Pelvic Pain

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Chapter 21 Pelvic Pain

Andrea J. Rapkin, Joseph C. Gambone

Pelvic pain is a frequent complaint in gynecology. It may be cyclic and associated with menstruation, sudden in onset (acute), or chronic, lasting for more than 6 months. Half of all menstruating women are affected by painful menstruation or dysmenorrhea, making it the most common type of pelvic pain. Ten percent of these women have severe symptoms necessitating time off from work or school.

image Dysmenorrhea

Dysmenorrhea may be primary, when there is no readily identifiable cause, or secondary to organic pelvic disease. The typical age range of occurrence for primary dysmenorrhea is between 17 and 22 years, whereas secondary dysmenorrhea is more common in older women.

PRIMARY DYSMENORRHEA

Pathophysiology

Primary dysmenorrhea occurs during ovulatory cycles and usually appears within 6 to 12 months of the menarche. The etiology of primary dysmenorrhea has been attributed to uterine contractions with ischemia and production of prostaglandins. Women with dysmenorrhea have increased uterine activity, which results in increased resting tone, increased contractility, and increased frequency of contractions. During menstruation, prostaglandins are released as a consequence of endometrial cell lysis, with instability of lysosomes and release of enzymes that break down cell membranes.

The evidence that prostaglandins are involved in primary dysmenorrhea is convincing. Menstrual fluid from women with this disorder have higher than normal levels of prostaglandins (especially prostaglandin F2α [PGF2α] and PGE2), and these levels can be reduced to below normal with nonsteroidal antiinflammatory drugs (NSAIDs), which are effective treatments. Infusions of PGF2α or PGE2 reproduce the discomfort and many of the associated symptoms such as nausea, vomiting, and headache. Secretory endometrium contains much more prostaglandin than proliferative endometrium. Women with primary dysmenorrhea have upregulated cyclooxygenase (COX) enzyme activity as a major cause of their pain. Anovulatory endometrium (without progesterone) contains little prostaglandin, and these menses are usually painless.

Figure 21-1 summarizes the relationships among endometrial cell wall breakdown, prostaglandin synthesis, uterine contractions, ischemia, and pain.

image

FIGURE 21-1 Postulated mechanism of pain generation in primary dysmenorrhea. Nonsteroidal anti-inflammatory drugs inhibit cyclooxygenase, the enzyme that catalyzes the formation of prostaglandins from arachidonic acid. Hormonal contraceptives that block ovulation significantly reduce the formation of prostaglandins. Both drugs mitigate this mechanism of pain and are effective treatment for primary dysmenorrhea.

(Modified from Dawood MY: Hormones, prostaglandins and dysmenorrhea. In Dawood MY [ed]: Dysmenorrhea. Baltimore, Williams & Wilkins, 1981.)

Clinical Features

The clinical features of primary dysmenorrhea are summarized in Box 21-1. Cramping usually begins a few hours before the onset of bleeding and may persist for hours or days. It is localized to the lower abdomen and may radiate to the thighs and lower back. The pain may be associated with altered bowel habits, nausea, fatigue, dizziness, and headache.

BOX 21-1 Features of Primary Dysmenorrhea

Initial Onset

About 90% experience symptoms within 2 years of menarche (i.e., when ovulation begins).

Duration and Type of Pain

Dysmenorrhea begins a few hours before or just after the onset of menstruation and usually lasts 48 to 72 hours.
Pain is described as cramp-like and is usually strongest over the lower abdomen and may radiate to the back or inner thighs.

Associated Symptoms

Nausea and vomiting
Fatigue
Diarrhea
Lower backache
Headache

Pelvic Examination Findings

Normal

Treatment

Box 21-2 lists the treatment options for primary dysmenorrhea. NSAIDs, which act as COX inhibitors, are highly effective in the treatment of primary dysmenorrhea. Typical examples include ibuprofen (400 mg every 6 hours), naproxen sodium (250 mg every 6 hours), and mefenamic acid (500 mg every 8 hours). Decreasing prostaglandin production by enzyme inhibition is the basis of all NSAIDs. Hormonal contraceptives such as oral contraceptive pills (OCs), patches, or transvaginal rings reduce menstrual flow and inhibit ovulation and are also effective therapy for primary dysmenorrhea. Extended cycle use of OCs or the use of long-acting injectable or implantable hormonal contraceptives or progestin-containing intrauterine devices minimizes the number of withdrawal bleeding episodes that users have. Some patients may benefit from using both hormonal contraception and NSAIDs.

BOX 21-2 Treatment of Primary Dysmenorrhea

General Measures

Reassurance and explanation

Medical Measures

Nonsteroidal antiinflammatory drugs
Hormonal contraceptives (including hormone-releasing intrauterine devices and vaginal rings)
Progestins
Tocolytics
Analgesics

Other Measures

Transcutaneous nerve stimulation
Acupuncture
Psychotherapy
Hypnotherapy

Resistant cases may respond to tocolytic agents (e.g., salbutamol), a calcium blocker (e.g., nifedipine), or high-dose continuous daily progestogens (especially medroxyprogesterone acetate or dydrogesterone). Nonpharmacologic pain management, particularly acupuncture or transcutaneous electrical stimulation, may be useful, as are psychotherapy, hypnotherapy, and heat patches. Surgical procedures such as presacral neurectomy and uterosacral ligament section have been largely abandoned.

If a patient fails to respond to hormonal contraception and NSAID therapy, the diagnosis of primary dysmenorrhea should be questioned and consideration given to a secondary cause. Ultrasonic imaging, laparoscopy, and hysteroscopy with directed biopsy should be performed to exclude pelvic disease.

SECONDARY DYSMENORRHEA

Pathophysiology

The mechanism of pain in secondary dysmenorrhea depends on the underlying (secondary) cause and in most cases is not well understood. Prostaglandins may also be involved in this type of dysmenorrhea, although NSAIDs and hormonal contraceptives that do not suppress menses altogether are less likely to provide satisfactory pain relief.

Clinical Features

The clinical features of some of the underlying causes of secondary dysmenorrhea are summarized in Box 21-3. In general, secondary dysmenorrhea is not limited to the menses and can occur before as well as after the menses. In addition, secondary dysmenorrhea is less related to the first day of flow, develops in older women (in their 30s or 40s), and is usually associated with other symptoms such as dyspareunia, infertility, or abnormal uterine bleeding.

BOX 21-3 Characteristics of Some Causes of Secondary Dysmenorrhea

Endometriosis

Pain extends to premenstrual or postmenstrual phase or may be continuous; may also have deep dyspareunia, premenstrual spotting, and tender pelvic nodules (especially on the uterosacral ligaments); onset is usually in the 20s and 30s but may start in teens.

Pelvic Inflammation

Initially pain may be menstrual, but often with each cycle it extends into the premenstrual phase; may have intermenstrual bleeding, dyspareunia, and pelvic tenderness.

Adenomyosis, Fibroid Tumors

Uterus is generally clinically and symmetrically enlarged and may be mildly tender; dysmenorrhea is associated with a dull pelvic dragging sensation.

Ovarian Cysts (Especially Endometriosis and Luteal Cysts)

Should be clinically evident

Pelvic Congestion

A dull, ill-defined pelvic ache, usually worse premenstrually, relieved by menses; often a history of sexual problems

Treatment

Management consists of the treatment of the underlying disease. The treatments used for primary dysmenorrhea (Box 21-2) are often helpful. Other specific treatments are discussed in the chapters dealing with the underlying causes.

image Acute Pelvic Pain

Acute pain is sudden in onset and is usually associated with significant neuroautonomic reflexes such as nausea and vomiting, diaphoresis, and apprehension. It is important for the gynecologist to be aware of both the gynecologic and nongynecologic causes of acute pelvic pain (Box 21-4). Delay of diagnosis and treatment of acute pelvic pain increase the morbidity and even mortality.

BOX 21-4 Causes of Acute Pelvic Pain

Gynecologic

Adnexal accidents (e.g., ovarian cyst torsion, rupture, hemorrhage)
Acute infections (e.g., endometritis, pelvic inflammatory disease)
Pregnancy complications (e.g., ectopic gestation, abortion)

Nongynecologic

Gastrointestinal (e.g., appendicitis, enteritis, or intestinal obstruction)
Genitourinary (e.g., cystitis, ureteral stones, urethral syndrome)
Other (e.g., pelvic thrombophlebitis, vascular aneurysm, porphyria)

Adnexal accidents, including torsion or rupture of an ovarian (Figure 21-2) or fallopian tube cyst, can cause severe lower abdominal pain. Normal ovaries and fallopian tubes rarely undergo torsion, but cystic or inflammatory enlargement predisposes to these adnexal accidents. The pain of adnexal torsion can be intermittent or constant, is often associated with nausea, and has been described as reverse renal colic because it originates in the pelvis and radiates to the loin. An enlarging pelvic mass is found on examination and ultrasound with decreased or absent blood flow to the adnexa on Doppler ultrasound studies. The need for surgical intervention is common and urgent.

image

FIGURE 21-2 Torsion of an ovarian cyst.

(From Clement PB, Young RH: Atlas of Gynecologic Surgical Pathology. Philadelphia, WB Saunders, 2000.)

Functional ovarian cysts (e.g., corpus luteum or follicular cysts) may rupture, causing leakage of fluid or blood that causes acute pain from peritoneal irritation. When there is significant associated bleeding, the pain may be followed by a hemoperitoneum and hypovolemia. Surgical intervention is mandatory in this setting, after adequate resuscitation with packed red cells and intravenous fluids.

Acute reproductive organ infections such as endometritis or salpingo-oophoritis (commonly referred to as pelvic inflammatory disease [PID]) can present acutely. Rupture of a tubo-ovarian abscess is a surgical emergency that can progress to hypotension and oliguria after initially presenting with diffuse lower abdominal pain. Pelvic infection is covered in greater detail in Chapter 22.

Several complications of early pregnancy, such as ectopic gestation (see Chapter 24) and threatened or incomplete abortion can cause acute pelvic pain and are generally associated with abnormal bleeding. Ectopic tubal pregnancies produce pain as the fallopian tube dilates and ruptures into the abdominal cavity and can be life-threatening when not diagnosed expeditiously.

Nongynecologic causes of acute lower abdominal pain (see Box 21-4) are frequently seen in the differential diagnosis when a woman presents with pelvic pain. Appendicitis is a common gastrointestinal cause of acute lower abdominal pain that eventually localizes to the right lower quadrant of the abdomen (McBurney’s point). The unilateral intensity of the pain usually differentiates it from salpingo-oophoritis. Rupture of an infected appendix into the pelvic cavity can have a significant adverse effect on female fertility. Diverticular abscess is also not uncommon but usually occurs in postmenopausal women.

Acute cystitis and ureteral stone formation (lithiasis) and passage are both frequently painful. Urethral syndrome can present acutely and become chronic over time when not recognized and treated. Urinary tract disorders are covered in more detail in Chapter 23.

image Chronic Pelvic Pain

Chronic pelvic pain (CPP) refers to pelvic pain of more than 6 months’ duration that has a significant effect on daily function and quality of life. CPP includes reproductive and nonreproductive organ–related pelvic pain that is primarily acyclic. Although CPP is an enigmatic entity, it is one of the most common presenting complaints in a gynecologic practice. As a health problem, it results in great cost to society in terms of hospital services, loss of productivity, and human misery.

Obviously, not all lower abdominal and low back pain is of gynecologic origin. Careful evaluation is needed to distinguish gynecologic pain from that of orthopedic, gastrointestinal, urologic, neurologic, and psychosomatic origin. The relationship between pelvic pain and the underlying gynecologic pathology is often inexplicable and frequently thought to be psychosomatic. The discovery of the role of prostaglandins in primary dysmenorrhea, however, formerly believed to be a neurotic affectation, calls for caution when making a diagnosis of psychosomatic pelvic pain. There is still much to be learned about the mechanisms involved in the production and perception of pelvic pain.

image Anatomy and Physiology

The pain fibers to pelvic organs are shown in Table 21-1. Painful impulses that originate in the skin, muscles, bones, joints, and parietal peritoneum travel in somatic nerve fibers, whereas those originating in the internal organs travel in visceral nerves.

TABLE 21-1 NERVES CARRYING PAINFUL IMPULSES FROM THE PELVIC ORGANS

Organ Spinal Segments Nerves
Perineum, vulva, lower vagina S2-4 Pudendal, inguinal, genitofemoral, posterofemoral cutaneous
Upper vagina, cervix, lower uterine segment, posterior urethra, bladder trigone, uterosacral and cardinal ligaments, rectosigmoid, lower ureters S2-4 Pelvic parasympathetics
Uterine fundus, proximal fallopian tubes, broad ligament, upper bladder, cecum, appendix, terminal large bowel T11-12, L1 Sympathetics through hypogastric plexus
Outer two thirds of fallopian tubes, upper ureter T9-10 Sympathetics through aortic and superior mesenteric plexus
Ovaries T9-10 Sympathetics through renal and aortic plexus and celiac and mesenteric ganglia
Abdominal wall
T12-L1
T12-L1
L1-2

Iliohypogastric
Ilioinguinal
Genitofemoral

Visceral pain is more diffusely spread than somatic pain because of a phenomenon called viscerosomatic convergence and the lack of a well-defined projection area in the sensory cortex for its identification. Viscerosomatic convergence occurs in all second-order neurons in the dorsal horn of the spinal cord that receive visceral input. No second-order neurons in the dorsal horn receive only visceral input. The viscerosomatic neurons have larger receptive fields than do the somatic second-order neurons, and the number of somatic second-order neurons vastly exceeds the number of viscerosomatic neurons. Visceral pain is therefore usually referred to the skin, which is supplied by the corresponding spinal cord segment (referred pain). For example, the initial pain of appendicitis is referred to the epigastric area, as both structures are innervated by the thoracic cord segments T8, T9, and T10.

The structures of the female genital tract vary in their sensitivity to pain. The skin of the external genitalia is exquisitely sensitive. Pain sensation is variable in the vagina; the upper segment is somewhat less sensitive than the lower. The cervix is relatively insensitive to small biopsies but is sensitive to deep incision or to dilation. The uterus is quite sensitive. The ovaries are insensitive to many stimuli, but they are sensitive to rapid distention of the ovarian capsule or compression during physical examination.

image Patient Evaluation

HISTORY

A pain history should be obtained during the first visit. Characteristics of the pain, including its location, radiation, severity, and alleviating and aggravating factors as well as effects on menstruation, level of stress, work, exercise, and intercourse should be determined. Symptoms related to the gastrointestinal, genitourinary, and musculoskeletal and neurologic systems should be elicited. This process can be guided by the Pain History Mnemonic outlined in Box 21-5.

BOX 21-5 Pain History Mnemonic (OLD CAARTS)

From Rapkin AJ, Howe CN: Chronic pelvic pain: A review. In Family Practice Recertification. Monroe Township, NJ, Medical World Communications, 2006, pp 59-67.

Onset: When and how did the pain start? Does it change over time?
Location: Localize specifically—Can you put a finger on it?
Duration: How long does it last?
Characteristics: Cramping, aching, stabbing, itching
Alleviating/aggravating factors: What makes it better (e.g., position change, medication, stress reduction)or worse (e.g., menstrual cycle, stress, specific activity)?
Associated symptoms:

Gynecologic (e.g., dyspareunia, dysmenorrhea, abnormal bleeding, discharge)
Gastrointestinal (e.g., constipation, diarrhea, bloating, gas, rectal bleeding)
Genitourinary (e.g., urinary frequency, dysuria, urgency, incontinence)
Neurologic: specific nerve distribution of the pain

Radiation: Does the pain move to other areas of the body?
Temporal: What time of day? —relationship to daily activities
Severity: Scale of 0 to 10 (from no pain to the most severe imaginable)

PHYSICAL EXAMINATION

The examination of the abdomen should be performed gently to prevent involuntary guarding, which may obstruct the findings. The patient should be asked to point to the exact location of the pain and its radiation, and an attempt should be made to duplicate the pain by palpation of each abdominal quadrant. The severity of the pain should be quantified on a 0 to 10 scale (0 = no pain, 10 = hitting thumb with a hammer).

A gentle but thorough pelvic examination should be performed with an attempt to reproduce and localize the patient’s pain. The examination may be suggestive of specific pelvic pathology. For example, patients with endometriosis may have a fixed retroverted uterus with tender uterosacral nodularity. Chronic salpingitis may be suggested by bilateral, tender, irregularly enlarged adnexal structures. A prolapsed uterus may account for pelvic pressure, pain, or low backache.

The abdominal wall should be examined for evidence of myofascial trigger points and for iliohypogastric (T12, L1), ilioinguinal (T12, L1), or genitofemoral (L1, L2) nerve entrapment. Each dermatome of the abdominal wall and back is palpated with a fingertip, and points of motion tenderness or “jump signs” are marked with a pen. The patient is asked to tense the abdominal muscles by performing a straight-leg raising maneuver (both legs raised at least 6 inches with both knees straight) or a partial sit-up. Points that are still tender or more tender or that reproduce the patient’s pain suggest that the etiology of the pain is in the abdominal wall, generally nerve entrapment, impingement, or trigger point pain, and should be injected with 2 to 3 mL of 0.25% bupivacaine. Chronic abdominal wall pain is confirmed if the pain level is reduced by at least 50% and outlasts the duration of the local anesthetic.

FURTHER INVESTIGATIONS

Psychological evaluation should be requested if an obviously traumatic event has occurred with the onset of pain; if there is obvious depression, neurosis, psychosis, or secondary gain; or to aid in the planning of pain management sessions. The latter may involve cognitive behavioral and stress reduction therapy.

Laboratory studies are of limited utility in the diagnosis of CPP, although a complete blood cell count, erythrocyte sedimentation rate (ESR), and urinalysis are indicated. The ESR is nonspecific and will be increased in any type of inflammatory condition, such as subacute salpingo-oophoritis, tuberculosis, or inflammatory bowel disease. Patients who are engaging in sexual intercourse should have a pregnancy test if they have a uterus and are not postmenopausal. Pelvic ultrasonography should be performed because the pelvic examination may miss an adnexal mass, particularly in obese patients and those who are unable to relax for the complete examination. If bowel or urinary signs and symptoms are present, an abdominal and pelvic computed tomography (CT) scan, endoscopy, cystoscopy, or CT urogram may be useful. Similarly, if there is clinical evidence of musculoskeletal disease, a lumbosacral x-ray, CT, magnetic resonance imaging, or orthopedic consultation may be in order.

Diagnostic laparoscopy is the ultimate method of diagnosis for patients with CPP of undetermined etiology. Laparoscopic examination and bimanual examination may differ in 20% to 30% of cases. Laparoscopy should only be performed if no etiology for the pain can be identified.

image Differential Diagnosis

ORGANIC CAUSES OF CHRONIC PELVIC PAIN

Of women with CPP who are subjected to diagnostic laparoscopy, about one third have no apparent pathology, one third have endometriosis, one fourth have adhesions or stigmata of chronic PID, and the remainder have other causes (Box 21-6).

BOX 21-6 Gynecologic Causes of Chronic Pelvic Pain

Endometriosis
Salpingo-oophoritis (pelvic inflammatory disease)
Ovarian remnant syndrome
Pelvic congestion syndrome
Cyclic pelvic (uterine) pain
Myomata uteri (degenerating)
Adenomyosis
Adhesions

Endometriosis

Endometriosis may be missed visually at the time of diagnostic laparoscopy in as many as 20% to 30% of women who have the disease proven histologically, so it is justifiable to initiate treatment based on a presumptive diagnosis of the disease once other etiologies have been ruled out.

The size and location of the endometriotic implants do not appear to correlate with the presence of pain, and the reasons for the pain are not fully understood.

Chronic Pelvic Inflammatory Disease (PID)

Chronic PID may cause pain because of recurrent exacerbations that require active antibiotic therapy or because of hydrosalpinges and adhesions between the tubes, ovaries, and intestinal structures. Before ascribing symptoms to adhesions, one must have specifically noted adhesions in the area of pain localization because some patients with extensive pelvic adhesions discovered incidentally during surgery for other reasons are asymptomatic.

Ovarian Pain

Ovarian cysts are usually asymptomatic, but episodic pain may occur secondary to rapid distention of the ovarian capsule. An ovary or ovarian remnant may occasionally become retroperitoneal secondary to inflammation or previous surgery, and cyst formation in these circumstances may be painful. Some women, for unknown reasons, may develop multiple recurrent hemorrhagic ovarian cysts that appear to cause pelvic pain and dyspareunia on an intermittent basis.

UTERINE PAIN

Adenomyosis (or endometriosis interna) may cause dysmenorrhea, dyspareunia, and menorrhagia, but rarely does it cause chronic daily intermenstrual pain. Uterine myomas usually do not cause pelvic pain unless they are degenerating, undergoing torsion (twisting on their pedicles), or compressing pelvic nerves. On occasion, a submucous leiomyoma may attempt to deliver through the cervix, which may cause considerable pelvic pain akin to childbirth. Uterine myomas may cause pain from rapid growth or infarction during pregnancy.

Pelvic pain is not likely to be caused by variations in uterine position, but deep dyspareunia may occasionally be associated with uterine retroversion, especially when the uterus is fixed in place by scarring or adenomyosis. The pain has been ascribed to irritation of pelvic nerves by the stretching of the uterosacral ligaments as well as to congestion of pelvic veins secondary to retroversion. The dyspareunia is typically worse during intercourse in the missionary position and is improved in the female superior position. A tender uterus that is in a fixed retroverted position usually signifies other intraperitoneal pathology, such as endometriosis or PID, and diagnosis rests on laparoscopic findings.

Pelvic Congestion Syndrome

The concept of a pelvic congestion syndrome still has many proponents. This entity has been described in multiparous women who have pelvic vein varicosities and congested pelvic organs. The pelvic pain is worse premenstrually and is increased by fatigue, standing, and sexual intercourse. Many women with this condition are noted to have a uterus that is mobile, retroverted, soft, boggy, and slightly enlarged. There may be associated menorrhagia and urinary frequency. Dilated veins may be seen on venographic studies. Factors other than venous congestion may be involved, however, because most women with pelvic varicosities have no pain. Surgery for this condition, consisting of hysterectomy and oophorectomy, may be beneficial for women who have completed their families, as are ovarian hormone suppression (decreased blood flow to the pelvic organs) and cognitive behavioral therapy.

Genitourinary Pelvic Pain

A variety of genitourinary problems result in pelvic pain. Urinary retention, urethral syndrome, trigonitis, and interstitial cystitis are prime examples. Urinary urgency, frequency, nocturia, and pelvic pain may suggest early interstitial cystitis. A thorough genitourinary evaluation is an important part of the workup for CPP. As many as one in five women have interstitial cystitis.

Gastrointestinal Pain

Gastrointestinal sources of CPP include penetrating neoplasms of the gastrointestinal tract, irritable bowel syndrome, partial bowel obstruction, inflammatory bowel disease, diverticulitis, and hernia formation. Because the innervation of the lower intestinal tract is the same as that of the uterus and fallopian tubes, the patient’s complaint of pelvic pain may be confused with pain of gynecologic origin. Irritable bowel syndrome is the most common gastrointestinal cause of pelvic pain.

Neuromuscular Pain

Pain of neuromuscular origin, which is experienced as low back pain, usually increases with activity and stress. Trigger points and myalgia of the pelvic floor muscles can cause pelvic pain, vulvodynia, and dyspareunia. Chronic low back pain without lower abdominal pain is seldom of gynecologic etiology. Fibromyalgia, or generalized myofascial pain syndrome, can also cause pelvic pain. On occasion, neuromuscular symptoms are accompanied by a pelvic mass, and surgical exploration may reveal a neuroma or bony tumor. Entrapped or compromised nerves in the abdominal wall (iliohypogastric and ilioinguinal nerve most commonly) or pelvic floor (pudendal nerve) are often unrecognized sources of pain. The nerves may become entrapped after surgery or physical trauma, pregnancy and delivery, or occupational injury.

PSYCHOLOGICAL FACTORS

A pathologic diagnosis may not be made in about one third of patients with CPP, even after laparoscopy, which has led to the postulation that psychological factors may be etiologic. The patients have been assumed to be anxious, neurotic, anorgasmic, and insecure in their roles as women or as mothers. When subjected to the Minnesota Multiphasic Personality Inventory (MMPI), these patients have shown a greater degree of anxiety, hypochondriasis, and hysteria than control subjects. The profiles are similar, however, in patients who have chronic pain with organic pathology, indicating that chronic pain per se engenders a complex, debilitating, psychological response. Chronic pain patients with and without pathology tend to feel depressed, helpless, and passive. They withdraw from social and sexual activity and are preoccupied with pain and suffering. Many have posttraumatic stress disorder from emotional, physical, or sexual trauma. Women with CPP are also at risk for chronic fatigue syndrome.

Pain Perception Factors

Chronic pain is characterized by physiologic, emotional, and behavioral responses that are different from those of acute pain. Although both acute and chronic pain consists of a stimulus and a psychic response, for acute pain these may be adaptive and appropriate, whereas for chronic pain this may not be the case. In fact, the response to chronic pain may be greatly affected by learning. The patient’s reaction to pain and the reaction of significant others to the patient and her pain may be so reinforcing that the behavior may persist even after the painful stimulus has resolved. In acute pain, the pain perception, suffering, and behavior are usually commensurate with the degree of sensory input. In chronic pain, the suffering and behavioral responses to a given sensory input may be quite exaggerated and may persist even after the stimulus has remitted.

Modulation of Sensation

Pain impulses are subjected to a large amount of modulation en route to and within the central nervous system. The first synapse in the dorsal horn is an important focus of enhancement, inhibition, or facilitation. Modulation of sensations may also occur within the spinothalamic system, the descending inhibitory neurosystems, and the frontal cortex. Various neurotransmitters and neuromodulators are present in the dorsal horn and at other higher levels of the neuraxis. Excitatory modulators include substance P, glutamate, aspartate, calcitonin gene-related peptide, and vasoactive intestinal peptide. Inhibitory neuromediators include endogenous opioid peptides, norepinephrine, serotonin, and γ-aminobutyric acid (GABA). Nerve axons that have been compromised after inflammation as well as stretch or crush injury also develop abnormal sodium channels. These changes play an important role in the development of allodynia (pain with gentle touch) and hyperalgesia (pain with stimuli that are not normally painful) in many women with CPP.

Within this context, anxiety and other psychological states are also considered to be facilitators or inhibitors of neurologic transmission. It is possible that many forms of CPP, in particular those without sufficient pathology, may result from modulation of afferent impulses or abnormality of descending inhibition in the dorsal horn, spinal cord, or brain.

image Management

When treating patients with CPP, a therapeutic, supportive, and sympathetic (but structured) physician-patient relationship should be established. The patient should be given regular follow-up appointments and should not be told to call only if the pain persists. This reinforces pain behavior as a means of procuring sympathy and medical attention.

A negative evaluation or the finding of pathology not amenable to therapy (e.g., dense pelvic adhesions) does not mean that the patient should be discharged from care without therapy directed toward her symptoms. After initial reassurance that there is no serious underlying pathology, and education as to the likely mechanisms of pain production, including central nervous system factors, symptomatic therapy should be undertaken. The symptoms of pain should be approached with the seriousness and direction afforded to any other condition.

TEAM MANAGEMENT

The most productive strategy for the management of patients with CPP is referral to a multidisciplinary pain clinic or creation of a multidisciplinary team within a specific practice setting. The personnel at such a facility should include a gynecologist, a psychologist who also has expertise in chronic pain and sexual and marital counseling, a physical therapist with pelvic floor muscle expertise, and for more complex cases, an anesthesiologist. An acupuncturist is often helpful for referrals. It is the role of the psychologist to provide cognitive behavioral pain management and stress reduction, assertiveness training, and adaptive coping strategies. Marital and sexual counseling or psychiatric referral for psychopharmacology may be needed as well. This aspect of therapy is crucial because many of these patients have become severely depressed and often are interpersonally, sexually, and sometimes even occupationally withdrawn. Depression may be secondary to pain, but without treatment of the depression, the pain may persist. Relaxation, cognitive, and behavioral therapies are employed to replace the pain behavior and its secondary gain with effective behavioral responses. Multidisciplinary management has been shown to be more effective than traditional gynecologic management. When a designated multidisciplinary pain clinic is not available, it is important to involve other specialists by referral.

MEDICAL AND SURGICAL MANAGEMENT

The gynecologist continues to assess progress, coordinate care, and provide periodic gynecologic examinations. In the initial stages of therapy, a trial of ovulation with or without menstrual suppression with combined hormonal contraception (pills, patches, rings; cyclic or continuous), high-dose or intrauterine progestins or a gonadotropin-releasing hormone agonist may be helpful. Ovulation with or without menstrual suppression is especially helpful in patients who have midcycle, premenstrual, or menstrual exacerbation of pain and in those who have ovarian pathology, such as parovarian adhesions or recurrent functional cyst formation. NSAIDs are also useful. Pharmacologic approaches to increase inhibitory neuromodulators such as norepinephrine, serotonin (5-HT), and GABA or sodium channel blockers are frequently used in the form of tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors, anticonvulsants, or other GABA-ergic agents and local anesthetics.

Surgical procedures that have not proved effective for CPP without pathology include unilateral adnexectomy for unilateral pain or total abdominal hysterectomy, presacral neurectomy, and uterine suspension for generalized pelvic pain. Lysis of adhesions is also usually nonproductive, with the possible exception of the situation in which the site of adhesions, visualized by the laparoscope, specifically coincides with the localization of pain. However, pelvic adhesions often recur after surgical lysis. Without proof of organic pathology or a reasonable functional explanation for the pelvic pain, a thorough psychosomatic evaluation should be carried out before a surgical corrective procedure is considered.

ANESTHESIA

Acupuncture, nerve blocks, and trigger-point injections of local anesthetics may provide prolonged pain relief. Acupuncture has been used successfully for dysmenorrhea, and trigger-point injections and nerve blocks with local anesthetics have been used successfully for pelvic pain. Acupuncture probably increases spinal cord endorphins. In patients who complain of pelvic pain, trigger points are usually found on either the lower abdominal wall, lower back, or vaginal and vulvar areas. A significant percentage of patients with pelvic pain have abdominal wall trigger points or nerve entrapments that respond to biweekly injections of a local anesthetic (usually up to five injections is sufficient). Anesthesia of trigger points (Figure 21-3) may abolish pain by lowering the impulses from the area of referred pain, thereby diminishing the afferent impulses reaching the dorsal horn to a level below the threshold for pain transmission. Local anesthetic nerve blocks on a repeated basis for areas of nerve impingement combined with instructions to patients about alteration in physical activity can be helpful. When needed, a prescription for nerve threshold–altering medications, as mentioned previously, can be given. These interventions can downregulate neural hypersensitivity and permanently decrease or eliminate pain.

image

FIGURE 21-3 Trigger point injection technique for the abdominal wall in a patient with chronic pelvic pain.

(From Auerbach PS: Wilderness Medicine, 5th ed. Philadelphia, Mosby, 2007.)

SUGGESTED READING

American College of Obstetricians and Gynecologists (ACOG) Committee on Practice Bulletins. ACOG Practice Bulletin No. 51. Chronic pelvic pain. Obstet Gynecol. 2004;103:589-605.

Gambone J.C., Mittman B.S., Munro M.G., et al. Consensus statement for the management of chronic pelvic pain and endometriosis: Proceedings of an expert panel consensus process. Fertil Steril. 2002;78:961-972.

Peng P.W., Tumber P.S. Ultrasound-guided interventional procedures for patients with chronic pelvic pain: A description of techniques and review of the literature. Pain Physician. 2008;11(2):215-224.

Rapkin A.J., Howe C.N. Chronic pelvic pain: A review. Parts 1 and 2. In: Family Practice Recertification. Monroe Township, NJ: Ascend Media; 2006:49-56. 59–67

Tu F.F., Holt J., Gonzales J., Fitzgerald C.M. Physical therapy evaluation of patients with chronic pelvic pain: A controlled study. Am J Obstet Gynecol. 2008;198:272-277.

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