A 28-year-old woman from Delhi presents with secondary amenorrhea of 6 months' duration. She reports regular cycles until 8 months ago, when she underwent dilation and curettage (D&C) for evacuation of a molar pregnancy. Since then, she has had no menses. On examination, she is afebrile, vital signs are stable, and pelvic examination is unremarkable. FSH is 6.2 mIU/mL, LH is 5.8 mIU/mL, estradiol is 45 pg/mL, and prolactin is 12 ng/mL (normal). Pelvic ultrasound shows a thin endometrium (2 mm) with no focal lesions. Hysteroscopy reveals dense adhesions involving the anterior and posterior uterine walls. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Asherman Syndrome ### Key Clinical Features Presented - **Secondary amenorrhea** (6 months duration) following **uterine instrumentation** (D&C for molar pregnancy) - **Normal gonadotropins** (FSH 6.2, LH 5.8 — both in normal range) - **Normal estradiol** (45 pg/mL — ovarian function intact) - **Normal prolactin** (12 ng/mL) - **Thin endometrium** on ultrasound (2 mm) - **Dense intrauterine adhesions** on hysteroscopy (diagnostic finding) ### Pathophysiology **Key Point:** Asherman syndrome results from intrauterine adhesions (synechiae) that obliterate the endometrial cavity, preventing normal endometrial growth and menstruation despite intact ovarian function and normal gonadotropin-releasing hormone (GnRH) axis. **Mnemonic: ASHERMAN = Adhesions + Scarring + Hysteroscopy + Endometrial + Removal + Molar/post-Abortion + Amenorrhea + Reproductive loss** ### Etiology in This Case D&C for molar pregnancy is a **high-risk procedure** for Asherman syndrome because: 1. Molar tissue is highly invasive and damages the basalis layer 2. Aggressive curettage required to remove molar tissue causes further endometrial trauma 3. Inflammation and subsequent scarring lead to adhesion formation **Clinical Pearl:** Any uterine instrumentation (D&C, myomectomy, hysteroscopic surgery, endometrial ablation) can cause Asherman syndrome, but post-molar evacuation and post-abortion curettage carry the highest risk (~15–20%). ### Diagnostic Approach | Finding | Asherman Syndrome | Sheehan Syndrome | Hypothalamic Amenorrhea | PCOS | | --- | --- | --- | --- | --- | | **FSH/LH** | Normal | ↓↓ (low) | ↓ (low-normal) | Normal or ↑ LH | | **Estradiol** | Normal | Low | Low-normal | Normal | | **Prolactin** | Normal | ↑ (elevated) | Normal | Normal | | **Endometrium** | Thin, atrophic | Thin, atrophic | Normal | Normal | | **Hysteroscopy** | Adhesions | N/A | N/A | N/A | | **History** | Uterine instrumentation | Postpartum hemorrhage/shock | Stress, weight loss, exercise | Irregular cycles, hirsutism | ### Why This Is Asherman Syndrome 1. **Temporal relationship**: Amenorrhea began immediately after D&C (uterine instrumentation) 2. **Intact ovarian function**: Normal FSH, LH, and estradiol indicate the hypothalamic-pituitary-ovarian (HPO) axis is functioning 3. **Normal prolactin**: Rules out Sheehan syndrome (postpartum pituitary necrosis) 4. **Hysteroscopic findings**: Dense adhesions are **pathognomonic** for Asherman syndrome 5. **Thin endometrium**: Reflects endometrial scarring and loss of functional endometrial tissue **High-Yield:** Asherman syndrome is a **uterine (outflow tract) cause of secondary amenorrhea** — the ovaries are working, but the endometrium cannot respond. ### Management Algorithm ```mermaid flowchart TD A["Secondary amenorrhea post-D&C"]:::outcome --> B["Check FSH, LH, prolactin, estradiol"]:::action B --> C{"Gonadotropins and estradiol normal?"}:::decision C -->|Yes| D["Pelvic ultrasound"]:::action D --> E{"Thin endometrium + history of instrumentation?"}:::decision E -->|Yes| F["Hysteroscopy"]:::action F --> G{"Adhesions present?"}:::decision G -->|Yes| H["Asherman syndrome confirmed"]:::outcome H --> I["Hysteroscopic adhesiolysis"]:::action I --> J["Estrogen therapy + mechanical separation"]:::action J --> K["Repeat hysteroscopy to prevent re-adhesion"]:::action ``` ### Treatment 1. **Hysteroscopic adhesiolysis** (lysis of adhesions under direct visualization) 2. **Estrogen therapy** (high-dose conjugated estrogens or transdermal estradiol) to promote endometrial proliferation 3. **Mechanical barrier** (Foley catheter, hyaluronic acid gel, or intrauterine device) to prevent re-adhesion 4. **Repeat hysteroscopy** (2–4 weeks post-treatment) to assess healing and prevent recurrence **Clinical Pearl:** Success rates for restoring menstruation are 40–80%, depending on the extent of adhesions. Fertility outcomes are worse with more extensive adhesions. [cite:Park 26e Ch 8; Yen & Jaffe's Reproductive Endocrinology 8e Ch 12]