Chronic pain management
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Chronic pain management

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  • Tremendous progress has been made in pain management through the increased understanding of the physiologic mechanisms of pain and the pathologic basis of pain syndromes. Along with an increasing awareness of the epidemiology of pain comes a heightened appreciation for the impact of pain on individuals, families and society. Attitudes toward pain and its treatment have deep roots that can be traced to environmental factors, cultural influences, physician training and even genetics. A natural outgrowth of awareness and understanding is the development of new products for pain management—new drugs, new formulations of existing drugs, and alternate drug-delivery systems (e.g., patient-controlled analgesia, epidurals, transdermal devices).
  • More than merely a disagreeable sensation resulting from a noxious event, pain is a multidimensional experience. Pain perception is complex, subjective, and influenced by physiologic, social, psychologic, and spiritual processes. The International Association for the Study of Pain (IASP) Subcommittee on Taxonomy defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage, or both.” This definition encompasses the sensory experience of pain and consideration of an individual’s affective and cognitive response and illustrates that the relationship between pain and tissue injury is neither uniform nor constant. Chronic pain has been described as persistent or recurrent pain, lasting beyond the usual course of acute illness or injury and adversely affecting the patient’s well-being. Thus, it is not merely a temporal extension of acute pain, and its management requires a shift in therapeutic strategy. Chronic pain occurs in cancer, in progressive diseases, in slowly evolving or nonprogressive conditions, and as a result of injury or neurologic damage. It also occurs in the absence of an easily identifiable underlying lesion. American Society of Anesthesiologists. Practice guidelines for pain management: a report by the American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiol. 1997;86:995-1004. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:19-21. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms . 2nd ed. Seattle, WA: IASP Press; 1994:3-4. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:3.
  • Many attempts have been made to classify pain syndromes based on a variety of dimensions. Ideally, a classification scheme should be mutually exclusive and completely exhaustive for the data to be incorporated. Every element in a classification should fit into one and only one place. Expert-based classifications develop preconceived categories and force individuals into the most appropriate one, even if not all characteristics defining the category are present. Examples of such systems include the International Classification of Diseases ( ICD-10 ) and the current procedural terminology (CPT) coding scheme. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:19-21.
  • This system is the most comprehensive approach to classification of chronic pain syndromes; it is intended to standardize descriptions of pain syndromes and provide a point of reference. The system establishes a 5-digit code that assigns a unique number to each chronic pain diagnosis. The digital code (1 through 9 within each “axis”) is first, followed by letters used as suffixes, if necessary. Axis I: concerned with regions; if patient has pain in more than one region, use two codes Axis II: concerned with systems, such as nervous system, respiratory, musculoskeletal, etc.; some details open to debate, but practicality should prevail Axis III: deals with characteristics of pain Axis IV : filled in according to the patient’s report of severity or chronicity of the illness Axis V: concerns mechanisms involved in pain production and is most open to debate. Letters (a, b, c, d, etc.): Since some syndromes have same final five-digit code, a letter may be added to the sixth place to distinguish them. It could indicate acute vs chronic conditions, but usually merely indicates the first of several conditions to be described with the same five digits. An example: Mild postherpetic neuralgia of T5 or T 6, 6 months’ duration = 303.22e Axis I: Thoracic region Axis II: Nervous system (central, peripheral, or autonomic); physical disturbance/dysfunction Axis III: Continuous or nearly continuous, fluctuating severity Axis IV: Mild severity of 1 to 6 months Axis V: Trauma, operation, burns, infective, parasitic (one of these) Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:19-21. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle, WA: IASP Press; 1994: 3-4.
  • Because more than 40% to 50% of patients in routine practice settings fail to attain relief from pain, chronic pain is considered a major health care and social problem of epidemic proportions. Chronic pain is the most frequent cause of suffering and disability that seriously decreases quality of life and the second most frequent complaint that brings people to physicians’ offices in North America. American Pain Society. Chronic pain in America: Roadblocks to relief. 2001. http://www.ampainsoc.org/whatsnew/conclude_road.htm Gitlin MC. Chronic non-cancer pain: an overview of assessment and contemporary management. J La State Med Soc . 1999;151(2):93-8. Glajchen M. Chronic pain: Treatment barriers and strategies for clinical practice. J Am Board Fam Pract. 2001;14:211-18. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:242.
  • Pain is one of the most common reasons that people seek medical help, yet it is frequently undertreated. The undertreatment of pain has a tremendous impact on individuals and society in terms of lost productivity, needless suffering, and burgeoning health care expenditures. Chronic pain sufferers are having difficulty finding physicians who can effectively treat their pain. Almost one half have changed doctors since their pain began; almost one fourth have changed doctors at least three times. The level of frustration is significantly higher in patients who have severe pain, where the majority have changed doctors at least once in their attempt to seek some relief from pain, and one out of every three people have changed three times or more. Their primary reason for changing physicians was that they still suffered unbearable pain even after treatment. The study cited above, Chronic Pain In America: Roadblocks To Relief, was conducted for The American Pain Society, The American Academy of Pain Medicine, and Janssen Pharmaceutica, L.P. by Roper Starch Worldwide Inc. in January 1999; details are posted on the American Pain Society website. American Pain Society. Chronic pain in America: Roadblocks to relief. 2001. http://www.ampainsoc.org/whatsnew/conclude_road.htm Glajchen M. Chronic pain: Treatment barriers and strategies for clinical practice. J Am Board Fam Pract. 2001;14:211-18. Lister B. Dilemmas in the treatment of chronic pain. Am J Med . 1996;101(suppl 1A):S25-S55. Portenoy RK: Opioid therapy for chronic nonmalignant pain: clinicians’ perspective. J Law Medicine Ethics . 1996;24:296-309.
  • A lack of basic knowledge about pain management strategies and a reluctance to prescribe opioids contribute to the inadequate treatment of chronic pain by health care professionals. Myths about opioids learned in training persist in practice—assumptions that tolerance, side effects and addiction are inevitable and unmanageable, and the misconception that there is a ceiling dose (i.e., maximum safe dose), all contribute to creating barriers to adequate treatment. Health care system barriers, including fear of regulatory scrutiny and prohibitive reimbursement policies, as well as patient barriers, such as fear of addiction or the assumption that pain is inevitable, also contribute to undertreatment. American Pain Society. Chronic pain in America: Roadblocks to relief. 2001. http://www.ampainsoc.org/whatsnew/conclude_road.htm Glajchen M. Chronic pain: Treatment barriers and strategies for clinical practice. J Am Board Fam Pract. 2001;14:211-18. Lister B. Dilemmas in the treatment of chronic pain. Am J Med . 1996;101(suppl 1A):S25-S55. Portenoy RK: Opioid therapy for chronic nonmalignant pain: clinicians’ perspective. J Law Medicine Ethics. 1996;24:296-309. Weinstein SM, Laux LF, Thornby JI et al. Medical students attitudes toward pain and the use of opioid analgesics: Implications for changing medical school curriculum. South Med J. 2000;93(5):472.
  • Inadequate pain management for minority patients may result both from physician- and patient-related factors. Some barriers that contribute to substandard pain management in ethnic and racial minority patients include: greater difficulty in assessing pain because of differences in language and cultural backgrounds physicians’ perceptions that patients in minority groups have fewer financial resources to pay for prescriptions physicians’ perceptions about a higher potential for drug abuse in minority groups Inadequate treatment may also result from the patients’ fear of aggressive treatment, their lack of assertiveness in seeking treatment, and a lack of expertise in treating pain patients at the sites used by many patients belonging to minority groups. These findings highlight the importance of conducting aggressive research and presenting timely and focused physician education programs to improve pain treatment for all people and to eliminate the disparities in pain treatment for ethnic and racial minorities. Bonham VL. Race, ethnicity, and pain treatment: striving to understand the causes and solutions to the disparities in pain treatment. J Law Med Ethics . 2001;29:52-68. Review. Glajchen M. Chronic pain: Treatment barriers and strategies for clinical practice. J Am Board Fam Pract. 2001;14:211-18.
  • Because of the barriers discussed earlier, until the late 1980’s most physicians felt that there was no role for long-term opioids in chronic pain management. In 1986 Portenoy and Foley described their retrospective experience treating 38 patients with chronic nonmalignant pain with opioids, with favorable outcomes in all patients. Other studies during the past 15 years have had similar outcomes. Opioids have become a mainstay of cancer pain therapy and have growing acceptance in the treatment of chronic nonmaligant pain. In 2000, Joranson and colleagues published the results of a retrospective survey of DAWN (Drug Abuse Warning Network) medical records from 1990 to 1996 to evaluate the proportion of drug abuse related to opioid analgesics and the trends in medical use and abuse of five opioid analgesics (fentanyl, hydromorphone, meperidine, morphine, oxycodone) used to treat severe pain. The abuse levels for each of the analgesics studied were less than 1% of the total DAWN mentions and declined during the study period despite substantial increases in medical use. The investigators concluded that the trend of increasing medical use of opioid analgesics to treat pain does not appear to contribute to increases in the health consequences of opioid use. Another important development in the treatment of chronic pain with opioids has been the recent surge in the medical and regulatory communities of published guidelines for the management of pain, which identify opioid therapy as accepted treatment for chronic pain management. Joranson DE, Ryan KM, Gilson AM, et al. Trends in medical use and abuse of opioid analgesics. JAMA. 2000;283:1710-1714. Portenoy RK, Foley KM. Chronic use of opioid analgesics in non-malignant pain. Pain. 1986; 25(2):171-86. Joranson DE, Ryan KM, Gilson AM, Dahl JL. Trends in medical use and abuse of opioid analgesics. JAMA. 2000;283(13):1710‑1714.
  • Since the early 1960’s, developments have taken place that can rectify some of the deficiencies in the understanding and treatment of pain that existed even in the early 20 th century. Research has given us a greater understanding of the pathophysiology underlying many chronic pain syndromes. This understanding has led to advances in drug therapies, the use of multimodal therapies, and the belief that in some cases the optimal treatment of chronic pain is best managed by a multidisciplinary team. A pioneer and giant in the field of pain therapy, J ohn Bonica, established the first multidisciplinary pain clinic, the Multidisciplinary Pain Center, at the University of Washington in 1960. Patient’s rights movements have been supported by documents such as the Joint Commission on Accreditation of Healthcare Association’s (JCAHO) Pain Standards for 2001 , which states that all patients have the right to the appropriate assessment and management of pain. Joint Commission on the Accreditation of Healthcare Organizations. Patient Rights and Organization Ethics. Referenced from the Comprehensive Accreditation Manual for Hospitals, Update 3, 1999. http://www.jcaho.org/standards_frm.html Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:3-15.
  • In the last several years, health-policymakers, health professionals, regulators, and the public have become increasingly interested in providing better pain management. In fact, the U.S. Congress has named this decade the Decade of Pain Control and Research. Medical and regulatory communities have been making great strides to address concerns about undertreatment of chronic pain, many of them issuing published guidelines for the management of pain and identifying opioid therapy as accepted treatment for chronic pain management . American Academy of Pain Medicine and American Pain Society. The Use of Opioids for the Treatment of Chronic Pain: A Consensus Statement , 1996. www.ampainsoc.org American Medical Association. AMA Report 11 of the Council on Scientific Affairs (A-99), April 2001. http://www.ama.assn.org/ama/pub/article/2036-2341.html American Society of Anesthesiologists. Practice Guidelines for Pain Management: A Report by the American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiology. 1997;86:995-1004. Jacox A, Carr DB, Payne R, et al. Management of Cancer Pain. Clinical Practice Guideline No. 9. In: AHCPR Publication No. 94-0592. Rockville, MD. Agency for Health Care Policy and Research, U.S. Department of Health and Human Services. Public Health Service, 1994. Joint Commission on the Accreditation of Healthcare Organizations. Patient Rights and Organization Ethics. Referenced from the Comprehensive Accreditation Manual for Hospitals , Update 3, 1999. http://www.jcaho.org/standards_frm.html The Federation of State Medical Boards of the United States, Inc. Model Guidelines for the Use of Controlled Substances for the Treatment of Pain . May 1998. http://www.fsmb.org World Health Organization: Cancer Pain Relief, with a Guide to Opioid Availability. 2nd ed. Geneva: WHO; 1996.
  • Numerous surveys from the United States and Europe during the last decade have shown that 30% to 50% of adult patients in active therapy for a solid tumor experienced chronic pain. With advanced disease, the prevalence of pain increased to 90%. A recent survey by the IASP concluded that the inferred mechanism of pain is neuropathic in 40% of cases. In a very large survey of institutionalized elderly patients with cancer, the prevalence of pain was 27.4%, and pain was associated independently with age, gender, race, marital status, functionality, and cognitive status. Cancer pain is often associated with psychological distress and functional impairment. Unrelieved pain may significantly impaired quality of life . In the AIDS population, the prevalence rates range from 25% to 80%. This broad range reflects differences in populations studied and pain assessment methodologies. Bernabei R, Gambassi G, Lapane K, et al: Management of pain in elderly patients with cancer. JAMA. 1998;279:1877-1882. Caraceni A, Portenoy RK, a working group of the IASP Task Force on Cancer Pain. An international survey of cancer pain characteristics and syndromes. Pain . 1999;82:263-274. Cleeland CS, Gonin R, Harfield AK, et al: Pain and its treatment in outpatients with metastatic cancer. N Engl J Med. 1994;330:592-596. Heim HM, Oei TP: Comparison of prostate cancer patients with and without pain. Pain. 1993; 53:159-162. Portenoy, RK: Cancer pain. Pathophysiology and syndromes. Lancet. 1992; 339:1026-1031. Portenoy RK, Kornblith AB, Wong G, et al: Pain in ovarian cancer. Prevalence, characteristics, and associated symptoms. Cancer . 1994;74:907-915. Serlin RC, Mendoza TR, Nakamura Y, et al: When is cancer pain mild, moderate or severe? Grading pain severity by its interference with function. Pain. 1995;61L277-284.
  • In the clinical setting, underlying mechanisms for pain can only be inferred, not established, and the overall classification tends to simplify complex processes. However, classifications based on inferred pathophysiology are clinically useful and have become widely accepted. Nociceptive Pain. Appears to be consistent with the ongoing activity in peripheral nociceptors (primary afferent neurons that respond selectively to noxious stimuli). The degree of nociceptor activation is inferred from the extent of the tissue damage, so nociceptive pain is said to be consistent with apparent degree of tissue injury. Somatic pains are those related to ongoing activation of somatic primary afferents. Visceral pains are those related to activation of the primary afferent neurons that innervate viscera. Neuropathic Pain. Believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system. The classification is based on inferred location of the pain “generator” (peripheral or central) and types of mechanisms involved. Three major categories have been recognized: deafferentation pain, sympathetically-maintained pain, and peripheral neuropathic pain. Deafferentation pains are presumably related to pathophysiologic processes in the CNS. Subtypes include pain caused by injury to the brain or spinal cord, phantom pain, postherpetic neuralgia, and pain caused by root avulsion. This type of neuropathic pain is less common in cancer patients. Sympathetically-maintained pain is defined as a pain presumed to be sustained by efferent activity in the sympathetic nervous system. A sympathetic nerve block is needed to establish the diagnosis of sympathetically-maintained pain. This type of pain appears to occur most frequently in the setting of a complex regional pain syndrome (CRPS), which refers to a regional pain syndrome in which pain is associated with focal autonomic dysfunction (vasomotor instability, swelling, sweating) and/or trophic changes (thinning of the skin, changes in hair growth, bone and subcutaneous tissue losses). Peripheral neuropathic pain is usually caused by a focal peripheral nerve injury, or by a diffuse injury (polyneuropathy). Portenoy, RK. Definitions and Principles of Assessment. In Pain in Oncologic and AIDS Patients . 3 rd ed. Newtown, PA: Handbooks in Health Care Co.; 2000:25-26.
  • Syndrome identification is useful to identify the etiology and pathophysiology of the pain and the extent of the underlying disease, to clarify the need for further evaluation, and to refine the prognosis and guide therapy. Pain syndromes can be acute or chronic. Acute cancer pain is almost always directly related to diagnostic interventions. Chronic cancer pain syndromes can be related to tumor infiltration or compression, related to treatment, or unrelated to cancer or its therapy. Approximately 75% of cancer pain syndromes result from a direct effect of the neoplasm. Careful assessment of the etiology is necessary because the determination of nociceptive versus neuropathic and whether the pain in caused by the cancer, the treatment, or is unrelated, can influence therapy selection. Portenoy, RK. Definitions and Principles of Assessment. In: Pain in Oncologic and AIDS Patients , 3 rd ed. Newtown, PA: Handbooks in Health Care Co.; 2000:25-26. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:192. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle, WA: IASP Press; 1994:3-4.
  • Acute pain induced by diagnostic procedures (biopsies) and various cancer therapies (surgery, radiation, chemotherapy) is not a difficult diagnostic problem. Chronic pain, however, tends to be more difficult to diagnose and treat. The intensity and severity of the pain must be accurately assessed and communicated to avoid undertreatment. The pathophysiology involved in the pain syndrome helps to distinguish between nociceptive (somatic and visceral) and neuropathic pain. Tumor type and stage often provide clues as to the type of pain problem — for example, infiltration of peripheral nerves, soft tissue, bone, hollow organs, mucosa, solid organs (necrosis), and occlusion of vasculature. Certain pain syndromes are associated with specific tumors, for example, pancreatic (abdominal), ovarian (abdominopelvic and low back), prostate (bone), breast (bone, lung, liver, brain). Patterns of pain can also be helpful in diagnosis. Incident pain is related to an activity or event, end-of-dose failure is commonly associated with a dosage interval that is too long, and spontaneous pain has no relationship to activities or events. Severe pain syndromes are useful in determining the best therapeutic approach. Among those syndromes are bone metastases, visceral pain, neuropathic (central and peripheral), back pain and spinal cord compression. Cleeland CS, Syrjala KL. How to assess cancer pain. In: Turk D, Melzack R, editors. Pain Assessment. New York: Guilford Press; 1992:360-87. Jacox A, Carr DB, Payne R, et al. Management of Cancer Pain. Clinical Practice Guideline Number 9. AHCPR Publication No. 94-0592, Rockville, MD. Agency for Health Care Policy and Research, US Department of Health and Human Services, Public Health Service; March 1994. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996. Turk DC, Okifuji A. A cognitive-behavioral approach to pain management. In: Wall PD, Melzack R., eds. Textbook of Pain, 4th ed. Edinburgh, Scotland: Churchill Livingston; 1994;1431-1444. Wall PD, Melzack R. Textbook of Pain . 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:540.
  • The treatment plan should begin with an assessment to identify the cause of the pain and potentially treatable organic conditions, some of which may be alleviated with primary treatment. Pharmacologic and nonpharmacologic interventions may incorporate a multidisciplinary team approach to improve functionality and quality of life. Depression, mood disturbance, and sleep disorders are frequent in cancer patients with pain syndromes. The pharmacologic management of chronic pain includes three broad categories of analgesics. The opioids are the mainstay drugs for moderate-to- severe pain associated with medical illness. The nonopioid drugs include acetaminophen and the nonsteroidal anti-inflammatory drugs. Adjuvant analgesics are drugs with primary indications other than pain, but which may be analgesic in selected circumstances. When cancer pain does not fit into a well-defined pain syndrome, the World Health Organization (WHO) Analgesic Ladder can be effectively used. However, this ladder has limited applicability for well-defined syndromes for which specific therapies have been demonstrated to be effective, for example, antidepressants, anticonvulsants and most recently the N-methyl-D-aspartate (NMDA) agents (high dose dextromethorphan) for neuropathic pain and NSAIDs for bone pain and pain that includes an inflammatory component. The central component to most regimens for treatment of moderate-to-severe cancer pain is a long-acting opioid with a short-acting opioid prescribed for breakthrough pain. Jacox A, Carr DB, Payne R, et al. Management of Cancer Pain. Clinical Practice Guideline Number 9. AHCPR Publication No. 94-0592, Rockville, MD. Agency for Health Care Policy and Research, US Department of Health and Human Services, Public Health Service; March 1994. Lucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management. Cancer Pract. 2002;10(suppl 1):S14-S20.
  • 08/13/12 12:24 PM An approach to the selection of drugs for use in managing cancer pain has been developed by the Cancer Relief and Palliative Care Program of the World Health Organization (WHO). This approach, known as the “analgesic ladder,” uses a stepwise selection of analgesics (nonopioids, opioids, and adjuvant analgesics), based on the severity of pain. This slide represents an adaptation of the WHO ladder. Patients with mild to moderate pain are first treated with an NSAID. If a specific indication for an adjuvant drug exists, the NSAID is combined with the appropriate adjuvant drug. Patients who present with moderate to severe pain, or who fail to achieve adequate relief after a trial of an NSAID, are treated with an opioid conventionally used for pain of this severity, which typically is combined with an NSAID and may be co-administered with an adjuvant, if indicated. Patients who present with severe pain or who fail to achieve adequate relief following appropriate administration of drugs on the second rung of the analgesic ladder should receive an opioid conventionally selected for severe pain. This treatment may also be combined with an NSAID or an adjuvant drug, as indicated. These simple guidelines have gained widespread acceptance in the treatment of cancer pain. Trials of this approach suggest that 70-90% of patients can achieve adequate relief of cancer pain without additional treatments. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:563-589.
  • Low back pain is the most common cause of workdays missed because of disability related to pain, and the condition that most often leads to disability claims. In addition, it is the most common cause of activity limitation in the working years (ages 18 to 55) in the U.S. and in every other developed country that has been studied. Low back pain is the second most frequent reason for physician visits, the fifth most frequent reason for hospitalization, and the third-ranking reason for surgical procedures. The annual incidence of low back pain in the United States is 5% of the adult population; at any point in time 7 million individuals are experiencing low back pain. Low back pain has a lifetime prevalence of 60% to 85%. Annual U.S. health care costs related to low back pain amount to $33 –$50 billion. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:242. Wall PD, Melzack R. Textbook of Pain. 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994 .
  • Back pain is a condition that arises from a large heterogeneous spectrum of diseases. A major issue is that the actual pathophysiologic causes of the pain are unknown. There is reasonable evidence that overt instability causes the pain and elimination of that instability will reduce pain. The strongest evidence is that root compression is associated with the pain, and decompression is a satisfactory treatment for many patients. However, for the majority of patients with chronic back pain, the association of the pain with structual abnormalities is weak. Back pain may originate from many spinal structures, including vertebrae and laminae, facet joints, meninges, nerves, or muscles. Pain receptors in the fibrous covering of the intervertebral disk or the membrane lining the vertebral bones may become inflamed from an acute traumatic event such as a whiplash injury or lifting a heavy object. The central nervous system may become sensitized over time as well. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain . 3 rd ed. Baltimore: Lippincott Williams Wilkins ; 2001:242.
  • Patients experiencing back pain and sciatica should receive a comprehensive assessment and prompt, effective treatment. These patients are heavy users of medical resources and are consistently disabled from pain. In fact, throughout the world specialized facilities exist to deal with the millions of patients suffering from chronic back pain. Regardless of the cause of the pain, these patients present with similar complaints and findings. They are preoccupied with pain, and pain is the cause of their impairment. A very high percentage of pain patients are depressed and anxious, and there is an unusually high incidence of psychiatric diagnoses in this population. An even larger number have features that are consistent with personalaity disorder. Drug misuse is common among them, but addictive behavior is rare. Wall PD, Melzack R. Textbook of Pain . 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:540.
  • A careful history and physical examination are often necessary for the diagnostic evaluation of a patient with back pain and sciatica. A medical history of unexplained weight loss, fever, cancer, infection, etc, may give clues to an underlying systemic or organ disease. Family and psychosocial history, such as depression, substance abuse, or job dissatisfaction, may be associated with persistent and unexplained back pain syndrome. To help with the differential diagnosis, the assessment of pain should consist of the following: description, duration, and severity/intensity of pain, along with an account of any alleviating or aggravating factors. Response to previous pharmacologic therapy is helpful in assessing future management strategies. Observe patient behavior during the interview to determine if actions are consistent with the description of pain. Physical examination should consist of musculoskeletal and neurologic evaluations. Clinicians should focus on musculoskeletal deformities, areas of tenderness, range of motion, and neurologic function. Imaging is important in chronic pain patients. Plain x-rays with flexion/extensions are important. MRI is best for most screening. CT can be used if bony pathology is suspected. Wall PD, Melzack R. Textbook of Pain . 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:541.
  • As mentioned earlier, chronic back pain results from a heterogeneous group of disorders with contributions from nociceptive, neuropathic, and psychologic sources. To evaluate the validity of a therapeutic approach, clear outcome measures are required, and these are not yet available for chronic back pain. Some of the multifactorial measures suggested are patient ratings, return to work, and increased function. Because there is still a scarcity of verifiable treatment outcomes, the best we can do is offer a review of the techniques that have widely accepted clinical use. Analgesic and adjuvant medications Physical therapies Neural stimulation Psychologic management Multidisciplinary pain centers A majority of people working in the field of chronic low back pain feel that a subset of patients with chronic low back pain should be treated in a multidisciplinary pain center, in which pharmacologic, psychologic, and physical therapies are integrated into an individualized plan for each patient. The goals of these groups center more on physical rehabilitation than on symptom control only. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:140-141.
  • Osteoarthritis (OA), also referred to as degenerative joint disease (DJD), is the most common form of arthritis. The syndrome is more common in men than women in the under-45 age group, but reverses (more common in women than men) in the over-45 age group. Age is the most powerful risk factor for osteoarthritis (OA) in the United States. It is estimated that 80% of individuals older than 55 years have radiographic evidence of OA, although only 25% report the symptoms to their doctors. The U.S. is growing older—the over-65 age group represented only 4% of the population in 1900, but accounted for 12.4% in 1988 and is projected to account for 22% by the year 2030. As the age of our population has increased, so has the prevalence of arthritis. About 43 million individuals (1 in 6) have arthritis, and most are older than 45 years. By the year 2020, 59.4 million persons in the U.S. will be affected by arthritis, thus increasing chronic disability and costs by more than 25%. Elders MJ. The increasing impact of arthritis on public health. J Rheumatol. 2000;60(suppl):S6-S8. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain . 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:503-504. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms . 2nd ed. Seattle, WA: IASP Press; 1994:48.
  • In addition to a progressive deterioration of the joint, including loss of articular cartilage and increased number of chondrocytes, frequently the patient history will include prior trauma, accidents, or microtraumas. Degeneration of the articular cartilage can also occur secondary to another disease (rheumatoid arthritis, gout arthritis and psoriatic arthritis). In truth, the anatomical causes of OA remain unclear, but any theory must take into account the fact that the principal structure involved in OA, the articular cartilage, contains few pain-sensitive fibers; thus, pain must be arising from other tissues. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:506. Wall PD, Melzack R. Textbook of Pain. 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:497.
  • Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:506-507.
  • The typical patient with osteoarthritis (OA) is middle-aged or elderly and complains of pain in the knee, hip, hand or spine. The patient usually has pain and stiffness in and around the affected joint and some limited function. Pain typically worsens with use of the affected joint and is alleviated with rest. Pain at rest or nocturnal pain is a feature of severe OA. Morning stiffness lasting less than 30 minutes is common. Patients with OA of the hip may complain of problems with gait. Pain can vary greatly in site and nature, sometimes making early diagnosis difficult. The pain may be felt in the area of the buttock, groin, thigh or knee and can vary in character from a dull ache to a sharp, stabbing pain. Hip stiffness is common, particularly after inactivity. Early physical signs of OA of the hip include restriction of internal rotation and abduction of the affected hip, with pain occurring at the end of the range of motion. Patients with OA of the knee often complain of instability or buckling, especially when descending stairs or stepping off curbs. Patients with OA of the hands may have problems with manual dexterity. The physical exam should include a careful assessment of the affected joints, surrounding soft tissue and bursal areas. Crepitus, which is felt on passive range of motion, is a frequent sign of OA of the knee. Periarticular disorders, such as anserine, infrapatellar or prepatellar bursitis, should be ruled out. These disorders can be mistaken for OA. Patients with erosive OA may have signs of inflammation in the interphalangeal joints of the hands. This inflammation can be mistaken for rheumatoid arthritis, which causes similar joint swelling. However, OA generally does not have an inflammatory component, except in advanced disease. Radiographs usually confirm the diagnosis of OA, although the findings are nonspecific. The key radiographic features of the disease are a loss of joint space and the presence of new bone formation. Most routine blood tests are normal in patients with uncomplicated OA. Analysis of synovial fluid usually reveals a white blood cell count of less than 2,000 per mm 3 (2.03 10 9 per L). Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:509. Manek J, Lane NE. Osteoarthritis: current concepts in diagnosis and management. Am Fam Physician . 2000;61:1795-804.
  • Treatment of osteoarthritis should be individualized. Comorbid conditions such as cardiac disease, hypertension, peptic ulcer disease or renal disease must be considered, as should the patient's needs and expectations. A wide range of treatment options are available for managing osteoarthritis pain. The American Pain Society published their guidelines for the treatment of arthritis in March 2002: those guidelines are summarized on this slide. In 2000, The American College of Rheumatology also published criteria for the treatment of osteoarthritis of the hip, knee and hand. Generally, the ACT treatment options are as follows: Nonpharmacologic Management ·          Patient education ·          Exercise ·          Assistive devices ·          Weight management   Pharmacologic Management ·          Acetaminophen ·          NSAIDS; COX-2 inhibitors ·          Glucosamine ·          Topical/local analgesics ·          Intra-articular corticosteroid injections ·          Surgery ·          Opioids American College of Rheumatology. Recommendations for the Medical Management of Osteoarthrits of the Hip and Knee. Arthritis and Rheumatism. 2000;43:1905-1915. Arthritis Pain Guideline Panel. Guideline for the Management of Pain in Osteoarthritis, Rheumatoid Arthritis and Juvenile Chronic Arthritis . Glenview, IL: American Pain Society; 2002. Manek J, Lane NE. Osteoarthritis: current concepts in diagnosis and management. Am Fam Physician . 2000;61:1795-804.
  • Fibromyalgia syndrome is not a subtype or form of arthritis. Although it is associated with widespread pain, joint swelling and inflammation are not obvious. The soft tissues that are painful in this syndrome appear to be the ligaments, muscles, bursae, tendons, and fascia. In 1990, the American College of Rheumatology established criteria for the diagnosis of fibromyalgia syndrome, including a history of widespread musculoskeletal pain of more than 3-months’ duration and pain upon palpation of specific tender points (11 of 18, with 9 bilateral). The locations of the tender points include the occiput, cervical spine, trapezius, supraspinatus, second rib, lateral epicondyle extensor muscle, gluteal region, greater trochanter, and knees (all bilateral). In view of the tenderness in these areas at stimuli not normally painful, some have viewed fibromyalgia syndrome as a disorder of “widespread allodynia.” Fibromyalgia syndrome has been reported in all age groups and in many ethnic groups. In adults, the syndrome is 4 to 7 times more common in women than in men. The highest prevalence is in women between 50 and 60 years old. Even though the syndrome may occur in association with other disorders such as systemic lupus erythematosus or rheumatoid arthritis, its presentation is not a “transition” to one of these or other disorders. Loeser JDF, Butler SH, Chapman CR, et al. Bonica’s Management of Pain . 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:581. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:145-151. Wall PD, Melzack R. Textbook of Pain. 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:579-580.
  • The current accepted model for fibromyalgia is that of a complex hyperalgesic pain syndrome in which central sensory abnormalities, peripheral pain generators, and psychoneuroendocrine dysfunction combine to generate a broad spectrum of patient symptoms and distress. The etiology of fibromyalgia is still unknown. Nevertheless, important discoveries in the last decade of the 20 th century have added to the knowledge of the psychologic, neurogenic, and muscular abnormalities present in the disorder. Three distinctive suggested etiologies are currently suggested. Psychologic Factors. While it is true that many patients with fibromyalgia may be depressed or anxious, depression or anxiety are not believed to be the cause of fibromyalgia syndrome. In fact, they may be a result of the presence of chronic pain. An association with previous major depression in patients and families may suggest a genetic factor. Muscle Abnormalities . Even though patients complain of muscle tenderness, no histologic abnormalities in muscle have been identified by electron microscopic studies of patients with fibromyalgia syndrome. Central Nervous System (Neurogenic) Hypothesis . Significant efforts have been made to demonstrate CNS abnormalities in individuals with fibromyalgia syndrome. Substance P levels in the cerebrospinal fluid have been reported to be higher in patients with fibromyalgia than in controls. Lower than normal levels of metabolites of serotonin have been found in the cerebrospinal fluid of patients with fibromyalgia syndrome compared with controls. Elevated levels of nerve growth factor in the cerebrospinal fluid recently have been demonstrated in patients with fibromyalgia but not in those with other painful conditions. Nerve growth factor may play a huge role in the persistent pain associated with fibromyalgia syndrome through neuroplasticity and neuromodulation. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:581. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:149-152. Wall PD, Melzack R. Textbook of Pain. 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:579-580.
  • It has been suggested that the typical patient with fibromyalgia syndrome is a middle-aged woman who complains to her doctor that “everything hurts.” In evaluating a patient, care must be taken to distinguish between a myofascial syndrome trigger point and a tender point (which occurs in fibromyalgia). Although some individuals with fibromyalgia syndrome may have an occasional trigger point upon examination, the two disorders are not synonymous. Other symptoms associated with fibromyalgia are throbbing occipital pain of muscle contraction headache, prolonged morning stiffness, chest wall pain, breast area pain, low back pain or sciatica-like radiation of pain, bursitis, tendonitis, irritable bowel, diarrhea, constipation, frequency/urgency. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:550.
  • The 1990 guidelines for a diagnosis of fibromyalgia are the most widely used criteria. A diagnosis consists of one historical feature and one physical finding. The historical feature is widespread pain of 3 months or more. Pain is considered widespread when all of the following are present: pain in the left and the right sides of the body, pain above and below the waist. Additionally, axial skeletal pain must be present (cervical spine or anterior chest or thoracic spine or low back). In this definition, shoulder and buttock pain is considered as pain for each side. The physical feature is pain in 11 of 18 tender point sites on digital palpation. The 18 tender points are: occiput, low cervical, trapezius, suprespinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knees. Digital palpation should be done with an approximate force of 4 kg. For a tender point to be considered “positive,” the patient must state that the touch was painful, not just tender. The presence of a second clinical disorder does not rule out the diagnosis of fibromyalgia. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms . 2nd ed. Seattle, WA: IASP Press; 1994:46. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:146. Wall PD, Melzack R. Textbook of Pain. 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:580. Wolk, M. The diagnosis and treatment of fibromyalgia. http://www.systoc.com/CMEcourses/wolk (accessed 5/23/02)
  • Generally the treatment of fibromyalgia sydrome (FMS) is unsatisfactory, yet there are many therapeutic options that can lessen the degree of pain, improve functionality and help patients cope with the disorder. Often a great deal of relief is provided simply by explaining the nature of the syndrome and reducing the patient’s anxiety by ruling out a more serious, life-threatening condition—assuring the patient that FMS will not cause crippling or reduced life expectancy. The first, and possibly most important, step in treatment is patient education and support, both by the physician and medical staff, as well as a FMS support group, if possible. Equally important for the FMS patient is exercise, as deconditioned muscles are more prone to microtrauma, and inactivity leads to dysfunctional behavioral traits. All FMS patients need to have an ongoing home exercise program with muscle stretching, gentle strengthening and aerobic conditioning. It is important to remember that exercise for the FMS patient is health training, not sports training; should be non-impact exercise; should be done for a total of 30 minutes each day (10-minute or 15-minute sessions are fine); and strength training should be concentric and avoid eccentric muscle contractions. Pharmacologic treatments have been used with varying degrees of success in FMS patients, the most effective drugs being tricyclic antidepressants and analgesics. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:159. Wall PD, Melzack R. Textbook of Pain. 3 rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:580.
  • Effective management of pain relies on a comprehensive assessment that defines the characteristics, etiology, and the underlying pathophysiology of the pain. Etiology. Defining the underlying organic activity that may be contributing to the pain may clarify the nature of the disease, indicate a prognosis, or suggest the use of specific therapies. Pathophysiology. Animal and clinical research suggest that the clinical presentation and the response to therapy of a particular pain syndrome may be determined by factors linked to the underlying mechanism of the pain. Although the classification that can be derived from such observations may be oversimplistic, it has clinical utility and so has become widely accepted. Using this scheme, the predominating pathophysiology of pain can be broadly defined as nociceptive, neuropathic, and idiopathic. Characteristics. The patient should be asked to describe the characteristics of the pain in terms of temporal aspects, intensity, topography, and exacerbating/relieving factors. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:11.
  • 08/13/12 12:24 PM Chronic pain is not just a prolonged version of acute pain. It often occurs in the absence of ongoing illness or after healing is completed, and often begins with an injury that causes inflammation and CNS changes. The injured area heals, scar tissue is formed, and the inflammation recedes. But for an unknown reason, the nervous system undergoes multiple changes that perpetuate the pain experience, continuing to send pain signals to somatic muscles. The nervous system reacts to the memory of the original injury and sends signals like those sent in response to that original injury. These signals become a recurring and disabling message that remind the patient of the original injury. As pain signals are repeatedly generated, neural pathways undergo physiochemical changes that make them hypersensitive to the pain signals and resistant to antinociceptive input. The pain signals can become embedded in the spinal cord, like a painful memory. This is why the c urrent perception of pain can be influenced by prior experience of chronic pain. Marcus D. Treatment of nonmalignant chronic pain. Am Fam Physician. 2000;61:1331-1338; 1345-1346.
  • The physiology of normal pain transmission involves some basic concepts that are necessary in order to understand the pathophysiology of abnormal or nonphysiologic pain. These include the concept of transduction of the first-order afferent neuron nociceptors. The nociceptor neurons have specific receptors that respond to specific stimuli if a specific degree of amplitude of the stimulus is applied to the receptor in the periphery. If sufficient stimulation of the receptor occurs, then there is a depolarization of the nociceptor neuron. The nociceptive axon carries this impulse from the periphery into the dorsal horn of the spinal cord to make connections directly, and indirectly, through spinal interneurons, with second-order afferent neurons in the spinal cord. The second-order neurons can transmit these impulses from the spinal cord to the brain. Second-order neurons ascend mostly via the spinothalamic tract up the spinal cord and terminate in higher neural structures, including the thalamus of the brain. Third-order neurons originate from the thalamus and transmit their signals to the cerebral cortex. Evidence exists that numerous supraspinal control areas—including the reticular formation, midbrain, thalamus, hypothalamus, the limbic system of the amygdala and the cingulate cortex, basal ganglia, and cerebral cortex—modulate pain. Neurons originating from these cerebral areas synapse with the neuronal cells of the descending spinal pathways, which terminate in the dorsal horn of the spinal cord. Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.
  • 08/13/12 12:24 PM Pain signals in the form of electrical impulses are carried by peripheral nerves called nociceptors (C-fibers) that synapse with neurons in the dorsal horn of the spinal cord. The pain signal is then transmitted via the spinothalamic tract to the cerebral cortex, where it is perceived, localized, and interpreted. The body’s pain-relieving, or antinociceptive, system balances out the pain-sensing system. When pain signals transmitted by peripheral nerves, or nociceptors , arrive in the brain, they activate neurons in the periaqueductal gray matter of the brain and the nucleus raphe magnus of the brainstem, which release endorphins and enkephalins. In addition to pain signals, other stimuli can trigger activation of the anti-nociceptive system, such as exercise, meditation, and comforting or reassurance. This explains the utility of many of the behavioral components of pain management programs. Image adapted with permission: Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35(7): 45-52, 59. ©The McGraw-Hill Companies, Inc. Illustration by Seward Hung. Besson, JM. The neurobiology of pain. Lancet. 1999;353:1610- 1615 .
  • Nociceptive pain is presumably related to ongoing activation of primary afferent neurons responsive to noxious stimuli. The activation of the nociceptors is related to tissue damage, although the relationship between pain and tissue damage is neither uniform nor constant. Nociceptive pain includes somatic pain and visceral pain. Somatic pain refers to ongoing activation of somatic afferent neurons. Bone pain is a typical example of this type of pain. Visceral pain is related to the activation of the primary afferent neurons that innervate viscera. Liver capsular pain is an example of visceral pain. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:581. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:11. Loeser JDF, Butler, SH, Chapman CR et al. Bonica’s Management of Pain, 3 rd Ed., Baltimore, Lippincott Williams Wilkins , 2001. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:219-247.
  • Neuropathic pain is believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system. It includes numerous clinical entities, which vary in their presentation pathophysiology and treatment. The classification is based on inferred location of the pain “generator” (peripheral or central) and types of mechanisms involved. Three major categories have been recognized: deafferentation pain, sympathetically-maintained pain and peripheral neuropathic pain. Deafferentation pains are presumably related to pathophysiologic processes in the CNS. Subtypes include pain caused by injury to the brain or spinal cord, phantom pain, postherpetic neuralgia and pain caused by root avulsion. Sympathetically-maintained pain is defined as a pain presumed to be sustained by efferent activity in the sympathetic nervous system. A sympathetic nerve block is needed to establish the diagnosis of sympathetically-maintained pain. This type of pain appears to occur most frequently in the setting of a complex regional pain syndrome. The term complex regional pain syndrome (CRPS), also known as reflex sympathetic dystrophy or causalgia , refers to a regional pain syndrome in which pain is associated with focal autonomic dysfunction (vasomotor instability, swelling, sweating) and/or trophic changes (thinning of the skin, changes in hair growth, bone and subcutaneous tissue losses). Peripheral neuropathic pain is usually caused by a focal peripheral nerve injury or by a diffuse injury (polyneuropathy). Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:83, 87, 93.
  • Idiopathic pain persists in the absence of an identifiable organic substrate and is believed to be excessive for the organic processes that exist. This type of pain is uncommon in mentally ill patients. A subgroup of patients with idiopathic pain presents positive evidence of a predominant psychologic contribution to the pain. These pains are described as psychogenic or are labeled with a specific psychiatric diagnosis. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3 rd ed. Baltimore: Lippincott Williams Wilkins; 2001:19-21. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms . 2nd ed. Seattle, WA: IASP Press; 1994. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:11.
  • The goal of pain assessment is the development of a pain-oriented problem list, which, in addition to characterizing pain, prioritizes other physical and psychosocial problems that may influence therapy or be amenable to primary treatment. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:563-589.
  • In order to make a comprehensive evaluation, the physician must take a detailed history from the patient. Temporal Features. Temporal features include onset, duration, frequency and constancy of the pain. Pain can be acute or chronic. Chronic pain may be punctuated by breakthrough pains (transitory acute pain). Intensity. Pain intensity should be measured validly and repeatedly using a simple scale. (See next slide) Topography. Pain can be described as focal, multifocal, generalized, referred. Focal pain s are usually well circumscribed, at the site of the lesion. Referred pains are experienced at a site remote from the presumed lesion. Pains can be referred from an injury in any deep tissues, including viscera, muscle, bone and peripheral or central nervous system. Quality. Descriptors of pain quality can be clues to underlying mechanisms. Somatic pains are often described as aching, throbbing or sometimes stabbing. The quality of visceral pains will vary according to the organ. In injury to hollow viscus, the pain is often described as cramping or gnawing. Neuropathic pains are usually described as dysesthesic (lancinating, burning, electric-shock-like, tingling). Exacerbating/Relieving Factors. Factors that aggravate or relieve pain may be useful for diagnostic purposes and treatment: they can be categorized as volitional or spontaneous. Pain induced by light touch on normal skin (allodynia) suggests a neuropathic component. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse, 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:566-567.
  • A number of excellent unidimensional tools exist that measure only pain intensity and have the advantages of being brief, easy to administer, and sensitive to treatment effects. Such tools include a visual analog scale (VAS), most often a 10-cm line anchored at one end by the description “no pain” and at the other end by “worst possible pain,” on which the patient marks the line at the point that best describes their pain intensity. Also used is a numerical rating scale (NRS) [“On a scale of 0 to 10, in which 0 is no pain and 10 is the worst pain imaginable, how severe is your pain?]. The categorical scale allows the patient to choose from four categories of intensity, from “none” (0) to “severe” (7-10). Cleeland, CS. Pain Research Group University of Texas M.D.Anderson Cancer Center. BPI Copyright 1991. Jacox A, Carr DB, Payne R, et al. Management of Cancer Pain. Clinical Practice Guidelines No. 9. AHCPR Publication No. 94-0592. Rockville, MD. Agency for Health Care Policy and Research, U.S. Department of Health and Human Services. Public Health Service, March 1994. Cleeland
  • A “faces” scale may be useful for patients who are unable to use NRS or VAS scales, such as children, the elderly, or patients with dementia. The Brief Pain Inventory is a straightforward and easily administered tool that provides the practitioner with information about pain history, intensity, location, quality, and interference. It includes a number of questions, each of which is answered by the patient on a scale of 1 to 10. Included are questions about pain characteristics as well as functionality. It also includes the simple body outlines above, on which the patient is asked to mark the areas of greatest pain. Cleeland, CS. Pain Research Group University of Texas M.D.Anderson Cancer Center. BPI Copyright 1991. Wong DL, Hockenberry-Eaton M, Wilson D, Winkelstein ML, Schwartz P. Wong’s Essentials of Pediatric Nursing. 6 th ed. St Louis, Missouri: Mosby, Inc.; 2001:1301. Reprinted by permission .
  • Primary Therapy . The first issue is the feasibility of primary therapy. For cancer pain, for example, radiotherapy, chemotherapy, or surgical resection may be options. Pharmacotherapy . Pharmacotherapy for pain falls into three broad groups: nonsteroidal anti-inflammatory agents (NSAIDS), opioid analgesics, and adjuvant analgesics. Rehabilitative Approaches. In certain chronic pain syndromes (e.g., low back pain, osteoarthritis, fibromyalgia), physical and occupationial therapy could be an integral part of pain management, depending upon the pathophysiology of the pain. Physical therapy is useful in increasing functioning and decreasing disability. Psychologic Interventions . Psychological approaches are underutilized in pain management, where there is often a strong association between mood and pain. Psychologic interventions may be helpful in reinforcing “well” behaviors, decreasing pain, and teaching coping and relaxation skills. Anesthesiological Approaches. I nvasive anesthesiologic techniques are designed to interrupt nociceptive transmission either by delivering local anesthetics, opioids, and other neuromodulatory drugs in close proximity to neural structures or directly into the spinal fluid, or by neural blockade. Neurostimulatory Techniques. Neurostimulator therapies, such as transcutaneous electrical nerve stimulation (TENS) and dorsal column stimulation (DCS), may have beneficial effects in some patients. Surgery. Surgical approaches are considered in selected cases, including refractory pain from neuroma or nerve entrapment. Neurodestructive techniques such as cordotomy or thalamotomy are rarely used. Complementary and Alternative Medicine Approaches/Lifestyle Changes. These interventions emphasize self-control, coping and adaptation and are diverse in scope, practice, and acceptability. Some are considered mainstream pain therapy, such as relaxation, nutritional support, and acupuncture. Others, such as homeopathy and naturopathy, have no scientific basis and generally are not accepted in routine medical practice. Health care professionals should remain open, express concerns about benefits and harms of these therapies, and provide support if patients pursue this approach. Improved nutrition, proper exercise, and stress reduction are important to proper pain management. Ferrell BA, Bradley LA, Cooney LM, et al. The management of chronic pain in older persons. AGS Panel on Chronic Pain in Older Persons . J Am Geriatr Soc. 1998;46:635-651. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:563-589. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996. Tasker RR. Surgical approaches to chronic pain. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:290-305. Turk DC. Psychologic issues in chronic pain. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:325, 330, 334.
  • Opioid Analgesics . Opioids are the mainstay drugs for moderate-to-severe pain associated with medical illness. Opioid analgesics can be classified as pure mu-agonists or agonist-antagonists based on their receptor interactions. The agonist-antagonist class can be subdivided into a mixed agonist-antagonist subclass and a partial agonist subclass. Because of their ceiling effect for analgesia and potential for reversing analgesia from pure agonists in physically-dependent patients, the agonist-antagonist drugs are not preferred for treating chronic pain. Nonopioid Analgesics. N onopioid analgesics include acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDS). They are usually used for mild-to-moderate pain. They have an additive effect when combined with opioids. There is substantial variability in the response of individual patients to different drugs. The selective COX-2 inhibitors (celecoxib, rofecoxib, valdecoxib, oncloxicam) have a more favorable GI safety profile than the nonselective COX-1 and COX-2 inhibitors. The nonselective drugs vary in toxicity. Drug selection should be influenced by drug-selective toxicities, prior experience, cost, and convenience. Adjuvant Analgesics. Adjuvant analgesics are drugs that have other primary indications but may be analgesic in specific circumstances. In the medically ill, adjuvant analgesics are more commonly used in the treatment of neuropathic pain. Drug selection should be guided by the risks associated with the therapy and the possibility of secondary benefits for symptoms other than pain. Sequential trials and dose titration are usually necessary. The appropriate use of adjuvant analgesics requires the clinician to know the approved indications, side effects, time-action relationship, pharmacokinetics, and specific guidelines for use in pain treatment. Cashman JN. The mechanisms of action of NSAIDS in analgesia. Drugs. 1996;52(suppl 5):S13-S23 . Galer BS. Painful poplyneuropathy. Neurologic Clinics. 1998;16(4):791-811. Hanks GW, Portenoy RK, MacDonald N, et al. Difficult pain problems. In: Doyle D, Hanks GW, MacDonald N, eds. Oxford Textbook of Palliative Medicine . Oxford: Oxford University Press; 1998:454. Langman MJ, Jensen DM, Watson DJ, et al. Adverse upper gastrointestinal effects of rofecoxib compared with NSAIDs. JAMA. 1999;282:1929-1933. Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper gastrointestinal effects of celocoxib in rheumatoid arthritis: a randomized controlled trial. JAMA. 1999;282:1921-1928.   Stein C. The control of pain in peripheral tissues by opioids. N Engl J Med. 1995;332:1685-1690.
  • Unlike the NSAIDS, acetaminophen has minimal anti-inflammatory effects. It may be less effective for pains with an inflammatory process and bone pain. Its safety profile is better than the NSAIDS. Among the more serious adverse effects, acetaminophen can cause hepatotoxicity, the risk of which is increased with liver disease or chronic alcoholism. Acetaminophen does not inhibit platelet function, and is preferred if the risk of bleeding is high. Gilman AG, Goodman LS, et al. The Pharmacological Basis of Therapeutics . 8 th ed. Elmsford NY: Pergamon Press; 2001 .
  • See notes for Slide #49. Drugs in this class are as follows: Chemical Class Generic Name Selective Cox-2 Inhibitors celecoxib, rofecoxib, valdecoxib, oncloxicam Non-Acidic nambumetone Acidic Salicylates aspirin, diflunisal, choline magnesium, trisalicylate, salsalate Acetic Acids indomethacin, tolmetin, sulindac, diclofenac, ketorolac Oxicams piroxicam Fenamates mefenamic acid, meclofenamic acid Proprionic Acids ibuprofen, naproxen, fenoprofen, ketoprofen, flurbiprofen, oxaprozin
  • The existence of ceiling doses for the NSAIDS imply that these drugs have limited maximal efficacy. The maximal efficacy may vary across drugs and with the type of pains. They are usually useful for mild to moderate pain, with a better efficacy in pain related to an inflammatory process and bone pain. They have an additive effect when combined with opioids. There is a substantial variability in the response of individual patients to different drugs. The selective COX-2 inhibitors present a more favorable gastrointestinal safety profile than the nonselective COX-1 and COX-2 inhibitors. The nonselective drugs vary in toxicity. Drug selection should be influenced by drug-selective toxicities, prior experience, cost, and convenience. Cashman JN. The mechanisms of action of NSAIDS in analgesia. Drugs. 1996;52(suppl 5):S13-S23. Langman MJ, Jensen DM, Watson DJ, et al. Adverse upper gastrointestinal effects of rofecoxib compared with NSAIDs. JAMA. 1999;282:1929-1933. Simon LS, Weaver AL, Graham DY, et al. Anti-inflammatory and upper gastrointestinal effects of celocoxib in rheumatoid arthritis: a randomized controlled trial. JAMA . 1999;282:1921-1928.    
  • Drugs commonly used for neuropathic pain include anticonvulsants (gabapentin, valproate, phenytoin, carbamazepine, clonazepam, topiramate, lamotrigine, oxcarbazepine and others); antidepressants (tricyclics, SSRI’s, and others); local anesthetics (mexiletine); corticosteroids (dexamethasone, prednisone); alpha-2 adrenergic agonists (tizanidine, clonidine); NMDA-receptor antagonists (dextromethorphan, ketamine); topical agents (local anesthetics, capsaicin, NSAIDs); and miscellaneous drugs (baclofen, calcitonin, and others). Lucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management. Cancer Pract. 2002;10(suppl 1):S14-S20 .
  • Gabapentin is the most widely used anticonvulsant for pain. The usual effective dose varies widely, from 600 mg to 3600 mg; occasional patients require doses as high as 6000 mg/day. Many other anticonvulsant drugs have established analgesic effects in diverse neuropathic syndromes. They may be particularly useful in predominantly stabbing or paroxysmal pains but are used for all types of neuropathic pain. Carbamazepine has been the most studied but its use often is limited in the cancer population due to risk of leukopenia. Experience with newer anticonvulsants (lamotrigine, topiramate, tiagabine, oxcarbazepine, zonisamide and others) is still limited, but the existing data suggest that these drugs have analgesic effects as well.   Galer BS. Painful poplyneuropathy. Neurologic Clinics. 1998;16(4):791-811. Rosner H, Rubin L, Kestenbaum A. Gabapentin adjunctive therapy in neuropathic pain. Clin J Pain. 1996;12:56-58.
  • Antidepressants, particularly the tricyclics, have been the best studied and most widely used adjuvant analgesic drugs. Their analgesic effect has been established in many pain disorders. The SSRIs (selected serotonin reuptake inhibitors) and other newer antidepressants seem to be better tolerated, but their analgesic profile has not been clearly demonstrated, except for few drugs. Analgesic effects are not dependent on their antidepressant effect.   Monks R, Mersky H. Psychotropic drugs. In: Wall PD, Melzack R, eds. Textbook of Pain, 4 th ed. New York: Churchill Livingston; 1999:1155-1186.
  • Corticosteroids are commonly used to treat cancer pain, especially when secondary to nerve compression or infiltration. They also have been shown to improve appetite, nausea, malaise, and overall quality of life. Adverse effects increase with the dose and duration of use, and chronic use is usually reserved for patients with advanced illness. Dose escalation is appropriate for worsening symptoms, particularly at the end of life. In nonmalignant pain, long-term use is limited to inflammatory disorders such as rheumatoid arthritis. Lucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management. Cancer Pract. 2002;10 (suppl 1):S14-S20.
  • Clonidine and tizanidine have established analgesic effects and may be tried in any type of chronic pain. Their use in medically ill patients generally has been limited to refractory neuropathic pain. Efficacy in neuropathic pain has been proved in a controlled study of epidurally administered clonidine. Tizanidine, an antispasticity drug, also has analgesic properties and is less likely to cause hypotension than systemically administered clonidine. Max MB, Lynch SA, Muir J, et al. Effects of desipramine, amitriptyline, and fluoxetine on pain in diabetic neuropathy. N Engl J Med. 1992;326:1250-1256 . Sindrup SH, Gram LF, Brosen K, et al. The selective serotonin reuptake inhibitor paroxetine is effective in the treatment of diabetic neuropathy symptoms. Pain . 1990;42:135-144 .
  • Recent preclinical studies have demonstrated that binding of glutamate at the N-methyl-D-aspartate (NMDA) receptor is involved in mechanisms that may underlie neuropathic pain. Three NMDA antagonists are commercially available in the US: ketamine (a dissociative anesthetic), dextromethorphan (an antitussive), and amantadine (an antiviral). They all have been shown to have analgesic properties. Additional experience is needed to determine their role in neuropathic pain associated with serious medical illness. Herry DA, Plummer JL, Goulrlay GK, et al. Ketamine as an adjunct to morphine in the treatment of pain. Pain. 1995;62:119-121. Nelson KA, Park KM, Robinovitz E, et al. High-dose oral dextromethorphan versus placebo in painful diabetic neuropathy and postherpetic neuralgia. Neurology. 1997;48:1212-1218. Pud D, Eisenberg E, Spitzer A, et al. The NMDA receptor antagonist amantadine reduces surgical neuropathic pain in cancer patients: a double blind, randomized, placebo controlled trial. Pain. 1998;75:349-354.
  • Opioid analgesics can be classified as pure agonists or agonist-antagonists based on their receptor interactions. Pure (full) agonists (e.g., codeine, fentanyl, hydrocodone, hydromorphone, methadone, morphine, oxycodone) do not have a ceiling effect: their effectiveness is not limited with increasing doses. Full agonists do not reverse or antagonize the effects of other full agonists given simultaneously. The agonist-antagonist class can be subdivided into a mixed agonist-antagonist subclass and a partial agonist subclass . Partial agonists are selective agonists at the mu receptor, but they have limited efficacy at this site. Mixed agonist-antagonists are weak antagonists at the mu receptor and agonists at the kappa receptor. Because of their ceiling effect for analgesia and their potential for reversing analgesia from pure agonists in physically dependent patients, the agonist-antagonist subclass of drugs are not preferred for the treatment of chronic pain. Jacox A, Carr DB, Payne R, et al. Management of Cancer Pain. Clinical Practice Guideline Number 9. AHCPR Publication No. 94-0592, Rockville, MD. Agency for Health Care Policy and Research, US Department of Health and Human Services, Public Health Service; March 1994. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:83-125.
  • Short-acting opioids have a fast onset of action for titration to analgesic effect, making them useful for breakthrough pain , but they require frequent dosing to achieve adequate control of chronic pain. A rapid onset of effect usually is unnecessary for the treatment of pain that is continuous; however, even in chronic pain states analgesic requirements may fluctuate. Transient severe pain on a baseline of chronic pain is called breakthrough pain , and may be caused by activity or procedures ( incidental pain ) or may be unpredictable. Short-acting opioids should be used in conjunction with extended-release opioids to control breakthrough pain. For persistent continuous pain, extended-release formulations or drugs with long half-lives are preferred over short-acting agents, as they facilitate patient adherence with treatment regimens, provide consistent levels of analgesia, and allow the patient to focus less on pain and pain medications. Patients and caregivers need to be warned that extended-release preparations become immediate-release if tablets are crushed or chewed, increasing the potential for overdose. Extended-release oral formulations are available for several opioids, including morphine and oxycodone. A continuous-release transdermal formulation of fentanyl is designed to provide effective pain control for up to 72 hours. An alternative to these pharmaceutically designed long-acting formulations is methadone, which may only require dosing every 8 hours due to its long half-life. However, this same property makes it somewhat challenging to titrate initially, especially in older patients with unpredictable and variable pharmacokinetics and increased opioid sensitivity. Lucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management. Cancer Pract. 2002;10(suppl 1):S14-S20.
  • Numerous extended-release formulations are available in different countries. The oral drugs allow dosing 1 to 3 times per day and the transdermal drugs allow dosing every 2 to 3 days. Usually, steady-state is approached with these formulations within a few days and dose adjustments are best made in this time frame. Lucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management. Cancer Pract. 2002;10(suppl 1):S14-S20. Weinstein SM, Anderson PR, et al. Cancer Management: A Multidisciplinary Approach . 5 th ed. P\\S\\L Consulting Group, Inc.; 2001.
  • Drug Selection. Choice of an opioid may be influenced by pain severity, previous exposure, drug or formulation availability, patient preferences and underlying condition (liver function, renal function), or cost. There is substantial individual variation in the response to different opioids. For this reason, sequential trials of opioids may be needed to identify the opioid that offers the best balance between analgesia and side effects. Conventionally used for moderate pain in patients with limited opioid exposure: codeine, hydrocodone, tramadol Conventionally used for moderate-to-severe pain: fentanyl, hydromorphone, morphine, methadone, oxydocone The principles in published guideilines must be understood to optimize the likelihood of successful outcomes: titrate one drug at a time; continue titration until significant pain relief or intolerable side effects; continue use if significant pain relief with acceptable side effects. Dosing. Opioid dose titration over time is critical to successful opioid therapy. The goal of therapy is to increase dose until pain relief is adequate or intolerable/unmanageable side effects occur. With opioids, there is no maximal (ceiling) or “correct” dose. Treat Side Effects. For most patients, the goal during long-term therapy is to identify a favorable balance between analgesia and opioid side effects. The common side effects are constipation and mental clouding. Other side effects occur less often. Manage the Poorly Responsive Patient. A patient cannot be said to be not responding unless the dose has been increased to the point of treatment-limiting side effects. Responsiveness varies with characteristics of a particular patient and his or her particular pain. No evidence exists that any particular characteristic imparts opioid resistance. Weinstein SM, Anderson PR, et al. Cancer Management: A Multidisciplinary Approach . 5 th ed. P\\S\\L Consulting Group, Inc.; 2001.
  • The route of administration is selected based on clinical judgment and experience. Many routes are available: oral, sublingual, oral transmucosal, transdermal, rectal, subcutaneous, intravenous, epidural, intrathecal. The route should be chosen according to the availability, needsand preferences of the patient. The oral and transdermal routes are preferred, when possible. Infusions (subcutaneous, intravenous) and transdermal routes are particularly useful when patients are unable to swallow or absorb opioid drugs. Intraspinal opioids should be used in highly selected patients, mainly when intolerable side effects prevent effective systemic therapy. Lucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management . Cancer Pract. 2002;10(suppl 1):S14-S20 .
  • Fixed-schedule (around-the-clock) dosing is preferred over as-needed dosing in the treatment of continuous or frequently recurring pain. The most common therapy involves coadministration of a long-acting drug on a fixed-schedule or around-the-clock regimen, with a short-acting drug offered “as needed” for breakthrough pain. An as-needed regimen may also be appropriate for opioid-naïve patients, patients with rapidly changing pain, and patients with intermittent pains. The size of the rescue dose is usually in the range of 5% to 15% of the total daily dose, administered every 3 hours as needed; studies of the oral transmucosal fentanyl formulation have not confirmed this ratio, however, and dosing with this drug should be started low and then titrated. Individualization of the scheduled opioid dose through a process of dose titration is critical to a successful outcome. Dosing adjustments can be in the range of 25% to 100%, depending on the severity of the pain and concern about opioid toxicity, or can be guided by the amount of rescue drug taken during the prior day. As the dose of the scheduled opioid is increased, the dose of the rescue also should be increased to maintain the dose as a percentage of the total daily dose. Side effects must be treated. In opioid-naïve patients or patients with limited exposure, the starting dose of an opioid used for severe pain is usually equivalent to morphine sulfate 5 to 10 mg parenterally every 4 hours. When there is a drug change, the starting dose is calculated according to the equianalgesic table. When oral transmucosal fentanyl is used, the starting dose should be 200 μg or 400 µg, irrespective of the total daily dose. For an oral rescue dose, the interval usually is every 2 to 3 hours. With intravenous or subcutaneous administration, the minimum interval can be as short as 10 to 15 minutes. Most short-acting opioids need to be administered every 3 to 4 hours, controlled-released every 8 to 12 hours, and sustained-released every 24 hours. Because of its long half-life, methadone is usually effective with a 6-12 hour dosing interval. The transdermal fentanyl system can be administered every 48 to 72 hours.   American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain. 4 th ed. Skokie, Illinois: American Pain Society; 1998.
  • The equianalgesic table describes relative potencies for different opioids and routes. Information about relative potency is needed whenever opioid drugs or routes of administration are changed. Although the information in the equianalgesic table is quite useful, it has limitations. The relative potency data were established on single-dose studies in selected populations, and they may be different when applied to chronic use. The heterogeneity of the population and variability in response, which occurs in part because of incomplete cross-tolerance, need to be considered in the clinical setting. When switching drugs, the equianalgesic dose must be reduced by 25 to 50%. The exceptions to this are transdermal fentanyl and methadone. When using the equianalgesic table included in the package insert for transdermal fentanyl, the calculated equianalgesic dose should not be reduced. When switching to methadone, it is necessary to reduce the calculated equianalgesic dose by 75% to 90%.
  • Individualization of opioid dose through titration is the key to the success of opioid therapy. Dose titration is achieved though incremental adjustment of the dose until a satisfactory balance between analgesia and side effects is achieved, or side effects preclude further dose adjustment. There is no ceiling effect to the analgesia provided by pure agonist opioids, and the maximal dose is unimportant as long as the patient achieves an acceptable balance between pain relief and side effects. Typically, doses stabilize for long periods during chronic pain therapy, however dose escalation is often required to maintain acceptable analgesia. In the medically ill patient this is usually due to the worsening of the clinical status of the condition. This underscores the need for ongoing assessment and outcomes monitoring. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:563-589.
  • The principles of good medical practice should guide the prescribing of opioids. An initial evaluation should include a pain history, a directed physical examination, and assessment of coexisting diseases or conditions. Evaluation of pain-related disturbances in physical functioning, psychological functioning, social functioning, and role functioning (e.g., ability to work) is an essential part of the comprehensive pain assessment.. A review of previous medical treatments and relevant medical history can aid in the diagnosis of chronic pain and reveal psychiatric disturbances that may require referral to a psychologist or psychiatrist. A history of previous appropriate and illicit drug use may help determine the adequacy as well as efficacious orinefficacious use of previous drug therapy for pain conditions. Practitioners should ask targeted questions about substance abuse (including alcohol) to determine the specific drugs and whether use is remote, recent, or ongoing. A history of substance abuse, including opioid abuse, does not necessarily contraindicate use of opioids for the treatment of pain, though such patients will require special consideration. Goals and Expectations Often, goals and expectations of clinicians and patients are different. Patients may feel that the only reasonable goal of drug therapy is complete pain relief and complete function. The practitioner’s expectation may be a decrease in pain sufficient to allow improved functio from rehabilitative therapy. Direct discussions are needed to increase understanding of the patient’s goals and expectations before a treatment plan is formulated. Haadox JD, Johanson D, Angarola RT, et al. The use of opioids for the treatment of chronic pain. A consensus statement from the American Academy of Pain Medicine and the American Pain Society; 1997. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:19-39.
  • A trial of opioids for chronic pain will determine whether treatment is effective and tolerable. Using the same principles of pain assessment and patient evaluation, the patient should be examined periodically to review efficacy and side effects of treatment, including whether analgesia is adequate and functional status is improved. Periodic reexamination is also necessary to reassess the nature of the pain complaint (e.g., worsening or new complaint) and to determine if opioid therapy is still indicated. The examination should also include an assessment of opioid misuse, and the patient should be referred for specialized care if abuse is suspected. One useful pnemonic for assessing and documenting outcomes for patients on opioid therapy is the so-called “4-A’s.” The 4-A’s should be monitored and recorded for every patient: Analgesia: pain relief; improved sleep and mood Activities of Daily Living (ADLs): measures of functional capacities Adverse Events: (constipation, sedation, nausea, pruritis, sexual dysfunction) Aberrant-Related Behaviors: (early refill requests, manipulative behavior, “lost” or “stolen” prescriptions, missed appointments) American Pain Society. Chronic Pain in America: Roadblocks to Relief . Available at: www.ampainsoc.org . Accessed March 18, 2002. Passik SD, Weinreb HJ. Managing chronic nonmalignant pain: overcoming the obstacles to the use of opioids. Adv in Ther . 2000;17:70-83. Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997.
  • Surveys in the cancer population suggest that 10% to 30% of patients will experience a poor response to an optimally titrated opioid regimen. Poorly-responsive patients can be considered for a variety of alternative opioid strategies. These include: 1) management of opioid side effects (e.g., a psychostimulant for opioid-induced sedation or mental clouding), 2) use of a pharmacologic approach to reduce the systemic opioid requirement (either a trial of intraspinal therapy or coadministration of a nonopioid or adjuvant analgesic), 3) opioid rotation, or 4) a trial of a nonpharmacologic approach to reduce the opioid requirement (eg, a stimulatory, rehabilitative, anesthesiologic, surgical, or complementary approach). Comparative studies of these strategies have not been conducted, and selection of one over another involves a detailed assessment, careful judgments about risks and benefits, and discussion of patient preferences. Opioid dose titration over time is critical to successful opioid therapy Goal: Increase dose until pain relief is adequate or intolerable and unmanageable side effects occur No maximal or “correct” dose Responsiveness of an individual patient to a specific drug cannot be determined unless dose was increased to treatment-limiting toxicity Mather LE. Trends in the pharmacology of opioids: implications for the pharmacotherapy of pain. Eur J Pain. 2001;5(suppl A):S49-S57 .
  • Opioid rotation is common practice and is based on the clinical observation of large individual variation in the response to different opioids. Guidelines for switching drugs assure safety and yield a reasonable starting dose of the new drug, which then must be titrated. Indelicato RA, Portenoy RK. Opioid rotation in the management of refractory cancer pain. J Clin Oncol. 2002;20(1):348-52 Mather LE. Trends in the pharmacology of opioids: implications for the pharmacotherapy of pain. Eur J Pain. 2001;5(suppl A):S49-S57 .
  • For most patients, the goal during long-term therapy is to identify a favorable balance between analgesia and opioid side effects. Common side effects are constipation and mental clouding. Other side effects occur less often. Tolerance to some side effects of opioids (e.g. nausea, somnolence, mental clouding) occurs soon after initiation of therapy, but some side effects occur less often but may persist. Estimates of the incidence of these side effects depend on the patient population and drug. Prevention is the best course of action for constipation. A prophylactic bowel regimen should be initiated with opioid therapy in most patients who are elderly or predisposed to constipation. While constipation is common with both oral and transdermal opioid use, studies have suggested that the transdermal route of administration has a lower incidence of constipation than the oral route. Mild sedation and impaired cognitive performance should also be anticipated when opioids are initiated. Patients should be instructed that until tolerance to these effects develops, they should not drive and should take precautions to avoid falls or accidents. Pycho- stimulant drugs such as methylphenidate and dextroamphetamine may counteract drowsiness. Although nausea often resolves spontaneously, several approaches can be used in its management. If nausea is associated with vertigo or markedly exacerbated by movement, antivertiginous drugs may be given. In other cases, metoclopramide or dopamine antagonists are appropriate. Pruritis may be treated with antihistamines. Ahmedzai S, Brooks D. Transdermal fentanyl versus sustained-release oral morphine in cancer pain: preference, efficacy, and quality of life. J Pain Symptom Manage . 1997;13: 254-261. Portenoy RK. Opioid analgesics. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996.
  • Research is targeted at the isolation of novel compounds that will produce profound central antinociceptive effects by acting on the following receptors: Excitatory amino acids (EAAs) glutamate and aspartate, as well as several neuropeptides—such as substance P, calcitonin gene-related peptide, cholecystokinin, and neurokinin—are the neurotransmitters of nociception found on the C-fibers entering the dorsal horn of the spinal cord. By acting on several receptors such as N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, kainate, the metabotropic receptors, and the neurokinin receptors, these neurotransmitters can induce central sensitization. Blockade of the N-type (neuron-specific) calcium channels within the dorsal horn represents an alternative for intrathecal analgesia with opioids or local anesthetics. An N-type calcium channel blocker (ziconotide) derived from the venom of a predatory marine snail soon may be available for clinical use. The activation of CNS adenosine A 1 receptors also is pertinent to pain control, as demonstrated by intrathecal administration of adenosine in animal models. Similarly, recent studies evaluated the role of cannabinoids, not only as antiallodynic and antihyperalgesic agents, but also as potentiators of opioid analgesia. Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59. LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management . Cancer Pract. 2002;10(suppl 1):S14-S20 .
  • Some membrane components, recently identified and anticipated to be relevant to the various pathogeneses of pathologic pain and targets for analgesic drugs discovery, are the sensory neuron specific tetrodotoxin-resistant (TTX-R) voltage-gated sodium channels, opioid receptors, the vanilloid receptors (VRs), and the serotonin receptors. In the DRG, 2 types of TTX-R voltage-gated sodium channels have been identified: the PN3 and NAN. After peripheral-nerve or tissue injury, the abnormal processing of pain may be contributed to alterations in the sodium channel expression and function. The activation threshold of nociceptors also may be lowered by a direct modulation of heat or by mechanotransducer receptor proteins. The VR-1 receptor, for example, contributes to heat detection. Others among the emerging peripheral nociception channel and receptor targets include the following: The alpha-2 adrenergic receptors—For example, the topical application of an alpha-2 adrenergic agonist causes local inhibition of noradrenaline release by acting on the adrenergic alpha-2 autoreceptors of the sympathetic endings. The proton-sensitive channels—The H + -gated channel that is cloned is the acid-sensing ionic channel (ASIC), which is a member of the amiloride-sensitive/degenerin family and is expressed in some brain neurons, as well as in nociceptive neurons. The ASIC is transiently activated by rapid extracellular acidification (below pH 6.5) and desensitizes within a few seconds. The nerve growth factor (NGF) receptor—An example is the tyrosine kinase (TrKA) receptor for NGF. The TrKA-NGF complex is internalized and retrogradely transported to the DRG cell body, where it initiates gene transcription that promotes upregulation of channels involved in pain transmission. The N- or T-type current calcium channels—Following axonal injury, altered Ca ++ signaling may contribute to hyperexcitability leading to neuropathic pain. The purine receptors—Purinoceptors on sensory nerve terminals may be acted upon by ATP released from different cell types, thereby contributing to the initiation of pain . Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.
  • The two major anesthetic approaches are neuraxial drug administration and neural blockade. Opioids, local anesthetics, and clonidine are routinely infused in continuous epidural or subarachnoid infusion for refractory cancer pain. This approach is mainly indicated for patients who have focal or multifocal pains that are below midchest and have been refractory to systemic pharmacotherapy. There is a wide variability among clinicians as to the technique used to implement a treatment trial and the approach to long-term therapy. Clonidine, administered in combination with opioid and local anesthetic, has been proven to be beneficial for neuropathic pain in a controlled clinical trial. Neural blockade by local anesthetic may be diagnostic, prognostic, or therapeutic. With therapeutic blocks, the duration of analgesia is variable and they often needed to be repeated. Neurolysis is occasionally considered, especially in advanced disease. The value of neurolytic celiac blockade is supported by extensive clinical experience and usually is offered early in the treatment of patients with pain due to pancreas cancer. Trigger point injections are often considered when focal pain originates from focal areas in muscle or connective tissue. Eisenach JC, DuPen S, Dubois M, et al. Epidural clonidine annalgesia for intractable cancer pain. Pain. 1995;61:391-400. Patt RB, Cousins MJ. Techniques for neurolytic neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural Blockade . Philadelphia: Lippincott Raven; 1998.
  • Neurostimulatory Approaches Stimulation of afferent pathways may produce analgesia. Transcutaneous electrical nerve stimulation (TENS) is a well-known application of this principle. Other approaches include counterirritation, acupuncture, percutaneous nerve stimulation, dorsal column stimulation, and deep brain stimulation. Data are limited at the present time. Considering their safety, trials of the less invasive techniques often may be warranted (TENS, acupuncture); the invasive approaches are considered for carefully selected patients. Surgical Procedures Denervation of a painful area can be accomplished by ablation of specific peripheral or central nervous system structures at any level of the neuraxis. Like chemical neurolysis, surgical neuroablative procedures now are rarely considered.  Cordotomy, the most common approach, can provide prolonged relief to more than two thirds of patients with pain from unilateral nociceptive lesions but may be much less effective in neuropathic pain, especially deafferentation syndromes. Complications are uncommon but can be serious (mirror pain, weakness, dysesthesia syndrome). Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:19-39.
  • 08/13/12 12:24 PM Psychologic Treatments Three psychologic approaches—behavioral, biofeedback, and cognitive-behavioral—are used most commonly for the treatment of chronic pain. Most often these are provided in the context of other therapy, including pharmacologic and rehabilitative. Studies have evaluated each of these treatments and shown them to have effects, to varying degrees, on pain, disability, and psychosocial adjustment. Rehabilitative Approaches Physiatric therapies include diverse modalities: physical therapy; occupational therapy; medicinal diathermy; cryotherapy; and use of orthoses, prostheses, and assistive devices. These therapies may help to alleviate pain and increase function. Heat and cold therapy can help musculoskeletal pain, and exercise may have analgesic effects in some cases (44). Immobilization by splinting or bracing a painful part may improve comfort. Assistive devices lessen the burden on limbs and may improve function and comfort. Clinical experience supports their use in the cancer population but data to that effect are lacking. Redd WH, Montgomery GH, DuHammel RN. Behavioral intervention for cancer treatment side effects. J Natl Cancer Inst. 2001;93(11):810-23.
  • To optimize the use of opioid therapy, clinicians also must have familiarity with the principles of addiction medicine. This begins with an understanding of the definitions of physical dependence, tolerance, addiction, and pseudoaddiction.
  • To optimize the use of opioid therapy, clinicians must be familiar with the principles of addiction medicine. This begins with an understanding of the definitions of physical dependence, tolerance, addiction and pseudoaddiction . Physical dependence is a pharmacologic effect characteristic of opioids whereby withdrawal or abstinence syndrome manifests upon abrupt discontinuation of the medication. Neither the dose nor the duration necessary to produce this phenomenon are known, however it is assumed that physical dependence occurs within days of continuous opioid use. Patients may be successfully weaned from opioid therapy by gradual downward titration . It is important for the physician to distinguish physical dependence from addiction. Addiction is a compulsive disorder in which an individual becomes preoccupied with obtaining and using a substance, the continued use of which results in a decreased quality of life. Addiction is suggested when drug use is characterized by compulsive drug-taking, craving, loss of control over the drug, and continued use despite harm. American Academy of Pain Medicine and American Pain Society. The Use of Opioids for the Treatment of Chronic Pain: A Consensus Statement. 1996. National Institute on Drug Abuse. Prescription Drugs and Their Abuse. NIDA Research Report Series. US Department Of Health And Human Services, National Institutes of Health, 2001 . Passik SD, Weinreb HJ. Managing chronic nonmalignant pain: overcoming the obstacles to the use of opioids. Advances in Therapy. 2000;17:70-83. Portenoy RK. Opioid therapy for chronic nonmalignant pain: A review of the critical issues. J Pain Symptom Manage. 1996;11:203-217.
  • Tolerance is defined as the need for increasing doses of opioids to maintain effect. Although tolerance to analgesia is often seen as a restriction to opioid therapy in chronic pain patients, clinical experience in cancer patients and other chronic pain patients indicates that doses of opioids needed to maintain analgesic effect (after initial dose titration) remain stable over time or increase due to worsening disease, not because the opioid is having less effect. It should be noted that the term tolerance does not apply when increased doses are needed because of increased pathology (eg, evolving neuropathic processes. Tolerance to other effects of opioids develops at different rates. For example, tolerance to some side effects (e.g., nausea) develops soon after initiation of therapy, while tolerance to others (e.g., constipation) may develop slowly or not at all. Tolerance to the reinforcing effects of opioids, and the consequent need to increase the dose of opioids to maintain these effects, may contribute to addiction, but it appears that tolerance to analgesic effects does not. Pseudoaddictive behaviors mimic those of true addition, but in reality may reflect undertreatment. This may include drug-seeking behavior, taking larger than prescribed doses, and running out of medications prematurely, tolerance, and withdrawal. Although adequate pain relief should eliminate the abnormal behavior if it is truly pseudoaddictive, it is important to recognize that pseudoaddiction and addiction can coexist. Passik SD, Weinreb HJ. Managing chronic nonmalignant pain: overcoming obstacles to the use of opioids. Adv Ther. 2000;17(2):70-83. Passik SD, Portenoy RK. Substance abuse issues in palliative care. In Berger A, Portenoy RK, Weissman D, eds. Principles and Practice of Supportive Oncology . 2nd ed. Philadelphia, PA: Lippincott-Raven Publishers; 1998. Portenoy RK. Opioid therapy for chronic nonmalignant pain: A review of the critical issues. J Pain Symptom Manage. 1996;11:203-217.
  • If the definition of addiction is clear, the question that should be asked is, What is the risk for iatrogenic addiction in patients without a known history of addiction during opioid treatment for pain? The literature suggests that the risk is minor during the treatment of acute pain and chronic cancer pain (possibly because cancer is a disease of older patients and those who have the disease and no history of drug abuse probably lack the biologic predisposition to addiction). The literature pertaining to chronic nonmalignant pain cannot adequately clarify this question. The probability of addiction, overall, presumably is small but likely to be influenced by a number of predictors. These predictors have not yet been empirically established; based on clinical experience, they may include a personal history of substance abuse, family history of substance abuse, age, personality factors, family dynamics, and social factors. Passik SD, Portenoy RK. Substance abuse issues in palliative care. In Berger A, Portenoy RK, Weissman D, eds. Principles and Practice of Supportive Oncology. 2nd ed. Philadelphia, PA: Lippincott-Raven Publishers; 1998. Passik SD, Portenoy RK: Substance abuse issues in psycho-oncology. In Holland J, et al. Handbook of Psycho-oncology. 2nd ed. Oxford: Oxford University Press; 1998:576-586.
  • From the clinical perspective, an initial assessment for the occurrence of aberrant drug-related behavior is needed. This may require a variety of strategies, including communication with the pharmacy or with others, urine drug screening, or specific rules governing prescription acquisition or follow-up. If aberrant drug-related behaviors are occurring, the assessment must be broad enough to determine whether they reflect the development of an addictive disorder or some other problem. This latter point highlights the certainty that not all aberrant drug-related behavior is addiction. Passik SD, Portenoy RK. Substance abuse issues in palliative care. In Berger A, Portenoy RK, Weissman D, eds. Principles and Practice of Supportive Oncology. 2nd ed. Philadelphia, PA: Lippincott-Raven Publishers; 1998. Passik SD, Portenoy RK: Substance abuse issues in psycho-oncology. In Holland J, et al. Handbook of Psycho-oncology . 2nd ed. Oxford: Oxford University Press; 1998:576-586.
  • There are numerous types of aberrant drug-related behaviors. They can be considered on a continuum or, based solely on clinical experience, broadly divided into categories that are more or less of concern. The more worrisome behaviors, such as multiple episodes of prescription “loss” despite warnings or the forging of prescriptions are presumably more likely to be related to addiction. Studies are needed to clarify the predictive value of these behaviors for a formal diagnosis of addiction (or substance dependence disorder). Passik SD, Portenoy RK. Substance abuse issues in palliative care. In Berger A, Portenoy RK, Weissman D, eds. Principles and Practice of Supportive Oncology. 2nd ed. Philadelphia, PA: Lippincott-Raven Publishers; 1998. Passik SD, Portenoy RK: Substance abuse issues in psycho-oncology. In Holland J, et al. Handbook of Psycho-oncology. 2nd ed. Oxford: Oxford University Press; 1998:576-586.
  • There is an absence of well-articulated management strategies for chronic pain patients receiving opioids who exhibit aberrant behavior. Nevertheless, some general principles may be applied, reflecting both proactive and reactive strategies. On the proactive side, physicians must clearly communicate to their patients the expectations of therapy and limits of acceptable and unacceptable behavior. These guidelines should be written and given to the patient and may take the form of a treatment contract that stipulates the type(s) of medications to be used, the sole pharmacy to be used to fill prescriptions, contingences for random urine and blood tests, and continued assessment of the chronic pain condition. On the reactive side, physicians must be prepared with an arsenal of strategies to respond to aberrant behaviors if they arise. This will include requiring frequent visits and prescribing of small quantities of drug. Given the relatively decreased potential of misuse of long-acting (e.g., methadone) and sustained-release opioids (e.g., transdermal fentanyl) in chronic pain patients, these may be preferred over short-acting opioids. Aberrant behaviors that appear during therapy must be comprehensively assessed so that if a differential diagnosis of addiction is made, the patient may be appropriately referred to an addiction specialist for treatment. Mironer YE, Brown C, Satterwaite JR, et al. Relative misuse potential of different opioids: A large pain clinic experience. American Pain Society. 2000. Abstract. Passik SD, Weinreb HJ. Managing chronic nonmalignant pain: overcoming obstacles to the use of opioids. Adv Ther . 2000;17(2):72.   Portenoy RK, Payne R: Acute and chronic pain. In: Lowinson JH, Ruiz P, Millman RB, eds. Comprehensive Textbook of Substance Abuse. 3rd ed. Baltimore, MD: Williams & Wilkins; 1997:78. If patients do engage in aberrant drug-related behaviors, management may take any number of turns and should be based on knowledge of the appropriate laws and regulations and diagnostic considerations.
  • Long-term opioid therapy is an extremely valuable approach to the treatment of chronic pain. Clinicians who manage this therapy must be able to perform a careful assessment and reassessment, administer these drugs knowledgeably, monitor outcomes (including the potential for aberrant drug-related behavior), and address negative outcomes. Documentation of multiple outcomes is essential.

Chronic pain management Chronic pain management Presentation Transcript

  • Module 1 Progress in Chronic Pain Management Understanding, Impact, Awareness and Advances A National Pain Education Council Program
  • What is Pain?PAIN: an unpleasant sensory and emotionalexperience associated with actual or potential tissuedamage, or described in terms of such damage,or both.CHRONIC PAIN: persistent or recurrent pain,lasting beyond the usual course of acuteillness or injury, or more than 6 months, andadversely affecting the patient’s well-being.(American Society of Anesthesiologists, 2002; Loeser et al, 2001; Merskey H et al, 1994; Portenoy et al, 1996)
  • Pain Classification Schemes • Anatomy or Body Location (low back pain) • Duration (acute, chronic) • Etiology (somatogenic, psychogenic) • Body System (e.g., myofascial, rheumatic, causalgic) • Severity (0-10 scale) • Mechanism (e.g., tissue injury, nervous system injury)(Loeser et al, 2001)
  • Multidimensional Classification of Pain IASP expert multi-axial classification of chronic pain• Axis I: Regions• Axis II: Systems• Axis III: Temporal Characteristics• Axis IV: Patient’s Statement of Intensity• Axis V: Etiology Example: Mild postherpetic neuralgia of T5 or T 6; 6 months’ duration = 303.22e Axis I: Thoracic region Axis II: Nervous system (central, peripheral, or autonomic); physical disturbance/dysfunction Axis III: Continuous or nearly continuous, fluctuating severity Axis IV: Mild severity of 1 to 6 months Axis V: Trauma, operation, burns, infective, parasitic (one of these) (Loeser et al, 2001; Merskey et al, 1994)
  • Prevalence and Impact of Chronic Pain on Society • Chronic pain is one of the most common conditions for which people seek medical treatment • 35% of Americans suffer from chronic pain • >50 million Americans are partially or totally disabled by chronic pain • 50 million workdays are lost per year • $100 billion is the estimated annual cost in lost productivity, medical costs, and lost income(American Pain Society, 2001; Gitlin, 1999; Glajchen 2001; Loesser et al, 2001)
  • Undertreatment of Chronic Pain• >40% to 50% of patients in routine practice settings fail to achieve adequate pain relief• In a recent study of 805 chronic pain sufferers, >50% had to change physicians to achieve relief because the physician: – was unwilling to treat pain aggressively – did not take the patient’s pain seriously – had inadequate knowledge about pain treatment(American Pain Society, 2001; Glajchen, 2001; Lister, 1996; Portenoy, 1996)
  • Common Barriers toTreatment of Chronic Pain Physician-Related • Limited knowledge of pain pathophysiology and assessment skills • Biases against opioid therapy and overestimation of risks • Fear of regulatory scrutiny/action Patient-Related • Exaggerated fear of addiction, tolerance, side effects • Reluctance to report pain: stoicism, desire to “please” physician • Concerns about “meaning” of pain (associate increased pain with worsening disease) System-Related • Low priority given to pain and symptom control • Limits on number of Rxs filled per month & number of refills allowed • Reimbursement policies(American Pain Society, 2001; Glajchen, 2001; Lister, 1996; Portenoy RK, 1996 ; Weinstein et al, 2000)
  • Ethnic and Racial Barriersto Treatment• Language or cultural differences make pain assessment more difficult• Physicians’ perceptions and misconceptions: – minority-group patients have fewer financial resources to pay for prescriptions – higher drug-abuse potential among minority groups• Patients’ lack of assertiveness in seeking treatment• Lack of treatment expertise at many sites at which minority-group patients are treated• Relative unavailability of opioids in some communities (Bonham, 2001; Glajchen, 2001)
  • Evolving Attitudes TowardOpioid UseHistorically, opioids were emphasized in terminally ill patients, andde-emphasized in chronic nonmalignant pain management.However, from the 1980’s to the present :• Attitudinal/perceptual changes on opioid use in nonmalignant chronic-pain treatment• More use of long-term opioid therapy in diverse pain syndromes – slowly growing evidence base – acceptance by pain specialists – acceptance by government and medical associations – increased reassurance from the regulatory community(Joranson et al, 2000; Portenoy et al, 1986)
  • Recent DevelopmentsIn Pain Management• Greater understanding of the pathophysiology underlying chronic pain syndromes• Scientific breakthroughs in molecular biololgy; insight into pain at the molecular level• Advances in drug therapy (drug delivery technologies)• Multimodal therapy• Multidisciplinary teams, shared decision-making that includes patients• Patients’ rights movement(JCAHO, 1999; Loeser et al, 2001)
  • Recent Organized Support for the Treatment of Pain National Organizations Issue Guideines • U.S. Agency for Health Care Policy and Research (HCPR)—1992 • U.S. Department of Health and Human Services—1994 • AAPM/APS Consensus Statement—1996 • American Society of Anesthesiologists—1997 • WHO; FSMB—1998 • AMA; APS (sickle-cell anemia)—1999 • American Pain Society: Clinical Guideline for Arthritis—2002 State-Led Initiatives • Legislation in form of Intractable Pain Acts (>10 states by 1999) • Guidelines for pain management (>18 states by 1999) • State Cancer Pain Initiatives(AAPM/APS, 1996; AMA, 2001; ASA, 1997; FSMB, 1998; JCAHO, 1999; WHO, 1996)
  • Module 2 Progress in Chronic Pain Management Chronic Pain Syndromes: Cancer Chronic Low Back Pain Osteoarthritis Fibromyalgia A National Pain Education Council Program
  • Cancer Pain Epidemiology • Cancer pain is highly prevalent – 30%-50% of those in active therapy – 75%-90% of those with advanced disease – approximately 25% of those in nursing homes(Bernebei et al, 1998; Caraceni et al,1999; Cleeland et al, 1994; Heim et al, 1993; Portenoy, 1994; Portenoy et al, 1992;Serlin et al, 1995)
  • Cancer Pain Inferred Pathophysiology • Nociceptive: deemed consistent with apparent degree of tissue injury – Somatic: related to ongoing activation of somatic primary afferents – Visceral: related to activation of primary afferent neurons that innervate viscera • Neuropathic: sustained by aberrant somatosensory processing in the peripheral nervous system or CNS(Portenoy, 2000)
  • Cancer PainDiagnosis: Clinical Considerations• Acute or chronic• Nociceptive, neuropathic or mixed pain – tumor-related (e.g., metastatic bone disease, nerve compression or infiltration) – treatment-related (chemotherapy, radiation or surgery) – unrelated to cancer or treatment(Portenoy , 2000; Portenoy et al, 1996)
  • Cancer Pain Principles of Assessment • Pain History – chronicity – intensity and severity – pathophysiology and mechanism – tumor type and stage of disease – pattern of pain and syndrome • Physical and Neurologic Examination • Radiographic Findings(Cleeland CS et al, 1992; Jacox et al, 1994; Portenoy et al, 199; Turk et al, 1994; Wall et al, 1994)
  • Cancer PainTreatment Considerations• Identify the cause of the pain• Primary treatment if indicated• WHO ladder combined with etiology-specific therapies for syndromes – pharmacologic and nonpharmacologic interventions – long-acting + short-acting opoids – adjuvant medications for neuropathic pain – NSAIDs and steroids can be helpful when there is an inflammatory component to pain(Jacox et al, 1994)
  • WHO Guidelines for Cancer Pain GOAL: Freedom From Pain STEP 3 • Step 3: Opioids for moderate-to-severe pain +/- non-opioid +/-adjuvant Pain Persists therapy STEP 2 • Step 2: Opioids for mild- to- moderate pain +/- non- Pain Persists opioid +/- adjuvant therapy • Step 1: Non-opioid +/- STEP 1 adjuvant therapy 08/13/12(Adapted from Portenoy et al, 1997)
  • Chronic Low Back PainEpidemiology• 60%–85% lifetime prevalence• Second most common complaint to prompt medical evaluation• Leading cause of long-term work disability• Most common reason for early Social Security disability in US• U.S. indirect costs: $33 billion annually• Disability and costs related to pain, not to the disease process (Loesser et al, 2001; Wall et al, 1994)
  • Chronic Low Back PainPathophysiology• Activation and sensitization of the nerve root nervi nervorum from root compression/traction• Sensitization of the nociceptors of the annulus fibrosus, periosteal spinal structures, and ligaments, due to acute inflammation, e.g., status post-trauma• Hyperalgesia (deep spinal and dermatomal) due to central sensitization (Loesser et al, 2001)
  • Chronic Low Back Pain Clinical Characteristics • Preoccupation with pain • Consistently disabled from pain • Depression and anxiety are common • High incidence of psychiatric diagnoses • Drug misuse is common, but addiction relatively rare (Wall et al, 1994)
  • Chronic Low Back Pain Diagnosis • History – medical, psychosocial – pain: location, duration, severity, alleviating/ aggravating influences • Physical Examination – posture and range-of-motion evaluation – routine neurologic and vascular exams • Imaging Studies – X-rays with flexion/extension – MRI – CT in some (Wall et al, 1994)
  • Chronic Low Back PainTreatment Considerations• Analgesic Medications• Adjuvant Analgesics• Physical Therapy Approaches• Neural Stimulation• Psychologic Management• Multidisciplinary Pain Centers (Portenoy et al, 1994)
  • Osteoarthritis(Degenerative Joint Disease)Epidemology• Most common form of arthritis worldwide• Occurs most in women and in adults over age 45• Occurs in 80% of people over 55 years of age• Affects >40 million people in US (1 in 6)• 23% experience limitation of activities• Cost in medical care and lost wages ~$95 billion(Elders, 2000; Loeser et al, 2001; Merskey et al, 1994)
  • OsteoarthritisPathophysiology• Progressive loss of articular cartilage• Chondrocytes produce metalloproteinases that degrade cartilage and cause fissuring, pitting, erosion, and denuded areas• Subchondral bone thickens and osteophytes, or bone spurs, form• Synovium thickened (contains moderate amount of lymphocytes, plasma cells)• Joint capsule and ligaments hypertrophied(Loesser et al, 2001; Wall et al, 1994)
  • OsteoarthritisClinical Characteristics• Deep aching pain, poorly localized• May occur in one or two joints or be generalized• Pain occurs in involved joint and is relieved by rest• Joint stiffness in morning and after periods of inactivity• Aching “night pain” is common• If pain is severe on activity and asymptomatic at rest, evaluate for neurogenic claudication (Loesser et al, 2001)
  • Osteoarthritis Diagnosis • History: age, functionality, degree of pain, stiffness, time of occurrence (e.g., morning, at rest, during activity) • Physical examination: range of motion, tenderness, bony enlargement of joint • Laboratory findings: radiograph, CBC, synovial fluid analysis(Loesser et al, 2001; Manek et al, 2000)
  • Osteoarthritis Treatment Considerations: First, perform a comprehensive assessment of pain and function Mild-to-moderate pain Acetaminophen Moderate-to-severe pain COX-2 NSAIDS Severe arthritis pain: COX-2 Opioids drugs and non-specific NSAIDs do not provide substantial relief Drug therapy ineffective and Surgical Treatment function severely impaired(ACR, 2000; APS, 2002; Manek et al, 2000)
  • Fibromyalgia Syndrome Epidemiology • 4–7 times more common in adult women than in men; highest prevalence in women 50–60 yrs • Approximately 2% of general population in U.S. and Canada have symptoms that could meet ACR criteria • Long-term follow-up studies suggest that fibromyalgia is not a syndrome representing a transition from one disorder to another(Loesser et al, 2001; Portenoy et al, 1996; Wall et al, 1994)
  • Fibromyalgia Syndrome Pathophysiology Etiology is unknown: 3 views of pathophysiology have emerged: • Central Nervous System (neurogenic) – generalized pain – increase in CSF substance P – decrease in serum and CSF serotonin • Muscle Pathology – decreased oxygen tension and blood flow – abnormal muscle biopsies – weakness • Psychopathology – anxiety, depression(Loeser et al, 2001; Portenoy et al, 1996; Wall et al, 1994)
  • Fibromyalgia SyndromeClinical Characteristics• Pain (musculoskeletal tenderness)• Lightheadedness, dizziness, syncope• Fatigue• Chronic insomnia; sleep disturbance• Cognitive deficits/short-term memory loss• Depression/anxiety• Numbness, dysesthesia in hands and feet(Loeser et al, 2001)
  • Fibromyalgia SyndromeDiagnosisBased on the 1990 ACRclassification guidelines:• 1 historical feature + 1 physical finding• Historical feature = widespread (axial) pain of 3 months or more• Physical finding = pain in at least 3 of the 4 body segments + a finding of at least 11 tender points on digital palpation of 18 designated tender points(Merskey et al, 1994; Portenoy et al, 1996; Wall et al, 1994; Wolk M, 2002)
  • Fibromyalgia Syndrome Treatment: A Multidisciplinary Approach • Patient Education – reading materials, videos, support groups • Physical Exercise – low-grade (muscle stretches, aerobic conditioning) • Pharmacologic Therapies – tricyclic antidepressants, NSAIDS, topical capsaicin, opioids* *Drug therapies have been used with varying degrees of success in treating fibromyalgia.(Portenoy et al, 1996; Wall et al, 1994)
  • Pathophysiology of Pain• Inferred from characteristics, etiology or pathophysiology• Types – nociceptive – neuropathic – idiopathic• Therapeutic implications(Portenoy et al, 1996)
  • Pathophysiology of Chronic Pain • In chronic pain, the nervous system remodels continuously in response to repeated pain signals – nerves become hypersensitive to pain – nerves become resistant to antinociceptive system • If untreated, pain signals will continue even after injury resolves • Chronic pain signals become embedded in the central nervous system(Marcus, 2000)
  • Peripheral and Central Pathways for Pain Ascending Tracts Descending Tracts Cortex Thalamus Midbrain Pons Medulla Spinal Cord (Brookoff, 2000)
  • Pain-Sensing System in the Malfunction in Chronic Pain Pain Acute pain: Sensing Pain-sensing signals are initiated in response to aIn chronic pain, stimuluspain signals are • They elicit a pain-generated relieving responsewithoutphysiologicsignificance Chronic pain: Pain signals are generated for no reason and may be intensified • Pain-relieving mechanisms may be defective or deactivated (Illustration: Seward Hung, 2000)
  • Nociceptive PainPresumably results from ongoing activation of primaryafferent neurons responding to noxious stimuli• Pain consistent with degree of tissue injury• Described as aching, squeezing, stabbing, throbbing• Subtypes: – Somatic: related to activation of somatic afferent neurons – Visceral: related to activation of visceral afferent neurons(Loeser et al, 2001; Portenoy et al, 1996)
  • Neuropathic Pain• Initiated by a primary lesion in the nervous system; believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system• Independent of obvious ongoing nociceptive activation• Burning, shooting, electrical quality; may be aching, throbbing, sharp• Subtypes: – Presumed “central generator”  deafferentation pain (central pain, phantom pain)  Sympathetically-maintained pain – Presumed “peripheral generator”  Polyneuropathies and mononeuropathies (Portenoy et al, 1996)
  • Idiopathic and Psychogenic Pain Idiopathic Pain • Usually exists in the absence of an identifiable physical or psychologic pathology that could account for pain • Uncommon in patients with progressive illness Psychogenic Pain • Presents positive evidence of a predominant psychologic contribution and may be labeled with a specific psychiatric diagnosis(Loeser et al, 2001; Merskey et al, 1994; Portenoy et al, 1996)
  • Module 3Progress in Chronic Pain Management: Therapeutic Modalities for Chronic Pain Management AssessmentA National Pain Education Council Program
  • Pain Assessment • Characterize the pain • Characterize the disease, relationship between pain and disease and potentially treatable etiologies • Clarify syndromes and infer pathophysiology • Determine need for urgent therapy • Identify other needs • Develop a therapeutic strategy(Portenoy et al, 1997)
  • Pain AssessmentComponents• History: temporal features, intensity, topography, quality, exacerbating/alleviating factors• Physical Exam: determine existence of underlying pathology• Lab and Radiographic Tests: appropriate to pain syndromeAssessment Tools• Pain Intensity Scales: VAS, NAS, “faces” scale• Multidimensional Pain Measures: Brief Pain Inventory, McGill Pain Questionnaire(Portenoy et al, 1997)
  • Pain Intensity Rating Scales • Visual Analogue Scale (VAS) No pain ----------------------------------- Worst pain • Numerical Rating Scale 0 ------------------------------------------- 10 No pain Worst pain imaginable • Categorical Scale None (0) Mild (1 – 4) Moderate (5 – 6) Severe (7 – 10) (Cleeland, 1991; Jacox et al, 1994)
  • Pain Intensity Rating Scales• Pain Faces Scale 0 2 4 6 8 10 No Hurts Hurts a Hurts Hurts a Hurts as hurt just a little bit even whole much as little bit more more lot you can imagine• Brief Pain Inventory Shade areas of worst pain Put an X on area that hurts most(Cleeland, 1991; Wong et al, 2001)
  • Module 3Progress in Chronic Pain Management Therapeutic Modalities for Chronic Pain Management: Treatment A National Pain Education Council Program
  • Therapeutic Optionsfor Chronic Pain Management • Pharmacotherapy • Rehabilitative Approaches • Psychologic Interventions • Anesthesiological Approaches • Neurostimulatory Techniques • Surgery • Complementary/Alternative Approaches • Lifestyle Changes (Portenoy et al, 1997)
  • Chronic Pain Management: Pharmacotherapy Analgesics • Nonopioids • Adjuvant Analgesics • Opioids(Cashman, 1996; Hanks et al, 1998; Galer, 1998; Stein, 1995)
  • Nonopioid Analgesics:Acetaminophen• Minimal anti-inflammatory effect• Fewer adverse effects than other nonopioid analgesics• Adverse effects: – renal toxicity – risk of hepatotoxicity at high doses; • increased risk with liver disease or chronic alcoholism• No effect on platelet function(Gilman et al, 2001)
  • Nonopioid Analgesics: NSAIDSMechanism of Action• Inhibit both peripheral and central cyclo- oxygenase, reducing prostaglandin formation• 2 isoforms of COX – COX-1: Constitutive, physiologic – COX-2: Inducible, inflammatory
  • Nonopioid Analgesics: NSAIDS• Major recent advance: COX-2 selective NSAIDS• COX-2 selective inhibitors have better GI safety profile; no change in platelet function• Drug selection should be influenced by drug-selective toxicities, prior experience, convenience, cost• Great individual variation in response to different drugs• Use with caution in patients with renal insufficiency, congestive heart failure or volume overload (Cashman, 1996: Langman et al, 1999; Simon et al, 1999)
  • Adjuvant Analgesics Adjuvant Analgesics for Neuropathic Pain CLASS EXAMPLESAnticonvulsants gabapentin, valproate, phenytoin, carbamazepine, clonazepam, topiramate, lamotrigineAntidepressants amitriptyline, desipramine, nortrip- tyline, paroxetine, citalopram, othersLocal Anesthetics mexiletineCorticosteroids dexamethasone, prednisoneα-2 Adrenergic Agonists tizanidineNMDA-Receptor Agonists dextromethorphan, ketamineTopicals lidocaine, lidocaine/prilocaine, capsaicinMiscellaneous baclofen, calcitonin
  • Adjuvant Analgesics: AnticonvulsantsCommon Characteristics• Most clinical experience: gabapentin, carbamazepine, phenytoin, valproate, clonazepam• Limited data on efficacy of newer anticonvulsants• Used as an analgesic, dosing schedule is similar to anticonvulsant indication• Large inter-/intra-individual variability in analgesic responseGabapentin• Usual first-line drug for neuropathic pain• Favorable safety profile• Positive controlled trials in PHN/diabetic neuropathy• No controlled studies in cancer patients• Usual starting dose 100-300 mg/day• Titration to identify responders/nonresponders• Usual effective dose 600-3600 mg/day; higher doses sometimes beneficial(Galer, 1998; Rosner et al, 1996)
  • Adjuvant Analgesics:Antidepressants• Evidence is best for tricyclics• SSRI/atypical antidepressants better tolerated• Proven efficacy for all types of neuropathic pain, but often preferred for continuous dysesthesias• Analgesic doses for tricyclics is usually less than the antidepressant dose(Wall et al, 1999)
  • Adjuvant Analgesics: Corticosteroids • Shown to improve pain, appetite, nausea, malaise, quality of life in cancer patients • In the cancer population, indicated for refractory neuropathic pain, and other indications: bone pain, bowel obstruction, capsular pain, lymphedema, headache • In non-cancer pain, long-term use is limited to inflammatory conditions • Usual drugs are prednisone and dexamethasone(Lucas et al, 2002)
  • Adjuvant Analgesics:α-2 Adrenergic Agonists • Evidence of nonspecific analgesic effects • Established analgesic effect of epidural clonidine in neuropathic cancer pain • Tizanidine usually better tolerated (starting dose 1-2 mg/day; usual maximum dose up to 40 mg/day)(Max et al, 1992; Sindrup et al, 990)
  • Adjuvant Analgesics:NMDA-Receptor Antagonists• N-methyl-D-aspartate receptor involved in neuropathic pain• Commercially-available drugs in the U.S.: ketamine, dextromethorphan, amantadine – Ketamine: dissociative anesthetic; can be used p.o. or IV/SC infusion – Dextromethorphan: antitussive; starting dose 120 mg/day; maximum daily dosage one gram – Amantadine: starting does 100 mg b.i.d.(Herry et al, 1995; Nelson et al, 1997; Pud et al, 1998)
  • Opioid Therapy: Classes of Opioids Pure (Full) Agonists: Preferred for Chronic Pain • Bind to opioid receptor(s) • No antagonist activity • No ceiling effect Agonist-Antagonists • Ceiling effect for analgesia • Can reverse effects of pure agonists – mixed agonist-antagonists (butorphanol, nalbuphine, pentazocine, dezocine) – partial agonists (buprenorphine) Antagonists • Reverse or block agonist effects of pure opioids • Naloxone has been used to treat opioid overdose, addiction(Jacoxet al, 1994; Portenoy et al, 1996)
  • Opioid Therapy: Drug SelectionShort-Acting Opioids Long-Acting Opioids• Hydrocodone/APAP • Transdermal Fentanyl• Hydromorphone • Methadone• Morphine • Extended-release• Oxycodone w or w/o morphine APAP • Oxycodone CR• Oral transmucosal fentanyl• Tramadol (Lucas et al, 2002)
  • Opioid Therapy: Drug SelectionAdvantages of Long-Acting Opioids• Fewer peaks and troughs – sustained pain relief• Dosed less often, improved adherence• Potentially improved patient satisfaction and quality of life (Lucas et al, 2002; Weinstein et al, 2001)
  • Opioid Therapy: Prescribing Principles • Drug Selection: Elements to Consider – Severity of pain, previous exposure, availability, patient’s preference, renal/liver function, cost • Dose to Optimize Effects – Fixed schedule (or around-the-clock) vs as-needed dosing; rescue doses • Treat Side Effects – Goal: balance between analgesia and side effects • Manage the Poorly Responsive Patient – Consider a variety of alternative strategies(Weinstein et al, 2002)
  • Opioid Therapy: Route of Administration • Oral / Transdermal • Rectal • Parenteral (IV, SC) • Intraspinal (epidural, intrathecal)(Lucas et al, 2002)
  • Opioid Therapy: Dosing • By-the-clock (fixed-schedule) dosing with long-acting opioid plus an “as-needed” short- acting “rescue” opioid (usually 5%–15% of total daily dose, q 2-3 h prn) • Baseline dose increases: 25%–100% or equal to “rescue” dose use • Increase “rescue” dose as baseline dose increases(American Pain Society, 1998)
  • Equianalgesic Table PO/PR (mg) Analgesic SC/IV/IM (mg) 30 Morphine 10 4–8 Hydromorphone 1.5 20 Oxycodone - 20 Methadone 10 - Fentanyl 100 μg/h parenterally and transdermally ≡ 4 mg/h morphine parenterally; 1 μg/h transdermally ≡ 2mg/24h morphine PO
  • Equianalgesic ConversionsExample:• Patient receiving a total 24-hr dose of morphine 180 mg PO• What is the equivalent 24-hour dose of PO hydromorphone?• Morphine 30 mg PO = Morphine 180 mg PO• Hydromorphone 7.5mg PO X• X = Hydromorphone 45 mg PO (6-8mg PO q 4hr)• Determine starting dose of new drug based on this calculation
  • Conversion Chart for Starting Dose of Transdermal Fentanyl Fixed-combination short-acting opioids (6/day): – Lorcet 5 mg/500 mg – Lortab 5 mg/500 mg – Percocet 5 mg/325 mg One 25 mcg/h – Percodan 5 mg/325 mg transdermal – Tylenol + Codeine 30 mg/325 mg fentanyl – Tylox 5 mg/500 mg patch/3 days – Vicodin 5 mg/500 mg (72 hours) Long-acting opioids(2/day): Multiple patches may be used – OxyContin 20 mg for doses exceeding 100 mcg/h. Doses up to 6oo mcg/h have – MS Contin 30 mg been evaluated in clinical trials.(Adapted from Duragesic PI, 2001)
  • Opioid Titration• Dose titration over time is key to successful opioid therapy• There is no ceiling dose for pure-agonist opioids. Titrate dose upward for maximum pain relief with acceptable side effects• Consider rescue medication for breakthrough pain• Responsiveness of an each patient to each drug varies• If a patient does not respond well on one opioid, it is important to try another (opioid rotation) (Portenoy et al, 1997)
  • Opioid Therapy: Patient Selection • Thorough Evaluation – pain history – physical exam – coexisting conditions • Review of Previous Medical/Pain History – any psychological disturbances – chronic pain history • Substance Abuse History (including alcohol) – remote, recent or ongoing – patient goals/expectations • consistent with physician’s? • feasible/reasonable? (Haddox et al, 1997; Portenoy et al, 1996)
  • Opioid Therapy:Monitoring Outcomes Monitoring the 4 A’s • Analgesia (pain relief) • Activities of Daily Living (psychosocial functioning) • Adverse Effects (side effects) • Aberrant Drug-Taking (addiction-related outcomes)(American Pain Society, 2002; Passik et al, 2000; Portenoy et al, 1997)
  • Opioid Therapy: Managing thePoorly Responsive Patient If dose escalation increases adverse effects • Side-effect management • Pharmacologic strategy to lower opioid requirement – spinal route of administration – add nonopioid or adjuvant analgesic • “Opioid rotation” – nonpharmacologic strategy to lower opioid requirement(Mather, 2001)
  • Opioid Therapy: Managing thePoorly Responsive Patient Opioid Rotation • Based on large intra-individual variation in response to different opioids • Reduce equianalgesic dose by 25%–50% with provisos: – reduce less if pain severe – reduce more if medically frail – reduce less if same drug by different route – reduce transdermal fentanyl less (no cutback from equianalgesic dose) – reduce methadone more: 75%–90%(Indelicato et al, 2002; Mather, 2001)
  • Opioid Therapy: Managing Side Effects • Common – Constipation – Somnolence, mental clouding • Less Common – Nausea – Sweating – Myoclonus – Amenorrhea – Itch – Sexual dysfunction – Urinary retention – Headache(Ahmedzai et al, 1997; Portenoy, 1996)
  • Novel Drug Therapies forTreatment of Pain Central Nociception: Emerging Analgesic Targets • Excitatory amino acid and NK receptors • N-type Ca++ receptors • N-acetylcholine receptors • Adenosine (A1) receptors • Cannabinoid (CB1) receptors(Pappagallo M)
  • Novel Drug Therapies forTreatment of Pain Peripheral Nociception: Emerging Analgesic Targets • Sensory neuron specific Na+ channels (eg, PN3, NAN) • Opioid receptors • Vanilloid receptors • Serotonin receptors • Alpha-adrenergic receptors • Proton-sensitive channels (pH-sensitive) • Nerve–growth-factor receptors (*TrKA, p75) • N- or T-type Ca++ channels • Purine receptors *TrKA = tyrosine kinase(Pappagallo M)
  • Chronic Pain Management: Nonpharmacologic Approaches Anesthetic Approaches • Neuraxial Drug Administration – opioids, local anesthetics, and/or clonidine via continuous epidural or intrathecal infusion • Neural Blockade – temporary block – neurolytic block(Eisenach et al, 1995; Patt et al, 1998)
  • Chronic Pain Management:Nonpharmacologic Approaches Neurostimulatory Approaches • TENS (transcutaneous electrical nerve stimulation) • Acupuncture • Dorsal Column Stimulation Surgical Procedures • Peripheral Nerve Procedures – peripheral neurectomy – rhizotomy • CNS Procedures – cordotomy (Portenoy et al, 1996)
  • Chronic Pain Management:Nonpharmacologic Approaches Psychologic Treatments • Behavioral treatment • Biofeedback • Cognitive-Behavioral Treatment Rehabilitative Approaches • Physical/Occupational Therapy • Heat/Cold Therapy (diathermy, cryotherapy) • Prostheses • Assistive Devices(Redd et al, 2002)
  • Module 4Progress in Chronic Pain Management Substance Abuse Issues in Chronic Pain Management A National Pain Education Council Program
  • The Terminology of Abuse• Physical Dependence – Abstinence syndrome induced by administration of an antagonist or by dose reduction – Usually unimportant if abstinence is avoided – Assumed to exist after few days’ dosing but actually highly variable – Does not independently cause addiction• Addiction – Disease with pharmacologic, genetic, psychosocial elements – Fundamental features: loss of control, compulsive use, use despite harm – Diagnosed by observation of aberrant drug-related behavior (AAPM/APS, 1996; NIDA, 2001; Passik et al, 2000; Portenoy, 1996)
  • The Terminology of Abuse• Tolerance – Diminished drug effect from drug exposure – Varied types: associative vs. pharmacological – Tolerance to analgesia is seldom a problem in the clinical setting: • Tolerance rarely “drives” dose escalation • Tolerance does not cause addiction• Pseudoaddiction – Aberrant drug-related behaviors driven by uncontrolled pain – Reduced by improved pain control – Complexities • How aberrant can behavior be before it is inconsistent with pseudoaddiction? • Can addiction and pseudoaddiction coexist?(Passik et al, 1998; Passik et al; Portenoy RK, 1996)
  • Risk Assessment for Addiction Low Addiction Risk • Acute pain • Cancer pain • Patients without abuse background or psychopathology Chronic Noncancer Pain • Probability of addiction is small – surveys that include patients with abuse or psychopathology show mixed results • Predictors of addiction may include – history of substance abuse – Age – personality factors – family dynamics and social factors(Passik et at, 1998; Passik et al, 1998)
  • Diagnosing and Monitoring Aberrant Behaviors Two-Step Monitoring Approach • Step 1: Are there aberrant drug-related aberrant behaviors? • Step 2: If yes, are these behaviors best explained by the existence of an addiction disorder? Differential Diagnosis • Addiction/pseudoaddiction • Other psychiatric disorders (e.g., borderline personality disorder) • Mild encephalopathy • Family disturbances • Criminal intent(Passik et at, 1998; Passik et al, 1998)
  • Drug-Related Behavior Predictive of AddictionProbably More Predictive Probably Less Predictive• Selling prescription drugs • Aggressive complaining• Prescription forgery • Drug hoarding when symptoms• Stealing or “borrowing” drug from milder another person • Requesting specific drugs• Injecting oral formulation • Acquisition of drugs from other• Obtaining prescription drugs from medical sources non-medical source • Unsanctioned dose escalation• Multiple episodes of prescription “loss” once or twice• Concurrent abuse of related illicit • Unapproved use of the drug to drugs treat another symptom• Multiple dose escalations despite • Reporting psychic effects not warnings intended by the clinician• Repeated episodes of gross • Occasional impairment impairment or dishevelment (Passik et al, 1998)
  • Addressing AberrantDrug-Related Behavior • General Management Principles – know laws and regulations – structure therapy to match perceived risk • Proactive Strategies – communicate goals of therapy – provide written guidelines (treatment contract) – assess often • Reactive Strategies – require frequent visits and small quantities of drug – use of urine toxicologies – long-acting drugs with no rescue doses – relate to addiction-medicine community (sponsor, program, addiction-medicine specialist, psychotherapist)(Mironer et al, 2000; Portenoy et al, 1997; Passik et al, 2000)
  • Conclusions• Chronic pain is common and undertreated• Identify chronic pain patients who would most likely benefit from opioid therapy and use it responsibly• Implement opioid treatment with a plan for ongoing monitoring• Assess and monitor pain, side effects, and drug-related behaviors• Adjust dosage• Manage side effects