Module 2.1.2 (Management of Pain) Flashcards
What is the acute pain pharmacotherapy guidelines in eTG?
What is used for post-operative pain management?
Where pain is predictable
- Use regular paracetamol and NSAIDS
Moderate to severe post-op pain
- Add pregabalin
- Add prn opioids
> PCA (patient controlled analgesia)
> If opioids are used for >7 days a slower taper may be required
Major surgery
- Epidural or intrathecal analgesia, peripheral nerve blocks, field blocks, wound infiltration
What is used for chronic (non-cancer) pain management?
Multidisciplinary care is the gold standard
- Pain education
- Psychology strategies
- Physiotherapy strategies
- Lifestyle measures
> Sleep hygiene, nutrition, stress mx, smoking cessation
- Medications as “scaffolding”
> Improve day-to-day function and quality of life
> Provide support while non-pharmacological treatment strategies are built up
> Targeted treatments if available (eg DMARDS in RA)
- Surgery
> E.g. joint replacement in OA
For chronic pain management;
A) What is used in nociceptive pain?
B) What is used in neuropathic pain?
C) What is used in nociplastic pain?
A)
- Simple analgesia
- TCA
- SNRI
- Opioids – limited evidence of benefit, many harms
B)
- TCA
- SNRI
- Gabapentinoids
- Lidocaine patch
- Capsaicin
- Clonidine
- Ketamine etc
C)
- TCA
- SNRI
- Gabapentinoids
> fibromyalgia
> caution effects on cogntion and fatigue may worsen some pain states over time
> use low doses
Chronic noncancer pain is often contributed to by more than one pain type (i.e. mixed pain) or multiple mechanisms within a single pain type. What is used if patients unable to use first line strategies (self-mangement strategies) for:
A) nociceptive pain
B) neuropathic pain
C) chronic noncancer pain
A)
- Paracetamol and NSAIDS for nociceptive pain
B)
- Adjuvants for neuropathic pain.
C)
- Opioids have a limited role in the management of chronic noncancer pain (see later slides)
Wahat NSAIDs to use in chronic non-cancer pain?
Celecoxib, naproxen, ibuprofen
Which adjuvants to use for neuropathic pain? How to use?
For neuropathic pain
- Gabapentinoids, TCA’s, SNRI’s
- Start at low dose and titrate slowly to improve tolerability
- May need to use 2 adjuvants if only a partial response
Do BZD, zolpidem and zopiclone have a role in chronic non-cancer pain?
No role in chronic non-cancer pain
Opioids in chronic non-cancer pain?
Opioids provide little, if any, benefit for chronic noncancer pain and cause significant harm
- Long-term use of opioids interferes with a patient’s ability to psychologically resolve negative emotions and reduces their problem-solving skills
- Opioids can reduce a patient’s motivation to participate in self-management strategies (e.g. exercise)
can consider, short term trial
> Buprenorphine patches, morphine, oxycodone, tapentadol or tramadol
Non pharmacological techniques for pain
A) physical
B) social techniques
C) pyschological
A)
- Physiotherapy Muscle relaxation Biofeedback Invasive techniques Injections and nerve blocks Electrical stimulation Neurosurgical procedures Acupuncture Ice/heat packs
B)
- Community support OT Self-help group Work retraining
C)
- Assertiveness training Behaviour modification Education Hypnosis Meditation Family therapy Distraction techniques
Early mobilization in acute pain should be done except when?
Except in cases of unstable fractures, spinal cord injuries and catastrophic injuries
> Gentle restoration of active range of motion
> Gradual introduction of functional activities
Example of passive treatments?
laser, ultrasound, acupuncture, massage, ice and heat
- Are not a substitute for active participation and offer little to rehabilitation on their own
- Discourage reliance on passive modalities – need to be used in combination with active treatments
Physical therapy encourages the body to make its own endogenous opioids like endorphins, enkephalins, dopamine, noradrenaline and serotonin
true or false
True
What is the most commonly prescribed psychological treatment for chronic pain?
Most commonly prescribed psychological treatment for chronic pain is CBT
- Assists people living with chronic pain
to reconceptualise their pain –>
how their thoughts (cognitions)
reciprocally interact with their actions
(behaviours)
- assists in identifying realistic and
practical goals, reinforces progress
and acknowledges effort and
achievement
What are the four Rs in analgesic prescribing
Right drug
- Type of pain - nociceptive/neuropathic
- Severity and expected duration of pain
Right dose
- Age, weight, renal and hepatic function
Right route
- Speed of onset –> aim of therapy
- Ability to swallow/absorb
Right interval
- Type of formulation
For paracetamol:
A) When is it used?
B) What happens in overdose?
C) What factors may increase risk of hepatotoxicity with paracetamol
D) When to reduce dose to 2-3 g per 24 hours?
A)
- Mild to moderate pain
- Less effective than NSAIDs, good safety profile when used at recommended doses
B)
Potentially life-threatening
C)
- Depleted glutathione stores (eg prolonged fasting or malnutrition)
- Treatment with hepatic enzyme inducers
- Severe renal, hepatic or cardiac impairment
- Dehydration
- Chronic alcohol intake
D)
- Weight < 50 kg
- ALT >50
- Prolonged fasting/malnourished
- Concurrent hepatic enzyme inducing medication
- Chronic etOH
- Dehydrated
- >65 years old
FOr NSAIDs;
A) when is it used
B) which has highest risk of CV events and lowest?
C) whats best for GI factors
D) risk factors
A)
Mild to moderate pain due to inflammation and tissue injury
- Synergistic with opioids and paracetamol
B)
- Diclofenac highest risk, naproxen lowest risk
C)
- Cox-2 selective best, then ibuprofen then diclofenac
D)
>65yo, high dose NSAID, concurrent use of aspirin, SSRIs, corticosteroids or anticoagulants, alcohol overuse, smoking, gord, h.pylori, CVD disease, HTN, waist cirumference, diabetes
When to use opioids in chronic non-cancer pain?
Opioids should only be considered for patients with chronic non- cancer pain once non-pharmacological therapies and non-opioid medicines have been optimised.
Which of the opioids are used for:
A) mild to moderate pain
B) moderate to servere pain
C) severe pain/severe chronic pain
A)
- Codeine – mild to moderate pain
- Tramadol – moderate pain
B)
- Tapentadol – moderate to severe pain
- Buprenorphine – moderate to severe pain
C)
- Morphine – severe pain
- Oxycodone – severe pain
- Hydromorphone – severe pain
- Methadone – severe chronic pain
- Pethidine – severe pain
- Fentanyl – severe pain
What are the indications of opioids?
Acute or cancer pain.
- May also be used for dyspnoea in palliative care
- Cough suppressant (codeine and derivatives)
What are the precuations for opioids?
Other medications that cause CNS/respiratory depression –additive effects
Hx seizures – increased risk of seizures (avoid pethidine and tramadol)
GI – caution in patients with ileus (avoid codeine and oral medication)
Renal impairment
- Avoid codeine, pethidine (accumulation of toxic metabolites)
- Oxycodone, tapentadol, fentanyl preferred (with dose adjustment)
Hepatic impairment
- Dose adjustment may be required –risk of coma
- Caution with Targin (oxycodone/naloxone)
Elderly
- Start low, go slow (increased risk of adverse effects)
Children and breastfeeding
- Avoid codeine
Patients at risk of Opioid induced ventilatory impairment
- Hx of obstructive airways disease (eg COPD or OSA)
- Utilise CPAP or supplemental O2 where appropriate
Who is codeine contraindicated in?
- Children <12 years of age
- <18 years undergoing tonsillectomy and/or adenoidectomy for obstructive sleep apnoea as deaths have occurred
- Breastfeeding (infant death has occurred)
What is codeine metabolised to?
Codeine metabolised to morphine by CYP2D6
- Normal metabolism 30mg codeine to 3mg morphine
- Poor metabolisers – no effect from codeine
> 6–10% of Caucasians and 1–2% of Asians
- Ultra-rapid metabolisers – increased risk of adverse effects
> Up to 10% of Caucasians, 1–2% of Asians, 21% of people from the Middle East and 29% of Ethiopians
Pharmacology of Tramadol
Metabolite O-desmethyltramadol acts on the µ-opioid receptor
Tramadol also inhibits reuptake of serotonin and noradrenaline
- useful in neuropathic pain
May be used in combination with more potent opioids
Contributes to serotonin syndrome
Lowers seizure threshold (can cause CNS stimulation)
Also metabolised by CYP2D6
Intra-individual variation in response and drug interactions
Reduce dose in renal impairment
Pharmacology of Tapentadol
Mu receptor agonist
Also inhibits noradrenaline reuptake
- Useful in neuropathic pain
Strong analgesic activity
Less CNS and GI AE’s
Reduce dose in moderate to severe hepatic impairment
Does not require metabolic activation
Why may Buprenorphine be used?
Partial agonist
- Ceiling effect on respiratory depression
- Less CNS, GI and dependence AE’s
- May precipitate withdrawal symptoms in opioid dependent people
- Effect is not reversed by naloxone in usual doses
- Caution in severe renal impairment and mod-severe hepatic impairment
What is the 1st line opioid? What is the AE?
Morphine 1st line opioid
- Oral, IV, IM, SC, epidural, intrathecal
- Other opioids may be used where adverse effects of morphine are unacceptable or there is concern about the effect of active metabolites
> Accumulates in renal impairment (esp. M6G) prolonging CNS fx
> Commonly causes itch (histamine release), N &V
> Delayed sedation due to delayed crossing of BBB
Compare oxycodone with morphine. What are the forms in comes in?
Better tolerated, quicker onset, more potent than morphine
- Reduce dose in moderate to severe renal impairment
IR and SR
- Oxycontin: Caution in swallowing disorders and abuse potential
- Targin: Contains naloxone (reduced constipation and abuse potential)
Pharmacology of fentanyl. What forms does it come in?
Potent synthetic opioid
- Good in renal impairment (no active or toxic metabolites)
- Caution – may contribute to serotonin toxicity
- Well tolerated
> IV = quick onset, short duration and patient controlled analgesia (IV)
> Transdermal patch = chronic pain only, not in opioid native patients, 24-72 hours to maximal effect.
> Lozenges, sublingual and buccal tablets – not interchangeable
> Intranasal
Pharmacology of hydromorphone
Potent opioid – 5x stronger than morphine
Reduce dose in moderate renal/hepatic impairment
Injection, mixture, tablets, SR tablets
Pharmacology of pethidine? Why not recommended?
Contributes to serotonin toxicity
Lowers seizure threshold
Toxic metabolite (norpethidine)
- May occur within 24 hours of starting pethidine.
- Early signs include anxiety and agitation; tremor, muscle twitching and seizures may occur later
Pharmacology of methadone
Also has NMDA antagonist effects
- Benefits in hyperalgesia, chronic pain
Watch for QT prolongation and CYP3A4 interactions
Complicated kinetics
- Long and variable t ½ (15-60h) –> autoinduction of hepatic enzymes with chronic use
- Complicated dose equivalence = pain specialist
What to do if adverse effects of opioids is limiting ability to control pain?
Control symptoms of adverse effect
Reduce dose of opioid
Add adjuvant/non-opioid
Switch to an alternate opioid (opioid rotation)
What are the adverse effects of opioids?
Nausea, vomiting (give antiemetic initially – improves with time)
Constipation/gastroparesis (give laxative ongoing, watch diet, mobility and fluids)
Itch (change opioid - avoid morphine, fentanyl ok)
Confusion/hallucinations (reduce dose, change opioid – caution tramadol, consider if pain causing symptoms or opioid)
Dry mouth (good oral hygiene)
Urinary retention
What is the most serious AE of Opioids
Respiratory depression
- Most serious adverse effect
- Decreased sensitivity to CO2
- Best judged by degree of sedation (use sedation score)
- RR reduction a late and unreliable indicator
- Worsen OSA
What are the long term adverse effects of opioids?
Immune compromise
Neuroendocrine symptoms
- Oedema, gynecomastia, amenorrhoea, osteoporosis, low testosterone
- Long term use of opioids suppresses the HPA axis resulting in suppression of all hormones – monitor hormone levels
Opioid induced hyperalgesia
Affects mood and sleep quality
What is opioid tolerance? what happens?
Decrease in drug effect over time, such that an increase in dosing is required to have the same effect
> Differential diagnosis: opioid induced hyperalgesia
- Increased dose doesn’t help the pain
- Pain can be widespread
- Opioid use increases the levels of pain
summary for acute pain management
A tolerable level of pain that allows optimal physical and emotional function
- Early mobilisation
Multimodal pharmacotherapy
- Early control of pain
- Simple analgesia, adjuvants, inhaled analgesics, local anaesthetics, opioids where necessary
- Opioids – use for minimum time, have plan
Whole person approach
Manage acute pain well to avoid acute –> chronic
Summary of paharmacological management?
Multi-modal analgesia
- Synergistic or additive effects, ↓doses and ↓AE’s, opioid sparing
Simple analgesia
- Paracetamol - risk in overdose, caution hepatic impairment -
- NSAIDS - contraindications and co-morbidities
Opioids
Adjuvants
Summary of opioids?
Tramadol
- Serotonin toxicity, lowers seizure threshold
Tapentadol
- NRI (neuropathic pain)
Buprenorphine
- Partial agonist. Available patch and sublingual
Morphine and oxycodone
- Standard opioids. Watch Targin® in hepatic impairment
Fentanyl and hydromorphone
- Potent
Pethidine
- Serotonin toxicity, lowers seizure threshold, toxic metabolite
Methadone
- NMDA antagonist, QT prolongation, pain specialist only
Explain the concept of nociceptive pain. Provide examples of the different subtypes of nociceptive pain including the tissues affected and the characteristics of the pain.
Nociceptive pain is “physiological” pain arising from stimulation of superficial or deep nociceptors by noxious stimuli such as tissue injury or inflammation. Subtypes include somatic and visceral pain. Somatic pain can be superficial or deep Visceral pain originates from the walls of visceral organs.
