(Radiographics. 1999;19:1089-1092.)
© RSNA, 1999
US Case of the Day1
Ramesh Avva, MD,
Hemendra R. Shah, MD and
Teresita L. Angtuaco, MD
1 From the Department of Radiology, University of Arkansas for Medical Sciences, 4301 W Markham St, Little Rock, AR 72205. From the 1998 RSNA scientific assembly. Received November 20, 1998; revision requested December 10 and received January 26, 1999; accepted January 26. Address reprint requests to T.L.A.
Index Terms: Placenta, US, 857.1298 • Pregnancy, complications, 857.824
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HISTORY
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A 19-year-old woman with a history of persistent vaginal bleeding and an intrauterine mass was referred to our institution. The patient had undergone dilation and curettage 3 months earlier for a missed abortion. Laboratory tests revealed a ß–human chorionic gonadotropin level of less than 2 mIU/mL and anemia with a hemoglobin value of 9.9 and a hematocrit of 28.8. Transabdominal and transvaginal pelvic ultrasonography (US) were performed.
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FINDINGS
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Initial transabdominal US images showed an echogenic mass in the uterus filling the endometrial cavity (Fig 1). Transvaginal US images depicted the endometrial mass in more detail and showed multiple anechoic areas. In addition, the mass appeared to invade the posterior myometrium up to the serosal surface (Fig 2a). Color Doppler US revealed intense hypervascularity of the mass (Fig 2b). There was no evidence of extension of the mass into the surrounding soft tissues, and no adnexal masses were identified. Because of clinical suspicion for a vascular malformation, pelvic angiography was performed. This study helped confirm the vascular nature of the mass but did not demonstrate typical findings for vascular malformation.
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Figure 1a. (a) Longitudinal transabdominal US image of the pelvis shows an echogenic mass with central anechoic areas filling the uterine cavity (arrow). (b) On a transverse transabdominal US image of the pelvis, the uterine contour is maintained. There is no evidence of extension of the mass into the parametria.
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Figure 1b. (a) Longitudinal transabdominal US image of the pelvis shows an echogenic mass with central anechoic areas filling the uterine cavity (arrow). (b) On a transverse transabdominal US image of the pelvis, the uterine contour is maintained. There is no evidence of extension of the mass into the parametria.
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Figure 2a. (a) Longitudinal transvaginal US image of the uterine fundus shows invasion of the mass into the myometrium but not beyond the serosal border (arrowheads). (b) Color Doppler US image of the uterine fundus demonstrates intense vascularity of the mass, causing suspicion for a vascular malformation.
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Figure 2b. (a) Longitudinal transvaginal US image of the uterine fundus shows invasion of the mass into the myometrium but not beyond the serosal border (arrowheads). (b) Color Doppler US image of the uterine fundus demonstrates intense vascularity of the mass, causing suspicion for a vascular malformation.
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DIAGNOSIS: Placenta increta.
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DISCUSSION
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In a normal pregnancy, the placenta is formed at the implantation site by a combination of the chorion frondosum from the developing embryo and the decidua basalis. When the decidua is partially or completely absent, abnormal placental implantation may occur. Depending on the location of the implantation, the condition is referred to as placenta accreta, placenta increta, or placenta percreta. If the placental villi extend beyond the confines of the endometrium and attach to the superficial aspect of the myometrium, the term placenta accreta is used. Placenta increta refers to a situation in which the villi invade the myometrium, whereas the term placenta percreta is used if the villi advance into the serosa or parametria. Although this classification scheme is widely accepted, the majority of the published literature discusses these abnormalities collectively as placenta accreta.
Placenta accreta occurs in approximately 1 in 7,000 pregnancies with a range of 1:540 to 1:70,000 being reported (1). Placenta accreta is the most common form of placental invasion (76% of cases), followed by placenta increta (18%) and placenta percreta (6%) (1,2). The primary risk factors for placenta accreta are placenta previa, advanced maternal age, and prior cesarean section. In a study by Miller et al (2), placenta previa was seen in nearly all cases of placenta accreta, and in its absence the diagnosis was uncommon. Advanced maternal age and prior cesarean section were the only other independent risk factors for placenta accreta in patients with placenta previa. These factors increase the risk of placenta accreta by affecting the decidual layer. In placenta previa, the placenta implants in the lower uterine segment where the decidual reaction is less complete. Previous cesarean sections cause scars within the myometrium. If the placenta implants at these sites, the decidual layer tends to be deficient, thus allowing placental extension into the myometrium. Other causes of uterine scarring such as endometritis, Asherman syndrome, and previous dilatation and curettage may be seen in some cases of placenta accreta.
Accurate prenatal diagnosis of placenta accreta is vital because this abnormality is an important cause of significant hemorrhage in the immediate postdelivery period with resultant maternal and fetal morbidity and mortality. However, the diagnosis is not usually made prospectively. The present case was especially interesting because of the time interval between the antecedent pregnancy and the onset of symptoms. As in most cases of vaginal bleeding, US was performed for initial evaluation. US criteria for the diagnosis of placenta accreta have been reported. These include loss of the retroplacental hypoechoic zone, interruption of the hyperechoic border between the uterine serosa and bladder, presence of mass-like tissue with echogenicity similar to that of the placenta, and the visualization of prominent vessels or lakes within the placenta or myometrium (3). In the present case, both prominent vasculature and loss of the retroplacental clear space were observed. False-positive results can occur at US with these criteria due to technical factors. For example, in anterior placentas, excessive compression with the transducer and improper gain settings for near-field scanning may obliterate the retroplacental clear space (4). These technical problems may be minimized with use of transvaginal US (5).
Magnetic resonance (MR) imaging has also been used to diagnose placenta accreta. On T2-weighted MR images, the mass is hyperintense and may be heterogeneous, reflecting the degree of hyalinization of the placenta. In addition, T2-weighted MR images are useful in the assessment of focal thinning of the myometrium and interruption of the junctional zone (6). Recently, Levine et al (7) completed a prospective study comparing US with MR imaging in the diagnosis of placenta accreta. The sensitivity and specificity of US were 86% and 92%, respectively. When MR imaging was included, sensitivity increased to 100%. Gray-scale US was typically sufficient in cases in which the retroplacental clear zone was greater than 2 mm in diameter. In cases in which this area was less than 2 mm, placental location determined which technique was most useful. MR imaging was most beneficial in posterior placenta because this anatomic area is sometimes difficult to evaluate with US.
Definitive treatment for placenta accreta consists of hysterectomy with possible resection of adjacent organs if percreta is present. In certain instances, however, conservative treatment may be used, especially if uterine preservation is desired. Conservative measures include curettage, oversewing of the placental bed, and ligation of the uterine arteries or the anterior divisions of the internal iliac arteries. The risks associated with a conservative approach include delayed hemorrhage and infection (2). In one case, a patient who was treated conservatively for placenta accreta experienced mild delayed bleeding and development of a placenta increta (8). Case reports of cytotoxic therapy with methotrexate have shown mixed results (9,10). Interventional radiology has proved useful in the treatment of obstetric hemorrhage. Angiographic embolization of the uterine or internal iliac arteries and their branches has been performed with good results in conjunction with surgical therapy (11) or in cases in which hemorrhage persisted despite medical and surgical treatment (12).
Our patient subsequently underwent hysterotomy and removal of the mass. Pathologic analysis revealed placental tissue invading the myometrium but not extending into the serosal surface. Follow-up conventional and color Doppler US performed 6 weeks after surgery showed a normal uterus with no residual area of hypervascularity (Figs 3, 4).
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Figures 3, 4. (3) Follow-up longitudinal transabdominal US image of the uterus obtained 6 weeks after surgery demonstrates normal endometrial echogenicity (arrow) with normal uterine contour. (4) Follow-up transvaginal color Doppler US image of the uterine fundus shows surgical scarring and minimal vascularity in the posterior myometrium.
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Figures 3, 4. (3) Follow-up longitudinal transabdominal US image of the uterus obtained 6 weeks after surgery demonstrates normal endometrial echogenicity (arrow) with normal uterine contour. (4) Follow-up transvaginal color Doppler US image of the uterine fundus shows surgical scarring and minimal vascularity in the posterior myometrium.
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References
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Breen JL, Neubecker R, Gregori CA, Franklin JE. Placenta accreta, increta, and percreta: a survey of 40 cases. Obstet Gynecol 1977; 49:43-47.[Abstract/Free Full Text]
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Miller DA, Chollet JA, Goodwin TM. Clinical risk factors for placenta previa-placenta accreta. Am J Obstet Gynecol 1997; 177:210-214.[Medline]
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Finberg H, Williams J. Placenta accreta: prospective sonographic diagnosis in patients with placenta previa and prior cesarean section. J Ultrasound Med 1992; 11:333-343.[Abstract]
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Wheeler TC, Anderson TL, Kelly J, Boehm FH. Placenta previa increta diagnosed at 18 weeks' gestation: report of a case with sonographic and pathologic correlation. J Reprod Med 1996; 41:198-200.[Medline]
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Rosemond RL, Kepple DM. Transvaginal color Doppler sonography in the prenatal diagnosis of placenta accreta. Obstet Gynecol 1996; 88:653-654.[Abstract]
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Amoh Y, Watanabe Y, Saga T, et al. Retained placenta accreta: MRI and pathologic correlation. J Comput Assist Tomogr 1995; 19:827-829.[Medline]
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Levine D, Hulka CA, Ludmir J, Li W, Edelman RR. Placenta accreta: evaluation with color Doppler US, power Doppler US, and MR imaging. Radiology 1997; 205:773-776.[Abstract/Free Full Text]
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Davis JD, Cruz A. Persistent placenta increta: a complication of conservative management of presumed placenta accreta. Obstet Gynecol 1996; 88:653-654.
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Arulkumaran S, Ng CSA, Ingemarsson I, Ratnam SS. Medical treatment of placenta accreta with methotrexate. Acta Obstet Gynecol Scand 1986; 65:285-286.[Medline]
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Jaffe R, DuBeshter B, Sherer DM, Thompson EA, Woods JR. Failure of methotrexate treatment for term placenta accreta. Am J Obstet Gynecol 1994; 171:558-559.[Medline]
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Dubois J, Garel L, Grignon A, Lemay M, Leduc L. Placenta percreta: balloon occlusion and embolization of the internal iliac arteries to reduce intraoperative blood losses. Am J Obstet Gynecol 1997; 176:723-726.[Medline]
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Greenwood LH, Glickman MG, Schwartz PE, Morse SS, Denny DF. Obstetric and nonmalignant gynecologic bleeding: treatment with angiographic embolization. Radiology 1987; 164:155-159.[Abstract/Free Full Text]
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HISTORY
FINDINGS
