Sonographic Evaluation of the Normal and Abnormal Placenta

The Institute for Advanced Medical Education is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

The Institute for Advanced Medical Education designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit(s) TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

These credits are accepted by the American Registry for Diagnostic Medical Sonography (ARDMS).

Faculty:
Lyndon M. Hill, MD
Professor Obstetrics and Gynecology
Medical Director Ultrasound
Magee Women's Hospital
Pittsburgh, PA

Course: Sonographic Evaluation of the Normal and Abnormal Placenta

Target Audience: Physicians, sonographers and others who perform and/or interpret obstetrical ultrasound.

System requirements: In order to complete this program you must have a computer with a recent version of Internet Explorer or Netscape, and a printer, which is configured to print from the browser.

For any questions or problems concerning this program or for problems related to the printing of the certificate please contact IAME at 802.824.4433 or email us.

Estimated Time for Completion of tutorial: One hour
Date of Release:
October 9, 2006
Date of Review:
June 10, 2012
Expiration Date: June 30, 2015

Disclosure: In compliance with the Essentials and Standards of the ACCME, the author of this CME tutorial is required to disclose any significant financial or other relationships they may have with the manufacturer(s) of any commercial product(s) or provider(s) of any commercial service(s) discussed in this program.

Dr. Lyndon Hill discloses no relevant financial relationships with commercial interests.

IAME discloses no relevant financial relationships with commercial interests. 

 

IAME Statement on Privacy and Confidentiality

 

Sonographic Evaluation of the Normal and Abnormal Placenta
Lyndon M. Hill, MD
Professor Obstetrics and Gynecology
Medical Director Ultrasound
Magee Women's Hospital
Pittsburgh, PA

(DIRECT TO QUIZ)

Objectives
After completing this course, the participant should be able to:

  • Describe the development of the normal placenta and its' sonographic appearance.
  • Identify the changes that occur in the placenta with intrauterine growth restriction.
  • Apply diagnostic ultrasound to identify placenta previa, abruption and other abnormalities that are the potential source of fetal disease and / or compromise.

Introduction
The placenta evolves rapidly over a short period of time. Its response to injury is limited. Fortunately, the placenta has significant reserve capacity; the fetus may be relatively unaffected until 30% of the placenta is no longer functional1.

Placental Development
The placenta evolves both structurally and functionally throughout pregnancy. In the first half of the 1st trimester, the embryo develops in an environment with a lower oxygen concentration than the fetus. The formation of villi begins around day 13 after conception; fetal placental capillaries are detectable by 3 weeks post conception. A transudate from maternal plasma bathes the trophoblastic plugs2. A true intervillus blood flow is not well established until 12 weeks' gestation. By 14 weeks' gestation uterine artery velocity increases; there is continuous intervillous flow; and end diastolic flow appears in the umbilical artery3.

The eventual position and shape of the normal placenta is due to the degeneration of villi from all areas, except those with the best blood supply. As a result, villi in the lower uterine segment tend to atrophy, while villi develop within the uterine fundus. This process is referred to as trophotropisim (tropho [Greek], to feed; tropic [Greek], turn toward) 4 .

Placental Volume

The placenta should be considered a fetal organ. Intrauterine growth restriction (IUGR) is preceded by reduced placental growth in the first half of pregnancy 5 . In early onset IUGR there is a failure to develop a normal placental villous tree, as well as a failure by the placenta to respond to hypoxia with trophoblastic proliferation and angiogenesis 6 .

Enlarged "jelly-like" Placenta

Enlarged "jelly-like" placentas have a prevalence of 0.6 to 7.6% 7 (Fig. 1). The range in the estimated frequency is due to variation in terminology between authors. In general, these placentas contain numerous sonolucent spaces with turbulent flow; the placental weight is < 10th percentile. They are associated with IUGR, pre-eclampsia and elevated 2nd trimester maternal serum alphafetoprotein 8 . Defective transformation of the spiral arteries results in a globular "jelly-like" placenta. Because of the poor vascularity, the majority of jelly-like placentas are located laterally.

Figure 1 - Jelly-like globular placenta associated with 2nd trimester intrauterine growth restriction.

To view an enlargement, click on the image.

 

Intervillous Thombosis

The intervillous space varies in size (0.3 to 3.0 cm) 9 . With uterine contractions, spiral artery flow is altered, resulting in a change in the shape of the intervillous space. The slow turbulent flow within the intervillous space, as well as the spiral artery's entrance into the intervillous space can be appreciated with color Doppler. One or more intervillous spaces are visualized in 2.2% of placentas between 15 and 34 weeks' gestation 10 .

An intervillous thrombus (Fig. 2), therefore, consists of coagulated maternal and fetal blood within an intervillous space. These lesions occur in up to 40% of placentas; they are not associated with an increase in fetal morbidity. Sonographically, they are initially isoechoic. As fibrin accumulates around its periphery, an intervillous thrombus becomes increasingly echogenic 11,12 .

Figure 2 - Intervillous thrombus (arrow).

To view an enlargement, click on the image.

 

Subamniotic Cysts

These cysts are frequently located close to the placental cord insertion (Fig. 3). The cysts may be simple or complex. If the cysts are larger than 4.5 cm or > 3 in number, the frequency of intrauterine growth restriction may be increased 13 .

Figure 3 - Subamniotic cyst (arrow) at the placental cord insertion (a, longitudinal; b, transverse).

To view an enlargement, click on the image.

 

Placenta Previa

In mid-gestation the placenta occupies 50% of the uterine surface. By 40 weeks' gestation, the placenta occupies 17 - 25% of the uterine volume 14 . This, in part, explains the decreasing prevalence of placenta previa as gestation advances.

The incidence of placenta previa is approximately 6% in the 1 st trimester 15 and 0.5% at term 15 .

Predisposing factors for placenta previa are outlined on Table I. The recurrence risk for placenta previa increases with each cesarean section (Table II) 16 . A prior cesarean section does not affect the site of placental implantation. The association between a prior cesarean section and placenta previa is due to a lack of resolution of a previa, suggesting that trophotropism is affected by lower uterine segment scarring 17 .

Table I. Predisposing factors for placenta previa.

Advanced maternal age
Multiparity
Prior cesarean section
Uterine curettage
Maternal cigarette smoking

 

Table II. Prevalence of placenta previa after cesarean sections 16

Cesarean Sections

Prevalence Placenta Previa (%)

1

0.65

2

1.80

3

3.00

4

10.00

 

With transvaginal sonography, Farine et al 18 reported a 100% sensitivity and negative predictive value for the sonographic diagnosis of placenta previa (Fig. 4). If the placenta extends over the internal cervical os by >= 2.5 cm at 20 - 23 weeks' gestation, Becker et al 19 had a 100% cesarean delivery rate (12 cases) (Fig. 5).

 

Figure 4 - Placenta previa. The placeta extends over the internal cervical os by 2.6 cm (+. . .+).   Figure 5 - Complete placenta previa (PL = placenta; cx = cervix).
To view an enlargement, click on the image.

 

Low-lying Placenta

Transvaginal sonography has been used to define a low-lying placenta as < 2.0 cm from the internal cervical os 20 (Fig. 6). Openheimer et al 20 did not have to perform any cesarean sections for vaginal bleeding when the placenta was > 2 cm from the internal cervical os (14 cases). However, 7 of 8 patients with a placental edge < 2 cm from the internal cervical os required a cesarean section for bleeding. The only patient in this group who did not have a cesarean section had a scan to delivery interval of 11 weeks. If the lower edge of a low-lying placenta is thick (> 1 cm) there is a higher risk of hemorrhage, emergency cesarean section and placenta accreta 21 .

Figure 6 - Low-lying placenta. The placental edge is 18 mm (+. . .+) from the internal cervical os.

To view an enlargement, click on the image.

 

Placental Abruption

Placental abruption has been defined as the premature separation of a normally implanted placenta after 20 to 24 weeks' gestation. External vaginal bleeding is not always present; approximately 40% of cases have concealed retroplacental hemmorhage (Fig. 7). The incidence of placental abruption is determined by the prevalence of high-risk patients at a given institution and is between 1/50 and 1/270 deliveries. The recurrence risk after 1 or 2 prior placental abruptions is 5.6% and 17%, respectively 22,23,24 . Factors that have been associated with placental abruption are outlined in Table III 25 .

Figure 7 - There is a 9.2 x 2.8 x 5.4 cm anterior retroplacental abruption between the markers.

To view an enlargement, click on the image.

 

Table III. Factors associated with placental abruption.

Advanced maternal age
Multiparity
Maternal vascular disease
Smoking
Prior placental abruption
External trauma
Cocaine use
Prolonged rupture of membranes
Uterine leiomyomas
Severe growth restriction

 

The sensitivity of an ultrasound examination for detecting placental abruption is between 25% and 50% 24,26,27 . However, if a retroplacental clot is visualized, the positive predictive value is quite high. In one study, if the delivery was within 2 weeks of positive ultrasound finding, the diagnosis was confirmed in every case. Because of its low sensitivity, the primary role of an ultrasound examination is to exclude a diagnosis of placenta previa.

Some of the numerous sonographic manifestations of placental abruption are outlined in Table IV 24,28,29 . Retroplacental abruptions generally have a worse prognosis than abruptions without a contained hemorrhage. Chronic or recurrent abruption with subsequent placental insufficiency can result in fetal growth restriction 30 .

Table IV. Sonograhic signs of placental abruption.

Retroplacental mass
Intraplacental mass
Diffuse placental thickness
Rounded placental edge
Separation of placental edge
Intra-amniotic hemorrhage
Preplacental or subamniotic mass
Blood in the fetal stomach
Intermembranous clot in twins

 

Succenturiate Placental Lobe

There may be one to several succenturiate or accessory placental lobes (Fig. 8). They each would have a vascular connection to the main body of the placenta. The incidence of succenturiate placental lobes is approximately 5% 31 . Villous atrophy results in the isolation of a placental lobe from the main body of the placenta. The primary concern with a succenturiate placental lobe is that the vessel connecting to the main placental body traverses the cervix (vasa previa). The second complication associated with a succenturiate placental lobe is the potential retention of the accessory lobe within the uterus after delivery 32 .

Figure 8 - Posterior succenturiate placental lobe.

To view an enlargement, click on the image.

 

Placenta Accreta

With placenta accreta the decidua basalis does not separate the myometrium and trophoblast. As a result the placenta adheres directly to the myometrium (accreta), grows into the myometrium (increta); or grows completely through the myometrium (percreta).

The incidence of placenta accreta has increased markedly over the past 70 years. In the 1930's the reported incidence was approximately 1 case/30,000 deliveries 33,34 . Wu 35 has recently reported an incidence in 1/533 deliveries. This marked increase is due to the increase in cesarean sections. With the increase in cesarean sections, there has also been an increased incidence of placenta previa - an additional risk factor for placenta accreta 34 . Usta et al 36 have reported a 6.3% rate of placenta accreta with placenta previa.

The loss of the hypoechoic interface between the placenta and myometrium was one of the first sonographic signs associated with placenta accreta. However, the isolated loss of this clear space as the only sign of placenta accreta has subsequently been found to have a low positive predictive value for placenta accreta between 15 weeks' gestation and term 37 .

When placenta accreta is present, the placenta has irregularly shaped vascular sinuses (lacunae) that have detectable low velocity blood flow (Fig. 9). Placental lacunae have been detected in cases of placenta accreta as early as 15 weeks' gestation. Placental lacunae have been reported to have a 93% sensitivity and positive predictive value for placenta accreta 38 .

Figure 9 - Placenta accreta. Irregularly shaped vascular lacunae (arrows) are present within the placenta.

To view an enlargement, click on the image.

 

The interface between the bladder and uterus is usually fairly thick. In patients with placenta accreta, varicies give the appearance that the bladder wall is interrupted (Fig. 10). This sonographic sign has a 93% sensitivity for detecting placenta accreta 38 .

Figure 10 - Placenta accreta. The interface between the bladder and uterus appears interrupted because of the bladder wall varicies.

To view an enlargement, click on the image.

 

The presence of a gestational sac in the lower uterine segment at 10 weeks or earlier is a 1 st trimester sonographic sign associated with palcenta accreta 37 .

Placental Chorioangioma

Chorioangiomas are detected in 1% of placentas evaluated pathologically after delivery. However, those that are large enough to be clinically significant occur only once in every 3,500 to 9,000 pregnancies 39,40 . In the past, only chorioangiomas > 5 cm were considered large enough to produce fetal complications 41 . More recently, it has been determined that the vascularity of a tumor, rather than its size, determines the likelihood of fetal complications 42 . Chorioangiomas are most commonly detected around the placental cord insertion. As they enlarge, chorioangiomas protrude into the amniotic cavity (Fig. 11).

Figure 11 - Placental chorioangioma. The feeding vessel to the chorioangioma can be appreciated with color Doppler.

To view an enlargement, click on the image.

 

Color Doppler should be used to evaluate a placental mass for blood flow. Chorioangiomas that produce fetal effects have either significant internal flow or a large feeding vessel 41 (Fig. 11). Their echo pattern may vary from isoechoic with the placenta to having a mixed echodense/echospared appearance due to the type and degree of degenerative changes that may have occurred. Fibrotic degeneration of a chorioangioma reduces the amount of blood flow through the lesion and is, therefore, considered a good prognostic sign.

The fetal effects from a vascularized chorioangioma are outlined in Table V. Non-immune hydrops results from the shunting of blood to the tumor and secondary high-output failure. Hemolytic anemia may also contribute to fetal hydrops 43 . Polyhydramnios is associated with the amount of vascular flow to the chorioangioma rather than to its size 42 . It has been hypothesized that the associated polyhydramnios is due to a transudate through the walls of the abnormal vessels within the chorioangioma. The fluid then passes through the placenta to the amniotic cavity.

Table V. Potential fetal effects of placental chorioangiomas.

Non-immune hydrops
  •  Anemia
  •  Thromocytopenia
  •  Cardiomegaly
  •  Pleural effusions
  •  Ascites
  •  Anasarca
Polyhydramnios
Pre-term labor
Intrauterine growth restriction

 

Conclusion

The placenta should be evaluated, not only as a necessary organ for fetal growth the development, but also as a potential source of fetal disease and/or compromise.

 

References

  1. Fox H. Pathology of the placenta. Clin Obstet Gynaecol 1986;13:501-519.
  2. Foidant J-M, Hustin J, Dubois M, Schaaps J-P. The human placenta becomes haemochorial at the 13 th week of pregnancy. Int J Dev Biol 1992;36:451-453.
  3. Jurkovic D, Jauniaux E, Campbell S, Pandya P, Cardy DI et al. Coelocentesis: a new technique for early prenatal diagnosis. Lancet 1993;341;1623-1626.
  4. Lauria MR, Smith RS, Treadwell MC, Comstock CH, Kirk JS et al. The use of second trimester transvaginal sonography to predict placenta previa. Ultrasound Obstet Gynecol 1996;8:337-340.
  5. Hafner E, Metzenbauer M, Höfinger D, Menkel M, Gassel R et al. Placental growth from the first to the second trimester of pregnancy in SGA-foetuses and pre-eclamptic pregnancies compared to normal foetuses. Placenta 2003;24:336-342.
  6. Kingdom J, Huppentz B, Seaward G, Kaufmann P. Development of the placental villous tree and its consequences for fetal growth. Eur J Obstet Gynecol Reprod Biol 2000;92:35-43.
  7. Raio L, Ghezzi F, Cromi A, Nelle M, Dürig P et al. The thick heterogeneous (jelly like) placenta: a strong predictor of adverse pregnancy outcome. Prenat Diagn 2004;24:182-188.
  8. Jauniaux E, Ramsey B, Campbell S. Ultrasonographic investigation of placental morphologic characteristics and size during the second trimester of pregnancy. Am J Obstet Gynecol 1994;170:130-137.
  9. Hoogland HJ. The ultrasound display of intervillous circulation. Placenta 1987;8:537-544.
  10. Reis NSV, Brizot ML, Schultz R, Nomura RMY, Zugaib M. Placental lakes on sonographic examination: correlation with obstetric outcome and pathologic findings. J Clin Ultrasound 2005;33:67-71.
  11. Jauniaux E, Campbell S. Ultrasonographic assessment of placental abnormalities. Am J Obstet Gynecol 1990;163:1650-1658.
  12. Harris RD, Cho C, Wells WA. Sonography of the placenta with emphasis on pathologic correlation. Sem Ultrasound CT and MRI 1996;17:66-89.
  13. Brown DL, DiSalvo DN, Frates MC, Davidson KM, Genest DR. Placental surface cysts detected on sonography. Histologic and clinical correlation. J Ultrasound Med 2002;21:641-646.
  14. Young GB. The peripatetic placenta. Radiology 1978;128:183-188.
  15. Hill LM, DiNofrio DM, Chenevy P. Transvaginal sonographic evaluation of first trimester placenta previa. Ultrasound Obstet Gynecol 1995;5:301-303.
  16. Clark SL, Loonings PP, Phelan JP. Placenta previa/accreta and prior cesarean section. Obstet Gynecol 1985;66:88-92.
  17. Laughon SK, Wolfe HM, Visco AG. Prior cesarean and the risk for placenta previa on second-trimester ultrasonography. Obstet Gynecol 2005;105:962-965.
  18. Farine D, Peisner D, Timor-Tritsch IE. Placenta previa - is the traditional diagnostic approach satisfactory? J Clin Ultrasoud 1990;18:328-330.
  19. Becker RH, Vonk R, Mende BC, Ragosch V, Entezami M. The relevance of placental location at 20 - 23 gestational weeks for prediction of placenta previa at delivery: evaluation of 8,650 cases. Ultrasound Obstet Gynecol 2001;17:496-501.
  20. Openheimer LW, Farine D, Ritchie JWK, Lewinsky RM, Telford J et al. What is a low-lying placenta? Am J Obstet Gynecol 1991;165:1036-1038.
  21. Ghourab S. Third-trimester transvaginal ultrasonography in placenta previa: does the shape of the lower placental edge predict clinical outcome? Ultrasound Obstet Gynecol 2001;18:103-108.
  22. Hibbard EM, Jeffcoate TNA. Abruptio placentae. Obstet Gynecol 1966;27:155-167.
  23. Pritchard JA, Mason R, Corley M, Pritchard S. Genesis of severe placental abruption. Am J Obstet Gynecol 1970;108:22-27.
  24. Jaffe MH, Schoen WC, Silver TM, Bowerman RA, Stuck KJ. Sonography of abruptio placentae. AJR 1981;137:1049-1054.
  25. Kramer MS, Usher RH, Pollack R, Boyd M, Usher S. Etiologic determinants of abruptio-placentae. Obstet Gynecol 1997;89:221-226.
  26. Sholl JS. Abruptio placentae: clinical management in nonacute cases. Am J Obstet Gynecol 1987;156:40-51.
  27. Glantz C, Purnell L. Clinical utility of sonography in the diagnosis and treatment of placental abruption. J Ultrasound Med 2002;21:837-840.
  28. McGahan JP, Philipps HE, Reid MH, Oi RH. Sonographic spectrum of retroplacental hemorrhage. Radiology 1982;142:481-485.
  29. Walker JM, Ferguson DD. The sonographic appearance of blood in the fetal stomach and its association with placental abruption. J Ultrasound Med 1988;7:155-161.
  30. Nyberg DA, Mack LA, Benedetti TJ, Cyr DR, Schuman WP. Placental abruption and placental hemorrhage: correlation of sonographic findings with fetal outcome. Radiology 1987;164:357-361.
  31. Benirshke K, Kaufman P. Placental shape aberrations. In: Benirshke K, Kaufman P (eds): Pathology of the human placenta. New York , Springer-Verlay, 1995, p. 394.
  32. Jeanty P, Kirkpatrick C, Verhoogen C, Struyven J. The succenturiate placenta. J Ultarsound Med 1983;2:9-12.
  33. Miller D, Chollet J, Goodwin T. Clinical risk factors for placenta previa - placenta accreta. Am J Obstet Gynecol 1997;177:210-214.
  34. Armstrong CA , Harding S, Matthews T, Dickinson JE. Is placenta accreta catching up to us? Aust NZJ Obstet Gynaecol 2004;44:210-213.
  35. Wu S, Lockerginsky M, Hibbard JU. Abnormal placentation: twenty-year analysis. Am J Obstet Gynecol 2005;192:1458-1461.
  36. Usta IM, Hobeika EM, Musa AAA, Gabriel GE, Nassar AH. Placenta previa-accreta: Risk factors and complications. Am J Obstet Gynecol 2005;193:1045-1049.
  37. Comstock CH, Lee W, Vettraino IM, Bronsteen RA. The early sonographic appearance of placenta accreta. J Ultrasound Med 2003;22:19-23.
  38. Comstock CH, Love JJ, Bronsteen RA, Lee W, Vettraino I et al. Sonographic detection of placenta accreta in the second and third trimester of pregnancy. Am J Obstet Gynecol 2004;190:1135-1140.
  39. Sepulveda W, Aviles G, Carstens E, Corral E, Perez N. Prenatal diagnosis of solid placental masses: the value of color flow imaging. Ultrasound Obstet Gynecol 2000;16:554-558.
  40. Prapos N, Liang R-I, Hunter D, Copel JA, Lu L-C et al. Color Doppler imaging of placental masses: differential diagnosis and fetal outcome. Ultrasound Obstet Gynecol 2000;16:559-563.
  41. Zalel Y, Weise B, Gamzu R, Schiff E, Shalmon B et al. Chorioangioma of the placenta. Sonographic and Doppler flow characteristics. J Ultrasound Med 2002;21:909-913.
  42. Jauniaux E, Ogle R. Color Doppler imaging in the diagnosis and management of chorioangiomas. Ultrasound obstet Gynecol 2000;15:463-467.
  43. Hata T, Inubashiri E, Kanenishi K, Akiyama M, Tanaka H et al. Three-dimensional power Doppler aniographic features of placental chorioangioma. J Ultrasound Med 2004;23:1517-1520.

TAKE THE QUIZ


Our online courses are free of charge.


If you wish to earn CME credit then you will be asked to make payment by major credit card after successful completion of the quiz. The charge is $25 for one credit, $60 for four credits and $80 for eight credits. If you purchase multiple credits you may take them at any time.

If you are using a voucher please enter your email address exactly as you did when you made your original purchase.

IAME Statement on Privacy and Confidentiality