MANAJEMEN NYERI
Definisi Nyeri dari IASP
(International Association for the Study of Pain)
Pain (Nyeri) adalah suatu
pengalaman sensorik dan
emosional yang berkaitan
dengan kerusakan jaringan
atau diduga ada kerusakan
jaringan
 Nyeri adalah pengalaman
sensorik yang berkaitan
dengan aktivasi nociceptor
dan lintasan nyeri
 Nyeri adalah suatu
pengalaman emosional
 Kerusakan jaringan tidak
mesti ada
 JENIS NYERI

Neuropathic Pain Mixed Pain

Inflammatory 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
components (musculoskeletal,
(either peripheral or
cutaneous or visceral)2
central nervous system)1

Examples Examples
Peripheral Examples
• Post herpetic 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
• Cancer pain • Postoperative visceral pain
• Posttraumatic neuropathy
Central • Carpal tunnel
Common descriptors2
• Posts troke pain syndrome
• 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
Ascending Pain
Transmission
Pathway
The ascending neural pain
pathway is only a 3 neuron
relay
The major convergence point is
the ventral posterior lateral
nucleus of the thalamus, which
relays the signal to limbic and
cortical areas

Ascending Pain Pathway (Purves, 2001).

Descending Pain
Modulation
Pathway
The Descending Pain
Pathway – The
Periaqueductal Grey
(PAG) is the major
convergence point.

Descending pain pathway (Purves, 2001).

 Targets of Pain Therapies
Pharmacotherapy
Non-opioid analgesics
Opioid analgesics
Nerve Blocks
Adjuvant analgesics (neuropathic,
musculoskeletal)

Acetaminofe Electrical Stimulation

n
Transcutaneous electrical nerve
stimulation (TENS)
Percutaneous electrical nerve
stimulation (PENS)

Alternative methods
Acupuncture
(NSAID) Physical Therapy
Chiropractics
Gottschalk et al., 2001
Surgery
  Thick, myelinated, fast
conducting neurons
 Mediate the feeling of
initial fast, sharp, highly
localized pain.
 Very thin, unmyelinated,
slow-conducting
 Mediate slow, dull, more
diffuse, often burning
pain.

Rabaan
Tekanan
Chemical mediators are released from damaged
tissue and inflammatory cells. Some
inflammatory mediators directly activate
nociceptors, while others act together to sensitize
the pain pathway.
 INFLAMMATION
l biological response to injury or
foreign substances
l acute and chronic inflammation
l components:
cellular response
biochemical mediators
 MECHANISMS OF INFLAMMATION

CELLULAR MECHANISMS:
Acute inflammation
PMN
Chronic inflammation
lymphocytes
monocytes
 MECHANISMS OF INFLAMMATION

BIOCHEMICAL MEDIATORS
 vasoactive amines
 plasma proteases (complement, kinins)
 arachidonic acid metabolites (PG, LT)
 lysosomal constituents
 oxygen derived free radicals
 cytokines
 growth factors
 MEDIATORS OF INFLAMMATION

Arachidonic Acid Metabolites

Prostaglandins
Leukotrienes
 GENERATION OF EICOSONOIDS

Phospholipids
Phospholipase

Arachidonic Acid
5-lipoxygenase cyclooxygenase

5-HPTE PGG2
peroxidase
LTB4 LTC4
PGH2

TXA2 PGI2 PGE2 PGF2 PGD2

BIOLOGICAL EFFECTS OF
PROSTAGLANDINS
PGE2 Vasodilatation, pain sensitization,
gastric cytoprotection
PGF2 Bronchoconstriction, uterine
contraction
PGI2 Inhibit platelet aggregation,
gastric cytoprotection
TxA2 Platelet aggregation
 Roles of COX-1 and COX-2

Arachidonic acid
COX-1
COX-2
“Constitutive”

PGs
PGs Inducible Constitutive

· GI cytoprotection · Inflammation · Renal function

· Platelet activity · Pain
· Renal function · Fever
 NON-COX SELECTIVE NSAIDS

 Carboxylic acids
[salicylates, meclofenamate, diflunisal]
 Indoleacetic acids
[indomethacin, sulindac]
 Propionic acids
[ibuprofen, fenoprofen, ketoprofen,
dexketoprofen, flurbiprofen]
 Naphthalene acetic acids
[naproxen]
NON-COX SELECTIVE NSAIDS
[CONT’D]

 Diclofenac
 Etodolac
 Nabumetone
 Oxaprozin
 Ketorolac
 COX - 2 INHIBITORS

 Celecoxib
 Rofecoxib
 Valdecoxib
 Meloxicam*
*(less COX-2 selective)
 DEXKETOPROFEN

 Merupakan garam tromethamine dari S-(+)-2-(3-benzoylphenyl)

propionic acid.
 Pertama kali digunakan pada tahun 1996.
 Dikembangkan dari molekul ketoprofen.
 Merupakan inhibitor COX-1 dan COX-2, dimana aktivitas
hambatan terhadap keduanya bersifat seimbang, sehingga
efek hambatan deksketoprofen terhadap pembentukan PGE2
cukup bermakna.
 Termasuk golongan nonselektif NSAID
 BEBERAPA PENELITIAN
TENTANG DEXKETOPROFEN
 KETESSE

Dexketoprofen trometamol - Ampul 50 mg, Tablet 25 mg

Indications:
Acute musculoskeletal pain, dysmenorrhea, toothache & post-op pain.
Dosage:
Tab 12.5 mg 4-6 hrly or 25 mg 8 hrly. Post-op pain 25 mg 8 hrly.Max dose: 75 mg.
Amp 50 mg/mL IV/IM 8-12 hrly. Max dose: 150 mg.
Contraindications:
History of asthma attack, bronchospasm, acute rhinitis or nasal polyp, urticaria or
angioneurotic edema, gastric ulcer or chronic dyspepsia, gastric bleeding, Crohn's
disease or ulcerative colitis, severe cardiac failure, moderate to severe renal
dysfunction, severe liver dysfunction, haemorrhagic diathesis, coagulation disorders &
anticoagulant therapy. Pregnancy & lactation.
Special precautions:
History of drug allergy, oesophagitis, gastritis & peptic ulcer. Haematological changes,
SLE or mixed-type connective tissue diseases. Abnormal liver, renal or liver function.
Diuretic therapy. May impair ability to drive or operate machinery. Children, elderly.