblast). A space in the blastocyst forms, which is the early amniotic cavity. Syncytiotrophoblastic cells secret erosive enzymes, allowing the blastocyst to completely implant and erode endometrial blood vessels by the end of the second week (Figure 7-4). Lacunae in the syncytiotrophoblast coalesce to form lacunar networks at the embryonic pole, forming the intervillous space. Chorionic villi invade the decidua basalis and enlarge the intervillous space. As maternal vessels are further eroded by syncytiotrophoblast, maternal blood bathes the lacunar network.¹

Placenta and Fetal Membranes

Differentiation of the trophoblastic cells occurs at approximately 5 days after conception into the cytotrophoblast and the syncytiotrophoblast. The syncytiotrophoblast secretes human chorionic gonadotropin and is responsible for proteolytic invasion into the decidua. As trophoblastic tissue proliferates, chorionic villi cover the entire chorionic sac. With continued sac growth, villi of the decidua capsularis are compressed and degenerate, yielding the chorion laeve, or smooth chorion, which eventually becomes the chorionic membrane. The villous chorion (chorion frondosum) or the fetal portion of the placenta is anchored to the maternal component (decidua basalis) by the cytotrophoblastic shell (Figure 7-5).⁶ The chorion frondosum can be recognized sonographically in the first trimester as a thickened region of echogenic tissue bordering a portion of the gestational sac, indicating the site of the developing placenta. As the pregnancy grows, the decidua capsularis projects into the uterine cavity and fuses with the decidua parietalis, eliminating the uterine cavity. Sonographically, this is depicted as a gestational sac (Figure 7-6). Clinically, it is important to remember that this membrane fusion is a weak attachment, and blood from the intervillous space can dissect the fused chorionic membrane away from the decidua parietalis, yielding hematoma formation (Figures 7-7A through C). The amniotic sac fuses with the chorionic leave, forming the amniochorionic membrane (Figures 7-8A and B, and 7-9).⁶

Spiral endometrial arteries in the decidua basalis bathe the intervillous space with maternal blood for nutrient and gas exchange. Endometrial veins drain this space (Figure 7-10).⁶ Deoxygenated fetal blood reaches the placenta through the 2 umbilical arteries, and oxygenated blood returns to the fetus through the single umbilical vein.

The early gestational sac is covered by chorionic villi visible by transvaginal sonography as a hyperechoic rim at about 4 to 4 1/2 weeks’ menstrual age (Figure 7-11A). The early placenta formed by proliferation of villi is seen in Figure 7-11B. By 9 to 10 weeks, the diffuse granular echotexture of the placenta is clearly apparent at sonography, and this texture is produced by echoes emanating from the villous tree, which is bathed in maternal blood (Figure 7-11C). The placenta retains this general sonographic appearance throughout the pregnancy, with the notable exception of calcium deposition.

Placental Calcification

Placental calcium deposition is common, may be extensive, and is a normal physiologic process that occurs throughout pregnancy.⁷ During the first 6 months, the calcification is microscopic; macroscopic plaques typically appear in the third trimester, most commonly after 33 weeks.^8,9 The calcium is deposited primarily in the basal plate and septa but is also found in the perivillous and subchorionic spaces.⁷ Plaques of calcium are readily detected at sonography as echogenic foci that do not produce significant acoustic shadows (Figure 7-12). The circular configuration seen in heavily calcified placentas results from septal calcifications.

Placental calcification has been studied by histologic,^10,11 chemical,¹² radiographic,⁸ and sonographic⁹ techniques with the following conclusions. The incidence of placental calcification increases exponentially with increasing gestational age, beginning at about 29 weeks (Figure 7-13).^8-10,12 More than 50% of placentas show some degree of calcification after 33 weeks.⁹ Placental calcification is more common in women of lower parity^8-10 and is probably related to maternal serum calcium levels.^7,13 Placental calcification is also more common in late summer and early fall deliveries, when maternal serum calcium levels are highest.^12,13 There is no proof that placental calcification has any pathologic or clinical significance.^7,14,15

Classification of macroscopic placental lesions can be grouped by their appearance, pathogenesis, or functional significance.⁷ As such, placental lesions may be due to (1) disturbances of maternal blood flow to or through the placenta; (2) disturbances of fetal blood flow to or through the placenta; (3) thrombi and hematomas; and (4) nonvascular lesions.⁷

Maternal blood pooling in the perivillous and subchorionic space is a normal finding visualized sonographically as anechoic or hypoechoic areas within the placenta. Slow flow can be demonstrated in these spaces. Eventually, fibrin deposition occurs. Macroscopic lesions that have been diagnosed sonographically consist of subchorionic fibrin deposition, intervillous thrombosis, perivillous fibrin deposition, and septal cysts (Figure 7-14).

Subchorionic Fibrin Deposition

A layer of subchorionic fibrin is noted in the majority of placentas.⁷ These anechoic or hypoechoic areas are visualized in approximately 15% of obstetric sonograms (Figure 7-15) and correspond to areas of subchorionic fibrin deposition between the chorionic plate and placental villi.¹⁶ Histologically, the fibrin is attached to the underside of the chorionic plate and is usually not clinically significant.⁷ Subchorionic fibrin is the result of pooling and stasis of maternal blood in the intervillous space beneath the chorion, leading to thrombosis and secondary fibrin deposition. Slow flow is often visible with real-time sonography (Figure 7-16). Subchorionic blood pooling and fibrin deposition may be quite prominent at sonography (Figure 7-17); it is important to recognize this entity so as not to confuse it with a chorioangioma.

Intervillous Thrombosis

Intervillous thromboses are intraplacental (villous-free) areas of hemorrhage, entirely within the intervillous space, with a variable gross appearance that depends on the age of the lesion.⁷ Fresh lesions are dark red, but with aging change to brown, yellow, and finally white. Usually, there are visible laminations that microscopically consist of layers of fibrin. Both fetal and maternal red blood cells are present, suggesting that a leakage of fetal cells from a villous tear stimulates maternal coagulation.¹⁷ Intervillous thromboses have a reported incidence that varies widely in the literature (3%-50%) in term, uncomplicated pregnancies.⁷

At sonography, intervillous thromboses appear as anechoic or hypoechoic intraplacental lesions that vary in size from a few millimeters to several centimeters (Figure 7-18).^18,19 No visible flow is identified sonographically. They may extend to the subchorionic space or the basal plate. These thrombi have no effect on placental function but pinpoint a site of bleeding into the intervillous space.⁷

Perivillous Fibrin Deposition

Perivillous fibrin deposition results from pooling and stasis of blood in the intervillous space. The lesions consist of nonlaminated plaques, varying in color from brown to white depending on age (Figure 7-19). Sonographically, they appear as intraplacental anechoic or hypoechoic lesions. Almost all full-term placentas contain some degree of perivillous fibrin deposition, visible macroscopically in most as fine speckling.⁷ In a percentage, the fibrin deposition is more extensive, forming a large, plaque-like lesion. Perivillous fibrin deposition and plaques are of little clinical significance.⁷

Maternal Lakes

“Maternal lakes” are frequently observed during obstetric ultrasound; they are anechoic lesions in the placenta that correspond to blood-filled spaces at delivery. This entity is not described in the pathology literature. We believe that maternal lakes represent an early stage of intervillous thrombosis and/or perivillous fibrin deposition before the fibrin is laid down. Flow can be demonstrated in some of these lesions at real-time sonography and color-flow Doppler examination (Figure 7-20). It is likely that in those lesions with particularly active flow, less fibrin is deposited so that the lesion is “empty” on gross inspection at delivery (Figure 7-21). Aberrant blood flow to the placenta may result in an increased number of maternal lakes, as has been described in cases of placenta accreta (see later discussion).

Infarcts

Placental infarcts result from a disruption or occlusion in the maternal vascular supply leading to a localized area of ischemic villous necrosis. Infarcts occur most commonly at the base of the placenta and vary in size from a few millimeters to many centimeters. Macroscopically, infarcts have a triangular shape, with the base of the triangle adjacent to the basal plate.^7,20 Although small infarcts are found in 10% to 25% of placentas of uncomplicated pregnancies, they occur with increased frequency in pregnancies complicated by preeclampsia and essential hypertension.⁷ Small infarcts affecting 5% or less of the parenchyma have little clinical significance in women with healthy parenchyma and adequate placental reserve. Extensive placental infarction is characteristic of an abnormal vascular tree and severely compromised uteroplacental circulation, and it is a reflection of maternal vascular diseases such as antiphospholipid syndrome, lupus erythematosus, and other thrombophilic entities.⁷

Placental infarcts cannot be documented at sonography unless they are complicated by hemorrhage.²¹ Maternal floor infarction is a distinct pathologic entity described in the 1960s and portrayed as a marked increase in fibrinoid deposits of the decidual floor (maternal surface) with encasement of villous tips rendering them sclerotic and avascular.^22,23 The etiology of this condition is unknown,²³ and this entity is not an infarct but a “massive basal plate fibrin deposition.”⁷ Pregnancy complications including fetal growth restriction, oligohydramnios, preterm birth, and stillbirth have been described in association with this placental lesion and may recur in subsequent pregnancies.^24,25 Maternal floor infarction is difficult to diagnose prenatally and may appear as increased echogenicity and thickening along the maternal surface of the placenta and continuing through the placental body in pregnancies complicated by fetal growth restriction and oligohydramnios.²⁵

Gestational Trophoblastic Disease

Neoplasms of the gestational trophoblast may be divided into those with villi (complete mole, partial hydatidiform mole, and coexistent mole and fetus) and those without villi (persistent trophoblastic neoplasia, including choriocarcinoma, invasive mole, and placental site trophoblastic tumor) (Table 7-1).

The complete hydatidiform mole is characterized by replacement of the placenta with enlarged, hydropic villi and the lack of an embryo. Complete moles are usually paternally derived and believed to result from abnormal fertilization of an empty ovum by either a single sperm with duplication of the paternal haploid set of chromosomes (46,XX) or 2 spermatozoa (dispermy), resulting in a heterozygous karyotype (46,XY or 46,XX).^22,27,28

At sonography, the uterus is filled with echogenic material containing multiple anechoic vesicles (bunch of grapes) of different sizes (Figure 7-22). The vesicles enlarge with advancing gestational age. Early in pregnancy, transvaginal sonography is helpful in diagnosing hydatidiform mole. A viable fetus may coexist with a complete mole in the case of a dichorionic twin pregnancy with one normal fetus and a coexisting complete mole. Elevated maternal serum β-human chorionic gonadotropin (β-hCG) levels are found with hydatidiform mole. Persistent trophoblastic neoplasia may occur in women with complete hydatidiform moles; therefore, serum β-hCG levels must be followed to ensure that they decrease to zero after evacuation of the mole, and appropriate follow-up is warranted.²⁷