Editor’s Introduction
Pelvic pain is a condition which is much more common than perceived by the medical and general community. Because it affects the most private aspects of human life such as sexuality and reproduction, patients are not willing to discuss it with their families, friends, and loved ones. Medical providers are also very likely to dismiss the symptoms and blame it on a psychological or psychiatric conditions. Chronic pelvic pain is real, it is common, and it is almost always due to some identifiable disease or injury. Patients with pelvic pain need to be heard and treated with dignity and respect, and the majority of them can be helped.
Pain is one of the most feared and dreaded human sensations. It is derived from the Latin poena – punishment. Pain, thirst, and hunger responses are considered to be the most primordial of human emotions [Reference Denton1]. Unlike higher emotions such as love, hate, and anger, these primordial sensations involve lower brain regions such as the medulla, midbrain, and hypothalamus. Pain may occur as an acute event or as a persistent, long-term symptom. While acute pain or nociception serves as an alert of trauma and impending damage, chronic pain is a disease and can easily become one of the most debilitating conditions that one can endure.
In 1979 the International Association for the Study of Pain (IASP) defined pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” [Reference Williams and Craig2]. This definition is incomplete because it excludes the clinically significant social and cognitive components of pain. Also, describing pain merely as an unpleasant sensation minimizes patient suffering and may influence bias in the approach of practitioners.
Over the years our understanding of pain has changed dramatically. The pain experience is characterized by tremendous interindividual variability. By definition, pain is a subjective and personal experience, inherently making clinical practice and research challenging. A multitude of biological and psychological factors contribute to these differences: genetic, psychosocial, and demographic processes inherently influence each other, contributing to the overall pain experience. Historically, pain researchers have focused intellectual pursuits on legitimizing these differences.
Nociceptive pain originates in damaged tissues, usually secondary to a noxious stimulus, and neuropathic pain is caused by a disease of the nervous system. Superficial nociceptive pain originates in the pain receptors (nociceptors) located in the skin. Deep nociceptive pain may be either somatic or visceral. Deep somatic nociceptors located in the muscles, tendons, ligaments, bones, and blood vessels usually produce dull and poorly localized pain. Deep visceral nociceptive pain originates in the visceral receptors and may be well localized; however, this localization rarely corresponds with the area of injury because of pain referral patterns. This phenomenon is commonly seen in conditions such as painful bladder syndrome, in which presenting symptoms may include back or vulvar pain. Neuropathic pain may originate in the peripheral or central nervous system, as a result of disease or intrinsic malfunction. Peripheral neuropathic pain is more common, producing sensations of burning, tingling, electrical shocks, or pins and needles. Table 1.1 outlines common terms used in clinical descriptions of abnormal pain function.
| Allodynia | Pain in response to the stimulus that is normally non painful |
| Hyperalgesia | Exaggerated response to a stimulus that is normally painful |
| Central sensitization | Up-regulation of central nervous system, causing the sensation of higher intensity pain with less provocation. Allodynia and hyperalgesia are signs of central sensitization |
| Analgesia | Absence of pain in response to painful stimulus |
| Dysesthesia | An unpleasant abnormal sensation. May be spontaneous or evoked |
| Paresthesia | An abnormal sensation. Unlike dysesthesia it does not need to be unpleasant |
| Hyperesthesia | Increased sensitivity to stimulation |
| Allotriesthesia | Pain caused by the sensation of a foreign body in the absence of a foreign body |
| Neuralgia | Pain in the distribution of the nerve. By definition it does not require nerve injury |
| Neuritis | Pain caused by inflammation of the nerve |
| Neuropathy | A disturbance of function or pathological change in a nerve |
| Noxious stimulus | A stimulus that is strong enough to damage normal tissues, usually prompting a reactive pain response |
| Peripheral sensitization | Increased sensitivity to an afferent nerve stimulus. Occurs after injury to the area, which results in the flare-up response |
| Nociceptive pain | Pain originating in the pain receptors in the skin (superficial), muscles, tendons, blood vessels (deep), or visceral organs, usually secondary to a noxious stimulus |
| Neuropathic pain | Pain originating in the peripheral or central nervous system, resulting from disease or intrinsic malfunction |
| Wind-up phenomenon | Perceived increase in pain intensity due to repetitive painful stimulus. Caused by activation of normally dormant receptors |
| Viscerosomatic convergence | Noxious stimulus to the viscera triggers pain referred to somatic sites |
| Viscerovisceral convergence | Noxious stimulus to the viscera triggers pain referred to other visceral sites |
| Functional somatic syndrome | Physical symptoms that are poorly explained. Encompasses conditions like chronic fatigue, fibromyalgia, irritable bowel syndrome, tension headache, and others |
| Somatization | Manifestation of mental phenomena as physical symptoms |
| Conversion disorder | Neurological symptoms such as numbness, blindness, or paralysis in the absence of organic cause and traced back to a psychological trigger |
Acute pain is an essential evolutionary sensation that prompts a change in position or behavior, usually in response to some noxious stimulus, with the goal of preventing any further damage to tissues. Pain has been studied in numerous animal species, including fish and invertebrates such as the fruit fly. Across species, it has been demonstrated that acute pain serves not only as a warning of external trauma, but also as a symptom of numerous internal disease processes. In humans, acute pain may serve as a lifesaving symptom of medical emergencies such as myocardial infarction. Chronic pain, on the other hand, does not always serve a clear essential purpose and can actually become a disease of its own. The general mechanism of chronic pain has clear differences from that of acute pain. The majority of patients who experience tissue trauma with acute pain will heal without any sequelae. After physical healing is complete, a small percentage of these patients will continue to experience pain. Chronic pain may result from a number of other mechanisms including degenerative disease resulting from aging or overuse, and abnormal or insufficient healing following acute physical trauma. Chronic pain may also present as a primary condition, lacking any identifiable cause. It is theorized that in some instances, the central nervous system may produce independent pain input without an external or internal pain stimulus. Regardless of origin, the mechanism of chronic pain generally has some relation to musculoskeletal or nervous system function.
Maladaptive plasticity changes in the nervous system that lead to a disruption in function, producing a disease state, have been described in a large number of clinical trials and animal studies. Additionally, these changes may also occur in sensory conduction pathways between the peripheral and central nervous system, resulting in the development and maintenance of chronic pain. Central sensitization represents the manner in which pain is uncoupled from the clear noxious stimulus that defines acute nociceptive pain. Instead, the features of pain are reflective of the functional state of the central nervous system, the memory of persistent pain, and the associated sensory conduction pathways. Central sensitization results in an alteration of the induction, spatial extent, intensity, and duration of pain [Reference Woolf3].
A key difference between an acute episode of pain and chronic pain is that the persistence of this sensation can lead to a number of adverse sequelae including physical suffering, sleep disorders, fatigue, and substance abuse. Because chronic pain and mood control share the same neurotransmitters, these patients often suffer from mood disorders such as depression, bipolar disease, obsessive–compulsive disorder, and posttraumatic stress disorder. Persistent pain can also lead to significant social concerns including difficulty with intimacy, strain on personal relationships, and poor professional performance. Decline in physical activity in patients with chronic pain often causes weight gain, deconditioning, and other secondary morbidities.
Prevalence and Impact of Chronic Pain
The prevalence of chronic pain is difficult to estimate. In the industrialized world anywhere from 20% to 50% of people suffer from pain for more than 6 months during some point in their lifetime. In the United States the prevalence of chronic pain is approximately 30.7%, translating to an estimate of 90 million people living in pain. Chronic pelvic pain affects 5.7%–26.6% of reproductive-age women, with variation in these numbers influenced by population characteristics [Reference Ahangari4]. It is estimated that one in seven women meet clinical criteria of chronic pelvic pain at some point in their lives. In women the prevalence of chronic pelvic pain is higher than that of asthma, diabetes, and coronary artery disease and almost as high as that of back pain [Reference Zondervan and Barlow5].
This vast number of affected individuals has led to significant social and economic sequelae. The total annual cost associated with pain in the United States has been estimated to be between 560 and 635 billion dollars, which is higher than the combined annual cost associated with heart disease and cancer. Other studies estimate the economic impact of chronic pain to be 3% of GDP.
Between 1999 and 2016, more than 630,000 people died from a drug overdose in the United States. In 2016, an estimated 48.5 million persons in the United States reported use of illicit drugs or misuse of prescription drugs in the past year, of which 4.3% were prescription pain relievers; this translates to 2 million individuals [6]. In 2017 healthcare providers wrote on average 58.5 prescriptions per 100 persons. Even though opioid prescribing continued to decrease through 2017, more efforts are needed to help healthcare providers adopt and maintain safe prescribing habits.
The Diagnostic Challenges of Chronic Pelvic Pain
Chronic pelvic pain is a common and often underdiagnosed condition occurring in both women and men. Although this book specifically focuses on chronic pelvic pain in women, chronic pain in men is equally frequent and devastating, with similar challenges in diagnosis and management.
The International Pelvic Pain Society defines chronic pelvic pain as pain located in the pelvis, persisting for 6 months or longer, with or without association with menstrual cycles and severe enough to cause functional disability [Reference Howard7]. Up to one in seven women meet this clinical criterion over the span of their lifetime. Despite this high prevalence, the condition remains relatively underdiagnosed and untreated. This is at least in part due to the suboptimal education of clinicians on the subject of female chronic pelvic pain. In the United States, most medical school curricula lack even a single lecture dedicated to chronic pelvic pain in women, and postgraduate obstetrics and gynecology training tends to limit this training to endometriosis and painful bladder syndrome. This approach produces clinicians who are ill prepared for the diagnosis and management of the wide range of gynecological and nongynecological conditions that can lead to chronic pelvic pain.
Most women with pelvic pain have more than one condition contributing to their pain, further complicating diagnostic workup. This is commonly true in the case of endometriosis. Dr. Fred Howard, a pioneer in the area of chronic female pelvic pain in the United States, made an observation in his practice that more than three-quarters of patients with endometriosis and pelvic pain have another etiology contributing to their pain, in addition to their endometriosis. This means that if the only intervention offered to these women is treatment of endometriotic lesions, more than half will likely not experience adequate improvement in their chronic pain.
The diagnosis of pelvic pain is further challenged by the fact that many patients with chronic pelvic pain do not have easily identifiable pathology. The American College of Obstetricians and Gynecologists (ACOG) highlights bloodwork, ultrasonography, cystoscopy, sigmoidoscopy, colonoscopy, and laparoscopy as potential workup modalities that may be helpful in working toward a diagnosis in patients with chronic pelvic pain, based on presenting symptoms [8]. It has been reported that up to 30% of women with pelvic pain have completely normal findings on laparoscopy [Reference Howard9]. In the remaining 70% of patients the most common surgical findings were lesions consistent with endometriosis and adhesions. The severity of endometriosis and adhesions tends to be only marginally correlated with the severity of chronic pelvic pain [Reference Vercellini, Fedele, Aimi, Pietropaolo, Consonni and Crosignani10]. Only deep infiltrating endometriosis has been shown to be associated with more pain [Reference Fauconnier, Chapron, Dubuisson, Vieira, Dousset and Bréart11]. In light of the inconsistent findings in the clinical workup of patients with chronic pelvic pain, ACOG has previously concluded that “few, if any of the diseases thought to cause chronic pelvic pain meet traditional epidemiological criteria of causality”[12].
A final key point is that more than 70% of the causes of chronic pelvic pain may be nongynecological, further contributing to diagnostic challenges. Musculoskeletal causes of pain are often overlooked in the evaluation and workup of chronic pelvic pain, and data regarding the true prevalence are limited. Based on a retrospective, cross-sectional study conducted using a population in a single chronic pelvic pain specialty clinic, Tu et al. estimated that the prevalence of pelvic floor musculoskeletal disorders in their patients was 14%–22% [Reference Tu, Sanie and Steege13]. Based on our practice experience, which is approaching two decades of work, this is a gross underestimation. Up to 74% of patients with chronic pelvic pain will have an identifiable abdominal wall trigger point with proper clinical evaluation, and 71% have focal areas of pain along the pelvic floor muscles (ie. levator ani, obturator interni) and piriformis muscles on vaginal exam [Reference Slocumb14]. The most common musculoskeletal contributor to chronic pelvic pain is spasm of the pelvic floor muscles. This spasm may be primary or secondary. Causes of primary spasm are unknown but it may be due to genetic abnormalities or inherent diseases of the muscles that make them more prone to spasm. Secondary spastic pelvic floor may result from irritation of pelvic viscera, physical pelvic trauma, or psychological insult. Irritation of the pelvic viscera may be associated with endometriosis or pelvic inflammatory disease (PID). Accidents, athletic activity, or simply overworking pelvic and lower extremity muscles can lead to pelvic trauma. Pelvic surgery and childbirth with seemingly uncomplicated clinical course may provoke pelvic floor muscle spasms. Psychological insult may include psychological trauma and sexual violence. Musculoskeletal causes of pain will be discussed in detail in Chapter 20.
Another common cause of chronic pelvic pain is painful bladder syndrome. It will be discussed in detail in Chapter 9. Painful bladder syndrome is also often referred to as interstitial cystitis or bladder pain syndrome. This syndrome often coexists with other pelvic pain disorders. Painful bladder syndrome is not simply a disease of the bladder; it is a condition mediated by the intricate connection between the viscera, muscles, and central nervous system. Table 1.2 lists a number of other gynecological and nongynecological conditions that may manifest as chronic pelvic pain.
We hope that this text will serve as a primary resource for addressing the challenges that clinicians face in caring for chronic pelvic pain patients. The following chapters will assist in defining the theories and components of chronic pelvic pain development. They will also provide diagnosis and management algorithms that can be used to optimize the care for these patients.
Five Things You Need to Know
Chronic pelvic pain is defined as pain located in the pelvis, persisting for 6 months or longer, with or without association with menstrual cycles and severe enough to cause functional disability.
In the industrialized world anywhere from 20% to 50% of people suffer from pain for more than 6 months during some point in their lifetime.
Up to 70% of patients with chronic pelvic pain have a nongynecological cause of their pain.
More than 60% of patients with chronic pelvic pain treated in general obstetrics/gynecology practice do not have a proper diagnosis.
Most patients with chronic pelvic pain have multiple reasons for pain: endometriosis, interstitial cystitis, and irritable bowel syndrome coexist in many of these patients.
