Acute pain management gunadi bandung

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pain management with highlight on etoricoxib use in daily practice

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Acute pain management gunadi bandung

  1. 1. From clinical evidence to clinical practice 1 Reumatologi Klinik Bandung 2013
  2. 2. Pain – an unpleasant sensory & emotionalexperience associated with actual & potentialtissue damage, or described in terms of suchdamage, or both.(International Association for the Study of Pain)
  3. 3. DescartesStimulus response model Ascending pain N + N Spinal cord
  4. 4. Nociception (noxious stimuli)Neuropathic (functional abnormalitiesof the nervous system)
  5. 5. LocationDurationFrequencyUnderlying causeIntensity
  6. 6. • Acute pain –<30 days’ duration• Chronic pain - >6 months• Subacute pain – from the end of the first month to the beginning of the seventh month of continued pain• Recurrent acute pain – persists over an extended period of time but occurs mainly as isolated episodes
  7. 7. ➢ VAS=0->4➢ VAS=4->7➢ VAS>7
  8. 8. Interventional Neural Blockade Potent opioid +/- adjuvant Weak +/- adjuvant opioidSimple +/- adjuvantanalgesia
  9. 9. • attempt to determine etiology of pain• causative or symptomatic treatment• the definitive cure of the pain syndrome
  10. 10. • Patient interview • Patient examination – Pain history – General – Medical history examination – Drug history – Systems – Social history examination
  11. 11. • Goal of therapy – minimal pain & maximal function• nonpharmacologic treatment options (kind words, a gentle touch, just being present)• pharmacologic treatment
  12. 12. Non Opioids  Paracetamol  NSAIDS  COX 2 inhibitorsOpioids  Weak  Strong Naloxone 13 Reumatologi Klinik Bandung 2013
  13. 13.  Acetaminophen (Paracetamol) Non-steroidal anti inflammatory drugs (NSAIDS) COX 2 inhibitors 14 Reumatologi Klinik Bandung 2013
  14. 14.  Effects › Anti-inflammatory › Analgesic › Anti-pyretic › Anti-platelet 15 Reumatologi Klinik Bandung 2013
  15. 15. NSAIDS COX 2 INHIBITORS Diclofenac (Voltaren)  Celecoxib (Celebrex) Mefenamic Acid  Etoricoxib (Arcoxia) (Ponstan)  Parecoxib (Dynastat) Ibuprofen ( Osdtarin)  Meloxicam ( Movicox) Naproxen (Gesiprox) Ketoprofen (Kaltrofen, Profenide) Ketorolac (Toradol) 17 Reumatologi Klinik Bandung 2013
  16. 16. • sole treatment for mild to moderate pain• adjunct to other analgesics for more severe pain• for both acute & chronic pain
  17. 17.  Postoperative – mild to moderate pain  Orthopedic – acute low back pain1,2  Dental – periodontitis  Oral surgery – 3rd molar surgery  Gynecological – dysmenorrhea  Urological – renal colic1 Griffin et al. Do NSAIDs help in acute or chronic low back pain? Am Fam Physician 2002;652 Tulder et al. Non-steroidal anti-inflammatory drugs for low-back pain. The Cochrane Database of Systematic Reviews 2000, Issue 2. Art. No.: CD000396. DOI: 10.1002/14651858 Vimolluck Sanansilp, Siriraj
  18. 18.  Ceiling effect to analgesia Adverse effects › Gastric ulceration › Reduction in renal blood flow › Platelet inhibition › Allergic reactions  Bronchospasm  Cross allergy is common Gastritis and functional thrombocytopenia are common with therapeutic doses Precautions – prolonged use can lead to › Renal failure › Increased risk of myocardial infarct and stroke 20 Reumatologi Klinik Bandung 2013
  19. 19. More GI side toxicity Anti-thromboticLess GI side effect Thromboxane Inhibition ( COX-1 mediated )Prothrombotic Prostacyclin Inhibition ( COX-2 mediated ) Celecoxib Diclofenac Ibuprofen ASA Etoricoxib Naproxen
  20. 20.  Drug : Class effect ? No Individual properties ? : Dose Ye Dose- s related Molecule/Chemistry Yes Half-life Yes Effect to BP & sodiumYe s Ye Duration of Rx s
  21. 21. 39,984 patients screened 5283 patients not randomized 34,701 patients randomized to treatment Etoricoxib 60 and 90 mg pooled Diclofenac 150 mg 17,412 started treatment 17,289 started treatment ITT Population ITT Population Not included in Not included in per protocol population per protocol population 223 (1.3%) <75% compliant 463 (2.7%) <75% compliant 388 (2.2%) took nonstudy 362 (2.1%) took nonstudy NSAID >10% of time NSAID >10% of time 16,819 (96.6%) 16,483 (95.3%) in per protocol population in per protocol populationITT=intention-to-treat; NSAID=nonsteroidal anti-inflammatory drug.Adapted from Cannon CP, et al. Lancet. 2006;368:1771–1781.
  22. 22. Primary End Point 7 Etoricoxib 60 and 90 mg pooled (320 events) 6 Diclofenac 150 mg (323 events) Cumulative Incidence, 5 Etoricoxib vs diclofenac HR=0.95 (95% CI: 0.81, 1.11) % (95% CI) 4 3 2 1 P=0.496 0 0 6 12 18 24 30 36 42 MonthsPatients at riskEtoricoxib 16,819 13,359 10,733 8277 6427 4024 805Diclofenac 16,483 12,800 10,142 7901 6213 3832 815CV=cardiovascular; PP=per protocol; CI=confidence interval; HR=hazardratio.Adapted from Cannon CP, et al. Lancet. 2006;368:1771–1781.
  23. 23. mITT (14 Days) Analysis In Patients With OA In Patients With RA 15 Etoricoxib 60 mg OA 15 Etoricoxib 90 mg RA Diclofenac 150 mg OAa Diclofenac 150 mg RA Etoricoxib 90 mg OA Diclofenac 150 mg OAbMean Change ±SE Mean Change ±SE 10 10 5 5 0 0 –0.5 –0.5 BL1 4 8 12 16 20 24 28 32 36 BL1 4 8 12 16 20 24 28 32 36 Months Months mITT=modified intention-to-treat; OA=osteoarthritis; RA=rheumatoid arthritis; SE=standard error; BL=baseline. a For etoricoxib 60 mg cohort. b For etoricoxib 90 mg cohort.
  24. 24. mITT (14 Days) Analysis Etoricoxib Diclofenac 150 mg 3.0 P<0.001 P=0.030 P=0.027 2.53 2.43 2.5 2.16 2.0Patients, % 1.63 1.61 1.5 1.11 1.0 0.5 0.0 60 mg vs Diclofenac 90 mg vs Diclofenac 90 mg vs Diclofenac Osteoarthritis Rheumatoid ArthritismITT=modified intention-to-treat; CI=confidence interval.a Difference in proportions (95% CI).
  25. 25. 3.0 Etoricoxib 60 and 90 mg pooled (176 events) Diclofenac 150 mg (246 events) All confirmed 2.5 eventsa Cumulative Incidence, Etoricoxib vs diclofenac HR=0.69 (95% CI: 0.57, 0.83) P=0.0001 2.0 % (95% CI) 1.5 1.0 Complicated events P=0.561 0.5 Etoricoxib vs diclofenac HR=0.91 (95% CI: 0.67, 1.24) 0 0 6 12 18 24 30 36 42GI=gastrointestinal; ITT=intention-to-treat;Months CI=confidence interval; HR=hazardratio.Patients at risk for upper GI events, no.Etoricoxib 17,412 13,704 10,972 8400 6509 4063 821a These included uncomplicated 10,396Diclofenac 17,289 13,190 (perforation, ulcer, and bleeds) and 8027 6306 3867 820complicated (perforation, obstruction, and bleeds) events.Adapted from Laine L, et al. Lancet. 2007;369:465–473; Cannon CP, et al.Lancet. 2006;368:1771–1781.
  26. 26. mITT (14 Days) Analysis 3.0 Etoricoxib P=0.284 Diclofenac 150 mg 0.50 (–0.36, 1.37)a 2.5 2.30 2.0 1.80Patients, % P=0.895 1.5 0.04 (–0.49, 0.57)a P=0.696 0.07(–0.24, 0.37)a 1.02 0.98 1.0 0.81 0.75 0.5 0.0 60 mg vs Diclofenac 90 mg vs Diclofenac 90 mg vs Diclofenac Osteoarthritis Rheumatoid Arthritis mITT=modified intention-to-treat; CI=confidence interval. a Difference in proportions (95% CI).
  27. 27. Etoricoxib 20 Diclofenac 150 mg P<0.001b 15 12.56Rate/100 PY P<0.001b P<0.001b 10 8.20 7.42 6.83 5 3.79 4.15 0 60 mg/day vs 90 mg/day vs 90 mg/day vs Diclofenac Diclofenac Diclofenac Patients With OA Patients With RAGI=gastrointestinal; AEs=adverse events; mITT=modified intention-to-treat; PY=patient-years;OA=osteoarthritis; RA=rheumatoid arthritis; COX=cyclooxygenase.a Events within 1 year of treatment; bFor both COX proportion hazard and stratified log-rank test.
  28. 28. Is an NSAID needed ? Inflammation ? Yes No Use non-pharmacologic Is there a contraindication to NSAID ?or other pharmacologic Rx Yes - Renal insufficiency ( CrCl < 30 ) - Allergic reaction - Concurrent GI injury No Is there a reason that a classical NSAID cannot be used ? - GI risk+ & Bleeding risk No Yes Use classical NSAID Use COX-2 inhibitor ( or classical NSAID + PPI+) No Is patient at increased risk for CV events ? YesSelect NSAID on the basis of GI risk Avoid NSAID esp. COX-2 inhibitor
  29. 29. 32Reumatologi Klinik Bandung 2013

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