Define and describe the sites, clinical features, diagnosis and management of endometriosis.

Severity of disease correlates poorly with severity of pain.

Definition

Endometriosis is the presence of functioning endometrial tissue (glands and stroma) outside the uterine cavity. Being hormonally responsive, it bleeds cyclically at the ectopic sites, producing inflammation, adhesions and pain.

Endometriosis - Sites & Theory

Sites

Most often within the pelvis — the ovary (forming a "chocolate cyst"/endometrioma), the pouch of Douglas, the uterosacral ligaments, the pelvic peritoneum, the recto-vaginal septum and the bladder; rarely at distant sites (umbilicus, scars, lung).

Theories of Origin

Sampson's retrograde menstruation theory (the most accepted), coelomic metaplasia, and lymphatic/ vascular dissemination, with a contribution from genetic and immunological factors.

Pathology

The ectopic deposits bleed cyclically, producing small "powder-burn"/blue-black lesions on the peritoneum and chocolate cysts (endometriomas) in the ovary (altered, tarry, retained blood), with surrounding fibrosis and dense adhesions. Microscopy shows endometrial glands and stroma with haemosiderin-laden macrophages.

Clinical Features

The classic triad is secondary dysmenorrhoea, deep dyspareunia and infertility, with chronic cyclical pelvic pain; there may be cyclical bowel/bladder symptoms. The severity of symptoms correlates poorly with the extent of disease.

Examination

A fixed retroverted uterus, tender nodularity of the uterosacral ligaments and pouch of Douglas, and a tender adnexal (ovarian) mass.

Investigations

• Ultrasound for an endometrioma; MRI for deep/extensive disease.
• Serum CA-125 may be mildly raised (non-specific).
• Laparoscopy is the gold standard for diagnosis (powder-burn deposits, endometriomas, adhesions) and allows staging (revised ASRM) and biopsy.

Complications

Infertility (the major concern — from adhesions and distorted tubo-ovarian anatomy), chronic pelvic pain, rupture or torsion of an endometrioma, dense pelvic adhesions with bowel/ureteric involvement, and rare malignant change in an endometrioma.

Management

• Medical (to suppress cyclical activity) — NSAIDs for pain; combined oral pills, progestins, the levonorgestrel-IUS, GnRH analogues (with add-back) and danazol.
• Surgical — laparoscopic ablation/excision of deposits, cystectomy of endometriomas and adhesiolysis; definitive surgery (hysterectomy with bilateral salpingo-oophorectomy) for severe disease in women who have completed their family.
• Infertility — surgery improves fertility in mild disease; assisted reproduction (IVF) for those who do not conceive.

WHY Endometriosis Causes Pain That Is Cyclical and Progressive

Understanding why the symptoms of endometriosis take the form they do follows directly from what the disease is: functioning endometrial tissue in an abnormal site. Because this ectopic tissue responds to the same hormonal cycle as the endometrium, it proliferates under oestrogen and bleeds at menstruation — but the blood has nowhere to escape. It therefore collects locally, causing inflammation, and — as this is repeated month after month — fibrosis, scarring and dense adhesions. Every symptom follows. The pain is cyclical, beginning a day or two before the period and worst during it (secondary dysmenorrhoea), and it is progressive, worsening year by year as the adhesions build up. Deposits in the pouch of Douglas and on the uterosacral ligaments cause deep dyspareunia and dyschezia; adhesions distort the tubes and ovaries and impair oocyte release and transport, causing infertility (present in up to 30–50% of women with the disease); and repeated bleeding into the ovary forms a 'chocolate' cyst (endometrioma). Note the classic paradox: the extent of the disease correlates poorly with the severity of the pain. Understanding that this is normal tissue behaving normally in the wrong place explains the whole clinical picture.

WHY Treatment Aims to Suppress Oestrogen — and its Limits

A useful concept is why the medical treatment of endometriosis is essentially the induction of a hormonal state in which the disease cannot thrive. Since the ectopic tissue is oestrogen-dependent, all medical treatments work by removing the cyclical oestrogen stimulus — either by producing a steady, progestogen-dominant state (the continuous combined pill, progestogens, the LNG-IUS) or by inducing a temporary, reversible pseudo-menopause (GnRH agonists). This suppresses the tissue, prevents its cyclical bleeding, and relieves the pain — which is why the disease also regresses naturally in pregnancy and after the menopause. But this approach has two important limits. First, the treatments are contraceptive — so they cannot be used by a woman who is trying to conceive, which is precisely the group in whom endometriosis-related infertility matters most; for her, the treatment is surgical (laparoscopic ablation/excision of deposits and adhesiolysis) or assisted reproduction. Second, medical treatment suppresses but does not cure: symptoms typically recur when it is stopped. Understanding that the disease is oestrogen-driven — and that suppressing oestrogen also suppresses fertility — explains both the logic and the frustration of treating endometriosis.

• Endometriosis = functioning endometrial tissue outside the uterus (commonest sites: ovary — chocolate cyst; pouch of Douglas; uterosacral ligaments).
• It bleeds cyclically with no escape → inflammation, fibrosis and adhesions — hence progressive, cyclical pain.
• Classic symptoms: secondary dysmenorrhoea, deep dyspareunia, chronic pelvic pain, dyschezia and infertility; the extent of disease correlates poorly with the pain.
• Diagnosis: laparoscopy is the gold standard (powder-burn deposits, chocolate cysts, adhesions); ultrasound shows endometriomas.
• Treatment: suppress oestrogen (continuous COC, progestogens, LNG-IUS, GnRH agonists) for pain; surgery (laparoscopic ablation/excision) if fertility is desired or medical treatment fails.