Medical School · Year 3 · Obgyn · includes a quiz and discussion video

Seminar 15: Uterine Disorders

OB/GYN Clerkship

Learning Objectives

By the end of this seminar, students will be able to:

1. Classify uterine leiomyomas by FIGO type and location, correlate fibroid position with symptom profile, and select appropriate management strategies
2. Recognize adenomyosis based on clinical presentation and characteristic imaging findings and differentiate it from leiomyomas
3. Distinguish endometrial hyperplasia with and without atypia, assess malignancy risk, and apply progestin-based treatment protocols
4. Stage endometrial cancer using the FIGO system and describe treatment approaches by stage and histologic type
5. Evaluate and manage pelvic organ prolapse using the POP-Q staging system with conservative and surgical options
6. Classify Mullerian anomalies, recognize their impact on reproductive outcomes, and identify indications for surgical correction

Seminar Outline

Section 1: Uterine Leiomyomas (Fibroids)

Uterine leiomyomas are the most common benign tumors of the female reproductive tract, with a cumulative incidence of 70 to 80 percent by age 50 based on pathologic and imaging studies. The prevalence is significantly higher in Black women, who develop fibroids at younger ages, with larger tumors, and with greater symptom severity compared to white women. Leiomyomas are hormonally responsive, growing under the influence of both estrogen and progesterone, which explains their tendency to enlarge during reproductive years and regress after menopause. Risk factors for fibroid development include early menarche, nulliparity, obesity, family history, and African American race, while protective factors include parity and smoking, the latter likely through its anti-estrogenic effects.

The FIGO classification system categorizes leiomyomas by their anatomic location relative to the uterine wall, which is critical for predicting symptoms and guiding management. Types 0 through 2 are submucosal fibroids that distort the endometrial cavity, with type 0 being entirely intracavitary, type 1 having less than 50 percent intramural extension, and type 2 having 50 percent or more intramural extension. Types 3 and 4 are intramural fibroids that lie entirely within the myometrium, with type 3 contacting but not distorting the endometrial surface. Types 5 through 7 are subserosal fibroids, with type 7 being entirely pedunculated and attached to the uterine serosa. Type 8 includes fibroids in atypical locations such as cervical or parasitic fibroids. This classification system directly informs surgical planning, as submucosal fibroids are amenable to hysteroscopic resection while intramural and subserosal fibroids require abdominal approaches.

The symptom profile of leiomyomas depends primarily on their size, number, and location within the uterus. Heavy menstrual bleeding is the most common symptom and is most strongly associated with submucosal fibroids, which increase the endometrial surface area and disrupt normal endometrial hemostasis. Bulk symptoms including pelvic pressure, urinary frequency, urinary retention, and constipation result from mass effect on adjacent organs, particularly with large intramural and subserosal fibroids. Reproductive consequences include subfertility, particularly when submucosal fibroids distort the endometrial cavity, and increased risk of miscarriage, preterm labor, and malpresentation during pregnancy. Pain symptoms including dysmenorrhea and dyspareunia are less common but may occur with fibroid degeneration, torsion of a pedunculated fibroid, or impingement on adjacent structures.

Diagnosis of leiomyomas relies on imaging, with ultrasound as the primary modality and MRI providing detailed mapping when surgical planning requires precise characterization. Transvaginal ultrasound demonstrates well-circumscribed, hypoechoic masses with variable echogenicity depending on the degree of calcification and degeneration. MRI provides superior soft tissue contrast and allows precise measurement of fibroid number, size, and location relative to the endometrial cavity and uterine serosa, making it invaluable for preoperative planning in complex cases. Saline infusion sonography evaluates the degree of submucosal fibroid extension into the endometrial cavity, which determines the feasibility of hysteroscopic resection. Hysteroscopy provides direct visualization of the uterine cavity and allows concurrent surgical treatment of submucosal fibroids.

<image>Panel A: Leiomyoma epidemiology showing 70 to 80 percent prevalence by age 50, racial disparities with higher incidence and severity in Black women, hormonal responsiveness to estrogen and progesterone, and risk factors (early menarche, nulliparity, obesity, family history). Panel B: FIGO classification diagram showing submucosal types 0 through 2 (distort cavity), intramural types 3 and 4 (within myometrium), subserosal types 5 through 7 (outer surface to pedunculated), and type 8 (cervical, parasitic) with surgical approach correlation. Panel C: Symptom-location correlation showing heavy menstrual bleeding (submucosal), bulk symptoms (intramural, subserosal), reproductive impact (submucosal cavity distortion), and pain (degeneration, torsion, impingement). Panel D: Imaging modalities showing transvaginal ultrasound (primary, hypoechoic well-circumscribed), MRI (detailed mapping, preoperative planning), saline infusion sonography (submucosal extension assessment), and hysteroscopy (direct visualization and treatment).</image>

Section 2: Fibroid Management

Observation is appropriate for asymptomatic fibroids, which represent the majority of leiomyomas and do not require treatment. Monitoring with periodic imaging, typically annually or when new symptoms develop, ensures that significant growth or new symptoms are identified promptly. Perimenopausal women with mild symptoms may be counseled that fibroids are expected to shrink after menopause as estrogen and progesterone levels decline. Indications for transitioning from observation to active management include the development of heavy menstrual bleeding causing anemia, significant bulk symptoms affecting quality of life, rapid growth raising concern for sarcoma (though this is extremely rare), or reproductive failure attributed to fibroid location.

Medical management of symptomatic fibroids aims to reduce bleeding and fibroid volume through pharmacologic manipulation. Nonsteroidal anti-inflammatory drugs reduce menstrual blood loss and associated dysmenorrhea but do not affect fibroid size. Tranexamic acid, an antifibrinolytic agent, reduces menstrual blood loss by approximately 50 percent and is taken only during menstruation. Hormonal contraception, including combined oral contraceptive pills and the levonorgestrel intrauterine device, reduces menstrual bleeding but does not reliably shrink fibroids. Gonadotropin-releasing hormone agonists produce a hypoestrogenic state that can reduce fibroid volume by 30 to 50 percent within 3 to 6 months, but use is limited to 6 months due to bone loss, and fibroid regrowth occurs after discontinuation. Newer oral gonadotropin-releasing hormone antagonists with hormonal add-back therapy allow longer-term use while managing bleeding and fibroid symptoms.

Procedural and uterine-sparing surgical options address symptomatic fibroids while preserving the uterus for women who desire future fertility or prefer to avoid hysterectomy. Uterine artery embolization is an interventional radiology procedure that delivers particulate embolic agents into the uterine arteries, reducing fibroid blood supply and causing ischemic necrosis, with symptom improvement in 80 to 90 percent of patients. MRI-guided focused ultrasound uses high-intensity ultrasound energy to thermally ablate fibroid tissue noninvasively. Myomectomy surgically removes fibroids while preserving the uterus and is the preferred approach for women desiring future pregnancy. Hysteroscopic myomectomy is appropriate for submucosal fibroids with significant intracavitary extension, while abdominal or laparoscopic myomectomy addresses intramural and subserosal fibroids. Myomectomy carries a risk of recurrence, with approximately 15 to 30 percent of patients developing new fibroids requiring additional treatment.

Hysterectomy provides definitive treatment for symptomatic fibroids and eliminates the possibility of recurrence. Indications include failure of conservative management, completed childbearing with persistent symptoms, very large fibroid burden, and concern for malignancy such as rapidly growing fibroids or sarcoma. The surgical approach is selected based on uterine size, fibroid distribution, and surgeon experience, with options including vaginal, laparoscopic, robotic-assisted, and abdominal hysterectomy. Vaginal and laparoscopic approaches are preferred when feasible due to shorter recovery, reduced pain, and lower complication rates. In cases where uterine sarcoma is a concern, power morcellation should be avoided due to the risk of disseminating unrecognized malignancy, and an en bloc removal technique with contained extraction is preferred.

<image>Panel A: Observation criteria showing asymptomatic fibroids (no treatment needed), periodic imaging monitoring, perimenopausal expectant management (postmenopausal regression), and indications for transitioning to active treatment (anemia, bulk symptoms, rapid growth, reproductive failure). Panel B: Medical management options showing NSAIDs (reduce bleeding, no size change), tranexamic acid (50 percent bleeding reduction during menses), hormonal contraception (bleeding reduction), GnRH agonists (30 to 50 percent volume reduction, 6-month limit), and oral GnRH antagonists with add-back (longer-term option). Panel C: Uterine-sparing procedures showing UAE (embolic agents, 80 to 90 percent symptom improvement), MRgFUS (thermal ablation, noninvasive), hysteroscopic myomectomy (submucosal), abdominal or laparoscopic myomectomy (intramural, subserosal), and 15 to 30 percent recurrence rate. Panel D: Hysterectomy showing indications (failed conservative treatment, completed childbearing, sarcoma concern), approach selection (vaginal, laparoscopic, robotic, abdominal), minimally invasive preference, and avoidance of power morcellation when sarcoma suspected.</image>

Section 3: Adenomyosis

Adenomyosis is a condition defined by the presence of endometrial glands and stroma within the myometrium, resulting in uterine enlargement and a range of debilitating symptoms. The condition most commonly affects women of reproductive age, with a peak incidence in the fourth and fifth decades of life. Risk factors include multiparity and prior uterine surgery, including cesarean delivery and curettage, which may facilitate the invasion of endometrial tissue into the myometrial layer. Adenomyosis frequently coexists with other uterine pathology including leiomyomas and endometriosis, and distinguishing adenomyosis from fibroids has important implications for treatment selection, as the conditions respond differently to medical and surgical interventions.

The clinical presentation of adenomyosis centers on two cardinal symptoms: heavy menstrual bleeding and progressive dysmenorrhea. The heavy menstrual bleeding is caused by the increased uterine surface area, impaired myometrial contractility, and altered endometrial vascularity associated with the ectopic endometrial tissue. Dysmenorrhea is characteristically progressive, worsening over time, and may begin before menstrual flow and persist throughout the period. Dyspareunia may occur, particularly with deep penetration, reflecting uterine tenderness. Physical examination classically reveals a diffusely enlarged, globular, and tender uterus that is symmetrically enlarged rather than irregularly contoured as with fibroids. The uterus may be two to three times the normal size.

Diagnosis of adenomyosis has been historically made on the hysterectomy specimen, but advances in imaging have enabled reliable preoperative diagnosis. Transvaginal ultrasound demonstrates a heterogeneous myometrium with poorly defined endometrial-myometrial borders, myometrial cysts representing ectopic endometrial glands, and the characteristic "venetian blind" shadowing pattern created by the diffusely altered myometrial echotexture. MRI is considered the most accurate imaging modality and demonstrates thickening of the junctional zone, the interface between endometrium and myometrium, exceeding 12 millimeters, which is considered diagnostic. The clinical diagnosis is made by integrating characteristic symptoms with supportive imaging findings, as no single noninvasive test is perfectly sensitive or specific. Definitive histologic confirmation requires examination of a hysterectomy specimen.

Treatment of adenomyosis is guided by symptom severity, reproductive goals, and response to conservative measures. Medical management includes hormonal therapy with combined oral contraceptive pills to reduce bleeding and pain, the levonorgestrel intrauterine device which produces local progestin-mediated endometrial suppression and is particularly effective for adenomyosis-related bleeding, and gonadotropin-releasing hormone agonists for short-term symptom relief. Pain management with nonsteroidal anti-inflammatory drugs provides symptomatic relief during menstruation. Hysterectomy remains the only definitive treatment for adenomyosis and is appropriate for women with severe symptoms who have completed childbearing. Adenomyomectomy, the excisional removal of adenomyotic tissue while preserving the uterus, has been described as a conservative surgical option, but its efficacy is limited by the diffuse nature of the disease and the inability to completely resect all affected tissue without compromising uterine integrity.

<image>Panel A: Adenomyosis pathology showing endometrial glands and stroma invading the myometrium, peak incidence in the 40s, risk factors (multiparity, prior uterine surgery), and frequent coexistence with leiomyomas and endometriosis. Panel B: Clinical presentation showing heavy menstrual bleeding (increased surface area, impaired contractility), progressive dysmenorrhea (worsening over time), dyspareunia (deep penetration tenderness), and physical examination findings (diffusely enlarged, globular, tender uterus). Panel C: Diagnostic imaging showing transvaginal ultrasound (heterogeneous myometrium, myometrial cysts, venetian blind shadowing), MRI (junctional zone thickening greater than 12 mm), and principle that definitive diagnosis requires hysterectomy histology. Panel D: Treatment options showing medical management (OCP, levonorgestrel IUD, GnRH agonists, NSAIDs), hysterectomy (definitive, completed childbearing), and adenomyomectomy (limited by diffuse disease, compromised uterine integrity).</image>

Section 4: Endometrial Hyperplasia

Endometrial hyperplasia is classified by the 2014 World Health Organization system into two categories based on the presence or absence of cytologic atypia, which determines the risk of progression to endometrial carcinoma. Hyperplasia without atypia, previously encompassing both simple and complex hyperplasia, carries a malignancy risk of 1 to 3 percent and represents a low-risk condition that is highly responsive to progestin therapy. Atypical hyperplasia, which demonstrates cytologic atypia including nuclear enlargement, rounding, and loss of polarity, carries a risk of concurrent or progressive endometrial cancer of 25 to 40 percent, making it a premalignant condition that generally warrants hysterectomy. The distinction between these two categories on endometrial biopsy is the single most important factor determining management and prognosis.

The pathogenesis of endometrial hyperplasia is driven by unopposed estrogen exposure without adequate progesterone to counteract estrogen's proliferative effect on the endometrium. Exogenous unopposed estrogen replacement therapy in women with an intact uterus is a well-established cause that has been largely eliminated by the standard practice of combining estrogen with progestin. Endogenous estrogen excess occurs in obesity through peripheral aromatization of androgens to estrogen in adipose tissue, in polycystic ovary syndrome through chronic anovulation, and with estrogen-producing ovarian tumors such as granulosa cell tumors. Tamoxifen exerts estrogenic effects on the endometrium despite its anti-estrogenic action on breast tissue. Nulliparity and continuous cycling without the protective effect of pregnancy-related progesterone exposure also contribute to risk.

The clinical presentation of endometrial hyperplasia is most commonly abnormal uterine bleeding, the character of which depends on the patient's menopausal status. Postmenopausal women typically present with any amount of vaginal bleeding, which mandates evaluation regardless of the quantity. Premenopausal women present with heavy or prolonged menstrual bleeding, intermenstrual bleeding, or irregular cycles. Some patients are asymptomatic, with hyperplasia discovered incidentally on endometrial biopsy performed for other indications or on imaging showing thickened endometrium. The clinical challenge is that the symptoms of hyperplasia overlap completely with those of other causes of abnormal uterine bleeding, making tissue diagnosis essential.

Diagnosis of endometrial hyperplasia requires histologic examination of endometrial tissue obtained through one of several methods. Office endometrial biopsy using a disposable sampling device such as a Pipelle is the most common initial diagnostic procedure and has a sensitivity of approximately 90 percent for detecting hyperplasia and cancer. Transvaginal ultrasound demonstrating a thickened endometrium, exceeding 4 millimeters in postmenopausal women, prompts tissue sampling but cannot distinguish hyperplasia from cancer or even benign causes of thickening. Dilation and curettage provides a more comprehensive endometrial sample than office biopsy and is indicated when office biopsy is technically insufficient or when results are discordant with clinical suspicion. Hysteroscopy with directed biopsy allows visualization of the endometrial cavity and targeted sampling of suspicious areas, providing the most accurate diagnosis.

<image>Panel A: WHO 2014 classification showing hyperplasia without atypia (1 to 3 percent malignancy risk, progestin-responsive) and atypical hyperplasia (25 to 40 percent concurrent or progressive cancer risk, generally warrants hysterectomy) with cytologic atypia features (nuclear enlargement, rounding, loss of polarity). Panel B: Unopposed estrogen pathogenesis showing exogenous estrogen therapy, endogenous excess from obesity (peripheral aromatization), PCOS (chronic anovulation), estrogen-producing tumors (granulosa cell), and tamoxifen (estrogenic endometrial effect). Panel C: Clinical presentation by menopausal status showing postmenopausal bleeding (any amount mandates evaluation), premenopausal heavy or irregular bleeding, and asymptomatic incidental discovery on biopsy or imaging. Panel D: Diagnostic methods showing office endometrial biopsy (Pipelle, 90 percent sensitivity), transvaginal ultrasound (thickened endometrium prompts sampling), D&C (comprehensive sample when office biopsy insufficient), and hysteroscopy with directed biopsy (most accurate, targeted sampling).</image>

Section 5: Endometrial Hyperplasia Management

Management of hyperplasia without atypia is primarily medical, with progestin therapy as the cornerstone of treatment. The levonorgestrel-releasing intrauterine device is the preferred first-line therapy due to its superior efficacy compared to oral progestins, with regression rates of approximately 90 percent at 6 months. The local progestin delivery produces high endometrial concentrations with minimal systemic side effects, and the device simultaneously provides contraception and endometrial protection. Alternative progestin regimens include oral medroxyprogesterone acetate at 10 to 20 milligrams daily for 12 to 14 days per month in a cyclic regimen, or continuous oral progestin for more robust suppression. Follow-up endometrial biopsy at 3 to 6 months assesses the histologic response, and most cases resolve with adequate progestin therapy.

Management of atypical hyperplasia differs fundamentally because of the high risk of concurrent or progressive endometrial cancer. The standard recommendation is total hysterectomy with bilateral salpingo-oophorectomy, as approximately 25 to 40 percent of patients with atypical hyperplasia on biopsy are found to have invasive cancer on the final hysterectomy specimen. For women who strongly desire future fertility and are willing to accept the risks of conservative management, a fertility-sparing approach using high-dose progestins with the levonorgestrel intrauterine device or oral megestrol acetate at 40 to 160 milligrams daily may be considered. This conservative approach requires close surveillance with endometrial biopsy every 3 months to document regression, and the patient must be counseled that progression to cancer may occur despite therapy. Once childbearing is complete, hysterectomy is recommended regardless of the response to progestin therapy.

Progestin agents used for endometrial hyperplasia differ in their route of administration, dosing, and side effect profiles. The levonorgestrel intrauterine device is preferred for both non-atypical and atypical hyperplasia due to its superior local drug delivery and high regression rates. Oral medroxyprogesterone acetate is dosed at 10 to 20 milligrams daily and may be administered cyclically for 12 to 14 days per month or continuously. Megestrol acetate at 40 to 160 milligrams daily is a high-dose option used primarily for atypical hyperplasia in the fertility-sparing setting. All progestin regimens require follow-up tissue sampling to confirm regression, and the duration of therapy depends on the histologic response and the patient's risk factors for recurrence. Patients who achieve complete regression should continue progestin therapy or undergo close surveillance, as recurrence rates are significant.

Risk reduction strategies for endometrial hyperplasia address the modifiable factors that contribute to unopposed estrogen exposure. Weight loss reduces peripheral estrogen production from adipose tissue aromatization and is particularly important for obese women with hyperplasia, in whom even modest weight loss can improve endometrial health. Treatment of polycystic ovary syndrome with measures that restore regular withdrawal bleeding, including combined oral contraceptive pills or cyclic progestins, protects the endometrium from prolonged estrogen exposure. Women receiving estrogen replacement therapy for menopausal symptoms must always have a progestin component to counterbalance the endometrial effects of estrogen. Combined oral contraceptive pills provide endometrial protection for premenopausal women at risk and should be considered for long-term risk reduction in appropriate candidates.

<image>Panel A: Hyperplasia without atypia management showing levonorgestrel IUD (preferred, 90 percent regression at 6 months), oral medroxyprogesterone (10 to 20 mg daily, cyclic or continuous), follow-up biopsy at 3 to 6 months, and expected resolution with adequate progestin therapy. Panel B: Atypical hyperplasia management showing hysterectomy with BSO (standard, 25 to 40 percent concurrent cancer), fertility-sparing option (high-dose progestins, LNG-IUD or megestrol), surveillance biopsy every 3 months, and hysterectomy after childbearing completion. Panel C: Progestin agent comparison showing LNG-IUD (superior local delivery, high regression rates), oral MPA (10 to 20 mg, cyclic or continuous), megestrol (40 to 160 mg, high-dose for atypical), and requirement for follow-up tissue sampling with significant recurrence rates. Panel D: Risk reduction strategies showing weight loss (reduces peripheral aromatization), PCOS treatment (restore regular withdrawal bleeding), progestin with ERT (endometrial protection), and OCP for premenopausal risk reduction.</image>

Section 6: Endometrial Cancer

Endometrial cancer is the most common gynecologic malignancy in the developed world, with approximately 65,000 new cases annually in the United States. The peak incidence occurs between ages 60 and 70, though the increasing prevalence of obesity has shifted the age distribution toward younger women. Risk factors mirror those of endometrial hyperplasia, as both conditions share the pathogenetic pathway of unopposed estrogen exposure. The overall prognosis is favorable when diagnosed at an early stage, with 5-year survival rates exceeding 80 percent for stage I disease, reflecting the fact that most endometrial cancers present with postmenopausal bleeding that prompts early evaluation and diagnosis.

Endometrial cancer is classified into two broad clinicopathologic types with distinct molecular profiles, clinical behaviors, and prognoses. Type I endometrial cancer, predominantly endometrioid histology, accounts for approximately 80 percent of cases and is associated with estrogen exposure, obesity, and endometrial hyperplasia. Type I cancers are typically lower grade, present at an earlier stage, and carry a more favorable prognosis. Type II endometrial cancer includes serous and clear cell histologies, is not estrogen-driven, and tends to occur in older, thinner women without the typical risk factor profile. Type II cancers are biologically aggressive, often present at an advanced stage, and have a significantly worse prognosis than type I cancers. Recent molecular classification incorporating four genomic subtypes further refines prognosis and is increasingly guiding adjuvant treatment decisions.

FIGO staging of endometrial cancer is surgically determined and provides the most important prognostic information. Stage I disease is confined to the uterine corpus, with stage IA involving less than 50 percent myometrial invasion and stage IB involving 50 percent or more. Stage II involves invasion of the cervical stroma. Stage III encompasses regional spread including pelvic and para-aortic lymph node involvement, adnexal involvement, and vaginal metastasis. Stage IV represents distant disease, with stage IVA involving the bladder or bowel mucosa and stage IVB indicating distant metastases including peritoneal, omental, or inguinal lymph node disease. The surgical staging procedure includes total hysterectomy, bilateral salpingo-oophorectomy, and sentinel lymph node assessment or full lymphadenectomy, with peritoneal washings and omental sampling performed based on histologic grade and type.

Treatment of endometrial cancer is primarily surgical, with adjuvant therapy determined by surgical stage and pathologic features. Stage I low-grade endometrioid cancer confined to the inner half of the myometrium may require no adjuvant therapy after surgical staging, as the risk of recurrence is very low. Higher-grade or more deeply invasive stage I tumors and stage II disease are typically treated with adjuvant vaginal cuff brachytherapy or pelvic external beam radiation to reduce the risk of locoregional recurrence. Stage III disease requires a combination of surgery, radiation, and often systemic chemotherapy, typically with carboplatin and paclitaxel. Stage IV disease is managed primarily with systemic chemotherapy, with radiation used for palliation or local control. Immunotherapy with immune checkpoint inhibitors has emerged as an important treatment option for advanced or recurrent endometrial cancers, particularly those with mismatch repair deficiency or high microsatellite instability.

<image>Panel A: Endometrial cancer epidemiology showing most common gynecologic malignancy, 65,000 annual US cases, peak at ages 60 to 70, obesity shifting age distribution younger, and greater than 80 percent 5-year survival for stage I. Panel B: Type I versus type II comparison showing type I (endometrioid, 80 percent, estrogen-related, lower grade, better prognosis) and type II (serous or clear cell, non-estrogen, aggressive, advanced stage, worse prognosis) with emerging molecular subtypes. Panel C: FIGO staging showing stage I (confined to uterus, IA less than 50 percent invasion, IB 50 percent or more), stage II (cervical stroma), stage III (regional spread to nodes, adnexa, vagina), and stage IV (bladder, bowel, distant metastases) with surgical staging components. Panel D: Treatment by stage showing stage I low-grade (surgery alone), stage I high-grade and stage II (adjuvant radiation), stage III (surgery plus radiation plus chemotherapy), and stage IV (chemotherapy, immunotherapy for MSI-H and dMMR, palliative radiation).</image>

Section 7: Endometrial Polyps

Endometrial polyps are focal overgrowths of the endometrium composed of glands, stroma, and a vascular pedicle that project into the uterine cavity. They are found in 10 to 40 percent of women presenting with abnormal uterine bleeding and are a common cause of both premenopausal and postmenopausal bleeding. Risk factors include advancing age, obesity, and tamoxifen use, with tamoxifen-associated polyps tending to be larger, more often multiple, and carrying a higher risk of atypical or malignant transformation. The overall malignancy risk in endometrial polyps is 1 to 3 percent, increasing with patient age, postmenopausal status, and polyp size exceeding 1.5 centimeters.

The clinical presentation of endometrial polyps varies depending on the patient's menopausal status and the size and location of the polyp. Intermenstrual bleeding is a common presentation, as the polyp may outgrow its blood supply or develop surface ulceration. Heavy menstrual bleeding occurs when polyps increase the endometrial surface area or disrupt normal hemostatic mechanisms. Postmenopausal bleeding caused by a polyp mandates evaluation to exclude concurrent hyperplasia or malignancy. Many polyps are asymptomatic and are discovered incidentally during imaging performed for other indications or during evaluation for infertility, where polyps have been implicated as a potential cause of implantation failure.

Diagnosis of endometrial polyps utilizes imaging techniques that visualize the endometrial cavity. Transvaginal ultrasound may show a focal area of endometrial thickening, and a feeding vessel on Doppler imaging may be visualized in some cases. Saline infusion sonography provides superior visualization by distending the cavity with fluid, which outlines the polyp and distinguishes it from diffuse endometrial thickening. Hysteroscopy is the gold standard for diagnosis, allowing direct visualization of the polyp, assessment of its size and attachment, and the opportunity for concurrent removal. Office endometrial biopsy may miss polyps due to the blind nature of the sampling technique, and a negative biopsy does not exclude a polyp when imaging is suggestive.

Treatment of endometrial polyps is guided by the patient's symptoms, menopausal status, and risk factors for malignancy. Small, asymptomatic polyps in premenopausal women may be observed, as some polyps resolve spontaneously, though this approach requires follow-up imaging to confirm regression or stability. Hysteroscopic polypectomy is the treatment of choice for symptomatic polyps, polyps in postmenopausal women, and polyps in women being evaluated for infertility. The procedure allows complete removal under direct visualization with minimal risk of complications and provides tissue for histologic examination to exclude hyperplasia or malignancy. Recurrence of polyps after polypectomy is possible and occurs in approximately 10 to 15 percent of patients, and long-term follow-up or prophylactic measures such as the levonorgestrel intrauterine device may be considered in patients with recurrent polyps or ongoing risk factors.

<image>Panel A: Endometrial polyp characteristics showing focal endometrial overgrowth with glands, stroma, and vascular pedicle, 10 to 40 percent prevalence in women with AUB, risk factors (age, obesity, tamoxifen with larger and multiple polyps), and 1 to 3 percent malignancy risk increasing with age and postmenopausal status. Panel B: Clinical presentation showing intermenstrual bleeding (surface ulceration), heavy menstrual bleeding (increased surface area), postmenopausal bleeding (mandates evaluation), and asymptomatic incidental discovery (during infertility evaluation or imaging). Panel C: Diagnostic imaging showing transvaginal ultrasound (focal thickening, feeding vessel), saline infusion sonography (fluid outlines polyp, distinguishes from diffuse thickening), hysteroscopy (gold standard, direct visualization), and limitation of office biopsy (may miss polyps). Panel D: Treatment approach showing observation (small, asymptomatic, premenopausal, follow-up imaging), hysteroscopic polypectomy (treatment of choice, symptomatic, postmenopausal, infertility), pathologic assessment (exclude malignancy), and 10 to 15 percent recurrence rate with prophylactic LNG-IUD consideration.</image>

Section 8: Pelvic Organ Prolapse

Pelvic organ prolapse encompasses a spectrum of conditions in which the pelvic organs descend from their normal anatomic positions due to weakening of the pelvic floor support structures. Anterior vaginal wall prolapse, or cystocele, involves descent of the bladder into the vaginal canal. Posterior vaginal wall prolapse, or rectocele, involves herniation of the rectum into the vagina. Uterine prolapse describes descent of the uterus into and potentially beyond the vaginal canal. Vaginal vault prolapse occurs after hysterectomy when the vaginal apex descends. Enterocele represents herniation of the small bowel into the upper vagina, often occurring in conjunction with vaginal vault prolapse. These conditions frequently coexist, and a comprehensive examination of all vaginal compartments is necessary to identify all sites of prolapse.

Risk factors for pelvic organ prolapse are both obstetric and non-obstetric, with vaginal delivery being the single most important modifiable risk factor. Multiparity produces cumulative damage to the pelvic floor muscles, connective tissue, and pudendal nerve, with each vaginal delivery incrementally increasing the risk. Aging causes progressive loss of tissue elasticity and muscle strength, contributing to prolapse even in nulliparous women. Obesity increases chronic intraabdominal pressure on the pelvic floor, and chronic cough from conditions such as chronic obstructive pulmonary disease produces similar mechanical stress. Connective tissue disorders including Ehlers-Danlos and Marfan syndromes increase prolapse risk by compromising the structural integrity of the pelvic support tissues. Prior hysterectomy and prior prolapse repair are also risk factors for subsequent prolapse.

The Pelvic Organ Prolapse Quantification system provides a standardized, reproducible method for staging prolapse severity. Stage 0 represents no prolapse, with all vaginal points well above the hymenal ring. Stage I describes descent to greater than 1 centimeter above the hymen. Stage II involves descent to within 1 centimeter above or below the hymen. Stage III describes descent greater than 1 centimeter below the hymen but less than total vaginal length minus 2 centimeters. Stage IV represents complete eversion of the vaginal vault or total procidentia. The system uses specific anatomic reference points measured in centimeters relative to the hymen, providing objective and reproducible measurements that allow longitudinal tracking and comparison of surgical outcomes.

The symptoms of pelvic organ prolapse are determined by the type and severity of prolapse and its impact on adjacent organ function. The most characteristic symptom is the sensation of a vaginal bulge or the feeling of "something coming down" or protruding from the vagina. Pelvic heaviness and pressure worsen throughout the day and with prolonged standing or exertion. Urinary symptoms are common and include stress incontinence, urgency, frequency, and difficulty voiding, with some women needing to manually reduce the prolapse to empty the bladder. Bowel symptoms include constipation, incomplete evacuation, and the need for vaginal splinting to facilitate defecation. Sexual dysfunction including dyspareunia and body image concerns affects quality of life and should be actively inquired about during the clinical assessment.

<image>Panel A: Prolapse types showing cystocele (bladder into anterior vagina), rectocele (rectum into posterior vagina), uterine prolapse (uterus descending into vaginal canal), vaginal vault prolapse (apex descent after hysterectomy), and enterocele (small bowel into upper vagina) with frequent coexistence. Panel B: Risk factors showing vaginal delivery (most important, cumulative with parity), aging (tissue elasticity loss), obesity (chronic intraabdominal pressure), chronic cough (mechanical stress), connective tissue disorders (Ehlers-Danlos, Marfan), and prior hysterectomy or prolapse repair. Panel C: POP-Q staging system showing stage 0 (no prolapse), stage I (greater than 1 cm above hymen), stage II (within 1 cm of hymen), stage III (greater than 1 cm below hymen), and stage IV (complete eversion or procidentia) with anatomic reference points. Panel D: Symptom profiles showing vaginal bulge sensation, pelvic heaviness worsening with standing, urinary symptoms (incontinence, voiding difficulty, manual reduction), bowel symptoms (constipation, splinting), and sexual dysfunction (dyspareunia, body image concerns).</image>

Section 9: Prolapse Management

Conservative management is appropriate for women with mild prolapse, those who are not bothered by their symptoms, and those who prefer to avoid or defer surgery. Observation alone is sufficient for asymptomatic prolapse, as the condition does not invariably worsen and treatment is driven by symptoms rather than anatomic findings. Pelvic floor muscle exercises, also known as Kegel exercises, strengthen the levator ani complex and may slow the progression of prolapse and improve mild symptoms, though they are unlikely to reverse significant prolapse. Weight loss reduces the chronic intraabdominal pressure that contributes to prolapse progression. Vaginal estrogen therapy may improve tissue integrity in postmenopausal women and is often used in conjunction with pessary management.

The pessary is a silicone device inserted into the vagina to provide mechanical support for prolapsed organs, and it represents the most effective nonsurgical treatment for pelvic organ prolapse. The ring pessary is the most commonly used type and is effective for mild to moderate prolapse of all compartments. The Gellhorn pessary provides more robust support for severe prolapse but may be more difficult for patients to remove and replace independently. Pessary fitting is typically a trial-and-error process, with the largest comfortable device selected to maximize support while maintaining patient comfort and allowing voiding and defecation. Regular follow-up every 3 to 6 months is essential for pessary care, during which the device is removed, cleaned, and the vaginal mucosa inspected for erosion or ulceration. Complications of neglected pessaries include vaginal erosion, infection, fistula formation, and incarceration.

Surgical management of pelvic organ prolapse offers a range of procedures selected based on the prolapse compartment, severity, and the patient's goals regarding sexual function and uterine preservation. Anterior colporrhaphy repairs cystocele by plicating the fibromuscular tissue of the anterior vaginal wall, while posterior colporrhaphy addresses rectocele through similar tissue reinforcement. Vaginal hysterectomy with uterosacral ligament suspension is appropriate for uterine prolapse when the patient does not desire uterine preservation. Abdominal or laparoscopic sacrocolpopexy, in which a synthetic mesh bridges the vaginal vault to the sacral promontory, is considered the gold standard for vaginal vault prolapse repair due to its superior durability and lower recurrence rate. Colpocleisis is an obliterative procedure that closes the vaginal canal and is appropriate for women who are not sexually active and desire the simplest and most durable surgical option.

Surgical considerations include the significant recurrence rate and the evolving role of mesh in prolapse repair. Prolapse recurrence after native tissue repair occurs in approximately 30 percent of patients over time, reflecting the underlying tissue weakness that contributed to the original prolapse. The use of transvaginal synthetic mesh for prolapse repair has been significantly restricted following FDA actions due to complications including mesh erosion, chronic pain, and dyspareunia. Abdominal mesh placement, as in sacrocolpopexy, has a better safety profile and remains the preferred approach for apical prolapse repair. Concurrent incontinence procedures may be performed at the time of prolapse repair, as prolapse reduction may unmask latent stress urinary incontinence that was previously occluded by the prolapsing tissue. Preoperative discussion of sexual function is essential, as some procedures may affect vaginal caliber and depth.

<image>Panel A: Conservative management showing observation (asymptomatic prolapse, symptom-driven treatment), pelvic floor exercises (strengthen levator ani, slow progression), weight loss (reduce intraabdominal pressure), and vaginal estrogen (improve tissue integrity in postmenopausal women). Panel B: Pessary management showing ring pessary (most common, mild to moderate prolapse), Gellhorn pessary (severe prolapse, more difficult self-management), trial-and-error fitting process, 3 to 6 month follow-up schedule, and complications of neglect (erosion, infection, fistula, incarceration). Panel C: Surgical options showing anterior and posterior colporrhaphy (cystocele and rectocele repair), vaginal hysterectomy with uterosacral suspension (uterine prolapse), sacrocolpopexy (gold standard for vault prolapse, mesh to sacrum), and colpocleisis (obliterative, non-sexually active patients). Panel D: Surgical considerations showing 30 percent recurrence rate with native tissue repair, transvaginal mesh restrictions (erosion, pain, dyspareunia), abdominal mesh safety profile (sacrocolpopexy), unmasking of latent stress incontinence with prolapse reduction, and preoperative sexual function discussion.</image>

Section 10: Mullerian Anomalies

Mullerian anomalies result from abnormal development, fusion, or resorption of the Mullerian ducts during embryogenesis and encompass a spectrum of uterine, cervical, and vaginal malformations. Mullerian agenesis, also known as Mayer-Rokitansky-Kuster-Hauser syndrome, represents complete failure of Mullerian duct development and presents with congenital absence of the uterus and upper two-thirds of the vagina in a phenotypically female individual with normal ovarian function and a 46,XX karyotype. The unicornuate uterus results from failure of one Mullerian duct to develop, producing a single-horned uterus with a functional cavity on one side, sometimes with a rudimentary contralateral horn. Uterus didelphys results from complete failure of fusion of the two Mullerian ducts, producing two complete uteri, each with its own cervix, and often with a longitudinal vaginal septum. The bicornuate uterus results from partial fusion failure, creating a heart-shaped uterus with two horns and a single cervix.

The septate and arcuate uterus result from failure of resorption of the midline septum after successful Mullerian duct fusion. The septate uterus is the most common congenital uterine anomaly and has the most significant reproductive implications, with the fibrous or muscular septum dividing the uterine cavity partially or completely. The arcuate uterus represents a mild indentation of the fundal endometrium and is generally considered a normal variant without significant clinical impact. The septate uterus is associated with increased rates of first-trimester miscarriage, attributed to implantation on the relatively avascular septum, as well as preterm delivery and malpresentation. The distinction between bicornuate and septate uterus is critical because their management differs fundamentally: the septate uterus is treatable with minimally invasive hysteroscopic resection, while the bicornuate uterus requires open metroplasty, which is rarely performed.

The clinical presentation of Mullerian anomalies varies from primary amenorrhea to recurrent pregnancy loss to incidental discovery. Mullerian agenesis presents with primary amenorrhea and absent vagina in an adolescent with otherwise normal pubertal development. Obstructive anomalies such as a non-communicating uterine horn or an obstructed hemivagina may present with cyclical pain, hematometra, or endometriosis. Unicornuate and bicornuate uteri are associated with preterm labor, malpresentation, and cervical insufficiency. The septate uterus most commonly presents with recurrent pregnancy loss, particularly first-trimester losses. Many women with Mullerian anomalies are asymptomatic, and the anomaly is discovered incidentally during imaging for other reasons or during evaluation for infertility or recurrent loss.

Diagnosis of Mullerian anomalies relies on imaging, with MRI considered the gold standard for accurate classification. Transvaginal ultrasound, particularly three-dimensional ultrasound, can identify many anomalies and is an appropriate initial screening study. MRI provides detailed assessment of the uterine fundal contour, cavity morphology, and myometrial thickness, allowing reliable differentiation between septate, bicornuate, and other anomalies. Hysteroscopy evaluates the internal cavity but cannot assess the external contour, and it must be combined with laparoscopy or imaging to distinguish a septate from a bicornuate uterus. Treatment is anomaly-specific: the septate uterus may be treated with hysteroscopic septoplasty, which has been shown in observational studies to reduce miscarriage rates, though randomized trial data remain limited. Mullerian agenesis is managed with vaginal dilation therapy as first-line treatment, with surgical creation of a neovagina reserved for patients who do not respond to dilation. Other anomalies are generally managed based on their specific reproductive or symptomatic consequences.

<image>Panel A: Mullerian anomaly spectrum showing agenesis (absent uterus and upper vagina, 46 XX), unicornuate (single horn with or without rudimentary horn), didelphys (two complete uteri, two cervices), and bicornuate (partial fusion failure, heart-shaped, single cervix). Panel B: Septate and arcuate uterus showing septate (most common anomaly, fibrous or muscular septum, first-trimester miscarriage association) and arcuate (mild fundal indentation, normal variant) with critical distinction from bicornuate for management (hysteroscopic resection versus open metroplasty). Panel C: Clinical presentations showing primary amenorrhea (agenesis), cyclical pain with obstruction (non-communicating horn, obstructed hemivagina), preterm labor and malpresentation (unicornuate, bicornuate), recurrent pregnancy loss (septate), and incidental discovery (asymptomatic). Panel D: Diagnostic approach showing 3D ultrasound (initial screening), MRI (gold standard, fundal contour, cavity morphology, myometrial thickness), hysteroscopy plus laparoscopy (cavity plus external assessment), and treatment options (hysteroscopic septoplasty, vaginal dilation for agenesis, anomaly-specific management).</image>

Summary

• Uterine leiomyomas affect 70 to 80 percent of women by age 50, with submucosal fibroids most strongly associated with heavy menstrual bleeding, and hysterectomy as the definitive treatment
• Fibroid management spans medical therapy (GnRH modulators, tranexamic acid), procedural options (UAE, myomectomy), and surgery (hysterectomy), selected based on symptoms and fertility goals
• Adenomyosis is characterized by endometrial tissue within the myometrium, presenting with progressive dysmenorrhea and heavy bleeding, with hysterectomy as the only definitive treatment
• Endometrial hyperplasia without atypia carries a 1 to 3 percent malignancy risk and responds to progestin therapy, with the LNG-IUD as the preferred agent
• Atypical endometrial hyperplasia carries a 25 to 40 percent risk of concurrent cancer and generally warrants hysterectomy, with fertility-sparing progestin therapy as an alternative with close surveillance
• Endometrial cancer is the most common gynecologic malignancy, with type I (endometrioid, estrogen-related) having better prognosis than type II (serous, clear cell)
• Endometrial polyps are treated with hysteroscopic polypectomy and carry a 1 to 3 percent malignancy risk that increases with age and postmenopausal status
• Pelvic organ prolapse is staged using the POP-Q system, with vaginal delivery as the primary risk factor, and managed with pessary or surgery (sacrocolpopexy as gold standard for vault prolapse)
• Prolapse surgery has a 30 percent recurrence rate with native tissue repair, and transvaginal mesh has been restricted due to complications
• Mullerian anomalies are best classified by MRI, with the septate uterus being the most common and most amenable to hysteroscopic correction

Key Terms

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