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Pain Management in the Hospital

Pain Management in the Hospital. Rog Kyle, MD Medical University of South Carolina 2/7/12. Objectives. Differentiate acute, chronic, somatic, neuropathic, referred, and visceral pain syndromes. Differentiate tolerance, dependence, addiction, and pseudo-addiction.

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Pain Management in the Hospital

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  1. Pain Management in the Hospital Rog Kyle, MD Medical University of South Carolina 2/7/12

  2. Objectives • Differentiate acute, chronic, somatic, neuropathic, referred, and visceral pain syndromes. • Differentiate tolerance, dependence, addiction, and pseudo-addiction. • Explain the indications and limitations of non-pharmacological, pharmacological, and adjuvant methods of pain control in the hospitalized patient. • Explain the indications and limitations of opioid pharmacotherapy. • Determine equianalgesic dosing for pharmacologic therapy as needed.

  3. Key Messages • Chronic pain is a significant problem in the elderly • There are many different mechanisms involved in generation and perception of pain • Both non-opioid and opioid options are available for managing pain. • Different classes of medication and non-pharmacotherapies are available for the management of pain syndromes • Opioids have a narrow therapeutic window and their use must be weighed carefully in the management of chronic, non-cancer pain

  4. Types of pain • Tolerance, dependence and addiction • Medications

  5. Types of Pain

  6. Nociceptive Pain • Nociceptors = pain fiber sensitive to noxious stimuli • Somatic – injury to tissues, well localized • Visceral – injury to organs (stretch receptors), poorly localized • Referred – afferent visceral fibers + somatic to same spinothalamic pathway

  7. Neuropathic pain • Abnormal neural activity secondary to disease, injury, or dysfunction • Persists without ongoing injury (trigeminal neuralgia, DM neuropathy) • Types: • Sympathetic – from peripheral nerve injury with autonomic changes • “New” term – Complex Regional Pain Syndrome (CRPS) • Type I = RSD • Type II = causalgia • Peripheral autonomic pain – • Same but without autonomic change (PHN) • Central Pain (spinal cord injury)

  8. Tolerance, Dependence, Addiction

  9. Tolerance • Tolerance - increase the dose to maintain equipotent analgesic effects • Associative - linked to environmental clues and involves psychological factors • Adaptive - involves down-regulation or desensitization of opioid receptors, or both

  10. Tolerance • Repeated administration of opioids • Desensitization or down-regulation • Sensitization – similar to neuropathic pain with increased sensitivity to pain

  11. Can’t distinguish the hyperalgesia due to opioid treatment from the hyperalgesia due to worsening neuropathic pain • It is often impossible to distinguish between pharmacologic tolerance and abnormal pain sensitivity • Both lead to escalation of opioid therapy that ultimately fails

  12. Dependence • Rapid discontinuation of opioid following prolonged administration produces symptoms • Dysphoria • Anxiety • Mood volatility • Hypertension • Tachycardia • Sweating

  13. Dependence • Psychological dependence • Extreme behavior (craving) associated with procuring/consuming drug • High vs. withdrawal • Physical dependence • class-specific withdrawal syndrome that can be produced by abrupt cessation or rapid dose reduction of a drug (or administration of an antagonist)

  14. Addiction • Physical and psychological dependence • Chronic relapsing disorder characterized by persistent drug-seeking and drug-taking behaviors • Impaired control over use, compulsive use, continued use despite harm and craving

  15. Medications

  16. NSAIDS

  17. Wide variety • 60 million Rx’s/yr • Clinical efficacy of equipotent doses is similar • Individual responses highly variable – especially toxicity • cox-1 vs. cox-2 • naprosyn may have greatest relative cardiovascular safety profile • diclofenac - available as a topical patch for pain due to trauma and as a gel for treatment of painful joints • sulindac – increased hepatotoxicity • indomethacin - GI and central nervous system adverse effects may be more frequent or severe than with other NSAIDs • ketorolac - risk of gastropathy is increased when use exceeds five days • piroxicam – high GI toxicity • celecoxib – no antiplatelet function. Increased CV risk above 200mg/day

  18. Utility of NSAIDS • Variations in patient response • Generally indicated in mild to moderate pain • Mostly for pain of somatic origin although has a CNS effect as well • Each trial should last a couple weeks • May have an opioid sparing effect as adjunct • Use at the maximum anti-inflammatory dose • Protein bound – may interfere with other protein bound drugs (dilantin. coumadin)

  19. Utility of NSAIDS • Noted variability in the response to NSAIDS between patients • Does not appear related to serum concentrations • Degree of Cox inhibition doesn’t correlate with effect • Non-prostaglandin effects may predominate in some patients • Switching between classes of NSAIDS may be beneficial

  20. Tricyclic Antidepressants

  21. Utility in pain management • Most useful in neuropathic pain • None of the TCA’s carries an indication for pain management • Used frequently in variety of settings • Amitriptyline most widely studied • Anti-depressant effects may alleviate depression associated with chronic pain • May have synergy with opioids • Switching TCA’s based on effect and/or side effects can be tried…but often frustrating

  22. Mechanism of action • Generally unknown • Theories involve action on serotonin, norepinephrine receptors (TCAs with the greatest effect upon serotonin seem to have the greatest analgesic effect) • May potentiate endogenous opioid system • However, potent serotonin RI’s have no analgesic effect of their own • Can take weeks to work

  23. Side effects • Anticholinergic (amitriptyline > nortriptyline) • Also GI, CV, neurologic (esp. sedation – maybe a +’ve) • Anticholinergic and CNS effects may diminish in days to weeks – “ride it out”

  24. Anticonvulsants

  25. Utility in pain management • Can be very effective, particularly in neuropathic pain • Wide variation in use among pain specialists, except with carbamazepine for trigeminal neuralgia • Gabapentin is frequently a first choice as levels do not need monitoring

  26. Mechanism of action • Theories include membrane stabilization (phenytoin), inhibition of repeated neuronal discharges (carbamazepine), GABA inhibition enhancement (valproic acid, clonazepam), GABA mimetics (gabapentin, pregabalin).

  27. Adjuvant medications

  28. Benzodiazepines • Good choice when anxiety complicates pain management (esp’ly cancer patients) • Clonazepam particularly useful in neuropathic pain (GABA potentiation) • Drawbacks well known • Addictive potential is significant • Potentiates sedation and respiratory depression

  29. Antispasmodics • Painful muscle spasm, myoclonic jerks can accompany a variety of pain conditions (and opioids) • toxicity of morphine • Mechanism of action may reflect their sedative effects more than direct muscle effect • Commonly used – cyclopenzaprine, carisoprodol, baclofen, methcarbamol

  30. SSRI/SNRI • Often tried when TCA side effects limit utility • May be treating depression – not an uncommon consequence of life with chronic pain • Venlafaxine has been shown to be similar to imipramine in one study of painful neuropathy • Duloxetine approved for diabetic peripheral neuropathy • Depression is probably undertreated in chronic pain patients in general (cancer and non-cancer pts)

  31. Opioids

  32. Opioids • Role in treatment of pain is well established for acute pain, malignant pain and care of the terminally ill • Role in chronic non-cancer pain is more controversial • WHO Ladder

  33. Opioids • WHO Ladder • Moderate to severe - fixed dose schedule and not on a “prn” basis • Stepwise approach • Adjuvants useful in enhancing analgesia and controlling side effects

  34. Opioids • Equi-analgesic dosing

  35. http://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdfhttp://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdf

  36. Opioids • Equianalgesic dosing • Equianalgesic conversion • MUSC pharmacy recommends 50% dose reduction for cross tolerance (others recommend 25-50%) except for methadone and fentanyl (see below)

  37. http://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdfhttp://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdf

  38. Opioids • Equianalgesic dosing • Equianalgesic conversion • Methadone conversion ratio

  39. http://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdfhttp://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdf

  40. Opioids • Equianalgesic dosing • Equianalgesic conversion • Methadone conversion ratio • Fentanyl conversion

  41. http://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdfhttp://www.musc.edu/pharmacyservices/medusepol/OpioidAnalgesicConversionChart.pdf

  42. Therapeutic failures and adverse outcomes • One of the fundamental principles of pain management is that the dose of an opioid should be increased until maximal analgesia is achieved with minimal side effects • What to do when this doesn’t work? • Identifying causes of treatment failure • Progression of underlying illness • Pharmacologic tolerance • Increased pain sensitivity

  43. PCA • Efficacy established in post-op pain • Morphine, hydromorphone, fentanyl • Higher pt satisfaction, better pain control, higher amount of opioid overall

  44. PCA • Morphine • Metabolites (morphine-6-glucuronide) accumulate in renal failure = sedation, respiratory depression • Fentanyl • Less histamine release = better in hypotension, bronchospasm • Inactive metabolites (hepatic), Safe in ESRD • Hydromorphone • Safe in ESRD • High concentration/low volume

  45. PCA Conversion • When converting from a PCA to an oral regimen in patients requiring long term pain control • Give approximately 50% of 24 hr total opioid use as a long acting oral formulation and 50% as breakthrough oral formulation • Reduce dose 25-50% to account for cross tolerance if switching opioid

  46. Side Effects • Depressed respiratory drive • Depressed consciousness, hallucinations • Hypotension • Nausea, vomiting • Ileus, constipation • Urinary retention

  47. Examples – Equianalgesic Dosing • Convert a patient requiring 120 mg of p.o. morphine and 20 mg i.v. morphine to p.o. oxycodone • 20 mg i.v. morphine = 60 mg p.o. morphine • 120 mg + 60 mg = 180 mg morphine/24 hr • Ratio 3:2 for morphine:oxycodone (po) = 120 mg oxycodone • Reduce by 25-50% = 10-15 mg oxycodone po Q4H

  48. Examples – Methadone Conversion • Convert a patient taking 300 mg MS Contin BID and 60 mg MSIR Q4H to methadone • Total oral morphine/24 hrs = 960mg • Conversion ratio is 16 for 960 mg = 960/16 = 60 • Reduce by 50% for cross tolerance = 30 • Given Q8H = 30/3 = 10 mg Q8H methadone

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