Howard T. Sharp
Science has produced many drugs, therapies, and surgeries in attempts to relieve the suffering associated with chronic pelvic pain (CPP). Unfortunately, only modest success has been achieved. This likely is due, in part, 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 such as gastroenterology, urology, neurology, or psychiatry are consulted. Patients eventually may be referred to centers specializing in CPP or empiric pain management, wherein neurolytic or opioid therapy may be commenced without finding a specific cause for pain.
Along the course of therapy and referral, frustration is often a byproduct of treating a supposedly remediable pain state only to have pain persist. Furthermore, a confusing aspect of CPP is that its definition implies that no etiology can be found; however, most textbooks list several causes for CPP (adhesions, endometriosis, pelvic inflammatory disease [PID], etc.). Therefore, the clinical challenge is to decipher which of the following is most likely:
1. A defined pain state exists but has been improperly diagnosed and treated.
2. A defined pain state exists, has been correctly identified, but happens to be present in an incidental form.
3. A neuropathic pain processing state is present.
GLOSSARY
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.
CPP
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, which is influenced by genetic differences, experiences, gender, anxiety, or expectation. The perception of and response to pain are believed to be determined by four simultaneous processes which 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, endometriosis, inflammatory bowel disease, or surgery may cause adhesions; yet, in up to 50% of cases there may be no significant antecedent event. Although adhesions commonly are 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 surgical treatment of adhesions. First, in a prospective study which involved second-look laparoscopy following laparotomy for reproductive surgery, 51% of patients developed de novo adhesions. Therefore, the possibility exists that treating adhesions may lead to more adhesions. Secondly, there is evidence to suggest that the lysis of adhesions may not result in significant pain relief. A randomized, prospective study of patients with CPP and known stage II to IV (moderate to severe) pelvic adhesions assessed the efficacy of surgical adhesiolysis on patients with CPP. Patients either underwent minilaparotomy adhesiolysis or no treatment. At 9- to 12-month follow-up, using the McGill Pain Scale to compare outcomes, there was no difference in the treatment group (n = 24) compared with 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. This small study lacks the power to answer definitively the question as to whether treatment of adhesions is beneficial.
In a case-control study of 100 consecutive laparoscopies in patients with CPP and 88 laparoscopies for infertility, pelvic adhesions were found more often in the control group (26% versus 39%). Trimbos and others studied 200 asymptomatic women undergoing laparoscopic sterilization and found a 14% incidence of pelvic adhesions. In a prospective cohort study of 102 women undergoing laparoscopy, wherein the surgeons were blinded as to the indications, which were pain (64%), infertility (35%), previous abnormal findings (19%), and sterilization (15%), adhesion scores were no different in the CPP group compared with 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 exhibiting CPP syndrome. CPP syndrome was defined as having at least four of the following (a) pain longer 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), (e) altered family role.
Laparoscopic pain mapping under conscious sedation provides additional information to better define whether a patient's adhesions are associated with pain. This technique employs local anesthesia at trocar sites in combination with intravenous opioids and benzodiazepines to enable the conscious patient to tolerate laparoscopic surgery. Pelvic structures can be mapped using a verbal analog pain scale (VAPS) from 0 to 10 to determine whether pain can be generalized to the pelvic viscera or to a focal point or adhesion. It is important to distinguish between surgically induced pain and pain which truly mimics the patient's chronic pain.
Taking these studies into consideration we can learn some valuable lessons. (a) The more surgery that is performed, the more likely adhesions are to occur. (b) Adhesions may be present in asymptomatic patients. (c) Adhesions may be incidental in symptomatic patients. (d) Although some case series have shown some benefit to adhesiolysis, the only randomized clinical trial of adhesiolysis in patients with CPP showed no treatment benefit. (e) Conscious sedation pain mapping surgery may better enable us to determine which adhesions are painful. (f) 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 disorders. Not only is there little correlation between the extent of disease and the degree of pain, but it often is 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 which 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 involvement of 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 nonsteroidal antiinflammatory drugs (NSAIDs), oral contraceptive pills (OCPs), danazol, progestins, or gonadotropin-releasing hormone (GnRH) agonists. These medications have been shown to reduce the size of endometriotic lesions and, thus, the stage; however, they have not been shown to eliminate disease. 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, such as an NSAID or OCP, is selected as first-line therapy.
Oral contraceptive pills may be used in a cyclic (standard) or continuous fashion. Continuous use refers to the ingestion of active pills every day for 3 to 6 months, rather than allowing menses to occur during placebo administration. This usually allows the patient to avoid the dysmenorrhea which may occur with the cyclic regimen. If OCPs are not effective after 3 months, danazol (600–800 mg/d) 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 to have study design adequate for inclusion. The reviewers concluded that danazol is effective in treating the symptoms and signs of endometriosis; however, its use is limited by the occurrence of androgenic side effects. GnRH agonists such as leuprolide or goserelin generally are 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 with the use of add-back therapy (addition of norethindrone acetate with or without conjugated equine estrogens).
Surgery generally is 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 treat only 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 recurrent symptoms 12 months after surgery.
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 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 to the lack of any corroborating studies.
Hysterectomy with or without adnexectomy may be appropriate in cases in which 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 annually in the United States alone. It clearly can 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 subsequently have normal-appearing reproductive organs and whose culture results are 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.
One study estimated that as many as 15% to 25% of patients with PID will go on to have CPP (relative risk = 3.0–5.0). There are no good studies addressing how to treat patients with laparoscopy-negative, culture-negative presumed persistent PID. They, therefore, often are treated with NSAIDs, neurolytic agents, or opioids. The patient's partner should be treated, also, to avoid reinfection. Persistent hydrosalpinx usually is treated surgically by salpingectomy.
Myofascial Pain
Myofascial pain is common in patients with a history of abdominal trauma or multiple surgeries and often is overlooked as a cause for CPP. Myofascial pain syndrome is a heterogeneous pain-producing disorder characterized by localized, reproducible, hyperirritable trigger points within a muscle or its investing fascia. The clinical sign of the trigger point is that it is tender when compressed, and has characteristic referred pain patterns, referred tenderness, motor dysfunction, or autonomic dysfunction.
Abdominal wall myofascial pain is detected best 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 treated successfully with icing, stretching exercises, and with local anesthetic injection. One to two milliliters of a 50:50 mixture of 1% lidocaine and 0.25% bupivacaine 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 patients with CPP who had trigger point injections. Most patients obtained relief within five injections. Physical therapy also has been successful in treating myofascial pain syndrome.
Pelvic Congestion
Patients with pelvic congestion syndrome typically complain of pelvic pain and aching which becomes progressively worse throughout the day, and they also may complain of dyspareunia or postcoital aching. Pelvic congestion syndrome as a cause for CPP has been a controversial entity since it was first described by Taylor in 1949. 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 co-workers proposed a more objective method of diagnosing pelvic varicosities 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 pelvic congestion syndrome. Subsequent studies by these authors propose diagnostic criteria for pelvic congestion syndrome and pathophysiologic mechanisms for pain production. It has been postulated that pain from vascular congestion is caused by vasoactive nociceptive peptides, such as substance P and calcitonin gene-related peptide. In a study by Reginald and colleagues of patients with venographically diagnosed pelvic congestion syndrome 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. They hypothesized that vasoconstriction allows clearance of nociceptive vasoactive peptides.
Conservative treatment of pelvic congestion includes medroxyprogesterone acetate in 30- to 50-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.
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder affecting approximately 15% of adults in the United States, yet only 25% of persons with questionnaire-detected IBS actually seek health care. It has been defined as lower abdominal pain, which is present for at least 12 weeks (not necessarily consecutive) out of the past year, that cannot be explained by structural or biochemical abnormalities. At least two of the following clinical features are needed for diagnosis: (a) pain relief with defecation, and onset associated with a change in (b) frequency or (c) consistency of stools.
Theories to explain a putative mechanism for IBS include visceral hyperalgesia, infection, an imbalance of neurotransmitters, and psychological factors. More recently, growing evidence suggests that these patients have a gastrointestinal sensory-reflex dysfunction as a common pathophysiologic mechanism, which may be manifested by different forms depending upon specific pathways involved. This may explain why some individuals are more pain prone, while others may be more prone to have diarrhea or constipation.
Rectal and sigmoid balloon distension studies have shown a lower threshold for pain, referred to as visceral hypersensitivity, in patients with IBS compared with controls. However, when balloon testing is performed, only 40% to 60% of patients with IBS report pain at levels of distension below the range of normal values; therefore, gut wall distension my not be the only stimulus to cause IBS.
Therapy for IBS involves treating symptoms, whether one is diarrhea prone or constipation prone. Diarrhea-prone patients respond to loperamide, hyoscyamine, and desipramine, whereas constipation-prone patients respond to fiber therapy or cisapride. Patients with a pain predominance may be treated with tricyclic antidepressants, NSAIDs, anticholinergic agents, calcium channel blockers and, in some cases, opioid analgesics. Newer agents are under development, such as visceral antinociceptive agents, κ-opioid agonists, and 5HT3 and 5HT4 receptor antagonists.
Patients who have rectal bleeding, persistent occult fecal blood, or failure of medical therapy should be referred to a gastroenterologist to rule out malignancy or inflammatory bowel disease.
Ovarian Remnant Syndrome
Ovarian remnant syndrome may result from incomplete removal of ovarian tissue at the time of oophorectomy and can be associated with CPP in premenopausal women. Patients with this syndrome usually have a history of extensive endometriosis or pelvic inflammatory processes, resulting in a technically difficult oophorectomy. Cyclic pelvic pain caused by ovarian remnant syndrome most commonly is associated with the development of ovarian follicles within hormonally active ovarian tissue. This diagnosis is suspected when serum levels of follicle-stimulating hormone and luteinizing hormone are normal. Hormone replacement therapy should be discontinued at least 10 days before assessing serum gonadotropin levels. Clomiphene citrate and GnRH agonists have been used to stimulate ovarian tissue, which assists in making an ultrasonographic diagnosis of ovarian remnant syndrome.
Surgical treatment usually requires extensive intraperitoneal adhesiolysis and retroperitoneal dissection to remove all ovarian tissue. In a series of eight patients treated surgically for ovarian remnant syndrome, three required large bowel resection, cystotomy was performed in three and a ureteroneocystostomy in one, and one required a small bowel resection. Outcome data regarding postoperative pain relief after surgical resection are limited to small case series, but cure rates as high as 90% are reported.
Residual Ovary Syndrome
Residual ovary syndrome originally was described by Grogen in 1958. It is characterized by the development of pain in one or both ovaries conserved at the time of hysterectomy, theoretically caused by perioophoritis with a thickened ovarian capsule. It has been postulated that pain is produced by the cyclic expansion of the ovary encased in adhesions.
The most common complaint in women with residual ovary syndrome is chronic lower abdominal pain, dyspareunia, and radiation of pain to the back or anterior thigh. A tender mass may be palpated on bimanual examination. This syndrome may occur in as many as 3% of women who have undergone hysterectomy with ovarian conservation. Treatment typically has been oophorectomy rather than lysis of adhesions, to avoid recurrent adhesion formation. Care should be taken to avoid ureteral damage, because retained ovaries often are near the ureter. Outcome data are limited regarding pain relief after surgery for retained ovaries (level 3 data). Postoperative pain relief has been reported in over 80% of patients after oophorectomy.
Pain of Uterine Origin
In the United States, approximately 18% of hysterectomies are performed for CPP, with endometriosis cited as the most common indication. Carlson and co-workers demonstrated significant reduction in pain following hysterectomy for CPP of all causes. In patients with pelvic pain who underwent hysterectomy, 85% complained of frequently occurring pain preoperatively, compared with 13% at 12 months postoperatively. In a prospective cohort study comparing surgical to nonsurgical treatment, 49% of medically managed patients with CPP had continued symptoms compared with 3% treated by hysterectomy. Moreover, 25% of patients in the nonsurgical group underwent hysterectomy within 1 year.
Stovall and others reported a 78% success rate in patients undergoing hysterectomy for pelvic pain of presumed uterine origin. In this retrospective study, patients were excluded for nonuterine pain such as endometriosis. A prospective multicenter cohort of 308 women undergoing hysterectomy for CPP reported resolution of pain in 74% and improvement in 21%. Risk factors for continued pain included age 30 or younger, history of pelvic inflammatory disease, and use of public assistance. These studies are helpful because they underscore the importance of investigating other, nongynecologic causes for CPP, and they provide guidelines for preoperative counseling.
Hysterectomy may be indicated in the absence of significant pathology, as long as a diagnostic laparoscopy has been performed, and the patient's pain has persisted for longer than 6 months with a serious negative impact on the quality of life. Prior to undergoing a hysterectomy the patient should be treated medically (oral contraceptives, NSAIDs, and induced amenorrhea) and should be evaluated for urinary, gastrointestinal, musculoskeletal, and psychological causes for pain. Possible causes of pain of uterine origin are listed in Table 43.1.
|
|
|
TABLE 43.1. Possible causes of pain of uterine origin |
PSYCHOLOGICAL ASPECTS OF CHRONIC PELVIC PAIN
Patients sometimes get the message “your pain is all in your head.” Whether patients are actually told this or whether they hear this is irrelevant. This concept reflects what physicians were taught historically as the somatic model of pain, wherein there was a direct relationship between tissue damage and pain intensity. This model does not account adequately for the discrepancy between objective physical findings and the perception of pain severity. A more contemporary approach recognizes the central models of pain, which include the effect of peripheral nociception and central pathways that determine disability and distress.
The psychological aspects of CPP can be significant. It is, therefore, worthwhile to distinguish among co-morbid states such as depression, anxiety, and panic attacks. It often is helpful to obtain consultation from an interested psychiatric health care professional. However, some screening tests can be done by primary care physicians, such as the Beck Depression Inventory or Zung Depression Index.
Clinical depression associated with CPP usually is manifested by sleep disturbance (insomnia or hypersomnia), loss of interest in pleasurable activities, guilt feelings, loss of energy, diminished concentration, appetite changes (decreased or increased), psychomotor changes, and possible suicidal ideation. The mainstays of therapy include the use of serotonin reuptake inhibitors, tricyclic antidepressants, and psychotherapy. Clinicians who prescribe these medications should be aware of diagnostic criteria for depression and be familiar with the side effects and contraindications of these medications.
PATIENT HISTORY
A thorough patient history is one of the most helpful tools in the evaluation of patients with CPP. The COLDERR acronym may be used to gain a general understanding of the patient's history of present illness.
· Character—What does the pain feel like? (sharp, dull, crampy)
· Onset—Does the pain come on suddenly or gradually? Is it cyclic or constant?
· Location—Is the pain localized or diffuse?
· Duration—How long has the pain been present and how has it changed over time?
· Exacerbation—What activities or movements make it worse?
· Relief—What medication, activities, and positions make it better?
· Radiation—Does the pain radiate anywhere (back, groin, flank)?
There are several important aspects of taking a detailed pain history and reviewing organ systems. Comprehensive history and physical examination forms are available through the International Pelvic Pain Society Web site and can be downloaded at www.pelvicpain.org. Establishing whether the pain is cyclic or not is helpful is narrowing the list of possible causes (Table 43.2). If the patient has poor insight into the nature of her pain, a pain calendar may be used prospectively to chart her symptoms during the month.
|
|
|
TABLE 43.2. Cyclic causes for chronic pelvic paina |
Reviewing past surgeries is helpful for gaining information about which organs can be eliminated from consideration and what effect surgery had on their pain. It may help establish a causal relationship between surgery and pain, which is common among patients with myofascial pain syndrome.
A thorough review of systems is important to exclude nongynecologic causes for CPP. Gastrointestinal complaints should be explored with specific questions about bowel frequency, consistency, associated pain, and to exclude a history of blood in the stool, which would alert the clinician to rule out neoplasm (Table 43.3). Likewise, urinary complaints such as dysuria, hematuria, nocturia, enuresis, and increased frequency should be probed for urologic causes of CPP (Table 43.4).
|
|
|
TABLE 43.3. Gastrointestinal causes for chronic pelvic pain |
|
|
|
TABLE 43.4. Urologic causes for chronic pelvic pain |
PHYSICAL EXAMINATION
Observing a patient's gait, body language, and facial expression can provide valuable information. Myofascial pain syndrome can result in or be a result of musculoskeletal dysfunction as seen with abnormalities in gait, body posture, leg lengths, or sacroiliac joint mobility. Such abnormalities warrant evaluation by a physiatrist or physical therapist.
A one-finger abdominal examination is performed on the anterior abdominal wall to detect trigger points, as described in the myofascial pain section. In addition, abdominal wall hernias may be diagnosed using this technique. Trigger points should be marked on the patient's skin with a soft pen tip and then mapped in the patient's chart for future comparison. Trigger points also may be found within the muscles of the back and buttocks.
A cotton-tipped applicator is useful in the examination of the vulvar vestibule to elicit painful areas or sites of vulvar vestibulitis. Special attention should be given to Bartholin ducts and Skene glands. On speculum examination, the vaginal fornices, or vaginal cuff in the posthysterectomy patient, can also be examined for tenderness using a cotton-tipped applicator. Any cervical discharge should be noted, examined by microscopy, and cultured. The posterior vaginal fornix should also be inspected visually to identify endometriosis. This sometimes is possible only with the aid of a tenaculum.
It is helpful to perform a “unimanual” examination prior to the bimanual examination to avoid “cross-contamination” from anterior abdominal wall pain signals. This consists of examining the vagina, cervix, and pelvic floor muscles with the hand in the vagina, without using the hand on the abdomen. The pelvic floor muscles should be examined individually to include the levator ani group, coccygeus, obturator internus, and the piriformis muscles. The uterus, tubes, and ovaries should be examined for localized pain. The pelvis should then be examined using the bimanual technique.
The rectovaginal examination is particularly useful to evaluate nodular or infiltrating endometriosis. If there is no tenderness in the cul-de-sac or along the uterosacral ligaments, yet endometriosis is strongly suspected, the patient should be reexamined during the menses.
PAIN MANAGEMENT
Pain management may include the use of NSAIDs, neurolytic agents, and narcotics. Knowledge of drug interactions, contraindications, and side effects are important aspects of successful pain management.
NSAIDs
NSAIDs are usually a safe category to start with, realizing there are several contraindications to these drugs, especially in patients with gastrointestinal disorders. The newer COX-2 (cyclooxygenase inhibitor-2) drugs have the advantage of fewer adverse effects on the gastrointestinal tract (Table 43.5).
|
|
|
TABLE 43.5. Oral NSAIDs |
Neurolytic Agents
Neurolytic agents encompass a number of drug categories used in the treatment of neuropathic pain, which include tricyclic antidepressants, serotonin reuptake inhibitors, and ion channel blockers. Table 43.6 lists some of these drugs which have been studied in patients with chronic pain.
|
|
|
TABLE 43.6. Oral Neurolytic Agents |
Narcotics
Narcotics often are thought of as appropriate for acute pain only; however, in some instances under careful supervision, patients with chronic pain may be candidates for narcotic therapy (Table 43.7). When narcotics are used, narcotic contracts are often helpful. Patients who demonstrate drug abuse behavior are not candidates for narcotic therapy. A patient who repetitively loses her prescription, uses multiple physicians for obtaining narcotic prescriptions, or routinely runs out of narcotics early is not considered a narcotic candidate. Patients who use narcotics over the long term should regularly report the symptoms on a VAPS and should report their degree of functionality. They should be encouraged regularly to wean from these agents.
|
|
|
TABLE 43.7. Oral narcotics |
Narcotic Agreements
When long-term narcotic therapy is used for pain management, it is useful to have the patient enter into a pain agreement to prevent misunderstandings and to help both the physician and patient comply with the federal laws regarding controlled substances.
When the agreement is entered, it is understood that if the patient terminates the agreement, the physician will discontinue narcotic therapy but will taper the medicine over a period of several days, as necessary, to avoid withdrawal symptoms. Also, a drug-dependence treatment program should be recommended. The patient agrees to describe the pain character and intensity, the effect of the pain on her daily life, and how well the narcotic is helping to relieve the pain. The patient also agrees not to use any illegally obtained controlled substances, and not share, sell, or trade medication with anyone.
Opioids, controlled stimulants, or antianxiety medication must not be obtained from any other doctor. The patient must agree to safeguard her pain medicine from loss or theft with knowledge that lost or stolen medicines will not be replaced. She should understand that prescriptions will be made only at the time of an office visit or during regular office hours and that no refills will be available during evenings or on weekends. This is helpful for covering physicians who receive calls from patients asking for narcotics. The pharmacy name, location, and telephone number are recorded and a log of the dosage, quantity, and prescription date is recorded in the patient's chart.
SUMMARY POINTS
· CPP is a complex entity, often without obvious, visible pathology.
· A distinction must be made between putative causes of CPP, which will respond to specific treatment, versus CPP associated with incidental pathology.
· Treatment of CPP with incidental pathology may result in failure and, in some cases, removal of otherwise normal organs. In such cases, treatment may take a more general and empiric course, resulting in the use of neurolytic medications and possibly the judicious use of narcotics.
SUGGESTED READINGS
Glossary and Contemporary Pain Theories
IASP Task Force on Taxonomy. Classification of chronic pain. Seattle: IASP Press, 1994;209–214.
Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965:150:971.
Putative Pain States
Diamond MP, Daniell JF, Feste J, et al. Adhesion reformation and de novo adhesion formation after reproductive pelvic surgery. Fertil Steril 1987:47:864–866.
Peters AA, Trimbos-Kemper GC, Admiraal C, et al. A randomized clinical trial on the benefit of adhesiolysis in patients with intraperitoneal adhesions and chronic pelvic pain. Br J Obstet Gynaecol 1992;99:59–62.
Rapkin AJ. Adhesions and pelvic pain: a retrospective study. Obstet Gynecol 1986;68:13–15.
Steege JF, Stout AL. Resolution of chronic pelvic pain after laparoscopic lysis of adhesions. Am J Obstet Gynecol 1991;165:278–281, discussion 281–283.
Stout A, Steege JF, Dodson WC, et al. Relationship of laparoscopic findings to self report of pelvic pain. Am J Obstet Gynecol 1991;164:73–79.
Stovall TG, Elder RF, Ling FW. Predictors of pelvic adhesions. J Reprod Med 1989:34:345.
Trimbos JB, Trimbos-Kemper GC, Peters AA, et al. Findings in 200 consecutive asymptomatic, healthy women having a sterilization. Arch Gynecol Obstet1990;247:121–124.
Endometriosis
Demco L. Mapping the source and character of pain due to endometriosis by patient-assisted laparoscopy. J Am Assoc Gynecol Laparosc 1998;5:241–245.
Hornstein MD, Surrey ES, Weisbery GW, et al. Leuprolide acetate depot and add-back in endometriosis: a 12 month study. Lupron add-back study group. Obstet Gynecol 1998;91:16–24.
Jacobson TZ, Barlow DH, Garry R, et al. Laparoscopic surgery for pelvic pain associated with endometriosis (Cochrane Review). Cochrane Database Syst Rev 2001;4:CD001300.
Koninckx P, Meuleman C, Demeye S, 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.
Martin D, Hubert G, Vander Zwaag R, et al. Depth of infiltrating endometriosis. J Gynecol Surg 1989;5:55.
Selak V, Farquuhar C, Prentice A, et al. Danazol for pelvic pain associated with endometriosis (Cochrane Review). Cochrane Database Syst Rev2001;4:CD000068.
Sutton CJ, Pooley AS, Ewen SP, et al. Follow-up report on a randomized controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal to moderate endometriosis. Fertil Steril 1997;68:1070–1074.
Pelvic Inflammatory Disease and Myofascial Pain
Slocumb JC. Neurological factors in chronic pelvic pain: trigger points and the abdominal pelvic pain syndrome. Am J Obstet Gynecol 1984;149:536–543.
Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual. Baltimore, Williams & Wilkins, 1983.
Pelvic Congestion Syndrome
Beard RW, Belsey EM, Lieberman MB, et al. Pelvic pain in women. Am J Obstet Gynecol 1977;128:566–570.
Beard RW, Kennedy RG, Gangar KF, et al. Bilateral oophorectomy and hysterectomy in treatment of intractable pelvic pain associated with pelvic congestion. Br J Obstet Gynaecol 1991;98:988–992.
Beard RW, Pearse S, Highman JH, et al. Diagnosis of pelvic varicosities in women with chronic pelvic pain. Lancet 1984;8409:946–949.
Reginald PW, Beard RW, Kooner JS, et al. Intravenous dihydroergotamine to relieve pelvic congestion with pain in young women. Lancet 1987;8555:351–353.
Stones RW, Loesch A, Beard RW, et al. Substance P: endothelial localization and pharmacology in the human ovarian vein. Obstet Gynecol 1995;85:273–278.
Stones RW, Rae T, Rogers V, et al. Pelvic congestion in women: evaluation with transvaginal ultrasound and observations of venous pharmacology. Br J Radiol 1990;63:710–711.
Stones RW, Thomas DC, Beard RW. Suprasensitivity to calcitonin gene-related peptide but not vasoactive intestinal peptide in women with chronic pelvic pain. Clin Autonomic Res 1992;2:343–348.
Taylor HC. Vascular congestion and hyperemia. Am J Obstet Gynecol 1949;57:211–230.
OVARIAN REMNANT SYNDROME
Grogen RH. Residual ovaries. Obstet Gynecol 1958;12:329–332.
Lafferty HW, Angioli R, Rudolph J, et al. Ovarian remnant syndrome: experience at Jackson Memorial Hospital. Am J Obstet Gynecol 1996;174:641–645.
Scott RT, Beatse SN, Illions EH, et al. Use of the GnRH agonist stimulation test in the diagnosis of ovarian remnant syndrome. J Reprod Med 1995;40:143–146.
Siddall-Allum J, Rae T, Rogers V, et al. Chronic pelvic pain caused by residual ovaries and ovarian remnants. Br J Obstet Gynaecol 1994;101:979–985.
Pain of Uterine Origin
Carlson KJ, Miller BA, Fowler FJ. The Maine women's health study: I. Outcomes of hysterectomy. Obstet Gynecol 1994;83:556–565.
Carlson KJ, Miller BA, Fowler FJ. The Maine women's health study: II. Outcomes of nonsurgical management of leiomyomas, abnormal bleeding, and chronic pelvic pain. Obstet Gynecol 1994;83:566–572.
Hillis SD, Marchbanks PA, Peterson HB. The effectiveness of hysterectomy for chronic pelvic pain. Obstet Gynecol 1995;86:941–945.
Stovall TG, Ling FW, Crawford DA. Hysterectomy for chronic pelvic pain of presumed uterine etiology. Obstet Gynecol 1990;75:676–679.
Wilcox LS, Koonin LM, Pokras R, et al. Hysterectomy in the United States, 1988–1990. Obstet Gynecol 1994;83;549–555.
