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2015: Pain Management - A Practical and Functional Approach-Lakkaraju


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Pain Management - A Practical and Functional Approach

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2015: Pain Management - A Practical and Functional Approach-Lakkaraju

  1. 1. Ravi Lakkaraju, MD Poway Spine and Pain Poway, CA
  2. 2.  The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage”  Pain is the single most common reason for patients to seek medical attention
  3. 3.  2000 – 13.1% of population over 65  2030 – 20% of population over 65  25-50% of community elders suffer chronic pain of some kind  45-50% of Nursing home residents suffer chronic pain
  4. 4.  Chronic pain effects approx. 100 million Americans  Roughly cost $635 billions annually  Incidence greater than Diabetes, heart disease and cancer combined.
  5. 5.  - sensitization of nociceptors  - Nerve damage  - Release of sensitizing humoral mediators
  6. 6.  In some conditions, nociception due to tissue damage may occur, but the patient may not perceive, or feel it  i.e., diabetic peripheral neuropathy  Conversely, the patient may perceive severe pain with no demonstrable evidence of tissue damage  i.e., trigeminal neuralgia
  7. 7.  Nociceptive – somatic (superficial, deep) and Visceral.  Neuropathic – painful mononeuropathies, polyneuropathies, Deafferentation pain, sympathetically maintained pain, central pain.  Mixed
  8. 8.  Acute pain  Chronic pain  Cancer pain  Chronic non-cancer pain (CNCP)  CPS (chronic pain syndrome)
  9. 9. 4 Basic Steps:  Transduction  Transmission  Modulation  Perception
  10. 10.  The process by which afferent nerve endings participate in translating noxious stimuli (e.g., a pinprick) into nociceptive impulses  Noxious stimulation is first carried by the faster A-delta fibers and then by the slower C fibers  Local injury can cause nociceptors to become hypersensitive to noxious stimuli, thereby creating a condition called sensitization
  11. 11. • The process by which impulses are sent to the dorsal horn of the spinal cord and the brain • Noxious stimulation is first carried by the faster A-delta fibers and then by the slower C fibers
  12. 12. • The process of dampening or amplifying pain- related neural signals • A variety of modalities can modulate these pathways”, including: • Systemic or neuro-axial injection of opioids • Electric stimulation, TENS, Acupuncture, Massage. • TCA’S, AED’s • Stress, Anxiety • Depression
  13. 13.  Refers to the subjective experience of pain  Results from the interaction of transduction, transmission, modulation  Dependent on the psychological aspects of the individual
  14. 14.  Neuropathic pain is pain due to damaged or dysfunctional nerves  The pathophysiology of neuropathic pain can have both peripheral and central mechanisms  it is doubtful that a single mechanism can account for all cases  The end result is pain that is experienced without evidence of noxious stimulus
  15. 15.  - Enhanced pain intensity  - Enlargement of pain areas  - Widespread hyperalgesia  - Enhanced disability
  16. 16.  - sensitization of central neural structures  - Dysfunction of endogenous pain modulation
  17. 17.  - Psychophysical Assessments  - Objective Assessments  - Measuring spread of pain and referred pain areas  - Measurement of endogenous modulation  - Measurement of Temporal Summation
  18. 18.  Can be classified mostly into 3 broad groups: - Curative/Disease modifying - Rehabilitative - Palliative
  19. 19.  Simplest and preferred when the identifiable pathophysiological process is present and becomes the target of treatment.  Typically pain should resolve once the underlying process resolves  Examples – ORIF, Appendectomy, Angioplasty for ischemia  Difficult to treat ‘upstream’ pathophysiologic process
  20. 20.  Appropriate when 2 conditions apply  - the curative model is not appropriate  - major goal of treatment is improving patient’s ability to function - Examples – multidisciplinary pain rehabilitation (PT, OT, counselling, biofeedback, CAM, vocational rehab, etc.,)
  21. 21.  Combination of Medication management to control pain  And/or  Less demanding rehabilitative therapies
  22. 22.  Low levels of pain can cause high functional impact, depression  Although pain threshold increases with age, tolerance for pain decreases.
  23. 23.  Multiple pain complaints, multiple medical problems, poor communication/under- reporting  Cognitive decline, depression, anxiety, insomnia, fatigue  Poor nutrition, poor tolerance to tests and procedures.
  24. 24.  Can be more reliable than just pain reporting, especially in low cognitive patients.  Facial expressions  Verbalizations  Body movements
  25. 25.  Changes in interpersonal interactions  Changes in activity patterns or routine  Mental status changes
  26. 26.  Decreased renal function (decrease in glomeruli, decrease in renal excretion, low GFR, higher serum drug levels)  Decreased hepatic function (decreased Cyt.P450 oxidation causing higher serum drug levels  Decreased serum protein, decreased functional binding to proteins – Less unbound drug, increased CNS effect.
  27. 27.  Two metabolites – M3G, M6G (6 is more active and leads to sedation, as this is renally excreted)  Elimination by hepatic metabolism to glucuronides  T1/2 is 2-4 hrs. may be elevated in elderly up to 15 hrs.
  28. 28.  Metabolized to normeperidine  Not reversible by naloxone  This leads to respiratory depression and excitatory neurotoxicity, anti-cholinergic effects, urinary retention  Blocks reuptake of NE and HT, can cause fatal reaction with concomitant SSRI (Fluoxetine)
  29. 29.  Decreased nerve conduction velocity (loss of myelin on axons, decrease axonal synapses)  Elderly adults rely on C-fiber input when reporting pain ; whereas, younger patients use C and A-delta.
  30. 30.  TENS, heat, acupuncture, relaxation techniques.  Exercise – targeted therapies with realistic achievable goals, should be integrated into daily routine and ADL’s, progress slowly as function and strength improve.  PT / OT , custom adaptive equipment as needed to decrease pain and improve function.
  31. 31.  ASA  Acetaminophen  NSAIDS  Tramadol  Opioids  Anti-Depressants  Anti-Epileptics  Local Anesthetics / Topicals
  32. 32.  NSAIDS – exercise caution due to renal, GI and CV risks  Anti-depressants and Anti-convulsants - adjunctive role in chronic pain especially neuropathic pain states. Dosing limited by side effects  Topical anesthetic / NSAID patches – limited penetration into the tissues, effective only at superficial targets
  33. 33.  Equalizing the ‘Pain Pendulum’  ‘Balance’ pain relief with risks associated with opioids.  (Not too much…not too little…just enough !!)
  34. 34.  Always administer tools for risk assessment (COMM, DIRE, ORT, SOAPP, SOAPP-R)  Have a clear written agreements / documentation / ‘opioid contract’  All opioid contracts should be simple and written at ‘6th or 7th’ grade level or even lower !  Written consent from patient that ‘contract’ was read and clearly understood by the patient.
  35. 35.  Opioid contract/Agreement sets precedence to ‘Rules/responsibilities on patients and reviews risks involved. Not a binding agreement but a good practice for every provider.  Templates of medication agreements can be downloaded from www.SanDiego-  Create function based treatment plans with goals, e.g, begin PT, document improvement in ADL’s and daily routine. Review partner or care-giver input apart from patients self report. Review therapy notes.
  36. 36.  Must have a good collaboration between patient and clinician  Apart from pain scores, goals should be realistic, meaningful and verifiable.  Treatment plan should be periodically re- assessed, modified based on goals and functional outcomes  Always have a ‘Exit strategy’ or plan termination that is mutually agreed upon by the patient.
  37. 37.  works on 3 receptors- mu, kappa, delta.  Exerts 3 actions – 1.inhibits transmission of nociceptive input from the periphery to the spinal cord, 2.activation of descending inhibitory pathways that modulate transmission in the spinal cord (pain “dampening”), 3. Alteration of limbic system activity.  Thus, opioids modify sensory and affective aspects of pain.
  38. 38.  Start at lowest possible dose for opioid –naïve patients – ‘start low go slow’  Opioid tolerant patients – select dose and medication on case by case basis. When converting from other opioid start at 50% equianalgesic dose and titrate per response.  May use ER/LA therapy alone, SA only, or a combination of ER/LA with a SA opioid.  Recommend not to use more than one SA concurrently.
  39. 39.  SA opioids typically have rapid onset (10-60 min) and relatively short duration (2-4 hrs)  ER/LA opioids have relatively slow onset (between 30 to 90 min) and relatively long duration of action (4 to 72 hrs)  Combination with non-opioid adjunctives can be beneficial and can have opioid sparing effects. But monitor for non-opioid drug toxicity.  No ‘ceiling’ effect for opioid analgesic dosing.  Selecting ‘Abuse-Deterrent’ formulations may minimize the opioid abuse.
  40. 40.  Phenanthrene (Morphine, codeine, Thebaine, Papaveretum)  Semi-synthetic (hydrocodone, hydromorphone, oxycodone, oxymorphone)  Synthetic (Fentanyl, Demerol, methadone)
  41. 41.  Buprenorphine  Butorphanol  Nalbuphine
  42. 42.  3 principal classes  - Mu 1, 2, 3  . 1-supraspinal analgesia  . 2-respiratory depression, physical dependence  -Kappa  . Sedation, spinal analgesia  Delta – Anti-depressant, dependence, Analgesia
  43. 43.  Morphine dose is used as a ‘standard’ for dose comparison of other opioids. Morphine equivalent daily dose (MEDD)  Recommend not to exceed >100 mg/day MEDD  exercise caution with morphine and Demerol use in renal insufficiency patients. Most other opioids eliminated by hepatic metabolism.  Codeine is a prodrug and not all patients convert it to an active form.
  44. 44.  When treating chronic pain with opioids, also be prepared to proactively treat side effects.  Common side effects include respiratory depression, sedation, mental clouding or confusion, nausea, vomiting, constipation, pruritus and urinary retention.  Side effects tend to subside with time with the “exception” of Constipation.
  45. 45.  Periodic urine drug screens (should be performed for the duration of COT)  244 un-intentional Rx drug related deaths in San Diego county in 2014, 5723 ER discharges related to pain killers in 2013  Utilizing ‘CURES’/PDMP system for monitoring and surveillance (CONTROLLED SUBSTANCE UTILIZATION REVIEW AND EVALUATION SYSTEM). Register by Jan 1st, 2016.  Can complete registration online at  Perform Pill counts at each visit, especially in high risk patients.
  46. 46.  July 2012, FDA released ‘final’ guidelines to REMS for ER/LA formulations.  2014-2015 – Government move to initiate an action plan to formulate ‘National Pain Strategy’(NPS)
  47. 47.  Urine drug screens typically done every 1-3 months.  More frequently done in high risk patients, e.g,  Prior history of addiction, past abuse, aberrant behavior, occupations demanding mental acuity, elderly, unstable or dysfunctional social environment, comorbid psychiatric or medical conditions  Sometimes daily or weekly monitoring may be necessary for patients at very high risk of adverse outcomes.  Urine specimens can be adulterated and should be aware.  Oral swab tests more easy to administer and can be more valuable than urine drug screens.
  48. 48. DRUG METABOLITES  Morphine  Codeine  Hydrocodone  oxycodone  Morphine, hydromorphone, codeine  Codeine, morphine, hydrocodone  Hydrocodone, hydromorphone, 6- hydrocodol  Oxycodone, oxymorphone  hydrocodone
  49. 49.  Screen for hypogonadism in patients on COT, especially with signs and symptoms of fatigue, mood changes, decreased libido, loss of muscle mass and osteoporosis.  Perform opioid rotation if lack of efficacy, side- effects of one opioid class, altered pharmaco- kinetics, changes in absorption.
  50. 50. CHRONIC PAIN PATIENT ADDICTED PATIENT  Medication use is not out of control  Medication use improves quality of life  Wants to decrease medication if adverse effects develop  Is concerned about the physical problem being treated with the drug  Follows the practitioner-patient agreement for use of the opioid.  May have left over medication  medication use is out of control  Medication use impairs quality of life  Medication use continues or increases despite adverse effects  Unaware of or in denial about any problems that develop as a result of drug treatment  Does not follow opioid agreement  Does not have left over medication. Loses prescriptions. Always has a story about why more drug is needed.
  51. 51.  Tolerance – decreased efficacy over time  Dependence – tolerance +withdrawal symptoms  Addiction – ‘neurobiological disease’. Strong genetic influence. Preoccupied with continued use despite harm  Pseudoaddiction – happens when pain is undertreated. “drug seeking” or “clock watching”. Usually resolves with effective pain management.
  52. 52. 0 1,000 2,000 3,000 4,000 5,000 6,000 7,000 8,000 Total Female Male Source: National Center for Health Statistics, CDC Wonder
  53. 53. 0 2,000 4,000 6,000 8,000 10,000 12,000 14,000 16,000 18,000 Total Female Male Source: National Center for Health Statistics, CDC Wonder
  54. 54. 0 5,000 10,000 15,000 20,000 25,000 Total Female Male Source: National Center for Health Statistics, CDC Wonder
  55. 55.  Reasons to terminate may include (healing or recovery from the treatment condition, intolerable side-effects, lack of response, discovery of abuse or misuse or addiction)  Typically 10% dose reduction per week. Slower taper will minimize unpleasant withdrawal symptoms.  Clonidine can be used. 0.1 – 0.2mg PO every 6 hrs daily or patch at 0.1mg/24 hours.  Drug rehab - Methadone
  56. 56.  Respiratory depression usually preceded by warning signs and can be prevented with careful monitoring  Take home Naloxone Rx for patients with high risk for overdose  . In 2014 FDA approved hand held auto- injector (Evzio) and can be used at home by family members or caregivers.
  57. 57.  Mu-1 agonist and NMDA antagonist  Analgesic duration of 4-6 hrs  Elimination t1/2 15-60 hrs  Can cause QT prolongation, Torsade de pointes
  58. 58.  Has been long used to treat addiction.  Long plasma elimination half life, relatively short analgesic half life makes it optimal for maintenance.  Has opioid and non-opioid receptor effects causing varied effects – ‘Broad spectrum opioid’  Metabolized by liver enzymes that differ from those associated with most other opioids, leading to drug-drug interactions.
  59. 59.  Significant genetic variations in the liver enzymes that metabolize methadone  Metabolism effected by cigarette smoking and alcohol consumption.  Lowest possible dose titration should be followed even for opioid tolerant patients.
  60. 60.  1 provider and 1 pharmacy for all controlled substances  Use CURES/PDMP  Use medication agreements when prescribing ‘COT’  Don’t mix opioids and CNS depressants/sedatives. Monitor polypharmacy  Implement multidisciplinary approach to treat chronic pain.