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Pelvic and Bladder Pain

This document was released in February 2023. This document will continue to be periodically updated to reflect the growing body of literature related to this topic.


KEYWORDS: Genitourinary Syndrome of Menopause, vulvodynia/vestibulodynia, clitorodynia/clitoral adhesions/clitoral phimosis, pelvic floor dysfunction, interstitial cystitis/bladder pain syndrome, and prostatitis.

At the end of this unit, the medical student will be able to:

  1. Understand the potential etiologies of pelvic and bladder pain and the various underlying causes including Genitourinary Syndrome of Menopause, vulvodynia/vestibulodynia, clitorodynia/clitoral adhesions/clitoral phimosis, pelvic floor dysfunction, interstitial cystitis/bladder pain syndrome, and prostatitis.
  2. Evaluate, diagnose, and differentiate between the different causes of pelvic and bladder pain.
  3. Outline treatments for causes of pelvic and bladder pain.

1. Overall Introduction

Pelvic and bladder pain can originate from a variety of conditions. These include Genitourinary Syndrome of Menopause, vulvodynia/vestibulodynia, clitorodynia/clitoral adhesions/clitoral phimosis, pelvic floor dysfunction, interstitial cystitis/bladder pain syndrome, prostatitis, and others. These conditions are discussed in detail in the following sections and are described in terms of etiology and epidemiology, diagnosis, and treatment options.

2.Genitourinary Syndrome of Menopause (GSM)

2.1 Etiology

Menopause results in the decrease of estrogens and androgens, which in turn contributes to atrophy of the vaginal and vulvar tissues and ultimately, various genital and urinary symptoms. These symptoms are collectively known as Genitourinary Syndrome of Menopause (GSM) and typically worsen over time without treatment.1-4 Besides menopause, GSM can also be caused by states of decreased estrogens and androgens including consumption of oral contraceptives and thyroid or pituitary disorders.

2.2 Diagnosis

Physical exam may reveal atrophy of the labia majora and/or minora as well as pubic hair thinning. Speculum exam may demonstrate narrowed vaginal introitus and pale vaginal epithelium lacking rugae.5

While the normal vaginal pH is 3.5-5.0, vaginal pH testing in women with GSM may be 5.5 or higher.5


2.3 Treatment6


Vaginal moisturizers

- Maintain vaginal integrity and elasticity if regularly used

Vaginal lubricants

- As needed, usually for sexual activity to relieve vaginal dryness and dyspareunia

- Three kinds: water, silicone, and oil-based

- Water-based lubricant needs repeated use due to evaporation

- Silicone-based lubricant is less likely to dry out but is more difficult to clean and may have an unpleasant taste and odor

- Oil-based lubricant should not be used with latex condoms due to possible condom breakage

Topical local vaginal estrogen

- Increases hormone levels locally without much systemic absorption6-7

- Improves vaginal symptoms such as dryness and dyspareunia in 2-3 weeks as well as recurrent UTIs

- Usage should be discussed for patients with active breast or endometrial cancer or on hormone depletion therapy

Vaginal DHEA suppositories

- Enzymes in vulva, vestibule, and vagina convert suppositories into estrogens and androgens, while endometrial tissue in uterus is not affected

-Treats dyspareunia


Selective estrogen receptor modulator (SERM) (ie ospemifene)

- Treats dyspareunia due to vulvovaginal atrophy

- Helpful for patients who prefer oral over vaginal treatments

- Contraindications: estrogen-dependent cancers, active or prior venous thromboembolism, previous stroke, and prior myocardial infarction or active heart disease

- Commonly reported adverse effects: hot flashes, vaginal discharge, muscle spasm

Systemic estrogen therapy

- Treats vasomotor symptoms, but patients may also require local estrogen treatments8

Non-Medication Treatments

Vaginal dilators

- May reduce pain with vaginal penetration through increased vaginal elasticity and decreased pain

- Can be self-taught or taught by pelvic floor physical therapist

CO2, Erbium laser, and radiofrequency devices

- Proposed to increase vascularization and connective tissue in vaginal canal to treat vaginal atrophy, dyspareunia, and vaginal laxity

- Actual efficacy of these treatments is unclear9-11

3. Vulvodynia/Vestibulodynia

3.1 Etiology and Epidemiology

Provoked vestibulodynia (PVD) is a condition in which patients experience superficial sexual pain of the vestibule, possibly caused by either an increased number of nerve endings in the vestibular mucosa, hormonal changes such as endometriosis treatment, hormonal birth control, infertility medications, menopause, or hypertonic pelvic floor dysfunction (PFD), and potentially others.13 PFD is caused by hypertonicity of the striated muscles surrounding the vagina, bladder, and anus, resulting in symptoms such as constipation, rectal fissures, urinary frequency, urgency, hesitancy, incomplete bladder emptying, or generalized vulvar vestibular pain. It occurs in approximately 8.3% of women.14


3.2 Treatment

Treatment depends on the underlying cause. Pain is often multifactorial, so a multidisciplinary approach may be required.


Sex therapy and/or cognitive behavior therapy (CBT)

- May be used in patients with significant anxiety or other psychological issues related to vulvodynia/vestibulodynia

Biomedical treatment modalities

- Include physical therapy, biofeedback, manual and electrical stimulation, internal massage, topical anesthetics, botulinum toxin injections, pudendal nerve blocks, and pudendal neuromodulation14

Discontinuation of hormonal contraceptives

- For patients using hormonal contraceptives, alternative options include non-hormonal contraception, local compounded testosterone 0.1%, or estradiol 0.01% in a methyl cellulose base 

Treatment of Vulvar Pathology

- Ultra-potent topical steroid clobetasol 0.05% ointment for vulvar dermatological conditions including lichen sclerosis16

- Consider vulvar or vaginal biopsy for diagnosis of underlying condition

Surgical intervention

- Indicated for refractory cases

- For severe PVD, may consider vulvar vestibulectomy16


4. Clitorodynia/Clitoral Adhesions/Clitoral Phimosis

4.1 Etiology and Epidemiology

Clitoral phimosis occurs in 22-33% of women, resulting in clitorodynia, muted orgasm, aversion to touch, or anorgasmia.17 Risk factors for clitoral phimosis include history of sexual pain, yeast infection, lichen sclerosis, low testosterone, blunt perineal/genital trauma, urinary tract infection, and other sexual dysfunctions such as persistent genital arousal disorder.

4.2 Diagnosis

Physical exam demonstrates clitoral prepuce attached to the glans and should include investigation of pain or hyposensitivity. If seen, thick white lichenoid changes may be biopsied.

4.3 Treatment

Treatment includes aggressive management of lichen sclerosis with topical steroid clobetasol 0.05% ointment and traction to reduce phimosis. Surgical treatment includes local anesthetic followed by lysis of adhesion or surgical dorsal slit procedure.

5. Pelvic Floor Dysfunction (PFD)

5.1 Etiology and Epidemiology

Pelvic floor dysfunction is caused by overactive, non-relaxing pelvic floor muscles, leading to dyspareunia, pelvic pain/pressure, voiding dysfunction, incomplete bladder emptying, sensory urgency, urinary incontinence, constipation, and dyschezia.19 It occurs in 14-78% of women who present with chronic pelvic pain20 and often occurs with dyspareunia as well.21,22 An initial injury usually precipitates a cycle of muscle pain and tension, potentially resulting in tissue inflammation and nerve damage. Common precipitating injuries include infection, muscle overload (ie competitive athletes or bladder/bowel dysfunction), local trauma/injury (ie vaginal deliveries or pelvic floor surgery), nervous system disorders (ie hyperalgesia), and comorbid pain disorders (ie vulvodynia, irritable bowel syndrome, temporomandibular joint dysfunction, fibromyalgia).

5.2 Diagnosis

5.2.1 History

Pain due to PFD is often described as episodic with an aching, throbbing, heavy, or pressured sensation and aggravated by stress. Patient’s chief complaint often includes dyspareunia, changes in urinary urgency, frequency, and dysuria, suprapubic/abdominal pain, changes in bowel function (ie dyschezia, constipation, incomplete stool evacuation, bloating, splinting posterior vagina, anal digitation, and hematochezia), and worsening pain with extended sitting.23 Past medical history may include urinary hesitancy that temporarily improves with urethral dilation, but cystoscopy is negative for urethral stricture, recurrent UTIs, especially in times of stress, with negative cultures, hip issues, and history of competitive athletics. Onset of symptoms can be precipitated by vaginal delivery (especially with laceration or episiotomy), pelvic surgery, or history of emotional, physical, or sexual abuse.

External physical exam may reveal lumbar lordosis, avoidance of sitting or sitting leaning to one side, pain on palpation of sacroiliac joint, and positive Fitzgerald’s test (pain with hip manipulation). Internal physical exam may reveal scars or incisions and one or more of the following indicating trigger points of pelvic floor muscles: palpable taut band, tender nodule in taut band, reproducible pain on palpation of tender nodule, or painful limit to stretch or full range of motion.20

5.3 Treatment

Treatment should be multidisciplinary with a focus on pelvic floor physical therapy and education.

Pelvic floor physical therapy

- Includes manual massage techniques, myofascial release, strain and counterstrain, joint mobilization, and trigger point massage for pain relief

- Thiele massage relaxes spastic pelvic floor muscles via application of digital pressure

- Effective in 59-80% of patients when appropriate physical therapy techniques are utilized

Trigger point/levator injections

- Local injections target tender myofascial trigger points and spastic pelvic floor

- Usually combination of local anesthetic (ie bupivacaine) and steroid (ie triamcinolone)

- Bupivacaine has longer myotoxicity risk and longer half-life

- Triamcinolone and other steroids target myalgia

- OnabotulinumtoxinA can be injected into spastic pelvic floor musculature to paralyze muscle (off-label use)24


- Intravaginal diazepam suppositories relax pelvic floor

- Relatively safe but prolonged half-life may result in accumulation of daily doses so may be more appropriate when administered as needed for physical therapy or intercourse25,26

- Other vaginal medications include ketamine and baclofen


- Off-label use for chronic refractory pelvic pain

- Thought to alleviate pelvic floor spasm by stimulating afferent nerve roots27

Other Conservative Treatments

- Includes cognitive behavioral therapy, relaxation and mindfulness therapy, and Transcutaneous Electrical Nerve Stimulation (TENS) units28


6. Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS)

6.1 Etiology and Epidemiology29

IC/BPS is a syndrome characterized by patient-reported lower urinary tract symptoms in the absence of other causes of bladder pain. Patients report an unpleasant sensation such as pressure, discomfort, or pain perceived to be related to the urinary bladder and associated with lower urinary tract symptoms for longer than 6 weeks without infection or other causes.30 The exact etiology of IC/BPS is unclear with possible mechanisms including defective urothelial permeability, inflammatory/infectious events, and changes of the hypothalamic pituitary adrenal axis and stress response. Some IC/BPS patients present with systemic symptoms including anxiety, depression, and chronic pain syndromes including migraines, fibromyalgia, and irritable bowel syndrome.31,32

IC/BPS occurs in about 2.7-6.5% of adult women and 1.9-4.2% of adult men in the U.S.1,33 and can occur concomitantly with pelvic floor dysfunction, levator ani pain, and hypertonic pelvic floor dysfunction.4,5

6.2 Diagnosis

Key symptoms include bladder or pelvic pain (ie pressure and discomfort) along with lower urinary tract symptoms (ie urgency, frequency, and/or nocturia). Unlike overactive bladder, IC/BPS patients will report pain worsening with bladder filling and voiding frequently to avoid or relieve their pain (as opposed to incontinence).

Basic assessment includes a comprehensive patient history, a bladder diary, symptom questionnaire, including a pain evaluation. The physical examination is imperative to rule out other source for the patient’s symptoms. Importantly, a urinalysis and culture must be obtained to rule out microhematuria or urinary tract infection. A post void residual is additionally an important basic assessment tool. If a patient is found to have evidence of a urinary tract infection, the bacteria should be treated and follow up assessment should be performed to ensure resolution of the patient’s symptoms after treatment.

In patients with complicated IC/BPS, imaging, cystoscopy, urodynamics, and specialist referral should be considered. In patients with a smoking history or a history of hematuria, a complete hematuria evaluation should be considered.34

As IC/BPS is a clinical diagnosis, there are no definitive tests that can rule out IC/BPS. However, cystoscopy can identify a subset of IC/BPS patients with Hunner lesions within the bladder, especially in men and women older than 50.8,15,35,36 Hunner lesions are circumscribed, reddened mucosal areas with small vessels extending towards a central scar and can rupture due to bladder extension, resulting in oozing of blood. Biopsy will show acute and chronic inflammation. This distinct subtype of IC/BPS usually responds favorably to treatment (fulguration and/or triamcinolone injection).30 In this patient population with persistent or refractory symptoms, oral cyclosporin A may be offered.

Clinically, relief from intravesical local anesthetics can indicate that the bladder contributes to a patient’s pelvic pain, which can help confirm the diagnosis of IC/BPS.

6.3 Treatment37

In patients with uncomplicated IC/BPS, imaging, cystoscopy and other testing are not required prior to initiation of treatment and may begin behavioral/nonpharmacologic treatments as well as oral or intravesical therapies.

IC/BPS is a chronic condition, so treatment is not usually curative but rather therapeutic and administered over an extended period of time. It is often multidisciplinary with any of the following components:

Behavioral/Nonpharmacologic Treatments

- Includes self-care practices/behavioral therapy, patient education (on normal bladder function and IC/BPS), physical therapy, imagery therapy8, stress management/coping strategies

- Behaviors that can worsen symptoms include specific foods or fluids irritating the bladder, certain exercises, tight-fitting clothes, sexual intercourse, and constipation

- Acupuncture/yoga, medication, non-pharmacological analgesia such as heat or cold over tender areas, and over-the-counter products like phenazopyridine34

Pain Management

- Includes non-steroidal anti-inflammatories, acetaminophen, urinary analgesics, and centrally-acting agents used for other chronic pain conditions (ie pregabalin and gabapentin)

- Opioids use is controversial

Oral Medications

- Includes tricyclic antidepressants (ie nortriptyline and amitriptyline), antihistamines (ie cimetidine and hydroxyzine), pentosan polysulfate, and cyclosporin A

- Systemic long-term glucocorticoids and long-term antibiotics should be avoided

- Amitriptyline works by blocking H1 receptor sand stabilizing mast cells; other tricyclic antidepressants block serotonin and norepinephrine re-uptake, although they are sedating

- Pentosan polysulfate is a heparin-like molecule that augments glycosaminoglycan layer of bladder urothelium and is the only oral medication FDA-approved for IC/BPS; adverse effects include increased liver enzymes, reversible hair loss, and potentially irreversible pigmentary maculopathy

- Cyclosporine A stymies activity and growth of T-cells and may work better for patients with Hunner lesions14,35,36

Intravesical Instillations

- Includes dimethyl sulfamethoxazole (DMSO), heparin, lidocaine, bupivacaine, and other local anesthetics for 6 weeks

- Bacillus Calmette Guerin (BCG) or resiniferatoxin are not recommended


- Cystoscopy under anesthesia possibly combined with short-duration, low-pressure hydrodistention

- Fulguration and/or injection of triamcinolone for Hunner lesions as well as possibly biopsy to rule out carcinoma in situ

Procedures for Refractory Condition

- Includes neuromodulation with intradetrusor injections of onabotulinum toxin A or neuromodulation with sacral nerve stimulation although evidence for efficacy is sparse23-25

Surgery (urinary diversion with or without cystectomy)

- Last resort due to long-term complications

- Seeks to increase functional capacity of bladder by diverting urinary stream

- Best for patients with end-stage, ulcerative IC/BPS and low bladder capacities (< 300 cc)


7. Prostatitis41

7.1 Etiology and Epidemiology

Prostatitis is characterized by infection of the prostate, usually caused by bacteria. It is the most common urologic condition in men younger than 50 with an estimated prevalence of 5% and the third most common in men older than 50.42-44 It is classified according to the NIH Classification of Prostatitis Syndromes as shown below45:


Category I - Identical to acute bacterial prostatitis

Category II - Identical to chronic bacterial prostatitis

Category III - Chronic Pelvic Pain Syndrome (CPPS) - defined by genitourinary pain without uropathogenic bacteria

Category IIIA (Inflammatory CPPS) - defined by excessive WBC in expressed prostate secretions or post-prostatic massage urine or semen

Category IIIB (Non-Inflammatory CPPS) - defined by no significant WBC

Category IV (Asymptomatic Inflammatory Prostatitis) - defined by significant WBC or bacteria in prostate specimens without symptoms


The etiology of prostatitis is likely multifactorial with possible causes including microbes, altered host defense mechanisms, ductal reflux, pelvic floor muscle abnormalities such as myofascial pelvic pain, intra-prostatic reflux, immunology, and prostate biopsy/urethral instrumentation. Microbes are usually gram-negative bacteria (65-80%) such as Escherichia coli, Pseudomonas aeruginosa, Serratia, Klebsiella, and Enterobacter. Gram-positive bacteria such as Enterococci comprise 5-10% of infections. A rare cause of prostatitis is tuberculosis. Altered host defense mechanisms include intraprostatic ductal reflux of urine into the prostate, phimosis, unprotected anal intercourse, indwelling catheters, and transurethral surgery. Alterations in prostate secretions may mitigate the normal anti-bacterial prostatic secretions. Dysfunctional voiding includes dyssynergic, high pressure voiding, which may lead to autonomic overstimulation of the perineal-pelvic neural system with chronic neuropathic pain as well as intraprostatic ductal reflux. Chronic muscular guarding of the pelvic floor may cause pelvic floor hypertonicity and subsequent pain. Intra-prostatic reflux causes retrograde invasion of urine and bacteria into the prostate.46 Immunology may play a role in the etiology of prostatitis due to elevated IgG, IgA, PSA, and interleukin-10 in these patients. Lastly, urologic procedures such as biopsy can have complications including prostatitis, so prophylactic antibiotics such as fluoroquinolone or cephalosporin are recommended for biopsy and simple cystourethroscopy.

7.2 Diagnosis

Prostatitis is characterized by pain of the suprapubic region, testicles, penis, and/or urethra as well as difficulty with urination, dysuria, painful ejaculation, and perineal pain. Accompanying symptoms may include fever, nausea, and vomiting. Note that acute prostatitis typically results in pain and infection symptoms, while chronic prostatitis primarily results in pain only. The NIH’s Chronic Prostatitis Symptom Index (NIH-CPSI) evaluates the symptoms and quality of life of patients with chronic prostatitis.47

History can include location of pain, lower urinary tract symptoms, STI history, recent instrumentation, and sexual dysfunction.48 Past medical history may include tuberculosis exposure or BCG therapy for bladder cancer, as these patients can have granulomatous prostatitis, leading to a nodular prostate on physical exam.49,50

Physical exam includes a digital rectal exam, which will typically indicate a tender, boggy, warm prostate in acute prostatitis and a tender prostate in chronic prostatitis. Physical exam of the abdomen, external genitalia, and perineum may reveal myofascial trigger points or musculoskeletal dysfunction of the pelvis and pelvic floor. Unlike acute bacterial prostatitis where aggressive prostate exam could cause sepsis, evaluation of chronic prostatitis requires expression of prostatic fluid. Acute prostatitis also requires urinalysis and urine culture.

The gold standard of diagnosis is the Meares-Stamey “four-glass test”, which examines the urethral bacteria, bladder urine, expressed prostatic secretions during prostatic massage, and any expressed prostatic secretions trapped in the urethra. These four samples are evaluated for leukocytes and culture.

7.3 Treatment



- Most commonly prescribed treatment for prostatitis

- Usually successful in acute bacterial prostatitis unless patient has abscess or anatomic abnormality of urinary tract

- Antibiotics predominantly used are fluoroquinolones


- Thought to block alpha-adrenergic receptors in bladder neck and prostate to relax and improve outflow obstruction, helping improve urine flow and decrease intra-prostatic ductal reflux

- Efficacy is unclear51

Anti-Inflammatory Medications

- Primarily used for chronic prostatitis

- Include non-steroidal anti-inflammatories, corticosteroids, and immunosuppressive drugs51

Hormonal Agents

- 5-alpha-reductase inhibitors may be used but are not first-line treatment

Physical Therapy, Prostate Massage, Phytotherapies, Combinations, and Alternative Medicine

- Physical therapy should be performed by specialists in pelvic floor physical therapy

- Use of these options should be patient-specific


8. Conclusions

There are many potential etiologies for pelvic and bladder pain. It is imperative to evaluate patients with bladder and pelvic pain thoroughly and rule out concerning pathology. A comprehensive history that includes a voiding diary, system questionnaire, and pain evaluation is important. A physical examination is required to rule out pathology or obvious source of pain should be performed. Basic evaluation with a urinalysis and culture as well as a post void residual should be obtained. Any patient with microhematuria should be further evaluated. Importantly, treatment decisions in patients with pelvic and bladder pain should be made after shared decision-making, with the patient informed of the risks, benefits and alternatives with initial treatment depending on severity of symptoms, clinical judgment, and patient preferences. Given that pelvic and bladder pain may be from multiple etiologies, simultaneous treatments and a multidisciplinary approach should be considered employed.


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Marisa Clifton, MD
Baltimore, MD

Isaac Elijah Kim, Jr., ScB
Providence, RI

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