PENGELOLAAN NYERI

JOKO MURDIYANTO

NYERI PERSALINAN
DIPANDANG DARI
SUDUT ANESTESI
JOKO MURDIYANTO

DEFINISI
Pain is Unpleasant sensory
and emotional experience
associated with actual or
potential tissue damage, or
describe in terms of such
damage (IASP)

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Pain Experience

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Pain is a personal, subjective experience that comprises :

Sensory-discriminative, Motivational-affective and Cognitiveevaluative dimensions
Ronald Melzack, Textbook of Pain 4th edition

What is Pain?

An unpleasant sensory & emotional experience associated with

actual or potential tissue damage, or described in terms of such
damage
The International Association for the Study of Pain

Subjective sensation
Pain Perceptions based on expectations, past experience, anxiety,
suggestions
Affective ones emotional factors that can affect pain experience
Behavioral how one expresses or controls pain
Cognitive ones beliefs (attitudes) about pain
Physiological response produced by activation of specific types of
nerve fibers
Experienced because of nociceptors being sensitive to extreme
mechanical, thermal, & chemical energy.
Composed of a variety of discomforts
One of the bodys defense mechanism (warns the brain that tissues
may be in jeopardy)
Acute vs. Chronic
The total person must be considered. It may be worse at night
when the person is alone. They are more aware of the pain
because of no external diversions.

Pain

Acute vs. Chronic

Acute pain is usually related to an
easily identified event or condition.
Chronic pain may or may not be
related to an easily identified
pathophysiologic phenomenon,
may be multifactorial, and may be
present for an indeterminate
period of time.

Where Does Pain Come From?

Cutaneous Pain sharp, bright,

burning; can have a fast or slow onset

Deep Somatic Pain stems from

tendons, muscles, joints, periosteum,
& b. vessels

Visceral Pain originates from

internal organs; diffused @ 1st & later
may be localized (i.e. appendicitis)

Psychogenic Pain individual feels

pain but cause is emotional rather than
physical

Pain Sources

Fast vs. Slow Pain

Fast localized; carried through A-delta axons in skin
Slow aching, throbbing, burning; carried by C fibers
Nociceptive neuron transmits pain info to spinal cord
via unmyelinated C fibers & myelinated A-delta fibers.
The smaller C fibers carry impulses @ rate of 0.5 to
2.0 m/sec.
The larger A-delta fibers carry impulses @ rate of 5
to 30 m/sec.

Acute vs. Chronic

What is Referred Pain?

Occurs away from pain site

Examples: McBurneys point, Kerrs sign

Types of referred pain:

Myofascial Pain trigger points, small hyperirritable

areas within a m. in which n. impulses bombard CNS &
are expressed at referred pain
Active hyperirritable; causes obvious complaint
Latent dormant; produces no pain except loss of ROM

Sclerotomic & Dermatomic Pain deep pain; may

originate from sclerotomic, myotomic, or dermatomic
n. irritation/injury
Sclerotome: area of bone/fascia that is supplied by a single

n. root
Myotome: m. supplied by a single n. root
Dermatome: area of skin supplied by a single n. root

Terminology

Noxious harmful, injurious

Noxious stimuli stimuli
that activate nociceptors
(pressure, cold/heat
extremes, chemicals)
Nociceptor nerve receptors
that transmits pain impulses
Pain Threshold level of
noxious stimulus required to
alert an individual of a
potential threat to tissue
Pain Tolerance amount of
pain a person is willing or
able to tolerate
Accommodation
phenomenon adaptation by
the sensory receptors to
various stimuli over an
extended period of time (e.g.
superficial hot & cold agents).
Less sensitive to stimuli.

Hyperesthesia abnormal
acuteness of sensitivity to
touch, pain, or other
sensory stimuli
Paresthesia abnormal
sensation, such as
burning, pricking, tingling
Inhibition depression or
arrest of a function
Inhibitor an agent
that restrains/retards
physiologic, chemical,
or enzymatic action
Analgesic a neurologic or
pharmacologic state in
which painful stimuli are
no longer painful

Questions to Ask about Pain

Pattern: onset & duration

Area: location
Intensity: level
Nature: description

Questions to Ask about

Pain
P Q R S T (ECG format)
Provocation How the injury occurred & what
activities the pain
Quality - characteristics of pain Aching
(impingement), Burning (n. irritation), Sharp
(acute injury), Radiating within dermatome
(pressure on n.)?
Referral/Radiation
Referred site distant to damaged tissue that
does not follow the course of a peripheral n.
Radiating follows peripheral n.; diffuse
Severity How bad is it? Pain scale
Timing When does it occur? p.m., a.m., before,
during, after activity, all the time

Questions to Ask about

L O CPain
ATES
L Location.
O Other Symptoms.
C Character: deep, burning, throbbing
A Aggravating and Alleviating factors.
T Timing.
E Effect: your daily routine?
S Severity.

Types of Nerves

Afferent (Ascending) transmit

impulses from the periphery to the
brain
First Order neuron
Second Order neuron
Third Order neuron
Efferent (Descending) transmit
impulses from the brain to the
periphery

First Order Neurons

Stimulated by sensory receptors

End in the dorsal horn of the spinal cord
Types
A-alpha non-pain impulses
A-beta non-pain impulses

Large, myelinated
Low threshold mechanoreceptor; respond to light touch

& low-intensity mechanical info

A-delta pain impulses due to mechanical pressure

Large diameter, thinly myelinated
Short duration, sharp, fast, bright, localized sensation

(prickling, stinging, burning)

C pain impulses due to chemicals or mechanical

Small diameter, unmyelinated
Delayed onset, diffuse nagging sensation (aching,

throbbing)

Second Order Neurons

Receive impulses from the FON in the dorsal

horn

Lamina II, Substantia Gelatinosa (SG) - determines

the input sent to T cells from peripheral nerve
T Cells (transmission cells): transmission cell that

connects sensory n. to CNS; neurons that organize

stimulus input & transmit stimulus to the brain

Travel along the spinothalmic tract

Pass through Reticular Formation

Types

Wide range specific

Receive impulses from A-beta, A-delta, & C

Nociceptive specific
Receive impulses from A-delta & C

Ends in thalamus

Third Order Neurons

Begins in thalamus
Ends in specific brain centers
(cerebral cortex)
Perceive location, quality, intensity
Allows to feel pain, integrate past
experiences & emotions and
determine reaction to stimulus

Descending Neurons

Descending Pain Modulation (Descending

Pain Control Mechanism)
Transmit impulses from the brain
(corticospinal tract in the cortex) to the spinal
cord (lamina)

Periaquaductal Gray Area (PGA) release

enkephalins
Nucleus Raphe Magnus (NRM) release serotonin
The release of these neurotransmitters inhibit
ascending neurons

Stimulation of the PGA in the midbrain & NRM

in the pons & medulla causes analgesia.
Endogenous opioid peptides - endorphins &

Neurotransmitters

Chemical substances that allow nerve impulses to move

from one neuron to another
Found in synapses
Substance P - thought to be responsible for the
transmission of pain-producing impulses
Acetylcholine responsible for transmitting motor nerve
impulses
Enkephalins reduces pain perception by bonding to pain
receptor sites
Norepinephrine causes vasoconstriction
2 types of chemical neurotransmitters that mediate pain
Endorphins - morphine-like neurohormone; thought to
pain threshold by binding to receptor sites
Serotonin - substance that causes local vasodilation &
permeability of capillaries
Both are generated by noxious stimuli, which activate
the inhibition of pain transmission
Can be either excitatory or inhibitory

Sensory Receptors

Mechanoreceptors touch, light or deep

pressure

Thermoreceptors - heat, cold

Krauses end bulbs ( temp & touch), Ruffini

corpuscles (in the skin) touch, tension, heat; (in
joint capsules & ligaments change of position)

Proprioceptors change in length or

tension

Meissners corpuscles (light touch), Pacinian

corpuscles (deep pressure), Merkels corpuscles
(deep pressure)

Muscle Spindles, Golgi Tendon Organs

Nociceptors painful stimuli

mechanosensitive
chemosensitive

Nerve Endings

A nerve ending is the termination of a nerve fiber

in a peripheral structure. (Prentice, p. 37)

Nerve endings may be sensory (receptor) or motor
(effector).
Nerve endings may be:
Respond to phasic activity - produce an impulse
when the stimulus is or , but not during
sustained stimulus; adapt to a constant stimulus
(Meissners corpuscles & Pacinian corpuscles)
Respond to tonic receptors produce impulses as
long as the stimulus is present. (muscle spindles,
free n. endings, Krauses end bulbs)
Superficial Merkels corpuscles/disks, Meissners
corpuscles
Deep Pacinian corpuscles,

Nerve Endings

Merkels corpuscles/disks Sensitive to touch &

vibration
Slow adapting
Superficial location
Most sensitive
Meissners corpuscles
Sensitive to light touch
& vibrations
Rapid adapting
Superficial location
Pacinian corpuscles Sensitive to deep
pressure & vibrations
Rapid adapting
Deep subcutaneous
tissue location

Krauses end bulbs

Thermoreceptor
Ruffini corpuscles/endings
Thermoreceptor
Sensitive to touch &
tension
Slow adapting
Free nerve endings Afferent
Detects pain, touch,
temperature,
mechanical stimuli

Nociceptors

Sensitive to repeated or prolonged

stimulation
Mechanosensitive excited by stress &
tissue damage
Chemosensitive excited by the release
of chemical mediators
Bradykinin, Histamine, Prostaglandins,
Arachadonic Acid
Primary Hyperalgesia due to injury
Secondary Hyperalgesia due to
spreading of chemical mediators

Pain Control Theories

Gate Control Theory
Central Biasing Theory
Endogenous Opiates Theory

Gate Control Theory

Melzack & Wall, 1965

Substantia Gelatinosa (SG) in dorsal horn of
spinal cord acts as a gate only allows one
type of impulses to connect with the SON
Transmission Cell (T-cell) distal end of the
SON
If A-beta neurons are stimulated SG is
activated which closes the gate to A-delta &
C neurons
If A-delta & C neurons are stimulated SG is
blocked which closes the gate to A-beta
neurons

Gate Control Theory

Gate - located in the dorsal horn of the spinal cord

Smaller, slower n. carry pain impulses
Larger, faster n. fibers carry other sensations
Impulses from faster fibers arriving @ gate 1st inhibit
pain impulses (acupuncture/pressure, cold, heat, chem. skin
irritation).
Brain

Gate (T
cells/ SG)

Pain
Heat, Cold,
Mechanical

Central Biasing Theory

Descending neurons are activated

by: stimulation of A-delta & C
neurons, cognitive processes,
anxiety, depression, previous
experiences, expectations
Cause release of enkephalins (PAG)
and serotonin (NRM)
Enkephalin interneuron in area of
the SG blocks A-delta & C neurons

Endogenous Opiates Theory

Least understood of all the theories

Stimulation of A-delta & C fibers causes

release of B-endorphins from the PAG & NRM

ACTH/B-lipotropin is released from the

anterior pituitary in response to pain broken
down into B-endorphins and corticosteroids

Mechanism of action similar to enkephalins

to block ascending nerve impulses

Examples: TENS (low freq. & long pulse

duration)

Goals in Managing Pain

Reduce pain!
Control acute pain!
Protect the patient from further
injury while encouraging
progressive exercise

Other ways to
control pain

Encourage central biasing motivation,

relaxation, positive thinking
Minimize tissue damage
Maintain communication w/ the athlete
If possible, allow exercise
Medications

Empat tahap fisiologi nyeri :

Proses transduksi Proses dimana suatu
rangsang nyeri (noxious stimuli) diubah menjadi
suatu aktifitas listrik, yang akan diterima oleh
ujung-ujung saraf.
Proses transmisi Sebagai perambatan rang
sang melalui saraf sensoris menyusul proses
transduksi.
Proses modulasi Proses dimana terjadi
interaksi antara sistem analgesik endogen
dengan asupan nyeri yang masuk ke kornu
posterior.
Persepsi Hasil akhir dari proses yang
kompleks dan unik yang menghasilkan suatu
perasaan yang subyektif.

Type or Category of Pain

3. Psychogenic
clear that
no somatic disorder
is present
1. Nociceptive
Caused by activity
in neural pathways
in response to potentially
tissue-damaging stimuli

fracture /
Postoperative
Ongoing or
impending injury

4. Mixed type
Caused by a
combination of both
primary injury or
secondary effects

2. Neuropathic
Initiated or caused by
primary lesion or
dysfunction
in the nervous sys.

sprain
Inflamation /
Infection
Muscle Stretch

strangulated
(scar tissue)
Sciatica

inflamed (infection )

Infiltrated or compressed
(tumors)

The Assessment of the Patient with Pain, Steven Richeimer, M.D. Director USC Pain Management, USC Medical Center, Los Angeles, CA, USA, 2007

1.

Goal
s

2.

3.

Pain Assessment

Metho
ds

1.
2.

Define the severity of

pain
Assist in the selection
of appropriate
analgesia
Evaluate the response
to treatment

Self Report
Team Approach

History
Past Medical History
Current Medications

The Methodology
of Pain Assessment

Physical Examination
Special Test
Psychological
Evaluation

The Assessment of the Patient with Pain, Steven Richeimer, M.D. Director USC Pain Management, USC Medical Center, Los Angeles, CA, USA, 2007

BASIC
LISTEN
2. LOCATE
3. LOOK
1.

Location: Patient or nurse marks drawing

Intensity: Patient rates the pain. Scale Used:

Quality: Use patints words, e.g. prick, ache, burn, sharp, hot etc.
Onset, duration, variations, rhythms (spontaneus or evoked):
Manner of expressing pain: (Pain Behaviour)
What relieves the pain?

What causes or increases the pain?

Effect of pain: (Note decreased function, decreased quality of life)
Accompanying symptoms (eg nausea)
Sleep
Appetite
Physical activity
Relation with others (eg irritability)
Emotion (eg anger, suicidal, crying)
Consentration
Other

Other comments:
Plan:

Pain Assessment Scales

Uni-Dimensional Scale
Only measures pain intensity
Appropriate for acute pain
The most common scale used in
outcome assessment (Analgesic
efficacy)

Verbal Rating Scale (VRS)

None, mild, moderate, severe
Numeric Rating Scale (NRS)
Visual Analog Scale (VAS)
Pictorial Scale

Multi-Dimensional Scale
Both intensity (severity) and
unpleasantness (affective)
Appropriate for chronic pain
Research /pathophysiology
Should be used in clinical
outcome assessment

McGill Pain Questionnaire (MPQ)

The Brief Pain Inventory (BPI)
The Memorial Pain Assessment Card

Photographic/Numeric Pain Scale

Modified
McGill Pain
Questionnaire
15 Minutes

Sensorik
Afektif
Evaluatif
Macam2
IRN
INS
71,4% Baik
28,6% Lumayan
dan sedang
(Meliala, 1999)

Treatment
Relief

General Activity
Mood
Walking ability

Worst

Normal work

Least

Relation with other people

Sleep

Average
Enjoyment of life
Right Now

Quicker and easier

Well established
reliability in cancer,
arthritis, and AIDs.
Sensory, affective and
functional status
Useful for treatment
response
Takes up to 15 min
Good choice for patients
with progressive
disease

ultimodal Pain Management

Coordinated use of medication & non medication
to control the pain
Consider the psycho-socio-cultural-spiritual aspects
Acute pain interventions
Treatment
Methods

Remove the
cause
of pain

Surgery
Splinting

Drug therapy

Non-opioid
Aspirin & other

NSAIDs
Paracetamol
Combinations

Opioid

High-tech

Morphine Epidural infusion

Local anaesthetic
Others
+ opioid

McQuary, 2000
An evidence-based resource for pain relief,

Physical
methods

Regional
analgesia

Low-tech
Nerve bloks
Local
anesthetic
+ opioid

Psychological
approaches

Physiotherapy Psychoprophylaxis
Manipulation
TENS
Acupunture
Ice

Relaxation
Hypnosis

Multimodal Analgesia
OPIOID
- Systemic
- Epidural
- Subarach
Ketamin,
Tramadol
COX-2, COX-3

PERCEPTION
Pain

MODULATION

Descending
modulation
Ascending
input

Dorsal
Horn

LOCAL ANESTHETIC
- Epidural
-Subarachnoid
-Peripheral nerve
block
Dorsal root
ganglion

TRANSMISSI
ON
Spinothalami
c
tract

Peripheral
nerve

LA
COX1
COX2

TRANSDUCTION

Peripheral
nociceptors

No single drug can produce optimal analgesia

adverse
effect
Adapted from Gottschalk A etwithout
al. Am Fam Physician.
2001;63:1981,
and Kehlet H et al. Anesth Analg. 1993;77:1049.

Trauma

WHO Pain Ladder

http://erlewinedesign.com/end-of-life-care/gfx/who_ladder.gif

AKIBAT KELOLA NYERI YANG TIDAK

ADEKUAT
1.Kardivaskuler
2.Paru

3.Gastrointestinal
4.Ginjal
5.Koagulasi
6.Imunologi
7.Otot

8.Psikis

1.Takikardi, Hipertensi,
Naiknya kerja jantung
2.Spasme otot nafas,
penurunan VC, atelektasis,
arterial hypoxemia,
naiknya risiko infeksi paru.
3.Ileus pascaoperasi.
4.Retensi urin, risiko oliguri.
5.Risiko tromboemboli.
6.Gangguan fungsi imunitas.
7.Kelemahan otot, kelelahan,
mobilitas terbatas, risiko
tromboemboli.
8.Ansietas, ketakutan,
frustasi, rasa tidak
nyaman.

Adult dosing guidelines for non-opioid

analgesics
DRUG
ROUTE

Paraaminophenols
Salicylates

DOSE
Oral
Oral

Ibuprofen
Ketoprofen
Indomethacin
Ketorolac

Oral
Oral
Oral
IV

Diclofenac Potassium
Meloxicam
Piroxicam
Elexoxib

Oral
Oral
Oral
Oral

500-1000 mg/4-6hr
max dose adults
4000 mg.
500-1000 mg/4-6hr
max dose adults
4000 mg.
400 mg/4-6hr.
25-50 mg/6-8hr.
25mg/8-12hr.
30mg initial.1530mg/
6-8hr not >5 days.
50 mg/8hr.
7.5-15 mg/24hr.
20-40 mg/24hr.
100-200 mg/12hr

Opioids Analgesic
1.Morphine iv dose 0.1 mg/kg with
additional doses of 0.05 mg/kg.
2.Meperidine iv dose 1 mg/kg with
additional doses 0.5 mg/kg.
3.Fentanyl iv dose 2 3 mcg/kg with
additional doses titrated by 0.5 mcg/kg
until desired level of analgesia is reached.

Paediatrics
Morphine (i.d. 0.05 0.1 mg/kg iv, then
titrate, maximum 10 mg/dose.
or
Fentanyl (i.d 1-2 g/kg, then titrate,
maximum 100 g/dose)

TERIMA KASIH
PERHATIANNYA
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