Pain Management
Pain Management
Pain Management
• Since 2008, Ministry of Health Malaysia implemented PAIN as 5th vital sign
“I think the simplest and probably the best definition of pain is what
the patient says hurts. I think that they may be expressing a very multi-
faceted thing. They may have physical, psychological, family, social and
spiritual things all wound up in this one whole experience. But I think
we should believe people and once you believe somebody you can
begin to under- stand, and perhaps tease out the various elements that
are making up the pain.”
Why ?
- Different types of pain respond to different types of analgesia
- To determine what type of pain in order to prescribe the right
analgesia
- Many may have mixed pain syndrome
Nociceptive pain
• Somatic pain
• Results from stimulation of skin, muscle, bone receptors
• Character is stabbing, throbbing, aching or pressure and usually are well-localized
• Eg bone cancer/metastasis, malignant skin ulcer
• Visceral pain
• results from infiltration, compression or the distension of thoracic or abdominal
viscera
• often poorly localized and may be described as gnawing, cramping, aching or sharp
• Referred pain
Neuropathic pain
• caused by injury to the peripheral and/or CNS
• pain occurs because the injured nerves either react abnormally to stimuli
or discharge spontaneously.
• character: burning, tingling, shooting or electric shock-like sensations.
• It may be associated with hyperalgesia, allodynia, or dysesthesia
• Eg
• Brachial plexopathy from pancoast tumour (pain radiating down upper limb)
• Lumbosacral plexopathy from large pelvic mass (pain radiating down lower limbs)
• Radicular pain from spinal metastasis (pain radiating around trunk like a belt/band)
• Facial pain/headache/trigeminal neuralgia (head and neck cancer)
Assessment
• P – Place / Site of pain (“Where is the pain?”)
• A - Aggravating factors (“What makes it worse?”)
• I – intensity (“How bad is the pain?” – use pain scale)
• N – Nature & Neutralizing factors (“What does it feel like?” & “What
makes it better?”)
Recommended Pain Scales
2. Opioids –
• drugs that are agonists at opioid receptor sites
• three types of opioid receptor (mu, kappa and delta)
• found in several areas of the brain and throughout the spinal cord
• Stimulation of opioid receptors results in a variety of responses, including analgesia,
respiratory depression, myosis, reduced gastrointestinal motility and euphoria
• receptor affinity – differences between opioids
• ‘weak’ opioids – dihydrocodeine, tramadol
• ‘strong’ opioids – morphine, fentanyl, oxycodone
…Classification of analgesics
3. Adjuvant analgesics
• do not function primarily as analgesics
• used in combination with opioids
• act to relieve pain in specific circumstances
• choice of adjuvant drug is generally guided by the nature of the underlying
pain
• Eg,
• Antidepressant/anticonvulsant – neuropathic pain
Principle of pain management
• WHO ANALGESIC LADDER according to pain intensity
• Step 1 (mild pain) – use non-opioid analgesics (Paracetamol, NSAIDs, COX-2
inhibitors)
• Step 2 (moderate pain) – use weak opioid analgesics +/- combination of step
1 drugs (tramadol, dihydrocodeine, codeine)
• Step 3 (severe pain) – use strong opioid analgesics (morphine, oxycodone,
fentanyl) +/- combination with step 1 drugs
Principle of pain management
The WHO method can be summarized in five phrases:
• Mild to moderate somatic pain may respond well to NSAIDs and COX-2 inhibitors where there
is strong inflammatory process
• Neuropathic pain may respond to opioid analgesics but often only partially and will require
addition of adjuvant analgesics
• Morphine is the drug of first choice for treatment of severe cancer pain
STEP 1
• Paracetamol
• NSAIDS
• risk/benefit
Paracetamol/acetaminophen
• analgesic and antipyretic
• lacks an anti-inflammatory effect
• mechanism of action remains unclear
• minimal toxicity at recommended doses
• Hepatotoxic if >4g / 24hrs
• increased risk if underlying liver disease
NSAIDS
• cyclo-oxygenase inhibitor : COX-1 or COX-2; inhibit production of
prostaglandins
• Aspirin not used - difficult to tolerate at analgesic doses due to its
side-effects
• high incidence of adverse events – GI and renal toxicity, CV events
• non-selective NSAIDs - GI effects common
• selective COX-2 inhibitors – less GI effects
Step 2 -‘weak’ opioid
• Codeine
• Codeine is a much weaker agonist at mu receptors than morphine
• Tramadol
• mixed mechanism - weaker agonist at mu receptors /noradrenaline and
selective serotonin-reuptake inhibitor (SSRI)
• A/E – nausea, vomiting, drowsiness, dizziness; tramadol may reduce
seizure threshold
STEP 3
• Morphine is the drug of first choice for treatment of severe cancer
pain
• no “ceiling effect”
• liver is the principal site of morphine metabolism
• products of morphine metabolism are eliminated by the kidney
• oral, rectal, SC, IV. Oral is the preferred route; next best s/c
• Immediate release(peak 1hr, effect 4hrs) vs modified-release/slow
release (peak 2-6hrs, effect 12 or 24hrs)
Principles of opioid prescription
Opioids are safe, effective and appropriate drugs for the management
of cancer pain, provided that:
• Appropriate starting doses and titration are observed
• The properties and relative potencies of different opioids are
understood
• Opioid-related adverse effects are monitored and managed
• Prescribers are aware that some types of pain are poorly responsive
to opioids and require other types of analgesics (adjuvant analgesics)
Starting morphine
• starting dose 5-10mg (usually 5mg) every 4 hours
• elderly/frail 2.5-5mg 4-6hrly
• In renal or liver impairment, lower dose (2.5-5mg) with longer internal
6-8hrly (Fentanyl is the safer opioid to use in renal impairment)
• ALSO prescribe PRN dose for breakthrough pain (same dose as regular
dose)
• After 24hrs, calculate total morphine dose (regular plus PRN)
• once pain is controlled , total morphine dose is divided by 2 and
prescribe nearest slow- release morphine dose 12hrly + prn doses
Opioid Side-effects
• Constipation – always prescribe prophylactic laxatives when using
regular opioid analgesia (lactulose, bisacodyl, senna)
• Nausea / Vomiting – occurs in first 1 week after starting. Treat with
metoclopramide 10mg TDS/QID
• Sedation – occurs during initial dose and normally subsides after a
few days.
Opioid toxicity
• rare
• precipitated by
• excessive increase in opioid dose
• dehydration or renal impairment/change in disease status – hepatic failure
• infection
• drug interaction
• signs and symptoms –
• Drowsiness
• Hallucinations (most commonly visual) • Confusion
• Vomiting
• Myoclonus
• Pinpoint pupils
• Respiratory depression (if severe)
• Naloxone (reversal agent) rarely used unless significant respiratory depression RR < 12
Opioid switching
• changing from morphine to another opioid or changing route of administration
• may be considered if :
• Pain is not well controlled despite optimal titration
• Intolerable side effects occur with morphine
• Renal impairment develops
• cannot swallow medication
• patient’s choice
• unwilling to take oral morphine regularly eg transdermal opioid – fentanyl
• Example
• oxycodone, diamorphine
• Fentanyl
• Buprenorphine
Common conversion factors for opioid
switching