KRT Lucas Meliala

Guru Besar Luar Biasa

Bagian Ilmu Penyakit Saraf
Fakultas Kedokteran Universitas Gadjah Mada,
Yogyakarta

Curriculum Vitae
Nama
Tempat/tanggal lahir
Alamat
Telepon
Fax.
Mobile
E-mail

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Prof. Dr. KRT. Lucas Meliala, SpKJ, SpS(K)

Pendidikan : Lulus Dokter tahun 1969,
Membang Muda (Sumut), 22 September 1941
alumnus FK-UGM
Jl. Nagan Lor 70, Jogjakarta
Lulus Spesialis Saraf & Jiwa tahun 1974
(0274) 450758
alumnus FK-UI, FK-UGM, FK Unair
(0274) 374052
Pekerjaan : Staf Fakultas Kedokteran UGM
0815 687 0584
bagian IP Saraf dan Jiwa sejak
lucasmeliala@yahoo.com
tahun 1968 sampai sekarang
Organisasi : 1999-sekarang : Ketua Pokdi Nyeri Perdossi
Anggota IASP, ENS
Ketua Governing board IPS

 Dalam praktek sehari-hari, nyeri banyak

ditemukan.
Masalahnya:

Jenis nyeri apa ??

 Nyeri nosiseptif
Somatik
Viseral

Nyeri non-nosiseptif
Neuropatik
Simpatetik

Nyeri fungsional

 Tipe nyeri lain yang spesifik:

Functional pain
Muscle pain
Colicky pain
Reffered pain
Post-operative pain

PENGERTIAN MODEL NYERI

PERILAKU NYERI
(PAIN BEHAVIOUR)

PENDERITAAN
(SUFFERING)

NYERI
(PAIN)

NOSISEPSI
(NOCICEPTION)

BIOMEDIKAL
(BIOMEDICAL)

BIOPSIKOSOSIAL
(BIOPSYCHOSOCIAL)
BYERS AND BONICA, 2001
MODIFIKASI PENULIS

PENYAKIT, KESAKITAN, ATAU

KEDUANYA
BERU

AME

Tanpa Ulkus
( tidak luka)

Ulkus (luka)

Nyeri perut
fungsional
yang kronik

Penyakit dan
kesakitan
Penyakit
tanpa
kesakitan

SAKIT

Kesakitan
tanpa
penyakit

SAKIT

Three year incidence of 10 common presenting symptoms and proportion

of symptoms with a suspected organic cause in US primary care

3 year incidence (%)

10

Organic Cause
8
6

4
2
0

Mayou & Farmer, 2002

 Pain of migraine differs from cancer pain

Cancer pain differs from the pain of
arthritis

Arthritis pain differs from the pain of

fibromyalgia

Multiple Pain Mechanisms

Nociception
Peripheral sensitization

Central sensitization
Ectopic excitability

Decreased inhibition/
Structural reorganization

Multiple Pain Symptoms

Spontaneous Pain

Superficial/Deep
Continuous/Intermittent

Evoked Pain
Thermal/Mechanical

Allodynia
Hyperalgesia

NOCICEPTIVE PAIN
Noxius Pheripheral Stimuli
Heat

Pain
Autonomic Response
Witdrawal Reflex

Cold

Brain

Intense
Mechanical
Force

Nociceptor sensory neuron

Heat
Cold
Modifikasi Meliala, 2005

Spinal cord

INFLAMMATORY PAIN
Inflammation
Macrophage

Spontaneous Pain
Pain Hypersensitivity
Reduced Threshold : Aliodyna
Increased Response : Hyperalgesia

Mast Cell
Neutrophil
Granulocyte

Brain

Nociceptor sensory neuron

Tissue Damage

Spinal cord

Modifikasi Meliala, 2005

PAIN SERIES OF EVENTS

PERCEPTION
PAIN

MODULATION
TRANSMISSION

TRANSDUCTION

NEUROPATHIC PAIN
Spontaneous Pain
Pain Hypersensitivity

Brain

Peripheral Nerve
Damage

Spinal cord Injury

Modifikasi Meliala, 2005

FUNCTIONAL PAIN
Spontaneous Pain
Pain Hypersensitivity
Brain

Normal Peripheral
Tissue and Nerves

Abnormal Central
Processing
Modifikasi Meliala, 2005

NYERI AKUT

Simtom

NYERI KRONIK

Disease

Sign :

Merengut
Postur abnormal
Doctor shopping
Dll

Simptom :

Ansietas
Depresi
Gangguan tidur
Marah, dll

Chronic Pain
The prevalence of musculoskeletal pain
increases with rising age.
Chronic pain is twice as common in people
aged more than 75 yo compared with the
25- to 34-yo group :
Arthritis

: increases tenfold

Musculoskeletal condition : increases fourfold

Schnitzer, 2006

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.

CHRONIC PAIN
Chronic pain patient has 4x to have emotional
disturbances:
Fear - avoidance behavior
Anxiety and sleep disturbance
Depression, helplessness, irritability, suicidal
risk
CNS toxicity due to inappropriate drug use
Loss of job, family and community status
CHRONIC PAIN IS A DISEASE ENTITY AND CAN KILL

Chronic Pain Defined by

Mechanisms
Peripheral (nociceptive)
Primarily due to
inflammation or damage
in periphery
NSAID, opioid responsive
Behavioral factors minor
Examples

Central (non-nociceptive)
Primarily due to a central
disturbance in pain
processing
Tricyclic responsive
Behavioral factors more
prominent
Examples

OA
Acute pain models (e.g.
third molar, postsurgery)
Mixed
RA
Neuropathic
Cancer pain

Fibromyalgia
Irritable bowel syndrome
Tension and migraine
headache
Interstitial cystitis /
vulvodynia, non-cardiac
chest pain / etc.

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%

Acute Pain (McQuay & Moore, 1999)

TREATMENT METHODS
Remove the cause
Of pain

Surgery
Splinting

Medication

Opioid
Morphine
others

Non-opioid
Aspirin & others
NSAIDS
Paracetamol
combinations

Regional
analgesia

Physical
methods

Low Tech
Nerve blocks
Local anaesthetic
opioid

High Tech
Epidural infusion
Local anaesthetic
opioid

Psychological
approaches

relaxation
psychoprophylaxis
hypnosis

physiotherapy
manipulation
TENS
Acupuncture
Ice

ANALGESIC MEDICATIONS
PRIMARY 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

Chronic Pain (McQuay & Moore, 1999)

TREATMENT METHODS

Analgesics

Conventional
NSAID
Parasetamol
to opioid
Unconventional
antidepressant
anticonvulsant
others

Block nerve transmission

Alternatives

Irreversible
surgery
Nerve destruction

Reversible
Local anaesthetic
steroid
opioid

Stimulators
Acupuncture
Hypnosis
Psychology

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 were
developed 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

Achieve pain control

Earlier is better

Keamanan kardiovaskuler NSAID

tergantung dari penghambatan COX-1
dan COX-2 di platelet

TXA2
Vasokontriksi
Agregasi Platelet
COX-1

PGI
Vasodilatasi
Disagregasi Platelet
COX-2

Pembagian cyclooxygenase inhibitor

Acetosal
Ketorolac

Ibuprofen
Nabumetone
Indomethacin
Etodolac
Piroxicam
Dexketo-

Diclofenac
Meloxicam
Nimesulide

COXIB

profen

COX-1
selective
inhibitor

Preferentially
COX-1
selective
inhibitor

Dual
COX
inhibitor

Preferentially
COX-2
selective
inhibitor
CV Incidence

GIT Incidence

COX-2
selective
inhibitor

The task of a doctor:

TO CURE IS SOMETIMES
TO TREAT IS OFTEN
TO COMFORT IS ALWAYS
A. Pare (1598)

NATURAL HEALING
All tissues, with the exception of
nerves,
heals by :
Fibrosis
Regeneration
Remodelling
Sukacita yang besar selalu didahului oleh penderitaan yang hebat

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.

 100 years ago found that aspirin be used

as :
Antiinflamation
Analgetic
Antiaggregation

65 years ago is known that aspirin have

gastrotoxicity effects

NSAID
Discovered about 40 years ago
Now, NSAID (NSAIDs) is in circulation and
growing, but failed to be better than aspirin

GI effects of NSAID
Nuisance symptoms
Heart-burn
Nausea
Dyspepsia
Abdominal pain
Mucosal lesions
Ulcer seen on endoscopy
Seriuous GI complications
Perforated ulcers
Bleeding

For Attention !!
Endoscopy results conducted on NSAID
users, 80% is the ulcer, but asymptomatic
and may heal

GI Complications in OA and RA
OA

RA

Hospitalizations

Hospitalizations

RA
Deaths

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

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

* Estimated
** Estimated from ratio of GI hospitalizations
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56

16500

Number of deaths

Number of Deaths associated with NSAID-induced GI

Damage, Compared with Other Causes, US
Population,1997

Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56

Percentage of People Who Are Unaware of NSAIDrelated 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

Percentage of Regular NSAID Users Who Expect to

Experience a Warning Sign Before a serious GI
Complication. Rx: Prescription; OTC: over-the -counter
Rx Users

OTC Users

32%

44%
56%

68%

Dont expect warning sign

Expect warning sign
Singh & Triadafilopoulos, The Journal of Rheumatology 1999, Vol.26, Suppl.56

Multimodal Analgesia
AN E XAM PLE

Opioid
doses of each analgesic
Improved anti-nociception
Potentiation

due to synergistic/
additive effects

May severity of side effects

NSAIDs,
COX-2 inhibitors,
regional blocks,
2-agonist

of each drug

Adapted from Kehlet H, Dahl JB. Anesth Analg., 1993;77:10481056.

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