Chronic Pain Flashcards
Chronic non-cancer pai
Heterogenous physical and psychological condition that
can have a significant impact on physical ability,
emotional well-being, and quality of life
May be pain that
● Persists beyond normal healing time
● Relates to chronic degenerative disease or persistent
neurologic condition
● Emerges and persists without an identifiable cause
Lots of conditions that fall under chronic pain
Pathophysiology - Revisited
Dysfunctional pain
or
Nociplastic pain
No known structual NS lesion
Or active periph inflaamm
Spontaneous pain with lack of stimulus, pain with non-painful stimuli
Maladaptive and potentiall persistent
Chornic pain often amix of nociceptive, nociplastic, neuropathic pain
Populations that bear more of the chronic pain
burden include
● Older adults
● Women
● Indigenous Peoples
● Veterans
● People who use drugs
Risk Factors
● Psychological vulnerability
(catastrophizing)
● Anxiety or depression
● Female sex
● Younger age (adults)
● Genetic predisposition
● Inefficient diffuse noxious
inhibitory control (DNIC)
● Descending pathway of pain
inhibition
● Nerve damage due to injury
or surgery
● History of poor acute pain
management
● History of poor response to
common analgesics
Complications
Chronic pain often presents as a complication of other
disease states, but may also result in its own complications:
● Deconditioning
● Hormonal effects
○ e.g., excess catecholamine production
● Neuropsychiatric symptoms
○ e.g., insomnia, memory loss, cognitive decline, depression
Overactivation of symp nervous system
Adrenaline release combined with cortisol
More anxiety or dread
Chronic Low Back Pain
3 trajectories
Low back pain is the leading cause of disability in the
world
One of the most common reasons that patients seek
care and a top reason for early retirement and
income poverty
3 trajectories: first is it quickly moves towards a state of no or very little pain
Ongoing moderate pain, fluctuating
- Variable intensities that wax and wane
Constant severe pain, persistent trajectory
There are many potential causes of low back pain
● Mechanical
○ e.g., degenerative joint disease, herniated disk, vertebral #, etc
● Non-mechanical spinal conditions
○ e.g., cancer, infection, inflammatory arthritis, etc
● Visceral disease (non-spinal disease with referred pain)
○ e.g., prostatitis, pelvic inflammatory disease, pancreatitis, etc
The majority of the time in chronic low back pain, there is
no identifiable active cause – but should still assess for
red flags`
Intiial assement for pt who may hve srious pathology or barriers to recovery and those that need further intervention
Chronic Low Back Pain
red flags
possible fracture: major trauma, such as MVA or fall from height
possible tumor or infection: recent fever chills unexplained weight loss
possible cauda equina syndrome: saddle anesthesia, numbess, recent onset of bladder dysfxn, sudden bilteral leg weakness
NIFTI
Tumor, infection
yellow flags
Psychosocial barriers
to recovery
belief that pain and activity are harmful
sickness behaviours
low or neg moods
see slide 13
Chronic Pain - Assessments
Accurate diagnosis
Identify iatrogenic factors
Psychiatric and psychosocial assessment
Gather the pain history
Goals of Therapy
● Treat underlying cause of pain
● Reduce pain
● Improve quality of life
● Improve function
● Improve other symptoms associated with pain
○ Sleep, mood, etc
What sort of tings would you like to do
If you give them opioids, tey may not be very functional
Treatment Algorithm
Using low back pain as
an example
Lots of diff nonpharm for perisstent nonspecific
As meds may not give as much benefit
nopharm more benefit, trial and error largely
Treatment AlgorithmNon-pharmacologic
Treatment
Self-management programs
● Activity
● Relaxation techniques
● Communication skills
● Modification of negative “self-talk” or
catastrophizing
● Education
● Sleep hygiene
● Stress management
● Cognitive behavioural therapy
● Physiotherapy
● Tai chi
Congitive is recommended commonly for psych therapies
Execise is beneficial for function, a bit for relief of pain
Small size effect for exercise
Potential for harm with spinal manipulation
Moderate effect with cognitive therapy
peer simplified chronic pain guidelne
slide 21
4 ps in pain manageent
prevention, psych, physical, pharmaceutical
musc therapy
Some evidence both mechanistic and otherwise
May help mitigate pain
Pharmacologic
Treatment
Tricyclic Antidepressants
Nortriptyline → Initial: 10 mg PO hs
Usual: 10-50 mg PO hs
Desipramine
Amitriptyline → Initial: 10-25 mg PO hs
Imipramine Usual: 25-100 mg PO hs
Start low and increase dose slowly (q1-2ks)
Adequate trial: ~2-4 weeks at adequate target dose
Initae one agent at a time not multiple
Nortriptyline secondary amine
Amitryptiline teritary
Secondary is less anticholingeric, better tolerated
Dont need to memorize dosing
Tricyclic Antidepressants
Evidence:
Neuropathic pain → NNT =3 (≥ 30% pain improvement)
NNH = 13 (ADR causing withdrawal)
30% pain improvement at least is minially clincally important
Chronic low back pain → may not significantly improve
pain or disability
Amitriptyline most studied, but nortriptyline generally
better tolerated
If there is NP componetnt (often there is), TCAs can be cisb==bsudered (prefered over trial of opioids)
Tricyclic Antidepressants
Adverse effects
● Drowsiness/sedation
● Confusion
● Dry mouth
● Hypotension
● Constipation
● Urinary retention
● Weight gain
27
● QTc prolongation/arrhythmia
2-3 hours before bedtime
Minimze residual sedation in the morning
In the AM
Unintentional overdoses not common
Low risk of seizures at therapeutic dose, at setting of OD risk is higher for seizures
Serotonin-Norepinephrine
Reuptake Inhibitors
Duloxetine → 30 mg PO once daily x 1 week, then
60 mg PO once daily
Venlafaxine XR → 37.5 mg PO once daily x 4-7 days,
then 75 mg PO once daily
(may need to get to 150-225 mg/d for benefit)
Allow ~ 1 week at each dose for tolerability
Adequate trial: at least 2-4 weeks at effective dose
Can go higher in these dosing ranges, haven’t seen much additional benefit for it above 60mg
More AE
150mg at least for benefit of pain, more NE kicks in
Better for bpain if you hit 5-HT AND NE
Duloxetine has higher NE activity at standard doses
Venlafaxine has higher 5HT activity, neeed higher dose to hit NE
Serotonin-Norepinephrine
evidence
Reuptake Inhibitors
Duloxetine
Chronic low back pain → NNT 7-8 (30-50% pain improvement)
NNH 6-12 (discontinue due to AE)
Also effective for other pain presentations
Venlafaxine
Evidence is scant
Magnitude of benefit varies
Usually not life threatening AE but du to tolerance, dizzine
Pt start on lower dose for tolerance reasons
Duloxetine better evidence usually preferref for chronic pain
Serotonin-Norepinephrine
Reuptake Inhibitors
Adverse effects
● GI
● Nausea
● Dry mouth
● Dizziness
● Sleep disruption, take in AM
Seizure risk with toxic doses
Risk of sertoonergic syndrome
Duloxetine is a moderate 2d6 inhibitor, venla is mild inhibitor
Drug Interactions
● Pharmacodynamic
○ Serotonergic
● Pharmacokinetic
○ CYP 2D6 (substrate + inhibitor)
○ CYP 3A4 (venlafaxine) (substrate)
○ CYP 1A2 (duloxetine) (substrate)
Gabapentinoids
Gabapentin → Initial: 100-300 mg PO HS (or 100 mg TID)
Increase by 100-300 mg per day (or weekly)
Usual: 600 mg PO TID-QID
(may require at least 900 mg/d for benefit)
(at least 1800 mg/d often needed in trials)
Pregabalin → Initial: 50-75 mg PO BID (or 25-50 mg TID)
Increase to 150 -300 mg PO BID
Titrate every 3-7 days, as tolerated, until at effective dose
Allow 1-2 weeks to assess benefit and tolerability
31 Adequate trial = ~3-4 weeks on adequate dose
KNOW MINIMUM EFFECTIVE DOSE = 900MG
Start 100-200 and slowly increase to it
Can go up to 3.6g/day
2.4g/day - usually would not be pushed further
More easy to dose; start dosing ranges where likely to be beneficial
300mg PO BID is max, 250mg is sweet spot w good ad==efficacy
Slow.ly weaned as can have withdrawal effect
Gabapentinoids
Evidence
Gabapentinoids may not improve pain or disability in
chronic low back pain and may increase risk of AEs
● DB, PC, RCT, N=108 from primary care/community settings
○ 67% F/U at 12 weeks
○ No significant difference in pain improvement or disability improvement.
Marked AEs gabapentin 55% vs placebo 32%
○ Pain. 2016;157(7):1499.
● SR → 3 RCTs (N=100) gabapentin vs placebo for lower back pain (+/- radiating
leg pain). No significant difference in pain improvement within 3 months
Chronic low back pain with opioids → may increase risk of
opioid-related deaths.
Neuropathic pain
● Gabapentin → NNT 7; NNH 8
● Pregabalin → NNT 5-8; NNH 14
Some benefit
If there is NP component - more likely to get benefit from gabapentinoid on board
Publication bias - exagerated beneif==fits from gabapentin
Gabapentinoids
Adverse effects
● Dizziness*
● Somnolence*
● Weight gain (? pregabalin > gabapentin)
● Euphoria/abuse (? gabapentin > pregabalin)
● ? ↑HF (dose-dependent ↑ peripheral edema)
More abuse potential w gabapentin, snort or inject at high dose
Not sure if cause edema or HF
No known metabolism interactions, there are both renally cleared
Check renal fxn if impaired
Topiramate
Initial: 25 mg po HS
Usual: 100 mg po BID (or 50 mg AM, 100 mg HS)
Increase dose weekly
Evidence
Chronic low back pain → may improve pain in short
term (very limited evidence)
Antiepiliptic
More in migraine prevention
Small dose then increased weekly
Scant evidence for it
CI may be beneficial or may cause harm
Topiramate
Adverse effects
● Drowsiness, dizziness, fatigue
● Ataxia, tremor
● Paresthesia
● Difficulty word-finding
● ↓ concentration
● Other non-CNS adverse effects
Lots of CNS AE
