Professional Documents
Culture Documents
DAN PERMASALAHANNYA
(Meliala, 2000)
Pain Is the 5th Vital Sign
Pain
Nosiseptif Intense
Mechanical
Nociceptor
Force
sensory neuron
Heat
Adaptif Inflammation
INFLAMANTORY PAIN
Spontaneous Pain
Pain Hypersensitivity
Macrophage Reduced Threshold : Aliodyna
Mast Cell Increased Response : Hyperalgesia
Neutrophil
Granulocyte
Brain
Spinal cord
Fungsional NOCICPTOR
Normal Peripheral
Tissue and Nerves
NOCICPTOR Abnormal Central
Processing
Prevalence of Acute Pain
1. Diener HC et al. J Headache Pain 2008; 9(4):225-31; 2. Todd KH, Miner JR. In: Fishman SM et al (eds). Bonica’s Management of Pain.
4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010; 3. Dix P et al. Br J Anaesth 2004; 92(2):235-7.
Epidemiology of Pain in
General Practice
• 1 in 3 patients reported pain
• Of patients in pain:
– 47.2% had acute pain
– Location of pain was mainly in musculoskeletal
areas and the limbs
– 2 in 3 pain patients had a drug prescription
• Pain was more frequent in women
Pain Intensity in
100% Pain Intensity
Neurologist
100%
15%
in other specialist 20%
80% 80%
7-10 (Severe)
60% 60%
57% 7-10 (Severe)
4-6
64%
(Moderate)
40% 4-6 (Moderate) 40%
0-3 (Mild)
20% 0-3 (Mild)
20%
28%
16%
0%
0%
All Pain Patients
All Pain Patients
17% 1% 6%
3%
Ladder 1 Ladder 2 Ladder 3 Adjuvant NA
Skrining dan Assessment
• Tergantung onset
• Tergantung tipe
• Tergantung intensitas
• Tergantung penyebab
• Tergantung ada/tidaknya komorbid
Prinsip Terapi
Discussion Question
PAIN
MODULATION
TRANSMISSION
TRANSDUCTION
19
Mechanism-Based Pharmacological Treatment
of Nociceptive/Inflammatory Pain
Brain
Step 1: NSAIDs
Step 1: acetaminophen
(4 g/day maximum dose;
4 h minimum interval between each 1 g dose)
Inadequate
analgesia
Step 2: coxib or nsNSAID
(make choice based on patient risk profile)
Inadequate
analgesia
Topical nsNSAID Step 3: add 1 of following:
Opioids
(with or without combined •Acetaminophen/codeine
(refer patient to pain clinic
oral acetaminophen, •Acetaminophen/tramadol
or specialist)
coxib or nsNSAID) •Tramadol
Coxib = COX-2 inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug
Ayad AE et al. J Int Med Red 2011; 39(4):1123-41.
23
Recommendations for Management of
Acute Pain
Acetaminophen
If ineffective
Add nsNSAIDs/coxibs
If ineffective
Add opioids
(preferably short-acting agents at regular intervals;
ongoing need for such treatment requires reassessment)
Baumann TJ. In: DiPiro JT et al (eds). Pharmacotherapy: A Pathophysiologic Approach. 5th ed. McGraw-Hill; New York, NY: 2002.
How do nsNSAIDs/coxibs work?
Arachidonic acid
COX-2 (induced by
COX-1 (constitutive)
inflammatory stimuli)
Coxibs BLOCK
Prostaglandins Prostaglandins
Gastrointestinal
cytoprotection, Inflammation, pain, fever
platelet activity
• Strategi gastroprotektif terbaik: Coxib + PPI (Targownik et al, 2008 Level III-2;
Chan et al, 2007 Level II).
• Tidak ada bukti klinis yang signifikan yang menyatakan bahwa coxib
memiliki efek inhibisi terhadap penyembuhan tulang. (Gerstenfeld &
Einhorn, 2004; Bandolier, 2004).
2. Golongan COX 2
Efek Anti Inflamasi Kuat
Efek Samping Cardiovascular BESAR
DEXKETOPROFEN
Efek Analgesik SETARA Cox 1
Efek Anti inflamasi SETARA Cox 2
Efek Samping GASTROINTESTINAL < Cox1
Efek Samping CARDIOVASCULAR < Cox2
Onset LEBIH CEPAT dari KETOPROFEN
Upper GI bleed risks for ns-NSAIDs (cont)
Ibuprofen
Diclofenac
Sulindac
Naproxen
Indomethacin
Ketoprofen
Piroxicam
1 10
Relative risk for upper GI bleed/perforation
Compared with not taking NSAIDs
Hernández-Diaz & Garcia Rodríguez, Arch Intern Med 2000 160: 2093-2099
Risk Factors for Gastrointestinal Complications
Associated with nsNSAIDs/Coxibs
History of GI bleeding/perforation
1
13.5
1
Concomitant use of anticoagulants 6.4
History of peptic ulcer
1
6.1
Age ≥60 years 2 5.5
Single or multiple use of NSAID 1 4.7
Helicobacter pylori infection
3
4.3
4
Use of low-dose ASA within 30 days 4.1
3
Alcohol abuse 2.4
Concomitant use of glucocorticoids 1 2.2
3
Smoking 2.0
0 5 10 15
Odds ratio/relative risk for ulcer complications
ASA = acetylsalicylic acid; coxib = COX-2-specific inhibitor; GI = gastrointestinal; NSAID = non-steroidal anti-inflammatory drug;
nsNSAID = non-specific non-steroidal anti-inflammatory drug; SSRI = selective serotonin reuptake inhibitor
1. Garcia Rodriguez LA, Jick H. Lancet 1994; 343(8900):769-72; 2. Gabriel SE et al. Ann Intern Med 1991; 115(10):787-96;
3. Bardou M. Barkun AN. Joint Bone Spine 2010; 77(1):6-12; 4. Garcia Rodríguez LA, Hernández-Díaz S. Arthritis Res 2001; 3(2):98-101.
Efektivitas digambarkan
dengan nilai NNT
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine.
Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
Hipnosis
Membayangkan
Plasebo
Musik/hiburan
Systemic
Opioid
Tricyclics
Anticonvulsan
NSAIDs
44
Assessment Ulang
Perform assessments
Yes
Pain is severe/disabling: requires opioids Refer to specialist
No
Treat appropriately
Lifestyle management
Interventional pain
Physical therapy Pharmacotherapy management
Occupational therapy
Education
Complementary therapies Biofeedback
Gatchel RJ et al. Psychol Bull 2007; 133(4):581-624; Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research.; National Academies
Press; Washington, DC: 2011; Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006.
Kesimpulan
• 38 th
• 1HSMRS nyeri punggung
bawah + kedua bokong
• ROM terbatas, terutama pada
gerakan fleksi dan rotasi.
• Nyeri tekan diatas vertebra
lumbal 4-5 dan dibokong (+).
• NPS 5-6
• Suhu tubuh 37.5 C.
P.1. Menurut Pendapat TS, bagaimana intensitas
nyeri pasien tersebut?
A. Nyeri ringan
B. Nyeri sedang
C. Nyeri berat
P2. Pemeriksaan penunjang yang dianjurkan:
A. Lumbal X-Ray
B. Lumbal CT Scan
C. Lumbal MRI
D. ENMG
E. Belum perlu
Causes of Low Back Pain
• Lumbar “strain” or “sprain” : 70%
• Degenerative changes : 10%
• Herniated disk : 4%
• Osteoporosis compression fractures : 4%
• Spinal stenosis : 3%
• Spondylolisthesis : 2%
• Spondylolysis, diskogenic LBP
or other instability : 2%
• Traumatic fracture : < 1%
• Congenital disease : < 1%
• Cancer : 0.7%
• Inflammatory arthritis : 0.3%
• Infections : 0.01%
• “Psychological” : ?
(Stoltz, 2003)
Red Flags
• Significant trauma history, or minor in older adults
• Nocturnal pain in supine position with history of cancer
• Bladder or bowel incontinence or dysfunction
• Constitutional symptoms:
• Fever / chills
• Weight loss
• Lymph node enlargement
• Risk factors for spinal infection
• Recent infection
• IV drug use
• Immunosuppression
A. Acetaminofen 3 x 1000 mg
B. K-diclofenac 2x 50 mg
C. Diazepam 3 x 2 mg
D. Morfin sulfat 2x10 mg
E. Metilpredisolon 8 mg-8mg-0mg
Summary of Evidence on Medications
for Acute Low Back Pain (Chou & Huffman, 2007)
Drug Net Effective Inconsistency Overall Comments
Benefit vs. ? Quality of
Placebo? Evidence
Acetaminophen Moderate Unclear Some Good Few data on serious adverse events
inconsistency
Antidepressants No evidence No evidence No evidence No evidence -
Antiepileptic drugs No evidence No evidence No evidence No evidence Evaluated only in patients with
radicular LBP
Tramadol Unable to No evidence Not applicable Poor The only trial compared tramadol with an
estimate NSAID not available in US
Kasus
A. 1-2 hari
B. 5 hari
C. 1 minggu
D. 10 hari
E. Tidak perlu bedrest, langsung aktifitas
P.6. Apakah boleh pijat?
A. Boleh
B. Tidak boleh
Semoga bermanfaat.