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Dr Hery Soebadiono Sp.S

RSK St Vinsentius A Paolo
SURABAYA
 Categorization of Pain Conditions
Central Pain Amplification
Nociceptive Pain Neuropathic Pain Inflammatory Pain

(ie, Burn) (ie, Herpes zoster) (ie, Rheumatoid arthritis) (ie, Fibromyalgia)

Noxious stimuli Neuronal damage Inflammation Abnormal pain

processing by CNS

Acute Pain Chronic Pain

Courtesy of Woolf C. Ann Intern Med. 2004;140:441-451.
3
Nociception: Neural Process of
Encoding Noxious Stimuli
 NOCICEPTION
•Between noxious stimulus and perception of pain lies a complex series of electrophysiology event,
collectively termed

•NOCICEPTION

•4 physiologic processes are involved:

1.Transduction
2.Transmission
3.Modulation
4.Perception
 Pain Perception
Depends on the balance between:
Excitatory system
Inhibitory system

(Cognitive, emotional, behavior)

 What is nociceptive pain?
• A sensory experience that occurs when specific
peripheral sensory neurons (nociceptors) respond to
noxious stimuli

• Painful region is typically localized at the site of injury

– often described as throbbing, aching or stiffness

• Usually time-limited and resolves when damaged

tissue heals (e.g. bone fractures, burns and bruises)
• Can also be chronic (e.g. osteoarthritis)
• Responds to conventional analgesics
Pain is a complex interaction that involves:

1. Cognitive
2. Emotional
3. Behavioral
 Nyeri  multidemensional
1. Sensory discriminative
 Menggambarkan kemampuan penderita
menceritakan dari mana asalnya nyeri.
 Seperti apa nyerinya: panas, cekot2, dll.
 Berat ringannya nyeri.
2. Cognitive demension
 Kemampuan membanding nyeri
sekarang dan masa lalu.
3. Affective or emotional demension
 Kemampuan penderita menggambarkan nyeri
seperti tidak menyenangkan, menderita sekali,
mengganggu dalam bekerja, dll.
4. Motivational Behaviour
 Menyebabkan penderita mencari pertolongan,
withdrawl reflex, dan escape behaviour.
 Nyeri bukan sensasi tunggal, tapi punya
banyak dimensi  tidak ada satu obat
yang mampu mengobati semua jenis
nyeri
Anger Anxiety

Fear
Depression
A

NOCICEPTIVE

Noxious Stimuli MELIALA, 2004

Acute Pain
 Acute Pain
 Generally sudden onset
– Certainly recent onset

– Usually has an obvious identifiable cause

• Injury/disease/iatrogenic (eg, surgery)

• Short duration (<1 month)
• Intensity generally variable and indicative
of severity of underlying condition or
situation
– Characteristic symptoms

• Redness, swelling, throbbing

– Characteristic behaviors
 Characteristics for Pain Treatment Facilities (IASP)
• 1. Pain Unit/ Pain Treatment Facility:
A generic term used to describe all forms of pain treatment facilities
without regard to personnel involved or types of patients served.
• 2. Multidisciplinary pain center:
An organization of health care professionals and basic scientists which
includes research, teaching and patient care related to acute and chronic
pain.
• 3. Multidisciplinary pain clinic:
A health care delivery facility staffed by physicians of different specialties
and other non-physician health care providers who specialize in the
diagnosis and management of patients with chronic pain. This type of
facility differs from a  Multidisciplinary Pain Center only because it does
not include research and teaching activities in its regular programs.
 Characteristics for Pain Treatment Facilities (IASP)

• 4. Pain clinic:
A health care delivery facility focusing upon the diagnosis and
management of patients with chronic pain. A pain clinic may specialize in
specific diagnoses or in pains related to a specific region of the body.
• 5. Modality-oriented clinic:
This is a health care facility which offers a specific type of treatment and
does not provide comprehensive assessment or management. Examples
include nerve block clinic, transcutaneous nerve stimulation clinic,
acupuncture clinic, biofeedback clinic, etc.
DOKUMENTASI
 KEBIJAKAN NYERI RS
• Tujuan pelayanan pasien nyeri:
1. Semua pasien nyeri mendapatkan pelayanan sesuai panduan
dan prosedur menejemen nyeri RS.
2. Menghindari dampak / risiko nyeri terhadap proses
penyembuhan
3. Memberikan kenyamanan pada pasien

• Dokter, perawat, fisioterapist yang terlibat dalam

penanganan nyeri telah mengikuti pelatihan menejemen
nyeri dan dinyatakan kompeten.
• Rumah sakit memiliki proses untuk mendidik staf
mengenai menejemen nyeri dengan melaksanakan
pelatihan manajemen nyeri
 DOKUMEN
Panduan Menejemen Nyeri
• PPK Nyeri Umum
• PPK Penyakit Nyeri
 Tim Nyeri RS
• Kolegium Nyeri (-)
• Komprehensif
– Anestesi : Nyeri Akut intensitas berat, Penguasaan obat
opioid, Familier dalam “Anestesi”, familier dalam
resusitasi
– Neurologi: Patofisiologi, mechanism based (central,
peripheral), pemeriksaan klinis dan penunjang klinis,
pain generator, familier dengan pendekatan personal
– Ortopedi, Rematologi dll
ALUR PENANGANAN NYERI RUMAH SAKIT
 Kebijakan Pelayanan Pasien Nyeri (TERDOKUMENTASI)

Asesmen Awal Nyeri Rawat Jalan Asesmen Awal Nyeri Rawat Inap

Periksa Pertama KALI Dan Setiap Kunjungan 24 Jam Pertama

Rencana Penatalaksanaan Pasien

Rencana Penatalaksanaan
Dengan Tujuan Terukur
Pasien Dengan Tujuan Terukur

Asesmen Ulang
Asesmen Ulang
Saat Kontrol
 Pain

Assessment of Disease Assessment of Pain

Diagnosis of Disease Diagnosis of Pain

Management of Disease Management of Pain

 The 3L Approach to Diagnosis

LISTEN
Patient verbal descriptors,
Q&A

LOCATE LOOK
Nervous system Sensory abnormalities,
lesion / dysfunction pattern recognition
 Pain Assessment

Assessment of Disease Assessment of Pain

1. Pain Intensity 2. Type of Pain 3. Comorbidity & Side Effects

Treatment
 STEP 1. PAIN INTENSITY
“An unpleasant sensory and emotional experience associated
with actual or potential tissue damage, or described in terms of
such damage.”

ACUTE PAIN CHRONIC PAIN

(<3 Mo) (> 3 Mo)

Multi-Dimensional Scale

Uni-Dimensional Scale McGill Pain Questionnaire (MPQ)

The Brief Pain Inventory (BPI)
The Memorial Pain Assessment Card
* Tool pengkajian nyeri

08/02/21
 NRS
PAIN
INTENSITY YES VRS Neonatal Infant Pain Scale (NIPS)
VAS 0 : No Pain
1-3 : Mild
4-5 : Moderate
6-7 : Severe
PATIENT ABLE
1-3 yo / Cognitive Disorder)
TO FLACC (Face, Legs, Activity, Cry and
COMMUNICATE Consolability)
WELL? (Score: 0-10)

3-8 yo
WB/Faces Pain Scale– Photographic
NO
(Score 0-10/no-Very Severe)

Sedation
Comfort Scale
9-17: Inadequate sedation and Pain Control
17-26 : Adequate Sedation and Pain Control
26-45: Over Sedation
 STEP 2. TYPE OF PAIN

Superficial Somatic Pain

Somatic
Nocicepthic Deep Somatic Pain
Visceral

Peripheral NP Hyper-Excitability
TYPE OF PAIN Neuropathic
Hyper-Excitability
Central NP
Loss of Inhibitory
FM
MFPS etc
Dysfunctional
Somatoform etc
 Elements for the physician

• Patient’s history
• characteristics of the pain,
• past and present pain managements strategies,
• past and present medical problems
• Physical examination :
• general site of pain
• musculoskeleteal system
• neurological system
• Diagnostic studies
• meant to supplement, not to replace a comprehensive
patient history and physical examination
 NEUROPATHIC PAIN

1. Pin Pricks
2. Electric Shock Like
3. Burning/Hot INTENSITY
4. Numbness
5. Alodinia

Gruccu G & Truini A, Tools for Assessing Neuropathic Pain, Plos Medicine, 2009
 Disfunctional Pain
Symptom Magnification Examination:

• Waddell signs: signs suggesting symptom magnification and

psychological distress:

– Superficial or non-anatomic or regional disturbance of motor or

sensory impairment
– Inconsistency
– Inappropriate/excessive verbalization of pain or gesturing
 STEP 3. COMORBIDITY

Gastrointestine

Cardiac
Vascular Brain
COMORBIDITY Peripheral

Renal

Respiratory

Contraindication And Side Effect

 MANAGEMEN NYERI NON FARMAKOLOGI

• Reduksi cemas: edukasi

• Distraksi - relaksasi: aktivasi retikuler menghambat stimulus
nyeri
• Terapi kognitif: melatih ketrampilan pengelolaan suatu
persepsi yang realistis
• Guide imagery hypnoterapi: konsentrasi untuk berimajinasi
dan visualisasi sesuatu yang indah/menyenangkan shg
membantu mengurangi nyeri dan mendorong relaksasi
 * Intervensi Nonfarmakologi

* Reduksi cemas * Immobilisasi

* Stimulasi Kulit * Posisioning
* Massage * Relaksasi
* Kompres dingin
* Distraksi
* Kompres Hangat
* Aromaterapi
* Stimulasi
Kontralateral * Hipnoterapi

AMAN, MURAH, TIDAK ADA EFEK SAMPING

08/02/21
 Pharmacology

• Efficacy and Effectivity (NNT, NNH, Selectivity,

Mechanism, Comparative Efficacy, Time to Re-
medication /half life)
• Safety (Comorbidity and Side Effects)
• Recommendation
• Cost
 The WHO Analgesic Ladder

Very severe Hydromorphone

WHO
Step III
Morphine
Oxycodone
Severe Fentanyl
Buprenorphine

Tramadol Tilidine
Codein
WHO Dextropropoxyphene
Step Moderate NSAIDs
II
COX II inhibitors

Acetylsalicylic acid
WHO
Step Mild Acetaminophene
I

Langford, 2002; Proceeding of the Grünenthal symposium

 Pain Assessment

Assessment of Disease Assessment of Pain

1. Pain Intensity 2. Type of Pain 3. Comorbidity & SE

Treatment

Non Pharmacology Pharmacology Interventional PM

Pure Analgetics NSAIDs Adjuvant Analgetics Opioid

Acetaminophen Anti- Anti- Opioid Atypical

Metampiron Ns NSAIDs Coxib Convulsant Deppresant - Opioid
Naproxen
INFLAMMATIO
N
Inflammation is a complex biological defense reaction
caused by tissue damage or injury or irritation

Can be elicited by numerous stimuli including:

infectious agents
antigen-antibody interaction ischemia
thermal and physical injury
 Mediators of Inflammation

1. Vasoactive amines (Histamine, Serotonin)

2. Platelet activating factor (PAF)
3. Complement system
4. Kinin system
5. Cytokines
6. Nitric oxide
7. Adhesion Molecules
8. Arachidonic acid metabolites:
•Prostaglandins (PGs)
•Thromboxane A2 (TXA2)
•HETE (hydroxy-eicosatetraenoic acid)
•Leukotrienes (LTs)
mediated by cyclooxygenases (COX)
• Cyclooxygenase-1 (COX-1) • Cyclooxygenase-2 (COX-2)

• Produces prostaglandins that • Produces prostaglandins that

mediate homeostatic functions mediate inflammation, pain, and
“HOUSEKEEPING” fever,mitogenesis in GI
epithelium
• Constitutively expressed, no • Induced “as needed” mainly in
inducer sites of inflammation by cytokines
needed • Sites: Brain, JG cells
• Plays an important role in
• Gastric mucosa proliferation
• Renal function
• Platelet aggregation and
antithrombogenesis
• Vascular endothelium
 Me c h a n is m o f Ac tio n
COX- 2 S e le c tivity o f NS AIDs

 Classification of NSAIDs based on COX selectivity

(1) irreversible inhibition of COX-1 and COX-2
- aspirin
(2) reversible competitive inhibition of COX-1 and COX-2
- ibuprofen
(3) slower, time-dependent inhibition of COX-1 and COX-2
- flubiprofen, indomethacin
(4) selective inhibition of COX-2
- celecoxib, rofecoxib, valdecoxib, etoricoxib, lumericoxib
 Me c h a n is m o f Ac tio n
COX Is o fo rm s

Type I COX (COX-1)

: constitutive form
- GI cytoprotection (prostacyclin)
- platelet aggregation (thromboxan A2)
- maintaining of renal blood flow (prostaglandin E2)
Type II COX (COX-2)
: inducible form during inflammation
- inflammation  fever, pain, headache
- constitutive in brain and renal cortex
- carcinogenesis
: both in the periphery and CNS
 Why *ns-NSAIDs can cause GI damage?
Arachidonic Acid
Glucocorticoids
(block mRNA expression)

COX-1 COX-2
(Constitutive) (Cytokine inducible)

x nsNSAIDs x

Purpose-designed COX-2
specific inhibitor
x
GI tract Inflammatory site:
Kidney • Macrophages
Platelet • Synoviocytes
• Endothelial cells

*ns = non-selective

nsNSAIDs: non selective Non Steroid Anti Inflammatory Drugs

Needleman P, and Isakson PC. J Rheumatol Suppl 1997;49:6-7; Flower RJ. Nat Rev Drug Discov 2003;2:179-191
 Need for effective and safer NSAIDs
• Mortality in patients suffering from an upper GI bleed or
perforation remains a concern particularly in those exposed to
NSAIDs1
• Most patients with OA requiring NSAIDs for pain control have
a high prevalence of GI risk factors2
• Evidence suggests co-therapy with a PPI does not prevent
NSAID damage to the lower GI tract3,4
– PPIs are not free of adverse events

• Clinical damage as a result of NSAID-induced lower

GI injury is now more clearly defined5
1.Straube S et al., BMC Gastroenterology 2009;9:41:1-7; 2.Lanas A et al., Ann Rheum Dis 2010;69:1453-8; 3.Goldstein JL et al., Clin Gastroenterol Hepatol
2005;3:133-141; 4.Goldstein JL et al., Ali Pharmacol Ther 2007;25:1211-1222; 5.Lanas A, Scarpignato C., Digestion 2006;73 (Suppl 1):136–50.
 CONDOR Study: Celecoxib 200 mg BID causes significantly
fewer GI events than diclofenac + PPI
Study

Clinically Significant Events Through the GI tract

10
population (ITT)
(n = 4484) 9
Celecoxib 200 mg bid (N=2238)

Cumulative Incidence of Adjudicated

8 Diclofenac SR 75 mg bid +
High 7
omeprazole 20 mg qd (N=2246)
GI
risk* 6

5 p<0.0001
H pylori OA/RA 4
negative diagnosis 3

1
Low
CV 0
risk† 0 30 60 90 120 150 180 210 240

Days From First Dose

In moderate to high GI risk patients taking NSAIDs for arthritis pain:

•Celecoxib demonstrated 4x lower risk of clinically significant GI AEs and lower
incidence of clinically significant anemia compare to Diclofenac + Omeprazole

Chan et al. Lancet. Early Online

11
Online Publication,
Publication, 17
17 June
June 2010
2010
 NSAID acidity is linked to increased
intestinal permeability1
Compound Acidity (pKa)
Valdecoxib2 9.8
-
Celecoxib3 9.7
a
Nimesulide3 6.4 • Chemical properties may also
c
contribute to the distinct effects of
Ibuprofen3 i 5.2 COX-2 inhibitors
Lumiracoxib4 d 4.7 • Celecoxib is a sulfonamide that is
Etoricoxib5
i 4.5 charged at physiologic pH
t • Etoricoxib is a sulfone with an acidic
Indometacin3 4.5
y pH
Naproxen (enteric coated)3 4.2
Diclofenac6 4.0
ASA (enteric coated)3
+ 3.5

1. Bjarnason I, Takeuchi K., J Gastroenterol 2009;44[Suppl XIX]:23–29; 2. Teagarden DL, Nema S., Biotechnology: Pharmaceutical Aspects
2007(5):1335-1346; 3. Bjarnason I et al., Aliment Pharmacol Ther 2007;26:95–106; 4. Rordorf CM et al., Clin Pharmacokinet
2005;44(12):1247-66; 5. Okumu A et al., Eur J. Pharm & Biopharm 2009;72:91-98; 6. Khazaeinia T et al., J Pharm Pharmaceut Sci
2003;6(3):352-359.
PRECISION:

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