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Wednesday, August 13, 2025

Endometriosis


Introduction

Endometriosis is a chronic, estrogen-dependent gynecological disorder characterized by the presence of functional endometrial-like tissue (glands and stroma) outside the uterine cavity. These ectopic implants can respond to hormonal fluctuations during the menstrual cycle, leading to inflammation, fibrosis, and adhesions.

The condition is a major cause of pelvic pain and infertility in women of reproductive age. While benign, endometriosis behaves in many ways like a neoplastic process, with the potential for local invasion and distant implantation, though without malignant histology in most cases.

Epidemiology

  • Prevalence: Estimated at 6–10% in women of reproductive age; higher (35–50%) in women with chronic pelvic pain or infertility.

  • Age: Most commonly diagnosed between 25–35 years.

  • Risk groups: More common in nulliparous women, women with early menarche, short menstrual cycles, or prolonged menstruation.

  • Family history: First-degree relatives have a 6–7-fold increased risk.

Etiology and Pathogenesis

The exact cause is not fully understood; multiple theories likely contribute:

1. Retrograde Menstruation (Sampson’s Theory)

  • Menstrual blood containing viable endometrial cells flows back through the fallopian tubes into the peritoneal cavity.

  • These cells implant and proliferate on peritoneal surfaces.

  • Explains pelvic distribution but not all cases.

2. Coelomic Metaplasia

  • Peritoneal mesothelial cells undergo metaplastic transformation into endometrial-like cells.

  • Could explain cases in premenarchal girls and in unusual sites.

3. Lymphatic or Hematogenous Spread

  • Endometrial cells spread via lymphatic or blood vessels to distant organs (lungs, brain, skin).

  • Explains rare extrapelvic lesions.

4. Stem Cell Theory

  • Bone marrow-derived stem cells differentiate into endometrial tissue at ectopic sites.

5. Immunological Factors

  • Impaired immune surveillance allows ectopic endometrial tissue to survive and grow.

Risk Factors

  • Early menarche (<12 years)

  • Short menstrual cycles (<27 days)

  • Heavy menstrual bleeding

  • Nulliparity

  • Family history of endometriosis

  • Low body mass index

  • High consumption of trans fats; low consumption of omega-3 fatty acids

Sites of Involvement

  • Pelvic sites: Ovaries (endometriomas), uterosacral ligaments, pouch of Douglas, pelvic peritoneum, fallopian tubes.

  • Extrapelvic sites: Bladder, bowel, abdominal wall, diaphragm, pleura, umbilicus, surgical scars.

  • Rare distant sites: Lung, brain, extremities.

Clinical Features

1. Pelvic Pain Syndromes

  • Dysmenorrhea: Often progressive and severe.

  • Chronic pelvic pain: Persists >6 months, may be cyclic or noncyclic.

  • Dyspareunia: Pain during deep sexual penetration.

  • Dyschezia: Pain during defecation, especially during menstruation.

  • Dysuria: Painful urination, especially with bladder lesions.

2. Infertility

  • Present in up to 30–50% of women with endometriosis due to adhesions, distorted pelvic anatomy, or inflammatory mediators affecting ovulation, fertilization, and implantation.

3. Other Symptoms

  • Bloating, fatigue, low back pain.

  • Site-specific symptoms if bowel or bladder involved (rectal bleeding, hematuria during menses).

Classification (Revised American Society for Reproductive Medicine – rASRM)

Staging is based on location, extent, and depth of implants; presence and severity of adhesions:

  • Stage I (Minimal): Few superficial implants.

  • Stage II (Mild): More and deeper implants.

  • Stage III (Moderate): Many deep implants, small endometriomas, filmy adhesions.

  • Stage IV (Severe): Large endometriomas, dense adhesions, extensive disease.

Note: Staging correlates poorly with symptom severity.

Diagnosis

Clinical Evaluation

  • Detailed history of menstrual cycle, pain characteristics, and infertility.

  • Pelvic examination may reveal:

    • Tender nodules in posterior vaginal fornix or uterosacral ligaments.

    • Fixed, retroverted uterus.

    • Adnexal masses (endometriomas).

Imaging

  • Transvaginal ultrasound: Best for detecting ovarian endometriomas (homogeneous, low-level echoes – “ground-glass” appearance).

  • MRI: Useful for deep infiltrating disease and mapping lesions.

  • Imaging has limited sensitivity for superficial peritoneal lesions.

Definitive Diagnosis

  • Laparoscopy with histologic confirmation: Gold standard.

    • Allows direct visualization of lesions (powder-burn, red flame, white scar appearances).

    • Enables simultaneous surgical treatment.

Management

Management depends on symptom severity, fertility desires, age, and disease extent.

1. General Principles

  • Aim: Pain control, suppression of disease activity, preservation or restoration of fertility.

  • Individualized treatment—no single “best” approach for all patients.

2. Pharmacologic Therapy

First-line for Pain Relief

  • Combined hormonal contraceptives (COCs):

    • Suppress ovulation, stabilize hormonal fluctuations, reduce menstrual flow.

    • Formulations: Ethinylestradiol + levonorgestrel, norethindrone acetate.

    • Continuous use may be more effective for pain suppression.

  • Progestin-only therapy:

    • Examples: Medroxyprogesterone acetate, norethindrone acetate, dienogest.

    • Mechanism: Induce decidualization and atrophy of endometrial tissue.

Gonadotropin-Releasing Hormone (GnRH) Agonists

  • Examples: Leuprolide acetate, goserelin, triptorelin.

  • Induce hypoestrogenism (“medical menopause”).

  • Limit use to 6 months without add-back therapy due to risk of bone loss.

GnRH Antagonists

  • Example: Elagolix.

  • Directly block GnRH receptors, leading to rapid suppression of estrogen.

Aromatase Inhibitors

  • Examples: Letrozole, anastrozole.

  • Reduce estrogen production from ovarian and peripheral tissues.

  • Often combined with progestins or GnRH analogs.

NSAIDs

  • Examples: Ibuprofen, naproxen.

  • Reduce prostaglandin-mediated pain; best for mild cases or adjunctive therapy.

3. Surgical Management

Conservative Surgery

  • Laparoscopic excision or ablation of lesions and adhesiolysis.

  • Improves pain and may enhance fertility.

  • Preferred for women desiring pregnancy.

Definitive Surgery

  • Total hysterectomy with bilateral salpingo-oophorectomy:

    • Reserved for severe, refractory disease in women who have completed childbearing.

  • May require postoperative hormonal therapy to prevent recurrence from residual disease.

4. Fertility Management

  • For minimal/mild disease: Surgical removal of lesions may improve spontaneous conception rates.

  • For moderate/severe disease: IVF may be indicated if pregnancy does not occur within 6–12 months after surgery.

5. Recurrence

  • Recurrence rates: 20–40% within 5 years after surgery without maintenance therapy.

  • Long-term hormonal suppression can reduce recurrence risk.

Complications

  • Chronic pelvic pain and reduced quality of life.

  • Infertility.

  • Adhesion formation leading to bowel or urinary obstruction.

  • Rare malignant transformation (e.g., endometrioid or clear cell ovarian carcinoma).

Prognosis

  • Chronic, recurrent condition; symptoms often improve after menopause.

  • With appropriate medical and/or surgical treatment, many women achieve satisfactory pain control and maintain fertility.





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