More than 21,000 women in the United States will receive a diagnosis of ovarian cancer (OC) in 2022. Although ovarian cancer accounts for only 1.1% of new cancer diagnoses, it accounts for 2.3% of all cancer deaths annually and has a 5-year relative survival rate of 49.1%.

 The median age at diagnosis is 63 years, with the highest incidence of ovarian cancer occurring in White women (11.3 per 100,000), followed by Asian/Pacific Islander women (9.4 per 100,000) and Black women (9.0 per 100,000).

The vast majority of ovarian cancers occur in the epithelium, with a smaller fraction originating in stromal cells and germ cells (

The epithelial cancers can be divided into type I and type II tumors. Whereas the type I tumors (endometrioid, clear cell, low-grade serous, and mucinous) typically behave in a more indolent fashion, the type II tumors, primarily composed of high-grade serous carcinomas, behave much more aggressively with early and widespread dissemination.

Of all the epithelial carcinomas, high-grade serous carcinoma accounts for 60% to 80% of cases, followed by mucinous carcinoma (5%-10%), endometrioid carcinoma (7%-10%), clear cell carcinoma (8%-12%), carcinosarcoma (5%), and other more rarer histologies.

Symptoms associated with ovarian cancer can be vague. Both the type I and II cancers are associated with abdominal pain, bloating, or gastrointestinal symptoms such as a change in bowel habits.

 Patients with symptoms should undergo pelvic/abdominal imaging and serum cancer antigen (CA) 125 testing. 

Unfortunately, there are no proven diagnostic screening tests (imaging or tumor markers) that have been able to improve early diagnosis or decrease disease-specific mortality.

Although theories for development of ovarian cancer have arisen based on knowledge of risk and protective factors, understanding of the sites of origin has been enhanced by knowledge of molecular factors and genetic predisposition. 

Proposed theories for ovarian carcinogenesis include incessant ovulation, gonadotropin stimulation, retrograde menstruation, and tubal inflammation. The concepts behind these theories and proposed pathways involved can overlap (

Development from incessant ovulation is a hypothesis that more frequent ovulatory cycles lead to the formation and growth of dominant follicles that produce high levels of estrogen-rich fluid, induce minor trauma from the act of ovulation, and result in surrounding epithelial proliferation, inflammation, wound repair, and increased amounts of DNA damage. Cumulatively, these events are believed to contribute to premalignant transformation. 

Epidemiologic studies that demonstrate reduced risk of ovarian cancer in women who experience fewer ovulatory cycles due to breastfeeding, pregnancy, or oral contraceptive use provide the most convincing evidence.

The same sequence of inflammation and wound repair supports the inclusion cyst theory of ovarian cancer. This theory proposes that ovarian cancer is the result of ovarian surface epithelium invagination into stromal inclusion cysts that are surrounded by a gonadotropin-rich environment that may induce precursor lesions to become cancer.

Lack of consistent and definitive evidence placing patients undergoing in vitro fertilization at significantly increased risk of ovarian cancer, however, does not bolster the incessant ovulation theory.

Convincing evidence points to the fallopian tube as the origin of many ovarian cancer cases. A group of Dutch investigators first reported serous tubal intraepithelial carcinomas (STICs) lesions in prophylactically removed fallopian tubes, many taken from women with 

The most convincing evidence of STIC as a precursor to ovarian cancer is the similar morphologic and molecular (

 mutation) profiles of the STICs and high grade serous ovarian carcinoma lesions.

 Up to 60% of fallopian tubes in patients with ovarian cancer demonstrate STIC at the time of hysterectomy or previous gynecologic surgery, demonstrating a role as a precursor.

Chronic inflammation of the tubes has also been proposed as carcinogenic based on exposure of the fallopian tube epithelium to retrograde menstruation or infectious and inflammatory agents.

Large population studies have demonstrated that occluding the tube via tubal ligation or the patient having had a previous salpingectomy can decrease the incidence of ovarian cancer by 28% and 35% (HR, 0.72, 0.65, respectively).

Endometrioid and clear cell ovarian epithelial cancers are known to be associated with endometriosis. Because of their anatomic location, the fallopian tubes are thought to be integral to the development of endometriosis-related cancers, as endometriotic foci are believed to pass through the tubes to reach the adnexa. 

Previous studies have identified occlusive tubal ligation as protective against development of endometrioid/clear cell etiologies, reporting up to a 50% reduction in these histologies, which supports the theory of endometriotic efflux as a potential contributor to nonserous ovarian histologies.

Although endometriosis itself is not considered a premalignant condition, there are many components of endometriosis that make malignant transformation plausible. For instance, endometriotic lesions are associated with chronic inflammation and cytokine release that are thought to precipitate the malignant transformation of implants to cancer. 

Because of overlapping risk factors between endometriosis and ovarian cancer (early menarche, late menopause, nulliparity), the rate of ovarian cancer among patients with known endometriosis is higher than that of the general population. 

A Swedish study found that compared with controls, patients with endometriosis were 1.3 to 2.0 times more likely to develop ovarian cancer and to receive a diagnosis at a younger age.

 Fortunately, given the propensity for development of symptoms, the majority of patients who receive a diagnosis of endometriosis-associated ovarian cancer—commonly endometrioid or clear cell histologies—frequently have stage I disease as compared with the general population who receive a diagnosis of ovarian cancer at stage III or above.

The overall lifetime risk of developing ovarian cancer in the general population is 1.3% to 1.5%, with a majority of cases occurring in the later years of life.

 Age and family history are the most important risk factors. 

Events that decrease the number of ovulatory events are known to reduce the risk of ovarian cancer, such as the number of pregnancies (increased protection with more pregnancies), breastfeeding, and use of oral contraceptives.

 Taking combined oral contraceptives (COCPs) that avert ovulation for at least 5 years can reduce a woman’s risk of ovarian cancer by up to 50% over a period of 30 years.

Approximately 18% to 24% of patients with ovarian cancer have a genetic predisposition due to inheritance of germline mutations. The widespread use of germline testing on patients with incident cancers has led to the identification of an increasing number of genes associated with cancer. In addition to 

 have been identified as genes associated with breast or ovarian cancer. 

Deleterious mutations in these genes are believed to occur in only 1% of families with a history of ovarian cancer, but if these mutations are present, patients have a 2.5% to 6.0% lifetime risk of developing serous ovarian cancer.

 Although this risk is higher than that of the general population, most of this cancer risk manifests at older ages. 

For this reason, risk-reducing salpingo-oophorectomy (RRSO) is typically recommended for patients aged 45 to 50 years.17,18 A summary of genetic mutations and overall risk for development of associated cancers is included in 

The most common germline mutations associated with the development of ovarian or fallopian tube cancer are in 

, genes involved in the homologous recombination DNA repair pathway. These mutations are propagated in an autosomal dominant fashion. Approximately 16% to 18% of patients with ovarian serous carcinoma have a germline 

 carriers, approximately 2% to 3% of cancers develop before 40 years of age, but this incidence increases to 20% by age 50, and increases even more after age 50. Hence, recommendations are for 

 carriers to undergo bilateral RRSO when they are aged 35 to 40 years.

The risk of ovarian cancer in patients with 

 disease [mutation] is lower than in those with 

disease [mutation], with approximately 2% to 3% of cases occurring by age 50, so RRSO is recommended for women aged 40 to 45 years. RRSO has been found to decrease the risk of OC by 75% to 95% but also contributes to the reduction in hormone production that is protective against development of breast cancer.

 Although the absolute risk of ovarian cancer is decreased, there is still a small risk of peritoneal carcinoma in 

 A trial (GOG-0199) by the Gynecologic Oncology Group reported a 2.6% rate of occult STIC or small invasive carcinomas in patients at increased risk who underwent RRSO. This number is thought to reflect the residual risk of peritoneal carcinoma that was not initially detected from RRSO procedures.

Patients with Lynch syndrome (hereditary nonpolyposis colorectal cancer syndrome) are at high risk of developing colorectal cancer and endometrial cancer (up to 70%) in addition to a lifetime risk of developing ovarian cancer that ranges from 10% to 13%.

Patients with Lynch syndrome are more likely to develop lower-grade, epithelial histology ovarian cancer and are more likely to develop early-stage disease (85% are stage I or II at diagnosis). Because of their lifetime risk of developing ovarian cancer, RRSO is recommended at age 40 or after completion of childbearing, as the risk of ovarian cancer prior to age 40 is less than 1%.

Understanding the origins of ovarian/fallopian tube cancer and subsequent risk of development of cancer allows for preemptive intervention regardless of whether the patient is desirous of future fertility.

Although there are no guidelines on preventive interventions to reduce the risk of endometriosis-associated cancers, hormone use is recommended for endometriosis-related pelvic pain with the goal of reducing estrogen input. 

Reduction in estrogen exposure to decrease ovulation and endometriotic implant stimulation can theoretically interrupt the inflammatory cascade thought to contribute to ovarian cancer precursors. In the population at increased risk for ovarian cancer, COCP use has been associated with a decreased risk of ovarian cancer in 

 However, this use must be weighed against the possible risk of breast cancer, which is still unknown.

The largest impact in terms of risk reduction occurs in patients or their family members with deleterious mutations conferring increased risk. Germline testing of patients with a new diagnosis of ovarian or fallopian tube cancer can identify mutations that lead to preventive measures and cascade testing of family members. Becauase of multifactorial causes, uptake of genetic testing has been much less frequent than recommended.

For women with a family history or genetic predisposition, recommendations exist for prophylactic surgery. 

 carriers, given the risk of ovarian cancer at earlier age onset, RRSO is recommended for women aged 35 to 40 years. 

 carriers, RRSO should occur between the ages of 40 and 45 years. For other genes (

) where there is a less than 10% risk of developing ovarian cancer, RRSO is recommended for patients aged 45 to 50 years.

 The risk of occult malignancy at the time of surgery for 

For women at average risk for ovarian cancer, salpingectomy at the time of hysterectomy for other indications or for sterilization may be protective. Data in non–

 gene carriers who underwent tubal ligation or salpingectomy have demonstrated up to a 35% risk reduction for ovarian cancer.

But in women 50 years or younger, the risk of all-cause mortality makes salpingo-oophorectomy less advisable unless there is a significant family history of ovarian cancer.

This, in conjunction with the knowledge that a significant proportion of cancers may arise from the fallopian tubes, raises the question of salpingectomy for risk reduction. The prospective SOROCk trial (NCT04251052) examining elective bilateral salpingo-oophorectomy (BSO) or salpingectomy in 

Bilateral RRSO in women with a genetic predisposition or family history of ovarian cancer has been shown to decrease the risk of ovarian cancer by up to 95%.

Approximately 3% to 8% of women who undergo RRSO for genetic predisposition will have an incidental STIC lesion found on permanent pathology, but women who have BSO for benign indications have incidental rates of less than 1%.

 If STIC lesions are identified incidentally, comprehensive evaluation of the abdominal cavity and peritoneal washings should be performed to ensure there is no evidence of disseminated disease. 

However, there are no definitive recommendations for surgical staging if a STIC lesion is incidentally found; in fact, the largest study examining outcomes in isolated STIC in RRSO patients reports limited utility of surgical staging because clinical outcomes associated with observation were favorable.27 Once identified, management with surveillance pelvic ultrasound and CA125 testing are reasonable approaches to monitoring.

The most important aspects of gynecologic care in the prevention of ovarian/fallopian tube cancer are extensively reviewing family history and facilitating cascade genetic testing for patients and families identified with genetic mutations. 

Use of COCPs is associated with risk reduction even in carriers of genetic mutation and curb inflammation that contributes to risk in disease entities. Salpingectomy has been associated with reduced risk of cancer but its contribution compared with RRSO is currently under study in carriers of genetic mutations. 

Cancer stat facts: ovarian cancer. National Cancer Institute Surveillance, Epidemiology, and End Results Program. Accessed November 25, 2021. https://seer.cancer.gov/statfacts/html/ovary.html

Kurman RJ, Shih IeM. The origin and pathogenesis of epithelial ovarian cancer: a proposed unifying theory. 

. 2010;34(3):433-443. doi:10.1097/PAS.0b013e3181cf3d79. PMID:20154587; PMCID:PMC2841791

Seidman JD, Vang R, Ronnett BM, Yemelyanova A, Cosin JA. Distribution and case-fatality ratios by cell-type for ovarian carcinomas: a 22-year series of 562 patients with uniform current histological classification. 

. 2015;136(2):336-340. doi:10.1016/j.ygyno.2014.12.018. Epub 2014 Dec 17. PMID:25528497

Dilley J, Burnell M, Gentry-Maharaj A, et al. Ovarian cancer symptoms, routes to diagnosis and survival - population cohort study in the ‘no screen’ arm of the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS). 

. 2020;158(2):316-322. doi:10.1016/j.ygyno.2020.05.002. Epub 2020 Jun 17. PMID:32561125; PMCID:PMC7453382

Menon U, Gentry-Maharaj A, Burnell M, et al. Ovarian cancer population screening and mortality after long-term follow-up in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomized controlled trial. 

. 2021;397(10290):2182-2193.doi:10.1016/S0140-6736(21)00731-5. Epub 2021 May 12. PMID:33991479; PMCID:PMC8192829

Otsuka I. Mechanisms of high-grade serous carcinogenesis in the fallopian tube and ovary: current hypotheses, etiologic factors, and molecular alterations. 

. 2021;22(9):4409.doi:10.3390/ijms22094409. PMID:33922503; PMCID:PMC8122889

Collaborative Group on Epidemiological Studies of Ovarian Cancer; Beral V, Doll R, Hermon C, Peto R, Reeves G. Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23,257 women with ovarian cancer and 87,303 controls. 

. 2008;371(9609):303-314. doi:10.1016/S0140-6736(08)60167-1. PMID:18294997

Babic A, Sasamoto N, Rosner BA, et al. Association between breastfeeding and ovarian cancer risk. 

. 2020;6(6):e200421. doi:10.1001/jamaoncol.2020.0421. Epub 2020 Jun 11. PMID:32239218; PMCID:PMC7118668

Scully RE. Pathology of ovarian cancer precursors. 

. 1995;23:208-218. doi:10.1002/jcb.240590928. PMID:8747398

Rizzuto I, Behrens RF, Smith LA. Risk of ovarian cancer in women treated with ovarian stimulating drugs for infertility. 

. 2019;6:CD008215. doi:10.1002/14651858.CD008215.pub2. Update in: 

. 2019 Jun 18;6:CD008215. PMID:23943232; PMCID:PMC6457641

Piek JM, van Diest PJ, Zweemer RP, et al. Dysplastic changes in prophylactically removed fallopian tubes of women predisposed to developing ovarian cancer. 

 2001;195(4):451-456. doi:10.1002/path.1000. PMID:11745677

Salvador S, Gilks B, Köbel M, Huntsman D, Rosen B, Miller D. The fallopian tube: primary site of most pelvic high-grade serous carcinomas. 

. 2009;19(1):58-64.doi:10.1111/IGC.0b013e318199009c. PMID:19258943

Falconer H, Yin L, Grönberg H, Altman D. Ovarian cancer risk after salpingectomy: a nationwide population-based study. 

. 2015;107(2):dju410. doi:10.1093/jnci/dju410. PMID:25628372

Sieh W, Salvador S, McGuire V, et al; Ovarian Cancer Association Consortium. Tubal ligation and risk of ovarian cancer subtypes: a pooled analysis of case-control studies. 

. 2013;42(2):579-589.doi:10.1093/ije/dyt042. PMID:23569193; PMCID:PMC3619957

Melin A, Sparén P, Persson I, Bergqvist A. Endometriosis and the risk of cancer with special emphasis on ovarian cancer. 

. 2006;21(5):1237-1242.doi:10.1093/humrep/dei462. Epub 2006 Jan 23. PMID:16431901

Sainz de la Cuesta R, Eichhorn JH, Rice LW, Fuller AF Jr, Nikrui N, Goff BA. Histologic transformation of benign endometriosis to early epithelial ovarian cancer. 

. 1996;60(2):238-244.doi:10.1006/gyno.1996.0032. PMID:8631545

Tung N, Domchek SM, Stadler Z, et al. Counselling framework for moderate-penetrance cancer-susceptibility mutations. 

. 2016;13(9):581-588. doi:10.1038/nrclinonc.2016.90. Epub 2016 Jun 14. PMID:27296296; PMCID:PMC5513673

Song H, Dicks E, Ramus SJ, et al. Contribution of germline mutations in the RAD51B, RAD51C, and RAD51D genes to ovarian cancer in the population. 

. 2015;33(26):2901-2907.doi:10.1200/JCO.2015.61.2408. Epub 2015 Aug 10. PMID:26261251; PMCID:PMC4554751

Zhang S, Royer R, Li S, et al. Frequencies of BRCA1 and BRCA2 mutations among 1,342 unselected patients with invasive ovarian cancer. 

. 2011;121(2):353-357. doi:10.1016/j.ygyno.2011.01.020. Epub 2011 Feb 15. PMID:21324516

Kauff ND, Satagopan JM, Robson ME, et al. Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation. 

. 2002;346(21):1609-1615. doi:10.1056/NEJMoa020119. Epub 2002 May 20. PMID:12023992

Sherman ME, Piedmonte M, Mai PL, et al. Pathologic findings at risk-reducing salpingo-oophorectomy: primary results from Gynecologic Oncology Group Trial GOG-0199. 

. 2014;32(29):3275-3283. doi:10.1200/JCO.2013.54.1987. Epub 2014 Sep 8. PMID:25199754; PMCID:PMC4178524

Watson P, Bützow R, Lynch HT, et al. The clinical features of ovarian cancer in hereditary nonpolyposis colorectal cancer. 

. 2001;82(2):223-228.doi:10.1006/gyno.2001.6279. PMID:11531271

Bonadona V, Bonaïti B, Olschwang S, et al. Cancer risks associated with germline mutations in 

. 2011;305(22):2304-2310.doi:10.1001/jama.2011.743. PMID:21642682

Schrijver LH, Antoniou AC, Olsson H, et al; Hereditary Breast and Ovarian Cancer Research Group Netherlands and International BRCA1/2 Carrier Cohort Study. Oral contraceptive use and ovarian cancer risk for 

 mutation carriers: an international cohort study. 

. 2021;225(1):51.e51-51.e17.doi:10.1016/j.ajog.2021.01.014. Epub 2021 Jan 22. PMID:33493488; PMCID:PMC8278569

Cusimano MC, Ferguson SE, Moineddin R, et al. Ovarian cancer incidence and death in average-risk women undergoing bilateral salpingo-oophorectomy at benign hysterectomy. 

. 2022;226(2):220.e1-220.e26. doi:10.1016/j.ajog.2021.09.020doi:10.1016/j.ajog.2021.09.020. Epub 2021 Sep 24. PMID:34563499

Rabban JT, Garg K, Crawford B, Chen LM, Zaloudek CJ. Early detection of high-grade tubal serous carcinoma in women at low risk for hereditary breast and ovarian cancer syndrome by systematic examination of fallopian tubes incidentally removed during benign surgery. 

. 2014;38(6):729-742. doi:10.1097/PAS.0000000000000199. PMID:24820399

Wethington SL, Park KJ, Soslow RA, et al. Clinical outcome of isolated serous tubal intraepithelial carcinomas (STIC). 

. 2013;23(9):1603-1611.doi:10.1097/IGC.0b013e3182a80ac8. PMID:24172097; PMCID:PMC4979072

Articles

Family history assessment, genetic screening are key to prevention.

Clues to the origins of ovarian cancer

Soft markers are minor ultrasound findings identified in the midtrimester that commonly do not represent a structural abnormality. These may be normal variants but are noteworthy because of their association with an increased aneuploidy risk. Commonly identified soft markers include echogenic intracardiac focus; echogenic bowel; choroid plexus cyst(s); single umbilical artery; urinary tract dilation; shortened humerus, femur, or both; thickened nuchal fold; and absent or hypoplastic nasal bone

Contemporaneously with the advancement in aneuploidy detection with soft markers was the development of improved serum screening methods to predict aneuploidy risk.

 The introduction of cell-free DNA (cfDNA) techniques greatly improved the ability to screen for common aneuploidies. Given the high sensitivity and specificity of cfDNA for trisomies 21, 18, and 13 across all age groups, in 2020, the American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine endorsed the option of cfDNA screening for all patients.

What is the initial approach when an isolated soft marker is identified?

“Isolated” is a soft marker that has been identified in the absence of any fetal structural anomaly, growth restriction, or additional soft marker, following a detailed obstetrical ultrasound examination. Identification of a soft marker is an indication for a detailed obstetrical ultrasound examination (Current Procedural Terminology code 76811) to ensure the finding is isolated. 

The decision to perform a detailed examination should be made through a shared decision-making framework. In the case of multiple soft markers or structural abnormalities, the approach to evaluation should be individualized.

If an isolated soft marker is confirmed, subsequent evaluation and counseling depend on prior aneuploidy screening results, additional risk factors for aneuploidy, and associations with nonaneuploid conditions.

Traditionally, the presence or absence of specific soft markers was used to modify the probability of trisomy 21 and 18 for high-risk patients.

However, the relative importance of this approach has evolved rapidly with improved prenatal screening techniques. 

The detection rates for aneuploidy with commonly employed serum screening strategies (ie, first-trimester screen, integrated screen, sequential screen, contingent screen, or quad screen) are high. 

cfDNA is the single best screening test for the common trisomies (trisomies 21, 18, and 13), and the posttest probability of a common aneuploidy after negative cfDNA screening is very low.

 Although a range of positive likelihood ratios (LRs) for a particular aneuploidy exists for each soft marker, even when the highest positive LRs are applied to a population that has previously had a negative cfDNA result, the risk of trisomy 21 is negligibly affected.

Only diagnostic testing removes residual risk for aneuploidy detection. 

Thus, a patient may elect diagnostic testing for any indication. However, we do not recommend diagnostic testing for aneuploidy solely for the evaluation of an isolated soft marker following a negative serum or cfDNA screening result (grade 1B). 

Similarly, if a pregnant person has undergone diagnostic testing and the results indicate a normal karyotype, identification of a soft marker is insignificant with regard to aneuploidy and should be reported as such.

Some pregnant people may decline any aneuploidy screening following a shared decision-making process that incorporates accurate information, accessible health care resources, and the patient’s clinical context, values, beliefs, and potential anxiety created by the identification and discussion of a soft marker.

Each practice should establish a standardized protocol for how the identification of an isolated soft marker will be documented and managed for patients who have previously declined aneuploidy screening. 

These protocols should ensure patients are informed prior to the ultrasound examination of how findings will be handled to enhance shared decision-making and patient autonomy.

What is the counseling and management regarding soft ultrasound markers?

Table 1 summarizes the definition, prevalence, range of LRs, evaluation, and follow-up for commonly identified soft markers. 

 summarizes recommendations for the evaluation and management of isolated soft ultrasound markers for aneuploidy in the
second trimester. 

Benacerraf BR, Frigoletto FD Jr, Cramer DW. Down syndrome: sonographic sign for diagnosis in the second-trimester fetus. 

 1987;163(3):811-813. doi:10.1148/radiology.163.3.2953039

Benacerraf BR, Gelman R, Frigoletto FD Jr. Sonographic identification of second-trimester fetuses with Down’s syndrome. 

. 1987;317(22):1371-1376. doi:10.1056/NEJM198711263172203

Benacerraf BR, Mandell J, Estroff JA, Harlow BL, Frigoletto FD Jr. Fetal pyelectasis: a possible association with Down syndrome. 

Lockwood C, Benacerraf B, Krinsky A, et al. A sonographic screening method for Down syndrome. 

. 1987;157(4 Pt 1):803-808. doi:10.1016/s0002-9378(87)80059-5

Malone FD, Canick JA, Ball RH, et al. First-trimester or second-trimester screening, or both, for Down’s syndrome. 

. 2005;353(19):2001-2011. doi:10.1056/NEJMoa043693

American College of Obstetricians and Gynecologists’ Committee on Practice Bulletins—Obstetrics; Committee on Genetics; Society for Maternal-Fetal Medicine. Screening for fetal chromosomal abnormalities: ACOG practice bulletin, number 226. 

. 2020;136(4):e48-e69. doi:10.1097/AOG.0000000000004084

Nyberg DA, Luthy DA, Resta RG, Nyberg BC, Williams MA. Age-adjusted ultrasound risk assessment for fetal Down’s syndrome during the second trimester: description of the method and analysis of 142 cases. 

. 1998;12(1):8-14. doi:10.1046/j.1469-0705.1998.12010008.x

Gil MM, Accurti V, Santacruz B, Plana MN, Nicolaides KH. Analysis of cell-free DNA in maternal blood in screening for aneuploidies: updated meta-analysis. 

. 2017;50(3):302-314. doi:10.1002/uog.17484

Filly RA. Obstetrical sonography: the best way to terrify a pregnant woman. 

. 2000;19(1):1-5. doi:10.7863/jum.2000.19.1.1

Filly RA, Norton ME. Obstetric sonography: why are we still terrifying pregnant women? 

. 2018;37(9):2277-2278. doi:10.1002/jum.14572

In this consult series, experts from SMFM discuss the evaluation and management of soft ultrasound markers for aneuploidy.

SMFM Consult Series #57: Evaluation and management of soft ultrasound markers for aneuploidy

Thrust into the front lines of the pandemic, we were called upon to not only care for patients with COVID-19 but to do so against the backdrop of ongoing nonelective care. Put simply, obstetrics never stopped. As we reflect on the heroic work of our colleagues and friends, it is interesting to frame our experiences through ebbs and flows of case counts for the past 2 years. 

We saw community burden through a unique lens given constant patient volume, access to COVID-19 testing in outpatient and inpatient areas with integrated electronic health records, early universal testing at delivery for mothers and exposed infants, and screening for those admitted during antepartum care.

Indeed, being in the labor and delivery department the past 2 years often felt like one was the canary in the coal mine. As COVID-19 surges came and went, we felt that the day-to-day rise in number of positive cases we diagnosed foreshadowed the rise in hospitalizations. 

Taking this to our statisticians, we asked them to see whether they could prove our hypothesis. The statistics were more complex than we expected.

At Parkland Hospital in Dallas, Texas, where there are nearly 12,000 births per year, the service was testing as many as 50 women a day. A time series analysis was used to compare the number of new COVID-19 cases in obstetrics and the number of new COVID-19 cases hospitalized in the Dallas–Fort Worth trauma service area. 

The Kwiatkowski-Phillips-Schmidt-Shin test was used to test the assumption of stationarity in both data sets. This assumption indicates that each time series has no dependence on the time it is being observed (no trend, seasonality, etc). 

The data were determined to be stationary, and the Granger causality test was used to determine whether the obstetrics COVID-19 counts at differing lags in addition to the changing hospital census counts were useful for forecasting the hospital census count in the future. 

A lag of 1 would indicate using obstetrics counts 1 day prior, a lag of 2 would be using the obstetrics counts 2 days prior, and so on. We tested to see how far out the obstetric case counts became the “canary.” Lags of 1 to 7 days were tested to assess the usefulness of the prior week of obstetrics data in forecasting the Dallas–Fort Worth hospital census. 

 values were adjusted using the Bonferroni method to control the inflated type I error rate due to multiple testing. Statistical significance is indicated
by 

Interestingly, the data proved our point. The obstetric COVID-19 cases 1 day prior forecasted hospital census increases in our metroplex (

We believe the same could be done with continued ongoing local surveillance, but that is not yet a reality because most community testing is done for an indication rather than universally. That is, community testing availability waxes and wanes in response to a recognized surge. 

Although these data are limited in predicting a surge far in advance, the labor and delivery department statistics did serve as a safety signal for the community. Ob-gyns were the canaries in the coal mines of COVID-19 community burden. We hope to use this insight and similar data in the future to guide targeted responses to disease spread. 

Obstetrics and gynecologists (ob-gyns) are tough.

Ob-gyns: canaries in the coal mine for COVID-19

Sexual assault affects more of those around us than we know, from coworkers to friends and family to the individual across from you in the coffee shop.

In the United States, a sexual assault is committed every 68 seconds. One of every 6 women in the US has been the victim of an attempted or completed rape, and 1 in 33 men in the US has been a victim of an attempted or completed rape.

 Only 25 of every 1000 perpetrators go to prison, according to the Rape, Abuse & Incest National Network.

Sexual assault can happen anywhere, with 55% of sexual assaults occurring at or near the victim’s home, 15% in an open public place, 12% at or near a relative’s home, 10% in an enclosed public area (eg, parking garage/lot), and 8% on school property.

April is Sexual Assault Awareness and Prevention Month, an excellent time to educate and equip ourselves and our patients with strategies to help prevent and protect victims of sexual assault.

Sometimes an individual may be a bystander to sexual assault. Common reasons for bystanders not intervening in situations include not wanting to cause a scene, wanting to mind their own business, or thinking someone else will step in.

However, there are ways to lend a hand in preventing sexual assault from happening in the first place by implementing active bystander intervention strategies.

Whether it’s stepping in when an individual acts aggressively or giving a friend a ride home when they’ve had too much to drink, active bystander intervention is integral to helping prevent
sexual assault.

By being a more proactive bystander, we can help prevent sexual assault and thus create a safer environment for ourselves and those around us.

Statistics. RAINN. Accessed February 23, 2022. 

Practicing active bystander intervention. RAINN. Accessed February 23, 2022. 

https://rainn.org/articles/practicing-active-bystander-intervention?_ga=2.126991567.39737792.1645629250-193895623.1645629250

Help prevent sexual assault

The study was conducted at the Menopause Clinic of King Chulalongkorn Memorial Hospital in Bangkok, Thailand, between November 2018 and May 2019.

Recruitment included a total of 200 postmenopausal women—aged 50 to 65—all with a 12-month history of amenorrhea or oophorectomy. Researchers excluded women who underwent recent hair loss treatments.

Each participant was evaluated for female pattern hair loss (FPHL), based on Ludwig's classification, using standardized global photography in all 6 views and trichoscopy for hair density and diameter.

A team of 3 dermatologists reevaluated all pictures to confirm FPHL, assessing 178 postmenopausal women for hair-loss patterns. The average age was 58.8 years and the time since menopause was 9.2 years.

A total of 82% of these participants had never used menopausal hormone therapy (MHT), while 5% were current MHT users. In addition, 4% of women had diabetes mellitus, 2% had a history of polycystic ovary syndrome (PCOS), and 8% had thyroid diseases.

The prevalence of FPHL was 52.2%, whereas the severity of FPHL by Ludwig grades 1, 2, and 3 were 73.2%, 22.6% and 4.3%, respectively.

Low self-esteem was a common factor that increased with FHPL severity, detected in 60% of the women. All women with Ludwig 3, in fact, indicated low self-esteem.

The median of total and terminal hair density in the FPHL group was significantly lower than in the normal hair group. The median of vellus hair density in the FPHL group, however, was significantly higher than in the normal hair group at the mid-scalp area.

More than half of postmenopausal women experience female pattern hair loss, according to a cross-sectional study in the journal Menopause.

Vol 67 No 4

Clues to the origins of ovarian cancer

SMFM Consult Series #57: Evaluation and management of soft ultrasound markers for aneuploidy

Ob-gyns: canaries in the coal mine for COVID-19

Help prevent sexual assault

Study shows strong correlation between female pattern hair loss and BMI in postmenopausal women

Postmenopausal vulvovaginal discomfort

Efficacy of combined oral contraceptives for treating depression in premenstrual women