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What is Pain ?

Apa itu Nyeri ?


(Pain)
Pain derived from Latin (poena)
signify a penalty or punishment

Pain is a sensation that


hurt
discomfort
distress
agony

Nyeri adalah suatu perasaan inderawi


yang tidak menyenangkan.
Nyeri adalah perasaan yang
subyektif
Nyeri adalah perasaan yang sangat subyektif.
Tak ada orang lain yang dapat mengetahuinya,
termasuk dokter, kecuali pasien itu sendiri.
Berbeda dengan penyakit lain seperti, parkinson,
kebutaan atau struma yang langsung dapat diamati.
Hanya penderita nyerilah yg tahu persis apa yg
dirasakan.
Oleh karena itu kita harus percaya apa yang dikatakan
pasien.
Nyeri adalah Racun bagi Tubuh Kita
Racun akibat rangsang
Mekanik Suhu Kimiawi

Kerusakan Jaringan

Terlepasnya berbagai mediator


H , K , ATP, Prostaglandin, Bradikinin,
Serotonin, Substance P, Histamine.
Cytocaines
Rangsang bagi nosiseptor

Transmisi ke SSP Nyeri Akut


via afferent pathways
4
Unrelieved Pain can Lead
to...

Insomnia Anxiety Depression

Anorexia Immobility
Prof.Hyodo, Japan

Adam was put into sleep, before Eva was


creating from Adams rib.
First concept of Pain by Descartes
in 17th Century
(Specifisity
Theory)
Pain was
faithfully
transmitted
from periphery
to brain
1965-
Progress in understanding pain
MELZACK and WALL GATE CONTROL THEORY

PAIN MODULATION
1965 MELZACK and WALL mengajukan suatu
hipotesis yg dikenal sbg
GATE CONTROL THEORY
Brain

GATE CONTROL SYSTEM


A
-
+ +
ACTION
SG DHN SYSTEM
- - +

C
Prof.Hyodo, Japan
Modulation

20th century
Pain

X Inhibition
CNS Modulation
Excitation

Example:
Nociception Stress Induced Analgesia

1. Nociception without pain


Stress induced analgesia
The role of modulation
Pain modulation can be triggered by
the meaning of injury

Injury for merit


Injury for honor
SENSITIZATION THEORY
( Periphery or Centrally )
Clifford J. Woolf (1990)

Neuron bukan seperti kabel yang kaku,tetapi sangat mudah berubah seperti plastik
(neuroplasticity )
Central sensitization plasticity of NS membuka demensi baru
tentang teori nyeri, dimana susunan syaraf pusat dapat berubah,
sehingga persepsi nyeri yang timbul tidak lagi mencerminkan
kwalitas dari noxious stimulus
Sensitization after the surgery or
tissue injury

HYPERALGESIA

ALLODYNIA
Trigeminal Neuralgia
panthom pain
Post Herpetic Neuralgia
Accepted by IASP in 1979 ( Harold MERSKEY )

Pain is unpleasant sensory and


emotional experience
-ascociated with actual or potential tissue damage or
- describe in term of such damage.

Pain is associated with actual or potential tissue


damage
Actual tissue damage Potential tissue damage

Nociceptive Pain (Pain due to a Nociception) pain


that is elicited by activation of nociceptors (Noxious Stimuli)
Acute Pain; Pain vanish after tissue healed
Nociceptive pain
Is pain that is elicited by activation of nociceptors .
Nociceptive pain is pain due to a nociception.
Nociception has 5 components
1. Transduction
2. Conduction
3. Modulation
4. Transmission
5. Perception
ciceptive Pain Neuron III
Persepsion

Transduction

Mechanic Conduction
al Transmission

Modulation
Neuron II
Therma
l
Neuron I

Chemica
l

Modified by AHT
What is a nociceptor?
Nociceptors are peripheral sensory
neurons that respond selectively to
noxious stimuli. (Nociceptors = pain receptors,
noci = injury)
or A number of receptors/channels that sense
damage

VR1 - vanilloid receptor family


ASICs - respond to low pH
P2X receptors - respond to ATP
TRPs receptors respond temp.
EPs receptors - prostaglandins,PGs
Characteristic of A and C-fiber
A Fiber
Rapid Conduction
Mechano Glu
Thermal
Nociceptors First Pain

C-Fiber
Slow Conduction Glu
Polimodal
Nociceptors Secound Pain
sP
Nociceptors;is characterized
by their response;
1. A-delta Mechanothermal nociceptors
Respond to mechanical and thermal stimuli.
display rapid conduction.
Produced first pain and well localized.
Ad fibers respond to this naciceptors.

2. C-fiber Polimodal nociceptors


Respond to mechanical, thermal and chemical.
Slow conduction.
Produced second pain and diffuse.
C fibers respond to this receptor.

Exist in many tissues, skin, muscle, pariosteum, joints, and viscera,


except brain.
It is important to know that two distinct
responses to a noxious stimulus FIRST
PAIN and SECOND PAIN
First pain: sharp and
pricking, well-localized and
brief. Responded by
A Fiber mechanoreceptors ,
First Pain
conveyed by Ad fiber.
Second Pain Second pain: dull and
diffuse and prolonged .
Responded by polimodal
C Fiber nociceptors , conveyed by C
fiber
Two sensory afferent neurons
1.Large myelinated A fibers, very fast conduction velocity. Respond
to innocuous stimuli
2.Small myelinated A & C unmyelinated fibers, have slow conduction
velocity. Respond to noxious stimuli

Large
fibers
A
Dorsal root
ganglion Dorsal Horn

Small
fibers
A
C Peripheral sensory
Nerve fibers

1.Tranduction
2. CONDUCTION
DHN of SC
3.Modulation in DHN Plays a big role in pain
perception
Is the first gate to
control pain.
Nociception (Pain) is
born in DHN

Lehmann, K. A.: From the first stimulus to pain memory. UN. Cologne, 2000 31
Modulation
Acending/Descending
Cortex
Modulatory Systems

PAG
Opioids

NRM LC

5-HT - - Enkephalin - Norepinephrine

Opioids
Pain

Modulation
Descending
modulation Dorsal Horn

Ascending Dorsal root ganglion Conduction


input

Transduction
Spinothalamic Peripheral
tract nerve

Trauma
Peripheral
nociceptors

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
Acute Pain
common pain
associated with
tissue injury
settles when
tissues heal or
vanish after
healing proccess.
Pain

Inhibition
CNS Modulation
Excitation

Nociception exp. normal situation


2. Nociception with Pain
ACUTE
PAIN

postoperative pain
traumatic pain
Acute Pain

Increased Shallow Increased Peripheral/


Anxiety
sympathetic GI effects breathing catabolic central
and fear
activity demands sensitisation

Myocardial Atelectasis Poor wound


O2 GI motility hypoxaemia healing/muscle Sleeplessness, Neuro-
hypercarbia breakdown helplessness plasticity
consumption

Weakness Psycho-
Myocardial Delayed and impaired logical
Pneumonia
ischaemia recovery rehab. distress

Chronic
GI = gastrointestinal
pain
Surgery

Tissue damage Nociceptive PAIN


Inflamed tissue input

Surgery has a biphasic insults to the body


1. Trauma to tissue
2. Inflammatory response
Setiap kerusakan jaringan selalu diikuti
dengan proses inflamasi
1
Painful stimulus
Prostaglandins
meningkatkan sensitizasi
jaringan nyeri.
Pain-sensitive tissue

Prostaglandin
2
Blood vessel
1 Substance P Bradykinin
Mast cell

Histamine
vasodilatasi
kemerahan dan panas.
Bradykinin
3
Substance P
2
3 Histamine memicu
terbentuknya degranulasi
Nociceptor oleh sel mast
pembengkakan
Sensitisasi perifer
COX-2 and peripheral
sensitization
Tissue injury

Neuron
firing threshold
COX-2 expressed decreases
EP
receptor PKA
PGE2
PKC

Increased
P
neuronal
membrane NaV1.8
excitability TTx-resistant
sodium channel
1.Peripheral sensitization

ASIC/BNC
2 .Central Sensitization
Spontaneous Allodynia
Hyperalgesia
Tissue damage pain
Primary Hyperalgesia

CENTRAL
PERIPHERAL SENSITIZATION
ACTIVITY

Decreased Increased
threshold to spontaneous
peripheral Expansion of activity
Nerve damage stimuli receptive
field

Secondary Hyperalgesia
So, after the surgery there is a
change in NS

what we called:

Neuro-Plasticity of the Nervous


System
Neuro-Plasticity of the NS
Central
sensitization

Spinal wind-up Histamine, Leukotrienes,


Norepinephrine, Cytokines,
Bradykinin,
Prostaglandins,
Neuropeptides, 5-HT,
Purines, H+/K+ions

Secondary
hyperalgesia

Peripheral Primary hyperalgesia


sensitization
After the injury the NS will changed neuro-plasticity
Secondary hyperalgesia

Primary hyperalgesia
CENTRAL SENSITIZATION
1. Perubahan pada
nociceptive pathway

Stimulasi noxious akan


menyebabkan rasa nyeri
bertambah (hyperalgesia) dan
stimulasi non-noxious akan
dirasakan sebagai nyeri
(allodynia)
Woolf, C. 2011. Pain, 152, S2 - 15
Peran NSAID pada nyeri
Nosisepsi
Sensitisasi
Mediator inflamasi
sentral
Histamine, Bradykinin
Leukotrienes, Cytokines,
Prostaglandins,
5-HT, H+/K+ions

NSAID
(Cox1 or Cox2)

Sensitisasi sensitisasi
Nosiseptor
perifer
ALLODYNIA
HYPERALGESIA
H .Primer
PROLONGED PAIN
REFERRED PAIN H .Secunder

CLINICAL PAIN
(PATHOPHYSIOLOGICAL
PAIN )
Vanished
after healing X Chronic
Pain (1 %)
Possible Analgesia OPIOID
- Systemic
PERCEPTION - Epidural
- Subarachnoid
Pain Ketamin, Tramadol,
agonist
COX-2, COX-3? LOCAL ANESTHETIC
- Epidural
MODULATION - Subarachnoid
Descending
modulation Dorsal Horn - Peripheral nerve block
Ascending CONDUCTION/
input TRANSMISSION LA
Steroids
COX-1
Spinothalamic COX-2
Peripheral
tract TRANSDUCTION
nerve
TRANSMISSION

Trauma
Peripheral
nociceptors

No single drug can produce optimal analgesia without adverse effect

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
Target Point of Analgesic Drugs
Ketamin
Paracetamol

Perception

Opioids
Gabapentinoids
Clonidine

Corticosteroids
NSAIDs
Modulation Transduction COXIBs
Local Anesthetic

Transduction

DRG

Transmission
Modulation
Local
anesthetics
COXIBs
Post herpetic Neuralgia Low Back Pain
LBP
Paindescribed in terms of such
damage
beyond the healing period
no more tissue damage Chronic Pain

Pain

Inhibition
CNS Modulation
Excitation

X Example: Phantom Pain


Nociception Neurophatic Pain

3. Pain without nociception


NYERI NOSISEPTIF

Api
NYERI INFLAMASI

Air Hangat

?
NYERI PATOLOGIS

Tanpa rangsangan
J. Loeser
(1980) PAIN BEHAVIOR

SUFFERING

PAIN

NOCICEPTION

Concept of nociception, pain, suffering and pain behavior


Behavioral
characteristics
Facial expressions- grimace(meringis)
clenched teeth, wrinkled forehead, crying.
Body movements -restlessness,
immobilization, muscle tension, protective
movement.of body parts
Social interaction- avoidance of
conversation & contacts.
Pain behavior
`
Chronic Pain is a
Biopsychosocial Phenomenon
Cognitive therapies
`functional restoration
Antidepressants/
Pain Behaviors
psychotropics
Opioids
Suffering Relaxation
Opioids Spiritual
Adjuvan drugs
Pain Perception
Neural-augmentation Local blocks
Ablative Surgery NSAIDS
XXXXXXXX
Nociception Opioids
Central Physical
Sensitisation Modalities

Loeser JD.Cousins MJ.Med J Aust. 1990;153;208-212,216


Acute pain Chronic pain

Nociceptive pain Neuropathic pain Dysfunctional pain


Somatic Pain Fibromyalgia
Visceral Pain Irritable bowel Synd.
Biomedical vs. Biopsychosocial
Management Pain

Acute pain Chronic Pain


Goal of treatment is goal of treatment is to
improve function in
to obtain pain relief
occupational, social and
emotional domains; pain
relief is de-emphasised.
Biomedical vs. Biopsychosocial
Management Pain

Acute pain Chronic Pain


Patient is ill, and Patient is not ill, and
therefore should should maintain normal
be free from activity levels as far as
normal possible
responsibilities
Biomedical vs. Biopsychosocial
Management Pain

Acute pain Chronic Pain


primary responsibility primary responsibility for
for improvement lies improvement lies with
with the doctor; the patient - patients
patients role is role is active.
passive.
Chronic Pain Syndromes
Develop: KINESIOPHOBIA
Avoidance of certain movements due to a fear
of reinjury or increased pain (Kori et al.,
1990)
One of the most destructive beliefs common
among those with chronic pain syndromes.
Usually leads to a variety of PROTECTIVE
BEHAVIORS which further impair
functioning.
M. Clark, Ph.D., 2000
Two great obstacles

In treating chronic pain


1. Fear avoidance behaviour
(Kinesiophobia = takut bergerak)
2. Passive treatment
(menginginkan pembedahan or massage)
(CRPS) Complex Regional
Pain Syndrome
Even Peripheral Changes of CRPS
are Result of Central Sensitization!
Possible causes of chronic pain

Neuropathic Pain Nociceptive Pain


Mixed Pain
Pain initiated or caused by a Pain with Pain caused by injury to
primary lesion or dysfunction neuropathic and body tissues
in the nervous system
nociceptive (musculoskeletal,
(either peripheral or
central nervous system)1 components cutaneous or visceral)2

Examples Examples
Peripheral Examples
Postherpetic neuralgia Pain due to inflammation
Trigeminal neuralgia Low back pain with Limb pain after a fracture
Diabetic peripheral neuropathy radiculopathy Joint pain in osteoarthritis
Postsurgical neuropathy Cervical radiculopathy Postoperative visceral pain
Posttraumatic neuropathy Cancer pain
Central Carpal tunnel syndrome Common descriptors2
Poststroke pain Aching
Common descriptors2 Sharp
Burning Throbbing
Tingling
Hypersensitivity to touch or cold 1. International Association for the Study of Pain. IASP Pain Terminology.
2. Raja et al. in Wall PD, Melzack R (Eds). Textbook of pain. 4th Ed. 1999.;11-57
Potential Models of Chronic
Pain
Myofascial pain
Low back pain
Osteoarthritis
Fibromyalgia
Mixed-model population
Neuropathic pain*
Cancer pain*
Panthom pain
etc.
TheraQuest
Treatment of Chronic Pain

Argoff
WRAMC Feb1, 2005
2nd Order Neuron Changes
In Persistent Pain States
PREGABALIN
Seperti gabapentin, pregabalin digunakan
sebagai anti konvulsant dan anti neuropatic, di
opproved oleh FDA 2005
Lebih potent dari gabapentin sehingga dosis
lebih rendah SE lebih sedikit
Dosis dimulai dari 50, 75, 150, 300 dan 600mg

Dosis 150mg menurunkan opioid consumption


pada laparascopic cholecystectomy. dosis 300mg pada
hip-arthroplasty.
Pregabalin Binding
to Voltage-Dependent
Ca2+
Calcium Channels

Ca2+
IonIon
channel
channel Pregabalin
Ca2+ Ca2+ Gabapentin
Pregabalin/
Ca2+ binding site

Ca2+
-
Outside
the cell

+ + + +
Cell membrane

Inside
the cell

Ca2+
Pain is a more terrible lord of
mankind than even death
himself
Albert Schweitzer
TISSUE INJURY

Prostaglandins
Bradykinin

Leukotriens

PAIN Histamine

NSAID
(Cox1 or Cox2)
Common surgeries which may
develop to CPSP are:
1.Limb amputation
2.Thoracic surgery
3.Breast surgery
4.Herniorrhapy
5.Cholicystectomy
Why chronic pain, is so
danger ?
Because Chronic pain is
Biopsychosocial phenomenon,
Produce suffering
Difficult to treat
High cost
Reduce quality of Life

Acute Pain is
Biomedical problem
Alarm protection
A symptom of injury or disease
Chronic vs Acute Pain
Chronic Pain
is not prolonged acute pain
must be considered and treated as
a disease.
Acute and chronic pain have nothing in
common but the four-letter word pain
John Loeser
Phantom Limb Pain is a
CNS Disorder

Development
Noxious input from limb

Cortical pain memory

Amputation

Reorganisation of somatosensory cortex

Maintenance
Selective loss of C fibers
Ectopic input from neuroma
Ectopic input from DRG
Sympathetic activation

Phantom
pain
Flor&Birbaumer 2000
Phantom Limb Pain is a
Pain Memory!

In 57% of subjects with phantom pain, this


resembled preamputation pain.
somatosensory inputs of sufficient
intensity and duration can produce long- lasting
changes in central neural structures
Katz&Melzack, Pain 1990;43:319
So, what is chronic pain?

Chronic pain is a biopsychosocial


phenomenon,
but the bio component is usually not
classical nociception, but the result of
a neurologic disease!
Remembering;

Acute pain is a symptom, and chronic


pain is a disease, causing suffering.
Since acute pain and chronic pain are
different, they must be treated
differently.
Biomedical vs. Biopsychosocial
Management Pain
Acute pain 1 Chronic pain
goal of treatment is to goal of treatment is to
obtain pain relief improve function in
occupational, social and
emotional domains; pain
relief is de-emphasised
Biomedical vs. Biopsychosocial
Management of Pain

Acute pain 2 Chronic pain


patient is ill, and patient is not ill, and
therefore should be should maintain normal
free from normal activity levels as far as
responsibilities possible
Biomedical vs. Biopsychosocial
Management of Pain

Acute pain 3 Chronic pain


primary responsibility primary responsibility for
for improvement lies improvement lies with the
with the doctor; patient - patients role is
patients role is active.
passive.
Two great obstacles

In treating chronic pain


1. Fear avoidance behavior
(Kinesiophobia = takut bergerak)
2. Passive treatment
(menginginkan pembedahan or massage)
2nd Order Neuron Changes
In Persistent Pain States
(CRPS) Complex Regional
Pain Syndrome
Even Peripheral Changes of CRPS
are Result of Central Sensitization!
2nd Order Neuron Changes
In Persistent Pain States
PREGABALIN
Seperti gabapentin, pregabalin digunakan
sebagai anti konvulsant dan anti neuropatic, di
opproved oleh FDA 2005
Lebih potent dari gabapentin sehingga dosis
lebih rendah SE lebih sedikit
Dosis dimulai dari 50, 75, 150, 300 dan 600mg

Dosis 150mg menurunkan opioid consumption


pada laparascopic cholecystectomy. dosis 300mg pada
hip-arthroplasty.
Pregabalin Binding
to Voltage-Dependent
Calcium Channels
Ca2+

Ca2+
IonIon
channel
channel Pregabalin
Ca2+ Ca2+ Gabapentin
Pregabalin/
Ca2+ binding site

Ca2+
-
Outside
the cell

+ + + +
Cell membrane

Inside
the cell

Ca2+
Treatment Approach
Disease specific measures
Physiotherapy
Regional sympathetic blockade-
Intravenous Regional Sympathetic Block
Stellate ganglion block upper limb
Lumbar sympathetic block
Pharmacological
TENS & Acupuncture
Surgical
Adjuvant analgesics
Antidepressants:
Most useful in neuropathic pain
Tricyclic agents more effective (PHN, DN)
Side effects

Anticonvulsants :
Extremely useful in neuropathic pain e.g. Trigeminal
neuralgia and diabetic neuropathy

Refractory neuropathic pain


Neuroleptics:
Pts with marked agitation and psychotic symptoms
Corticosteroids:
Anti-inflammatory and possible analgesic effects

Antiarrhythmic drugs:
Lignocaine for chronic neuropathic pain
Mexiletine for diabetic neuropathy

Ketamine:
Analgesic effect on low dose

analgesic effects but the effect of opiod


Nitroglycerine:
Invasive Treatment
Modalities
Neuro Destructive Technique -
Aim To destroy Target nerve
To produce prolonged interruption of
Nociceptive pathways

Cryoanalgesia
Techniques Thermal Ablation with radiofrequency
coagulation
Chemical Neurolysis
Treatment Modalities
Invasive Techniques
Neural Blockade
Neurolytic Blocks
Implantation of Neurostimulator
Implantation of continuous drug delivery
systems
Treatment Modalities
Invasive
Neural Blockade-
Nerve Plexuses, Epidural Space,
Subarachnoid Space
Local Anaesthetics Bupivacaine,

Ropivacaine usually combined with into


spinal epidural space or steroid ,
peripheral block
Management modalities contd

Epidural steroid
injections
Stellate Ganglion Block
Management modalities contd

Lumbar sympathetic
neurolysis
Treatment modalities
Neurostimulation theory-
TENS- High frequency , low intensity
current stimulate nociceptive inhibitory
Afferents in dorsal horn- Alleviates pain
ACUPUNCTURE
Injury blocks flow of chi life force
Acupuncture releases these blocks
TENS
Acupuncture
Take home message
Chronic pain should be;
Recognized as an important health problem
Seriously affecting quality of life and ability
to work.
Should be treated with the same priority as
any underlying disease
Treated by mulstidisiplinary approach.
PAIN HAS BEEN EVOLVING

A Symptom of
A Disease Entity
Disease

Is a disease of
Nervous System.

Is a special disease
Since pain has become a special
disease

Its should be treated by a


specialist Pain Specilist
94
69

15
19

28
20

20
5 242

:: Population
Population (in
(in Million)
Million)
:: Pain
Pain specialist
specialist

Data from Asean-PS 20013


Fellow dari KMN (Konsultan Menejemen Nyeri), 2 angkatan, 2011dan 2012
KepMenkes 779/Menkes/Sk/VIII/2008 ttg
standar pelayanan anestesiologi dan
reanimasi di rumah sakit
Why it has to be an
anesthesiologist in PM?
We are working with various analgesic drugs in our
daily basis;
1. Non-opioid analgesic (NSAIDs)

2. Opioid analgesic

3. Local anesthetic

4. We had been trained in regional blocks for


analgesia.
5. So we are mastering in pain pathway.

6. Regional blocks is the basic of intervention pain


management
Intervention Pain
Management
Recovery

Operation

Strong
opioids

Weak
Opioids +/-
Non- Non-
opioids opioids +/-
adjuvant
Nonpharmacological
methods
Intervention Pain
Management
Recovery

Operation

Strong
opioids

Weak
Opioids +/- World of mistery
Non- Non-
opioids opioids +/-
adjuvant
Nonpharmacological
methods
Intervention Pain
Management

Recovery

Operation
IPM
Strong
opioids

Weak
Opioids +/-
Non- Non-
opioids opioids +/-
adjuvant
Nonpharmacological
methods
Intervention Pain
Management

IPM
Interventional Pain Management are some minimally
invasive procedures which gives permanent/long term
pain relief.
It fills the gap between pharmacologic management of
pain & more invasive operation procedure.
Intervetion Pain Management in Holland

St. Anna Hospital | W. Halim | Cervicogenic Headache| 2013


IASP Task Force on Guidelines for Pain
Treatment Facilities, 1990

A. According to available personnel and resources :

1. Multidisciplinary Pain Centre


2. Multidisciplinary Pain Clinic
3. Pain Clinic
1. Multidisciplinary Pain Center
The largest and most complex of pain treatment facility
A wide array of health care specialist is required
Exist as component of MEDICAL SCHOOL
Organization of health care professional include :
Patient care ( acute & chronic )
Teaching
Research
e.g Multidisciplinary pain center Seattle , USA and
Sydney, Australia
2. Multidisciplinary Pain Clinic
3. Pain Clinic
Is a simple Pain Treatment Facility
Focusing on management of chronic pain
May specialized on specific diagnose or
syndrome or modalities that it is used
A pain clinic may be large or small, but it
should never be a label for an isolated
solo. practitioner
Pain Clinic

1. According to the modality


Modality-Oriented Clinic
Nerve block clinic Anesthesiologist
Biofeedback clinic Psychologist
Acupuncture clinic Acupuncturist
etc
Pain Clinic

2. According to the syndrome


SyndromeOriented Clinic
Headaches Clinic Neurologist
Low back pain Clinic Orthopedics
Facial pain Clinic Oral Surgery, ENT
Arthritis pain Clinic Rheumatologist
etc
Why Treat Pain?
Pain relief is a basic human right!
suffering from pain
patient satisfaction
speed of recovery LoS cost
complications of unreleived pain
productivity and quality of life
development chronic pain
Pain is the fifth vital sign
Origin the term
Pain the fifth vital sign

Pain is common reason


for seeking medical care.

If pain is recorded for all


Dr. J. Cambell 1995
patients, finally we are
President of IASP,
focusing on the main
Coined the term fifth
cause for seeking medical
vital sign . care.

Quality of care means


Pain is measured
and treated.
Pain: The Fifth Vital Sign
Pulse
Pain:
Blood pressure The Fifth
Temperature Vital Sign

Respiratory rate

1995 American Pain Society (APS) designatedPAIN as the 5th vital sign
2000 JCAHO introduced PAIN as a new standard of pain management.
Sample Clinical Chart

Cburning Asharp
sensation stabbing
3.4.04 X 1.4.04
X
Bdullaching
X 1.4.04

Temperature

BloodPressure
Pulse
Respiration
Pain
Conclution

Absolutely we need Pain


Specialisty In Indonesia
No one can be a generalist like this man

is to specialize in everthing!
If you can feel pain you are alive.
If you can feel the pain of other
people, you are a human.
If you can treat the pain patient you
are a good doctor.
Prof. Hyodo, Japan
Modulation

20th century
PAIN HAS BEEN EVOLVING

Pain as a symptom Pain as a disease


of disease entity
Since pain has become a special
disease

Its should be treated by a


specialist Pain Specilist
The Role of A fiber
Although in normal condition A fiber does not
response to noxious stimuli, but it plays a big role
in NORMAL SENSATION.

Without A fiber, any noxious stimuli will perceive


as BURNING PAIN (TN, HZ)