Placenta, Cord, and Membranes




KEY TERMS



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Key Terms




  1. Basal plate: maternal surface of placenta.



  2. Chorioangioma: benign tumors arising from the fetal surface of the placenta.



  3. Chorionic plate: fetal surface of placenta.



  4. Complete placenta previa: occurs when the placenta completely covers the internal os.



  5. Extrachorial placenta (circummarginate and circumvallate): attachment of placental membranes to the fetal surface of the placenta rather than the villous placental margin.



  6. Low-lying placenta/low implantation: occurs when the inferior placental edge is within 2 cm of the internal cervical os.



  7. Placental abruption: separation of a normally implanted placenta.



  8. Succenturiate placenta: the presence of one or more accessory lobes separate from the main placental body.



  9. Trophotrophism: a dynamic process of placental remodeling where areas with poor vascularity atrophy and areas of good perfusion grow.



  10. Uterine synechia (amniotic sheets): broad-based tissue that extends into the amniotic cavity but is external to the amnion and chorion.



  11. Vasa previa: occurs when fetal vessels that run in the fetal membranes cross the internal cervical os.





INTRODUCTION



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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.




DEVELOPMENT OF THE PLACENTA: EMBRYOLOGY



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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




Figure 7-1.


Three portions of the decidua (basalis, capsularis, and vera or parietalis) are illustrated. Diagram shows the relation of the amniotic cavity to decidua and chorion before fusion. (Reproduced with permission from Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics, 23rd ed. New York: McGraw-Hill, 2010.)






Figure 7-2.


A: Intradecidual sign. The gestational sac (dark circle) does not deform the central uterine cavity and is embedded within the decidua. B: Double decidual sac sign. The gestational sac (dark circle) protrudes and displaces the central cavity. (Reproduced with permission from Laing FC, Brown DL, Price JF, et al. Intradecidual sign: is it effective in diagnosis of an early intrauterine pregnancy? Radiology. 1997 Sep;204(3):655-660.)





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




Figure 7-3.


Fertilization of the ovum occurs in the fallopian tube; the morula reaches the uterine cavity 3 days after fertilization. (Reproduced with permission from Moore KL, Persaud TVN, Torchia MG. The Developing Human: Clinically Oriented Embryology. 10th ed. Philadelphia: Saunders, 2016.)





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




Figure 7-4.


Erosive enzymes in the syncytiotrophoblast enable the blastocyst to completely implant and erode endometrial blood vessels. (Reproduced with permission from Moore KL, Persaud TVN, Torchia MG. The Developing Human: Clinically Oriented Embryology. 10th ed. Philadelphia: Saunders, 2016.)





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




Figure 7-5.


Chorion frondosum (fetal portion of the placenta) is anchored to maternal decidua basalis by cytotrophoblastic shell. (Reproduced with permission from Moore KL, Persaud TVN, Torchia MG. The Developing Human: Clinically Oriented Embryology. 10th ed. Philadelphia: Saunders, 2016.)






Figure 7-6.


Gestational sac. Axial view of a 5.5-week gestational sac with yolk sac (YS) and decidualized endometrium.






Figure 7-7.


A: Large subchorionic hematoma at 11+4 weeks’ gestation (arrow). B: Power Doppler reveals no active flow within the hematoma. C: Resolving subchorionic hematoma at 20 weeks’ gestation (arrow).








Figure 7-8.


A: Axial view of a first trimester pregnancy. Amniotic membrane (arrows); yolk sac (Y). B: First trimester intrauterine pregnancy with embryo (E) and amnion (arrow) identified.







Figure 7-9.


Amniotic sac fuses with the smooth chorion, forming the amniochorionic membrane. (Reproduced with permission from Moore KL, Persaud TVN, Torchia MG. The Developing Human: Clinically Oriented Embryology. 10th ed. Philadelphia: Saunders, 2016.)





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.




Figure 7-10.


Spiral arteries in the decidua basalis bathe the intervillous space with maternal blood. (Reproduced with permission from Moore KL, Persaud TVN, Torchia MG. The Developing Human: Clinically Oriented Embryology. 10th ed. Philadelphia: Saunders, 2016.)






PLACENTAL IDENTIFICATION



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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.




Figure 7-11.


Normal placental development. A: Transvaginal scan at 5.5 weeks showing gestational sac with hyperechoic rim (curved arrow) representing chorionic villi. B: Transvaginal scan at 9 weeks showing early placenta (arrow). Arrowhead, yolk sac. C: Transabdominal scan at 20 weeks showing typical diffuse granular echotexture of the placenta (P). Note relatively hypoechoic myometrium (M).







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.




Figure 7-12.


Placental calcification. A: Anterior placenta at 39 weeks contains prominent calcifications, especially in basal plate (arrows) and septa (arrowheads). (F, fetus.) B: Radiograph of tissue slice confirms presence of calcification. (Arrows indicate basal plate.) C: Photomicrograph of tissue stained for calcium shows deposits along the basal plate (arrows), in subchorionic area (arrowheads), and in perivillous space (open arrows).







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 parity8-10 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




Figure 7-13.


Placental calcification versus gestational age. (Reproduced with permission from Spirt BA, Cohen WN, Weinstein HM. The incidence of placental calcification in normal pregnancies. Radiology.1982 Mar;142(3):707-711.)






MACROSCOPIC LESIONS OF THE PLACENTA: NORMAL



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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).




Figure 7-14.


Common macroscopic lesions of the placenta. Subchorionic fibrin deposition (F) appears as laminated yellow-white plaques, sometimes associated with fresh blood. Intervillous thrombosis (I) appears as round to oval lesions varying from red to laminated white, depending on age. Perivillous fibrin deposition (P) is seen as nonlaminated plaques varying from brown to white depending on age. True infarcts (IN) appear as dark red to white nonlaminated lesions adjacent to basal plate.





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.




Figure 7-15.


Subchorionic fibrin deposition. A: Sagittal scan at 21.5 weeks shows multiple subchorionic anechoic/hypoechoic lesions (arrows). B: Transverse scan 90 degrees to central lesion in (A) showing subchorionic lesion (arrows) with vessel overlying it (arrowhead). C: Gross photograph of placenta showing multiple deposits of subchorionic fibrin corresponding to lesions seen at sonography (arrows). D: Section of placenta showing laminated subchorionic fibrin deposition (arrows) corresponding to lesions in (A). Note vessel (arrowhead) overlying central lesion (B).









Figure 7-16.


Subchorionic fibrin deposition. Anterior placenta (P) with prominent subchorionic blood pooling (arrows) at 21 weeks. The complex low-level echo pattern was seen in real time to represent slow flow.






Figure 7-17.


Subchorionic fibrin deposition. A: At 21 weeks, a prominent complex subchorionic lesion with a large cystic component is seen (arrows). No flow was demonstrated within. (P, placenta.) B: At 25 weeks, the solid component was smaller (curved arrow). (Arrows, overlying cyst; open arrow, umbilical cord; F, fetus.) Gross photographs of fetal surface (C) and cross section (D) of term placenta show opened cyst (arrows) adjacent to cord insertion. The cyst was formed by the chorion and contained clear fluid and fibrin (f). E: Photomicrograph confirms that the cyst wall is made up of chorion (arrow). (f, fibrin; P, placenta.)









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




Figure 7-18.


Intervillous thrombosis. A: Two irregular-shaped intraplacental hypoechoic lesions (arrows) are seen in this anterior placenta at 33 weeks; several similar lesions were noted in this placenta. B: Laminated fibrin, characteristic of intervillous thrombosis, is demonstrated in 2 adjacent lesions (arrows) after delivery. (P, placenta; F, fetus; black arrow, umbilical cord.)






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




Figure 7-19.


Centrally located plaque of perivillous fibrin that is irregularly shaped and yellow-white in color. (Reproduced with permission from Fox H, Sebire NJ. Pathology of the Placenta, 3rd ed. Philadelphia: Saunders; 2007.)





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).




Figure 7-20.


Maternal lake. A: Anterior placenta at 21 weeks contains hypoechoic intraplacental lesion (arrow). (P, placenta; F, fetus.) B: Flow is demonstrated with color-flow Doppler.







Figure 7-21.


Maternal lake. A: Sector scan at 35 weeks showing anechoic intraplacental lesion (arrows). (P, placenta.) B: At delivery, lesion (arrow) contained blood that fell out upon sectioning.






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




MACROSCOPIC LESIONS OF THE PLACENTA: ABNORMAL



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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).




Table 7-1ABNORMAL MACROSCOPIC LESIONS OF THE PLACENTA



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




Figure 7-22.


Hydatidiform mole. A: Sagittal scan of the uterus shows a diffuse vesicular echo pattern. B: Gross specimen demonstrates multiple grapelike cysts. (Part (B) Used with permission from Dr. David Jones, Department of Pathology, SUNY Health Science Science Center at Syracuse, New York.)

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Jan 12, 2019 | Posted by in GYNECOLOGY | Comments Off on Placenta, Cord, and Membranes

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