Chronic pelvic pain can be defined as cyclic or non-cyclic pain of six or more months in duration that localises to the anatomical pelvis and is severe enough to cause functional disability and require medical or surgical treatment.
Chronic pelvic pain can be defined as cyclic or non-cyclic pain of six or more months in duration that localises to the anatomical pelvis and is severe enough to cause functional disability and require medical or surgical treatment. It is the reason for 10% of all outpatient visits to a gynaecologist . It is responsible for approximately 40% of laparoscopies  and 10-15% of hysterectomies. While chronic pain may not always be curable, it can be managed so those patients attain normal or near-normal levels of function.
Endometriosis and adhesions are responsible for many cases of chronic pelvic pain in women but a significant number of patients have no obvious aetiology for their pain at the time of laparoscopy.
Physiology and anatomy
Pelvic pain is a poorly understood phenomenon. Acute pain is a protective mechanism that alerts the central nervous system to impending peripheral injury. Descartes originally maintained that pain was a simple signal from peripheral pain neurons to the brain (the ‘somatic theory’). Eventually, it became clear that pain is much more complex. The ‘gate theory’ proposes that peripheral nociceptive signals can be modulated by neurotransmitters that can be linked with mood states . These neurotransmitters include serotonin and endorphins. The ‘gateway’ to pain may be opened by depressive states as opposed to direct tissue irritation. Indeed, affective disorders are not uncommon after several months of pain. Thus, interacting psychological and physical factors are likely to be present early in the course of pain and attempts to separate those into a single cause and effect are usually unrewarding . The intensity of the pain may not be proportional to tissue damage, a common finding in chronic pelvic pain. A third theory, the ‘diathesis–stress’ model, proposes that some patients are at increased risk of experiencing chronic pain due to pre-existing vulnerabilities that may be acquired . This might explain why a disproportionate number of chronic pelvic pain patients report histories of sexual abuse.
The pelvic viscera receive neurons from both the sympathetic (thoracolumbar) and parasympathetic (craniosacral) systems. The corpus, cervix and proximal fallopian tubes transmit pain through sympathetic fibres that arise from T10–L1. These fibres include neurons that are part of the uterosacral ligaments, and eventually coalesce into the superior hypogastric plexus (presacral nerve). It should be noted that the presacral nerve does not receive fibres from the ovaries and lateral pelvic structures, which is why a presacral neurectomy is applicable only to midline pain.
The lateral pelvis transmits pain via parasympathetic neurons (nervi erigentes) arising from S2–S4. The presacral nerve divides into the hypogastric nerves that eventually form the inferior hypogastric plexus and this plexus subdivides into vesical, middle rectal and uterovaginal (Frankenhauser’s) plexuses. Frankenhauser’s plexus lies just lateral to the uterosacral ligaments and medial to the uterine arteries and receives pain sensations only from the corpus and vagina. Unlike presacral neurectomy, which can affect bladder and rectal function, transection of Frankenhauser’s plexus during a laparoscopic uterosacral nerve division should not result in constipation or bladder distension.
Approach to the patient
Women with chronic pelvic pain present unique challenges to the clinician. Unlike many gynaecological conditions that are relatively treatable, chronic pelvic pain may not be cured in a large number of patients. This is ultimately unsatisfying for both the patient and physician. In some cases, physicians may become frustrated and ascribe the patient’s pain to psychiatric disease. Many women are also told that they ‘have to live with their pain’. It is unacceptable to tell a patient that she must tolerate chronic pain and that nothing more can be done. It is also inappropriate to make patients feel that their pain is imaginary and ‘in their heads’.
A better approach is one in which the patient is informed that although their pain may not be cured, it can be managed. The chronic pain patient should also be told that their pain is real, even when our limited medical science has failed to elucidate the aetiology of that pain. Patients should be informed, however, that psychiatric support is available to them, not because they are ‘crazy’ but because all patients with chronic disease can benefit from supportive counseling and appropriate psychiatric intervention.
Ultimately, many patients with chronic pelvic pain benefit from sensitive physicians who are willing to spend the time necessary to alleviate what is often a significant threat to the patient’s quality of life. In many cases a multidisciplinary effort produces the best results.
The differential diagnosis of the patient with chronic pelvic pain are:
There is another condition, which may be related to complaints of pelvic pain in those individuals who have had pelvic surgery and now are re-experiencing pain. This is a syndrome whose parallel is the ‘phantom limb’ syndrome in amputees. A neuropathy may develop that is generated from regrowth of nerve tissue or development of a neuroma that causes a reinstigation of the firing of the neural elements in the brain which had previously identified an area as being a source of pain.
Evaluation of a patient with chronic pelvic pain
A complete history is taken and a physical examination performed. If the history and physical examination indicate that gynaecological features are not important, she is referred for evaluation of the other five factors involved in pelvic pain. If at the gynaecological examination abnormal ovarian findings are detected, then ultrasound is performed and the patient is treated accordingly. Laboratory tests are also performed and if they are abnormal, they are treated accordingly. In addition, empirical antibiotics are given if there is clinical evidence of infection in spite of negative cultures. In cases of cyclical pain, nonsteroidal anti-inflammatories (NSAIDs) are given. The patient is told to start the NSAIDs at the first day of the period or, if she can usually tell when she is going to start her period, she can preferably start the medication a day or two before the period [6-7]. This strategy is supported by the evidence that most of the prostaglandins are released during the first 48 hours of menstruation, thus accounting for the clinical features and timing of primary dysmenorrhoea. In this way, the pain receptors are blocked by the NSAID well before the prostaglandins are released and the patient will feel significantly less pain if the mediators of the pain are prostaglandins. The patient is then tried on a course of suppressive oral contraceptive therapy for a period of two to three months. Although there are no studies demonstrating the benefit of oral contraceptive therapy for chronic pelvic pain, this therapy is effective in patients whose major problem is primary dysmenorrhoea. If these therapies were not successful, a laparoscopy would then be advisable or alternatively, the patient could be tried on a three months course of GnRH analogue.
The physical examination differs from the classic bimanual examination. After a careful abdominal examination, one should initially palpate the pelvic structures with one hand on the lower abdomen, avoiding the use of the other hand until later in the examination. All painful areas should thus be recorded. Abdominal wall pain may be distinguished from visceral pain by the classic maneuver of having the patient tense their abdominal muscles. If the pain increases, it may be ascribed to an abdominal wall process, whereas visceral pain will decrease with abdominal muscle tensing. Finally, a bimanual examination may be done, with the most tender areas palpated last. Uterosacral nodularity may be assessed via a rectovaginal examination.
Investigations may include a pregnancy test, full blood count, high vaginal swab culture and endocervical swab for chlamydia and ultrasound, although the latter is often of limited value.
Irritable bowel syndrome
Irritable bowel syndrome (IBS) is a common cause of chronic pelvic pain. It is associated with many non-colonic features including dyspareunia and is more prevalent in young women. The diagnosis is made on the history alone and, although results of special investigations are by definition negative, the diagnosis should not simply be one of exclusion. One study found that many women with IBS consult gynaecologists rather than gastroenterologists but that these patients rarely had gynaecological pathology . Another study reviewing the prevalence of IBS in the gynaecological outpatient department at the University Hospital of South Manchester found that dyspareunia was strongly associated with IBS . There was also an increased prevalence of IBS in women referred for menorrhagia and intermenstrual bleeding. Of all women referred to the clinic for pelvic pain, 50% had symptoms suggesting IBS. It has been found that 34% of women who deny chronic bowel symptoms report a change in bowel habits with the onset of menstruation and a higher proportion of women with IBS report a worsening of bowel symptoms during menstruation [10-11]. Conversely, gynaecological disease may also be misdiagnosed as IBS  – a situation that can be clarified via hormone suppression.
To diagnose IBS the patient should have chronic pain and at least two (preferably three) of the following features:
Conscious pain mapping
This is a microlaparoscopic technique in which the patient is sedated but can respond to questions during surgery that allows the gynaecologist to better correlate operative findings with symptoms. It can help to distinguish abdominal wall pain from gynaecological pain and may facilitate identification of vague endometriotic lesions. In some cases, the patient may pinpoint painful areas in the pelvis that do not correlate with overt pathology . The utility of conscious pain mapping, which can be done in an outpatient clinic, is still debatable but appears promising.
Endometriosis is found in a high percentage of patients who are carefully screened to eliminate other potential causes of chronic pelvic pain. The prevalence of each American Fertility Society (AFS) class of endometriosis in patients with chronic pelvic pain was studied  (Table 1). For 130 patients in whom a laparoscopic diagnosis of endometriosis was made, six months of gonadotrophin-releasing hormone (GnRH) therapy was provided as the only treatment. After five years, 46.6% of treated patients were free of symptoms. These patients were evaluated by laparoscopy for two years and then followed very carefully with questionnaires for an additional three years. The recurrence rate of pain symptoms in five years was evaluated by AFS class  (Table 2). 53.4% of women treated with GnRH agonist alone had a recurrence of symptoms during the time period of study. 46.6% of women treated with GnRH analogues alone were cured and had no recurrence during the five-year time period of the study.
Thus, once a determination has been made that a patient has a gynaecological cause for the CPP, endometriosis is the most prevalent disease and minimal to mild endometriosis is most frequently found at laparoscopy. Minimal or mild disease is also that disease which most completely responds to GnRH agonist alone.
The question then occurs as to whether it is cost-effective and efficacious to initiate endometriosis specific GnRH agonist therapy prior to laparoscopic diagnosis on the basis of clinical judgment. A cost/benefit analysis comparing GnRH agonist therapy with laparoscopy for clinically diagnosed endometriosis was performed to determine if this is reasonable. A cost comparison of a two-month trial of GnRH therapy to diagnostic/therapeutic laparoscopy for all patients who failed treatment with oral contraceptives and NSAIDs and for whom a clinical diagnosis of endometriosis had been made was performed . The result of the study concluded that GnRH agonist as a diagnostic/therapeutic modality will save almost one half the total cost of treatment of endometriosis as a cause of pelvic pain. In addition, as a diagnostic/ therapeutic modality it will save 50% of the patients the need for an operative procedure.
Effectiveness of laparoscopy
All the risks of laparoscopy might be acceptable if the diagnosis and treatment by laparoscopy was much more successful than medical therapy. In a landmark article, the role of laparoscopy in chronic pelvic pain was evaluated. Less than 50% of women with chronic pelvic pain were found to be helped by diagnostic and operative laparoscopy. Both physicians and patients must recognise that laparoscopy is not the ultimate evaluation for chronic pelvic pain. In fact, about 40% of women with chronic pelvic pain had no apparent pathology at laparoscopy .
Treatment for negative laparoscopies
It is important that women with chronic pelvic pain and negative laparoscopies are provided an opportunity for treatment with GnRH agonist because endometriosis is the most likely diagnosis missed in such patients, if their disorder is gynaecological.
Pelvic congestion syndrome is not easy to diagnose. It tends to cause acute exacerbations in addition to the chronic pain . Unilateral pain increased by prolonged standing, walking or lifting and relieved by lying down is common. Other symptoms are postcoital ache that may last for a few days and, less commonly, actual dyspareunia. This condition is rarely diagnosed at laparoscopy, as the incompetent veins are retroperitoneal and usually empty in the supine position. The diagnosis can usually be achieved by pelvic venography. In one study, 91% of patients with chronic pelvic pain with a negative laparoscopy have venographic evidence of this condition . Hormonal suppression is the initial mode of treatment in women with suspected pelvic congestion. Thus, again, GnRH agonist would be useful for patients with negative laparoscopy. It is critical that patients are completely evaluated by psychological, gastrointestinal, urological, gynaecological, myofascial and musculoskeletal examinations to avoid the risk that they may undergo an unnecessary procedure.
The role of adhesions in chronic pelvic pain has been questioned. A retrospective study comparing asymptomatic infertile patients with women who had chronic pelvic pain did not reveal a significant difference in the density or location of adhesions. A randomised clinical trial on the benefits of adhesiolysis by laparotomy showed no benefit in patients with light or moderate pelvic adhesions. Patients with severe adhesions involving the intestinal tract benefited from this procedure .
Excision of endometriosis
Laser and cautery methods do not adequately treat deeply infiltrating endometriosis (often >5 mm invasive), whereas excision allows for therapeutic removal of lesions and corroborative histology. Excision of endometriotic lesions is generally with higher fertility rates than medical treatment with hormonal modulators. Hormonal modulation, however, can be successful in place of surgery for alleviating pelvic pain. There is no proven benefit to adjuvant medical therapy after extensive laparoscopic resection of endometriosis and it may decrease fertility rates as well. Ovarian endometriomas are a source of severe chronic pain  and their removal by stripping techniques or laser photovaporisation of the capsule provides gratifying results in terms of relief .
Role of presacral neurectomy
For patients with severe disabling central dysmenorrhoea, presacral neurectomy was effective in a well-controlled prospective study. Success rates of 73% in relieving dysmenorrhoea, 77% in relieving dyspareunia and 63% in relieving other pelvic pains were achieved by presacral neurectomy in 50 patients treated for chronic pelvic pain after failing to respond to oral contraceptives and NSAIDs . Uterosacral ligament resection did not increase the success rate over presacral neurectomy alone, which may be accomplished via laparotomy or laparoscopy. Presacral neurectomy has been associated with catastrophic haemorrhage from the middle sacral vessels. Patients should be apprised of potential long-term constipation and urinary retention.
Laparoscopic uterosacral nerve ablation
The division of these ligaments relieved pain in patients enrolled not only in retrospective studies, but also in patients in a randomised prospective study [24-26].
Laparoscopic uterosacral nerve ablation (LUNA) is accomplished more readily than presacral neurectomy but may be much less effective in the long term. As only the uterovaginal portion of the inferior hypogastric plexus is affected, bladder and bowel symptoms are avoided. However, as in presacral neurectomy, individual variations in technique affect efficacy rates and the lack of uniformity has clouded study results. Some surgeons divide the uterosacral ligaments with either laser or scissors; other practitioners resect much if not all of the ligaments and even make attempts at isolating Frankenhauser’s plexus itself. Some studies report excellent effectiveness but these involve small patient populations. If patients have endometriosis, it is possible that success may be influenced more by the resection of endometriosis than by concurrent LUNA. Ureteral injury has been reported in expert hands.
All uterine denervation procedures fail to treat lateral pain and are only indicated in patients who suffer central uterine pain. Furthermore, a presacral nerve block can result in similar pain relief as PSN without the attendant surgical morbidity.
Hysterectomy with bilateral oophorectomy was effective in women who failed to obtain long-term relief of pain with oral contraceptives and nonsteroidal anti-inflammatory medications. These women were diagnosed with pelvic congestion syndrome, although pathology revealed that 25% had adenomyosis. Of 99 women who underwent hysterectomy for chronic pelvic pain of at least six month’s duration and whose disease by symptoms and examination was confined to the uterus, 77.8% had significant improvement and 22.2% had persistent pain .
Once widely used for a multitude of gynaecological and non-gynaecological conditions, there is little to justify the routine use of uterine suspension. Occasional patients with symptoms attributable to an incarcerated uterus may benefit but this is largely anecdotal. Some surgeons believe that uterine suspension may prevent substantial ovarian adhesions after conservative surgery for endometriosis; again, this is unproven.
Chronic appendicitis does exist and can be the cause of chronic lower abdominal pain. In five recent reports, appendectomy resulted in relief of symptoms of right lower quadrant pain in selected patients [28-31]. In addition, there appears to be no correlation between visible pathology, histopathology and complaints of pain relieved by appendectomy.
Appendiceal endometriosis has been found in 3–5% of women with endometriosis. Fecaliths can also produce chronic pain without full-blown appendicitis.
Every patient with chronic pelvic pain is different. Some present initially to a gynaecologist and may receive definitive laparoscopic and/or medical treatment. Unfortunately, a great number of women are not helped by their initial provider and they typically migrate from one physician to the next in search of pain relief. It is not uncommon for such a patient to have seen four or more providers and receive several laparoscopies and laparotomies. By this time, a true pain syndrome exists in which there is a great degree of interference with daily activities. Further surgery is unlikely to benefit this patient, who is often dismissed as mentally impaired.
In these seemingly intractable cases, one specialist is not adequate to remedy a chronic pain syndrome and this is where a multidisciplinary effort is helpful. The patient can be seen jointly by gynaecologist, anaesthetist, psychiatrist and additional specialists who then combine their resources to manage the patient’s chronic pain syndrome. The goal is not always to ‘cure’ pain so much as to allow the patient to function more normally and have a better quality of life.
|AFS CLASS||percentage of patients with C.P.P.|
|Class I - Minimal Disease||42%|
|Class II - Mild Disease||36%|
|Class III - Moderate Disease||28%|
|Class IV - Severe Disease||4%|
|Total Class I and II||78%|
|Total Class III and IV||32%|
|AFS CLASS||Recurrence Rate|
|Class I - Minimal Disease||25.6%|
|Class II - Mild Disease||55.8%|
|Class III - Moderate Disease||42.8%|
|Class IV - Severe Disease||66.7%|
Coressponding author: Dr. Tarek A. Gelbaya
Address: Ardyia 92400, PO Box 420, Kuwait
E mail : firstname.lastname@example.org
1. Reiter RC. Chronic pelvic pain. Clin Obstet Gynecol. 1990;33:130-136.
2. Howard FM. The role of laparoscopy in chronic pelvic pain: promise and pitfalls. Obstet Gynecol Surv.1993; 48:357-387.
3. Melzack R. Neurophysiologic foundations of pain. In: Sternbach RA, Ed. The psychology of pain. New York: Raven Press, 1986: 1-24.
4. Schaffer CB, Donlon PT, Bittle RM. Chronic pain and depression: a clinical and family history survey. Am J psychiatry 1980; 137: 118-20.
5. Walker E, Katon W, Harrop-Griffiths J et al. Relationship of chronic pelvic pain to psychiatric diagnosis and childhood sexual abuse. Am J Psychiatry 1988; 145 75-80.
6. Prostaglandinas menstruales y dismenorrea su modulacion por antiinflamatorios no esteroideos. Aires B. Medicina. 1999; 59 (3): 259-64.
7. Tratamiento profilactico de la dismenorrea primaria con ibuprofen. Pedron Nuevo N, Gonzalez-Unzaga M, Medina Santillan R. Ginecol Obstet Mex 1998 June; 66:248-52.
8. Prior A, Whorwell PJ. Gynaecological consultation in patients with the irritable bowel syndrome. Gut. 1989; 30:996-998.
9. Prior A, Wilson K, Whorwell PJ, Faragher EB. Irritable bowel syndrome in the gynecological clinic. Survey of 798 new referrals. Dig Dis Sci. 1989; 34:1820-1824.
10. Whitehead WE, Cheskin LJ, Heller BR, et al. Evidence for exacerbation of irritable bowel syndrome during menses. Gastroenterology. 1990; 98:1485-1489.
11. Whitehead WE, Schuster MM. Gastrointestinal Disorders: Behavioral and Physiologic Basis for Treatment. San Diego, CA: Academic Press; 1985:155-177.
12. Mathias JR, Ferguson KL, Clench MH. Debilitating ‘functional’ bowel disease controlled by leuprolide acetate, gonadotropin-releasing hormone (GnRH) analog. Dig Dis Sci. 1989; 34:761-766.
13. Palter SF, Olive Dl. Office microlaparoscopy under local anaesthesia for chronic pelvic pain. J Am Assoc General Laparosc 1996; 3: 359-64.
14. Koninckx PR, Lesaffre E, Meuleman C, et al. Suggestive evidence that pelvic endometriosis is a progressive disease whereas deeply infiltrating endometriosis is associated with pelvic pain. Fertil Steril. 1991; 55: 759-765.
15. Waller KG, Shaw RW. GnRH analogues for the treatment of endometriosis: long-term follow-up. Fertil Steril. 1993; 59:511-515.
16. Carter JE. Cost effective management of women with chronic pelvic pain. Keio J Med. 1995; 44:96.
17. Mathias SD, Kuppermann M, Liberman RF, Lipschutz RC, Steege JF. Chronic pelvic pain: prevalence, health-related quality of life, and economic correlates. Obstet Gynecol 1996; 87: 321-7.
18. Beard RW, Reginald PW, Wadsworth J. Clinical features of women with chronic lower abdominal pain and pelvic congestion. Br J Obstet Gynaecol 1988; 95: 153.
19. Beard RW, Highman JH, Pearce S, Reginald PW. Diagnosis of pelvic varicosities in women with chronic pelvic pain. Lancet 1984; 2:946.
20. Steege JF, Stout AL. Resolution of chronic pelvic pain after lysis of adhesions. Am J Obstet Gynecol. 1991; 165:278-283.
21. Daniell JF, Kurtz BR, Gurley LP. Laser laparoscopic management of large endometriomas. Fertil Steril. 1991; 55:692-695.
22. Rock JA. Endometriosis and pelvic pain. Fertil Steril. 1993; 60:950-951.
23. Lee RB, Stone K, Magelssen D, et al. presacral neurectomy for chronic pelvic pain. Obstet Gynecol.1986; 68:517-521.
24. Daniell JF, Feste J. Laser laparoscopy. In: Kai WR, ed. Laser Surgery and Gynecologic Obstetrics. Boston, Mass: GK Hall; 1985:147-165.
25. Sutton CJG. Laser uterine nerve ablation. In: Donnez J, ed. Laser Operative Laparoscopy and Hysteroscopy. Leuven, Belgium: Nauwelaerts Printing; 1989:43-52.
26. Lichten EM, Bombard J. Surgical treatment of dysmenorrhea with laparoscopic uterine nerve ablation. J Reprod Med. 1987; 32:37-4
27. Stovall, TG, Ling FW, Crawford DA. Hysterectomy for chronic pelvic pain of presumed uterine etiology. Obstet Gynecol. 1990; 75:676-679.
28. Bryson K. Laparoscopic appendectomy. J Gynecol Surg. 1991; 7:93-95.
29. Fayez JA, Toy NJ, Flanigan TM. The appendix as the cause of chronic lower abdominal pain. Am J Obstet Gynecol. 1995; 172:122-123.
30. Al-Sailli M, Vilos GA. Retrospective evaluation of laparoscopic appendectomy in women with chronic right lower quadrant pain. J Am Assoc Gynecol Laparosc. 1995; 2:139-142.
31. Daniell JF, Kurtz BR, McTavish G, et al. Incidental appendectomy: preventive and therapeutic. Gynaecol Endosc. 1994; 3:221-223.
Editor's Note: The use of GnRHa therapy in undiagnosed endometriosis and for pelvic congestion is controversial and is not necessarily endorsed by the Editorial Board of OBGYN.net Chronic Pelvic Pain