2. Pain – an unpleasant sensory & emotional
experience associated with actual & potential
tissue damage, or described in terms of such
damage, or both.
(International Association for the Study of Pain)
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
10. • attempt to determine etiology of pain
• causative or symptomatic treatment
• the definitive cure of the pain
syndrome
11. • Patient interview • Patient examination
– Pain history – General
– Medical history examination
– Drug history – Systems
– Social history examination
12. • Goal of therapy – minimal pain &
maximal function
• nonpharmacologic treatment
options (kind words, a gentle touch,
just being present)
• pharmacologic treatment
17. • sole treatment for mild to moderate
pain
• adjunct to other analgesics for more
severe pain
• for both acute & chronic pain
18. Postoperative – mild to moderate pain
Orthopedic – acute low back pain1,2
Dental – periodontitis
Oral surgery – 3rd molar surgery
Gynecological – dysmenorrhea
Urological – renal colic
1
Griffin et al. Do NSAIDs help in acute or chronic low back pain?
Am Fam Physician 2002;65
2
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
19. 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
20. More GI side toxicity
Anti-thrombotic
Less GI side effect
Thromboxane Inhibition
( COX-1 mediated )
Prothrombotic
Prostacyclin Inhibition
( COX-2 mediated )
Celecoxib Diclofenac Ibuprofen ASA
Etoricoxib Naproxen
21. 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
22.
23. 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 population
ITT=intention-to-treat; NSAID=nonsteroidal anti-inflammatory drug.
Adapted from Cannon CP, et al. Lancet. 2006;368:1771–1781.
29. Etoricoxib
20 Diclofenac 150 mg
P<0.001b
15
12.56
Rate/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 RA
GI=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.
30. 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 ? Yes
Select NSAID on the basis of GI risk Avoid NSAID esp. COX-2 inhibitor