Management of chronic pelvic pain

^{Louise P. King, MD, JD, is director of research in the Division of Minimally Invasive Gynecologic Surgery, associate program director of the Fellowship in Minimally Invasive Gynecologic Surgery, and an assistant professor at Brigham and Women’s Hospital in Boston, Massachusetts. She is also director of reproductive bioethics at the Center for Bioethics and codirector of Ethics and Essentials of the Profession at Harvard Medical School in Boston. In addition, she is an affiliated faculty member at Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics at Harvard Law School in Cambridge, Massachusetts.}

Chronic pelvic pain (CPP) in womenis defined as nonmenstrual pain lasting greater than 6 months. It accounts for over 10% of referrals to gynecologists with an incidence rate between 5.7% and 26.6%.¹ CPP is a common indication for surgery leading to 12% of all hysterectomies and over 40% of gynecologic diagnostic laparoscopies, yet up to 35% of these laparoscopies add little to treatment.²

The optimization of care for women with CPP represents a priority and requires understanding the multifaceted etiology of pelvic pain and how to effectively diagnose and treat the condition. Few advances in technology have addressed this area of medicine and thus it represents a unique opportunity for innovation.

Diagnosis and underlying neuronal basis of pain

CPP may originate from both somatic and visceral structures which then converge in the spinal cord, leading to complex pelvic pain patterns.³ CPP often involves multiple organ systems resulting in pelvic organ “cross talk.” The convergence of visceral innervation in the dorsal horn can lead to 1 dysfunctional organ enhancing the pain of a second organ. One example is patients with endometriosis who have associated bladder pain syndrome and irritable bowel syndrome.⁴

Further complicating the picture, visceral pain may induce somatic pain through viscerosomatic convergence.⁵ This presents as pelvic floor tension myalgia or referred pain from specific organ locations.

Prolonged exposure to painful stimuli can cause somatic peripheral sensitization resulting in hyperalgesia. Central sensitization may lead to somatic dysfunction, especially of the pelvic floor muscles.⁶ The processing of sensory pain information by our brain is regulated by cognitive and affective interpretation. Emotional events such as trauma and sexual abuse may regulate our pain perception and lead to persistent pelvic pain.⁷

Given this level of complexity, it is no wonder that patients and health care professionals alike become frustrated as they try their best to parse out etiologies of pain and potential successful treatment. This represents an opportunity for the development of optimal online content and tracking to assist with diagnosis and understanding for both patients and health care professionals.

Patient evaluation

Evaluation begins with a thorough history and a detailed physical examination to tease apart contributing factors.⁸ The International Pelvic Pain Society has developed a detailed questionnaire, available for free on their website, to help providers obtain a pertinent history and guide the exam.⁹

A baseline ultrasound is frequently ordered but may be of limited value. However, patients with alarming symptoms such as hematochezia, postmenopausal bleeding, hematuria, or unexplained weight loss should be evaluated specifically for those symptoms with targeted imaging and possibly gastrointestinal (GI) endoscopy.

By contrast, specialized imaging protocols and experienced radiologists can reliably identify visceral sources of pain from ultrasound and magnetic resonance imaging (MRI), such as adenomyosis, deep infiltrating endometriosis, pelvic congestion syndrome, and pelvic adhesions.¹⁰

In the case of endometriosis, MRI or specialized ultrasound can identify endometriomas, obliterated posterior cul-de-sacs, deep infiltrating endometriosis, rectal endometriosis, and uterosacral ligament involvement.¹¹ That said, laparoscopy remains more accurate at detecting, diagnosing, and, hopefully concomitantly, treating endometriosis.¹² Musculoskeletal sources of pain may be evaluated by MRI or x-ray if suspected on examination.¹³

Treatment

Table 1. Potential Medical Therapy Regimens Specific to Suspected Endometriosis

GnRH, gonadotropin-releasing hormone; IUD, intrauterine device; NSAID, nonsteroidal anti-inflammatory drug; OCP, oral contraceptive.

The key to successful treatment of CPP for any patient is a holistic approach. Frequently, patients hope for a single cause and a single cure. However, this is highly unlikely. Helping patients accept that CPP is typically a multifactorial disease that can be difficult but not impossible to treat is essential.

Initiating a medication regimen to treat CPP as an empirical first step is reasonable, assuming all potential contributing causes are addressed. If a patient fails initial medical therapy, a laparoscopy should be undertaken in an effort to confirm and potentially surgically treat disease ahead of more aggressive regimens (Table 1)¹⁴.

Key points related to surgical intervention

A significant number of outpatient laparoscopic surgical procedures for women are performed to assess for pain but with little benefit.¹⁵ When the procedure is done without a specific plan to address pathology if found, the risks, albeit low, outweigh any benefit.

Specific to endometriosis, any surgeon who undertakes a laparoscopy should be prepared to proceed with excision of all visible lesions. Excision is likely superior to fulguration, especially in patients with deep infiltrating endometriosis.¹⁶ If a surgeon does not feel they could adequately treat apparent endometriosis, they should refer the patient to a surgeon who specializes, even for a diagnostic laparoscopy, to avoid unnecessary repeat surgeries.

Establishing normal anatomy is the ultimate goal of surgery when endometriosis, ovarian pathology, or adhesions are found. In the setting of advanced endometriosis or severe adhesions, this will typically involve fairly extensive lysis of adhesions including ureterolysis and enterolysis.

Typically, in stage 4 endometriosis, the posterior cul-de-sac is obliterated by bilateral endometriomas that may be adhered to each other as well as to the pelvic sidewalls and bowel. A combination of blunt and sharp dissection is helpful. Many surgeons also rely on either monopolar cautery, harmonic, or carbon dioxide laser to achieve dissection planes. A full knowledge of electrocautery and other energy sources is essential to achieve safe surgical dissection.

Endometriomas frequently rupture during this process. Copious irrigation and clearance of endometrioma fluid is important. The ideal method of treatment for endometriomas is not yet known. Recurrence of ovarian endometriomas is thought to be less frequent when ovarian cyst walls are removed, preserving normal parenchyma.^17-19

Yet, aggressive surgical resection of endometrioma cyst walls leads to a decrease in anti-Müllerian hormone (AMH). Decreased AMH is associated with decreased ovarian reserve and thus less success with potential stimulatory cycles during in vitro fertilization. Some authors have proposed instead that ovarian endometriomas should be drained and the posterior aspect of the wall cauterized.^20-22

Surgeons should discuss this evidence with patients and should carefully tailor surgery in consultation with patients to address their goals. For example, in a young patient with severe pain, the excision of endometrioma walls to decrease recurrence would be ideal, whereas for patients seeking fertility treatments, drainage and cauterization may be more suited.

Prevention of postoperative adhesions is a priority in patients with chronic pelvic pain. Surgical technique, hemostasis, and copious irrigation are likely helpful in decreasing the potential for adhesions. The evidence is not robust enough to date to support the use of various barrier methods to prevent adhesions in surgery for pain or subfertility.^23,24

Monopolar or preferably bipolar cautery can be used judiciously to address isolated areas of bleeding. If the bleeding is more diffuse in cystectomy, suturing remaining ovarian parenchyma in a purse string to achieve hemostasis through compression is likely preferred.²⁵

All efforts must be made to identify and address any potential area of injury at the time of surgery. Cystoscopy and sigmoidoscopy are valuable tools to assess for small areas of potential injury in instances when extensive adhesions to the bowel or lesions overlying the bladder have been addressed. Neither procedure can be completely relied upon to identify injuries that result from electrical or thermal injury, however, as delayed necrosis may not be identified.

Hysterectomy for CPP

Table 2. Potential Therapies

FODMAP, fermentable oligosaccharides, disaccharides, monosaccharides, and polyols; GI, gastrointestinal; GnRH, gonadotropin-releasing hormone; UAE, uterine artery embolization.

Hysterectomy is the most common surgery performed for CPP, yet there are no randomized controlled trials that specifically address its efficacy. Prospective and retrospective trials have shown that hysterectomy significantly relieves pain in women.^26,27

A laparoscopic approach for hysterectomy is preferred and can be accomplished even with very large uteri. If a particular surgeon is not well versed in laparoscopic hysterectomy, they should refer the patient to a specialist who can ensure access to all surgical options.

Integrative care

Adjunctive therapies can be highly beneficial for patients with CPP. A multidisciplinary approach is ideal. If there is no center for pelvic pain in the area, creating cooperative plans of care with other specialists will be of greatest benefit to patients and will achieve the best outcomes.

Psychological counseling can be helpful to address poor coping mechanisms and the potential development of situational or chronic depression.

Pelvic floor therapists can address specific muscular dysfunction but can also work with biofeedback as well as behavioral and relaxation feedback modalities. Pelvic pain clinics can address opiate dependence if this has become an issue over time. These clinics can also help with scheduled trigger point injections that might coincide with physical or pelvic floor therapy.

Patients will need to be counseled that they will require multiple visits over what is typically a long period of time. They also will have to make permanent behavioral changes to fully address their chronic pain.

Conclusions

CPP is a complex, potentially debilitating, and costly disorder that is poorly understood. Patients with this condition require extensive work-up, careful treatment plans, and counseling (Table 2). Whenever possible, referral to specialists is encouraged.

Acknowledgement:
Mario Castellanos, MD

References

1. Ahangari A. Prevalence of chronic pelvic pain among women: an updated review. Pain Physician. 2014;17(2): E141-E147.
2. Howard FM. Chronic pelvic pain. Obstet Gynecol. 2003;101(3):594-611. doi:10.1016/s0029-7844(02)02723-0
3. Cervero F. Visceral versus somatic pain: similarities and differences. Dig Dis. 2009;27 Suppl 1:3-10. doi:10.1159/000268115
4. Hoffman D. Central and peripheral pain generators in women with chronic pelvic pain: patient centered assessment and treatment. Curr Rheumatol Rev. 2015;11(2):146-166. doi:10.2174/1573397111666150619094524
5. Perry CP. Peripheral neuropathies and pelvic pain: diagnosis and management. Clin Obstet Gynecol. 2003;46(4):789-796. doi:10.1097/00003081-200312000-00008
6. Butrick CW. Pathophysiology of pelvic floor hypertonic disorders. Obstet Gynecol Clin North Am. 2009;36(3):699-705. doi:10.1016/j.ogc.2009.08.006
7. Alappattu MJ, Bishop MD. Psychological factors in chronic pelvic pain in women: relevance and application of the fear-avoidance model of pain. Phys Ther. 2011;91(10):1542-1550. doi:10.2522/ptj.20100368
8. Czerniak E, Biegon A, Ziv A, et al. Manipulating the placebo response in experimental pain by altering doctor’s performance style. Front Psychol. 2016;7:874. doi:10.3389/fpsyg.2016.00874
9. History and Physical Form. International Pelvic Pain Society. Accessed October 5, 2021. https://pelvicpain.org/
10. Juhan V. Chronic pelvic pain: An imaging approach. Diagn Interv Imaging. 2015;96(10):997-1007. doi:10.1016/j.diii.2015.07.010
11. Champaneria R, Abedin P, Daniels J, Balogun M, Khan KS. Ultrasound scan and magnetic resonance imaging for the diagnosis of adenomyosis: systematic review comparing test accuracy. Acta Obstet Gynecol Scand. 2010;89(11):1374-1384. doi:10.3109/00016349.2010.512061
12. Nisenblat V, Prentice L, Bossuyt PMM, Farquhar C, Hull ML, Johnson N. Combination of the non-invasive tests for the diagnosis of endometriosis. Cochrane Database Syst Rev. 2016;7:CD012281. doi:10.1002/14651858.CD012281
13. Aagesen AL, Melek M. Choosing the right diagnostic imaging modality in musculoskeletal diagnosis. Prim Care. 2013;40(4):849-861, viii. doi:10.1016/j.pop.2013.08.005
14. Mounsey A, Wilgus A, Slawson DC. Diagnosis and management of endometriosis. AFP. 2006;74(4):594-600.
15. Tu FF, Hellman KM, Backonja MM. Gynecologic management of neuropathic pain. Am J Obstet Gynecol. 2011;205(5):435-443. doi:10.1016/j.ajog.2011.05.011
16. Fritzer N, Tammaa A, Haas D, et al. When sex is not on fire: a prospective multicentre study evaluating the short-term effects of radical resection of endometriosis on quality of sex life and dyspareunia. Eur J Obstet Gynecol Reprod Biol. 2016;197:36-40. doi:10.1016/j.ejogrb.2015.11.007
17. Ouchi N, Akira S, Mine K, Ichikawa M, Takeshita T. Recurrence of ovarian endometrioma after laparoscopic excision: risk factors and prevention. J Obstet Gynaecol Res. 2014;40(1):230-236. doi:10.1111/jog.12164
18. Guzel AI, Topcu HO, Ekilinc S, et al. Recurrence factors in women underwent laparoscopic surgery for endometrioma. Minerva Chir. 2014;69(5):277-282.
19. Hart R, Hickey M, Maouris P, Buckett W, Garry R. Excisional surgery versus ablative surgery for ovarian endometriomata: a Cochrane Review. Hum Reprod. 2005;20(11):3000-3007. doi:10.1093/humrep/dei207
20. Somigliana E, Berlanda N, Benaglia L, Viganò P, Vercellini P, Fedele L. Surgical excision of endometriomas and ovarian reserve: a systematic review on serum antimüllerian hormone level modifications. Fertil Steril. 2012;98(6):1531-1538. doi:10.1016/j.fertnstert.2012.08.009
21. Raffi F, Metwally M, Amer S. The impact of excision of ovarian endometrioma on ovarian reserve: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2012;97(9):3146-3154. doi:10.1210/jc.2012-1558
22. Cohen A, Almog B, Tulandi T. Sclerotherapy in the management of ovarian endometrioma: systematic review and meta-analysis. Fertil Steril. 2017;108(1):117-124.e5. doi:10.1016/j.fertnstert.2017.05.015
23. Keckstein J, Ulrich U, Sasse V, Roth A, Tuttlies F, Karageorgieva E. Reduction of postoperative adhesion formation after laparoscopic ovarian cystectomy. Human Reproduction. 1996;11(3):579-582. doi:10.1093/HUMREP/11.3.579
24. Ahmad G, O’Flynn H, Hindocha A, Watson A. Barrier agents for adhesion prevention after gynecological surgery. Cochrane Database Syst Rev. 2015;(4):CD000475. doi:10.1002/14651858.CD000475.pub3
25. Song T, Kim WY, Lee KW, Kim KH. Effect on ovarian reserve of hemostasis by bipolar coagulation versus suture during laparoendoscopic single-site cystectomy for ovarian endometriomas. J Minim Invasive Gynecol. 2015;22(3):415-420. doi:10.1016/j.jmig.2014.11.002
26. Hartmann KE, Ma C, Lamvu GM, Langenberg PW, Steege JF, Kjerulff KH. Quality of life and sexual function after hysterectomy in women with preoperative pain and depression. Obstet Gynecol. 2004;104(4):701-709. doi:10.1097/01.AOG.0000140684.37428.48
27. Brandsborg B, Nikolajsen L, Hansen CT, Kehlet H, Jensen TS. Risk factors for chronic pain after hysterectomy: a nationwide questionnaire and database study. Anesthesiology. 2007;106(5):1003-1012. doi:10.1097/01.anes.0000265161.39932.e8