PAIN MANAGEMENT

WISNU SETYARI
  Etiological Factor
 Inflam/tissue damage/nerve lesion

 Pain Mechanism

 Pain Syndrome
 Post-op/ arthritic/ back / neuropathic pain
PAIN RECEPTOR
 SENSORY OF nerve ending that mediate
pain → NOCICEPTORS :
 CHEMO-RECEPTOR
 MECHANO-RECEPTOR

 ALGESIC or PAIN producing substance:

 Hypertonic saline, Ach, 5-HT, Histamin,
Bradykinin and Substance P
PAIN :

 INFLAMMATORY PAIN
 Acute
 Chronis

 NEUROPATHIC PAIN
 Trigeminal neuralgia
 Post herpetic pain
 Diabetic neuropathy, dll
 ACUTE & CHRONIC PAIN
 MILD – MODERATE PAIN :
 NSAID
 ACETAMENOPHEN
 COMBINATION NSAID & ACETAMINOPHEN

 MODERATE – SEVERE PAIN :

 COMBINATION OPIOID & NSAID/
ACETAMINOPHEN
 Aspirin
 Analgesic
 Antiinflammatory
 Inhibits COX
 Irreversible inhibitor of COX
 Nonselective inhibitor of COX (adverse
effects)
 Drug-drug interactions
 Reye’s syndrome
Ibuprofen and other NSAIDS

 Analgesic
 Antiinflammatory
 Reversible inhibitors of COX
 Nonselective inhibitor of COX
(adverse effects)
 Acetaminophen
 Analgesic
 Low effect on peripheral COX
 Few drug-drug interactions
 Not antiinflammatory
 Liver toxicity
 May inhibit COX selectively in central
nervous system
 Only weak inhibitor of peripheral COX
 Inhibits effects of substance P in CNS?
 Inhibits effects of glutamate in CNS?
 Opioids

 Work through opioid receptor mechanisms

 Analgesic >>>
 Adverse effects
• GI tract
• CNS
• Histamine release
•  cranial pressure
Some Opioid – Nonopioid
Combinations
 Codeine + Aspirin (Empirin)
 Codeine + Acetaminophen (Tylenol)
 Dihydrocodeinec+ Aspirin + caffeine
 Hydrocodone + Acetaminophen (Lortab )
 Oxycodone + Acetaminophen (Percocet)
 Pentazocine + Aspirin (Talwin compound)
 Propoxyphene + Acetaminophen (Wygesic
NSAID +Acetaminophen
 Greater analgesic effect than either
alone
 Avoids adverse effects of opioids
 Similar half lives for many NSAIDS
and acetaminophen
 Over-the-counter
 MYOFACIAL PAIN
DYSFUNCTION

 ANALGESIC
 TRICYCLIC ANTIDEPRESSANT
 CENTRALLY ACTING MUSCLE
RELAXANT
 GLUCOCORTICOID
TRICYCLIC ANTIDEPRESSANT
 AMITRIPTYLIN , NORTRIPTYLIN

 EFECTIVE IN SMALL DOSE

 INHIBIT PAIN TRANSMISSION
 Inhibit nociceptive pathway by blocking the re
uptake of serotonin & norepinephrine
 Act as sodium channel blocker similar local
anesthetic
 FOR CHRONIC PAINFUL CONDITION
 ADVERSE EFFECT :
 CONSTIPATION
 DRY MOUTH
 BLURRED VISION
 COGNITIVE CHANGE
 TACHICARDI
Central Muscle Relaxant

 DIAZEPAM
 METHOCARBAMOL
 CYCLOBENZAPRIN
 VERY LOW DOSE SHOULD BE USED
INITIALLY
 ADV.EFECT : SEDATION, DEPRESSION,
ADICTION
 NEUROPATHIC PAIN

 TRIGEMINAL NEURALGIA

 CARBAMAZEPIN
 PHENYTOIN
 VALPROIC ACID
 BACLOFEN
 LAMOTRIGIN
 POST HERPETIC PAIN

 NORTRIPTYLIN ( TCA )
 KETAMIN ( NMDA ANTAGONIST )
 GABAPENTIN ( ANTICONVULSANT )
 OPIOID
Topical Medication for
Orofacial Neurophatic Pain
 TOPICAL ANAESTHETIC:
 BENZOCAINE
 LIDOCAINE
 LIDOCAINE & PRILOCAINE

 NEUROPEPTIDE :CAPSAICIN

 NSAID :
 KETOPROFEN
 DICLOFENAC
 SYMPATHOMIMETIC AGENT
 CLONIDIN

 NMDA BLOCKING AGENT

 KETAMIN

 ANTICONVULSANT: CARBAMAZEPIN

 TCA : AMITRIPTYLIN

 ANTISPASMODIC: BACLOFEN
HEMOSTATIC

 HEMOSTASIS
NORMAL MECHANISM IN THE BODY
DESIGN TO PREVENT THE LOST OF
BLOOD AFTER INJURY.

 DENTISTRY INVOLVED PROCEDURES

CAUSING BLEEDING
 3 MAIN STEP HEMOSTASIS :

 1. VASOCONSTRICTION:
- LOCAL : THROMBOXANE
- SYSTEMIC : EPINEPHRIN

 2. FORMATION OF PLATELET

 3. FIBRIN CLOT
 TOPICAL TREATMENT

 DRESSINGS :
 GAUZE , SPONGES, PRESSURE,
COLLAGEN SHEET, ETC
→ TO PROMOTE PLATELET AGGREGATION

 CLOTTING FACTORS:
 TOPICAL THROMBIN → PROMOTE FIBRIN
FORMATION → CLOT
 ASTRINGENTS :
 ZINC, ALUMINIUM SALTS
→ DENATURE BLOOD / TISSUE PROTEIN
TO PROMOTE PLUG FORMATION

 VASOCONSTRICTOR :
 ADRENERGIC AGENT → EPINEPHRIN
→ PROMOTE VASOCONSTRICTION