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
What to do for opioid dependence?
Withdrawal symptoms occur if chronic treatment is stopped suddenly or an antagonist is given
- This is NOT addiction
- Gradually reduce doses before cessation
What guides opioid use in elderly patients?
Generally require lower doses
>80years ~half the dose of a younger person
Constipation – prophylactic laxatives required
More sensitive to CNS effects
> falls risk
What guides opioid use in chronic pain patients?
Consider their usual background analgesia plus new pain requirements (eg post-op)
- Multimodal analgesia
> Eg ketamine infusions
> May need higher doses of breakthrough opioids
What to use in patients who still require pain management?
Regional or epidural anaesthesia
- Ideally managed with input from addiction specialist liaising with regular prescriber and pain specialists
What to do before/during using opioids?
Assess pain intensity, cardiorespiratory status, level of sedation and adverse effects regularly –> monitor
Use small increments for dose increases
For SR products initially increase the dose (not the frequency) if required
- Occasionally an increase in frequency maybe appropriate
High dose or rapid IV admin may rapidly cause respiratory depression, circulatory collapse and even cardiac arrest
- Have naloxone and resus facilities available
consider take home naloxone for high risk patients
What is naloxone nasal spray used for? How long does it take to work? Who is it recommended for?
Naloxone is part of emergency rescue treatment for known or suspected opioid overdose. It can be administered via nasal spray or intramuscular injection and takes effect 2 to 5 minutes later.
- Naloxone nasal spray is recommended for patients at increased risk of opioid overdose or people who are likely to witness opioid overdose
When prescribing opioids for patients with increased overdose risk, incorporate strategies to minimise risk including coprescribing naloxone: high dose potent opioid use, hx substance use disorder, comorbidities that increase the risk of respiratory depression (eg OSA, renal or hepatic impairment)
What opioids to use in acute short term pain?
Consider if an IR (immediate release) opioid is needed in combination with paracetamol +/- NSAID +/- other analgesia
Both pain and the need for opioids should reduce over time
- Typically quite rapidly
- Short-stay and emergency department patients do NOT need SR opioids
- Patients shouldn’t need opioids for the entirety of their recovery
- Opioid supply should reflect anticipated need or follow-up – NOT pack size!
Sustained release opioids are NOT licenced or recommended for the management of acute pain
What opioids to use in chronic pain (cancer pain)?
Use a SR opioid regularly and calculate a prn IR dose for breakthrough or incident pain
Never use SR opioids prn!
Always use opioids in combination with other analgesics
Always have a plan for the use of opioids
Duration, expected outcome, review date
What are SR examples of opioids
Targin® SR (oxycodone/naloxone) usually bd
Oxycontin® SR (oxycodone) usually bd
MS Contin® or Kapanol® SR (morphine) usually bd
Norspan® patches (buprenorphine) change patch weekly
Fentanyl patches (potent opioid – not in opioid naïve) change every 3 days
Jurnista® SR (hydromorphone – potent opioid) usually once daily
Palexia® SR (tapentadol) usually bd
Tramadol SR usually bd (Durotram® is once a day)
What are IR examples of opioids?
Oxycodone IR tablets, capsules, liquid
Morphine IR tablets, liquid
Buprenorphine sublingual tablets
Fentanyl lozenges, sublingual and orally disintegrating tablets
Hydromorphone liquid and IR tablets
Tapentadol IR tablets
Tramadol IR capsules and liquid
What not to do for SR tablets
do not crush them
What are the harms of opioids?
- Constipation
- Death
- Depression
- Falls and fractures
- Hormonal effects
- Hyperalgesia
- Motor vehicle collisions
- Opioid use disorder
- Respiratory depression and sleep disordered breathing
- Tolerance, physical dependence and withdrawal
What are the ways to optimise non-pharmacological management before and during opioid trial
Active physiical therapies
- hydrotherapy
- exercise based physiotherapy
- occupational therapy
- activity pacing
Psychological therapies
- CBT
- relaxation training
Other treatment options
- acupuncture
What are the options for non-opioid treatrment in chronic-non cancer pain?
simple analgesia
- paracetamol and NSAIDs
TCA (amitryptilline and nortripytilline)
- for neuropathic pain
- nortriptyliine = less sedating
Gabapentinoids
- Adjuvant for neuropathic pain
- AE include drowsiness and peripheral oedema
SNRI (duloxetine and venlafaxine)
- Recommended for neuropathic pain
When is the risk of harm from opioids increased?
For patients with complex co-morbidities, and when co-prescribed with BZDs and other sedatives
> avoid prescribing opioids for these patients
What is BRAN
decision making process
- Benefits
- Risks
- Alternatives
- Nothing (what if we do nothing…)
How to set expectations when starting an opioid in chronic non-cancer pain?
Duration: acceptable trial period is up to 8 weeks, syccess or faulure should be determined within 2-4 weeks
Formulation and dose: start at a low dose, any response should be evident at oral morphine equivalent dose at less than 60mg
Treatment outcomes: agree on goals of opioids treatment and how these will be monitored, goals for physical and cognitive functioning
exit strategy: important to agree in which opioid treatment will be stopped
follow up: review patient every 1-2 weeks to monitor progress
How to start an opioid in chronic non-cancver pain? Tips and advice.
- Opioids have a time-limited benefit, generally no longer than 3 months
- Conside use of paracetamol for opioid sparing benefits
- Trial regular opioid free periods
What are the 5As in opioid therapy as a monitoring tool?
Activity
- What progress has been made in the patients functional goals
Analgesia
- How does the patient rate the pain over the last 24 hours
Adverse effects
- Constipation, nausea, dizziness, drowsiness etc
Aberrant behaviours
- Any problematic behaviour or signs of misuse/abuse
Affect
- Any changes to how the patient has been feeling
What are the four principles of motivational interviewing?
- Empathy
- Developing discrepancy
- Rolling with resistance
- Supporting self-efficacy
What are the five key skills for motivational interviewing?
- Open-ended questioning
- Affirmations
- Reflections
- Summarisations
- Elicit – provide – Elicit
Why is tapering of opioids good?
- Tapering has been shown to improve function without worsening pain
- Benefits of opioids reduce over time while risk of harms increase
- Pain management alternatives have fewer side effects
Who are the patients at risk of overdose?
Using >60 mg OMEDD (oral morphine equivalent daily dose) or >30mg OMEDD for certain populations (older patients)
- concomitant use with other CNS depressants (alcohol, benzodiazepines)
How to rapid taper for short term exposure in reponse to misuse or intolerable adverse effects?
reduce the daily dose by 10– 25% each week
How to slowly taper (eg after years of exposure)?
Reduce the daily dose by 10–25% each month
What to do for moderate to severe OUD (overuse of opioid)?
Rotation to opioid agonist treatment (OAT) may be more appropriate
- Taper may increase risk due to loss of tolerance
What is used for opioid agonist treatment?
May be a better long term option
- Methadone and buprenophrine are both effective in prescription opioid dependence
- Buprenorphine less restrictive and has a good safety profile
How to reduce opioid harms in community pharmacy?
- recommend and supply OTC nasal naloxone
- recommend staged supply where appropriate
- perform a chronic pain medscheck
- consider a HMR for the aptient
How to reduce opioid harms in hospital pharmacsists?
- Limit supply of opioids at discharge to clinical need by using new half pack sizes
- Adopt an opioid stewardship program in hospital
- Add information about the opioid to the discharge summary (including indication, intended duration and recommendation for GP to assess at next consultation)
All patients with moderate to severe cancer pain should try?
Opioid analgesia
- Once adequate control is achieved with immediate release products, consider conversion to slow release formulations
What to use for metastaic bone pain (cancer)
Radiotherapy, NSAIDS, bisphosphonates, corticosteroids, radioactive strontium-89
What to use for pain due to inflammation and oedema in confined spaces?
raised ICP, hepatic capsular pain, nerve compression/infiltration
- Dexamethasone
What needs to be kept in mind for opioid conversion?
GUIDE ONLY – need close monitoring
- Effectiveness
- Adverse effects
- Toxicity
Use 50-75% of calculated dose
> Monitor closely and titrate dose as necessary
> Have breakthrough opioid analgesia available
What is the equianalgesic dose of morphine for 200 micorgram buprenorphine tablet?
8-16 mg
When is a breakthrough (rescue) opioid used? How much sould be used?
In patients receiving long-acting opioid formulations for chronic pain (SR, transdermal), a “rescue” dose for breakthrough pain is recommended.
> an immediate-release form of the same opioid is used (e.g. morphine IR with morphine SR)>
- The size of the breakthrough dose should be 1/6th – 1/12th (5%-15%) of the patient’s 24-hour baseline opioid dose
> Inpatient setting, rescue doses can be provided IV every 15-30 minutes.
> Oral rescue doses can be offered as needed over the normal dosing interval of the drug (typically every 4 hours and not <1hr)
> If pain not controlled after 3 doses, overall management reviewed
What is an adjuvant?
An adjuvant is a substance that is not primarily used for the treatment of pain but can increase analgesia
Outline some information and what type of drugs are used in the folloowing adjuvant categories:
A) Antiepileptics
B) TCA
C) SNRI
D) Skeletal muscle relaxant
E) NMDA-receptor antagonists
F) Hormones, hormonal analogues
G) Biphosphonates
H) BZD
I) LA
J) Capsaicin
K) Botulinium toxin A (botox)
L) Alpha 2 agonists
M) Steroids
N) Inhaled agents
O) PEA (Palmitoylethanolamide)
sucrose, vitamin C and cannabinoids also used.
A)
Neuropathic pain
Carbamazepine (trigeminal neuralgia), gabapentin, pregabalin, valproate, topiramate, clonazepam
gabapentinoids: black box warning, caution in combo with other CNS depressants.
B)
Neuropathic pain, musculoskeletal pain (eg chronic nociceptive pain)
Amitriptyline, nortriptyline (least anticholinergic fx), doxepin
C)
Neuropathic pain, musculoskeletal pain (eg chronic nociceptive pain)
Duloxetine (most evidence – can use up to 120mg), venlafaxine, milnacipran
D)
Muscle spasms
Baclofen, diazepam
E)
Ketamine wafers and infusion
Neuropathic pain
F)
Calcitonin: Malignant bone pain, burn pain, phantom limb pain
Octreotide: Bowel obstruction (reduce secretions)
G)
IV bisphosphonates, denosumab
Bone pain in malignancy (also use NSAID, glucocorticoids, radium 223)
H)
Diazepam, midazolam, lorazepam
Skeletal muscle relaxant, antianxiety
I)
Lignocaine = Topical, 5% patch and infusion Patch for focal/regional pain
Flecainide = Refractory neuropathic pain
J)
Topical in refractory post-herpetic neuralgia and painful polyneuropathy
Cream and patches
K)
Local injection
L)
Clonidine
M)
Nerve compression, raised intracranial pressure, bone pain, bowel obstruction, lymphoedema
Prednisolone, dexamethasone
N)
Methoxyflurane
Nitrous Oxide (watch B12 and folate with regular use)
O) Endogenous anti-inflammatory (low levels in ppl with chronic pain)
For cannabis, what is THC and CBD?
Nabiximols (Sativex) is the only medicinal cannabis registered in Australia for spasticity in MS
THC (delta-9-tetrahydrocannabinol) – S8 Responsible for intoxicating and some therapeutic effects
CBD (Cannabidiol) – S4 if CBD only Wide range of pharmacological but no intoxicating effects
What is AE of THC?
At higher doses –> dizzy, “spaced out”, sedated
Increased appetite
Paranoia, severe anxiety and psychotic reactions
> Driving risk with THC
> Withdrawal (THC)
What is the AE of CBD?
Can reduce these AE’s – possible anxiolytic and antipsychotic effects
Well tolerated at high doses (up to 5000mg) – diarrhoea can be reported
Potent inhibitor of various CYP450 enzymes
> Interactions do not appear to be clinically significant in adults (risk in children with epilepsy) – more research required
What neuropathic pain? How to treat? What are the types?
Chronic and difficult to treat
Often refractory to simple analgesics, including NSAIDs
- Poor relief with opioids alone
- Antidepressants and antiepileptics (adjuvants) drugs of choice
Types: Peripheral neuropathy (e.g. postherpetic neuralgia (PHN), painful peripheral diabetic neuropathy) and central sensitisation pain syndromes (CRPS, CVPS, CWP)
What is used as 1st,2nd,3rd,4th,5th line treatment in neuropathic pain?
1st line
TCA’s SNRI’s Localised – lignocaine 5% patch
2nd line
Pregabalin, gabapentin
3rd line
Tramadol, tapentadol
4th line
Opioids
5th line
Valoprate, sublingual ketamine
What to use for trigeminal neuralgia (neuropathic pain)
Carbamazepine
What are interventional therapies for neuropathic pain?
Spinal stimulators
Percutaneous radiofrequency neurotomy
Epidural block Local anaesthetic and corticosteroid
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 for chronic non-cancer pain
Goals of care
To provide strategies to live a meaningful/functional life with pain
Biopsychosocial model or “whole person” approach
Multidisciplinary care is the gold standard
- Pain education
- Psychology strategies
- Physiotherapy strategies
- Lifestyle measures –> sleep hygiene, nutrition, stress mx, smoking cessation
> medications as scaffolding
- Medications only if demonstrated benefit – as part of overall plan
- Improve day-to-day function and quality of life
- Provide support while non-pharmacological treatment strategies are built up
> Limited evidence paracetamol + NSAIDS– only if nociceptic pain
> adjuvants for neuropathic pain
- Regular review and consideration of deprescribing
- Opioids – little benefit, significant harms
> Targeted treatments if available (eg DMARDS in RA)
Language guidelines for chronic pain
- Using language that is empowering, accurate, respectful and inclusive
- A cause of iatrogenic pain?
Summary of non-pharmacological techniques in acute and chronic pain
Non-pharmacological techniques
Physical, social and psychological –> imp in both acute and chronic pain
acute pain
> RICE = Relative rest, ice, compression, elevation AND Early mobilisation is important in most cases AND Discourage reliance on passive modalities
chronic pain
Physical therapies
> Encourage body to make it’s own endogenous opioids, reduce falls risk, reduces muscle atrophy and improves gait
> Meditative movement tx can help sleep, depression, fatigue and QOL
> Pacing vs boom and bust
> Discourage reliance on passive modalities
CBT
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
Summary of core competencies for pharmacists in the safe supply of opioids.
- Understand mandatory legislative requirements
- Recognise clinical side effects of opioids
- Recognise risks associated with interactions
- Provide appropriate patient education
- Identify when collaboration with a prescriber is necessary
- Determine when pain management is inadequate
- Evaluate and address overdose risk
Opioid epidemic, summary of chronic non cancer pain
Opioid analgesia attenuates with time, while the harm persists or increases with time and increasing doses
- AE’s in 80% patients on long-term opioids
- ↑ risk of harm if complex comorbidities or other sedative use
> Tapering opioids improves pain, function and QOL
> Regulatory changes –> Pack sizes, authority indications, 12 month review
Optimise non opioid management
- Active physical tx - pacing
- Psychological tx- CBT and mindfulness
- If appropriate other pharmacotherapy –> para/NSAID/TCA/gabapentinoids/SNRIs
Summary of opioid trial in chronic non-cancer pain
Trial of up to ~8 weeks, start with low dose, agree on goals of treatment (physical/functional goals), exit plan
- Review every 1-2 weeks, written opioid agreement
- 5 A’s – activity, analgesia, adverse effects, aberrant behaviours, affect
summary of tapering opioid in chronic non-cancer pain
To reduce risk of harm and improve pain, function and quality of life
- Especially if function has not improved, risk of opioid use disorder, risk of overdose
Engage with patient – patient must agree to taper – provide support –> motivational interviewing
- Open-ended questions, affirmations, reflective listening, summarise discussion
Taper
- Rapid taper for short-term exposure or in response to misuse or intolerable adverse effects: reduce the daily dose by 10–25% each week
- Slow taper (eg after years of exposure): reduce the daily dose by 10–25% each month.
- Aim to reduce to lowest effective dose (including cessation)
Opioid use disorder
- May need to consider buprenorphine/methadone
- Taper may increase risk due to loss of tolerance
Summary of cancer pain and palliative care
Paracetamol, NSAIDS, adjuvants, opioids
- Bone pain and inflammation
Opioid conversion
- Practice converting opioids – not exact– need to monitor
- Incomplete cross-tolerance -use 50-75% of calculated dose
Breakthrough opioids
- 1/6th – 1/12th (5%-15%) of 24-hour baseline opioid dose
Explain why neural plasticity can be problematic in chronic pain, and why acute pain is treated more aggressively than the cautious approach used in previous decades?
Neural plasticity is usually a good thing as it helps the nervous system to learn and adapt to changing requirements. However, in chronic pain neural plasticity may result in maladaptation.
> Nociceptors become more easily stimulated when there is continuous exposure to painful stimuli.
> Pro-inflammatory mediators when present for extended periods as seen in chronic inflammation will lead to excitation of neurons carrying pain signals.
> Persistent pain leads to neuronal fibres in the dorsal horn firing repeatedly
= When this occurs smaller pain-signals result in a greater pain response. It is one of the reasons acute pain is now treated more aggressively than in the past.
. Explain the difference between chronic and acute pain in terms of the aims of treatment.
In acute pain the aim is to treat the cause of the pain and provide rapid and effective analgesia to reduce the chance of transition to chronic pain.
In chronic pain medications are not expected to achieve resolution of pain, but instead a reduction in pain that allows the patient to function. Addressing functional impairment, depression, other psychosocial issues, and quality of life, are key goals of treatment for chronic pain.
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.
