|IMAGES IN ACADEMIC MEDICINE: REPUBLICATION
|Year : 2017 | Volume
| Issue : 3 | Page : 200-202
Ultrasound diagnosis of a molar pregnancy
Sharon Schreiber1, Laura Wallace1, Creagh T Boulger1, David P Bahner2
1 Department of Emergency Medicine, Wexner Medical Center at The Ohio State University, Columbus, OH, USA
2 OPUS 12 Foundation, Columbus, OH, USA
|Date of Web Publication||21-Apr-2017|
David P Bahner
Department of Emergency Medicine, The Ohio State University College of Medicine, Columbus, OH 43210
Source of Support: None, Conflict of Interest: None
We describe a case of a middle-aged female presenting with vaginal bleeding and elevated beta-human chorionic gonadotropin. Transvaginal ultrasound images were consistent with a molar pregnancy. This example highlights the benefit of including emergency ultrasound in the clinical management of suspected gestational trophoblastic disease.
The following core competencies are addressed in this article: Medical knowledge, Patient care.
Republished with permission from: Schreiber S, Wallace L, Boulger CT, Bahner DP. Bedside sonography primer: Ultrasound diagnosis of a molar pregnancy. OPUS 12 Scientist 2013;7(1):1-2.
Keywords: Bedside sonography, diagnostic imaging, molar pregnancy
|How to cite this article:|
Schreiber S, Wallace L, Boulger CT, Bahner DP. Ultrasound diagnosis of a molar pregnancy. Int J Acad Med 2017;3, Suppl S1:200-2
| Introduction and Case Presentation|| |
A 48-year-old Asian female presented to the emergency department at approximately 5 weeks of gestational age, by last menstrual period, with vaginal bleeding. Before 1 week, she had passed a large clot with tissue. She continued to have cramping and bleeding over the next week and saw her family doctor who found her to have an elevated beta-human chorionic gonadotropin (hCG) level. On emergency department presentation, her beta-hCG level was measured at 305,533 mIU/mL. A transvaginal ultrasound revealed a “snowstorm” appearance, with clustered grape-like cystic structures within a hypoechoic uterus, characteristic of a hydatidiform mole [Figure 1]. The patient was consented for suction dilatation and curettage and was taken to the operating room.
|Figure 1: Sagittal view of the uterus. Note the grape-like cystic structures within the hypoechoic uterus and absence of fetal tissue. The transducer used for this image contains a damaged crystal resulting in a black streak artifact (”fan-shaped” black shadow just to the right from mid-image)|
Click here to view
| Discussion|| |
Gestational trophoblastic disease (GTD) encompasses four main pathologies: Molar pregnancy (complete hydatidiform mole [CHM] and partial hydatidiform mole [PHM]), invasive mole, choriocarcinoma, and placental site trophoblastic tumor (PSTT). The term gestational trophoblastic neoplasia is a subset of GTD and refers to the latter three pathologies (invasive mole, choriocarcinoma, and PSTT). If left untreated, the mortality rate nears 100%.
This patient received a diagnosis of GTD based on ultrasound imaging. There are two general types of molar pregnancy: CHM and PHM. Complete moles are predominantly diploid androgenetic, from one haploid sperm that fertilizes an empty ovum (70–90%) and duplicates. Most PHMs are triploid, due to a normal egg that is fertilized by two sperm. CHMs tend to have higher hCG levels (>100,000 mIU/ml) than with PHMs (<100,000 mIU/ml). Another common differentiating factor between PHM and CHM is the presence of embryonic or fetal tissue. PHMs show clear signs of fetal or embryonic tissue, especially the presence of villous blood vessels, proliferation of hyperplastic cytotrophoblast, and syncytiotrophoblast, while these are absent in CHMs. In this case, the patient's hCG level and lack of fetal tissue led to a diagnosis of a complete mole.
In general, the incidence of molar pregnancy is 1 in 1500 live births. Several risk factors have been identified for molar pregnancy: age <20 or >40 nearly doubles the risk, prior molar pregnancy (associated with a 10–20-fold increase), previous spontaneous abortion can increase the risk by 2–3-fold, and diet that is low in animal fat and beta-carotene. In addition, there appears to be significant regional variation: Studies from North America, Australia, New Zealand, and Europe show an incidence between 0.57 and 1.1/1000 live births, while studies in the Southeast Asia and Japan suggest an incidence as high as 2/1000 live births. Finally, ovulation induction increases the risk of a combined pregnancy that consists of both a normal pregnancy and a molar pregnancy.
The initial presentation for molar pregnancy usually consists of abnormal and sometimes massive uterine bleeding as was seen in this case. However, due to elevated hCG, a patient may also present with acute hyperthyroidism, which can distract from a proper diagnosis.
Definitive treatment is operative removal of the pregnancy, usually with emergent dilatation and curettage, as patients may become unstable due to blood loss. A rapid diagnosis is therefore essential. While it is true that elevated hCG levels are an important finding of GTD, hCG levels alone can seldom differentiate a CHM from a normal intrauterine pregnancy or other pathologies. The diagnostic gold standard of GTD has traditionally been histological analysis. However, histological morphology alone is not completely reliable and is only possible with tissue removed during surgery. Genetic testing can not only be used to differentiate between a diploid sample and triploid but also requires surgical tissue sample. As such, ultrasonography greatly aids in the early diagnosis of molar pregnancy and has significantly decreased the morbidity and mortality of this condition. The classic ultrasound finding is the characteristic “snowstorm” appearance and clustered grape-like cystic structures within a hypoechoic uterus as was visualized in our patient.
Following dilation and curettage, postoperative complications can include toxemia, hyperthyroidism, and trophoblastic embolization. In particular, patients who are hyperthyroid secondary to the molar pregnancy must be managed carefully due to the increased risk of thyroid crisis during general anesthesia.
Once the mole is removed and the patient stabilized, the primary goals of treatment become prevention and early detection of a subsequent choriocarcinoma. In general, CHMs are more associated with choriocarcinoma (15–20%) than PHMs (1–5%). All patients treated for molar pregnancy should be monitored regularly for elevated hCG levels. In addition, as the presence of one molar pregnancy elevates the risk of a subsequent one, it is important to counsel the patient to seek medical attention sooner rather than later in the event of vaginal bleeding or missed period.
| Conclusion and Follow-Up|| |
In this case, the patient was found to have an invasive mole that was removed during surgery. This was confirmed on histologic diagnosis. She then underwent actinomycin D chemotherapy, followed by methotrexate. Her hCG level was monitored once per week and plateaued quickly once chemotherapy was begun. At her last follow-up, 6 months after her initial diagnosis, her beta-hCG level was >5.0 mIU/ml.
Justifications for re-publishing this scholarly content include: (a) The phasing out of the original publication after a formal merger of OPUS 12 scientist with the International Journal of Academic Medicine and (b) Wider dissemination of the research outcome(s) and the associated scientific knowledge.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Ma OJ, Mateer JR, Blaivas M. Emergency Ultrasound. 2nd
ed. New York: McGraw Hill; 2008.
Lurain JR. Gestational trophoblastic disease I: Epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole. Am J Obstet Gynecol 2010;203:531-9.
Ronnett BM, DeScipio C, Murphy KM. Hydatidiform moles: Ancillary techniques to refine diagnosis. Int J Gynecol Pathol 2011;30:101-16.
Sebire NJ. Histopathological diagnosis of hydatidiform mole: Contemporary features and clinical implications. Fetal Pediatr Pathol 2010;29:1-16.