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Summary Table

Feature	Detail
Risk Factors	Reproductive-age women (25-35 years), nulliparity, early menarche, late menopause, short menstrual cycles (<27 days), prolonged flow (>7 days), family history (first-degree relative), mullerian anomalies causing outflow obstruction
Etiology	Presence of functional endometrial glands and stroma outside the uterine cavity; most accepted theory is retrograde menstruation (Sampson theory)
Patient Presentation	Cyclic pelvic pain that worsens during menstruation (secondary dysmenorrhea), dyspareunia (deep), dyschezia, chronic pelvic pain, subfertility/infertility
Classic Physical Exam	Fixed, retroverted uterus; tender nodularity along the uterosacral ligaments on rectovaginal exam; adnexal mass (endometrioma)
Key Diagnostic Results	Transvaginal ultrasound showing "ground-glass" appearance of endometrioma; gold standard is direct visualization via laparoscopy with histologic confirmation
Management	First-line medical therapy: NSAIDs + combined oral contraceptives (COCs) continuously; second-line: GnRH agonists; surgical: laparoscopic excision/ablation of lesions; definitive: total abdominal hysterectomy with bilateral salpingo-oophorectomy
Keywords	"Cyclic pelvic pain," "secondary dysmenorrhea," "chocolate cyst," "powder-burn lesions," "infertility workup," "pain with menstruation and intercourse," "fixed retroverted uterus"

1. Pathophysiology

Endometriosis is defined by the implantation and growth of endometrial-type tissue (glands and stroma) outside the uterine cavity. These ectopic implants are most commonly found on the ovaries, uterosacral ligaments, posterior cul-de-sac (pouch of Douglas), and the pelvic peritoneum. Less commonly, they can appear on the bowel, bladder, and rarely at distant sites such as the lung (catamenial pneumothorax).

The most widely accepted explanation is the Sampson theory of retrograde menstruation: during menses, endometrial tissue refluxes through the fallopian tubes into the peritoneal cavity. Once there, these cells implant, proliferate, and respond to cyclic hormonal stimulation just like native endometrium. This is why the disease is fundamentally estrogen-dependent. Each menstrual cycle triggers proliferation and subsequent bleeding within these implants, causing a local inflammatory response, fibrosis, and adhesion formation.

The cyclical inflammation explains the hallmark symptom of progressive secondary dysmenorrhea. Pain worsens with each cycle because repeated bleeding leads to cumulative scarring and adhesion formation. Deep dyspareunia results from implants on the uterosacral ligaments and the cul-de-sac, which are mechanically stretched during intercourse. Dyschezia (painful defecation) occurs when implants involve the rectovaginal septum or bowel serosa, and these symptoms also follow a cyclic pattern, worsening perimenstrually.

Infertility in endometriosis is multifactorial. The inflammatory peritoneal environment is toxic to sperm and oocytes. Adhesions can distort tubal anatomy, impairing ovum pickup. Endometriomas within the ovary destroy normal follicular tissue. Additionally, there is evidence of impaired endometrial receptivity even when the eutopic endometrium appears structurally normal.

When an endometrioma forms within the ovary, repeated cyclic bleeding creates a cyst filled with old, hemolyzed blood, giving it a thick, dark brown appearance. This is the classic "chocolate cyst." Over time, these cysts can become quite large and are a frequent finding on imaging.

Other proposed theories include coelomic metaplasia (peritoneal cells transforming into endometrial tissue, which may explain rare cases in men on estrogen therapy or in pre-menarchal girls) and lymphatic/hematogenous spread (explaining distant implants in the lung or brain).

2. Classification and Clinical Manifestation

Revised American Society for Reproductive Medicine (rASRM) Staging

Stage	Description	Characteristics
I (Minimal)	Isolated implants, no adhesions	Few superficial peritoneal implants
II (Mild)	Superficial implants with minor adhesions	Total area of implants <5 cm, no significant adhesions
III (Moderate)	Deep implants, small endometriomas	Multiple deep implants, filmy and dense adhesions, small ovarian endometriomas (<2 cm)
IV (Severe)	Large endometriomas, dense adhesions	Large bilateral endometriomas, extensive dense adhesions, cul-de-sac obliteration

The stage does not correlate well with the severity of pain. A patient with Stage I disease can have debilitating pain, while a patient with Stage IV may be asymptomatic and discovered only during an infertility workup.

Clinical Manifestations By Location

Location of Implant	Clinical Feature
Ovary	Endometrioma (chocolate cyst), chronic pelvic pain, infertility
Uterosacral ligaments	Deep dyspareunia, palpable nodularity on rectovaginal exam
Cul-de-sac (pouch of Douglas)	Deep dyspareunia, dyschezia
Bladder/ureter	Cyclic dysuria, hematuria (catamenial hematuria), ureteral obstruction
Rectosigmoid/bowel	Cyclic dyschezia, hematochezia, rectal pain perimenstrually
Lung/diaphragm	Catamenial pneumothorax, cyclic hemoptysis (rare but highly testable)
Abdominal wall (scar)	Cyclic painful nodule at cesarean section or laparoscopy scar site

3. Diagnostic Workup

Test	Role	Key Findings
Clinical history and exam	Best initial step	Cyclic pelvic pain + tender nodularity on rectovaginal exam
Transvaginal ultrasound	Best initial imaging	Homogeneous "ground-glass" echogenicity within an ovarian cyst (endometrioma); cannot detect superficial peritoneal implants
Pelvic MRI	Second-line imaging	Better for deep infiltrating endometriosis (rectovaginal septum, bladder, bowel); characterizes endometriomas; useful for surgical planning
CA-125	Not recommended for diagnosis	May be mildly elevated but nonspecific; can be elevated in many conditions (ovarian cancer, PID, fibroids, pregnancy)
Laparoscopy with biopsy	Gold standard / most accurate test	Direct visualization of implants (powder-burn, blue-black, red, or clear vesicular lesions) with histologic confirmation showing endometrial glands and stroma

The diagnosis of endometriosis begins with clinical suspicion based on the triad of dysmenorrhea, dyspareunia, and infertility in a reproductive-age woman. A thorough history focusing on the cyclic nature of symptoms is the single most important clue. On pelvic examination, the classic finding is tender nodularity along the uterosacral ligaments, best appreciated on rectovaginal exam. A fixed, retroverted uterus suggests dense posterior adhesions.

Transvaginal ultrasound is the best initial imaging study. It is most useful for identifying ovarian endometriomas, which appear as well-defined cysts with homogeneous low-level internal echoes (the "ground-glass" pattern). However, ultrasound has poor sensitivity for superficial peritoneal implants and small deep lesions. A normal ultrasound does not rule out endometriosis.

MRI provides superior soft-tissue contrast and is particularly valuable when deep infiltrating endometriosis is suspected (bowel, bladder, ureteral involvement). It helps map disease extent before surgery. However, MRI is not routinely ordered as a first-line study.

CA-125 is sometimes measured but is not reliable for diagnosis. It lacks both sensitivity and specificity. It may be mildly elevated (typically 35-100 U/mL), but this finding can also be seen in ovarian malignancy, pelvic inflammatory disease, and other conditions. It is not recommended as a screening or diagnostic tool.

The gold standard remains laparoscopy with histologic confirmation. Visual inspection during laparoscopy reveals characteristic lesions: classic "powder-burn" or "gunshot" lesions (dark blue-black puckered nodules), red flame-like lesions (early active implants), or white scarred lesions (burned-out disease). Biopsy demonstrating endometrial glands and stroma confirms the diagnosis. In current practice, many clinicians initiate empiric medical therapy based on clinical suspicion without laparoscopy, reserving surgery for patients who fail medical management or who require a definitive diagnosis (e.g., infertility patients).

4. Management and Treatment

Setting	Treatment	Details
Empiric first-line (pain)	NSAIDs + continuous COCs	Ibuprofen 400-600 mg every 6-8 hours PRN; COCs taken continuously (skip placebo week) to suppress menstruation
Second-line hormonal	Progestins	Medroxyprogesterone acetate 10-30 mg/day orally, or depot medroxyprogesterone 150 mg IM every 3 months; norethindrone acetate 5 mg/day
Second-line hormonal	Levonorgestrel IUD	52 mg levonorgestrel intrauterine system; local progestin effect, suppresses implants
Third-line hormonal	GnRH agonists	Leuprolide 3.75 mg IM monthly or 11.25 mg IM every 3 months; maximum 6 months without add-back therapy due to bone loss
Add-back therapy	Norethindrone acetate 5 mg/day	Given concurrently with GnRH agonists to prevent hypoestrogenic side effects (bone loss, hot flashes, vaginal dryness)
Third-line hormonal	GnRH antagonists (oral)	Elagolix 150 mg daily (up to 24 months) or 200 mg twice daily (up to 6 months); dose-dependent bone density monitoring required
Surgical (conservative)	Laparoscopic excision/ablation	For failed medical therapy or infertility; excise/ablate visible implants, lyse adhesions, drain/excise endometriomas
Surgical (definitive)	TAH-BSO	Total abdominal hysterectomy with bilateral salpingo-oophorectomy; reserved for severe refractory disease in patients who have completed childbearing

Medical Management

The first step in management for a patient with suspected endometriosis and pelvic pain is empiric therapy with NSAIDs combined with continuous combined oral contraceptives. The COC is taken without the placebo week to achieve continuous ovarian suppression and prevent the cyclic hormonal fluctuations that drive implant activity. This approach eliminates withdrawal bleeding and reduces the inflammatory stimulus at ectopic sites.

If COCs fail after 3-6 months, the next step is to switch to progestin-only therapy. Options include oral norethindrone acetate (5 mg daily), depot medroxyprogesterone acetate (150 mg IM every 3 months), or a levonorgestrel-releasing IUD. Progestins work by inducing decidualization and subsequent atrophy of endometrial implants. Depot medroxyprogesterone and the levonorgestrel IUD are particularly useful because they often achieve amenorrhea.

GnRH agonists (leuprolide) represent third-line therapy. They work by initially stimulating, then downregulating the hypothalamic-pituitary-gonadal axis, creating a medical menopause state. This profoundly suppresses estrogen production, starving implants of their hormonal fuel. The key limitation is bone mineral density loss. Without add-back therapy, GnRH agonists should not be used for more than 6 months. Add-back therapy with norethindrone acetate (5 mg/day) allows extended use by providing just enough hormonal support to protect bones and reduce vasomotor symptoms while still keeping estrogen levels low enough to suppress endometriosis.

Oral GnRH antagonists (elagolix) are a newer option that offers dose-dependent estrogen suppression without the initial flare effect seen with GnRH agonists. At the lower dose (150 mg daily), partial estrogen suppression allows use for up to 24 months. At the higher dose (200 mg twice daily), more complete suppression limits use to 6 months without add-back.

Danazol, a synthetic androgen, is rarely used today due to androgenic side effects (hirsutism, acne, voice deepening, weight gain, hepatotoxicity). It is essentially historical but may still appear as a distractor.

Surgical Management

Conservative surgery via laparoscopy is indicated when medical therapy fails, when a tissue diagnosis is needed, or when infertility is the primary concern. Surgical goals include excision or ablation of all visible implants, lysis of adhesions, and restoration of normal pelvic anatomy. For endometriomas larger than 3-4 cm, cystectomy (excision of the cyst wall) is preferred over simple drainage and ablation because recurrence rates are lower and subsequent fertility outcomes are better.

Definitive surgery (TAH-BSO) is reserved for patients with severe, debilitating, treatment-refractory disease who have completed childbearing. If the ovaries are removed, estrogen replacement therapy can be considered, but there is a small risk of reactivating residual disease.

Infertility-Focused Management

For patients whose primary concern is infertility, the approach differs. Medical suppression of endometriosis (COCs, GnRH agonists) does not improve fertility and should not be used for this purpose. Instead, options include laparoscopic surgical treatment of implants and adhesions (improves spontaneous conception rates in mild-moderate disease) or proceeding directly to assisted reproductive technology (IVF), especially in moderate-to-severe disease or when other factors contribute.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Adenomyosis	Dysmenorrhea + heavy menstrual bleeding + uterine tenderness	Uterus is diffusely enlarged and boggy (globular); no adnexal mass; MRI shows junctional zone thickening >12 mm; endometriosis has focal implants, nodularity, and adnexal findings
Primary dysmenorrhea	Painful menstruation in young women	Begins at menarche, pain is not progressive, no abnormal exam findings, no associated infertility or dyspareunia
Chronic pelvic inflammatory disease	Chronic pelvic pain + adnexal tenderness + infertility	History of STI/PID, cervical motion tenderness, fever, purulent discharge; pain is not cyclic
Ovarian torsion	Acute pelvic pain + adnexal mass	Pain is sudden and unilateral, often with nausea/vomiting; Doppler shows decreased or absent blood flow; not cyclic
Ruptured ovarian cyst	Acute pelvic pain + adnexal pathology	Sudden onset, mid-cycle timing, free fluid in cul-de-sac on ultrasound; no cyclic pattern
Irritable bowel syndrome	Chronic pelvic/abdominal pain, pain with defecation	Symptoms related to bowel habits (diarrhea/constipation alternating), no relation to menstrual cycle, normal pelvic exam
Interstitial cystitis	Chronic pelvic pain + dyspareunia	Suprapubic pain, urinary frequency/urgency, symptoms worsen with bladder filling and improve with voiding; not cyclic with menses

6. Traps and High-Yield Pearls

The single most common way students lose points on endometriosis questions is by failing to recognize the cyclic nature of symptoms. The vignette will describe pelvic pain, dyspareunia, or even GI or urinary symptoms, but the distinguishing feature is that these symptoms worsen perimenstrually and follow a cyclic pattern. If the pain is constant and unrelated to the menstrual cycle, think of other diagnoses.

A second frequent trap involves confusing endometriosis with adenomyosis. Both cause dysmenorrhea in reproductive-age women, but adenomyosis presents with a diffusely enlarged, boggy, tender uterus and heavy menstrual bleeding (menorrhagia), whereas endometriosis presents with a normal-sized or fixed retroverted uterus, nodularity on rectovaginal exam, and adnexal endometriomas.

Students also commonly forget that the stage of disease does not predict pain severity. A vignette showing minimal laparoscopic findings does not exclude the diagnosis in a patient with classic symptoms.

On treatment questions, remember that hormonal suppression does not treat endometriosis-related infertility. If the vignette presents a patient whose chief complaint is inability to conceive, the answer is never "start OCPs" or "start leuprolide." The correct next step is either laparoscopic surgery or referral for assisted reproduction.

For the rare but testable scenario of cyclic hemoptysis or recurrent unilateral pneumothorax in a young menstruating woman, think of thoracic endometriosis (catamenial pneumothorax). This is a classic "if you know it, you get it" question.

Finally, when a vignette describes a painful nodule at a prior surgical scar (especially a cesarean scar) that enlarges and becomes tender during menstruation, the diagnosis is scar endometriosis. This is an increasingly tested topic and should be recognized immediately from the cyclic pain-at-scar pattern.

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