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Chronic pain management


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Chronic pain management

  1. 1. Module 1 Progress in Chronic Pain Management Understanding, Impact, Awareness and Advances A National Pain Education Council Program
  2. 2. 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)
  3. 3. 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)
  4. 4. 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)
  5. 5. 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)
  6. 6. 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)
  7. 7. 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)
  8. 8. 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)
  9. 9. 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)
  10. 10. 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)
  11. 11. 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)
  12. 12. Module 2 Progress in Chronic Pain Management Chronic Pain Syndromes: Cancer Chronic Low Back Pain Osteoarthritis Fibromyalgia A National Pain Education Council Program
  13. 13. 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)
  14. 14. 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)
  15. 15. 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)
  16. 16. 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)
  17. 17. 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)
  18. 18. 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)
  19. 19. 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)
  20. 20. 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)
  21. 21. 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)
  22. 22. 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)
  23. 23. Chronic Low Back PainTreatment Considerations• Analgesic Medications• Adjuvant Analgesics• Physical Therapy Approaches• Neural Stimulation• Psychologic Management• Multidisciplinary Pain Centers (Portenoy et al, 1994)
  24. 24. 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)
  25. 25. 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)
  26. 26. 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)
  27. 27. 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)
  28. 28. 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)
  29. 29. 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)
  30. 30. 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)
  31. 31. 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)
  32. 32. 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)
  33. 33. 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)
  34. 34. Pathophysiology of Pain• Inferred from characteristics, etiology or pathophysiology• Types – nociceptive – neuropathic – idiopathic• Therapeutic implications(Portenoy et al, 1996)
  35. 35. 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)
  36. 36. Peripheral and Central Pathways for Pain Ascending Tracts Descending Tracts Cortex Thalamus Midbrain Pons Medulla Spinal Cord (Brookoff, 2000)
  37. 37. 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)
  38. 38. 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)
  39. 39. 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)
  40. 40. 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)
  41. 41. Module 3Progress in Chronic Pain Management: Therapeutic Modalities for Chronic Pain Management AssessmentA National Pain Education Council Program
  42. 42. 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)
  43. 43. 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)
  44. 44. 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)
  45. 45. 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)
  46. 46. Module 3Progress in Chronic Pain Management Therapeutic Modalities for Chronic Pain Management: Treatment A National Pain Education Council Program
  47. 47. Therapeutic Optionsfor Chronic Pain Management • Pharmacotherapy • Rehabilitative Approaches • Psychologic Interventions • Anesthesiological Approaches • Neurostimulatory Techniques • Surgery • Complementary/Alternative Approaches • Lifestyle Changes (Portenoy et al, 1997)
  48. 48. Chronic Pain Management: Pharmacotherapy Analgesics • Nonopioids • Adjuvant Analgesics • Opioids(Cashman, 1996; Hanks et al, 1998; Galer, 1998; Stein, 1995)
  49. 49. 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)
  50. 50. 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
  51. 51. 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)
  52. 52. 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
  53. 53. 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)
  54. 54. 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)
  55. 55. 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)
  56. 56. 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)
  57. 57. 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)
  58. 58. 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)
  59. 59. 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)
  60. 60. 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)
  61. 61. 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)
  62. 62. Opioid Therapy: Route of Administration • Oral / Transdermal • Rectal • Parenteral (IV, SC) • Intraspinal (epidural, intrathecal)(Lucas et al, 2002)
  63. 63. 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)
  64. 64. 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
  65. 65. 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
  66. 66. 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)
  67. 67. 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)
  68. 68. 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)
  69. 69. 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)
  70. 70. 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)
  71. 71. 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)
  72. 72. 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)
  73. 73. 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)
  74. 74. 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)
  75. 75. 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)
  76. 76. 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)
  77. 77. 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)
  78. 78. Module 4Progress in Chronic Pain Management Substance Abuse Issues in Chronic Pain Management A National Pain Education Council Program
  79. 79. 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)
  80. 80. 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)
  81. 81. 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)
  82. 82. 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)
  83. 83. 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)
  84. 84. 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)
  85. 85. 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