{"paper_id":"79307010-8b5d-4269-9366-6fc6a43f260d","body_text":"Annals of Agricultural and Environmental Medicine 2016, Vol 23, No 2, 223–226\nwww.aaem.plREVIEW  ARTICLE \nChronic pelvic pain\nSlawomir Wozniak1\n1 3rd Department of Gynecology, Medical University, Lublin, Poland\nWozniak S. Chronic pelvic pain. Ann Agric Environ Med. 2016; 23(2): 223–226. doi: 10.5604/12321966.1203880\nAbstract\nIntroduction.  Chronic pelvic pain (CPP) affects about 10–40% of women presenting to a physician, and is characterised \nby pain within the minor pelvis persisting for over 6 months.  \nMaterials and method. The Medline database was searched using the key words ‘chronic pelvic pain’ and ‘pelvic congestion \nsyndrome’, published in English during the past 15 years.  \nThe condition markedly deteriorates the quality of life of the affected. Its aetiology has not been fully described and elucidated, \nalthough organic, functional and psychosomatic factors are implicated. Pain associated with parametrial varices was defined \nas pelvis congestion syndrome (PCS). Since the aetiology of CPP is complex, multi-directional diagnostic procedures are \nrequired.  \nResults. The main diagnostic methods employed are imaging examinations (ultrasound, computer tomography, magnetic \nresonance). Advances in interventional radiology considerably contributed to the CPP treatment. Currently, embolization \nof parametrial vessels is one of the most effective methods to relieve pain associated with pelvic congestion syndrome.  \nConclusions. Due to the complex aetiology of chronic pelvic pain, the most beneficial effects are obtained when the therapy \nis based on cooperation of the gynaecologist, physiotherapist, psychologist and interventional radiologist.\nKey words\nchronic pelvic pain, pelvic congestion syndrome, parametrial varices\nINTRODUCTION\nChronic Pelvic Pain (CPP)  is defined as continuous or \nintermittent pain located in the hypogastrium (minor pelvis) \npersisting for more than 6 months. CPP is a widespread \ncondition affecting about 1 in 6 adult females [1]. Increased \npain deteriorates the quality of life of the patients and requires \npharmacological treatment or surgical interventions. It is \nestimated that about 3.8% of women at any age and 12% of \nthose at reproductive age complain of chronic pain sensations \nin the minor pelvis region [2]. Data from the United Kingdom \nreveal that about 18% of women take one day of sick leave \nannually due to CPP. The findings reported by Perry et al. \nindicate that about 2–10% of women presenting to the \nGynaecological Outpatient Department suffer from CPP, of \nwhom about 20% undergo diagnostic laparoscopy. According \nto Gelbay et al., 10%-15% of CPP patients are qualified for a \nhysterectomy [3, 4, 5].\nThe aetiology of CPP has not been fully defined and \nelucidated. The causes are usually complex. Several pain-\ninducing factors are implicated. Acute pain is caused by \ntissue damage and decreases or subsides simultaneously \nwith healing. Since the aetiology of chronic pain is affected \nby some additional factors, it can persist long after the \ntissue  injury  has healed or occur despite its absence. \nThe  lesions  involve both the ascending and descending \ntracts of the central and peripheral nervous system. The \nimmunological factors inducing peripheral nervous system \ndysfunction and activating normally inactive fibres, including \ncytokines, such as tumour necrosis factor α (TNF-α) and \nchemokines.\nThe above-mentioned locally secreted factors cause \ndysaesthesia involving a larger area than primarily affected by \nthe pathology. Long-term pain can also enhance the primary \npain stimulus, which leads to visceral hyperalgesia. Surgery-\nrelated damage to nervous fibres, injury, or inflammation, \ncan induce or increase pain sensations [5, 6]. According to the \nRoyal College of Obstetricians and Gynaecologists (RCOG), \nthe aetiological factors causing pain can be divided into those \nthat are gynaecological and extra-gynaecological [7]. The \ngynaecological factors causing CPP include:\n•\t endometriosis / adenomyosis\n•\t pelvic congestion syndrome\n•\t uterine fibroids\n•\t ovarian tumours\n•\t pelvic inflammatory disease\n•\t post-operative or post-inflammatory adhesions.\nThe extra-gynaecological factors causing CPP are as \nfollows:\n•\t surgical (chronic appendicitis, adhesions)\n•\t urological (interstitial cystitis, chronic urinary \ninflammation, urolithiasis, urethra syndrome)\n•\t gastrointestinal (irritable bowel syndrome, constipations, \ninflammatory bowel diseases)\n•\t ortho-neuro-muscular (degenerative changes, \nneuropathies, prolapse of the nucleus pulposus, nerve \nincarceration)\n•\t psychosomatic (depression, sleep disorders, anxiety, \nmigraine with abdominal symptoms, history of sexual \nabuse)\n•\t neurological (nerve incarceration in the scar inducing \nchronic pain in the region supplied by the affected nerve; \nin about 3.7% of cases it is caused by a single Pfannenstiel \nincision).\nEndometriosis and adenomyosis are common causes of \nCPP. According to Neis, endometriosis is diagnosed in about \n1/3 of women with CPP and in less than 5% of those without \nCPP [8].\nAddress for correspondence: Slawomir Wozniak, 3rd Department of Gynecology, \nMedical University, Lublin, Poland\nE-mail: slavwo7572@gmail.com\nReceived: 17 April 2014; accepted: 18 July 2014\n\nAnnals of Agricultural and Environmental Medicine 2016, Vol 23, No 2\nSlawomir Woznia k. Chronic pelvic pain\nEndometriosis develops primarily in reproductive \nage women, between 15–49 years of age, yet may also be \ndiagnosed during puberty and after menopause. Typical \nsymptoms of endometriosis, as well as adenomyosis, include \ndysmenorrhoea, dyspareunia, and chronic pelvic pain [2]. The \nseverity of symptoms depends on the stage of endometriosis \naccording to the American Society for Reproductive Medicine \nClassification for Endometriosis (ASRM), size and number \nof endometriosis lesions, involvement of the Douglas sinus \nand number of surgical interventions in the pelvic region [9]. \nRandal et al. demonstrated that women complaining of CPP \nand with suspected endometriosis had significantly higher \nlevels of antiendometrial antibodies (AEAs), regulatory T \nlymphocytes (Tregs), nerve growth factor (NGF) in the area \naffected by endometriosis and vascular endothelial growth \nfactor (VEGF) [10]. The immune response is modulated, \namong other factors, by increased levels of estrogens, which \nis observed in patients with endometriosis. According to \nthe literature data, these mechanisms are likely to underlie \nCPP causing the ingrowth of nerve fibres to the endometrial \nectopic foci and neoangiogenesis in nerves. This mechanism is \nimplicated in the enhancement of pain sensations. Moreover, \navailable reviews regarding this issue indicate that pain \nis attributable to increased inflammation. The literature \nfindings demonstrate that women with endometriosis have \nhigher levels of inflammatory factors in the peritoneal fluid \nand blood serum [2, 11, 12]. Significantly higher levels of \nleptin and 6-keto-prostaglandin F1 alpha (6-KF) were found \nin the peritoneal fluid in women with endometriosis [13, \n14, 15]. According to Drosdzol-Cop et al., adolescent girls \ndiagnosed with endometriosis have statistically significantly \nhigher serum levels of interleukin 4 (IL-4). Moreover, \nsignificantly decreased levels of IL-2 and increased levels of \nIL-6, tumour necrosis factor – α (TNF-α) and glycodelin A, \nwere noted in the study group [16].\nPelvic congestion syndrome (PCS) is believed to be one of \nthe causes of CPP. The aetiology of PCS has not been fully \nexplained. The theory regarding the pain due to dilation of \nvenous vessels and reduced flow in pelvic vessels was first put \nforward by Taylor in 1949 [17]. One of PCS factors is likely to \nbe failure or lack of the valve system in the peri-ovarian and \nparametrial veins. The anomaly of vessels causes retrograde \nflow to the ovarian vessels, which results in visibly dilated \nveins and varices. The lack of valves near the ovarian vessel \nramification is found in about 15% of women; the failure of \nthe valve system is diagnosed in 40% of cases on the left side \nand in 35% of patients on the right side [18, 19]. Mechanical \nvessel compression impairs blood flow, e.g. improper position \nof the uterus or shift of the uterus can cause the compression \nof the left renal vein between the aorta and the inferior \nmesenteric artery. Veins can increase their volume by about \n60% and therefore symptoms are initially less distinct [20, 21].\nMoreover, 15% of women aged 20–50 are diagnosed with \npelvic varices, which are not always symptomatic. The risk \nfactors of pelvic congestion syndrome include the number \nof pregnancies >=2, varices of the lower limbs, polycystic \novary syndrome and hormonal disorders. Increased levels \nof estrogens correlate with the development of PCS. By \nweakening the vascular walls, estrogens may induce varices. \nThe incidence of PCS is found to be higher in women before \nmenopause. Hormonal changes occurring during pregnancy \nand the enlarging uterus increase the volume of pelvic veins \nby even 60%, slowing down the blood flow, causing the mass \neffect and compressing the adjacent nerves, which results \nin pain sensations. Moreover, the uterus may also compress \nvessels, which may lead to the development of pain and PCS \n[19, 20, 21].\nPCS is characterised by a chronic, dull, continuous pain, \nwhich often increases after intercourse, before or during \nthe first days of menstruation, in the standing and sitting \nposition, during pregnancy, and in cases of irregular \nmenstruation and perineal varices. In the majority of cases, \npain occurs on the side of venostasis, less frequently on the \nopposite side. PCS can also be accompanied by urinary \nsymptoms caused by perineal varices, lumbosacral pain, \nnausea, flatulence, cramping abdominal pains. The physical \nexamination reveals varices along the saphenous vein and \npain sensations in the ovarian projection.\nPelvic Doppler ultrasound is the first-line imaging \nexamination used for PCS diagnosis. In cases of PCS, the \nexamination shows enhanced flows within the minor pelvis \n[20, 21]. Park et al. visualised pelvic minor varices in 53% \nof the female population [22]. In the majority of centres, \ncomputer tomography with contrast has replaced venography \nfor imaging vessels of the minor pelvis. An alternative method \nwithout contrast is magnetic resonance imaging (MRI). MRI \nvisualises the dilated, tortuous vessels in the area of the \novary and uterus, which can reach the broad ligament of the \npelvis or the pelvic wall. The use of gadolinium increases the \nsensitivity of this examination by mapping the vessels of the \nminor, and precisely localises the pathology [21].\nLaparoscopy used for the diagnosis of CPP may not visualise \nthe dilated vessels. Increased abdominal pressure can \ncompress the vessels and mask the presence of pathologically \ndilated vessels. The results of diagnostic laparoscopy in PCS \nare normal in 80–90% of cases [21]. However, in certain cases, \nlaparoscopy enables visualisation of the causes of PCS, e.g. \nfoci of endometriosis.\nThe treatment of PCS is mainly dependent on the severity \nof pain. Symptomatically acting analgesics, i.e. non-\nsteroidal anti-inflammatory drugs, are used. In cases of \npain associated primarily with menstruation, contraceptive \npills are used to reduce the heaviness of menstruation or as \ncontinuous therapy to inhibit menstruation. Moreover, the \nuse of medroxyprogesterone for the treatment of PCS has \nbeen described in some prospective studies. Thanks to its \nvasoconstricting properties, six-month therapy alleviated \npain sensations and suppressed symptoms reported by \npatients. However, the effect was not long-lasting. Pain has \nalso been treated with gonadotropin-releasing hormone \n(GnRH) agonists with hormones used for hormone \nreplacement therapy (HRT), dihydroergotamine, goserelin, \ndanazol, and substances reconstructing the vascular wall \n[20, 23–26].\nOnce pharmacological treatment options have failed, \ninvasive methods are applied. Prior to the development of \ninterventional radiology, hysterectomy with salpingectomy \nor ovariectomy was performed. At present, one of the \nmost common methods providing satisfactory outcomes is \nembolization. The procedure was first used for the treatment \nof PCS by Edwards et  al. in 1993 [27]. An X-ray-guided \ncatheter is introduced through the femoral vein to the \nvaricose vein. Subsequently, an embolization spiral is inserted \ninto the dilated area, which closes the pathological vessel. \nProspective studies carried out by Kim et al., demonstrate \nthat during the 48-month observation period the procedure \n224\n\nAnnals of Agricultural and Environmental Medicine 2016, Vol 23, No 2\nSlawomir Woznia k. Chronic pelvic pain\nwas effective in 83% of cases. No beneficial effects were found \nin 13% of patients, whereas deterioration of symptoms was \nobserved in 4% of cases. There were no side-effects, such as \nabnormal menstruation or hormonal imbalance. Moreover, \nthe embolisation procedure did not reduce fertility in the \nexamined group. [21, 28].\nThe aetiology of CPP is complex and therefore multi-\ndirectional diagnostic procedures are required. The first \nstep involves history taking and physical examination. An \nimportant element of history taking is to determine the \nfactor inducing or increasing pain, and to assess the effects \nof pain on the quality of life as well as the way of coping with \nit. The diagnosis of CPP also includes imaging examinations, \ni.e. transabdominal and transvaginal ultrasound of the \nreproductive system and pelvis, computer tomography \n(CT), magnetic resonance imaging (MRI) and venography. \nUltrasound is used to exclude other organic changes that \ncould induce CPP, i.e. ovarian pathology, uterine fibroids, \nadenomyosis or dilated vessels of adnexa. The use of colour \nDoppler ultrasound enables visualisation of increased flow \nin the parametrial vessels. Park et al. have determined the \ndiagnostic CPP criteria for transvaginal and transabdominal \nultrasound examinations [7, 20, 21, 22], which include:\n•\t tortuous veins of the pelvis of a diameter >6 mm\n•\t slowed down or retrograde vascular flow\n•\t dilated, arched vein within the myometrium \ncommunicating bilaterally with pelvic varices\n•\t polycystic image of ovaries.\nThe diagnostic procedures for CPP also include biochemical \nblood tests, bacteriological tests, cystoscopy, and contrast \nexaminations of the large intestine. Diagnostic laparoscopy \nis performed in 40% of CPP cases. The procedure enables \nfinding the foci of endometriosis in 1/3 of cases and adhesions \nin ¼ of patients; however, in 1/3 of cases it does not visualise \nthe possible cause [29].\nBased on a meta-analysis by Latthe et al., the risk factors \nof chronic pelvic pain have been determined. They include: \ndysmenorrhoea in women < 30 years of age, Body Mass \nIndex (BMI)< 20, smoking, menarche at the age<12 years, \nlong menstruation cycles, prolonged and irregular menstrual \nbleedings, symptoms of premenstrual syndrome, infertility, \nhistory of sexual abuse, mental disorders (e.g. depression, \nanxiety, hysteria) [30, 31].\nThe treatment of CPP is multi-directional. The first stage \nalgorithms involve pharmacological therapy. Once ineffective, \ninterventional procedures are instituted. The pharmacological \nagents minimising pain include analgesics (NSAIDs, \nopioids), antibiotics, contraceptive pills, progestagens, \nGnRH agonists, danazol. According to the RCOG, hormonal \ntherapy should be used for 3–6 months. Reginald et al., who \nused dihydroergotamine in patients with PCS, observed \nreduced passive congestion and alleviated pain sensations. \nThe administration of 30 mg of medroxyprogesterone acetate \n(MPA) daily decreased the features of congestion within the \npelvis observed on venography and reduced the severity of \npain. The alternative method of PCS treatment is ovarian and \ninternal iliac vein embolization. Surgical procedures used \nto reduce CPP depend on the likely cause of complaints and \ninclude the following: removal or vaporisation of the vulval \nor vestibular abnormal tissue, caused by the inflammation \nof vestibular glands or vulvodynia, hysteroscopic removal of \nlesions visualised in the uterine cavity, myomectomy, lysis \nof intraperitoneal adhesions, removal of endometriosis foci, \ndisruption of conduction pathways – presacral neurectomy \n(PSN), laparoscopic uterine nerve ablation (LUNA) in cases \nof dysmenorrhoea, adhesions, in the course of endometriosis, \nadenomyosis, CPP of indiscernible causes, appendectomy, \nsurgical hernia ring closure, and trigger point therapy (local \nanaesthesia) [7, 24–26].\nData available in the Cochrane library compare the \npharmacological and non-pharmacological methods used \nto relieve chronic pelvic pain. The extent of pain reduction, \nquality of life, adverse side-effects and economic benefits \nwere evaluated in a randomised study. Several groups were \ndistinguished in which the following were used: changes in \nlifestyle, psychotherapy, physiotherapy, pharmacotherapy \n(non-steroidal anti-inflammatory drugs, DTA, progesterone, \nIUD, Danazol, GnRH analogues, drugs affecting venous \nvessels, antidepressants, antiepileptic drugs, analgesics), \nsurgical interventions (laparoscopy, hysterectomy, \noophorectomy).\nThe exclusion criteria were endometriosis, irritable \nbowel syndrome, primary dysmenorrhoea, pain syndrome \nassociated with chronic inflammation. Reduced pain was \nobserved in the groups treated with MDA and goserelin. \nOtherwise, the liberation of adhesions, sertraline and \nlaparoscopic disruption of conduction pathways did not \nresult in pain elimination [25, 26, 32, 33].\nCONCLUSIONS\nDue to the complex aetiology of chronic pelvic pain, the most \nbeneficial effects are obtained when the therapy is based on \ncooperation between the gynaecologist, physiotherapist, \npsychologist and interventional radiologist.\nFigure 1. Magnetic resonance scan showing enhanced, bilateral tortuous pelvic \nveins\n225\n\n\nAnnals of Agricultural and Environmental Medicine 2016, Vol 23, No 2\nSlawomir Woznia k. Chronic pelvic pain\nFigure 2. Gray-scale (a) and colour Doppler (b) ultrasound images demonstrate \ncongested pelvic veins\nREFERENCES\n1. Zondervan KT, Yudkin PL, Vessey MP. The community prevalence of \nchronic pelvic pain in women and associated illness behaviour.  Br J \nGen Pract. 2001; 51: 541–7.\n2. 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