essential points considering better treatment in pain management
TRANSCRIPT
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KRT Lucas Meliala
Guru Besar Luar Biasa
Bagian Ilmu Penyakit Saraf
Fakultas Kedokteran Universitas Gadjah Mada
Yogyakarta
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Curriculum Vitae
Nama : Prof. Dr. KRT. Lucas Meliala, SpKJ, SpS(K)
Tempat/tanggal lahir : Membang Muda (Sumut), 22 September 1941
Alamat : Jl. Nagan Lor 70, Jogjakarta
Telepon : (0274) 450758
Fax. : (0274) 374052
Mobile : 0815 687 0584
E-mail : [email protected]
Pendidikan : Lulus Dokter tahun 1969,alumnus FK-UGM
Lulus Spesialis Saraf & Jiwa tahun 1974
alumnus FK-UI, FK-UGM, FK Unair
Pekerjaan : Staf Fakultas Kedokteran UGM
bagian IP Saraf dan Jiwa sejak
tahun 1968 sampai sekarang
Organisasi : 1999-sekarang : Ketua Pokdi Nyeri Perdossi
Anggota IASP, ENS
Ketua Governing board IPS
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Dalam praktek sehari-hari, nyeri banyak
ditemukan.
Masalahnya:
Jenis nyeri apa ??
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Nyeri nosiseptif
Somatik
Viseral
Nyeri non-nosiseptif
Neuropatik
Simpatetik
Nyeri fungsional
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Tipe nyeri lain yang spesifik:
Functional pain
Muscle pain
Colicky pain
Reffered pain
Post-operative pain
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BIOMEDIKAL(BIOMEDICAL)
BIOPSIKOSOSIAL(BIOPSYCHOSOCIAL)
NOSISEPSI(NOCICEPTION)
NYERI(PAIN)
PENDERITAAN(SUFFERING)
PERILAKU NYERI(PAIN BEHAVIOUR)
PENGERTIAN MODEL NYERI
BYERS AND BONICA, 2001MODIFIKASI PENULIS
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PENYAKIT, KESAKITAN, ATAU
KEDUANYA
SAKIT
SAKITPenyakit
tanpa
kesakitan
Penyakit dan
kesakitan
Kesakitan
tanpa
penyakit
Ulkus (luka)Tanpa Ulkus
( tidak luka)
Nyeri perut
fungsional
yang kronik
BERU A M E
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Three year incidence of 10 common presenting symptoms and proportion
of symptoms with a suspected organic cause in US primary care
3yearincidence(%)
4
6
8
10
Organic Cause
2
0
Mayou & Farmer, 2002
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Pain of migraine differs from cancer pain
Cancer pain differs from the pain of
arthritis Arthritis pain differs from the pain of
fibromyalgia
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Multiple Pain Mechanisms
Nociception
Peripheral sensitization
Central sensitization
Ectopic excitability
Decreased inhibition/
Structural reorganization
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Multiple Pain Symptoms
Spontaneous Pain
Superficial/Deep
Continuous/Intermittent
Evoked Pain
Thermal/MechanicalAllodynia
Hyperalgesia
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Heat
Cold
Intense
Force
Mechanical
Heat
Cold
PainAutonomic Response
Witdrawal Reflex
Nociceptor sensory neuron
NOCICEPTIVE PAIN
Noxius Pheripheral Stimuli
Spinal cord
Brain
Modifikasi Meliala, 2005
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Macrophage
Neutrophil
Granulocyte
Tissue Damage
Spontaneous Pain
Pain Hypersensitivity
Reduced Threshold : AliodynaIncreased Response : Hyperalgesia
Nociceptor sensory neuron
INFLAMMATORY PAIN
Inflammation
Spinal cord
Mast Cell
Brain
Modifikasi Meliala, 2005
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PERCEPTION
MODULATION
TRANSMISSION
TRANSDUCTION
PAIN SERIES OF EVENTS
PAIN
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Spontaneous Pain
Pain Hypersensitivity
Peripheral Nerve
Damage
NEUROPATHIC PAIN
Spinal cord Injury
Brain
Modifikasi Meliala, 2005
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Normal Peripheral
Tissue and Nerves
FUNCTIONAL PAIN
Abnormal Central
Processing
Spontaneous Pain
Pain Hypersensitivity
Brain
Modifikasi Meliala, 2005
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NYERI AKUT Simtom
NYERI KRONIK Disease
Sign :
MerengutPostur abnormal
Doctor shopping
Dll
Simptom :
AnsietasDepresi
Gangguan tidur
Marah, dll
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Chronic Pain
The prevalence of musculoskeletal pain
increases with rising age.
Chronic pain is twice as common in peopleaged more than 75 yo compared with the
25- to 34-yo group :
Arthritis : increases tenfold Musculoskeletal condition : increases fourfold
Schnitzer, 2006
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Chronic Pain
Chronic pain is often produces suffering
not only in an individual experience but
also a cultural societies and make serious
disruption of their lives.
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CHRONIC PAIN
Chronic pain patient has 4x to have emotionaldisturbances:
Fear - avoidance behavior
Anxietyand sleep disturbanceDepression,helplessness, irritability, suicidal
risk
CNS toxicitydue to inappropriate drug useLoss of job,family and community status
CHRONIC PAIN IS A DISEASE ENTITY AND CAN KILL
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Chronic Pain Defined by
Mechanisms
Peripheral (nociceptive)
Primarily due to
inflammation or damage
in periphery NSAID, opioid responsive
Behavioral factors minor
Examples
OA
Acute pain models (e.g.third molar, post-
surgery)
RA
Cancer pain
Central (non-nociceptive) Primarily due to a central
disturbance in painprocessing
Tricyclic responsive
Behavioral facto rs mo reprominent
Examples
Fibromyalgia
Irritable bowel syndrome
Tension and migraineheadache
Interstitial cystitis /vulvodynia, non-cardiacchest pain / etc.
Mixed
Neuropathic
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BARRIERS TO PAIN MANAGEMENT
Inadequate pain assessment 76%Patient reluctance to report pain 62%
Patient reluctance to take opioids 62%
Physician reluctance to prescribe opioids 61%
Inadequate staff knowledge about pain
management
52%
Nursing staff reluctance to give opioids 38%
Excessive state regulation of analgesics 18%
Lack of psychological support services 11%
Lack of equipment 6%Lack of neurodestruction procedures 5%
Lack of access to wide range of analgesics 3%
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Acute Pain (McQuay & Moore, 1999)
TREATMENT METHODS
Remove the cause
Of painMedication Regional
analgesiaPhysical
methods
Psychological
approaches
Surgery
Splinting
Low Tech
Nerve blocks
Local anaesthetic
opioid
High Tech
Epidural infusion
Local anaesthetic
opioid
physiotherapy
manipulation
TENS
Acupuncture
Ice
relaxation
psychopro-
phylaxis
hypnosis
Non-opioid
Aspirin & others
NSAIDS
Paracetamol
combinations
OpioidMorphine
others
ANALGESIC MEDICATIONS
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ANALGESIC MEDICATIONSPRIMARY ANALGESICS
Acetminophen
Prostaglandin synthesis inhibitors Salicylates
Traditonal NSAIDs
COX-2-selective NSAIDs (coxibs)
Tramadol Opioids
Traditional
Mixed
ADJUVANT MEDICATIONS
Antidepressants
Anticonvulsants
Local anesthetics
Miscellaneous agents
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Chronic Pain (McQuay & Moore, 1999)
TREATMENT METHODS
Analgesics Block nerve transmission Alternatives
Conventional
NSAID
Parasetamol
to opioid
Unconventional
antidepressant
anticonvulsant
others
Reversible
Local anaesthetic
steroid
opioid
Irreversible
surgery
Nerve destruction
StimulatorsAcupuncture
Hypnosis
Psychology
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Treatment
Paracetamol should be used for the first line
analgesic agent due to its favourable side effect
and safety profile
COX-2 inhibitors and non selective NSAID weredeveloped with the goal of delivering pain relief
with caution on cardiovascular and or
cardiorenal risk
The additional of weak opioids is recommended
when greater analgesia desired
Schnitzer, 2006
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Achieve pain control
Earlier is better
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TXA2 PGI
VasokontriksiAgregasi Platelet
VasodilatasiDisagregasi Platelet
COX-2COX-1
Keamanan kardiovaskuler NSAID
tergantung dari penghambatan COX-1
dan COX-2 di platelet
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Pembagian cyclooxygenase inhibitor
Acetosal
KetorolacIndomethacin
Piroxicam
IbuprofenNabumetone
Etodolac
Dexketo-profen
Diclofenac
Meloxicam
NimesulideCOXIB
COX-1selective
inhibitor
PreferentiallyCOX-1
selectiveinhibitor
DualCOX
inhibitor
PreferentiallyCOX-2
selectiveinhibitor
COX-2selective
inhibitor
CV Incidence
GIT Incidence
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The task of a doctor:
TO CURE IS SOMETIMES TO TREAT IS OFTEN
TO COMFORT IS ALWAYS
A. Pare (1598)
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NATURAL HEALING
All tissues, with the exception ofnerves,
heals by :
Fibrosis
Regeneration
Remodelling
Sukacita yang besar selalu didahului oleh penderitaan yang hebat
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Bone :- heals well
- by remodelled over time
Muscle :- heals fairly well
- by fibrosis and no remodelling
Ligaments :- heal by fibrosis and scarring
Joint capsul :- is well innervated
- little is known of healing- scarring may reduce joint mobility
Disc :have a very limited blood supply
degenerate with repeated trauma
dehydrate fibrous replacement.
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100 years ago found that aspirin be used
as :
Antiinflamation
Analgetic
Antiaggregation
65 years ago is known that aspirin havegastrotoxicity effects
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NSAID
Discovered about 40 years ago
Now, NSAID (NSAIDs) is in circulation and
growing, but failed to be better than aspirin
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GI effects of NSAID Nuisance symptoms
Heart-burnNausea
Dyspepsia
Abdominal pain
Mucosal lesions
Ulcerseen on endoscopy
Seriuous GI complications
Perforated ulcers
Bleeding
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For Attention !!
Endoscopy results conducted on NSAID
users, 80% is the ulcer, but asymptomaticand may heal
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GI Complications in OA and RA
OAHospitalizations
RAHospitalizations
RADeaths
No. of patients 1283 3883 2921
Person-year of observation 3234 19,961 12,224
Person-year taking NSAID 2199 15,638 8471
No. of GI events 19 228 25
No. of GI events while taking
NSAID
16 205 19
Rate per year while taking NSAID
(%)
0.73 1.31 0.22
Rate per year while not taking
NSAID (%)
0.29 0.19 0.05
Relative risk while taking NSAID 2.51 6.77 4.21
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56
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NSAID-associated GI Hospitalizations and
Deaths:National Incidence Estimates
(United State)
Diagnosis No. of
Patients
Exposed
GI
Hospitalization
Rate/Year
No.of
Hospitalization
/Year
GI Death
Rate/Year
No.of
Deaths/Year
RA 2,000,000 1.3% 26,000 0.22% 4400
Probable
RA
3,000,000 0.7%* 21,000 0.11%** 3300
OA 8,000,000 0.7% 56,000 0.11%** 8800
Total 13,000,000 103,000 16500
* Estimated
** Estimated from ratio of GI hospitalizations
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56
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Number of Deaths associated with NSAID-induced GI
Damage, Compared with Other Causes, US
Population,1997
Numberofd
eaths
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56
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Percentage of People Who Are Unaware of NSAID-
related GI Complications in a Cohort of Regular NSAID
Users. Rx:prescription; OTC:over-the-counter
Aware of complications but unconcerned
Unaware of complications NSAIDs can cause
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56
P t f R l NSAID U Wh E t t
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Percentage of Regular NSAID Users Who Expect to
Experience a Warning Sign Before a serious GI
Complication. Rx: Prescription; OTC: over-the -counter
68%
32%
44%
56%
Dont expect warning signExpect warning sign
Rx Users OTC Users
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56
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doses of each analgesic
Improved anti-nociceptiondue to synergistic/additive effects
May severity of side effects
of each drug
Adapted from Kehlet H, Dahl JB.Anesth Analg.,1993;77:10481056.
Potentiation
Opioid
NSAIDs,COX-2 inhibitors,regional blocks,2-agonist
A N E X A M P L E
Multimodal Analgesia
Berbuatlah dan cintailah tanpa memperhitungkan kebahagiaanmu sendiri, dan engkau akan berbahagia sepanjang waktu
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