ULTRASOUND EVALUATION OF THE PLACENTA AND UMBILICAL CORD

19 ULTRASOUND EVALUATION OF THE PLACENTA AND UMBILICAL CORD





PLACENTA


The placenta is a fascinating but often ignored organ that provides primary support for the developing fetus. In The Diseases and Deformaities of the Foetus (1892), JW Ballantyne wrote




The same could be said in reference to sonography and the value of sonographic assessment of the placenta. Those who perform obstetric ultrasound (US) are encouraged to study this interesting, crucial structure because significant placental pathology may be found, often before the fetus is affected. Recognition of frequent anatomic variants and clinically important lesions of the placenta is highly valuable for optimal performance and interpretation of prenatal US.


This chapter reviews normal placental and umbilical cord development and anatomy, and presents common abnormalities of the placenta (including maternal and fetal processes) and cord, as shown by US, highlighted with pathologic correlation.



Normal Development and Anatomy


The recently released ovum is normally fertilized in the fallopian tube and reaches the uterine cavity as the morula, which rapidly evolves into the blastocyst. The blastocyst, in turn, attaches to and implants in the endometrium on day 5 to 6 after fertilization.2 The outer cell layer of the blastocyst, which will become the placenta, transforms to the trophoblastic cell mass that intermixes with endometrial cells (10th postovulatory day). The trophoblast shortly thereafter differentiates into the cytotrophoblast and syncytiotrophoblast. The latter cells erode into the endometrial glands and blood vessels.


Between 10 to 13 days after ovulation, lacunae or clefts appear among the rapidly proliferating trophoblastic cell mass. These spaces form the intervillous space, the wide channels where the transfer of gases and nutrients occurs between maternal and fetal circulations (Fig. 19-1). Early on, this proliferation of villi is characterized by a hyperechoic appearance on US, although a definitive placenta is only well seen after 10 to 12 weeks. Villi form from mesenchyme, and blood vessels that sprout into the primary villous stems, which then branch into secondary and tertiary villi. Around 8 weeks’ gestation, the villi oriented toward the endometrium (now called the decidua) continue to divide and grow as the chorion frondosum. The villi toward the endometrial cavity atrophy and form a smooth surface, the chorion laeve. The chorion normally apposes with the amnion at approximately 12 to 16 weeks.



True maternal blood flow is not established until 12 weeks of gestation; before then plasma (not blood) flow occurs in the intervillous space.2,3 Uteroplacental circulation occurs when uterine spiral arterioles, dislodging the trophoblastic plugs, are transformed into flaccid, dilated uteroplacental arterioles, creating low-pressure, low-impedance blood flow to the intervillous space, thereby establishing an adequate reservoir of oxygen and nutrients for support of the early fetus. Investigators have described normal and abnormal early placental/villous circulation at 8 to 12 weeks.4 Overall, there is a decrease in resistance to blood flow in the uterine circulation from early gestation to term in normal pregnancies.5


Sonographic evaluation of the placenta begins with localization. At US, the placenta may be visible as early as 10 weeks as a thickening of the hyperechoic rim of tissue around the gestational sac (Fig. 19-2). At 12 to 13 weeks, intervillous blood flow is easily demonstrable by color or power Doppler sonography. By 14 to 15 weeks, the placenta is well established and a prominent hypoechoic area, the retroplacental complex, composed of the decidua, myometrium, and uterine vessels, may be readily visualized (Fig. 19-3). At 16 to 18 weeks, small intraplacental arteries may be demonstrated with color or power Doppler US at low-flow settings. The third trimester placenta is a very vascular organ, and both retroplacental and intraplacental arteries are widely distributed and discernible at color or power Doppler imaging.





Placental Size/Shape


US can be used to assess placental size, thickness, and echotexture. Because the placenta is primarily a fetal organ, its size is often a reflection of the health and size of the fetus. The normal term placenta measures 15 to 20 cm in diameter with a volume of 400 to 600 mL.2 Although there is a broad range, normal placental thickness is approximately 1 mm per week of gestation.6,7 As a general rule, the placenta should be approximately equal in thickness (in millimeters) to the gestational age in weeks, +/− 10 mm. The term placenta should generally not be thicker than 45 mm, although some exceptions occur.6 Placental volume in the second trimester has been reported to be a predictor of abnormal fetal outcome, but the method of measurement is complex and not widely adopted.811 A thin placenta may be a marker for a small-for-dates fetus or a sign of growth restriction. Marked polyhydramnios may cause thinning of the placenta (Fig. 19-4). In the presence of marked polyhydramnios, a normal size placenta may in fact be abnormally thickened.



Placentomegaly has many causes. A small area of attachment to the uterus may cause artifactual thickening of the placenta, but careful and complete scanning of the maternal surface and insertion site can make this apparent (Fig. 19-5). The causes of a truly thick placenta may generally be divided into two categories, based on sonographic morphology: homogeneous and heterogeneous echotexture. Common causes of homogeneous thickening are diabetes mellitus (DM; typically gestational-onset DM), anemia, hydrops, infection (villitis) and, rarely, aneuploidy (Fig. 19-6A and B). If multiple small cystic spaces are seen within a thickened placenta, the differential diagnosis would include: triploidy, placental hemorrhage, villitis, mesenchymal dysplasia,12 and Beckwith-Wiedemann syndrome (Figs. 19-7 and 19-8).13 Heterogeneous thickening may be seen with intraplacental hemorrhage, which is further discussed in a later section.







Circumvallate Placenta and Succenturiate Lobe


Circumvallate placenta is an abnormality of placental shape whereby the membranes insert inward from the edge, toward the center of the placenta. The placenta is termed circummarginate if the fetal membrane insertion is flat. More often, the transition where the fetal vessels of the chorionic plate terminate has a raised or rolled edge, termed circumvallate.13,14 Circumvallate placenta is characterized by thickened, rolled chorioamniotic membranes peripherally. This condition may be complete (involving 100%) or partial, when only a portion of the placental circumference is involved. In general, circummarginate or partial circumvallate placentas are of no clinical (obstetric or fetal) significance. However, complete circumvallation has been associated with an increased risk of bleeding, low birth weight/intrauterine growth restriction (IUGR), oligohydramnios, preterm labor/delivery, placental abruption, and perinatal mortality. On US, an irregular placental edge with a heaped up appearance may be noted (Fig. 19-9).15,16 The thickened ridge of peripheral tissue, often found at pathologic inspection to be accompanied by chronic placental hemorrhage or infarction, merits consideration because of its unusual but fairly characteristic sonographic appearance (Fig. 19-10A and B). Of note, the classic US feature of a rolled-up placental edge can appear on some views as a linear structure protruding into the fluid-filled amniotic cavity, and thus can potentially be misinterpreted as a uterine synechia (Figs. 19-11A and B, and 19-12).17 It is possible to assess the degree of circumvallation sonographically by evaluating the entire placental edge over 360 degrees, with the transducer oriented radially to the placenta.






Succenturiate (or accessory) lobe of the placenta occurs in approximately 5% of pregnancies.14 This is recognized on US as a distinct, apparently separate mass of placental tissue, without recognizable bridging tissue.18 In these cases, there is a higher incidence of placental infarction and velamentous insertion of the umbilical cord. The most serious potential complication associated with this condition is when umbilical vessels supplying the succenturiate lobe cross the internal cervical os (vasa previa), to be covered in greater detail in a later section.



Placental Calcifications


It is known that the placenta can mature and calcify (recognized as the sonographic sign of aging) at a fairly reproducible rate. A sonographic classification system for grading placentas in utero according to maturational changes was developed by Grannum et al.19 Extensive research attempted to correlate the placental maturity assessed by US with lung maturity in the 1970s and early 1980s.20 Although early investigations were promising, it was later demonstrated that the US findings of placental maturation do not reliably predict fetal lung maturity. As a result, placental grading, which was in vogue for a time, is now rarely pursued because it is of little clinical value. Premature or accelerated placental calcification has been associated with several factors including chronic maternal hypertension, preeclampsia, IUGR, and maternal cigarette smoking (Fig. 19-13A and B).21




Focal Cystic/Hypoechoic Lesions


Cystic or hypoechoic lesions are frequent placental abnormalities, commonly noted after 25 weeks’ gestation. Although they may represent a variety of entities, small hypoechoic areas are often of no clinical significance (Fig. 19-14). They are more concerning if they are seen early in gestation, are numerous or large.22 Although they represent a variety of pathologic entities, common etiologies for hypoechoic placental lesions include: intervillous thrombus, and decidual septal cysts. Intervillous thrombi (IVT) are usually 1 to 2 cm in diameter and consist of coagulated maternal blood in the intervillous space, often surrounded by compressed or infarcted villi (Fig. 19-15). They are very common, with reported incidence of 30% to 40%.23 At times, IVT may appear as larger sonolucent lesions, which can cause some confusion and concern. Decidual septal cysts are usually less than 3 cm in diameter, with reported incidence of 20%. They usually occur near the subchorionic zone and result from degeneration of decidual cells within septa that extend from the decidual floor and support the placenta, resulting in cavities filled with homogeneous fibrinous fluid. Hemorrhage into the cavity may resemble IVT, and it is often difficult to distinguish these entities with US. Correct determination can be made at pathologic examination (Fig. 19-16).





Hypoechoic placental lesions may result from perivillous fibrin deposition, typically located at the periphery of the placenta, with macroscopically visible plaques occurring in 20% to 25% of uncomplicated pregnancies. Subchorionic fibrin deposition results in triangular or rectangular areas of fibrin deposited under the fetal surface of the placenta, with the base of the triangle along the chorion. At pathology, they are noted in approximately 20% of placentas. It has been observed that most placental surface cysts detected on sonography are related to cystic change in an area of subchorionic fibrin.24 These entities are usually of no clinical significance because they are typically associated with normal pregnancy outcomes, and have no distinguishing sonographic appearance other than their characteristic locations.


The processes described likely account for the commonly reported sonographic finding of placental or venous lakes that appear as sonolucent intraplacental spaces. On US, swirling internal echoes can sometimes be observed and their shape may be modified with change in maternal position or uterine contractions.25 Such hypoechoic cystic placental lesions, sometimes referred to as placental lakes, have variably been reported in association with maternal-fetal Rh incompatibility, elevated maternal serum alpha-fetoprotein levels, and edematous placentas (Fig. 19-17). They do not, however, appear to be of clinical concern because they have no proven effect on placental function or fetal health. Investigations into the clinical significance of these findings at routine obstetric US have revealed no associated risk of pregnancy complication or poor outcome.26 In a report of placental lakes seen on US between 15 and 34 weeks’ gestation in low-risk pregnancies, no significant difference in birth weight, gestational age at delivery, or adverse obstetric outcome was observed.27




Vascular Abnormalities


Placental infarction is a localized area of ischemic villous necrosis, resulting from interruption in maternal blood supply, more common at the periphery of the placenta. Most are roughly triangular in appearance at pathology, with the base of the triangle along the basal plate (Fig. 19-18). These have been associated with post-term pregnancies, maternal hypertension, and anticardiolipin antibodies. Most are due to thrombotic occlusion of an uteroplacental artery, less often from retroplacental hematoma stripping the placenta away from its blood supply. Most placental infarction is not readily detectable by US because it is isoechoic with adjacent placental tissue,28 unless there is associated hemorrhage in which case, the chronicity of the bleed will influence the echogenicity. In rare instances, acute placental infarction may be visible as a slightly hyperechoic region. Fortunately, most infarctions are small, affect less than 5% of the placenta, and are not clinically significant. When infarction occurs early, centrally or extensively (greater than 30% involvement of the placenta), it is strongly associated with pregnancy-induced hypertension, IUGR, preterm delivery and even fetal death.14,22 Power Doppler US is being investigated as a means to detect areas of placental ischemia or infarction manifest as areas of diminished blood flow.



A separate and distinct process, which is of clinical consequence and has been diagnosed by prenatal US is maternal floor infarction. This rare but important, clinically relevant condition is worth understanding and recognizing because it is associated with significant fetal risk and has been reported to recur in subsequent pregnancies. This type of infarction is characterized histologically by massive deposition of fibrin in the basal plate of the placenta, encasing the villi which become avascular and necrotic (Fig. 19-19). The resulting impaired perfusion of the intervillous space by maternal blood is associated with a high incidence of fetal morbidity and mortality. In one series, fetal death occurred in 40% of cases, preterm birth in 60%, and IUGR in 54% of live births.29 This condition has been diagnosed by prenatal US with hyperechoic areas corresponding to infarction, predominantly along the maternal surface, but extending through much of the placental tissue (Fig. 19-20 A and B). Interspersed hypoechoic areas of varying dimensions and marked placental thickening have been noted as well (Fig. 19-21A and B).30 One hallmark on sonography is the typical basal location near the decidua (maternal surface), which is relatively unique to maternal floor infarction.





Fetal artery thrombosis results in a triangular region of injury, with the base of the triangle fused with the basal plate of placenta, as seen at gross pathology. The reported incidence is 5% in normal placentas, increased in cases of maternal DM. There is an association with maternal coagulation disorders, and they may serve as a marker for thrombosis elsewhere in the fetal vascular system. However, these lesions are not detectable by prenatal US.



Hematomas


It is helpful to consider the location, etiology, sonographic appearance, and clinical impact when confronting blood collections related to the placenta (Fig. 19-22). Massive subchorionic thrombosis results from a large thrombus that strips the chorion away from villous tissue. This may result in a bulging protuberance that elevates and distorts the fetal surface of the placenta, sometimes referred to as a Breus mole (an unfortunate misnomer because this entity bears no relationship to a molar pregnancy or gestational trophoblastic disease). It is quite rare, with reported incidence of 0.05%. Its significance is controversial. In some cases, it may be associated with preterm delivery and spontaneous abortion, possibly due to venous compromise in the uteroplacental circulation.31 Sonographically, it appears as a hypoechoic or cystic area along the fetal surface of the placenta32 (Figs. 19-23A and B, and 19-24).





Subchorionic or marginal hematoma is a hematoma at the lateral margin of the placenta and has an incidence of 2% (Fig. 19-25). It occurs most often with placental implantation in the inferior uterus or lower uterine segment (LUS) and probably arises from rupture of uteroplacental veins. They can be associated with miscarriage and preterm labor but are generally of little significance. Rarely, preplacental or subamniotic hematomas may be seen, although even large hematomas in this location tend to be of little consequence to the fetus. However, some data suggest that this lesion may be of significance in causing fetal growth restriction and fetomaternal hemorrhage in some cases.33



Retroplacental hematomas, which can manifest as the clinical condition of placental abruption, are of greatest clinical consequence. They are likely due to rupture of a decidual arteriole with bleeding separating the basal plate of the placenta from the uterine wall. The reported incidence at pathology is 5% with threefold increased risk in patients with preeclampsia. This lesion often leads to basal plate necrosis and villous infarction. The reported associations include maternal hypertension/preeclampsia, obstruction of venous drainage of the placenta, cocaine abuse, cigarette smoking, anticardiolipin antibodies, blunt trauma, and chorioamnionitis. The clinical significance of such bleeds is related to the gestational age at onset and to their size: as expected, smaller hematomas have a larger impact on early (less than 20 wk) gestations, whereas large hematomas, which may cause significant infarction of villi, must strip more than 30% to 40% of placenta away from myometrium to have clinical implications.


When imaging the placenta, the retroplacental hypoechoic complex, composed of uteroplacental vessels (predominantly veins) and myometrium and measuring 1 to 2 cm in thickness (see Fig. 19-3), should be observed. When this region appears thicker, the possibility of retroplacental hemorrhage, focal myometrial contraction, or leiomyoma should be considered. Focal contractions are transient, typically changing in appear ance during the examination and myomas are usually distinguishable by their round shape, attenuation and internal vascularity on Doppler interrogation, not present within hematomas.



Placental Abruption


Placental abruption is characterized by spontaneous hemorrhage behind or within the placenta with premature separation of the normally implanted placenta from the uterus. The clinical condition (abruption) and the pathologic condition (hematoma) both refer to the abnormal accumulation of maternal blood within or beneath the placenta or membranes.34,35 The incidence of placental abruption is 0.5% to 1%.36,37 It is one of the leading causes of perinatal mortality, accounting for 15% to 20% of all perinatal deaths.38 If the bleeding is extensive, maternal cardiovascular shock and disseminated intravascular coagulopathy may develop. Associated maternal conditions linked with abruption are hypertension, preeclampsia, abdominal trauma (especially anterior placentas), cocaine abuse, cigarette smoking (twofold increase), alcohol use and advanced maternal age.3941


Occasionally, retroplacental or intraplacental hematomas are small and clinically silent (Fig. 19-26). Large hematomas are typically apparent and present clinically with classic features of sudden abdominal pain/cramping, vaginal bleeding, uterine tenderness and often with onset of labor. However, this reported classic presentation occurs in a minority of cases. It is important to remember that not all cases of abruption are identifiable as hemorrhage on US. The sensitivity of US in visualizing hemorrhage is reported to be approximately 50%, but the lack of a gold standard [pathology] limits this evaluation.42 In one series, retroplacental blood clot was seen by US in only 15% of the cases.41 Sonography of abruption may be relatively normal, noncontributory and potentially misleading because US may not be reflective of the gravity of the clinical situation. Given that US cannot always reliably identify this condition, particularly in the emergent setting, it may be ill-advised to perform a US examination and potentially delay management when there is a high clinical suspicion of placental abruption and urgent intervention is indicated.



Still, sonography, given its wide and quick availability, is the only reasonably accurate and practical method of evaluating placental abruption, when clinical circumstances allow.43,44 Rarely, magnetic resonance imaging (MRI) may be used to show hemorrhage, particularly in cases of chronic abruption, but the expense and limited availability preclude its frequent use. If abnormal, US may show a hypoechoic, subchorionic thickened area at the margin of the placenta.45 Doppler US can be useful in distinguishing acute hematoma from hypoechoic retroplacental uterine veins.


The most common site of separation is at the edge of the placenta, sometimes referred to as a marginal abruption or marginal hematoma, often with centrifugal extension away from the placenta. Rarely, this subchorionic hemorrhage may be difficult to differentiate from unapposed chorion and amnion, which may be normal up to 18 weeks of gestational age. The gravest prognosis is for gestations complicated by retroplacental hemorrhage, in which a significant (>30%-40%) placental detachment from the myometrium not uncommonly results in IUGR or fetal demise.22,46


The extent of placental detachment and the volume (sonographic estimate = L × W × H/2) and location of the bleed are the best predictors of pregnancy outcome. It seems fairly well documented that if a hemorrhage is visible at sonography, the patient is at higher risk than if no hematoma is seen in patients with vaginal bleeding.47 Ball et al found that the presence of a sonographically visible subchorionic hemorrhage increased the risk of placental abruption 11-fold and the risk of miscarriage or stillbirth two- to fourfold.48,49 In general, the worst outcomes are seen with retroplacental bleeds, hematomas larger than 50 mL, and greater than 50% placental detachment (Figs. 19-27 and 19-28).5052




The sonographic appearance of retroplacental hemorrhage varies, depending on age and location of the bleed. Characteristically, hemorrhage may be acutely (0-48 h) hyperechoic, becoming isoechoic at 3 to 7 days, followed by hypoechoic echotexture at 1 to 2 weeks.45 After 2 weeks, portions of the clot may become anechoic. Hematomas also tend to become smaller with age, although the rate of decrease is variable.



Placenta Previa


A frequent US finding is an early diagnosis of placenta previa that appears to move (“migrate”) away from the internal cervical os during the latter half of pregnancy (Fig. 19-29A and B). The term placental migration has been used, but it is somewhat misleading. Rather than moving, it is suggested that the placenta is carried toward the fundus, away from the os because of elongation of the uterus with differential growth primarily in the LUS, as gestation advances. Thus the majority of cases of potential previa resolve before term (Fig. 19-30A and B). Although a fairly high incidence of apparent previas has been reported in the second trimester, few true previas persist at term.5356




Placenta previa refers to a placenta that overlies or is proximate to the internal cervical os and is the most common cause of bleeding in the third trimester. The incidence of previa at term ranges from 0.5% to 1.0%, with greatly increased frequency in multiparous women, advanced maternal age, previous abortion, and prior cesarean section.13,39,57,58 It is theorized that the increased incidence in multiparous women results from the depletion of normal decidua by each subsequent pregnancy, leaving the scantier decidua in the LUS for implantation. And, the higher incidence with prior cesarean sections is attributable to scarring in the LUS that renders its growth/elongation impaired; hence, the placenta is unable to migrate away from the internal os. The rate of migration of the placental edge away from the cervical os, which may occur progressively throughout the third trimester, has been measured and may be useful in predicting the eventual route of delivery.59


The terminology used to describe types of placenta previa is often confusing and variably understood (Fig. 19-31). Complete placenta previa, the condition in which a portion of the placenta completely covers the internal os, is straightforward and widely accepted (Fig. 19-32A and B). The term central previa is used when the midportion of the placenta, not just the edge, completely covers the os. Partial previa is used when the placenta partially covers the internal os, a condition that, strictly speaking, can only be applied when the internal os is dilated to some degree. Marginal previa describes placental tissue that reaches the edge, but does not cover the internal os. Confusion arises when describing a placenta shown to encroach upon cervical stroma but not reach or cover the os. Such forms of previa may be difficult to delineate sonographically and to convey with current terminology (Fig. 19-33A and B). Many investigators have chosen to use the term incomplete placenta previa and to report the measured distance from the placental edge to the internal os (Fig. 19-34A and B). Low-lying placenta refers to one that extends into the LUS, usually more than 2 cm from the internal os, and does not cover or reach it.






The problem of potential or possible previa is one that has stimulated much investigation. Placenta previa is eminently detectable with US. Complete previa, with placenta completely covering the internal os, is typically readily diagnosed sonographically. It is worth noting that an overly distended maternal bladder or a transient myometrial contraction of the LUS can potentially mimic a true placenta previa (Fig. 19-35A to C).60 Awareness of these pitfalls can help avoid false-positive interpretations. The role and reliability of US in assessing previa has been particularly enhanced with the use of translabial and transvaginal techniques.53 With translabial (also referred to as transperineal) imaging, the patient empties her bladder and assumes the lithotomy position. The sector transducer, with sterile cover and gel applied, is placed at the vaginal introitus affording a detailed, accurate, quick and well-tolerated view of the cervix to ascertain length and placental location relative to the internal os. The improved spatial and contrast resolution of transvaginal and translabial techniques compared with transabdominal US results from less interposed soft tissue and diminished acoustic attenuation (Fig. 19-36A and B

Only gold members can continue reading. Log In or Register to continue

Mar 10, 2016 | Posted by in ULTRASONOGRAPHY | Comments Off on ULTRASOUND EVALUATION OF THE PLACENTA AND UMBILICAL CORD
Premium Wordpress Themes by UFO Themes