Kuliah

NYERI SOMATIK DAN VISERAL

dr. Resa Budi Deskianditya, Sp.N
Prodi Kedokteran FK UMP
1 November 2022
 Deffinition

Pain Pathway

Neuroanatomy of pain

outline Pain classification

Pain control theory

Visceral and referred pain

Pain assessment
 “An unpleasant physical and emotional
experience which signifies tissue damage or
potential for such damage” -IASP, 1979

Nyeri adalah pengalaman sensorik dan

Definition emosional yang berhubungan dengan
kerusakan jaringan / stimulus yang potensial
menimbulkan kerusakan jaringan
 IASP Announces Revised Definition of Pain
Jul 16, 2020

• “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual
or potential tissue damage,” and is expanded upon by the addition of six key Notes and the etymology of the
word pain for further valuable context.
1. Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and
social factors.
2. Pain and nociception
3. Through their life experiences, individuals learn the concept of pain.
4. A person’s report of an experience as pain should be respected.
5. Although pain usually serves an adaptive role, it may have adverse effects on function and social and
psychological well-being.
6. Verbal description is only one of several behaviors to express pain; inability to communicate does not
negate the possibility that a human or a nonhuman animal experiences pain.
 “The uncomfortable sensation of pain has caused man to seek an explanation,

using contemporary concepts to find a reason for this discomfort (1).”

• What is Pain?
• Pain can be defined as a somatic sensation of acute discomfort, a
symptom of some physical hurt or disorder, or even emotional
distress.
• It is a common human experience therefore the idea of pain and pain
management appear throughout history
 Pain is a crucial aspect of the body’s
defense mechanisms

What is
Pain? Pain “is a part of a rapid warning
relay instruction the motor neurons
of the central nervous system to
minimize detected physical harm
(2).”
• Nyeri à mekanisme menghindari keadaan
berbahaya, mencegah kerusakan lebih jauh,
mendorong proses penyembuhan
• Stimulus noksius : akar dari suatu nyeri
(Penar, 2000)
Sistem somatik

Bagian dari sistem saraf perifer yang bertanggung

jawab untuk membawa informasi sensoris dan
motorik dari dan ke sistem saraf pusat

Mentransimisikan informasi sensoris dan gerakan

volunteer
The experience of pain

Three systems interact 1. Sensory - 2. Motivational - 3. Cognitive - evaluative

usually to produce pain: discriminative system à affective system à system à overlies the
processes information determines the individuals learned
about the strength, individual´s approach- behaviour concerning
intensity, quality and avoidance behaviours the experience of pain.
temporal and spatial It may block, modulate,
aspects of pain or enhance the
perception of pain
“Pain Experience”

De
ty
x ie

pr
e
An

ss
ion
Phy
lta

Catastrophization
s ic a
Men

?????
Spiritual

So &
ma on
tiz c tati
a tio x pe esire
n E D

“Pain is a personal, subjective experience that comprises :

Sensory-discriminative, Motivational-affective and Cognitive-evaluative dimensions”
Ronald Melzack, “Textbook of Pain” 4th edition
 Elliott & Walton, 2018
Clinical Model of Triangulation
Socioenvironmental

Cognitive/Belief Sensorimotor
Dys-integration

Emotional/ Very
Affective
Low Nociceptive /
Low Physiological
Moderate
High
Very High
Central Nociplastic Peripheral Neuropathic
Neuroanatomy
 What Causes Pain?
• Pain is caused by the stimulation of pain
receptors which are free nerve endings.
• “Nocireceptors are pain receptors that are
located outside the spinal column in the
dorsal root ganglion and are named based
upon their appearance at their sensory ends.
These sensory endings look like the branches
of small bushes( 2).”
• There are two types of nocireceptors that
mediate fast or slow pain signals
• The perception of pain is when these
receptors are stimulated and they transmit
signal to the central nervous system via
sensory neurons in the spinal cord.

http://staff.washington.edu/chudler/gif/spiback1.gif
Pain Signaling

• These neurons release excitatory

neurotransmitters which relay signals from
one neuron to another.
• “The signals are sent to the thalamus, in
which pain perception occurs. From the
thalamus, the signal travels to the
somatosensory cortex in the cerebrum, at
which point the individual becomes fully
aware of the pain (2).”
 • The portions of the nervous system
responsible for the sensation and
perception of pain may be divided into
three areas:
Neuroanatomy • 1. afferent pathways
of pain • 2. CNS
• 3. efferent pathways

1. The afferent portion is composed of:

a) nociceptors (pain receptors)
b) afferent nerve fibres
c) spinal cord network
• Afferent pathways terminate in the dorsal horn of the
spinal cord (1st afferent neuron)
• 2nd afferent neuron creates spinal part of afferent
system
• The portion of CNS involved in the interpretation of
the pain signals are the limbic system, reticular
formation, thalamus, hypothalamus and cortex
• The efferent pathways, composed of the fibers
connecting the reticular formation, midbrain, and
substantia gelatinosa, are responsible for modulating
pain sensation
Back
Pain pathway
Normal Nerve Impulses Leading to Pain

Perceived pain

4
1 Descending
modulation
Ascending
input

Nociceptive afferent fiber

Spinal cord 2
Pain pathway
There are four processes in the pain pathway
1. Transduction
Noxious stimuli translated into electrical activity at sensory nerve
endings
2. Transmission
Propagation of impuses along spinothalic pathway
3. Modulation
Transmission is modified
4. Perception
Affective / motivational aspect
 Physiology of Pain Perception

• Transduction Injury Brain

• Transmission
• Modulation
• Perception
• Interpretation
• Behavior
Descending
Pathway

Dorsal
Peripheral Root
Nerve Ganglion

Ascending
Pathways
C-Fiber

A-beta Fiber Dorsal

Horn
A-delta Fiber
Spinal Cord
27 Adapted with permission from WebMD Scientific American® Medicine.
 Proses penjalaran nyeri

Persepsi :
Fenomena kimiawi psikologis
Lesi kompleks akspresi nyeri

Modulasi :
Sensitisasi nosiseptor : Modulasi potensial aksi
Kulit,otot, tulang, saraf, dll dari afferen di medula
Tranduksi : spinalis
Munculnya potensial aksi
dari stimulus

Transmisi :
Penjalaran pot.aksi dr perifer
Ke sentral
 • 1. Transduksi
• Konversi stimulus noksious termal, mekanik, atau
Nyeri kimia menjadi aktivitas listrik pada akhiran
serabut sensorik nosiseptif
nosiseptif • Menghasilkan PG, BK, H à merangsang produksi
SP
Transduction
 Transduction

External Heat VR1

Pain and auto-sensitization
Ca2+ Na+

mDEG ACTION
ACTION POTENTIAL
Mechanical POTENTIAL
Voltage gated sodium channels
P2X3
Stimuli
ChemicalATP
action potentials
Generator potentials

Woolf & Mitchel, 2001; Modifikasi Meliala, 2003

Peripheral Mediators of Inflammation

Thermal/

SP: vascular permeability; CGRP: long-lasting vasodilation

Proses inflamasi terjadi jika:
- adanya antigen
- adanya kegiatan makrofag dengan
mensekresi imun mediator
- keluarnya mediator histamin
- aktivitas enzim cyclooxygenase
- produksi prostaglandin
 • 2. Transmisi
• Transmisi merupakan aktivitas serabut saraf
menyusul proses transduksi berupa penyaluran
rangsang noksius melalui serabut saraf sensorik
aferen ke tingkat yang lebih tinggi
Nyeri • A-delta à bersinaps di LR I,II,V,X à Informasi
nosiseptif yang dihantarkan oleh traktus ini bersifat cepat,
tajam dan terlokalisir
• C à bersinaps di LR I,II,V à Informasi nyeri yang
dihantarkan oleh traktus ini bersifat informatif
dari pengalaman nyeri yang bersifat tumpul,
dalam, tidak terlokalisir
 NOCICEPTION and NOCICEPTORS
Nociception is the process by which intense thermal, mechanical or
chemical stimuli are detected by a subpopulation of peripheral nerve
fibers, called nociceptors
Type 1
(High heat Trsh)
A-∂ fiber
Type 2
Nociceptors (High Mechanical Trsh)

a bidirectional
signalling machine Peptidergic
(neuropeptides, Sub-P,
C-fibers CGRP, TrkA)

(All modalities) Non-Peptidergic

(GDNF, Artemin)
(Cellular and Molecular Mechanisms of Pain, Basbaum, Bautista et al, 2009)
 KHSP/m/detik
Nama Diameter
KHSP=Kecepatan Hantar Reseptor
(sistem letter) µm
Saraf Perifer
Aa 10-20 70-120 Eferen otot
Ab 6-12 30-70 Reseptor : Meissner, Ruffini, Paccini, Merkel; akhiran
sekunder spindel otot
(Mekanoseptor)
Ag 2-10 10-50 Eferen otot (intrafusal)
Ad 1-6 5-30 Reseptor untuk: mekanikal, termal, mekanotermal
(polimodal), reseptor rambut, reseptor visera.
(Mekano-nosiseptor)
C < 15 0,5-20 Reseptor C; reseptor polimodal C, reseptor visera,
reseptor panas, dingin dan mekanik
(Nosiseptor)
Nerve fibres
AFEREN SENSORIS DARI PERIFER KE
MEDULA SPINALIS
The image part with relationship ID rId2 was not found in the file.
Ascending Pathway
• Lateral spinothalamic tract
• Spinoreticular tract
• Spinomesencephalic tract
• Dorsal column postsynaptic spinomedullary pathway
• Propiospinal multisynaptic ascending systems
Nyeri nosiseptif

• 3. Modulasi
• Modulasi merupakan aktivitas saraf yang akan mengontrol
rangsang noksius sebelum dilanjutkan ke tingkat yang lebih tinggi.
• Sensitisasi Sentral >< Inhibisi Sentral
Descending Pain Modulation Pathways

pain modulating neurons from the cortex,

hypothalamus, midbrain periaqueductal gray and
rostral medulla alter pain response in the dorsal
horn of the spinal cord
Nyeri nosiseptif

• 4. Persepsi
• Persepsi merupakan proses akhir yang berupa aktivitas saraf
sensorik yang menghasilkan persepsi nyeri yang bersifat subjektif
Anger Anxiety

Fear
Depression
A

PSYCHOLOGICAL
B

NOCICEPTIVE

Noxious Stimuli MELIALA 2004

Pain clasification
Tipe nyeri berdasarkan onset

Kerusakan substansial
jaringan, mengaktivasi
Nyeri Akut hantaran nosiseptik
(trauma, tindakan
bedah, penyakit)

Tipe Nyeri
Neuropatik
Nosiseptik
Nyeri Kronis Viseral
Campuran
Acute vs Chronic Pain

Characteristic Acute Pain Chronic Pain

Cause Generally known Often unknown

Duration of pain Short, Persists after healing,

well-characterized ³3 months

Treatment Resolution of Underlying cause and pain

approach underlying cause, disorder; outcome is often
usually self-limited pain control, not cure
ASPEK FISIK NYERI AKUT NYERI KRONIK
Lokasi Jelas Difus, menyebar
Deskripsi Mudah Sulit
Durasi Pendek Terus berlangsung
Fisiologis Kond.alert (HR­,BP ­) Muncul puncak nyeri
Pengaruh pada istirahat Mengurangi nyeri Perburuk nyeri,kerusakan

Pengaruh pada kehidupan Nyeri akut Nyeri kronik

Pekerjaan Terkendali Dipertanyakan
Keluarga & relasi Menolong dan supportif Lelah, deteriorasi
Finansial Dpt dikendalikan Tekanan, bisa kekurangan

Mood ansietas., takut Depresi, marah, pts asa

Toleransi thd nyeri Biasanya terkendali Krg terkendali, pts asa
Respon dari dokter Positif/ memberi harapan Mrs disalahkan,> obat, F.up
menjemukan
Asuransi Terkendali Bervariasi, kesulitan ­
pengobatan Mencari penyebab & obat Fokus fungsi, manajemen
 Acute Pain
• Acute pain is short-term pain or pain with an easily identifiable cause
• Acute pain “is the body's warning of present damage to tissue or
disease. It is often fast and sharp followed by aching pain. Acute pain
is centralized in one area before becoming somewhat spread out. This
type of pain responds well to medications (2).”
 Chronic Pain
• Chronic pain is pain that last much longer than pain normally would
with a particular injury.
• Chronic pain can be constant or intermittent and is generally harder
to treat than acute pain.
• Pain can also be grouped by its source and related pain detecting
neurons such as cutaneous pain, somatic pain, visceral pain, and
neuropathic pain
• Opioid Analgesics can be used to treat many types of pain
Klasifikasi nyeri (Chapman, 2004)

Nosiseptif /
Neuropatik
Inflamatorik
Berdasarkan
Patofisiologi

Psikologik /
Idiopatik NOCIPLASTIC
Fungsional
Nociceptive vs Neuropathic Pain
Nociceptive Mixed Type Neuropathic
Pain Caused by a Pain
Caused by activity in combination of both
Initiated or caused by
neural pathways in primary injury and
primary lesion or
secondary effects
response to potentially dysfunction in the
tissue-damaging stimuli nervous system

CRPS*

Postherpetic
Postoperative
Arthritis neuralgia Trigeminal
pain
neuralgia
Sickle cell Neuropathic
Mechanical crisis low back pain Central post-
low back pain
Distal stroke pain
Sports/exercise polyneuropathy
injuries (eg, diabetic, HIV)
*Complex regional pain syndrome
 Nyeri nosiseptif (inflamatorik)
• Ditimbulkan oleh rangsang pada nosiseptor
• Nosiseptor : ujung saraf bebas yang berakhir
pada :
- kulit à deteksi nyeri kulit
- tendo dan sendi à deteksi nyeri
visceral
• Peka terhadap : mekanis, suhu, listrik,
kimiawi
(Heong, 2004; Richeimer, 2006)
Nyeri nosiseptif :
• Stimulasi singkat, tdk timbul kerusakan jaringan

Nyeri inflamatorik:
• Stimulasi kuat, kerusakan / lesi jaringan atau proses
inflamasi
• Dapat bersifat spontan atau dibangunkan
• Berguna utk proses penyembuhan
 NOCICEPTIVE PAIN
Noxius Pheripheral Stimuli
Pain
Heat Autonomic Response
Witdrawal Reflex
Cold
Brain

Intense
Mechanical
Nociceptor sensory neuron
Force

Heat

Spinal cord
Cold
 INFLAMMATORY PAIN
Spontaneous Pain
Inflammation Pain Hypersensitivity
Macrophage Reduced Threshold : Allodynia
Increased Response : Hyperalgesia
Mast Cell

Neutrophil
Granulocyte Brain

Nociceptor sensory neuron

Tissue Damage

Spinal cord
Nyeri neuropatik

• Nyeri neuropati : nyeri yg disebabkan oleh gangguan

fungsi / perubahan patologis di susunan saraf perifer dan
pusat
• Nyeri neuropati perifer : nyeri yang disebabkan gangguan
fungsi saraf tepi (radik, pleksus, serabut saraf)
• Nyeri neuropati sentral : nyeri karena lesi saraf sentral
(otak, batang otak, medula spinalis)
NEUROPATHIC PAIN

Spontaneous Pain
Pain Hypersensitivity

Brain

Peripheral Nerve
Damage

Spinal cord Injury

 Freezing, like the feet are on ice,
Burning, feeling like the feet are on fire although they feel warm to touch

Stabbing, like sharp knives Modified by Meliala 2006 Lancinating, like electric shocks
FUNCTIONAL PAIN

Spontaneous Pain
Pain Hypersensitivity

Brain

Normal Peripheral
Tissue and Nerves

Abnormal Central
Processing
 Elliott & Walton, 2018
AM e C Pa e
Socioenvironmental

Cognitive/Belief Sensorimotor
Dys-integration

Emotional/ Very
Affective
Low Nociceptive /
Low Physiological
Moderate
High
Very High
Central Nociplastic Peripheral Neuropathic
 Elliott & Walton, 2018
Purely Nociceptive
Socioenvironmental

Cognitive/Belief Sensorimotor
Dys-integration

Emotional/ Very
Affective
Low Nociceptive /
Low Physiological
Moderate
High
Very High
Central Nociplastic Peripheral Neuropathic
 Elliott & Walton, 2018
Clinical Model of Triangulation
NEUROPATHIC Socioenvironmental

Cognitive/Belief Sensorimotor
Dys-integration

Emotional/ Very
Affective
Low Nociceptive /
Low Physiological
Moderate
High
Very High
Central Nociplastic Peripheral Neuropathic
 Elliott & Walton, 2018
Clinical Model of Triangulation
NOCIPLASTIC Socioenvironmental

Cognitive/Belief Sensorimotor
Dys-integration

Emotional/ Very
Affective
Low Nociceptive /
Low Physiological
Moderate
High
Very High
Central Nociplastic Peripheral Neuropathic
 Terminology of Pain
• Pain
An unpleasant sensory and emotional experience
associated with actual or potential tissue damage,
or described in terms of such damage.
• Allodynia
Pain due to a stimulus which does not normally
provoke pain.
• Analgesia
Absence of pain in response to stimulation which
would normally be painful.
• Anasthesia dolorosa
Pain in an area or region which is anasthetic.
• Causalgia
A syndrome of sustained burning pain, allodynia, and
hyperpathia after a traumatic nerve lesion, often
combined with vasomotor dan sudomotor dysfunction
and later trophic changes.
• Central Pain
Pain initiated or caused by a primary lesion or
dysfunction in central nervous system.
• Dysesthesia
An unpleasant abnormal sensation, whether
spontaneous or evoked.
• Hyperalgesia
An increased response to a stimulus which is normally
painful.
• Hyperesthesia
Increased sensiticity to stimulation, excluding the special
senses.
• Hyperpathia
A painful syndrome characterized by an abnormally
painful reaction to a stimulus, especially a repetitive
stimulus, as well as an increased threshold.
• Hypoalgesia
Diminished pain in response to a normally painful
stimulus.
• Hypoesthesia
Decreased sensitivity to stimulation, excluding the
special senses.
• Neuralgia
Pain in the distribution of a nerve of nerves.
• Neuritis
Inflammation of nerve of nerves.
• Neurogenic Pain
Pain initiated or caused by a primary lesion,
dysfunction, or transitory perturbation in the
peripheral or central nervous system.
• Neuropathic Pain
Pain initiated or caused by primary lesion or
dysfunction in the nervous system.
• Neuropathy
A disturbance of function or pathological change in a
nerve: in one nerve, mononeuropathyl; in several
nerves, mononeuropathy multiplex; if diffuse and
bilateral, polyneuropathy.
• Nociceptor
A receptor preferentially sensitive to a noxious stimulus
or to a stimulus which would become noxious if
prolonged.
• Noxious Stimulus
A noxious stimulus is one which is damaging to normal
tissues.
• Pain Threshold
The least experience of pain which a subject can
recognize.
• Pain Tolerance Level
The greatest level of pain which a subject is
prepared to tolerate.
• Paresthesia
An abnormal sensation, whether spontaneous or
evoked.
• Peripheral Neurogenic Pain
Pain initiated or caused by a primary lesion or
dysfunction or transitory perturbation in the
peripheral nervous system.
• Peripheral Neuropathic Pain
Pain initiated or caused by a primary lesion or
dysfunction in the peripheral nervous system.
PAIN CONTROL THEORY
PAIN CONTROL: THEORY
• Gate Control Theory
• Melzack and Wall 1965
• A non-painful stimulus can block the transmission of a painful stimulus
• Substantia Gelatinosa: dorsal horn; acts as a gate for sensory info; A-beta
fibers vs. A-delta and C fibers
• T Cells: transmission cell that connects sensory nerves to afferent tracts;
receives from SG
• Example: rubbing injury; modalities
Theory of pain production and modulation

• Most rational explanation of painproduction and modulation

is based on gate control theory (created by Melzack and Wall)

• According to this theory, nociceptive impulses are

transmitted to the spinal cord through large A- delta and
small C- fibers
• These fibers create synapses in the SG

• The cells in this structure function as a gate, regulating

transmission of impulses to CNS

ØStimulation of larger nerve fibers (A-alfa, A-beta) causes

the cells in SG to "close the gate".
• A closed gate decreases stimulation of T-cells (the 2nd
afferent neuron), which decreases transmission of impulses,
and diminishes pain perception
 • Levels Model (Castel, 1979)
• Gate theory doesn’t cover it
all
PAIN • Three levels
CONTROL: • Involves higher “central”
THEORY control
• Endogenous Opiates
 Ascending
Influence • Similar to Gate Control Theory

LEVELS Pain
Control

THEORY: • Large diameter afferents synapse on

enkephalin interneurons

I Mechanics
• Release of enkephalins into synapse
of nociceptive pathways
• Enkephalins believed to inhibit
release of Substance P
• Prohibits synaptic transmission of
pain
 • Descending Influence Pain Control
• Higher brain centers modulate synaptic
transmission in dorsal horn

LEVELS
• Mechanics
• Stimulus is received in Peri-Aqueductal Gray
(PAG)

THEORY: • Third-order neurons from Raphe Nucleus are

activiated

II
• Dorsolateral tract descends from RN and
synapse on enkephalin interneurons in lamina
II releasing serotonin
• Release of enkephalins into 1st and 2nd
order afferent nociceptive pathway
LEVELS THEORY: III
• Beta-Endorphin Mediated Pain Control
• Release of beta-endorphins has analgesic response
• Mechanics
• Hypothalamus is stimulated and synapses with PAG
• Beta-endorphin released and activates dorsolateral tract
• Serotonin released and enkephalin influence
• Can be initiated by long term (20-40 min) electrical stimulation (motor level)
• High intensity w/ long pulse duration
 NORMAL TRANSMISSION
MODEL 1 - NORMAL TRANSMISSION
INNOCOUS OR NOXIOUS STIMULATION

Afferent Input

SP GluTAMATE

Ca2+

AMPA NK1

Postsyneptic activity

Normal Sensibility
Doubell et al., 1999
Modifikasi Meliala, 2003
 KERUSAKAN JARINGAN
SUPRESSED TRANSMISSION
INFLAMASI
MODEL 2 – Supressed Transmission
Activation of segmental and descending inhibitory systems
SENSITISASI
SSA MI Pg NOS
Si-Na+ Afferent Input
B AKTIFASI
ECT. DISC. 5HT
R-NE Adenosin
KORNU DORSALIS
Pengalaman
Kognitif Inhibisi
Behaviour desenden
Psikologik OTAK
Presynaptic
PAIN – NO PAIN
MOR GABA
SHT Adenocine

SP GluTAMATE Gly

Postsynaptic
Ca2+

NK1 AMPA MCR SHT GLYCINE

GABA
Postsyneptic activity

Reduced Sensibility
Doubell et al., 1999
Modifikasi Meliala, 2003
 FASCILITATED TRANSMISSION KERUSAKAN JARINGAN

Increased excitation/reduced inhibition

INFLAMASI

SENSITISASI
Afferent Input SSA MI Pg NOS
Si-Na+
B AKTIFASI
ECT. DISC. 5HT
R-NE Adenosin
KORNU DORSALIS
Pengalaman
Kognitif Inhibisi
Behaviour desenden
Psikologik OTAK
Ca2+
ATP
Ca2+ PAIN – NO PAIN
P2X3 VSCC GABA Adenocine
Presynaptic NMDA Reduced
Mg2+ MOR Presynaptic
Augmentation
SP GDNF GLUTAMATE SHT inhibition
mGluR

Increased transmitter release

Ca2+ Retrograde signale e.g.NO
Ca2+
Ca2+
Reduced
VSCC AMPA NMDA TrkB GABA MOR SHT Postsynaptic
Postsynaptic
NK1 Mg2+ inhibition
facilitation
mGluR S/T
Tyr

PKC Brc GLYCINE

Ca2+
PLC Postsyneptic activity

Doubell et al., 1999

Reduced Sensibility Modifikasi Meliala, 2003
 DESCENDING INHIBITION
BRAIN DESCENDENS

5HT

ENK
AFFEREN

SP-GLUTAMAT
NEURON TRANSMISI

Kornu Dorsalis

Meliala, 2005
 DESCENDING INHIBITION
NO PAIN
athway
To ing p
the brain Des cend

Serotonin/
Neurone of the Noradrenaline
Spinothalamic tract

µ-Receptor a2-Receptor

Pain transmitter

Spinal neurone

Afferent C fibers
Pain
Enkephalin Message
Kornu Dorsalis

Theraupeutic Approaches of Pain Management, 2004 Meliala, 2004

Pain assesment
Why It’s Important?
• To assist:
• Diagnosis
• Goals for clinical intervention and management;
• Effectiveness of a treatment programme
• Patient’s functional ability despite pain;
• Data for insurance, compensation and pension claims.
Pain assessment scales
Verbal pain intensity scale Visual analog scale

No Mild Moderate Severe Very Worst Worst

pain pain pain pain severe possible
No
pain possible
pain pain
pain

0–10 Numeric pain intensity scale “Faces” scale

0 1 2 3 4 5 6 7 8 9 10
No Moderate Worst 0 1 2 3 4 5
pain pain possible pain

1. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. 1996:8-10.
2. Wong DL. Waley and Wong’s Essentials of Pediatric Nursing 5th ed. 1997:1215-1216.
3. McCaffery M, Pasero C. Pain: Clinical Manual. Mosby, Inc. 1999:16.
Pain Yellow Flags
Analgetik
 The WHO Analgesic Ladder

Very severe Hydromorphone

WHO
Step III
Morphine
Oxycodone
Severe Fentanyl
Buprenorphine
Pain intensitiy Tramadol
Tilidine

Drugs
WHO Codein
Step II Moderate Dextropropoxyphene
NSAIDs
COX II inhibitors

Acetylsalicylic acid
WHO
Acetaminophene
Step I Mild

Langford, 2002; Proceeding of the Grünenthal symposium

 Vit B6 (Increase serotonin,
Epinephrin & GABA)

Vit B1 (Block Na Channel)

• Vit B12 (Block Cytokine)

• Vit B6 ( serotonin,Epinephrin &

GABA)
 Acute Pain (McQuay & Moore, 1999)
TREATMENT METHODS

Remove the cause Medication Regional Physical Psychological

Of pain analgesia methods approaches

Low Tech •relaxation

•Nerve blocks •psychopro-
•Surgery Opioid •Local anaesthetic
•Splinting phylaxis
•Morphine •hypnosis
± opioid
•others

Non-opioid High Tech •physiotherapy

•Aspirin & others •Epidural infusion •manipulation
NSAIDS •Local anaesthetic •TENS
•Paracetamol ± opioid •Acupuncture
•combinations •Ice
 ACUTE AND SEVERE PAIN

Recommended Significant Toxicity

Initial Dosing
Significant Sedation

Pain/Analgesia Threshold

Some Analgesia

Traditional
Initial Dosing No Analgesia

Analgesic dosing ladder

 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 Block nerve transmission Alternatives

Conventional Irreversible
•NSAID •surgery
Parasetamol •Nerve destruction
to opioid
•Stimulators
•Acupuncture
Unconventional Reversible •Hypnosis
•antidepressant •Local anaesthetic •Psychology
•anticonvulsant ±steroid
•others ±opioid
Visceral and Referred
Pain
 sensasi nyeri yang timbul akibat kerusakan organ
dalam, sering ditandai oleh sensasi dalam (deep),
tumpul (dull), sakit (aching)

Nyeri Nyeri yang berasal dari organ internal bersifat difusse

Visceral:
(menyebar) dan sulit dilokalisasi

Pasien sering menunjukkan lokasi nyeri yang bukan

berasal dari organ yang terganggu melainkan
menunjukkan daerah permukaan tubuh yang
berhubungan dengan organ tersebut
mechanism
2 mechanisms:
- Dermatomal rule
- Convergence-projection theory
• Dermatomal rule
When pain is referred, it is usually to a structure that developed from
the same embryonic segment of dermatome ass the structure in which
the pain orginates.
• For instance:
The heart and the inner aspect of left arm
Testicle and ureter+kidney
• Convergence-projection theory
Convergence of somatic and visceral pain fibers on the same second-
order neurons in the dorsal horn that project to the thalamus and then
to the somatosensory cortex
Referred pain
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Dermatome Kulit
Thank you