Interstitial Cystitis, feat. Dr. Edward Kim

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Here’s the RoshReview Question of the Week!

A 41-year-old woman presents to your office for dysuria. She states that she has been having persistent urinary urgency and frequency for the past six months. She reports discomfort with bladder filling, pain with urination, and relief after voiding. A review of her history reveals normal fluid intake. A workup for pelvic pain performed by her primary care provider and gastroenterologist was negative. On physical exam, you note suprapubic tenderness. Her urinalysis and culture are negative. Which of the following is the best therapeutic option?

Check out if you answered correctly at the links above!

Today we welcome Dr. Edward Kim to the podcast. He is a urogynecology fellow at the University of Pennsylvania, performing research on a challenging topic: interstitial cystitis. Dr. Kim is looking to recruit more patients into a study on quality of life and patient education in IC — if you have questions or someone to refer, let us know by emailing us or contacting us with the form on the website!

Overview

  • IC: kind of a misnomer!

    • There is no conclusive evidence that there is an inflammation nor distinct pathology in the bladder interstitium.

    • Contemporary thinking: chronic pain condition related to or perceived to be originating from the bladder.

      • Newer terminology has been proposed: bladder pain syndrome.

      • In clinical practice, some patients seem to prefer ‘interstitial cystitis’ because to them is sounds more like a more medical diagnosis and they don’t want to be labeled as having a pain syndrome. So IC/BPS are used interchangeably.

Epidemiology

  • Can affect men and women but more common in women.

    • High prevalence in age 40s.

    • Don’t know the precise prevalence given complexity of syndrome.

Clinical Presentation

  • Variable

  • Persistent urinary urgency, urinary frequency, and pain or discomfort related to voiding.

    • Note that we say pain or discomfort. Some patients describe what they’re feeling as discomfort and not pain.

    • Classic: patient with these symptoms who had been treated multiple times for urinary tract infections despite having negative urine cultures. They also may report going to the bathroom frequently or spending a lot of their day on the toilet to relieve their urgency and discomfort or pain.

      • Many of these patients may also have associated conditions like irritable bowel syndrome, fibromyalgia, and pelvic floor muscle dysfunction.

      • They also may have concurrent psychiatric comorbidities such as depression or anxiety.

Diagnosis

  • American Urological Association: “An unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder, associated with lower urinary tract symptoms of more than six weeks duration, in the absence of infection or other identifiable causes.”

    • In other words, IC is a clinical diagnosis and diagnosis of exclusion.

    • Differential diagnosis should include:

      • Infection

      • Overactive bladder

      • Bladder or urethral cancer, gynecologic cancer

      • Uterine fibroids with compression effect on the bladder

      • Bladder stone

      • Bladder diverticulum

      • Foreign material such as synthetic mesh or suture

      • Neurologic conditions that may cause urinary retention in particular

      • Other chronic pelvic pain conditions such as endometriosis.

    • This is why it’s important to perform a thorough history and physical and obtain a post void residual and urine tests as an initial evaluation to rule out these other etiologies.

  • Hunner lesions can be seen on cystoscopy.

    • They are specific for IC, but they only are seen in about 10% of patients with IC.

  • Potassium sensitivity test KCl is instilled into the bladder.

    • This is not performed anymore due to its low sensitivity and specificity and also it’s very painful!

  • Urodynamics is not typically used to diagnose IC but it can be done to rule out other etiologies.

Treatment

  • Management strategy is multi-faceted.

  • First-line treatments are patient education, behavior and diet modification, and general stress management.

    • There is good evidence behind teaching patients bladder retraining where they learn to increase the interval between each voids.

    • Avoidance of things like artificial sweetener, caffeine, alcohol, spicy food, citrusy or acidic foods can help with symptoms.

      • Doesn’t require elimination, but helps to make informed decisions about diet.

    • Applying heat or ice packs to the suprapubic or perineal regions can also be helpful.

    • Pelvic floor muscle tenderness or dysfunction on exam —> consider pelvic floor PT.

  • Second-line treatments include oral medications and bladder instillation.

    • PRN medication is usually pyridium or over the counter AZO.

      • Warn patients that their urine will turn orange and may stain clothing.

    • Daily medications, the most commonly used ones are: amitriptyline, hydroxyzine and pentosan polysulfate sodium (Elmiron).

      • Note that Elmiron is the only FDA approved medication for IC. However, use of Elmiron has been associated with macular eye disease. Thus, in 2020, the FDA inserted a warning label to reflect this and use of Elmiron has been declining.

      • Between amitriptyline and hydroxyzine, currently there is more data on amitriptyline. Some patients find amitriptyline helpful in controlling their symptoms but some cannot tolerate its sedative and anticholinergic side effects.

    • If there is inadequate response to medications, then bladder instillation can be considered. This involves instilling a mixture of local anesthetic, heparin, DMSO, etc. via a catheter. Usually this involves repeated treatments.

  • Third-line treatment is hydrodistention.

    • Hyper-distention of the bladder under anesthesia for about 10 minutes and emptying the bladder.

      • The thought is that sensory nerves in the bladder are disrupted due to the hyper distention.

      • For patients who see prolonged and significant benefit, repeat treatments are considered.

    • If on cystoscopy Hunner lesions are found, they can be addressed with cautery, resection or injection with steroids.

  • Fourth-line treatments include neuromodulation using Botulinum toxin A injection into the bladder and sacral neuromodulation.

    • These techniques have been used for overactive bladder and neurogenic bladder but recent clinical trials have reported efficacy for interstitial cystits. 

  • Fifth-line treatment is cyclosporine A. Use is limited due to its side effects and paucity of convincing data.

  • Sixth-line and last resort is surgical diversion of the bladder with or without cystectomy.

    • Fortunately, patients seldom have to go past fourth-line treatments. As with any chronic pain condition, it is a difficult journey for many of them and it is critical for providers to listen and empathize with them.

Female Sexual Dysfunction

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What is normal sexual response? 

  • Original landmark studies had a very linear model of “normal sexual response” 

    • Excitement → plateau → orgasm → resolution 

  • More contemporary model is non-linear and encompasses a variety of sequences of the original four stages of as well as other stages 

    • Estrogen plays a significant role in female sexual response, including maintenance of genital tissue sensitivity, elasticity, secretions, pH, etc, as well as urinary continence, pelvic floor muscle tone, and joint mobility 

    • Approximately 43% of American women report experiencing sexual problems, with higher prevalence in women aged 45-64

What are the different types of sexual dysfunction? 

Based on the DSM-V - 5 specific types of female sexual dysfunction:

  • Female sexual interest and arousal disorder 

    • Lack of or significant decrease in at least three of the following: 

      • Interest in sexual activity 

      • Sexual or erotic thoughts or fantasies 

      • Initiation of sexual activity and responsiveness to a partner’s initiation 

      • Excitement or pleasure during all or almost all sexual activity

      • Interest or arousal in response to internal or external sexual erotic cues 

      • Genital or nongenital sensations during sexual activity in almost all or all sexuall encounters 

    • Symptoms have persisted for a minimum of 6 months and cause clinically significant distress in individuals 

  • Female orgasmic disorder 

    • Marked delay in, marked infrequency of, or absence of orgasm, or markedly reduced intensity of orgamsic sensations in almost all or all occasions of sexual activity 

    • Symptoms have persisted for a minimum of 6 months and cause clinically significant distress in individuals  

  • Genito-pelvic pain/penetration disorder 

    • The persistent or recurrent presence of one or more of the following symptoms:

      •  Difficulty having intercourse 

      • Marked vulvovaginal or pelvic pain during intercouruse or penetration attempts 

      • Marked fear or anxiety about vulvovaginal or pelvic pain anticipating, during, or resulting from vaginal penetration 

    • Symptoms have persisted for a minimum of 6 months and cause clinically significant distress in individuals  

  • Substance/medication-induced sexual dysfunction 

    • Disturbance in sexual function that has a temporal relationship with substance/ medication initiation, dose increase, or discontinuation and causes clinically significant distress in the individual 

  • Other specified or unspecified sexual dysfunction

    • Distressing symptoms characteristic of sexual dysfunction that do not meet the criteria of one of the defined categories. The major distinction between specified and unspecified is whether the clinician specifies reason that the symptoms do not meet criteria for other classes 

    • One specified reason: genitourinary syndrome due to menopause 

How should we evaluate for FSD? 

  • Ask about it!

    • During routine visits, can ask questions about sexual function 

    • Ask broad, open-ended questions during routine history gathering 

    • “Many women experience concerns about sex. Are you experiencing any issues?” 

  • Initial approach if patient answers yes, or if FSD is a complaint 

    • Comprehensive History 

      • Should ask detailed history about patient’s sexual and gender identity 

      • Nature, duration, and onset of symptoms - also if symptoms cause distress 

      • If patient is using medications 

      • Partner factors (ie. number of current partners, their gender, health problems, sexual function problems) 

      • Relationship quality - communication about sexual concerns with partner, past and current abuse or violence experience

      • Pain/injuries/Body image 

    • Physical Exam

      • Often, there are not specific physical exam findings 

      • However, use of mirror and pointing out female anatomy for education is sometimes helpful 

      • Can also identify if there are areas that are causing pain 

How do we treat FSD? 

  • Psychological Interventions 

    • Relationship distress and partner sexual dysfunction can trigger sexual problems in other domains 

    • Options include sexual skills training, cognitive-behavioral therapy, mindfulness-based therapy, and couples therapy 

      • Sexual skills training: can include instructions in masturbation, other erotic stimulation, decrease feelings of guilt and shame with masturbation, as well as learning about anatomy (ie. clitoral stimulation)

      • Couples therapy: exercises to better communication with partner 

      • History of trauma - may need trauma-based psychotherapeutic approach  

    • Can consult or refer to mental health specialists with expertise in this area 

  • Medical therapy

    • Estrogen

      • Low-dose vaginal estrogen therapy is the preferred hormonal treatment for FSD due to genitourinary syndrome of menopause  

      • Low-dose systemic estrogen can be an alternative 

      • Other alternatives include Ospemifene for management of dyspareunia due to genitourinary syndrome of menopause 

    • Androgen Therapy

      • Short-term use of transdermal testosterone can be considered for treatment of postmenopausal women with sexual interest andd arousal disorders 

      • Need to appropriately counsel that there are risks (ie. acne, increased hair growth, virilization - may be irreversible) and long-term side effects are not known 

      • Can try for 3-6 months after baseline testosterone is tested and after 3-6 weeks of initial use 

      • Should be discontinued if no effect after 6 months 

    • Flibanserin 

      • Addyi on the market 

      • Serotonin receptor agonist/antagonist and was approved in 2015 by the FDA to treat hypoactive sexual desire disorder in premenopausal women without depression 

      • However, systematic review and meta-analysis of existing studies showed that overall quality of evidence for efficacy and safety were low, and there was minimal to no improvement in hypoactive sexual desire disorder with use 

      • Black box warning against alcohol use - increased risk of syncope and hypotension 

    • Sildenafil (Viagra) 

      • Not efficacious

      • Hypothesized that it may increase pelvic blood flow to clitoris and vagina, but has not been proven to work 

    •  Bupropion 

      • If patient has antidepressant-induced female sexual dysfunction, supplementation with bupropion may improve symptoms 

  •  Other 

    • For genito-pelvic pain and penetration disorders:

      • Education to help patient understand anatomy and etiology of their symptoms 

      • Vaginal dilators

      • Physical therapy (Pelvic PT) 

      • Intravaginal prasterone for treatment of postmenopausal women who have dyspareunia 

      • Lubricants and moisturizers 

        • Don’t cure the underlying cause, but may reduce or alleviate dyspareunia that is due to vaginal dryness 

          • Coconut oil is a good option, but do not use with condoms 

          • Tend to counsel more toward silicone-based lubricants because they do not dry out as quickly as water-based lubricants 

      • Vaginal lasers

        • Became a hot topic while we were senior residents and some people raved about them; latest evidence suggesting they’re not effective.

        • Vaginal CO2 fractional laser is inadequately studied for treatment of vulvovaginal atrophy 

        • Cost of treatment is rather high 

Endometriosis Part II: Treatment

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How do we treat endometriosis? 

  • Approach 

    • Should be based on severity of symptoms and make sure that other causes of pelvic pain are excluded 

    • Usually, medications are tried first because of the risks, recovery, and costs of surgery

    • Discussion of desire for fertility in the future can also help guide your management 

    • Review with patients that this is a chronic disease - it is not curable, but can be treated. Also, discuss that the road through treatment can be long, and that one mode of therapy that is effective for some, may not be effective for others 

  • Medical 

    • NSAIDS 

      • Can be used to treat primary dysmenorrhea, and is first line for that 

      • However, no high-quality data reporting its efficacy in endometriosis; however it is low-cost and readily available; usually combined with combined hormonal therapy 

    • Estrogen-progestin contraceptives 

      • First line treatment for endometriosis because can be used long-term, well tolerated, and are relatively easy to use 

      • No formulation has demonstrated superiority

      • Both cyclic and continuous dose appear to be effective at reducing pain, but two systemic reviews reported that continuous COC regimens were more effective at reducing pain than cyclic (meaning you take the active pills in one pack → move on to the next pack, skip the placebos) 

      • This is because COCs suppress ovarian function while they are being taken and can reduce endometriosis disease activity and pain 

      • Obviously, there are risks and benefits of taking COCs, and there are many people that cannot take COCs because of the estrogen component (check out our past episode!)

    • Progestins 

      • If people can’t take estrogen, then they can use progestin only therapy 

      • Most commonly = norethindrone acetate 5 mg by mouth daily, but can be increased by 2.5 until l15 mg daily is the max

      • Depo Provera - 150 mg IM injection q12 weeks 

      • Progestins inhibit endometrial tissue growth. It also doesn’t carry the risk of VTE with COCs, and avoids risk of bone loss and menopausal symptoms associated with GnRH agonists

      • However, side effects include increased breakthrough bleeding, weight gain (Depo Provera), mood changes 

      • Alternatives: Etonogestrel implant - observational trial of 41 women showed it decreased intensity of endometriosis-related pain

      • LNG-IUD - limited evidence, but postop IUD can reduce recurrence of dysmenorrhea in women with surgically confirmed endo 

    • Gonadotropin-releasing hormone agonists 

      • I.e., leuprolide; others are things like buserelin, goserelin, etc 

      • Meta-analysis shows they are more effective than placebo, and just as effective as other medical therapies 

      • Common doses: Leuprolide 3.75 IM qmonth or 11.25 mg q3 month 

      • However, remember that it is a GnRH AGONIST 

        • Initially, can worsen symptoms for a little bit due to initial surge of LH and FSH before eventually suppressing the HPO axis (warn patients about 7-14 days of worsening symptoms) 

      • To counteract the hypoestrogenic effects (ie. menopausal symptoms, vasomotor symptoms), usually will do add-back therapy with 5 mg oral norethindrone 

    • GNRH Antagonist 

      • Also suppress HPO axis, but does so immediately, without initial LH and FSH surge like agonists 

      • Also induces a hypoestrogenic state and can cause vasomotor symptoms, as well as leads to decrease in bone density  

      • Easier to dose because they are oral rather than IM 

      • Ex: elagolix (Orilissa), dosed 150 daily up to 200 mg twice daily 

    • Danazol

      • Can be effective in reducing pain, but not common because it can cause androgenic side effects  

    • Aromatase inhibitors 

      • Usually reserved for severe, refractory endometriosis-related pain 

      • Often used in combination with progestins 

      • Off-label use of AI 

      • Limited data overall, but does seem to decrease pain compared to placebo 

      • Similarly, can cause hypoestrogenic side effects 

    • Neuropathic pain treatments 

      • Can be used if there is still pain from endometriosis (see other below)  

  • Other 

    • Often, long-lasting pain from endometriosis can become chronic pain 

    • See our chronic pain episode → basically can lead to a cycle of lowered threshold of stimulus to cause pain, central sensitization 

    • May also need other therapy such as pelvic floor PT

    • May need neuropathic pain treatments (ie. gabapentin) to decrease sensitization. Remember to remind your patients that gabapentin does not take pain away immediately, and needs to be used consistently for several weeks 

  • A note on opioids 

    • Patients with endometriosis and pelvic pain may receive opioids for pain relief when presenting for treatment urgently 

    • Opioids should be used sparingly or avoided for endometriosis and CPP because they only treat symptoms and do not address the issue 

    • Can lead to dependence and overuse 

  • Surgical 

    • There are many, many surgeries out there for endometriosis, from simple ablation, to adhesiolysis, to nerve transections, to hysterectomies. We will cover a few 

    • Surgery offers the benefit of definitive diagnosis, but risks include damage to organs (especially if there is heavy burden of endometriosis as well as adhesions) like bladder and bowel

    • Most people will achieve initially pain relief after surgery - women who underwent operative laparoscopy were 3x more likely to report improvement in pain at 12 months than controls who had diagnostic laparoscopy (one study showed 73 vs 21%) 

    • However, nearly 20% of patient will undergo repeat surgery within 2 years because of recurrent symptoms, and risk of symptom recurrence is as high as 40% at 10 year follow up 

    • Risk factors for persistent or recurrent pain: incomplete excision, ovarian cyst drainage instead of cyst excision, and ovarian conservation

    • Endometriosis tends to get better with Menopause, and so longer latency to menopause gives more time for symptoms to recur 

    • Postoperative medical therapy: ASRM advises posteropative medical suppressive therapy for most women treated surgically 

      •  6-24 months of suppression can reduce symptom recurrence and thus potentially avoid need for multiple surgeries 

      • Best evidence comes from 2 systemic reviews: one using LNG-IUD, and another for postoperative use of COCs for prevention of relapse 

  • Surgical techniques

    • Laparoscopy generally favored over laparotomy because less invasive and improves visualization, with better recovery and shorter hospital stay, elss pain 

    • Conservative 

      • Excision or ablation of endometriosis lesions with intent of preserving the uterus and as much ovarian tissue as possible 

      • First line option for most people who want surgery for endometriosis because it preserves fertility and hormone production

      • Remember: even in young patients who don’t want fertility, hormone production is necessary for bone and cardiac health!  

      • Less invasive and morbid than definitive surgery, and there is documented short term efficacy 

      • 2014 systematic review: decreased pain and increased live birth rate after conservative surgery 

      1. Disadvantages: 

        1. Rate of recurrent symptoms is higher compared to definitive surgery 

        2. Rate of reoperation increases with time, whereas it is relatively stable with definitive surgery 

    1. Hysterectomy without oophorectomy 

      1. For patients who have debilitating symptoms and whom have completed childbearing 

      2. Failed both medical therapy and at least one conservative treatment procedure 

      3. Also reasonable if other indications for a hyst (ie symptomatic fibroids, prolapse, etc) 

      4. Effective treatment for pain symptoms from endometriosis, with reoperative rates that are relatively low (19% in one study, compared to 58% in people undergoing conservative therapy) 

      5. Disadvantages 

        1. Longer, more morbid surgery with higher rates of complication 

    2. Hysterectomy with oophorectomy

      1. Those who would benefit are those with extensive adnexal disease and those for whom the risks of reoperation outweigh the risks of premature menopause 

      2. Likely increases the efficacy of definitive surgery but is accompanied by quality of life issues and potential adverse outcomes due to early menopause 

      3. Reason to do it: endometriosis is an estrogen-dependent disease, and tends to get better with menopause 

      4. Early menopause (<44 years) is associated with increase risks of overall mortality, cardiovascular disease, neurologic disease, osteoporosis 

Endometriosis Part I: Evaluation and Diagnosis

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Be sure to check out our previous episode on chronic pelvic pain with Dr. Eva Reina to round out your CPP diagnosis skills!

What is endometriosis? 

  • Gynecologic condition where endometrial glands and stroma occur outside of the uterine cavity that can respond to hormonal shifts of the menstrual cycle.

    • Most within pelvis, but can occur elsewhere: bowel, diaphragm, and even in the pleural cavity 

    • Benign, but can cause dysmenorrhea, dyspareunia, chronic pain, and infertility 

  • Incidence

    • Occurs in 6-10% of reproductive age women, but is present in 38% of women with infertility and 71-87% of women with chronic pelvic pain! 

    • No data to suggest that endometriosis is increasing, but it is likely more recognized and being diagnosed more often now.

    • There is a familial association - first degree relatives of someone with endometriosis are at higher risk for also developing it, but the inheritance is likely polygenic-multifactorial 

  • Risk factors

    • Nulliparity, prolonged exposure to endogenous estrogen (ie. early menarche, late menopause)

    • Shorter menstrual cycles, heavy periods, obstruction of menstrual outflow

    • Increased height, lower BMI, and high consumption of trans unsaturated fats

      • This does not mean that you’re going to get endometriosis if you’re tall or have a low BMI! And you’re not going to treat it by stopping eating trans fats.

      • Association doesn’t equate to causation.

  • Etiology 

    • Endometriosis occurs when ectopic endometrial tissue implants, grows, and elicits inflammatory response 

    • Inflammatory response: COX-2 activity, overproduction of prostaglandins, and then chronic inflammation → triggers pain and causes infertility

      • Also why those with endometriosis will usually have flares that coincide with their menstrual cycle.

    • Nerve growth factor is also highly expressed in endometriotic lesions → increase density off nerve fibers → can explain increased sensitivity and pain 

      • Can also be explained by central sensitization (lowering threshold of pain) 

      • Go back go our CPP episode to remember what all these things are! 

    • Sampson’s Theory of Retrograde Menstruation - most popular/common theory where endometrial cells flow backwards through the fallopian tubes into the peritoneal cavity during menses

      • But, up to 90% of women HAVE retrograde menstruation, and not everyone has endometriosis 

      • Likely, there is a multifactorial cause of endometriosis, where ectopic endmoetrial tissue interacts with alterned immunity, imbalance of cell proliferation/apoptosis, aberrant signalling, and genetic factors 

      • There are certain genes that are statistically associated with endometriosis 

    • Chronic inflammation and endometriotic lesions can distort the pelvic anatomy through adhesions, endometriomas, and other substances lilke cytokines and prostaglandins that are “hostile” to normal ovarian function, fertilization, and implantation 

How do we evaluate for endometriosis? 

  • History and physical

    • Usually patient will present during reproductive years with pelvic pain (ie. dysmenorrhea or dyspareunia), infertility, or ovarian mass 

    • However, there are many people with endometriosis who are asymptomatic! 

    • Diagnosis is more likely to be made in people with symptoms 

      • Remember the “PPUBS” framework 

        • Pain - can you describe your pain? 

        • Periods - menstrual history; is the pain surrounding menstruation or line up with other parts of their menstrual cycle? 

        • Urinary symptoms - there can be endometriotic lesions on the bladder → frequency, urgency, pain with voiding 

        • Bowel - symptoms include diarrhea, constipation, dyschezia, and bowel cramping 

        • Sexual dysfunction - peritoneal or deeply infiltrating endometriosis can present with dyspareunia 

    • Physical exam: can be variable depending on location and size of implants

      • You may feel nodules in the posterior fornix, uterosacral ligaments,, adnexal masses, and immobility or lateral displacement of the cervix or uterus 

      • However, exam can be completely normal 

  • Rule out other causes for pelvic pain 

    • Labs - no pathognomonic lab for endometriosis 

      • CA125 can be elevated, but it’s not routinely ordered because other diseases can also elevate CA-125 levels 

      • It’s not specific and not helpful for endometriosis

    • Imaging 

      • Ultrasound is usually all you need - can see things like endometriomas, nodules, etc. 

      • Sometimes, can consider MRI

      • Imaging can help to rule out other causes of pelvic pain (ie. fibroids)  

  • Definitive diagnosis vs. presumptive diagnosis 

    • Presumptive diagnosis

      • Endometriosis is a pathologic diagnosis - meaning you need histology of a lesion biopsied during surgery 

      • Sometimes, if surgery is not desired or not yet possible, presumptive diagnosis can be made based on combination of signs, symptoms, and imaging findings 

      • Clinical diagnosis is enough to start therapy that is low risk and easily tolerated

      • If patients improve, can actually hold off on surgery 

    • Definitive diagnosis 

      • Surgery - usually indicated for persistent pelvic pain that does not respond to medical therapy, evaluation of severe symptoms that limit function, andd treatment of anatomic abnormalities 

      • Usually laparoscopy - can get definitive diagnosis and treatment 

        • Peritoneal lesions can appear like reddish or bluish irregularly shaped islands, “powder burn” lesions, white opacifications, translucent blebs

        • Allen-Masters syndrome = scarred or puckered peritoneal surface 

        • Dense fibrous disease 

        • Endometriomas 

    • Pathologic Categorizations 

      • Superficial peritoneal lesions 

      • Ovarian lesion (endometrioma) 

      • Deeply infiltrating - solid endometriosis situated more than 5 mm deep to the peritoneum 

    • Surgical Staging - this is to report operative findings. They do NOT correlate with presence or severity of symptoms. However, there are studies that have shown inverse correlation with advanced stages and prognosis for fertility treatment 

      • Stage I - minimal disease; ie. isolated implants, no significant adhesions 

      • Stage II - mild endometriosis with superficial implants that are < 5 cm in aggregate and are scattered on peritoneum and ovaries. NO significant adhesions 

      • Stage III - Moderate disease with multiple implants, both superficial and deeply invasive, peritubal and periovarian adhesions may be evidence  

      • Stage IV - severe disease; multiple superficial and deep implants, including large ovarian endometriomas. Filmy and dense adhesions are usually present

Chronic Pelvic Pain

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Today we welcome Dr. Eva Reina, who is a current PGY-3 at Brown/Women and Infants. Eva shares with us some information on one of the most clinically challenging topics in office gynecology: chronic pelvic pain.

In terms of the initial evaluation, using the PPUBS framework can be useful:

  • Pain: typical “can you describe your pain?”

  • Periods: a thorough menstrual history, which should always be part of your GYN history taking.

  • Urinary symptoms: timeline of symptoms with respect to urination, as well as triggers for any symptoms related to urination.

  • Bowels: constipation and diarrhea, depending on pattern, can relay problems such as IBS, IBD, or other functional GI disorders.

  • Sexual function: describing not only the nature of dyspareunia, but the timing and length of pain symptoms.

After history taking, a physical examination is the next important step. Particularly with the pelvic exam, starting with a single digit may be revelatory. Deep infiltrating endometriosis may be suggested by particular point tenderness. Bimanual examination can help to assess uterine size or concerns for adenomyosis. Speculum exam may not reveal much in the way of pain, but allows for testing for infectious etiologies.

We then discuss some of the mechanisms of chronic pelvic pain development:

Central Sensitization: Most patients with chronic pelvic pain do have multiple pain generators and may even be centrally sensitized: that is, amping up of a stimulus leading to a state of constant reactivity. This lowers the threshold of a stimulus to cause pain and also may maintain pain even after the initial insult has been removed. For instance, in population-based studies vulvodynia, IC, endo, IBS, migraines are commonly found together.

Cross-Talk:

  • The top-down phenomenon. The patient who has low back pain, migraines, fibromyalgia, and has now been referred to your office with chronic pelvic pain. 

  • The bottom-up phenomenon. 30 year old female who has “always had painful periods.” Stopped OCPs 5 years ago in order to achieve pregnancy. Presenting to your office for urinary symptoms (pain with bladder filling, urgency, frequency). 

  • Pelvic Organ Cross-Sensitization: Convergence of sensory input from the pelvic viscera, their associated striated sphincters, muscular components of the pelvic floor, lower abdominal wall, the muscular perineum and its corresponding cutaneous components. 

Afferent information from the major pelvic organs (e.g. bladder, bowels, and uterus) is conducted through the hypogastric, splanchnic, pelvic, and pudendal nerves to cell bodies in thoracolumbar and lumbosacral dorsal root ganglia. At first, these signals go up to the brain (central nervous system), and an efferent signal comes back down (e.g. reflexically removing your hand from a hot stove). 

Over time, if one doesn’t remove the noxious stimulus, the body thinks there must be nobody home to hear the fire alarm, let’s try the neighbor’s house. So, long-term, noxious afferent stimulation from an irritated pelvic organ (peripheral to central) leads to that sensory input traveling back down to the peripheral nervous system to pass the message along to a nearby pelvic organ that was not previously affected. This neurogenic “inflammation” via the central to peripheral pathway may even produce functional changes in the uninsulted organ with little evidence of an organic etiology (e.g. IBS, IC/PBS, vulvodynia). 

Where do the muscles come in? 

  • It is helpful to think of muscular spasm as a reactive phenomenon. If you uncover pelvic or abdominal wall myalgia, be sure to treat other primary pain generators BEFORE pelvic floor PT. If you don’t remove the stimulus, the patient is unlikely to make sustained forward progress in PT. 

  • Pelvic floor PT is hard to come by (shortage of well-trained providers) and it is uncomfortable both physically and mentally for patients. Thus it is difficult to motivate patients to return to pelvic floor PT after a previous failure of therapy.