presents with dysmenorrhea and chronic pelvic pain in younger women (age 25-35).
| Pathogenesis | • Ectopic implantation of endometrial stroma & glands outside uterus • Combination of cellular metaplasia and retrograde menstruation • Like normal endometrium, implants proliferate and shed during menses; however, because they have no outlet they can cause recurrent, slowly progressive pelvic inflammation, fibrosis and adhesions→ distortion of the adjacent pelvic anatomy | | --- | --- | | Clinical features | Pain locations and symptoms vary depending on implant location • Dyspareunia (MCC) particularly with deep penetration due to anatomic proximity • Dysmenorrhea (MCC) • Chronic pelvic pain • Infertility • Dyschezia • Cyclic dysuria, hematuria if involves the bladder | | Physical examination | • Immobile uterus • Anatomic distortion such as lateral cervical displacement • Cervical motion tenderness • Posterior fornix tenderness • Adnexal mass • Rectovaginal septum, posterior cul-de-sac, uterosacral ligament nodules or thickening | | Diagnosis | • Presumptive clinical dx → no improvement with medical therapy→ laparoscopy (Direct visualization & surgical biopsy) is required for definitive dx and is also therapeutic. |
Endometriosis is typically a benign condition and does not require further imaging (eg, CT scan) for evaluation or treatment.
<aside> 💡 Transvaginal ultrasound is often normal (except in those with an endometrioma) because lesions are too small to detect on imaging.
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A CT scan cannot definitively diagnose endometriosis because the lesions are too small to visualize, and a CT scan is not indicated in patients with a normal pelvic ultrasound.
Many patients have severe dysmenorrhea but seek medical attention only for infertility.
<aside> 💡 Not associated with amenorrhea
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Patients with dysmenorrhea and infertility due to suspected endometriosis require operative laparoscopy, which offers a definitive diagnosis (eg, visual inspection, biopsy) and improvement in pain symptoms and fertility.
Asymptomatic endometriosis (diagnosed incidentally during an unrelated surgery) require reassurance and observation only.
Indications for treatment of endometriosis include:
| Treatment | • Medical • Suppress ovulation and reduce menses (OCPs or GnRH agonists, aromatase inhibitors) • NSAIDs→ dec. inflammation) • Surgical resection • Laparoscopic fulguration of lesions improves fertility in patients with endometriosis. | | --- | --- |
Endometriosis is estrogen-responsive; however, it does not increase endometrial cancer risk because gland proliferation is outside the uterus (rather than an over proliferation of the endometrium).
Endometriosis have a slightly increased risk of epithelial ovarian cancer; however, endometriosis does not increase the risk of endometrial hyperplasia.
Intrauterine adhesions can result from pelvic inflammatory disease (eg, endometritis), which typically presents with abnormal uterine bleeding or vaginal discharge. Endometriosis is an extrauterine disease.
Endometriosis does not involve the hypothalamic-pituitary-ovarian axis and does not affect estrogen levels.
Continuous hormonal contraception (estrogen-progestin or progestogen-only contraceptives) together with NSAIDs is the first-line treatment in patients with endometriosis who do not want to conceive and have mild to moderate pelvic pain without complications. Continuous hormonal contraception stops the cyclical, estrogen-dependent growth of endometrial tissue, thereby reducing pelvic pain and the size of endometriotic lesions. Second-line treatment options include gonadotropin-releasing hormone agonists and androgens. Surgery is indicated for patients with expanding endometriomas, infertility, and refractory symptoms despite medical therapy, or if there is diagnostic uncertainty (e.g., to exclude malignancy).