For Physicians and Health Care Professionals
Case-Based Learning
These hypothetical cases are a way to promote thinking and learning about the many unusual ways chronic pelvic pain may present and the various approaches to evaluating and treating these issues.
Keep in mind that in the realm of chronic pelvic pain, there are few standardized protocols or guidelines on how to manage many problems. Often the cornerstone of effective evaluation and treatment lies in the Scientific Method, as you'll see in these cases.
Please feel free to contact Dr. Soffer with questions or comments. SofferWomensCare@gmail.com
Case #1
A hypothetical 53 yo postmenopausal F was referred to me for chronic generalized abdominal pain and bloating x2 years s/p IUD removal complicated by IUD breakage, requiring operative hysteroscopy to recover missing arm of IUD (documentation confirms all pieces of the IUD were accounted for and imaging not suggestive of retained pieces of IUD). History suggestive that pain flares tend to occur seasonally, worse spring/summer/fall than in winter, unclear why. Labs and imaging noncontributory. EMB & pap WNL. Pain refractory to NSAIDs, PT, diet modifications (tried gluten-free, dairy-free, IC diet x2 weeks each). Exam significant for generalized abdominal tenderness all four quadrants, point tenderness in RLQ, approx 5cm medial to ASIS and +tender pudendal nerves bilaterally. Bilateral pudendal nerve block relieved bloating sensation immediately and permanently, and relieved generalized abdominal pain (including bilateral upper quadrants). Point tenderness in RLQ remained, in fact worse than before pudendal nerve block. Trigger point injection with lidocaine 1% plain to block R ilioinguinal nerve relieved RLQ pain completely, and additionally relieved bloating which pt didn't even perceive immediately prior to injection. Weekly serial blocks to ilioinguinal nerve x4 weeks relieved pain long term, after figuring out her trigger was lifting heavy bags of mulch or fertilizer during gardening season. Dx: Abdominal cutaneous ilioinguinal nerve entrapment
Morals of the story:
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Red herrings are real, sometimes history can throw you off track. Have patients record their pain in detail, when flares happen, exacerbating and relieving factors VERY impt!
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Don't forget there are muscles and nerves in the area where we work. Correlation does not equal causation. Just because these pains were initially reported follow her IUD mishap doesn't mean that caused it.
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Referred pain should never been underestimated in terms of how far away the precipitating issue may be. MANY patients get relief of upper abdominal pain with pudendal nerve blocks.
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Sometimes a diagnostic pudendal nerve block may unmask the more localized pain that precipitated the generalized pudendal neuralgia in the first place. Whenever you find pudendal neuralgia, don't forget to ask yourself, "Why did this happen?" Sometimes it's something obvious like she is post-trauma (surgery, delivery, sexual assault, etc), but sometimes it's more subtle like repeated musculoskeletal injury from lifting mulch. Very often endometriosis patients will develop overlying pudendal neuralgia that persists even after endo is hormonally controlled.
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No shame in referring to a specialist. My love of treating chronic pelvic pain is rooted in helping these long-term sufferers get back to life. But it's also really fun to figure these weird scenarios out. If you're not into it, find someone who is. Many of these riddles can take awhile and some persistence.
Hypothetical 24 yo F with 3 yr h/o debilitating sporadic pelvic pain several times daily, rated 8-10/10. Flares awakened her from sleep and lasted hours. Exacerbating factors included intercourse, activity (walking, light aerobic exercise), prolonged sitting, menses. Relieving factors: none identified. No n/v/d/c, no urinary sx.
Had been seen by 14 gyns, 3 pain med specialists, several internists, 2 GI’s and a pain psych in the prior 3 years for this single issue.
Pain had been refractory to: Ibuprofen, opioids, gabapentin, elavil, cymbalta, acupuncture, empiric azithro/ceftriaxone (for presumed cervicitis), empiric Doxycycline (for presumed chronic endometritis) x2 rounds, psychotherapy. Pt unable to tolerate any real PT.
Hx significant for:
Chlamydia (s/p tx) age 19, neg TOC x3 on chart review
NSVD
LEEP, neg margins and normal paps since.
Dx hysteroscopy WNL.
No h/o autoimmune disease. No h/o vaginitis.
One long-term male partner, not sexually active x3 years 2/2 pain
Contraception: Nexplanon, c/b irregular spotting
Exam: Mild generalized abdominal pain in all four quadrants; exquisite point tenderness (elicits tears) from single-digit palpation at posterior fourchette, bilateral levators, bilateral pudendal nerves, cervix, uterus. Unable to assess adnexa 2/2 severe pain at posterior fourchette precluding proximal exam, but prior sonos WNL. +Hypertonic pelvic floor with +trigger points along puborectalis.
Approach:
-Remove Nexplanon and replaced with continuous OCPs for more consistent menstrual suppression (in case of endo vs adeno)
-Diagnostic pudendal nerve blocks: relieved generalized abdominal pain completely and long-term, but provided only short term relief of pain at posterior fourchette, levators, pudendal nerves and cervix.
-Trigger point injections 1% lido plain to trigger points at puborectalis resolved trigger points and hypertonic pelvic floor long term with 3 serial injections q2 weeks.
Though pudendal nerve blocks and TPI did demonstrate dramatic improvement in overall abdominal and pudendal pain, she still involuntarily teared up with gentle BME at the start of each visit, so I knew we hadn’t really addressed the crux of the issue. She had been referred to me with working dx of pelvic congestion syndrome, and although her story didn’t sound much like PCC, she did exhibit excessive bleeding with trigger point injections (coag workup neg).
As a reminder to those long-stumped by pelvic congestion syndrome (aka. all of us), PCC is generally considered likely 2/2 ovarian vein vs internal iliac vein insufficiency, which causes a heavy ache, usually unilateral (often L>R, thought due to L ovarian vein draining into L renal vein rather than IVC like the R side does), often antepartum/postpartum (maybe due to increased blood flow during pregnancy?), premenstrual or postcoital. Problem is, PCC has no defined diagnostic criteria. Since there is no designated ‘normal’ vein caliber, radiology doesn’t have a way to definitively call it PCC. And since the majority of women with subjective venous congestion on imaging are asymptomatic, it’s very hard to argue that IR should embolize veins in healthy young women. Thus, when I sent my pt for MRI and radiology ruled her venous congestion WNL, I did my best to argue her case. The first radiologist wasn’t swayed, neither was the chief. I requested a standing MRI (since veins go flaccid in many people when supine), which wasn’t a thing at our institution. I requested a referral outside our institution to get a standing MRI. That process would take time and further battle to demonstrate need.
Meanwhile, throughout this battle for a PCC dx, the pt continued to come q10-14 days for pudendal nerve blocks, which were the only thing keeping her pain relieved enough to be functional at work and home without narcotics. Then one day, after showing me her pain calendar which showed another sharp, sleep-awakening pain flare with no apparent trigger, I told her we were starting over. This just seemed too inconsistent with PCC. I had gotten in so deep navigating this pt through a bureaucratic care system that I felt like I had lost the forest for the trees and had forgotten where we started. So I retook her history, with pen and paper (not sure why it’s different than doing it on computer, but when histories are long and complicated, visual grouping of details really helps me). Seeing it in my own format made me realize how many holes were in the story. So I did the unthinkable: I read every note written in her extensive multidisciplinary chart. Literally hundreds of notes. And then finally I found the answer buried deep in there, and I tried the one thing I hadn’t tried yet. Ectocervical block at 12, 3, 6, and 9. Less than 4cc of lidocaine and her pain was gone. I saw her again 8 months later for an exacerbation (apparently prompted by break-thru spotting), again relieved with the same 3.5cc of lido to the ectocervix. I saw her again last week (now years later) for an exacerbation, her first in years. Between those visits she reported having zero pain. Able to have intercourse, exercise, work, play with her kid, etc etc. Her complaints of pain started after her LEEP (a detail she had long-since forgotten). Working dx: Ectocervical peripheral neuropathy s/p LEEP.
Pearls:
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It’s ok to be wrong. It’s not ok to give up.
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Notes have become prohibitively long in this era of insurance-required auto-populated junk. Though it has become truly onerous to read encyclopedically-thick notes to find the relevant info, it can be vital in complicated or refractory cases.
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Make your patient your partner in the quest for answers, rather than the victim of an ever-changing plan. It’s empowering for them, they’ll be less irritated about course corrections, and it’s 100% necessary for you to be effective. We rely on their observational powers and data collection quite a bit to guide our treatment.
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Block that ectocervix before your LEEPs (not paracervical; ectocervical). Never had a pathologist tell me it affected examination of the specimen, it really helps patients tolerate office LEEPs, and it will likely prevent peripheral and central sensitization. Even though we don’t really think of LEEPs as surgery, any injury to tissue can lead to sensitization syndromes and neuropathy.
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Remember that pudendal neuralgia and hypertonic pelvic floors can develop in response to other pain syndromes and overlapping pain sx can confuse the whole picture. When the pudendals are tender, block them, be happy with the improvement but don’t be satisfied. Keep looking for the primary cause of pain which caused the secondary pudendal neuralgia in the first place. Incomplete improvement after pudendal nerve block is a huge tell that you have two or more things contributing to pain.
Case #2
Case #3
Hypothetical 49 yo F with chronic sporadic abdominal and pelvic pain and deep dyspareunia x4 years s/p TLH/BSO c/b ureteral transection, s/p 2 subsequent surgeries for reinsertion and 1 for adhesiolysis (done to address chronic pain, without relief). Referring gyn and urologist noted significant adhesions in each case, subjectively worsening with each subsequent surgery.
Pain refractory to NSAIDs, premarin cream, narcotics, heat packs, physical therapy. Pt unable to tolerate Gabapentin due to daytime somnolence and unwilling to switch from SSRI (long effective for anxiety/depression) to cymbalta or elavil. No urinary issues s/p final reinsertion surgery.
Exam significant for generalized abdominal pain all four quadrants, no pain at perineal body or posterior fourchette, slightly tender and hypertonic pelvic floor, +tender bilateral pudendal nerves, and ++exquisite tenderness at apical cuff associated with palpation of subcentimeter nodule.
Pudendal nerve block relieved generalized abdominal pain, hypertonic pelvic floor, and pudendal nerve tenderness on exam with 3 serial blocks, but did little to relieve apical cuff tenderness.
Lidocaine block directly to apical cuff nodule (exquisitely painful block for pt to endure) relieved pain completely. Pt required 9 visits total, enduring a block to the nodule each visit, to achieve complete and lasting relief of deep dyspareunia and sporadic/vague abdominal pains.
Working dx: Traumatic Neuroma.
Let’s talk about a gynecologist’s favorite topic: NERVES!
There are 4 main types of acute peripheral nerve injuries: penetrating, crush, stretch, and ischemic. There are five grades of nerve injury, ranging from grade 1 (aka. neuropraxia), which is just focal demyelination, to grade 5 (aka neurotmesis), which is complete transection of a nerve. All the grades between are varying degrees of injury to the various layers of the nerve (remember endoneurium, perineurium, epineurium?). Different grades of injury may require different treatments and are associated with different prognoses.
Grade 1 nerve injury - neuropraxia - tends to occur due to compression or traction on a nerve. This may cause a conduction block proximal to the lesion, and may also cause distal muscle groups to be stimulated indefinitely (may lead to hypertonicity). Acute neuropraxia injuries (think ‘Saturday Night Palsy’ with your radial nerve crushed over the chair back during a drunken stupor) tend to resolve within a few weeks, since the nerve isn’t lastingly damaged and simply re-myelinates with time. Chronic neuropraxia injuries (think carpal tunnel) can develop lasting effects for the nerves and distal muscles.
When docs refer to pain ‘from adhesions,’ I assume they’re thinking about these kinds of stretch nerve injuries (neuropraxia) caused by pull from adhesions, which could theoretically be relieved by adhesiolysis. The thing is, I’ve never actually seen surgical adhesiolysis fix it. For the dozens of patients referred to me with working diagnoses of post-surgical adhesion pain, every one of them achieved lasting relief with pudendal nerve blocks or blocks directly to the nerves whose distributions demonstrated pain (and in one case the pain was relieved by remediation of mesh erosion). It’s possible abdominal nerve blocks (eg. ilioinguinal, iliohypogastric, genital branch of gen-fem nerve, etc) may be alleviating pain by hydrodissecting adhesions off the nerve, but again, surgical intervention is not typically the answer in my experience.
I suspect this patient’s issue was a grade 5 nerve injury - neurotmesis, complete transection of a nerve. Ask yourself: what happens when skin is transected? It heals. It’s not replaced with an exact replica of the skin like some fish and amphibians can do; the re-epithelialization may prevent infection and dehydration but lacks the hair follicles, sebaceous glands, and epidermal progenitor cells which are important for full skin function. A similar thing happens with nerve healing. The cut nerve crudely heals itself over to prevent infection, but it’s not the same organization or composition of the original nerve ending. The haphazard overgrowth of normal nerve components over the nerve stump will most often result in dysfunction in the form of conduction block. We’ve all seen this from patients who describe persistent numbness in their CS scar. Sometimes, unfortunately, instead of the nerve going silent when it scars over with a disorganized arrangement of nerve components, it can shoot off random nerve signals which may be experienced as tingling or pain. These ‘traumatic neuromas’ can also be distinguished by different types, but for gyn purposes, the important things to know are:
1) they might present up to 12 months after the injury (since this is really a result of the healing process)
2) palpation of the stump/nodule shoots pain along the distribution of the nerve (and may also cause referred pain elsewhere)
3) No standard tx, high tx failure rates and poor prognosis.
In the periphery, neurosurgeons, orthos and podiatrists tend to resect the neuroma and bury the cut edge of the nerve in an adjacent muscle belly where it is less likely to get recurrently stimulated and is in a protective microenvironment. But for those of us working in the pelvis, full of adjacent organs like the bowel, bladder, and countless vessels which could potentially harmed during exploration, we all know we’re not digging through a belly full of adhesions hoping to find a traumatic neuroma, and then hoping to find a safe way to bury it in muscle or cap it, etc. Other tx options, like massage and electrostimulation were also not good options for this pt since she could hardly tolerate palpation. I didn’t like the idea of cryo, due to burn risks to surrounding tissue or dehiscence, and systemic nerve therapies (gabapentin, elavil, cymbalta) were no-go’s as mentioned above. So I tried simple desensitization with recurrent lidocaine nerve blocks. Thankfully, it worked and the patient was pain-free and without dyspareunia by the end of our 9 visits.
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Some references for this topic (though much came from my textbooks - I’m so old fashioned):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593675/
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/nerve-injury