1.93 CME

Chronic Pelvic Pain: Diagnostic, Approach and Management

Speaker: Dr. Harika Chikkam

Consultant Obstetrician and Gynecologist, Laparoscopic and Robotic Surgeon, Kims Hospital, Bangalore

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Summary Listen

  • Chronic pelvic pain (CPP) is defined as continuous, non-psychogenic pain lasting over six months, affecting about 24% of reproductive-aged women. It is often misdiagnosed as gastrointestinal or spinal issues. Textbook definition specifies pain localized to the anatomic pelvis, severe enough to cause functional disability requiring medical care.
  • The etiology of CPP is diverse, including gynecological causes like endometriosis, adenomyosis, PID, adhesions, cysts, fibroids, and pelvic congestion syndrome. Gastrointestinal causes include IBS, IBD, and chronic constipation. Musculoskeletal factors such as myofascial pain and pelvic floor spasms, urological conditions like interstitial cystitis (bladder pain syndrome), psychological factors (anxiety, depression), and neurological issues like nerve entrapments can also contribute.
  • Pelvic pain can be non-cyclic (e.g., adhesions, endometriosis, remnant ovarian syndrome, pelvic congestion, ovarian neoplasm) or cyclic. Cyclic causes include primary dysmenorrhea, mid-cycle pain (ovulation), and secondary dysmenorrhea due to endometriosis, adenomyosis, uterine/vaginal anomalies, IUDs, polyps, or leiomyomas.
  • The physiology of chronic pain differs from acute pain. In CPP, there's a modulation and upregulation of nociceptors, leading to allodynia (pain from non-painful stimuli). Inflammatory lesions, like endometriosis, create a chronic neurogenic inflammation environment with continuous stimulation and plastic changes in the peripheral nervous system. Pelvic congestion syndrome involves dilatation and engorgement of pelvic veins, causing mechanical/ischemic pain and central sensitization. Prostaglandins are key mediators of pain during menstruation.
  • Acute conditions can transition to chronic pain, such as unresolved ectopic pregnancies, recurrent adnexal torsion, or persistent tubo-ovarian abscesses. Chronic adhesions, resulting from previous surgeries, PID, or endometriosis, can cause pain. Adhesiolysis for isolated adhesions is not routinely recommended unless associated with infertility or endometriosis; barrier materials and careful surgical technique can prevent formation.
  • Pelvic congestion syndrome presents with dull aching pain worsening on standing, post-coital pain, and vulvar/lower limb varicosities. Diagnosis is clinical and with Doppler ultrasound showing increased vascularity. Low-estrogen OCs offer short-term relief, but endovascular embolization is the preferred treatment.
  • Endometriosis is defined as the presence of endometrial glands and stroma outside the uterus, most commonly in pelvic viscera and peritoneum. It is found in 22-90% of patients with pelvic pain or infertility. It can cause cyclical GI symptoms and is strongly associated with infertility due to tubal immotility, adhesions, and ovarian impact. Classification includes ovarian, peritoneal, and deep infiltrating endometriosis (DIE), defined by depth of invasion (>5mm).
  • Localization of endometriosis lesions helps correlate with symptoms: uterosacral ligaments/Douglas pouch/posterior fornix cause dyspareunia, dysmenorrhea, back pain. Bladder involvement leads to urinary frequency, hematuria, painful urination. Ureteric nodules can be asymptomatic until causing hydronephrosis. Bowel lesions cause dyschezia, diarrhea, constipation, and painful defecation. Risk factors include early menarche, short cycles, nulliparity, Mullerian anomalies, while protective factors include multiparity, lactation, and increased BMI.
  • Endometriosis theories include retrograde menstruation (Samson's), coelomic metaplasia, immune dysfunction, genetic/hormonal/environmental factors, stem cell theory, metastatic theory, and endoinduction theory. Diagnosis involves detailed history, clinical exam, and imaging. Ultrasound is first-line; MRI maps disease extent using the IDEA protocol, dividing the pelvis into anterior, posterior, and middle compartments for implant mapping.
  • Classification systems like the #ENZIAN classification provide a comprehensive staging, addressing the limitations of the ASRM score. #ENZIAN categorizes lesions by peritoneum (P1-3), ovary (O1-3), tubal patency (T+/T-), and deep endometriosis (A for rectovaginal/retrocervical, B for lateral compartment/ligaments, C for rectal nodule). It also includes F for adenomyosis (FA), bladder (FB), intestine (FI), and ureter (FU), providing detailed mapping for surgical planning and patient counseling. The Endometriosis Fertility Index (EFI) scores patients post-surgery to predict fertility outcomes.
  • Medical management for endometriosis aims to suppress symptoms rather than cure the disease, as implants often reactivate post-treatment. Options include combined hormonal contraceptives, progestins (e.g., dienogest), GnRH agonists, and GnRH antagonists (e.g., relugolix with add-back therapy). These are given for specified durations (e.g., COCs 24-36 months, progestins/GnRH 24 months) with monitoring for side effects like bone density changes.
  • Surgical management is the gold standard, aiming for complete excision of endometriotic tissue via laparoscopy. Principles include complete lesion removal, nerve-sparing techniques, fertility preservation, and a compartmental approach. For peritoneal endometriosis, excision is preferred over ablation. Cystectomy is recommended for ovarian endometriomas. DIE excision involves a stepwise approach: sigmoid mobilization, ureterolysis, and posterior peritonectomy. Multidisciplinary care with urologists or colorectal surgeons is often necessary.
  • Adenomyosis, the presence of endometrial tissue within the myometrium, results from basal layer disruption and infiltration into the junctional zone. It's common in multiparous women over 40 with previous uterine surgery. Theories include direct invasion, reaction to trauma, metaplasia, and adult stem cell involvement. Patients present with heavy menstrual bleeding, dysmenorrhea, dyspareunia, and infertility. It often co-exists with fibroids and endometriosis.
  • Diagnosis of adenomyosis relies on ultrasound and MRI. Ultrasound criteria (User criteria) include direct signs like myometrial cysts, junctional zone thickening, subendometrial lines/buds, and focal adenomyomas; indirect signs include globular uterine enlargement, asymmetrical wall thickening, and heterogeneous myometrial texture. MRI provides detailed thickness of the junctional zone and extent of myometrial involvement (diffuse/focal).
  • Specific adenomyosis entities include adenomyoma (localized confluence of glands), cystic adenomyosis (hemorrhagic cyst without uterine communication), Focal Adenomyoma-like masses in the Outer Myometrium (FORM), Accessory Cavitated Uterine Mass (ACUM) from developmental anomalies, and juvenile cystic adenomyosis.
  • Medical management for adenomyosis involves NSAIDs, combined oral contraceptives, progestins (including IUCDs), and GnRH agonists/antagonists to induce hypoestrogenism and endometrial atrophy. Interventional and surgical options include microwave ablation, MR-guided focused ultrasound (HIFU) for thermal destruction. Fertility-sparing surgical techniques for adenomyomectomy range from traditional wedge resections to complex procedures like the transverse H-shaped incision, push technique, double/triple flap techniques for uterine wall reconstruction, and four-petal technique, aiming to preserve uterine integrity and reduce rupture risk in future pregnancies. Hysterectomy remains the definitive treatment in severe cases or when fertility is not desired.

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