Chronic Pelvic Pain



Chronic Pelvic Pain


Howard T. Sharp



Science has produced many drugs, therapies, and surgeries in an attempt to relieve the suffering associated with chronic pelvic pain (CPP). Unfortunately, only modest success has been achieved. This is likely in part due to the heterogeneity that exists in this ill-defined population of patients as well as our limited understanding of pain modulation. Often, when standard therapies fail or when no visible pathology can be identified, other specialties are consulted such as gastroenterology, urology, neurology, or psychiatry. Patients may eventually be referred to centers specializing in CPP or empiric pain management, wherein opioid therapy may be commenced without finding a specific cause for pain.

Along the course of therapy and referral, frustration is often a by-product of treating a supposed remediable pain state only to have pain persist. Clinically, part of the diagnostic challenge is to decipher whether (a) a defined pain state exists that has not yet been diagnosed or treated, (b) a defined pain state exists and has been identified correctly but happens to be present in an incidental form (e.g., asymptomatic endometriosis), and/or (c) a neuropathic pain processing state is present.

The focus of this chapter is to review several putative causes of pelvic pain that should be considered in patients who present with CPP and to review history taking, physical examination techniques, and treatment options.


Definitions



  • Allodynia: Pain due to a stimulus which does not normally provoke pain.*


  • Central pain: Pain initiated or caused by a primary lesion of dysfunction in the central nervous system.*


  • Chronic pelvic pain: Nonmenstrual pain of 6 months duration or greater, localized to the pelvis, anterior abdominal wall below the pelvis, or lower back, severe enough to result in functional disability or require medical or surgical treatment.


  • Dysesthesia: An unpleasant abnormal sensation, whether spontaneous or evoked.*


  • Endometriosis: The existence of two or more of the following outside of the endometrium: (a) endometrial epithelium, (b) endometrial stroma, (c) endometrial glands, (d) hemosiderin-laden macrophages.


  • Hyperalgesia: An increased response to a stimulus which is normally painful.*


  • Myofascial pain syndrome: A heterogeneous pain-producing disorder characterized by localized, reproducible, hyperirritable trigger points within a muscle or its investing fascia.


  • Neuropathic pain: Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the peripheral or central nervous system.*


  • Neuralgia: Pain in the distribution of a nerve or nerves.*


  • Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of damage.*


Contemporary Pain Theories

Until the 1960s, pain was considered a sensory response to tissue damage. It is now widely accepted that pain has a reactive or emotional as well as sensory component that is influenced by genetic differences, past experiences, gender, anxiety, or expectation. The perception of and response to pain are believed to be determined by four simultaneous processes that include transduction (depolarization of a peripheral sensory nerve ending to generate an impulse), transmission (neural events to carry the impulse), modulation (neural events that control transmission neurons), and perception (event processing influenced by behavioral and emotional factors).


The theory most widely accepted to explain the mechanism whereby pain transmission occurs was described by Melzak and Wall as the gate control theory. This theory suggests that the modulation of nociception at the spinal cord is mediated by descending signals for high centers within the brain through neurotransmitters. It describes a bidirectional gate at the level of the spinal cord rather than merely unidirectional pain transmission as previously held by the Cartesian theory.


Putative Pelvic Pain States


Adhesions

Pelvic inflammatory disease (PID), endometriosis, inflammatory bowel disease, or prior surgery may cause adhesions; yet, in up to 50% of cases, there may be no significant antecedent event. Though adhesions are commonly found in patients with CPP, it may be difficult to assess whether they are contributing to pelvic pain or are merely incidental findings.

Several studies have raised questions about the benefit of treating adhesions surgically in patients with CPP. In a prospective study of patients undergoing second-look laparoscopy following laparotomy for reproductive surgery, 51% of patients developed de novo adhesions, thus raising the possibility that treating adhesions may lead to more adhesions. There is evidence to suggest that the lysis of adhesions may not result in significant pain relief. Two randomized prospective studies have been conducted to evaluate the effect of adhesiolysis in patients with chronic pelvic or abdominal pain. Neither study has provided convincing evidence to support adhesiolysis as being beneficial for providing pain relief in patients with chronic pain. In the first study, patients in the treatment arm underwent adhesiolysis by minilaparotomy. At 9 to 12 months following surgery, there was no difference in McGill pain scales comparing the treatment group (N = 24) to controls (N = 24). After stratification, the authors acknowledged a trend toward a benefit in patients with well-vascularized or thick adhesions involving the intestinal tract, the pain hypothesis being symptoms of intermittent small bowel subileus. The second and larger study (N – 116) showed no difference in abdominal pain in the treatment and control groups at 1 year after surgery.

In a case-control study of 100 consecutive laparoscopies in patients with CPP compared with 88 patients used as controls who underwent laparoscopy for infertility, pelvic adhesions were more common in the control group (39% vs. 26%). In a study of 200 asymptomatic women undergoing laparoscopic sterilization, 14% of women were found to have pelvic adhesions. In a prospective cohort study of 102 women undergoing laparoscopy, wherein the surgeons were blinded as to the indications, that is, pain (64%), infertility (35%), previous abnormal findings (19%), and sterilization (15%), adhesion scores were no different in the CPP group compared with those found in controls.

In an uncontrolled prospective study of 30 women undergoing laparoscopic adhesiolysis for CPP with a mean follow-up interval of 8.2 months, there was an overall improvement of pain in 63%. There was a trend toward greater improvement in the group with CPP compared with the group with CPP syndrome. CPP syndrome was defined as patients having at least four of the following: (a) pain greater than 6 months duration, (b) previous treatments unsuccessful in relieving pain, (c) diminished physical activity (work, exercise, sex), (d) at least one vegetative sign of depression (sleep dysfunction, decreased appetite, psychomotor retardation), or (e) altered family role.

Based on these studies, the following should be considered: (a) adhesions can form after surgery, even if adhesiolysis was the main surgical objective; (b) adhesions may be present in patients who are asymptomatic with respect to pain; (c) adhesions may be incidental in patients who suffer from CPP; (d) while some case series have shown benefit to adhesiolysis, the randomized clinical trials of adhesiolysis in patients with chronic pelvic and/or abdominal pain have shown no treatment benefit; and (e) judgment is critical as to whether or not to perform surgery in patients who have had multiple laparoscopic procedures, weighing the risks and benefits.


Endometriosis

Endometriosis is one of the most enigmatic of gynecologic pain disorders. Not only is there little correlation between the extent of disease present and the degree of pain, but it is often found in asymptomatic women. The noted exception is deep infiltrating endometriosis in the rectovaginal septum, which has been shown to have a direct correlation to pain.

Endometriosis may have several appearances ranging from the more typical “powder burn,” blue-gray lesions to atypical lesions that may be clear, red, or white. Various explanations have been proposed to account for endometriosis-related pain, including inflammation, prostaglandin production, neuronal involvement, and adhesions. Data from conscious sedation laparoscopic pain-mapping have demonstrated areas of pain well beyond the visible endometriosis.

Symptoms associated with endometriosis include cyclic pelvic pain or dysmenorrhea. The pain associated with endometriosis may precede the menses, occur with menses, and continue after menses. Tenesmus may be associated with endometriosis involving the rectosigmoid colon. Other clinical manifestations may include dyspareunia or ovarian mass (endometrioma).

Conservative medical treatment is recommended as the initial therapy for endometriosis or presumed endometriosis. This may include the use of nonsteroidal anti-inflammatory drugs (NSAIDs), hormonal contraceptive
drugs, danazol, progestins, and gonadotropin-releasing hormone (GnRH) agonists. These medications may provide symptomatic relief and in some cases have been shown to reduce the size of endometriotic lesions and thus the stage. There are no convincing data to suggest that one form of medical suppressive therapy is superior to another. Usually, the agent with the lowest side effect profile is selected as first-line therapy, such as NSAIDs or hormonal contraceptive drugs.

Hormonal contraceptive drugs may be used in a cyclic (standard) or continuous fashion. Continuous use refers to delaying withdrawal menstruation for 3 to 6 months rather than allowing menses to occur during placebo administration. This usually allows the patient to avoid the dysmenorrhea that may occur with the cyclic regimen. If hormonal contraceptive drugs are not effective after 3 months, danazol (600 mg to 800 mg per day) or GnRH agonists may be used.

The use of danazol for endometriosis-associated pain was evaluated by Cochrane Database reviewers, wherein four trials were found with adequate study design for inclusion. The reviewers concluded that danazol is effective in treating the symptoms of endometriosis; however, its use is limited by the occurrence of androgenic side effects. GnRH agonists such as leuprolide or goserelin are generally used for 6 months if a favorable response is noted. The main concern about prolonged use of these agents is the loss of bone mineral density. The treatment window may be extended to 12 months or longer with the use of add-back therapy (addition of a progestin with or without estrogen).

Surgery is generally reserved for refractory cases. If surgery is to be performed, it should be tailored toward the patient’s reproductive wishes. If the patient desires to preserve her childbearing capacity, endometriotic lesions may be destroyed or removed by vaporization or excision laparoscopically or by laparotomy. It is argued by some that vaporization may only treat the “tip of the iceberg” with the potential to leave deep infiltrating endometriosis behind. To date, there are no convincing data to recommend one laparoscopic therapy over the other. Unfortunately, a significant number of patients treated conservatively (without hysterectomy and bilateral salpingo-oophorectomy) will develop returning symptoms 12 months postoperatively.

Laparoscopic surgery for the treatment of endometriosis-associated pain was reviewed in the Cochrane Database. Only one study was deemed adequate for evaluation; therefore, most of our current understanding stems from level 3 data (case series and opinions of experts). The review concluded that laparoscopic laser treatment of endometriosis was more effective than expectant treatment of endometriosis, but the reviewers included a caution about the interpretation of results due the lack of any corroborating studies. Hysterectomy with or without adnexectomy may be appropriate in cases where childbearing is no longer an issue.


Pelvic Inflammatory Disease

PID is a significant health problem (approximately 1 million cases per year) resulting in an expense of 3.5 billion dollars annually in the United States alone. It can clearly be a cause of acute pain, yet it also may be asymptomatic. The most likely mechanism for pain is from inflammation and distension of the fallopian tubes. A distended fluid-filled fallopian tube or hydrosalpinx will sometimes persist for months or years and may cause CPP. It is less clear why pain persists in patients with treated PID, who have subsequent normal-appearing reproductive organs, and are culture negative for causative microorganisms. It is theorized that the initial inflammatory insult may have started a cascade of signals within the pelvis, spinal cord, and brain, resulting in visceral neuropathic pain.

As many as 15% to 25% of patients with PID will go on to have CPP. There are no good studies addressing how to treat laparoscopy-negative, culture-negative patients with presumed persistent PID. The patient’s partner should be treated as well to avoid reinfection. Persistent hydrosalpinx usually is treated surgically by salpingectomy.


Myofascial Pain

Myofascial pain syndrome (MFPS) may represent the largest group of unrecognized and undertreated acute and chronic medical problems in clinical practice. It is estimated to have a prevalence of 30% in patients suffering from pain in general medical clinics and as high as 85% to 93% in pain specialty clinics. Myofascial pain is common in patients with a history of trauma or multiple surgeries and is often overlooked as a cause for CPP. MFPS is a heterogeneous pain-producing disorder characterized by localized, reproducible, hyperirritable trigger points within a muscle or its investing fascia. Clinically, trigger points are tender when compressed, have characteristic referred pain patterns, referred tenderness, motor dysfunction, or autonomic dysfunction.

Abdominal wall myofascial pain is best detected by isolating the rectus abdominus muscles by having the patient flex her abdomen by lifting her feet or head and shoulders off the examination table while in the supine position. A one-finger search along the anterior abdominal wall is performed to identify painful trigger points. When localized, trigger points can be successfully treated with icing, stretching exercises, and injection with local anesthesia. One to 2 mL of a 50:50 mixture of 1.00% lidocaine and 0.25% bupivicaine may be injected into the muscle and fascia with a 22- or 25-gauge needle to achieve a diagnostic and therapeutic block. Slocumb reported on the successful treatment of 89% of 131 CPP patients with trigger point injections. Most patients obtained relief within five injections. Physical therapy has also been successful in treating MFPS.



Pelvic Varicosity Pain Syndrome

Patients with pelvic varicosity pain syndrome (PVPS), formerly called pelvic congestion syndrome, typically complain of pelvic pain and aching that becomes progressively worse throughout the day. They also may complain of dyspareunia or postcoital aching. PVPS as a cause for CPP has been a controversial entity since it was first described. One reason for skepticism is the observation that some women who demonstrate dilated vessels at the time of surgery or during pregnancy are asymptomatic.

Beard and colleagues proposed a more objective method of diagnosing pelvic varicosities by using transcervical pelvic venography to measure vessel diameter, vessel tortuosity, and dye transit time, suggesting that vein diameter alone is not the only significant finding of PVPS. Subsequent studies by these authors propose diagnostic criteria for PVPS and pathophysiologic mechanisms for pain production. It has been postulated that pain from PVPS is caused by vasoactive nociceptive peptides such as substance P and calcitonin gene-related peptide. In a study by Reginald and associates of patients with venographically diagnosed PVPS injected with a potent vasoconstrictor (dihydroergotamine), a 35% reduction in vein diameter, decreased dye transit time, and up to 4 days of pain relief was demonstrated when compared with patients injected with placebo. The authors hypothesized that vasoconstriction allows clearance of nociceptive vasoactive peptides.

One randomized clinical trial showed benefit with the use of GnRH agonist therapy over medroxyprogesterone acetate in 30-mg daily doses. Ultimately, surgery may be necessary. In Beard’s series of 36 patients treated with hysterectomy and bilateral salpingo-oophorectomy, 67% obtained complete relief of pelvic pain. Only 1 of the remaining 12 patients had significant pain.


Painful Bladder Syndrome

Painful bladder syndrome (PBS), formerly known as interstitial cystitis, is a chronic inflammatory condition of the bladder characterized by urgency, frequency, or pain in the absence of a urinary tract infection or malignancy. In some series, up to 85% of women with pelvic pain presenting to gynecologists have this condition.

The diagnosis of PBS is controversial but is often made by distending the bladder cystoscopically under anesthesia. Intravesical instillation of potassium chloride, which usually is nociceptive in the presence of PBS, has also been used diagnostically. Questionnaires can be used as well. Treatment usually is individualized and multimodal, including diet, exercise, smoking cessation, transcutaneous electrical nerve stimulation, bladder training, medications, bladder distention, or bladder instillation.

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May 25, 2016 | Posted by in GYNECOLOGY | Comments Off on Chronic Pelvic Pain

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