Pain Management:

an introduction
Objectives

✤ Definition
✤ Classification
✤ Physiology
✤ Assessment
✤ Management
✤ Anesthesia and Pain
An unpleasant sensory or emotional
experience associated with actual or potential
damage, or described in terms of such
damage

International Association for The Study of Pain (IASP)

✤ Subjective phenomenon

✤ Tissue damage may not always lead to perception of

pain and perception of pain may not be related to tissue
damage

✤ Multidimensional

✤ pain location, intensity, temporal aspects, quality,

impact and meaning
Classification(s)

✤ Acute and Chronic Pain ✤ Inflammatory Pain,

Neuropathic Pain,
✤ Cancer Pain Idiopathic Pain
✤ Nociceptive and ✤ Neuropathic Pain
Neuropathic Pain
✤ Nociceptive Pain
✤ Visceral and Somatic
Pain
✤ Chronic Pain
Acute Pain
✤ Brief periods of time and is associated with temporary
disorders
✤ Pain of less than 3 to 6 months duration

Chronic Pain
✤ Continuous and recurrent
✤ Pain lasting for more than 3-6 months, or persisting
beyond the course of an acute disease, or after tissue
healing is complete.
Nociceptive
✤ Represents the normal response to noxious insult or injury of
tissues such as skin, muscles, visceral organs, joints, tendons, or
bones.
✤ Examples include:
✤ Somatic
✤ Musculoskeletal (joint pain, myofascial pain), cutaneous; often
well localized
✤ Visceral
✤ Hollow organs and smooth muscle; usually referred
Neuropathic
✤ Pain initiated or caused by a primary lesion or disease in the
somatosensory nervous system.
✤ Sensory abnormalities range from deficits perceived as numbness
to hypersensitivity (hyperalgesia or allodynia), and to paresthesias
such as tingling.
✤ Examples include,
✤ Diabetic neuropathy, postherpetic neuralgia, spinal cord injury
pain, phantom limb (post-amputation) pain, and post-stroke
central pain.
Inflammatory
✤ Activation and sensitization of the nociceptive pain pathway by a
variety of mediators released at a site of tissue inflammation.
✤ The mediators that have been implicated as key players are
proinflammatory cytokines such IL-1-alpha, IL-1-beta, IL-6 and TNF-
alpha, chemokines, reactive oxygen species, vasoactive amines, lipids,
ATP, acid, and other factors released by infiltrating leukocytes,
vascular endothelial cells, or tissue resident mast cells
✤ Examples
✤ Appendicitis, rheumatoid arthritis, inflammatory bowel disease,
and herpes zoster.
✤ Cancer Pain
✤ Genetic and environmental factors

✤ Sensitization resulting in persistent (chronic) pain

✤ Nociceptors

✤ Signal acute pain

✤ Chronically sensitized

✤ Persistent pathological pain disorders

Chronic pain
✤ Abnormal state and function of the spinal cord neurons: hyperactive
✤ Increased transmitter release by spontaneously active primary afferent
neurons
✤ Increased responsiveness of postsynaptic receptors (in part due to
phosphorylation of glutamate-activated NMDA receptors)
✤ Release of biologically active factors from activated glia.
✤ Aggravated by the loss of inhibitory interneurons involved in the
modulation of pain.
✤ Transduction

✤ Noxious thermal, chemical, or mechanical stimuli are

converted into an action potential.

✤ Transmission

✤ Conduction of action potential through the nervous

system via the first-, second-, and third-order neurons
(dorsal root ganglion, dorsal horn, and thalamus)
✤ Modulation

✤ Alteration of afferent neural transmission along the

pain pathway (inhibition or augmentation)

✤ Perception

✤ Integration of painful input into the somatosensory

and limbic cortices
Transmission

Aδ fibres
Fast, sharp and well localized sensation (first pain)

C fibres
Duller slower onset and often poorly localized sensation (second pain)
Modulation: Peripheral Modulation

mediated by release of algogens like histamine,

Primary
bradykinin, PGE2 and leukotrienes from damaged
Hyperalgesia
tissues.

✤ Nociceptors and their neurons display sensitization following

repeated stimulation.
✤ Decrease in threshold
✤ Increase in frequency response
✤ Decrease in response latency and spontaneous firing even after
cessation of the stimulus (after discharges)
Modulation: Peripheral Modulation

Neurogenic inflammation
Secondary
Triple response of flare, local edema and
Hyperalgesia
sensitization to noxious stimuli.

Antidromic release
of substance P (sP)
from collateral
axons of primary
afferent neurons.
Substance P
✤ degranulates histamine and
serotonin
✤ vasodilates blood vessels
✤ tissue edema and induces
formation of leukotrienes.
Modulation: Central Modulation

✤ Facilitate or inhibit pain.

✤ The mechanisms for facilitation
✤ Windup and sensitization of second order neurons.
✤ Receptive field expansion
✤ Hyper excitability of flexion responses.
✤ Neurochemical mediators
✤ sP , CGRP , VIP , cholecystokinin, angiotensin, galanin, L-glutamate
and L-aspartate.
Inhibitory mechanisms

Segmental inhibitory mechanism

✤ Activation of large afferent fibres subserving epicritic sensation

inhibitory WDR neuron and spinothalamic activity.
✤ Inhibitory neurotransmitters (amino acids)
✤ Glycine and γ-amino butyric acid (GABA)

✤ Segmental inhibition
✤ Mediated by GABA receptor activity
b
✤ Increases K+ conductance across the cell membrane.
 Supraspinal inhibitory mechanism

✤ Supraspinal structures

✤ Send fibres down the spinal

cord to inhibit pain at the level
of the dorsal horn.
✤ Periaqueductal gray, reticular
formation, and nucleus raphe
magnus (NRM).
✤ Pre-synaptically on the primary
afferent neurons
✤ Post-synaptically on second-
order neurons (or interneurons).
Supraspinal inhibitory mechanism

✤ Inhibitory pathways utilise monoamines

✤ Noradrenaline and Serotonin terminate on nociceptive

neurons in the spinal cord

✤ Spinal inhibitory interneurons which store and release opioids.

✤ Noradrenaline mediates this action through α2 receptors.

✤ Endogenous opiate system

✤ Enkephalins and β-endorphins (Presynaptically)

✤ Exogenous opiates act (postsynaptically)

Central Sensitization
Normosensitivity
Neuropathic Pain
Hyperalgesia
Allodynia
Why does chronic pain exist?

✤ Genetic and environmental factors

✤ Sensitization resulting in persistent (chronic) pain
✤ Nociceptors
✤ Signal acute pain
✤ Chronically sensitized
✤ Persistent pathological pain disorders
Chronic pain
✤ Abnormal state and function of the spinal cord neurons:
Hyperactive
✤ Increased transmitter release by spontaneously active primary
afferent neurons
✤ Increased responsiveness of postsynaptic receptors (in part due
to phosphorylation of glutamate-activated NMDA receptors)
✤ Release of biologically active factors from activated glia.
✤ Aggravated by the loss of inhibitory interneurons involved in
the modulation of pain.
✤ If sensitization persist

✤ Chronic pain and hyperalgesia

✤ Injury of the nervous system (chronic neuropathic

pain)

✤ Imaging studies

✤ Chronic pain is accompanied by permanent structural

alterations in specific brain areas that play a crucial role
in nociception
Acute Pain Chronic Pain

✤ Post-operative
✤ Cancer pain

✤ Obstetric - Labor
✤ Cancer related

✤ Burns
✤ From cancer therapy

✤ Trauma
✤ Cancer unrelated

✤ Infective / Inflammatory
✤ Non-cancer
conditions ✤ Nociceptive
✤ Ischaemic pain ✤ Neuropathic
✤ Visceral pain ✤ Idiopathic
Assessment and
Diagnosis
How to Asses and Diagnose

✤ Regularly screen all patients for pain and perform a comprehensive

pain assessment when pain is present
✤ Set the Stage.
✤ Understand that pain is a multidimensional phenomenon
✤ A thorough history and physical exam
✤ Include thorough neurological and musculoskeletal examinations.
✤ Additional testing, such as imaging and laboratory studies or
electrodiagnostic testing (EMG/nerve conductions)
✤ NIPS (Neonatal Infant Pain Score)
✤ Neonatus (0- 28 hari)
✤ Prematur usia konsepsi < 40 minggu
✤ FLACC (Face, Leg, Activity, Cry, Consolability) score
✤ Bayi 28 hari sampai 1 tahun
✤ Anak usia 1 -3 tahun atau yang belum bisa bicara
✤ Anak lebih 3 tahun menggunakan FACES score
✤ Behavioral Pain Score (BPS)
✤ Pasien penurunan kesadaran dan pasien ICU dalam
sedasi
NIPS (Neonatal Infant Pain Score)
Ekspresi Wajah Relaks 2
Meringis 1

Menangis Tidak menangis 0
Merengek 1
Menangis kencang 2

Pola napas Relaks 0
Perubahan pola nafas 1

Lengan Tertahan/Relaks 0
Fleksi/Ekstensi 1

Tungkai Tertahan/Relaks 0
Fleksi/Ekstensi 1

Respon rangsangan Tidur/tenang 0

Rewel 1
NIPS

✤ Nyeri ringan: > 2

✤ Nyeri sedang: 2 - 4
✤ Nyeri berat : 4 - 7
 Skala FLACCS

Wajah Tidak ada ekspresi yang khusus (seperti 0
senyum)
Kadang meringis atau mengerutkan dahi, 1
menarik diri
Sering / terus menerus mengerutkan 2
dahi, rahang mengatup, dagu bergetar

Posisi normal / rileks 0

Ekstremitas Tidak tenang, gelisah, tegang 1
Menendang atau menarik kaki 2

Berbaring tenang, posisi normal, 0
Gerakan bergerak mudah
Menggeliat-geliat, bolak-balik 1
berpindah, tegang
Posisi tubuh meringkuk, kaku / spasme 2
atau menyentak

 Skala FLACCS


Menangis Tidak menangis 0
Merintih, merengek, kadang mengeluh 1
Menangis tersedu-sedu, terisak-isak, 2
menjerit

Kemampuan Senang, rileks 0
Ditenangkan Dapat ditenangkan dengan sentuhan, pelukan, 1
atau berbicara, dapat dialihkan.
Sulit/ tidak dapat ditenangkan dengan 2
pelukan, sentuhan atau distraksi.
Skala FLACCS

✤ Nyeri ringan: < 4/10

✤ Nyeri sedang: 4 – 6
✤ Nyeri berat: > 7/10
 Behavioral Pain Scale (BPS)
Ekspresi Wajah
Tenang 1
Sebagian Muka menegang (Dahi mengerenyit) 2
Seluruh muka menegang (kelopak mata menutup) 3
Wajah menyeringai 4
Pergerakan atau posisi ekstremitas atas
Tenang 1
Menekuk sebagian didaerah siku 2
Menekuk total dengan disertai jari-jari mengepal 3
Menekuk total secara terus menerus 4
Toleransi terhadap ventilasi mekanik
Dapat mengikuti pola ventilasi 1
Batuk tetapi masih dapat mengikuti pola ventilasi 2
Melawan pola ventilasi 3
Pola ventilasi tidak ditoleransi 4
Skala BPS

✤ Nyeri ringan < 6/12

✤ Nyeri sedang 6-8
✤ Nyeri berat > 9/12
QISS-TAPED

Besides sensations you consider to be

Q Quality "pain," are there other unusual
sensations, such as numbness?
(Anxiety screen) Do you feel stressed or
I Impact nervous? Have you been particularly
anxious about anything? Do you startle
easily?
Does the pain move/radiate anywhere?
S Site Has the location changed over time?

How often are you in severe pain?

S Severity (hours in a day, days a week you have
pain)?
 Is there a predictable pattern? (e.g.,
Temporal always worst in the morning or in the
T
Characteristics evening? Does it suddenly flare up?)

What makes the pain worse? When do

Aggravating and you get the best relief? How much relief
A
Alleviating Factors do you get? How long does it last?

Have you tried spinal or other injections

Past Response, for pain treatment? What was done? Was
P
Preferences it helpful?

What are you most afraid of? (Uncovers

Expectations, specific fears, such as fear of cancer, which
E
Goals, Meaning should be acknowledged and addressed.)

Review imaging, laboratory and/or other

Diagnostics & test results as indicated
D
Physical Exam
Differential diagnosis for the
individual case
✤ Medical diagnoses related to the pain: underlying diagnoses causing pain (for
example; osteoarthritis, cellulitis, diabetic peripheral neuropathy, etc.)
✤ Pain type (acute, neuropathic, visceral, etc.), intensity, impact on quality of life and
function
✤ Medical comorbidities contributing to pain and/or affecting treatment:
✤ Cardiovascular, cerebrovascular or neuromuscular diseases
✤ Medications that may interfere with the usual choices of drug or nondrug
treatments. Some treatments may be contraindicated in patients on anticoagulants,
or with an uncorrected bleeding disorder, active infection, pregnancy,
immunosuppressive therapy, or other issues.
✤ Psychosocial issues and patient's ability to cope with pain
✤ Factors that impact treatment planning and may affect response to treatment include
depression, anxiety, negative emotions, past experiences, illness perception, alcohol
dependence, substance abuse and current social situations.
Management
Date
Principles

✤ Establishes goals, expectations, methods and time course

✤ Pain cannot be treated on the basis of pain intensity alone,
✤ Outline goals explicitly and discuss them carefully with the
patient.
✤ What is meaningful pain relief?
WHO Analgesic Ladder for Cancer Pain
Modified WHO Analgesic Ladder
✤ Fourth step

✤ Neurosurgical procedures such as brain stimulators.

✤ Invasive techniques,

✤ nerve blocks and neurolysis (eg, phenolization,

alcoholization, thermocoagulation, and radiofrequency

✤ Pediatric Pain Management

✤ Acute pain in emergency and postoperative

✤ Treatment of crises of chronic pain

✤ Moderate evidence

✤ transforaminal epidural steroid injections, lumbar

percutaneous adhesiolysis, and spinal endoscopy for
painful lumbar radiculopathy

✤ Limited evidence

✤ intradiscal treatments in low back pain.

✤ Medullar and peripheral stimulators

✤ Opioids

✤ Newer administration method

✤ Promoting opioid as a safe treatment for chronic

noncancer pain patients

✤ Methadone

✤ very useful in the treatment of cancer pain, chronic

noncancer pain, and refractory neuropathic pain that
does not respond to conventional treatment.

✤ rotation of opioids in cancer pain.

✤ Bidirectional fashion:

✤ Slower upward pathway for chronic pain and cancer pain,

✤ Faster downward direction for intense acute pain, uncontrolled

chronic pain, and breakthrough pain.

✤ One can ascend slowly one step at a time in the case of chronic
pain

✤ Increase the rate of climb according to the intensity of the pain.

✤ Start directly at the fourth step, in extreme cases, to control pain of

high intensity, using patient-controlled analgesia pumps for
continuous intravenous, epidural, or subdural administration.

✤ When the pain is controlled, one can “step down”

Treatment Principles and Methods

✤ Combine multiple modalities/disciplines

✤ Medications, invasive interventions, rehabilitation, integrative

medicine, as well as psychological, spiritual, and vocational/

occupational interventions
✤ There are very few situations when a multimodal approach

(combination of pharmacologic and nonpharmacologic

strategies) is not appropriate or necessary
✤ Educate and communicate with patients and caregivers
✤ Collaborative care, shared decision-making with their providers,

and chronic disease self-management have improved health

outcomes
✤ 5 Rs

✤ Right analgesic(s)

✤ Right route

✤ Right dose

✤ Right dosing interval (scheduled dosing vs PRN

dosing)

✤ Right message
Adjuvants
✤ Steroids ✤ Sodium channel blockers
✤ Anxiolytics ✤ N-methyl-d-aspartate receptor
antagonists
✤ Antidepressants
✤ Hypnotics
✤ Anticonvulsants
✤ Antiepileptic-like
gabapentinoids (gabapentin
and pregabalin)
✤ Membrane stabilizers
 Routes of Administration
✤ Use the oral route whenever possible
✤ Oral ✤ IV ✤ Except e.g. post op period,
✤ Rectal ✤ TTS ✤ Try other routes e.g.

✤ buccal, sublingual, or rectal routes

✤ SQ ✤ Neuraxial.
before initiating parenteral routes

✤ IM ✤ Others ✤ Parenteral:

✤ SQ and IV preferred & feasible for

short-term therapy

✤ Always avoid IM.

✤ Oral and transdermal: preferred

Nonpharmacologic Interventions

✤ Cognitive-behavioral approaches
✤ Passive relaxation with mental imagery, distraction, progressive

relaxation, biofeedback, hypnosis, and music therapy.

✤ Help patients understand more about their pain, alter their pain

behavior and coping skills, and change their perception of pain.

✤ Physical techniques
✤ Applications of heat and cold, massage, exercise, and

transcutaneous nerve stimulation.

✤ reduce pain by altering the physiologic response and providing the

patient with some sense of control over the pain.

Referral

✤ Active suicidal ideation or significant untreated affective disorder -

psychiatric and psychological referral
✤ Active addictive disorder, or aberrant drug-related behavior when an
addiction diagnosis is uncertain - addiction medicine referral
✤ When interventional (injection) approaches are considered for
diagnosis or treatment - referral to interventional pain specialist
✤ Suspected collagen-vascular disorder or other inflammatory/arthritic
process - rheumatology referral
✤ Suspected active/progressive neurologic disease - neurology referral.
Responsible Opioid Prescribing

✤ Evaluation of the patient

✤ Development of a treatment plan
✤ Informed consent and agreement for treatment
✤ Periodic review
✤ Consultation
✤ Maintenance of comprehensive medical records
✤ Compliance with controlled substances laws and regulations
 SUMMARY
✤ 1st step: is the good pain assessment.

✤ Pain medications must be taken

✤ when the pain is first perceived.

✤ Doses of opioids are increased:

✤ with the patient’s report of pain

✤ Adjuvant medications are used for:

✤ opioid non-responsive & neuropathic

pain.

✤ Non-pharmacologic approaches are always a

part of any pain management protocol.