ANALGESIA
CONSULTANT : DR T BULAYA
INTERN (JRMO) : DR C
MUPWAYA
OUTLINE
1. A DETAILED HISTORY
2. A COMPREHENSIVE PHYSICAL
EXAMINATION
3. METHODS OF PAIN ASSESSMENT
4. PAIN PATHOPHYSIOLOGY
5. PHARMACOLOGICAL INTERVENTION IN
PAIN MANAGEMET
INTRODUCTION
Pain is an unpleasant sensory and
emotional experience, associated with actual
or potential tissue damage, or described in
terms of such damage (The International
Association for the Study of Pain, IASP).
Etymology: “Pain” came from Latin
poena, "punishment, penalty" and as well
from Greek "ποινή" (poine), generally
"penalty", "punishment“.
FACTORS INFLUENCING PAIN
EXPERIENCE
1. AGE
2. GENDER
3. PERSONALITY
4. CULTURE
5. LEARNED BEHAVIOUR/PAST EXPERIENCE
6. BELIEFS/ATTITUDES
7. RELIGION/SPIRITUALITY
DETAILED Hx
PAIN ASSESSMENT
SOCRATES MNEMONIC
S – SITE (WHERE IS THE PAIN)
O – ONSET
C – CHARACTER
R – RADIATING
A – ASSOCIATED SYMPTOMS
T - TIME AND DURATION
E - EXACERBATING
S - SEVERITY
PHYSICAL EXAMINATION
LOOK, FEEL AND MOVE
LOOK
• PATIENT – FACIAL EXPRESSION, POSTURE,
MOVEMENTS, SWEATING
• SITE – INFECTION, INFLAMMATION, MUSCLE
WASTING
FEEL
• AVOIDING CAUSING PAIN TO THE PATIENT
MOVE
• RESPONSE TO ACTIVE OR PASSIVE MOVEMENT
• STIFFNESS? LIMITATIONS?
METHODS OF PAIN
ASSESSMENT
I. VERBAL RATING SCORE
II. NUMERICAL RATING SCORE
III. VISUAL ANALOGUE SCALE
IV. MCGILL PAIN QUESTIONNAIRE
PAIN PHYSIOLOGY
THE BODY’S NEURAL DETECTION OF PAIN IS
CALLED NOCICEPTION
NOCICEPTION INVOLVES THE RELAY OF
INFORMATION PERIPHERALLY FROM SPECIAL
RECEPTORS IN THE TISSUES TO THE BRAIN
THE PAIN SYSTEM HAS SEVERAL
COMPONENTS
PAIN PHYSIOLOGY
SPECIALISED RECEPTORS CALLED
NOCICEPTORS
FOUND IN PERIPHERAL TISSUES
DETECT STIMULI
FILTER INTENSITY AND TYPE OF
STIMULI
PRIMARY AFFERENT FIBRES
(TRANSMISSION)
A – DELTA AND C FIBRES
TRANSMIT NOXIOUS STIMULI TO CN
PHARMACOLOGICAL
INTERVENTION IN PAIN MANAGEME
World Health Organization (WHO) Pain
Ladder provides a structured approach to
treating pain, particularly in cancer and
palliative care.The WHO pain ladder follows
a step wise approach to prescribing
analgesic medications based on pain
severity.
PHARMACOLOGICAL INTERVENTION
IN PAIN MANAGEME
Step1:MildPain •Non-opioidanalgesics(e.g.
Acetaminophen,NSAIDs) •±Adjuvant
therapy(e.g.,antidepressants,anticonvulsant
s for neuropathic pain)
Step2:Moderate Pain •Weak opioids(e.g.
Codeine, tramadol) •±Non-opioid
analgesics •±Adjuvant therapy
Step3:Severe Pain •Strong opioids(e.g.
Morphine, fentanyl) •±Non-opioid
analgesics •±Adjuvant therapy
Drug Names &Classes
Non-Opioids(Step1) •Acetaminophen(Paracetamol) •Non-
SteroidalAnti-Inflammatory Drugs(NSAIDs) •Ibuprofen
•Naproxen •Diclofenac •Celecoxib(COX-2selective)
Weak Opioids(Step2) •Codeine •Tramadol
•Dihydrocodeine
Strong Opioids(Step3) •Morphine •Oxycodone •Fentanyl
•Hydromorphone •Methadone Adjuvant
Medications(usedatallsteps
•Antidepressants(e.g.,amitriptyline,duloxetine)–
forneuropathicpain •Anticonvulsants(e.g.
Gabapentin,pregabalin)–fornervepain
•Corticosteroids(e.g. Dexamethasone)–for inflammation-
related pain
PHARMACOLOGICAL INTERVENTION
IN PAIN MANAGEME
. Mechanism of action and side effects of Action
Each class of analgesics works differenintly to
relieve pain:
1. Non-Opioids(Step1) •Acetaminophen:Inhibits
cyclooxygenase(COX) enzymes in the CNS,reducing
pain and fever.
Side effects: Acetaminophen Liver toxicity (high doses)
2. NSAIDs:Inhibit COX-1and COX-2 enzymes,reducing
prostaglandin synthesis,leading to decreased
inflammation and pain
Side effects: •Gastric irritation,ulcers,and bleeding
•Kidney dysfunction •Increased cardiovascular
risk(someCOX-2inhibitors
PHARMACOLOGICAL INTERVENTION
IN PAIN MANAGEME
. Mechanism of action and side effects of Action Each class of
analgesics works differenintly to relieve pain:
3. . Opioids
(Step2&3) •Bind to mu-opioid receptors in the brain and spinal cord,
modulating pain perception. •Reduce neurotransmitter release in pain
pathways,leading to analgesia.
•Strong opioids(like morphine) have a high eraffinity for these receptors
compared to weak opioids(likecodeine).
Side effects: •Common: •Nausea, vomiting •Constipation
•Drowsiness,sedation •Respiratorydepression(dose-dependent) •Long-term
risks: •Tolerance and dependence •Risk of addiction (especially with
chronic use)
4. ). Adjuvant Drugs •Antidepressants:Increase serotonin and
norepinephrine levels in descending pain pathways.
•Anticonvulsants:Stabilize nerve membranes and reduce hyperexcitability
in neuropathic pain
Side effects: )•Antidepressants:Drowsiness,drymouth,weightgain
•Anticonvulsants:Dizziness,sedation Conclusion
CLASSIFICATION OF OPIOID
COMPOUNDS
Naturally occurring:
- Morphine
- Codeine
- Papaverine
- Thebaine
Semisynthetic:
- Heroin
- Dihydromorphone
- Thebaine derivatives (e.g., buprenorphine)
Synthetic:
- Morphinan series (e.g., butorphanol)
- Benzomorphan series (e.g., pentazocine)
- Phenylpiperidine series (e.g., pethidine, fentanyl,
alfentanyl, sufentanyl and remifentanyl)
COMPARATIVE POTENCY OF
OPIOIDS
- Morphine: 1
- Pethidine: 0.1
- Fentanyl: 100
- Alfentanyl: 10-25
- Sufentanyl: 500 – 1000
- Remifentanyl: 250
PETHIDINE
Mu-agonist
It has structural similarities to atropine and
may have some of their effects and side
effects (tachycardia, midriasis, dry mouth)
Duration of action: 120-150 min
It has an active metabolite – norpethidine –
with a strong potential to precipitate
seizures in compromised patients
It readily crosses blood-brain and placental
barrier
PETHIDINE
Dosages:
1-2 mg/kg IV, IM QID
Contraindications:
Renal failure
Hypovolemic patients
Those on MAOIs (monoamino oxidase
inhibitors) – may produce hypotension or
hypertension, convulsions, hyperpyrexia
and even coma
FENTANYL
Mu-agonist
Dose-dependent respiratory depressant
Cardiovascular stability is present
Duration of action: 30-45 min
No active potentially dangerous metabolite,
predominately metabolized in the liver and
2/3 of the dose is excreted in the urine
FENTANYL
Effects:
- Analgesia
- Deep sedation (in extremely high doses: 50-
150 mcg/kg)
Dosages:
- 0.5-100 mcg/kg IV
Special breathing support systems MUST be
available during fentanyl administration!
TRAMADOL
Has been in clinical use in Germany since the
late 1970s and has proven effective in both
experimental and clinical pain.
Is a synthetic, centrally acting analgesic
agent.
It acts as an opioid agonist with selectivity
for μ-receptor and also binds weakly to κ- and
σ-receptors.
Analgesic doses of tramadol are comparable
to those of pethidine.
TRAMADOL
Has 2 distinct but complementary
mechanisms of action:
1 – opioid – antagonised (about 30%) by
naloxone
2 – nonopioid – acts on monoamine system
to inhibit the reuptake of noradrenaline and
serotonin (5-hydroxytryptamine)
TRAMADOL
Effects on respiration
There is minimal (not clinically relevant)
respiratory depression at the recommended
dosages. However, depression may occur at
considerably exceeded dosages.
Effects on cardiovascular system
Postoperative IM tramadol (0.75-1.5 mg/kg)
decreases both heart rate and diastolic blood
pressure but not clinically relevant. Although there
is no effect on systolic blood pressure*.
* - Schaffer J, Kretz FJ et al. Nalbuphine and tramadol for control of postoperative pain in
children. Anaesthetist 1986;35:408-13.
TRAMADOL
Recommended dosages
- oral: 50-100 mg every 4-6 hrs.
The maximum recommended daily oral
dose is 400 mg.
- IM, IV: Safe and clinically effective – 1.0-1.5
mg/kg
Maximum IV dosage – 600 mg/day.
TRAMADOL
Not recommended for use:
- in patients < 12 years of age
- in patients who are receiving MAOIs or
within 2 weeks of their withdrawal
- During pregnancy or in lactating mothers
THANK YOU!
