Evaluation and Treatment of Chronic Pelvic Pain

Chronic pelvic pain is a multifactorial condition best managed through interdisciplinary care that integrates behavioral, pharmacologic, and surgical treatments using shared decision making.

Abstract

Chronic pelvic pain (CPP) is a complex and often debilitating condition that affects 15–26% of women worldwide. It is defined as pain perceived to originate from pelvic organs or structures that typically lasts longer than 6 months and is often associated with negative cognitive, behavioral, sexual, and emotional consequences. Chronic pelvic pain is not a single disease but rather a symptom with many potential causes, with most patients having multiple contributing conditions. This article provides an overview of the evaluation and management of CPP for obstetrician–gynecologists. We recommend an organ system–based approach to diagnosis, recognizing that any combination of gynecologic, gastrointestinal, musculoskeletal, urologic, neurologic, and vascular sources is a possible cause. Effective management integrates behavioral, pharmacologic, and surgical strategies tailored to the suspected pain mechanisms in each patient. Educating patients about pain physiology, including the interaction between peripheral pathology and central pain amplification, is essential. Although CPP is not always curable, patients can experience significant and meaningful improvement in pain, function, and quality of life through long-term interdisciplinary support. Establishing a strong therapeutic relationship, validating patients' experiences, and empowering patients to take an active role in their care are central to effective management. Shared decision making, collaborative goal setting, and establishing clear expectations support sustained engagement and functional improvement.

Chronic pelvic pain (CPP) is an often debilitating condition that affects 15–26% of women worldwide.¹ Although there is no consensus among professional societies on the definition of CPP or minimal duration of pain required for diagnosis, the American College of Obstetricians & Gynecologists defines it as, “pain symptoms perceived to originate from pelvic organs/structures typically lasting more than 6 months” that “is often associated with negative cognitive, behavioral, sexual and emotional consequences as well as with symptoms of lower urinary tract, sexual, bowel, pelvic floor, myofascial, or gynecologic dysfunction.”² There is wide variation in the frequency, pattern, and location of pain in patients with CPP. Pain may be intermittent or constant, exhibit a cyclical pattern that is temporally associated with the menstrual cycle (eg, ovulatory pain or dysmenorrhea), or can occur when not menstruating (nonmenstrual pelvic pain). Pain can also be localized to a single site or involve multiple pelvic regions. Furthermore, there is no consensus among professional societies regarding the minimum duration of pain required for diagnosis, with some defining CPP as pain lasting 3 months or longer and others using a threshold of 6 months or longer.³ The substantial symptom burden frequently leads to repeated surgical procedures and prolonged use of medical therapies. On average, individuals with CPP have a higher number of office visits, emergency department visits, hospitalizations, diagnostic testing, medication use (including opioids), and surgical procedures compared with those without CPP.^4,5 Despite these interventions, many experience persistent pain and distress and report feeling stigmatized and dismissed,^6,7 which contribute to impaired emotional health, reduced work productivity, and lower quality of life.^8,9

PATHOPHYSIOLOGY

Chronic pelvic pain is not a single disease but rather a symptom with many potential causes, often with multiple contributing conditions in affected individuals. These include disorders with identifiable gynecologic pathology (eg, endometriosis) and others better characterized as functional pain syndromes (eg, irritable bowel syndrome). Many conditions associated with CPP are part of the broader chronic overlapping pain conditions recognized by the National Institutes of Health, which include fibromyalgia, chronic fatigue syndrome, chronic migraine, chronic tension-type headache, temporomandibular joint disorder, chronic low back pain, irritable bowel syndrome, interstitial cystitis/bladder pain syndrome, vulvodynia, and endometriosis.¹⁰ Chronic overlapping pain conditions affect predominantly women and frequently co-occur in the same individual. For example, one insurance claims–based study reported that individuals with endometriosis have significantly elevated odds of co-occurring chronic pain conditions, including a 15.6-fold increase for vulvodynia, 18.6-fold for irritable bowel syndrome, 10-fold for fibromyalgia, fivefold for interstitial cystitis/bladder pain syndrome, and 3.2-fold for migraine headaches.¹¹ Chronic overlapping pain conditions share common risk factors and pathophysiologic mechanisms, most notably central nervous system sensitization that promotes chronic pain at multiple levels (ie, spinal, subcortical, cortical). The terms nociplastic pain, centralized pain, and central sensitization are overlapping concepts that have been used to describe this phenomenon.^11–13

Nociplastic pain mechanisms are thought to be a common feature of chronic overlapping pain conditions, including CPP. Chronic pelvic pain can result from any combination of the three pain mechanisms recognized by the International Association for the Study of Pain: nociceptive pain, caused by activation of nociceptors secondary to tissue injury or inflammation; neuropathic pain, caused by injury to the somatosensory nervous system; and nociplastic pain, attributed to altered pain perception associated with central nervous system amplification of ascending signals or loss of descending pain inhibition (Fig. 1).^13,14 These pain mechanisms are not mutually exclusive and likely occur across a continuum. The degree to which each mechanism contributes to CPP differs across chronic pain conditions and between individuals with the same condition(s); therefore, elucidating individual pain mechanisms is essential for informing effective and personalized treatment strategies. For example, endometriosis lesions can release proinflammatory cytokines that activate peripheral nociceptors (nociceptive pain) and can also directly compress or infiltrate nerves such as the obturator or sciatic nerve (neuropathic pain).¹⁵ Neuropathic pain can also occur as a result of sensitization of second-order neurons innervating adjacent structures, leading to cross-organ sensitization. The central nervous system can amplify and dampen the signals from the periphery, which may explain why there is little correlation between severity of pain symptoms and extent of pelvic pathology (eg, number, subtype, or location of endometriosis lesions) and why medications and surgery aimed at nociceptive pain mechanisms do not consistently alleviate pain.^16,17 The hallmark symptoms of nociplastic pain include widespread pain throughout the body with generalized sensory sensitivity—manifesting as heightened sensitivity to both internal and external painful and nonpainful stimuli (eg, increased bother with visual or sound stimuli)—along with common symptoms of fatigue, nonrestorative sleep, cognitive dysfunction, and mood disturbance.¹³ Risk factors for nociplastic pain include female sex, genetics or epigenetics, adverse childhood experiences, obesity, physical inactivity, and physical and emotional trauma and stressors.¹³ It is important to note that nociplastic pain is not a dichotomous construct but can occur in varying degrees among individuals and that its severity is linked to relevant clinical outcomes. For example, in patients with CPP, those with higher degrees of nociplastic pain are more likely to report greater pain intensity and functional disability and are less likely to respond to standard treatments aimed at removing or reducing nociceptive input (eg, surgical removal of endometriosis or hysterectomy).^16–18

Fig. 1. Conceptual model of mechanisms of pain in patients with chronic pelvic pain. Chronic pelvic pain can occur from any combination of nociceptive, neuropathic, or nociplastic pain. These pain mechanisms are not mutually exclusive and likely occur across a continuum, and the degree to which each mechanism contributes to persistent pain differs across chronic pain conditions and between individuals with the same condition(s). For example, nociceptive pain can occur as a result of endometriosis lesions, which release proinflammatory cytokines that activate peripheral nociceptors. Neuropathic pain can occur as a result of compression or infiltration of somatosensory nerves; it can also occur because of sensitization of second-order neurons innervating adjacent structures, leading to cross-organ sensitization. Nociplastic pain, which manifests as widespread pain, fatigue, memory difficulties, poor sleep, and generalized sensory sensitivity (heightened sensitivity to both internal and external painful and nonpainful stimuli), can be caused or exacerbated by nociceptive and neuropathic pain or can occur independently. These pathophysiologic processes interact and are associated with compromised function of the hypothalamic–pituitary and sympathetic–adrenal axes and systemic immune dysregulation, reflected in circulating monocytes and other white blood cells. Organ images created with ChatGPT4 and edited with Canva; all figure layouts and content were created by the authors.

As-Sanie. Evaluation and Treatment of Chronic Pelvic Pain. Obstet Gynecol 2026.

DIFFERENTIAL DIAGNOSIS OF CHRONIC PELVIC PAIN BY ORGAN SYSTEM

The evaluation and management of CPP is challenging because of its nonspecific and highly variable symptoms, which may result from a single condition or combination of chronic overlapping pain conditions. We recommend an organ system–based approach to the differential diagnosis, recognizing that most patients experience multiple sources of pain, with each requiring attention (Fig. 2). Because inadequately treated pain negatively affects quality of life, evaluation should not be delayed even when duration-based diagnostic criteria (eg, 6 months) have not been met. This review focuses on the most common nonmalignant gynecologic conditions associated with CPP in nonpregnant women. We also provide a brief overview of common nongynecologic contributors to identify and refer patients to other specialists when appropriate. Notably, patients with nongynecologic conditions such as irritable bowel syndrome, interstitial cystitis/bladder pain syndrome, or musculoskeletal pain can experience a cyclic exacerbation of their symptoms during menses, highlighting the overlap with gynecologic contributors and the importance of a thorough and nuanced diagnostic approach.¹⁹ Our approach reflects the recently developed International Federation of Gynecology and Obstetrics–International Pelvic Pain Society “R U MOVVING Some” classification system for CPP, an interdisciplinary, consensus-based framework designed to standardize terminology, to facilitate timely diagnosis, and to improve patient-centered care.³

Fig. 2. Differential diagnosis and example clinical features of conditions associated with chronic pelvic pain. NMPP, nonmenstrual pelvic pain; DYS, dysmenorrhea; DYSP, dyspareunia. Organ images created with ChatGPT4 and edited with Canva; all figure layouts and content were created by the authors.

As-Sanie. Evaluation and Treatment of Chronic Pelvic Pain. Obstet Gynecol 2026.

Gynecologic

The most common gynecologic pathologies associated with CPP include endometriosis, adenomyosis, and uterine leiomyomas. These have the shared traits of being estrogen-dependent conditions characterized by the painful triad of dysmenorrhea, nonmenstrual pelvic pain, and dyspareunia, as well as increased rates of infertility.^1,20

Endometriosis

Endometriosis, defined as the presence of endometrium-like tissue outside of the uterus, affects approximately 10% of reproductive-aged women, although the prevalence varies depending on patient symptoms and method of diagnosis.^15,21,22 It is identified in 28–49% of adults and 62–75% of adolescents presenting with pelvic pain or dysmenorrhea.^23,24 Risk factors include menarche before age 12, nulliparity, obstructive Müllerian anomalies, and a family history of endometriosis.²⁵ Endometriosis is classified into four subtypes: superficial peritoneal, deep, ovarian (endometriomas), and extrapelvic endometriosis.²⁶ These subtypes may occur alone or together, and distinguishing among them is important because subtype can influence management. Superficial peritoneal lesions are the most common, identified in approximately 80% of patients who undergo surgery.^21,27

The presence and severity of symptoms vary widely and do not correlate with the number, location, or subtype of lesions, except for dyspareunia, which is correlated with deep disease in the posterior cul-de-sac.^28,29 Approximately 90% of affected individuals report pelvic pain, with 55% experiencing severe symptoms.³⁰ Among these, 78.7% have dysmenorrhea, 69.4% experience nonmenstrual pelvic pain, and 44.9% report deep dyspareunia. Other symptoms include dyschezia (27%), infertility (26%), and moderate-to-severe fatigue (50%).^30,31 In less than 1% of patients with endometriosis, deep lesions can cause hydroureter or bowel obstruction; deep disease should be suspected when dyschezia, flank pain, or hematuria occur with cyclic pain.^32,33

Histologic confirmation has long been considered the gold standard for diagnosing endometriosis. However, multiple professional societies recommend making a clinical diagnosis based on symptoms, supported by physical examination and pelvic imaging.^34–38 This shift recognizes that requiring surgery may delay treatment, and in most cases, empiric hormonal therapy offers efficacy comparable with that of surgical removal of lesions. On examination, endometriosis may be suspected if there is posterior cul-de-sac tenderness or nodularity or decreased uterine mobility, findings present in up to 67–90% of patients with deep disease.³⁹ Transvaginal ultrasonography reliably detects ovarian endometriomas (93% sensitivity, 96% specificity) and has moderate sensitivity for deep lesions (79%) but low sensitivity for superficial lesions (65%).⁴⁰ Augmented pelvic ultrasonography, which evaluates the relative position of the ovaries and dynamic uterine sliding (eg, “kissing ovaries” and absence of uterine slide against the rectosigmoid suggest adhesions and deep endometriosis), is not widely performed in the United States but is supported by professional societies^34,37,38 given its accuracy in diagnosing deep endometriosis (88.4% sensitivity, 78.8% specificity).^41–43 Magnetic resonance imaging (MRI) with an endometriosis-specific protocol has 91–93.5% sensitivity and 86–87.5% specificity for endometriomas and deep endometriosis.⁴⁴ Notably, the absence of examination or imaging findings does not exclude the diagnosis of endometriosis.

Adenomyosis

Adenomyosis is an estrogen-dependent disorder characterized by the presence of endometrial epithelial cells and stromal fibroblasts within the myometrium, with associated hypertrophy and hyperplasia of surrounding smooth muscle.^45,46 Its prevalence in the general population is unknown, with reports ranging from 8.8 to 61.5% in women undergoing hysterectomy and 21–34% in women undergoing transvaginal ultrasonography for gynecologic symptoms.⁴⁷ Of individuals diagnosed by ultrasonography, 40–50% experience abnormal uterine bleeding, 30% report dysmenorrhea, and 33% are asymptomatic.⁴⁸ Adenomyosis can present as an enlarged, boggy, and tender uterus, although the absence of findings does not exclude adenomyosis.⁴⁸ Adenomyosis is diagnosed on transvaginal ultrasonography (81.8% sensitivity, 81.3% specificity) or MRI (sensitivity 46.1–74%, specificity 83–99.1%) by the presence of a thickened uterine junctional zone (more than 12 mm).⁴⁹ Adenomyosis and endometriosis frequently coexist. Cross-sectional studies report that 15–91.1% of individuals with endometriosis also have adenomyosis on imaging, which may contribute to persistent abnormal uterine bleeding and pain despite surgical removal of endometriosis lesion.^{45,48,50–52}

Uterine Leiomyomas

Uterine leiomyomas (fibroids) are benign tumors of the uterine myometrium with a lifetime prevalence of 40–89%, depending on method of diagnosis, patient age, and population characteristics.^53–55 About 25–50% of individuals with leiomyomas experience symptoms, most commonly heavy menstrual bleeding and pelvic pain.^53–55 In one survey of 3,000 individuals with leiomyomas, 75% reported dysmenorrhea, 33% nonmenstrual pelvic pain, and 29% dyspareunia, with 24–35% describing these symptoms as extremely bothersome.⁵⁶ Leiomyomas often coexist with endometriosis and adenomyosis,^57,58 making it challenging to determine the relative contribution of leiomyomas to pain symptoms. Transvaginal ultrasonography has 69% sensitivity and 98% specificity in diagnosing leiomyomas, which improves to 94% sensitivity and 97% specificity with saline infusion sonohysterography.⁵⁹ Although ultrasonography provides adequate information for most patients, MRI may be beneficial for preoperative planning and has high diagnostic accuracy.⁵⁹

Musculoskeletal

Common musculoskeletal contributors include high-tone pelvic floor dysfunction, abdominal wall myofascial pain, and pelvic girdle and hip pain.^60,61 High-tone pelvic floor dysfunction is identified in 58–79% of people with CPP.^62–64 Symptoms include nonmenstrual pelvic pain and dyspareunia, constipation, urinary frequency, and exacerbation with physical activity. High-tone pelvic floor dysfunction is diagnosed based on symptoms and signs, including tenderness to palpation of the pelvic floor muscles (eg, obturator internus, levator ani).⁶⁵ Abdominal wall myofascial pain can be identified as a positive Carnett sign (pain that worsens or stays the same with abdominal wall flexion) or as myofascial trigger points (focal, hypercontractile bands of skeletal muscle).^20,60 Pelvic girdle pain can arise from sacroiliac dysfunction or pubic symphysis pain.^60,61 These can be suspected by asymmetry in the iliac crest and pubic symphysis height. Hip pain can result from multiple orthopedic causes (eg, arthritis, labral tears) and typically presents with unilateral pain, worsened by weight-bearing activities.

Vulvar

Vulvodynia is estimated to occur in 8–16% of women.^66,67 Consensus guidelines define vulvodynia as “vulvar pain lasting ≥3 months, without a clear identifiable cause, which may have potential associated factors.”⁶⁸ The two most common subtypes are provoked vestibulodynia and generalized vulvodynia, which can occur in isolation or comorbid with other vulvar conditions. Provoked vestibulodynia is the most common subtype and is characterized by pain localized to the vulvar vestibule, often described as burning or stinging of the vulvar vestibule provoked by contact such as vaginal intercourse or tampon placement.⁶⁹ A cotton swab test can be performed by applying pressure to the mucosal surfaces of the vestibule to elicit provoked vestibulodynia. Consensus guidelines on optimal test technique and diagnostic sensitivity are yet to be established.⁷⁰ Generalized vulvodynia is typically associated with diffuse and constant pain, often exacerbated by activities that apply pressure to the vulva (eg, prolonged sitting or tight pants).

Persistent vulvar pain can also be caused by a specific disorder such as infection, trauma, hormonal deficiencies (eg, genitourinary syndrome of menopause, lactational amenorrhea), and neoplastic, neurologic, or iatrogenic pathologies after medical or surgical treatments to the vulva or long-term hormonal suppression.⁶⁸ Biopsies should be considered if there are blisters, erosions, ulcers, or edema.⁶⁸

Lower Urinary Tract

Interstitial cystitis/bladder pain syndrome is the most common lower urinary tract cause of CPP. It is defined by the American Urologic Association as an unpleasant sensation (pain, pressure, discomfort) lasting 6 weeks or longer perceived to be related to the bladder and accompanied by urinary frequency or urgency in the absence of other identifiable pathology. However, when hematuria is present, it warrants expedited workup because this suggests another cause, including possible malignancy. It is estimated that interstitial cystitis/bladder pain syndrome occurs in 2.7–6.5% of women, and in 15.5–78.3% of women with CPP.^71,72 Interstitial cystitis/bladder pain syndrome frequently co-occurs with other CPP conditions (48% have endometriosis and 30–75% have irritable bowel syndrome).^1,73,74 The American Urologic Association recommends diagnosing interstitial cystitis/bladder pain syndrome based on symptoms, with physical examinations and laboratory tests used to rule out other causes.⁷⁵ Cystoscopy and urodynamics should be reserved for uncertain diagnoses, in the setting of hematuria, or when risk factors for malignancy are present (eg, smoking).⁷⁵ The gynecologist may screen patients for interstitial cystitis/bladder pain syndrome and refer symptomatic patients to clinicians with urologic expertise for confirmation of diagnosis and treatment.

Gastrointestinal

Irritable bowel syndrome is the most prevalent gastrointestinal contribution to CPP, occurring in 8–41% of women with CPP.⁷⁶ Irritable bowel syndrome is diagnosed on the basis of symptoms using the Rome IV criteria: recurrent abdominal pain occurring for 6 months or longer with pain on average 1 d/wk or more in the past 3 months associated with at least two of the following: 1) defecatory pain, 2) change in stool frequency, or 3) change in stool form.⁷⁷ Although colonoscopy and laboratory tests are not required for diagnosis, they should be considered in patients with worrisome features such as hematochezia, unexplained weight loss, or family history of colon cancer. Given the rising incidence of gastrointestinal cancers in individuals younger than age 50 years—which is thought to be driven in part by increased incidence of obesity, Western diets (red meat, high saturated fat), and sedentary lifestyles⁷⁸—clinicians should consider malignancy in the differential diagnosis of symptomatic younger patients, even without a family history, when worrisome features are present.

Endometriosis of the bowel is estimated to occur in 5–12% of patients with endometriosis,⁷⁹ and patients with endometriosis have up to 18 times the risk of having irritable bowel syndrome.^11,80 Given the high coprevalence and overlap in symptoms between irritable bowel syndrome and bowel endometriosis, distinguishing the underlying cause of bowel symptoms can be challenging. Abdominal bloating, altered bowel habits, and pain with defecation are reported in 46–99% of patients with endometriosis⁸⁰; these symptoms are equally prevalent in patients with and without deep endometriosis³⁰ but may also reflect irritable bowel syndrome or inflammatory bowel disease. Thus, clinical evaluation should include identifying red-flag symptoms that warrant advanced imaging (pelvic MRI or augmented pelvic ultrasonography) to evaluate for bowel endometriosis and referral to a gastroenterologist to evaluate for and treat gastrointestinal pathologies.

Neurologic or Neuropathic

Neuropathic pain is defined as pain resulting from injury to the somatosensory nervous system. It is often described as burning, tingling, stinging, or shock-like and may be accompanied by paresthesia. Nerve entrapment syndrome, a subtype of neuropathic pain, occurs when a single nerve or nerve root is compressed, leading to symptoms localized to the dermatomal distribution of the affected nerve. In the pelvis, nerves of the lumbosacral plexus innervate the pudendal, sciatic, and gluteal regions.^20,81 Sacral nerve roots also include somatic and parasympathetic innervation. Thus, their compression can result in bowel, bladder, or pelvic floor dysfunction. Neuropathies are typically unilateral and may result from surgical trauma, deep endometriosis, or repetitive mechanical stress (eg, cycling leading to pudendal neuralgia). On physical examination, findings may include hyperesthesia, hypoesthesia, or allodynia along the affected dermatome. Involvement of the suspected nerve can often be confirmed by symptom relief after a targeted nerve block.

Pudendal neuralgia is one of the most recognized pelvic neuropathies but is rare, estimated to affect 1 in 100,000 individuals.⁸² It may result from mechanical or nonmechanical injury to the pudendal nerve and manifests as perineal or genital pain often accompanied by sexual, bladder, bowel, or autonomic dysfunction. Diagnosis is aided by the Nantes criteria, which include characteristic features such as pain localized to the pudendal distribution, exacerbation with sitting, absence of nocturnal awakening, lack of objective sensory loss, and relief after pudendal nerve block.⁸² Other pelvic neuropathic pain conditions may arise from injury to the genital or perineal branches of the iliohypogastric, ilioinguinal, genitofemoral, and posterior femoral cutaneous nerves.

Pelvic Venous Disorders

Pelvic venous disorders are thought to arise from reflux—typically involving the gonadal or internal iliac veins or obstruction—typically involving left renal or iliac veins. Symptoms described by patients with pelvic venous disorders include pelvic heaviness or pain, with symptoms potentially worsened by prolonged standing or activity, relieved by laying down, exacerbated by menses, and associated with prolonged postcoital aching pain. However, these are nonspecific and overlap widely with symptoms of multiple other CPP conditions.²⁰ When the left renal vein is affected, symptoms can include hematuria and left flank pain.⁸³ Physical examination findings are often normal but may include vulvar or perineal varicosities and tenderness on bimanual examination. Diagnosis is based on symptoms and imaging indicating parauterine or gonadal vessels more than 5 mm in diameter on venography or with demonstration of retrograde flow in gonadal vessels on pelvic venous duplex ultrasonography.⁸⁴ Given the absence of large epidemiologic studies on pelvic venous disorders, evidence-based guidelines are unavailable, and the prevalence of symptoms among individuals with dilated pelvic veins or coexisting conditions remains unknown.

EVALUATION

Establishing Therapeutic Relationship

Women with CPP frequently experience delayed diagnosis, dismissal, and repeated negative clinical encounters.^6,7,85–87 Thus, establishing a strong therapeutic relationship and empowering patients to take an active role in their care are critical for effective patient-centered management. Multiple professional societies recommend using a trauma-informed approach that actively engages patients in understanding how past trauma may influence current pain experiences.^1,20,88–90 Comorbid psychological conditions are highly prevalent and are associated with greater pain severity and reduced quality of life; however, it is essential to emphasize that CPP is not “in the patient's head” and is not solely explained by trauma or psychiatric disorders. Instead, chronic pain and psychologic symptoms often co-occur as a result of shared environmental, genetic, inflammatory, and neurobiological mechanisms.⁹¹ Integrating shared decision making, collaborative goal setting, and realistic discussions about long-term care expectations are essential; these strategies are associated with improved outcomes in individuals with CPP.¹ When feasible, longer appointments and short-interval follow-up support more thorough evaluations and help align patient and clinician expectations. These in turn improve adherence to therapy and treatment outcomes.¹

History

Providing time for patients to share their stories while validating the pain experience is key to establishing open communication.^1,20,92,93 Self-administered questionnaires are beneficial, particularly when completed before the appointment to allow more time for examination, counseling, and patient education. Box 1 provides suggested questions for taking a chronic pain history. Table 1 provides suggested questionnaires and educational tools to support symptom assessment and patient education. For busy clinicians, these tools are best used as flexible resources, with each health care professional selecting the components most relevant to their practice to streamline history taking, to enhance communication, and to guide management and patient education without excessive burden. Incorporating these resources into their clinical workflow may improve patient experience and support comprehensive care.

Box 1. Assessment of Clinical Symptoms and History.

Domain and questions

 Pain assessment: “OPQRST”

•   O: Onset: Did the pain start suddenly or gradually? Was it associated with any specific event?

•   P: Provocation, palliation: Worse or better with movement, vaginal intercourse or tampon use, full bladder, urination, bowel movement? Does it improve with heat, rest?

•   Q: Quality: Is it crampy, stabbing, heavy sensation, falling-out sensation, burning, stinging?

•   R: Region, radiation: Is the pain midline, one-sided, diffuse, around a surgical scar, in a dermatomal pattern? Does it radiate? Do you have pain in other locations of your body?

•   S: Severity: What is your average and worst pain on a 0–10 scale? During menses and when not bleeding?

•   T: Timing: Related to menses, ovulation? Is it constant or intermittent, with or without flares? For pain with intercourse, is it with entry or deep penetration or lingers after sex?

Associated symptoms

•   Urinary frequency, urgency, hematuria, nocturia?

•   Bloating, constipation, diarrhea, hematochezia?

•   Menstrual bleeding (are menses heavy, irregular, intermenstrual bleeding, postcoital bleeding?)

Prior Treatments

•   What medications, injections, interventions have you tried, including physical therapy, acupuncture, over-the-counter medications?

•   What surgeries did you have? What was found? If there was endometriosis, was it superficial or deep, and did your surgeon describe “stage” of endometriosis? Where was it located? Was it removed or were any lesions not treated?

•   Which treatments are you still using? Which treatments helped and for how long? Did you experience any side effects?

Patient perception and experience: “FIFE”

•   F: Feelings: explore depression, anxiety, pain catastrophizing (eg, do you worry that this pain will never go away?)

•   I: Ideas: What do you think might be causing this pain?

•   F: Function: Are there things that you used to do that you can't anymore?

•   E: Expectations: If we cannot fully take the pain away, what would meaningful progress or improvement look like for you?

Table 1.

Examples of Clinician and Patient Resources^*

It is important to remember that patients with CPP remain at risk for acute illness and new pathology such as appendicitis, pelvic inflammatory disease, and ovarian torsion. Thus, new or worsening symptoms should not be misattributed to their underlying chronic pain. Clinicians should partner with their patient's primary care physician and facilitate immediate investigation of red-flag symptoms, including hematuria, hematochezia, unexplained weight loss, early satiety, vomiting, or fever.

Physical Examination

A trauma-informed approach to the pelvic examination is recommended by multiple professional societies.^20,34,95 Patients should be empowered to pause or stop the examination at any time, emphasizing patient autonomy and comfort. Figure 3 summarizes a systematic approach to the physical examination, which progresses from observation of the patient in the standing and sitting positions to examination of the back and abdomen and finally a vulvar and pelvic examination. The back examination should include palpation of the sacroiliac joints and paraspinal muscles. The abdominal examination should include careful assessment of prior surgical scars and identification of abdominal mass(es), including those within prior surgical scars (eg, abdominal wall endometriosis, incisional hernia). Light and deep palpation should be performed in all four quadrants, the suprapubic and umbilical regions, and the pubic symphysis to identify pattern of pain (diffuse vs focal tenderness) and trigger points. The Carnett test helps differentiate abdominal pain caused by abdominal wall myofascial pain from an underlying visceral cause (Fig. 3). Pain that worsens or does not improve on flexion (positive test) suggests a musculoskeletal cause, whereas pain that improves with flexion (negative test) suggests a visceral pain source.

Fig. 3. Overview of physical examination of patients with chronic pelvic pain. *The Carnett test is performed by palpating the painful abdominal area with a single digit and asking the patient to contract abdominal muscles by lifting head and shoulders. A positive test suggests myofascial origin and is defined as pain that worsens or does not improve on flexion. A negative test suggests a visceral source of pain and occurs when pain improves with flexion. SI, sacroiliac. Data from Lamvu et al.³.

As-Sanie. Evaluation and Treatment of Chronic Pelvic Pain. Obstet Gynecol 2026.

For patients with vulvovaginal pain and dyspareunia, evaluation for provoked pain of the vulvar vestibule and perineum should be performed (see the Vulvar section for discussion of the cotton swab test). Single-digit palpation of the superficial and deep pelvic floor muscles assesses for resting tone, muscle bands and spasm, and tenderness. Pelvic floor myofascial pain is diagnosed when painful or contracted muscles are identified. Palpation of the posterior cul-de-sac assesses for nodularity, tenderness, tethering, and reduced mobility of pelvic structures; when present, these findings suggest deep endometriosis. Bimanual examination can identify large adnexal masses, leiomyomas, and uterine and cervical tenderness. Throughout the examination, tenderness to palpation should be correlated with the patient's pain symptoms to identify the anatomic sources contributing to their symptoms.

Imaging and Diagnostic Evaluation

The role of imaging is to identify structural causes and to rule out malignancy. Multiple professional society guidelines recommend transvaginal pelvic ultrasonography as the initial diagnostic test.^2,20,38,41 Magnetic resonance imaging is not cost effective in the initial evaluation of CPP⁹⁶ but may be considered to evaluate specific findings identified by history, examination, or ultrasonography such as concerns for deep endometriosis, extrapelvic endometriosis, or adnexal masses when ultrasonography is inconclusive.^43,97,98 Accuracy of all imaging modalities is influenced by imaging protocol and radiologist training in specific pelvic pathology (eg, deep endometriosis).⁴³ Thus, clear communication of the clinical indication and appropriate protocol selection are essential to optimize diagnostic yield.

Laboratory testing should be reserved for targeted symptom evaluation such as urinalysis for dysuria or hematuria. Evaluation with computed tomography, colonoscopy, and cystoscopy should be reserved for patients with concerning symptoms or imaging findings such as gastrointestinal or urinary tract bleeding or pelvic masses, with referral to a specialist with content expertise.¹

TREATMENT

CPP is best managed through an integrated approach that combines pharmacologic and nonpharmacologic treatments, with patients engaged as active participants in their care. The optimal sequence and combination of treatments remain unknown, resulting in a trial-and-error process. We recommend a holistic, personalized, interdisciplinary approach aimed at reducing pain and restoring function and quality of life, with a focus on treating all contributing conditions through patient-centered care and collaboration across specialties. The following section reviews treatment options commonly managed by gynecologists, although we emphasize the importance of coordinating care with the primary care physician and appropriate specialists for gastrointestinal, urologic, musculoskeletal, and neurologic conditions when indicated. Shared decision making involves evaluating treatment options collaboratively, integrating patient preferences and values, and managing treatment-related adverse effects, all of which may change over time. Shared decision making, clinician empathy, and clear communication—including explanation of treatment options and expectations, including that complete resolution of pain is not always achievable—are associated with better outcomes, treatment satisfaction, and health care utilization.^93,99,100

Pain Education

An essential first step in helping patients navigate CPP is educating patients about the pathophysiology of chronic pain, including the difference between acute and chronic pain and the interaction between organ-based pathology with central nervous system mechanisms that amplify and maintain pain.¹⁰¹ This includes reframing treatment as a multimodal process rather than a singular cure. Most patients with CPP have more than one contributing condition and will require more than one treatment modality.^1,20 Setting expectations that these conditions are chronic, are often overlapping, and require ongoing management—along with clear education on the underlying mechanisms and rationale for each treatment strategy—has been shown to improve patient satisfaction, engagement, and adherence.^20,102,103

Analgesics

Nonsteroidal anti-inflammatory drugs such as ibuprofen and naproxen are effective first-line treatments for dysmenorrhea and abnormal uterine bleeding but have not shown consistent efficacy in managing nonmenstrual pelvic pain or endometriosis-associated pelvic pain alone.¹⁰⁴ When used on a scheduled basis during menses, nonsteroidal anti-inflammatory drugs provide meaningful pain relief in approximately 45–53% of patients with dysmenorrhea and can reduce menstrual blood loss by an average of 40 mL per cycle.^105–107 However, chronic, long-term use is associated with risks, including gastritis, gastric ulceration, and renal injury, and should be approached with caution. Because of the lack of demonstrated efficacy and risk of dependency, multiple professional society and expert guidelines advise that opioids are not recommended for long-term management of CPP.^1,2,20

Hormonal Suppression

Hormonal suppression is first-line treatment for patients with estrogen-dependent gynecologic pain contributors (eg, endometriosis, adenomyosis, leiomyomas) and nongynecologic pain condition with symptoms that worsen during menses or ovulation such as cyclic flares of irritable bowel syndrome or interstitial cystitis/bladder pain syndromesymptoms.¹⁰⁸ First-line options include combined hormonal contraceptives (CHCs) or progestin-only methods because of their efficacy, tolerability, low cost, and favorable safety profile; gonadotropin-releasing hormone agonists and antagonists are considered second-line options.^20,38 Selection of therapy should be guided by shared decision making, incorporating patient preferences, side-effect profiles, and reproductive goals. There are a limited number of prospective comparative-effectiveness studies of hormonal suppression for the treatment of CPP, and most studies are in patients with endometriosis. However, evidence from three meta-analyses in patients with endometriosis suggests that all options are associated with improvement in dysmenorrhea, nonmenstrual pelvic pain, and dyspareunia, with clinically similar efficacy among the hormonal agents.^37,109,110 Systemic suppression with norethindrone acetate (with or without letrozole), dienogest, relugolix, and leuprolide—but not CHCs—also significantly reduces endometrioma size.¹¹¹ Continuous suppression to achieve amenorrhea is preferred given greater improvement in both dysmenorrhea and nonmenstrual pelvic pain.¹¹² It is important to note that hormonal therapies are not curative. In a systematic review of 58 studies, 11–19% of patients reported no pain relief and 5–59% had persistent symptoms despite treatment, with 25–34% experiencing recurrence within 1 year of discontinuation.¹¹³

Postoperative hormonal suppression after excision of endometriosis is associated with lower pain scores and reduced recurrence at 18 months.¹¹⁴ A 2024 randomized controlled trial reported a 40% reduction in pain at 3 years after conservative surgery with either postoperative long-acting progestins or CHC, with patients receiving long-acting progestins 33% less likely to undergo additional surgical procedures or second-line treatments compared with those who received CHCs.¹¹⁵

Selection between CHCs and progestin-only methods should be guided by shared decision making, particularly given evidence from a 2025 systematic review demonstrating comparable efficacy of both options for managing endometriosis-associated pelvic pain.¹¹⁰ However, given interindividual variability in efficacy and adverse effects, trials of multiple hormonal suppression strategies, switching within and across classes, are often necessary to identify the optimal regimen.¹¹⁶ Among progestin-only methods, norethindrone acetate (5–15 mg daily) and medroxyprogesterone (10–30 mg orally daily or 150 mg intramuscularly every 3 months) have demonstrated efficacy for endometriosis-associated pain,¹⁵ whereas norethindrone 0.35 mg daily does not reliably induce ovulation suppression or amenorrhea and is not recommended for CPP management. Progestin intrauterine devices have demonstrated efficacy in treating dysmenorrhea and CPP in patients with endometriosis¹¹⁷ but do not reliably suppress ovulation; therefore, they are not advised as monotherapy in patients with ovarian endometriomas or ovulation-related symptoms. In these cases, adding systemic hormonal suppression may be appropriate.

Gonadotropin-releasing hormone agonists and antagonists are appropriate second-line agents. These gonadotropin-releasing hormone modulators inhibit pituitary secretion of follicle-stimulating hormone and luteinizing hormone, leading to a profound hypoestrogenic state. Use of “add-back” therapy with combined estrogen-progestin or norethindrone acetate can reduce vasomotor symptoms and minimize bone mineral density loss without reduced efficacy in treating pelvic pain.¹¹⁸ It is important to note that none of these medications are approved by the U.S. Food and Drug Administration for use beyond 2 years in the United States because the safety and efficacy of extended therapy have not been evaluated beyond this duration. This limitation should be discussed with patients during shared decision making.

Pelvic Floor Physical Therapy

Pelvic floor physical therapy is a first-line treatment for patients with high-tone pelvic floor dysfunction, vulvodynia, and interstitial cystitis/bladder pain syndrome and also been shown to improve pain in patients with endometriosis and primary dysmenorrhea. Although most studies are small and outcomes vary by condition, pelvic floor physical therapy has been associated with 38–70% reduction in noncyclic pelvic pain and 10–58% improvement in sexual function, with approximately 60–80% of patients reporting meaningful pain relief after a full course of therapy.^71,119–127 Interventions include abdominal wall and pelvic floor muscle relaxation and stretching, connective tissue mobilization, trigger-point release, and targeted strengthening exercises. Patients should be counseled that pelvic floor physical therapy typically involves transvaginal assessment and manual myofascial release. It may be beneficial to counsel patients that they may experience a short-term increase in discomfort with pelvic floor physical therapy and discuss strategies to manage symptom flares. Patients should also be counseled that completing an entire course of therapy, typically lasting at least 8–12 weeks, and participation in their prescribed individual home exercise program are associated in greater degree and duration of symptom improvement.¹¹⁹ Additional barriers that may contribute to participation in pelvic floor physical therapy include out-of-pocket cost, scheduling constraints, and travel logistics.^128,129 Setting appropriate expectations may help support adherence to a full course of therapy.

Muscle Relaxants

Muscle relaxants may be useful for managing myofascial pain or acute pain exacerbations. Most agents, including cyclobenzaprine, methocarbamol, metaxalone, and orphenadrine, exert their effects through the central nervous system.¹³⁰ Tizanidine acts primarily at the spinal cord level, and baclofen targets skeletal muscle. Although muscle relaxants have not been specifically studied in CPP conditions, they may be considered in patients with myofascial pain such as high-tone pelvic floor dysfunction on the basis of extrapolated benefit from nonpelvic myofascial pain syndromes. These medications are typically administered orally; however, compounded vaginal suppository formulations have been described in pelvic pain populations despite their lack of evaluation in rigorous clinical trials. Existing studies on muscle relaxants address primarily short-term use (less than 6 weeks), with limited data on long-term efficacy and safety. However, two recent studies evaluated daily use of sublingual cyclobenzaprine in patients with fibromyalgia for 14 weeks and demonstrated significant sustained improvements in pain (46% of patients reporting meaningful reduction in daily pain), as well as sleep and fatigue, with low risk of serious adverse events.^131,132

Vaginal diazepam is an off-label option thought to target central and spinal mechanisms. Diazepam is a benzodiazepine and thus has muscle relaxant properties mediated through action on GABA receptors. Despite theoretical local effect when placed vaginally, systemic absorption exceeds 70% and has prolonged half-life as a result of bypassing first-pass metabolism.¹³³ Placebo-controlled trials have not shown clear benefit,^134,135 and risks include dependence and drug interactions. Given limited safety and efficacy data, use should be approached with extreme caution, and it should not be used concurrently with opioids, alcohol, or other medications that cause sedation.

Injections

Trigger-point injections with local anesthetics (eg, lidocaine, bupivacaine) can be used to treat abdominal wall or pelvic floor trigger points. Although the mechanism of action is not fully understood, the therapeutic benefit often exceeds the expected duration of the anesthetic. These injections may be a useful adjunct to pelvic floor physical therapy, particularly in patients with severe and focal pain on palpation of a muscle group, because they can reduce pain intensity by approximately 55% and facilitate greater participation in therapy.^136–138 The addition of corticosteroids to local anesthetics for myofascial trigger-point injections is not recommended by multiple professional societies.¹³⁹ Comparative studies have not shown superior efficacy compared with anesthetic alone, and repeated steroid injections carry risks of local soft-tissue atrophy and hyperpigmentation.¹³⁹

Nerve blocks with local anesthetic may be useful for both diagnosis and treatment of patients with neuropathic pain conditions such as pudendal neuralgia or cutaneous nerve entrapment, although data are limited. Nerve blocks performed under ultrasonography or computed tomography guidance or based on anatomic landmarks demonstrate similar efficacy in several studies.^140,141 Magnetic resonance neurography may provide more accurate image-guided treatment, but comparative studies are lacking, and these interventions should be performed by physicians with content expertise.⁸² Data evaluating efficacy of pudendal nerve blocks are low quality, drawn primarily from observational studies with short-term follow up.¹⁴² Between 60% and 80% of patients report short-term improvement after pudendal nerve block, with 26–50% of patients reporting sustained improvement at 3 months.^140,143,144 Regarding entrapment of the ilioinguinal, iliohypogastric, or genitofemoral nerves, evidence is similarly limited; however, small observational studies suggest that 46–79% of patients report significant pain relief after diagnostic or therapeutic nerve block.^141,145,146 The addition of corticosteroids does not appear to improve the efficacy of pudendal nerve block compared with local anesthetic alone¹⁴⁴ but may offer added benefit in image-guided nerve injections for postherniorrhaphy pain.¹³⁹

Botulinum toxin injections into the pelvic floor muscles may be considered in some patients with high-tone pelvic floor dysfunction. Although individual studies show mixed efficacy and modest benefit over placebo or anesthetic, a recent meta-analysis reported an approximately 25-point reduction (0–100 visual analog scale) in both pelvic pain and dyspareunia 12 weeks after injection.¹⁴⁷ Patients who experience benefit from a single injection of botulinum toxin can be reassured that, if symptoms recur, repeat injections are expected to provide comparable efficacy.¹⁴⁸ Dose of botulinum toxin has varied widely across studies, ranging from 40 to 300 units. Stratified meta-analysis indicated that botulinum toxin doses exceeding 100 units were more likely to result in statistically significant improvement in pain.¹⁴⁷ Given the potential benefit and low risk of adverse events, botulinum toxin may be appropriate as an option in patients with persistent symptoms despite pelvic floor physical therapy, muscle relaxants, or trigger-point injections.¹¹⁹

Topical Medications

Topical lidocaine 5% ointment applied to the vulva, labia, or posterior fourchette can decrease provoked or spontaneous pain in patients with vulvodynia.^149,150 In a randomized clinical trial, both topical overnight lidocaine and multimodal pelvic floor physical therapy were associated with significant reductions in pain and improvement in sexual function, with 39% and 78% of patients receiving topical lidocaine compared with pelvic floor physical therapy reporting being very much or much improved, respectively (P<.001).¹²⁴ Compounded topical preparations containing neuropathic agents (eg, amitriptyline, gabapentin) or muscle relaxants (eg, baclofen) are also used in clinical practice with anecdotal success but lack high-quality comparative evidence.

Neuromodulator Medications

Neuromodulators, including gabapentinoids, tricyclic antidepressants, and serotonin–norepinephrine reuptake inhibitors, have demonstrated efficacy in improving pain, sleep, and mood in patients with fibromyalgia, irritable bowel syndrome, or interstitial cystitis/bladder pain syndrome and can be considered in any patient with clinical symptoms that suggest nociplastic pain such as widespread pain, fatigue, pain hypersensitivity (hyperalgesia and allodynia), and limited response to peripherally targeted treatments.^151,152 However, only a few studies have evaluated these medications in gynecologic CPP, with mixed results. Their use is supported primarily by extrapolated benefit from other chronic overlapping pain conditions. Two double-blind, randomized, placebo-controlled trials, one in patients with CPP without pelvic pathology and another in those with vulvodynia, did not demonstrate superiority of gabapentin over placebo and reported higher rates of adverse effects, including sedation and dizziness.^153,154 Although data in gynecologic CPP are limited and mixed, neuromodulators may still be considered, particularly in patients with comorbid conditions such as interstitial cystitis/bladder pain syndrome or irritable bowel syndrome or those with features of nociplastic or neuropathic pain given the demonstrated benefit in other chronic overlapping pain conditions. Medication selection should be individualized and based on prior treatment exposure, coexisting symptoms, and patient preference. For example, serotonin–norepinephrine reuptake inhibitors may be preferred in patients with concurrent mood disorders, medications with sedating effects may benefit patients with sleep dysfunction, and cyclobenzaprine is preferred for those with myofascial pain. Medications should be initiated at low doses and titrated gradually on the basis of symptom response and tolerability. It is important to note that a lack of response to one medication does not preclude benefit from others within and across classes because each acts through different central mechanisms.

Nonpharmacologic Strategies

Nonpharmacologic therapies, including psychological and behavioral treatments, are among first-line treatments for chronic pain.^13,14 Although they are supported by high-quality evidence in other chronic overlapping pain conditions, most studies for CPP conditions are small and low quality.¹⁰² Guided therapy approaches, including cognitive behavioral therapy, acceptance and commitment therapy, and sex therapy, are associated with 24% reduction in pelvic pain, 29–62% reduction in dyspareunia, 11–38% improvement in sexual function, and 30% reduction in sexual distress.^{125,155–158} Exercise interventions, particularly yoga, have shown clinically significant improvements in pain intensity, mental health, and quality of life in patients with CPP conditions, including dysmenorrhea,^159–161 endometriosis,¹⁶² and interstitial cystitis/bladder pain syndrome.¹⁶³ Additional nonpharmacologic strategies that have been studied include acupuncture,¹⁶⁴ acupressure,¹⁶⁵ and dietary modification such as a “low inflammatory diet.”¹⁶⁶ Although evidence for these adjunct treatments is limited with variable efficacy across studies, they are low risk and may offer benefit for select patients when incorporated into a multimodal treatment plan.

Neuromodulation

Transcutaneous electrical nerve stimulation has been shown to reduce pain in a variety of chronic overlapping pain conditions, including dysmenorrhea, endometriosis, vulvodynia, and fibromyalgia.^167–170 It has also been shown to reduce fatigue in patients with fibromyalgia¹⁷¹ and to improve sexual function in individuals with vestibulodynia.¹⁷² Sacral neuromodulation has been shown to reduce pain intensity in patients with urogenital pain, and posterior tibial nerve stimulation can offer short-term relief.¹⁷³ Emerging approaches such as dorsal root ganglion and spinal cord stimulation show promise, although data remain limited.¹⁷³

Procedures for Vascular Causes

Patients with symptoms and imaging findings consistent with pelvic congestion syndrome or pelvic venous disorders may benefit from referral to interventional radiology for evaluation of endovascular treatment options. Although randomized controlled trials are currently underway,⁸³ existing evidence is limited to case series and observational studies, which indicate modest short-term benefit.^174,175

Surgery for Pelvic Pain

Surgical interventions for CPP aim to address identifiable anatomic pathology and should be considered when there is strong suspicion for conditions likely to benefit from operative treatment. The strongest evidence supports excision of endometriosis lesions and hysterectomy; other procedures, such as nerve release and vestibulectomy, may be considered in select patients, although high-quality comparative studies are lacking for most of these interventions.

Removal of Endometriosis

Professional society guidelines recommend offering surgery as treatment for endometriosis-associated pain if hormonal treatment is ineffective, has unacceptable side effects, or is contraindicated, including those with ovarian endometriomas with features concerning for malignancy and patients with deep endometriosis causing hematuria, hematochezia, or occlusion of the intestinal or urinary tract.^35–38 Surgical efficacy in improving pain varies by endometriosis subtype. Evidence supporting removal of superficial peritoneal lesions for pain relief is limited.¹⁷⁶ However, cystectomy for ovarian endometriomas is more effective than drainage or ablation in reducing dysmenorrhea, dyspareunia, recurrence of endometrioma, and the risk of repeat surgical intervention 2 years after surgery.¹⁷⁷ Similarly, excision of deep rectovaginal endometriosis is associated with reduction in dysmenorrhea, noncyclic pelvic pain, and dyspareunia 2 years after surgery.¹⁷⁸ However, surgery is not curative and has risks. In a systematic review of surgical removal of endometriosis without postoperative hormone treatment (n=2,652, analysis not stratified by endometriosis subtype), 25% of patients experienced persistent pain, 15.8% reported recurrent pain (pain improved and then recurred), and 8.1% experienced a postoperative complication at a median follow-up of 24 months.¹⁷⁹ Repetitive surgery is not routinely indicated or recommended, and there is no role for laparoscopy to diagnose but not treat endometriosis.³⁸ Patients who undergo surgery by high-volume endometriosis surgeons have lower rates of repeat surgery, fewer postoperative complications, and reduced health care utilization for endometriosis or pelvic pain in 9.5 years after surgery.¹⁸⁰ These findings support current recommendations that surgery for endometriosis, particularly deep endometriosis, be performed by experienced surgeons.^36,38 Postoperative hormone suppression is advised in individuals not seeking immediate pregnancy because it is associated with lower pain scores and reduced risk of endometriosis recurrence.¹¹⁴

Other Nonextirpative Surgeries

Vulvar vestibulectomy is the most studied surgical treatment for provoked vestibulodynia and can provide significant pain relief, particularly in patients unresponsive to conservative therapies. In the only randomized controlled trial, vestibulectomy resulted in greater pain reduction on the cotton swab test compared with electromyographic biofeedback or group cognitive behavioral therapy at 6 months; improvements in sexual function and psychologic outcomes were similar across all three groups.¹⁵⁷ At 2.5 years, clinical improvement was sustained for all treatment modalities; however, the severity of self-reported pain during intercourse was comparable, suggesting similar long-term outcomes for this patient-centered goal.¹⁸¹ Additional observational studies support the potential benefit of vestibulectomy, but the overall evidence is limited by small sample sizes, lack of comparison groups, short follow-up, and inconsistent outcome measures.⁶⁷ High-quality studies are needed to refine patient selection and to clarify long-term efficacy.

Surgical decompression of the pudendal nerve may be considered for patients with pain refractory to conservative treatments, with low-quality evidence suggesting moderate short-term benefit.¹⁴² However, long-term outcomes remain unclear. Given the elevated risk of severe complications, the procedure should be performed only by experienced surgeons.

Evidence supporting the efficacy of other conservative surgical interventions for CPP remains limited. For example, systematic reviews have found no benefit of adhesiolysis for management of abdominopelvic pain in the absence of bowel obstruction,^182,183 no benefit of laparoscopic uterosacral nerve ablation, and questionable utility of presacral neurectomy for management of CPP.^183,184

Hysterectomy

Multiple professional society guidelines support hysterectomy as an appropriate option for patients with treatment-resistant pelvic pain, intolerable side effects from medical therapy, and no desire for future fertility.^20,38 Evidence is limited by the lack of randomized trials, short follow-up, and inconsistent outcome measures. However, a 2025 systematic review (seven studies, n=12,247) reported that the incidence of persistent pain after hysterectomy ranged from 12% to 68%, with most studies around 25%, indicating that hysterectomy is not always curative.¹⁸⁵ Younger patients and those with chronic overlapping pain conditions, preoperative depression, or clinical symptoms of nociplastic pain (eg, widespread pain, fatigue) are at higher risk of persistent pain.^16,17,185 The presence of adenomyosis was not associated with reduced risk of persistent pain, and associations with endometriosis were variable.¹⁸⁵ This does not preclude offering surgical treatment for these individuals but underscores the importance of shared decision making to clarify goals, set realistic expectations, and discuss the potential need for adjunctive therapies after surgery, highlighting that hysterectomy can cure abnormal uterine bleeding but is not guaranteed to alleviate pelvic pain.

It is important to note that hysterectomy alone does not adequately treat endometriosis unless lesions are excised concurrently. Even with ovarian conservation, hysterectomy is associated with increased risks of cardiovascular, metabolic, and mental health disorders,^186–188 which should be discussed with patients before surgery. Ovarian preservation is recommended whenever possible because there is insufficient evidence that bilateral oophorectomy reduces subsequent treatment for CPP, even among patients with endometriosis.^185,189

CONCLUSION

Chronic pelvic pain is a common, multifactorial condition that requires a patient-centered, interdisciplinary approach. Like other chronic pain disorders, CPP is not always curable and often necessitates long-term support. Optimal management prioritizes multimodal treatment plans, which may include hormonal suppression, physical therapy, neuromodulators, behavioral therapies, and surgery, tailored to individual pain mechanisms and patient preferences. Establishing a strong therapeutic relationship, validating the pain experience, and empowering patients to engage actively in their care are critical. Shared decision making, collaborative goal setting, and having clear discussions about expectations support sustained engagement and functional improvement. Timely identification of patients appropriate for gynecologic management or specialist referral helps optimize outcomes while avoiding unnecessary delays and low-value care.

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