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Obstetrics and Gynecology›Condition·Updated Jul 11, 2026·v1

Endometriosis

Endometriosis is a chronic, estrogen-dependent inflammatory disorder affecting ~10% of reproductive-age women, characterized by ectopic endometrial tissue causing chronic pelvic pain and infertility. Diagnosis is often delayed (average 6.7 years); transvaginal ultrasound and MRI can diagnose advanced disease, while laparoscopy with histology remains the gold standard. Management combines first-line hormonal suppression (CHC or dienogest 2 mg daily), second-line GnRH antagonists with add-back therapy, and laparoscopic excision for refractory cases or fertility needs. Postoperative long-term suppression (especially LNG-IUS) reduces high recurrence rates. Endometriosis confers significantly increased risks of adverse pregnancy outcomes (preterm birth OR 1.63, placenta previa OR 3.03, SGA OR 1.27) and a modest increase in ovarian cancer risk (absolute lifetime risk <2-5%, no screening recommended). Multidisciplinary care, early recognition, and fertility-preserving strategies are critical to improving outcomes.

High Evidence516 references·9,842 words·40 min read·v1
endometriosischronic pelvic paindysmenorrheainfertilitydeep infiltrating endometriosisendometriomaprogesterone resistanceGnRH antagonistspontaneous hemoperitoneum in pregnancy

Quick Reference

RxDrug of choiceCombined hormonal contraceptive (continuous or cyclic) or progestin (dienogest 2 mg orally once daily) as first-line for pain. For second-line: oral GnRH antagonist with add-back therapy (elagolix 200 mg BID with estradiol 1 mg/norethindrone acetate 0.5 mg, or relugolix CT 40 mg/1 mg/0.5 mg once daily).
AltAlternativesLevonorgestrel-releasing intrauterine system (LNG-IUS) for postoperative recurrence prevention; GnRH agonists with add-back (limited to ≤6 months); aromatase inhibitors (letrozole 2.5 mg daily) for postmenopausal patients.
⊘AvoidNSAIDs after 20 weeks gestation; GnRH agonists without add-back for >6 months; danazol (androgenic side effects); ovulation suppression agents for infertility alone; unopposed estrogen therapy in postmenopausal women with endometriosis.
DxTest of choiceLaparoscopy with histologic confirmation is the gold standard for definitive diagnosis. Transvaginal ultrasound (TVS) is first-line imaging, with MRI reserved for inconclusive TVS or surgical mapping of deep disease.
ScKey scoreEndometriosis Fertility Index (EFI), postoperative score 0-10 predicting spontaneous pregnancy rates; cumulative pregnancy at 36 months ranges from 10% (EFI 0-2) to 69% (EFI 9-10).
→When to referRefer for surgical evaluation when medical therapy fails after 3-6 months, for deep infiltrating endometriosis requiring multidisciplinary surgery (bowel, bladder, ureter), for infertility with EFI <5 or age >38, or for adolescents with persistent dysmenorrhea despite empiric therapy.
Endometriosis is a chronic, estrogen-dependent condition causing pain and infertility; management combines hormonal suppression (CHC, progestins, GnRH antagonists with add-back) and laparoscopic excision, with attention to elevated risks of adverse obstetric outcomes (preterm birth OR 1.63, placenta previa OR 3.03) and low absolute risk of ovarian cancer (<2-5%). Early diagnosis and multidisciplinary care are essential to reduce diagnostic delay and improve quality of life.
Endometriosis is an estrogen-dependent chronic inflammatory disorder affecting approximately 10% of reproductive-age women, causing chronic pelvic pain and subfertility with an average diagnostic delay of 6.7 years. Driven by retrograde menstruation, progesterone resistance, and chronic inflammation, the disease presents in three phenotypes (superficial peritoneal, ovarian endometrioma, deep infiltrating) that require tailored management. First-line therapy includes combined hormonal contraceptives or progestins (e.g., dienogest 2 mg daily), with escalation to GnRH antagonists (elagolix, relugolix CT, linzagolix) with add-back therapy. Laparoscopic excision is indicated for refractory pain, large endometriomas, or fertility needs, with postoperative suppression to prevent recurrence. Endometriosis carries significantly elevated risks of adverse pregnancy outcomes (preterm birth, placenta previa) and a modest increase in ovarian cancer risk (absolute lifetime risk <2-5%). Multidisciplinary care and early diagnosis are critical to reduce disease burden.

Overview and Recommendations

Background

  • •Endometriosis is an estrogen-dependent chronic inflammatory disorder defined by the presence of endometrium-like tissue (glands and stroma) outside the uterine cavity, affecting approximately 10% of reproductive-age individuals worldwide, an estimated 9 million women in the United States. Untreated, it carries a substantial burden of chronic pelvic pain and subfertility, with diagnostic delay averaging 6.7 years from symptom onset and patients often consulting three or more clinicians before obtaining a definitive diagnosis.
  • •The disease presents in three major phenotypes that may coexist and are increasingly considered distinct diseases with different pathogenic mechanisms: superficial peritoneal endometriosis (most common, often in adolescents with clear or red lesions), ovarian endometriomas (bilateral in 30-50%, associated with a 54.3% reduction in AMH), and deep infiltrating endometriosis (DIE, infiltration >5 mm into subperitoneal tissue, involving rectovaginal septum, bowel, bladder, or ureters).
  • •Pathogenesis is driven by a tripartite mechanism: retrograde menstruation (supported by an 8.63-fold increased risk of retrograde uterine contraction pattern during menses), progesterone resistance (mediated by YAP1 upregulation of miR-21-5p suppressing progesterone receptor expression), and chronic inflammation with immune evasion, dysbiosis, and central sensitization that amplifies pain.
  • •Endometriosis is heritable with polygenic/epigenetic susceptibility; lesions can be clonal with acquired genetic instability. It is associated with a 1.3-fold increased risk of pregnancy loss, a 2-fold increased risk of , a 1.3-fold increased risk of , and a 1.5-fold increased risk of ovarian cancer (especially endometrioid and clear cell subtypes), with the highest risk among women with DIE and ovarian endometriomas (aHR 9.66).
  • •Classification uses three systems serving distinct purposes: revised ASRM staging (I-IV) for research and infertility prognosis (though it correlates poorly with pain severity), the #Enzian classification for compartment-based surgical mapping of deep disease (A: rectovaginal, B: uterosacral/cardinal, C: rectum), and the Endometriosis Fertility Index (EFI, 0-10) for predicting spontaneous pregnancy rates after surgery. No single system predicts all outcomes.

Evaluation

  • •Suspect endometriosis in any reproductive-age woman presenting with dysmenorrhea (often beginning before menses and persisting through flow), deep dyspareunia, nonmenstrual pelvic pain, or infertility, 90% of affected individuals report pelvic pain, and 26% experience infertility.
  • •Ask about pain timing and character: cyclic vs constant, relation to menstruation, dyschezia (painful defecation), diarrhea or constipation, dysuria, hematuria, or rectal bleeding. Inquire about family history (2.75-fold increased risk with affected sibling), previous pelvic surgeries, childhood adversity (HR 1.20-1.61), and fertility desires and duration of infertility.
  • •Perform a bimanual pelvic examination, ideally during menstruation when lesions are more tender and palpable, examine for tender nodules in the posterior fornix, fixed retroverted uterus, uterosacral ligament nodularity, and adnexal masses. Sensitivity is only 25-50%, so a normal examination does not exclude disease, especially superficial peritoneal endometriosis.
  • •Order transvaginal ultrasound (TVS) as first-line imaging, preferably with an endometriosis-trained sonographer. For DIE, TVS has pooled sensitivity 79-91% and specificity 94-98%; for ovarian endometriomas, detection rates exceed 90%. A negative TVS does not rule out superficial peritoneal disease but can diagnose advanced disease without laparoscopy.
  • •Obtain pelvic MRI when TVS is inconclusive or for surgical mapping of deep endometriosis; MRI has pooled sensitivity 91-94% and specificity 86-88% for DIE, and is less operator-dependent. MRI is not recommended as a primary screening tool due to cost.
  • •Check serum CA-125 (threshold ≥30 U/mL) as a rule-in test: pooled specificity is 93% (95% CI 89-95%) but sensitivity is only 52% (38-66%), with higher sensitivity for moderate-to-severe disease (63%) than minimal (24%). A positive result supports the diagnosis, but a negative result cannot rule out endometriosis.
  • •Consider diagnostic laparoscopy with histologic confirmation as the gold standard when imaging is negative but clinical suspicion remains high, or when surgical treatment is planned for pain or infertility. Direct visualization of endometriotic lesions followed by biopsy provides the highest diagnostic accuracy.
  • •Apply the structured diagnostic algorithm: Step 1, clinical suspicion based on symptoms; Step 2, pelvic examination and first-line TVS; Step 3, if TVS shows ovarian endometrioma or DIE, diagnosis is established without laparoscopy; Step 4, if TVS is negative or equivocal but suspicion high, obtain pelvic MRI; Step 5, if MRI is negative or suggests only superficial disease, offer diagnostic laparoscopy.
  • •Evaluate for coexisting conditions including (up to 85% of endometriosis patients, exacerbating uterine contractility and pain), irritable bowel syndrome (OR 3.5), and pelvic inflammatory disease (OR 5.9), these share symptoms and may be misdiagnosed or co-occur.
  • •Assess fertility status: document age, duration of infertility, ovarian reserve (AMH, antral follicle count), and prior pregnancy history. Postoperatively, calculate the Endometriosis Fertility Index (EFI) to predict spontaneous conception, cumulative pregnancy rate at 36 months ranges from 10% (EFI 0-2) to 69% (EFI 9-10).

Management

  • •Initiate first-line medical therapy for pain in premenopausal women not seeking immediate pregnancy: a combined hormonal contraceptive (CHC, continuous or cyclic) or a progestin-only agent such as 2 mg orally once daily. In network meta-analysis, dienogest reduced pelvic pain (SMD -1.20, 95% CI -1.78 to -0.61) and CHC reduced pain (SMD -0.67, 95% CI -1.25 to -0.09) versus placebo.
  • •If first-line therapy fails after 3-6 months of adherence, escalate to an oral GnRH antagonist with add-back therapy: 200 mg twice daily with estradiol 1 mg/norethindrone acetate 0.5 mg add-back, combination therapy (40 mg/1 mg/0.5 mg) once daily, or 200 mg daily with add-back. Dysmenorrhea responder rates at 3 months are 72-76% versus 20-24% with placebo.
  • •Do not use GnRH agonists (leuprolide, nafarelin) for more than 6 months without add-back therapy, lumbar spine bone mineral density loss exceeds 2% at 6 months. Add-back with estradiol 1 mg/norethindrone acetate 0.5 mg daily stabilizes BMD and can extend therapy safely.
  • •Refer for laparoscopic surgery when medical therapy fails, pain is refractory, large endometriomas (>3 cm) are present, or fertility is desired with resectable disease. Excision of lesions is preferred over ablation for deep disease and endometriomas, it allows histologic confirmation and more complete removal, and improves overall pain at 6 months (OR 6.58) and live birth rates (OR 1.94) versus diagnostic laparoscopy alone.
  • •For ovarian endometriomas, perform rather than drainage or ablation, cystectomy reduces recurrence (OR 0.12 with postoperative LNG-IUS). Preserve ovarian cortex to protect fertility; bilateral endometriomas reduce AMH by 54.3%. Avoid coagulation of the ovarian hilum to minimize damage to ovarian reserve.
  • •Stage surgically using rASRM and EFI, the EFI guides fertility counseling: if EFI ≥5, attempt natural conception for 6-12 months; if EFI <5 or age >38, proceed directly to ART without additional surgical delay. Ovulation suppression agents (GnRH agonists, progestins) do not improve pregnancy rates and should not be used for infertility alone.
  • •After surgery, initiate long-term hormonal suppression to prevent recurrence: CHC, progestin (dienogest 2 mg daily), or the (LNG-IUS). LNG-IUS is the most effective postoperative agent, reducing endometrioma recurrence (OR 0.12, 95% CI 0.02-0.63) and pain scores (MD -24.96 on VAS). Continue suppression until pregnancy is desired or menopause.
  • •In pregnancy, manage pain with paracetamol; avoid NSAIDs after 20 weeks (risk of and premature ductus arteriosus closure). GnRH agonists and hormonal contraceptives are contraindicated once pregnancy is confirmed. Classify pregnancies in women with stage III-IV endometriosis or DIE as high-risk and offer serial ultrasound for fetal growth, placental position, and cervical length.
  • •Acute management of spontaneous hemoperitoneum in pregnancy (SHiP), suspected by acute abdominal pain with hypovolemic shock, requires emergency laparotomy with oversewing of bleeding implants and possible concurrent cesarean delivery if the fetus is viable ≥24 weeks. SHiP incidence is 4.9 per 100,000 births with median blood loss 2000 mL; maternal mortality is low with prompt surgery.
  • •For postmenopausal women with residual disease or de novo pain, use progestogen monotherapy (oral micronized progesterone 200 mg/day or norethindrone acetate 5 mg/day) as preferred hormone therapy to avoid estrogen-driven reactivation. Aromatase inhibitors such as 2.5 mg daily may be used for refractory pain. External beam radiation (1500-2100 cGy) to ovarian remnants is a last-resort option.
  • •Monitor for recurrence: endometrioma recurrence after cystectomy reaches 27% at 24 months without suppression; pain recurrence after bowel resection for DIE is 24%, with reintervention in 19%. Counsel patients that the disease is chronic with high recurrence risk without ongoing hormonal suppression.
  • •Avoid: performing hysterectomy or as first-line treatment for pain (25% have recurrent pain post-hysterectomy); using danazol (androgenic side effects); performing laparoscopic uterine nerve ablation (LUNA), two large RCTs showed no benefit for endometriosis-associated pain; using GnRH antagonist monotherapy without add-back for >6 months (bone loss); and using ovulation suppression for infertility alone (no pregnancy benefit).
  • •Refer to a multidisciplinary team for deep infiltrating endometriosis requiring bowel, bladder, or ureteral surgery, shaving has fewer major complications than segmental resection (6.7% vs 24%). Refer to a fertility specialist if EFI <5 or age >38 with infertility. For adolescents, refer for laparoscopy if pain persists despite 3-6 months of empiric CHC or NSAID therapy.

Board Review — High Yield

  • •Sampson's hypothesis, retrograde menstruation is the primary pathogenic mechanism; supported by an 8.63-fold increased risk of retrograde uterine contraction pattern during menses in endometriosis.
  • •Triple classification system, rASRM (research), #Enzian (surgical mapping), EFI (fertility prognosis); no single system predicts all outcomes.
  • •Three phenotypes, superficial peritoneal, ovarian endometrioma (bilateral in 30-50%, reduces AMH by 54.3%), and deep infiltrating endometriosis (DIE, >5 mm infiltration), may represent distinct diseases.
  • •Progesterone resistance, mediated by YAP1 upregulation of miR-21-5p suppressing progesterone receptor; explains limited efficacy of progestin monotherapy.
  • •CA-125, rule-in test with 93% specificity but only 52% sensitivity; more useful in moderate-severe disease (63% sensitivity). Negative test does not rule out.
  • •GnRH antagonists with add-back, elagolix, relugolix CT, and linzagolix achieve 72-76% dysmenorrhea response at 3 months with <1% BMD decline over 2 years when used with add-back.
  • •Endometriosis Fertility Index (EFI), validated postoperative score guiding need for ART; EFI ≥5 → attempt natural conception 6-12 months; EFI <5 or age >38 → proceed to IVF.
  • •Spontaneous hemoperitoneum in pregnancy (SHiP), rare (4.9/100,000 births) but life-threatening; requires emergency laparotomy with oversewing of bleeding implants and possible cesarean delivery.
  • •Ovarian cancer risk, 4.2-fold increased risk, especially type I (endometrioid/clear cell, aHR 7.48); absolute lifetime risk <2-5%; routine screening not recommended.
  • •Diagnostic delay, averages 6.7 years from symptom onset, with patients consulting a mean of three clinicians before diagnosis; transvaginal ultrasound can diagnose advanced disease without laparoscopy.

Deep Dive — Evidence Details

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