This document provides biographical information about Dr. Rachmat Gunadi Wachjudi and discusses the pathophysiology and treatment of rheumatic pain. It notes that Dr. Wachjudi is the head of the Department of Internal Medicine at Dr. Hasan Sadikin Hospital Bandung. The document then discusses topics like acute pain in hospitals, prevalence of chronic pain, knee osteoarthritis, approaches to assessing and treating rheumatic pain, pharmacologic and non-pharmacologic pain management strategies, considerations for NSAID therapy, and providing a practical approach to managing rheumatic pain.

1. PendidikanPendidikan
-- Dokter umum FK UNSRI /RSMH PalembangDokter umum FK UNSRI /RSMH Palembang
-Internist FK UNPAD /RSHS BandungInternist FK UNPAD /RSHS Bandung
-Subspesialis Reumatologi : FKUI / RSCMSubspesialis Reumatologi : FKUI / RSCM
- Clinical Rheumatology and Osteoporosis Training-- Clinical Rheumatology and Osteoporosis Training-
Arthritis Foundation of WA-PerthArthritis Foundation of WA-Perth
Rachmat Gunadi WachjudiRachmat Gunadi Wachjudi
Lahir diLahir di GarutGarut 16 Januari 195516 Januari 1955
PekerjaanPekerjaan
Kepala Dep/SMF Ilmu Penyakit Dalam FK UNPAD/ RSKepala Dep/SMF Ilmu Penyakit Dalam FK UNPAD/ RS
dr Hasan Sadikin Bandungdr Hasan Sadikin Bandung
OrganisasiOrganisasi::
IDI, PAPDI, IRA, PEROSI, PERALMUNI, IPSIDI, PAPDI, IRA, PEROSI, PERALMUNI, IPS

2. ““Pain is a more terrible lordPain is a more terrible lord
of mankind than even deathof mankind than even death
itself”itself”
Dr. Albert Schweitzer (1875-1965)Dr. Albert Schweitzer (1875-1965)

3. Pathophysiologic approachPathophysiologic approach
Rheumatic Pain ManagementRheumatic Pain Management
Rachmat Gunadi WachjudiRachmat Gunadi Wachjudi
Departemen/SMF Ilmu Penyakit DalamDepartemen/SMF Ilmu Penyakit Dalam
FK UNPAD/RS Dr Hasan Sadikin BandungFK UNPAD/RS Dr Hasan Sadikin Bandung

4. Acute pain in hospitalAcute pain in hospital
Num be r P e rce nt
P ain pre se nt all o r m o st o f tim e1 024/3 162 33
P ain w a s s e ve re o r m o de rate 2 755/3 157 87
P ain w a s w o rs e than e x pe cte d 1 82/1051 17
Had to a sk fo r drugs 1 085/2 589 42
D rugs did no t a rrive im m e dia te ly4 55/1085 41
Bruster et al. BMJ 1994 309: 1542-6

5. Acute painAcute pain

6. ChronicChronic PPainain PPrevalence inrevalence in
EuropeEurope
 Pain at leastPain at least
moderatemoderate
 Pain at leastPain at least
6 months6 months
 One in fiveOne in five
adultsadults
affectedaffected
acrossacross
Europe hasEurope has
chronic painchronic pain
 One in threeOne in three
householdshouseholds
affected byaffected by
chronic painchronic pain
Breivik et al. Europ J
Pain 2006 10:287-333

7. ChronicChronic DDiseases andiseases and QQuality ofuality of LLifeife
Sprangers et al. J Clin Epidemiol 2000 53: 895-907
More negative impact

8. KneeKnee
OsteoarthritisOsteoarthritis

9. Identify and Treat UnderlyingIdentify and Treat Underlying
CauseCause
Management StrategiesManagement Strategies
Whenever possible, it is
important to identify and treat
the underlying cause of pain!

10. RheumaticRheumatic painpain assessmentassessment
 Nociceptive or neuropathic ?Nociceptive or neuropathic ?
 Articular or nonarticularArticular or nonarticular
 Inflammation or non-inflammationInflammation or non-inflammation
 Acute or chronicAcute or chronic
 The pattern and amount of involved jointThe pattern and amount of involved joint

13. Nociceptive vs Neuropathic PainNociceptive vs Neuropathic Pain
Nociceptive Neuropathic
Definition Pain caused by physiological
activation of pain receptors
Pain initiated or caused by a primary
lesion or dysfunction in the peripheral
or central nervous system
Mechanism Natural physiological transduction Ectopic generation central
sensitization and others
Localization Local + referred pain Confirned to innervation territory of
the lesioned nervous structure
Quality of
symptoms
Ordinary painful sensation New strange sensations
Treatment Good response (conventional
analgesics)
Poor response (conventional
analgesics)

14. Inflammation or noninflammationInflammation or noninflammation
SignSign InflammatoryInflammatory
ArticularArticular
NoninflammatoryNoninflammatory
ArticularArticular
inflammatoryinflammatory
NonarticularNonarticular
WarmthWarmth Yes, diffusely overYes, diffusely over
the jointthe joint
NoNo Sometimes, butSometimes, but
localized over thelocalized over the
structurestructure
OedemaOedema Yes, usuallyYes, usually
diffusely over thediffusely over the
joint (effusion)joint (effusion)
No joint effusion butNo joint effusion but
may be bonymay be bony
enlargementenlargement
Yes, but localized toYes, but localized to
particular structureparticular structure
rednessredness Rarely, if present,Rarely, if present,
the joint is diffuselythe joint is diffusely
redred
NoNo Rarely, but localizedRarely, but localized
TendernessTenderness Yes, over the jointYes, over the joint
lineline
Yes, over the jointYes, over the joint
lineline
Yes, over theYes, over the
particular structureparticular structure

15. The pattern and amount of involved jointThe pattern and amount of involved joint
 Symmetrical ?Symmetrical ?
 Large joint (shoulder, hip, knee)?Large joint (shoulder, hip, knee)?
 Small joint (wrist, MCP, PIP,DIP,MTP)?Small joint (wrist, MCP, PIP,DIP,MTP)?
 Monoarticular ( 1 joint)Monoarticular ( 1 joint)
 Oligoarticular ( 2-4 joints)Oligoarticular ( 2-4 joints)
 Polyarticular (> 4 joints)Polyarticular (> 4 joints)
 Involved axial skeleton (thoracic spine, sacroiliacInvolved axial skeleton (thoracic spine, sacroiliac
joints or costo-chondral joint?joints or costo-chondral joint?

16.  OsteoarthritisOsteoarthritis
 SLESLE
 Rheum arthritisRheum arthritis
 Gouty arthritisGouty arthritis
 Soft tissue RheumSoft tissue Rheum
 Systemic sclerosisSystemic sclerosis
 SpondyloarthritisSpondyloarthritis 1%7%
3%1%
6%
13%
69%
The most prevalentThe most prevalent
rheumatic ailmentrheumatic ailment

17. Treatment approaches
Invterentional
pain
management
Neurostimulation
Pharmacotherapy
Physical
rehabilitation
Physio-& Medical
Training Therapy
Lifestyle
Surgical
Complementary
/ alternative
Psychology
Treatment approach

18. Non pharmacologicNon pharmacologic
 Patient EducationPatient Education
 Self management programSelf management program
 Psychosocial measuresPsychosocial measures
 Weight management (if overweight)Weight management (if overweight)
 PhysiotherapyPhysiotherapy
 Occupational therapyOccupational therapy
 Aids (eg. Shoe wedges, patella-taping,Aids (eg. Shoe wedges, patella-taping,
cushioned training shoes, stick)cushioned training shoes, stick)

19. Pharmacologic therapyPharmacologic therapy
 Analgesic and anti-inflammatoryAnalgesic and anti-inflammatory
 Intra-articular corticosteroidsIntra-articular corticosteroids
 Intra-articular hyaluronic acidIntra-articular hyaluronic acid
 DMOADs, DMARDs, Immune modulatorsDMOADs, DMARDs, Immune modulators

20. AnalgesicsAnalgesics
 Non narcotic: acetaminophenNon narcotic: acetaminophen
 Opioid related analgesics:Opioid related analgesics:
TramadolTramadol
PropoxyphenePropoxyphene
codeinecodeine
 Opioid analgesics (may be topical)Opioid analgesics (may be topical)

21. Anti-inflammatoryAnti-inflammatory
 NSAIDs :NSAIDs :
Conventional (non selective Cox-2 inhibitors)Conventional (non selective Cox-2 inhibitors)
Selective Cox-2 inhibitorsSelective Cox-2 inhibitors

22. PolypharmacyPolypharmacy
 Co morbidityCo morbidity
 Side effectsSide effects
 Drug interactionsDrug interactions
 ComplianceCompliance

23. The scissors or the barber ?The scissors or the barber ?

26. Choice of NSAIDChoice of NSAID ::
nonselective >< selective COX-2nonselective >< selective COX-2
inhibitorsinhibitors
 Not differ in efficacyNot differ in efficacy
 Cox-2 selective inhibitors have less GI toxicityCox-2 selective inhibitors have less GI toxicity
 Concomitant low dose ASA: reduced the advantageConcomitant low dose ASA: reduced the advantage
 No preferential use for patients at risk for NSAID-No preferential use for patients at risk for NSAID-
induced renal failureinduced renal failure
 Non selective NSAID + ASANon selective NSAID + ASA  diminished thediminished the
effect of ASA on platelet functioneffect of ASA on platelet function
 Cox-2 selective cost moreCox-2 selective cost more

27. Initiating therapyInitiating therapy
 Base line laboratory examination isBase line laboratory examination is
essential prior to initiating long-termessential prior to initiating long-term
treatment with NSAIDstreatment with NSAIDs
 CBC, electrolytes, creatinine, LFTsCBC, electrolytes, creatinine, LFTs

28. Monitoring therapyMonitoring therapy
 Check LFTs every 6-12 wkCheck LFTs every 6-12 wk
 Periodically monitor CBCPeriodically monitor CBC
 In a patient at risk for renal toxicity:In a patient at risk for renal toxicity:
electrolytes and creatinine should beelectrolytes and creatinine should be
monitored closelymonitored closely

29. Special precautionsSpecial precautions
 Risk factors for GI toxicityRisk factors for GI toxicity
 Risk factors for hemodynamicallyRisk factors for hemodynamically
mediated NSAID induced renal failuremediated NSAID induced renal failure
 Severe anemiaSevere anemia
 Selective Cox-2 are safer forSelective Cox-2 are safer for
thrombocytopeniathrombocytopenia
 NSAIDs can worsen heart failureNSAIDs can worsen heart failure

30. Risk factors for GI toxicityRisk factors for GI toxicity
 Age > 60 yearAge > 60 year
 History of PUB and UGI bleedingHistory of PUB and UGI bleeding
 Concomitant steroidConcomitant steroid
 AnticoagulationAnticoagulation
 Prolonged use of max dose NSAIDProlonged use of max dose NSAID
 Comorbidity (cardiovascular, renal insuff,Comorbidity (cardiovascular, renal insuff,
hepatic impairment, diabetes,hepatic impairment, diabetes,
hypertension)hypertension)

31. Risk factors for NSAID inducedRisk factors for NSAID induced
renal failurerenal failure
 Intrinsic renal diseaseIntrinsic renal disease
 Volume depletionVolume depletion
 Diuretic useDiuretic use
 CirrhosisCirrhosis
 Heart failureHeart failure
 Concomitant ACE inhibitorConcomitant ACE inhibitor
 Advanced ageAdvanced age

32. Special precautionsSpecial precautions
 NSAIDs can induce an elevation in bloodNSAIDs can induce an elevation in blood
pressure and can blunt antihypertensivepressure and can blunt antihypertensive
effects (B blockers, ACE I, diuretics)effects (B blockers, ACE I, diuretics)
 Drug interactions (Binding sites onDrug interactions (Binding sites on
plasma)plasma)
 NSAIDs combinationNSAIDs combination  increase toxicityincrease toxicity
(OTC, patients)(OTC, patients)
 NSAIDs should be discontinue prior toNSAIDs should be discontinue prior to
surgery (5X half-life)surgery (5X half-life)

33. Special precautionsSpecial precautions
 Aspirin and other NSAIDs can trigger attacksAspirin and other NSAIDs can trigger attacks
of severe asthma and marked nasalof severe asthma and marked nasal
congestion (COX-2 selective ?)congestion (COX-2 selective ?)
 Should be avoid during pregnancy (ifShould be avoid during pregnancy (if
possible) Esp. in the third trimesterpossible) Esp. in the third trimester

34. Practical pointsPractical points
 Pain patophysiology ?Pain patophysiology ?
 Sumber nyeri ?Sumber nyeri ?
 Diagnosis ?Diagnosis ?
 Derajat nyeri ?Derajat nyeri ?
 Profil pasien ? Umur dllProfil pasien ? Umur dll
 Riwayat pengobatan nyeriRiwayat pengobatan nyeri
 KomorbiditasKomorbiditas
 Pemilihan modalitas terapiPemilihan modalitas terapi
 Keselamatan pasienKeselamatan pasien

35. Terimakasih atas perhatiannyaTerimakasih atas perhatiannya
Balikpapan Rheumatology UpdateBalikpapan Rheumatology Update
Pilih obat yang tepat untuk nyeri reumatik sesuai patofisiologi