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Polycystic ovarian syndrome

Increasing age

Estrogen-secreting tumor

Endometrial hyperplasia

Unopposed estrogens

Tamoxifen use

GENERALPREVENTION

In young women who are obese or anovulatory, the risk of endometrial cancer can be reduced by taking oral contraceptive pills, permanently losing weight, or taking cyclic progesterone to prevent unopposed estrogen’s effects on the uterus.

Estrogen replacement therapy should always include progesterone unless the woman has had a hysterectomy.

Cigarette smoking has been associated with a lower risk of type I endometrial cancer; however, it is not recommended secondary to its many health risks and increase risk of type II endometrial cancer.

COMMONLYASSOCIATED CONDITIONS

Endometrial hyperplasia: 1–25% will progress to endometrial adenocarcinoma:

–Simple without atypia

–Complex without atypia

–Simple with atypia

–Complex with atypia

43% with complex hyperplasia with atypia have concurrent endometrial

cancer.

Endometrial cancer patients should be screened regularly for breast and colon cancer per routine screening guidelines.

Patients who have breast or colon cancer are at increased risk for endometrial cancer.

Granulosa cell tumors of the ovary produce estrogen; these patients will have an increased risk of endometrial cancer.

DIAGNOSIS

HISTORY

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Endometrial cancer

–Postmenopausal bleeding is the most frequent sign. Any spotting or abnormal discharge mandates evaluation.

–Premenopausal patients with history of anovulation and heavy, irregular, or prolonged periods that fail multiple medical managements mandate evaluation.

Sarcoma

–Mixed müllerian sarcoma: bleeding and prolapsing tissue, pain (2)[C]

–Leiomyosarcoma: pelvic pain, pressure, uterine mass, abnormal bleeding

PHYSICALEXAM

Pelvic exam: enlarged uterus, fixed

DIFFERENTIALDIAGNOSIS

Atypical complex hyperplasia: a premalignant lesion of the endometrium

Cervical cancer

Ovarian cancer invading the uterus

Endometriosis

Adenomyosis

Leiomyoma

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

Liver and renal function tests

Transvaginal ultrasound usually shows increased endometrial thickness (>4 mm in postmenopausal patients or in patients with irregular or heavy periods if >35 years of age, 100% NPV) (1)[A].

Levels of cancer antigen 125 (CA-125) may be elevated when intraabdominal disease is present (1)[A].

Chest x-ray (CXR): Most common site of metastases is the lung.

Mammogram and colonoscopy: Endometrial cancer is associated with breast and colon cancer.

Routine preoperative MRI, CT, or PET scan: not recommended (3)

Follow-Up Tests & Special Considerations

Endometrial cancer is mostly localized to the uterus; therefore, preop evaluation for metastasis is not needed unless metastasis is already suspected (2)[A].

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CT scan, PET/CT, MRI, CA-125: not part of the routine evaluation but may be needed if metastasis is suspected, patient is a poor operative candidate, or pathology returns high grade (G3 endometrioid, papillary serous, clear cell, carcinosarcoma) (2)

MRI has been reported to show the depth of myometrial penetration accurately but is not always cost-effective (6)[A].

Diagnostic Procedures/Other

Office endometrial biopsy (90% accurate): If negative with high suspicion for cancer or patient continues to have bleeding, a dilation and curettage (D&C) is necessary (2)[B]. Endometrial stromal sarcoma and leiomyosarcoma rarely are diagnosed preoperatively. Any patient with history of irregular, heavy, or prolonged periods should undergo endometrial biopsy prior to endometrial ablation procedures.

Fractional D&C is 99% accurate except in cases of sarcoma.

If surgical approach is favored, D&C with hysteroscopic guidance is recommended over D&C alone, due to its ability to pick up discrete lesions (2)[A].

Meta-analyses suggest hysteroscopic peritoneal dissemination of malignant cells. Unknown significance of that dispersion.

Test Interpretation

Federation of Gynecology and Obstetrics Staging System: revised 2009

–Stage I (confined to corpus uteri)

A: No or <1/2 myometrial invasion

B: Invasion ≥1/2 the myometrium

–Stage II: Tumor invades cervical stroma but does not extend beyond the uterus.

–Stage III: Local and/or regional spread

A: Uterine serosal and/or adnexal invasion

B: Vaginal and/or parametrial involvement

C: Metastases to pelvic and/or para-aortic lymph nodes

IIIC1: +Pelvic nodes

IIIC2: +Para-aortic lymph nodes positive pelvic lymph nodes

–Stage IV: Tumor invades bladder and/or bowel mucosa and/or distant metastases:

A: Tumor invades bladder and/or bowel mucosa.

B: Distant metastases, including intra-abdominal metastases and/or

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inguinal lymph nodes (1)[A]

Uterine sarcoma criteria for diagnosis: mitotic index, cellular atypia, and areas of coagulative necrosis separated from tumor (7)[C]

TREATMENT

GENERALMEASURES

Main treatment for uterine cancer is surgery.

Radiation is used to prevent tumor recurrence at the vaginal cuff.

MEDICATION

First Line

Endometrial

–Chemotherapy for advanced or recurrent disease incurable with surgery and radiation

Paclitaxel + carboplatin (2)[B]

Doxorubicin + cisplatin + paclitaxel

Hormonal therapy

–Medroxyprogesterone acetate: for recurrence or metastases

–Megestrol (Megace) 160 mg/day for at least 2 months for women with premalignant lesions, atypical complex hyperplasia, or well-differentiated endometrial cancer in patients desiring fertility. Follow with D&C to determine cancer resolution.

–Levonorgestrel-containing intrauterine device: as mentioned earlier for patients who desire future fertility

Sarcoma

– Chemotherapy

Doxorubicin as single agent or in combination (7)[A]

Hormonal

–Tamoxifen or aromatase inhibitors; not fully studied, +/− progesterone

–Progesterones

ADDITIONALTHERAPIES

Radiation therapy

Nonoperative candidates: radiation therapy alone

Low risk: no adjuvant radiation therapy

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Intermediate risk: Consider adjuvant vaginal brachytherapy; reduces local recurrences but has no effect on overall survival

Vaginal brachytherapy is equivalent to whole pelvic radiation in regards to overall survival (3).

High risk: chemotherapy and radiation therapy in some cases (6,8)[A]

SURGERY/OTHER PROCEDURES

Surgical staging

Extrafascial hysterectomy and bilateral salpingo-oophorectomy

Cytologic washings

Pelvic and para-aortic lymph node dissection

Omental sampling, as indicated, and for papillary serous (3)

Optimal tumor debulking (1)[A], survival advantage

LAP2 trial: minimally invasive and laparotomy similar 5-year survival (3)

Geriatric Considerations

Older (and obese) patients may be at high risk for surgery. Alternative radiation or progesterone therapy can be considered.

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Admission criteria/initial stabilization

–Excessive vaginal bleeding

–Preoperative stabilization

Nursing: routine; ensure postoperative pain is controlled.

Postsurgical criteria: pain controlled, tolerating diet, ambulating, and voiding

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Follow-up visit with speculum and rectovaginal exam every 3 to 6 months for 2 years, then every 6 months for 3 years, and then annually for life (2)[C]

Patient Monitoring

Annual CXR is no longer recommended.

CT scan or PET/CT scan of the chest, abdomen, and pelvis should be used

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only to investigate suspicion of recurrent disease, not routinely.

Control comorbid conditions.

DIET

As tolerated and according to comorbidities

PATIENT EDUCATION

After surgery:

No intercourse for ~6 weeks

No lifting >10 to 15 lb

No driving until pain free

Do not expect resumption of full activity for 6 weeks.

PROGNOSIS

5-year survival rates

(6)[A]

COMPLICATIONS

Surgical: excessive bleeding, wound infection, lymphedema, deep vein thrombosis (DVT), and damage to the urinary or intestinal systems Radiation: diarrhea, ileus, bowel obstruction or fistula, radiation cystitis,

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proctitis, vaginal stenosis, DVT

Chemotherapy: per the drug given

REFERENCES

1.Creasman W. Revised FIGO staging for carcinoma of the endometrium. Int J Gynaecol Obstet. 2009;105(2):109.

2.American College of Obstetricians and Gynecologists. Endometrial cancer. Obstet Gynecol. 2015;125(4):1006–1026.

3.Sorosky JI. Endometrial cancer. Obstet Gynecol. 2012;120(2 Pt 1):383–397.

4.Burke W, Orr J, Leitao M, et al; for Society of Gynecologic Oncology Clinical Practice Committee. Endometrial cancer: a review and current management strategies: part I. Gynecol Oncol. 2014;134(2):385–392.

5.Burke W, Orr J, Leitao M, et al; for Society of Gynecologic Oncology Clinical Practice Committee. Endometrial cancer: a review and current management strategies: part II. Gynecol Oncol. 2014;134(2):393–402.

6.Humber C, Tierney J, Symonds P, et al. Chemotherapy for advanced, recurrent or metastatic endometrial carcinoma. Cochrane Database Syst Rev. 2005;(4):CD003915.

7.Gadducci A, Cosio S, Romanini A, et al. The management of patients with uterine sarcoma: a debated clinical challenge. Crit Rev Oncol Hematol. 2008;65(2):129–142.

8.Einhorn N, Tropé C, Ridderheim M, et al. Asystematic overview of radiation therapy effects in uterine cancer (corpus uteri). Acta Oncol. 2003;42(5– 6):557–561.

ADDITIONALREADING

SEE ALSO

Cervical Malignancy

Algorithm: Pelvic Pain

CODES

ICD10

C54.1 Malignant neoplasm of endometrium

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C55 Malignant neoplasm of uterus, part unspecified

C54.2 Malignant neoplasm of myometrium

CLINICALPEARLS

Most common presenting symptom is abnormal uterine bleeding.

Any patient with history of irregular, heavy, or prolonged periods should undergo endometrial biopsy.

Primary cause is unopposed estrogen.

Endometrial thickness on transvaginal ultrasound of <5 mm makes endometrial cancer very unlikely.

Primary treatment is with surgery, with possible chemotherapy ± radiation.

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ENDOMETRIOSIS

Andrew G. Alexander, MD Maegen Dupper, MD

Kenneth A. Ballou, MD

BASICS

DESCRIPTION

Endometriosis is a common but potentially painful and debilitating estrogendependent gynecologic condition affecting women of predominately reproductive age (1)[A].

Symptoms and signs generally consist of pelvic pain and decreased fertility. Due to estrogen-dependent implants of endometrial tissue found outside the uterus. Although endometriomas have been recorded in liver, bowel, umbilicus, lung, and other tissue, the most common pathologic sites are:

–Peritoneum (bladder, cul-de-sac, pelvic walls, ligaments, and fallopian tubes)

–Ovaries

–Rectovaginal septum

Ectopic endometrial implants proliferate and slough with the menstrual cycle.

Stage I (minimal) to IV (severe). Staging is useful in therapeutic planning but does not correlate with pain severity.

EPIDEMIOLOGY

Prevalence

Female only

Affects 11% of fertile women

Found in 30–50% of infertile women

Found in 50–60% of women and adolescent women with pelvic pain

Pediatric Considerations

Endometriosis may begin with puberty as endometrial implants are dependent on ovarian hormones. This can lead to debilitating pelvic pain and severe dysmenorrhea associated with missed school, social, and family activities.

Pregnancy Considerations

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The presence of endometriosis decreases fecundability from 15–20% per month to 2–10% per month. 25–50% of infertile women have endometriosis. However, pelvic endometriosis generally improves during pregnancy.

Geriatric Considerations

Although menopause often results in a resolution of symptoms, pelvic endometriosis may extend into menopause and may be exacerbated by hormone replacement therapy (HRT).

ETIOLOGYAND PATHOPHYSIOLOGY

Not fully understood; several factors are believed to play a role, including immunologic changes and genetic predisposition in the presence of abnormal proliferating endometrial tissue implants causing chronic peritoneal inflammation.

Theories include:

–Sampson theory: Retrograde menstruation results in peritoneal implantation and disease.

–Halban theory: Distant disease is probably caused by hematogenous/lymphatic dissemination or metaplastic transformation.

–Coelomic metaplasia: Coelomic epithelium remains undifferentiated in the peritoneal cavity and differentiates to form functioning endometrium.

Endometrial-associated infertility is multifactorial:

–Pelvic inflammation

–Anatomic disruption of pelvic structures (Involvement of the fallopian tube may cause isthmic tubal obstruction.)

–Proliferation and activation of peritoneal macrophages (may predispose to gamete phagocytosis)

–Alteration in eutopic endometrium

Genetics

Odds ratio of symptomatic endometriosis with a first-degree affected relative is 7.2. Those with affected first-degree relatives have a 26% chance of severe manifestations versus 12% if no first-degree affected relatives.

RISK FACTORS

Family history

Menstruation and ovulation Delayed childbirth

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