Fellowship revision > Pain > Flashcards
Pain Flashcards
What is an example of a pain assessment tool for patients who are elderly or have cognitive impairment?
What’s the score range?
Domains?
Abbey pain scale
0-18
Vocalisation
Facial expression
Change in Body Language
Behavioural Change
Physiological change
Physical changes
What are appropriate paediatric doses of oxycodone, fentanyl & morphine postoperatively?
All only if SS<2:
oxycodone 0.1-0.2mg/kg PO 2-3hourly prn
fentanyl 0.1-0.2microg/kg 5-minutely IV prn (pain protocol)
morphine 20-30microg/kg IV 5-minutely pain protocol or 0.1-0.3mg/kg PO q4h
gabapentin paediatric dose?
5mg/kg PO BD
How to manage buprenorphine overdose?
remove patch (slow offset approx 12 hrs), give naloxone (may require higher doses & longer duration infusion)
Describe the anatomy of the stellate ganglion
sympathetic ganglion
on either side of the root of the neck
formed by fusion of inferior cervical ganglion with 1st & occasionally 2nd thoracic ganglion
only supplied by efferent sympathetic fibres from ipsilateral sympathetic chain (which lies inferiorly) along with 1st & 2nd thoracic segmental anterior rami
anteriorly: subcut tissue, SCM, subclavian artery, carotid sheath
posteriorly: anterior scalene, sheath of brachial plexus, neck of 1st rib, TP of C7, vertebral artery, longs Colli
laterally: sup intercostal vein & artery, ventral rams of T1
medially: prevertebral fascia, vertebral body of C7, does, Tx duct
inferiorly: pleural dome over lung apex
Describe the anatomy of the stellate ganglion
sympathetic ganglion
on either side of the root of the neck
formed by fusion of inferior cervical ganglion with 1st & occasionally 2nd thoracic ganglion
only supplied by efferent sympathetic fibres from ipsilateral sympathetic chain (which lies inferiorly) along with 1st & 2nd thoracic segmental anterior rami
anteriorly: subcut tissue, SCM, subclavian artery, carotid sheath
posteriorly: anterior scalene, sheath of brachial plexus, neck of 1st rib, TP of C7, vertebral artery, longs Colli
laterally: sup intercostal vein & artery, ventral rams of T1
medially: prevertebral fascia, vertebral body of C7, does, Tx duct
inferiorly: pleural dome over lung apex
What is CRPS type 1?
occurs following an initiating event (eg. trauma or injury) with little or no nerve injury
What is CRPS type 2?
nerve injury= the causative factor to the pain
What are some indications for stellate ganglion block?
Chronic pain conditions- eg. CRPS type 1 & 2, HZ affecting face & neck, refractory chest pain or angina, phantom limb pain
Vascular disorders of the upper limb- eg. Raynaud’s, vasospasm, scleroderma, frost bites, embolic phenomenon, trauma
What are some contraindications to stellate ganglion block?
unable to consent
local infection or neospasm
anatomical or vascular anomalies
recent MI
anti-coagulated pts or those with coagulopathy
glaucoma
severe emphysema
cardiac conduction block
pre-existing contralateral phrenic nerve palsy (may precipitate resp distress)
What are some conditions associated with sympathetically maintained pain?
occlusive arterial diseases
diabetes mellitus
venous ulceration
neuropathic conditions eg. CRPS, postherpetic neuralgia or after peripheral nerve lesion
What are some complications of stellate ganglion blockade?
Horner’s syndrome (which does indicate successful stellate ganglion block)
damage to adjacent structures (vascular (carotid artery, IJV, inf thyroid artery), neurological (vagus nerve, brachial plexus root), PTx, chylothorax, oesophageal perforation)
inadvertent spread of LA (intravascular, neuraxial/brachial plexus, hoarseness from RLN injury, elevated hemidiaphragm from phrenic nerve blockade)
LAST
Infection
What are some contraindications to stellate ganglion block?
unable to consent
local infection or neospasm
anatomical or vascular anomalies
recent MI
anti-coagulated pts or those with coagulopathy
glaucoma
severe emphysema
cardiac conduction block
pre-existing contralateral phrenic nerve palsy (may precipitate resp distress)
what are the sedation score grades?
0= wide awake
1= easy to rouse
2= easy to rouse but unable to remain awake
3= difficult to rouse
To what should opioid be titrated? why?
sedation score <2, given that a score of 2 indicates early OIVI
describe the concept of multimodal analgesia?
combinations of analgesics with different sites or modes of action may improve analgesia & pt satisfaction & reduce requirements, hence adverse effects (eg. respiratory & GI complications, PONV, sedation, dizziness & LOS) & improves mobilisation cf opioids- evidence in TKA, UL ortho surgery, spinal surgery, laparoscopic sleeve gastrectomy, open gastrectomy, cardiac, LSCS, rhinoplasty. Multimodal analgesia incorporates PRE-EMPTIVE or PREVENTIVE pain psychoeducation
Does depth of anaesthesia (BIS 30-40 vs 45-60) have any effect on post-op pain or opioid requirement?
No
What are benefits of pre-emptive or preventive pain psycho-education?
reduce pain intensity, analgesic use, LOS, anxiety, CPSP
An important component of multimodal analgesia
Spinal level for cystoscopy with ureteric stent?
T10; innervation ureters T12-L2 (pain), T10-L1 sympathetic), urethra somatic pudendal (S2-4), parasympathetic S2-4, sympathetic T12-L2
What are some ways to measure pain?
Categorical (quick & simple, useful in elderly or visually impaired & some children)
eg.
verbal descriptor scale- mild/mod/severe/excruciating (can convert to numeric scores, good correlation btwn VDS & VAS but VAS is more sensitive measure of pain treatment outcome (easier to detect differences btwn treatments). also limited by cultural/linguistic differences in interpretation.
pain “relief”: none/mild/mod/complete
Visual analogue scale: >=70mm is “severe”, 0-5 is no pain, 5-44 mild pain 45-69 moderate pain. reduction in pain intensity 30-35% clinically meaningful. simple & quick, avoid imprecise descriptive terms but unsuitable for can aged <5yo, require coordination.
Verbal NRS correlates well with VAS- doesn’t require equipment
Pain meter: 5 coloured emoticon faces on slide ruler, less variance than scores with VAS
Functional activity scale score: 3-level ranked categorical score:
A= able to undertake activity without limitation due to pain
B= mild limitation (pt can do the activity but experiences mod-severe pain)
C= unable to complete an activity due to pain, pain Rx-related adverse effects
Chirldren:
Faces pictorial scales
FLACC scale: Faces, Legs, Activity, Cry, Consolability
Specific tools (eg. NPQ) for neuropathic pain
PS45 Statement on Patients’ Rights to Pain Management and Associated Responsibilities)
enhanced pain management has been associated with improved outcomes after surgery & trauma, more successful rehab in pts w persistent pain & potentially improved survival of pts w Ca p+
All pts w pain har right to have their complaint of pain respected, thoroughly assessed, timely management or referral, in setting goals regarding their pain management, if required multi-D teams to address physical & psychological aspects of pain management. to have risks/benefits/alternatives of possible interventions explained to them.
they have responsibility to engage openly w healthcare providers, to participate actively in their care & decisions, to consider best-practice advice.
Pain, acute & chronic definition
placebo definition
an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
acute pain= Pain of recent onset & probable limited duration, usually has identifiable temporal & causal relationship with injury or disease, generally considered to last up to 7 days, its duration reflects the mechanism & severity of underlying inciting events. “subacute” is 7-30 days.
chronic= pain which has persisted beyond the expected time of healing of an injury & there may not be a clearly identifiable cause- pain receptors fire even in absence of tissue damage. Descending facilitatory influences may contribute to development & maintenance of chronic pain.
chronic postsurg pain is that which develops or increases in intensity after surgical procedure, in the area of the surgery, persists beyond the healing process (ie. lasts @ least 3/12), not better explained by another cause eg. infection, malignancy or pre-existing pain condition.
particularly common where nerve trauma is inevitable or surgical field richly innervated.
risk factors:
pre-op: pre-exisiting pain, female, preop anx, younger adults, opioid use esp if ineffective
intra: surg w incr nerve damage
postop: poorly controlled pre-op pain, radiation or neurotoxic chemo, dep/anx
placebo= inert substance w therapeutic response
Pain history
assess pain with sociopsychobiochemical model; recognition of physiological, psychological & environmental factors influencing.
History: general medical Hx
Specific “pain history”:
site: main location/radiation
circumstances ass’d w onset (trauma/surgery)
character: sensory descriptors, neuropathic characterists, affective descriptors
intensity (at rest, on movement, aggravating/relieving factors, continuous/intermittent)
ass’d syptoms (eg. nausea)
-effect of pain on functional activities & sleep: FUNCTIONAL ASSESSMENT TOOL eg: FAS
Treatment: current & prev pharm & non-pharm, effects/outcomes, health professionals consulted
prior existing pain or medical conditions, Rx & outcome
BELIEF regarding causes of pain, expectations/preferences regarding pain management & outcomes
pre-emptive & preventive analgesia
pre-emptive: administer analgesia prior to tissue damage aiming to limit development of subacute or chronic pain by limiting acute pain & cascade of sensitisation- aim to prevent wind-up. ?IV lignocaine, esmolol.
preventive: effects of analgesia last longer than DOA- ketamine
What’s neuropathic pain?
pain initiated or caused by primary lesion or dysfunction in the nervous system. May be a component of acute or chronic pain. Eg. CRPS1 (acute minor trauma), 2 (nerve injury), post-stroke pain, trigeminal neuralgia, painful diabetic neuropathy. Pain due to: 1. lowered threshold for activation of injured afferent (ectopic discharges- due to Na+ & Ca++ channel alterations). 2. locally released nerve growth factor= sproutings of other axons to denervated area 3. increased peripheral input results in sensitisation in spinal cord (primary hyperalgesia, agg by loss of inhibitory mechanisms & reactive changes in adjacent tissues). 4. A-B fibres sprout from laminae III & IV & move into superficial DH so normally painless sensatios are perceived as painful (tactile allodynia). 5. Wind-up (increased acrivity of glutamate in DH due to C-fibre smulation). 6. downregulation of DH orpiod receptors & decr opioid sensitivity. 7. Loss of tonic (-) form GABA & glycine- GABA A mainly post-syn, GABAB mainly pre.
PS41: position statement on acute pain management
Framework for acute pain management:
-Education: at undergraduate level & multi-D, patient & their carer, verbal & nonverbal communication influences pt pain experience
-Assessment: regular, for efficacy & adverse effects.
Functional assessment as well as pain intensity to base analgesic regimen adjustments
consideration of impact of new medical or surgical issue or non-opioid responsive pain if unexpected pain levels despite Rx
consider psych factors/past experiences contributing to pain experience; non-pharmacological interventions for them
all pts on opioids are @ risk of OIVI; monitor (minimum SS). mitigate & have strategies for managing OIVI where possible.
-Pharmacologic therapies:
multi-modal analgesics & Rx for their side-effects
titratable dose regiments
avoid long-acting opioid preparations unless a demonstrated need, close monitoring & a cessation plan in place
Analgesic stewardship programs
order sets are recommended (combine meds, monitoring & meds for adverse effects)
-deliver of safe & effective acute pain management:
hospitals to ensure necessary governance, HCW training, staffing & documentation for opioid & specialised analgesia delivery techniques
multi-D approach for pts w complex medical & psych co-morbidities
ANZCA-accredited hospitals must have an acute pain service with: qualified staff w expertise in acute pain Mx, close multi-D liaison, protocols for Rx & adverse reactions, regular R/V, after hours r/v service
QA: regular audits for effectiveness of Rx & adverse events (outcomes overseen by qualified specialist & hospital R/V committee w mechanism to deal w & prevent adverse event recurrence.
research, education ongoing
ANALGESIC STEWARDSHIP:
opioid stewardship= coordinated interventions designed to improve, monitor & evaluate use of opioids to support & protect human health
strives for a balance btwn analgesia sufficient to facilitate pt recovery & restoration of function & minimisation of analgesia-related harms to pts & others
relies on education but also system-focused strategies such as forcing functions, barriers & automation & also standardisation & protocols, warnings, reminders & checklists.
so it’s both individual practitioners & healthcare system as a whole.
considers before, during admission & at time of discharge.
recognition of pts @ higher risk of poorer postop pain control:
younger female, smoking, preop anxiety & depression, pain catastrophising, preop pain & preop opioid use. pts w acute pain trajectories not decreasing over the first few postop days are predictive of chronic postsurg pain & persistent postdischarge opioid use
regular pain assessment is vital however chasing unidimensional pain scores w opioids & raising expectations in pts, carers & staff that arbitrarily define “acceptable” levels of pain or even elimination of pain can lead to prescription of excessive opioid & risk OIVI, persistent postdischarge opioid use & opioid misuse & diversion.
more important than unidimensional pain scores is assessment of how acute pain affects function. functional limitation due to pain means that re-evaluation of therapy is required.
to assist w achieving functional goals, time prn IR opioid so the near maximum effect of the dose occurs @ the time of the designated activity (“activity-based analgesia”).
unexpected pain despite appropriately-prescribed Rx or pain that suddenly increases suggests development of new med/surg issue, psychological issue or pain thats not opioid responsive, for which alternate analgesia should be considered.
pain scores shouldn’t be disregarded, but pain score trajectory assists w Ax of pt progress.
Most significant opioid adverse effects:
1. OIVI: due to sedation, depression of central resp drive, UA obstruction. risks hypoxic brain damage & death. peak risk is within 24hrs of surgery, most events are preventable.
can usually avoid w careful titration of dose against effect, careful observation & monitoring.
SNORING should not be assumed to be normal sleeping; such pts should have their level of sedation assessed on a regular basis.
RR & SpO2 aren’t direct measures of adequacy of ventilation, there’s no good evidence or correlation w PaCO2 (a direct measure of OIVI)
-Pt-related risk factors (*assume all pts are @ risk!)
older age
female
sleep disordered breathing
obesity
renal impairment
pulm disease (esp COPD)
cardiac disease
DM
HTN
neurologic disease
2+ comorbidities, genetic variations in opioid metabolism
opioid-tolerant (likely due to differential tolerance to opioids)
-Modifiable risk factors:
co-administration of sedatives
multiple opioids (this DOESN’T include verified doses of opioids pts took for Mx of chronic pain)
continuous infusion of opioids
initiation of long-acting opioid preparations
multiple prescribers
inadequate nursing Ax or responses
reliance on a unidimensional pain scores alone to Ax adequacy of analgesia, “chasing” pain scores
using opioids for pain that’s not opioid-responsive
OIVI risk is less w tramadol, tapentadol & patches of buprenorphine
To manage OIVI risk:
-avoid modifiable risk factors
-appropriate monitoring & early escalation of care where OIVI noted
SEDATION SCORE
2. persistent post-discharge opioid use
3. opioid misuse & diversion
PS41: position statement on acute pain management
IT_PM 1.10
Outline the problems in managing acute pain for patients with chronic prior exposure to opioids
Framework for acute pain management:
-Education: at undergraduate level & multi-D, patient & their carer, verbal & nonverbal communication influences pt pain experience
-Assessment: regular, for efficacy & adverse effects.
Functional assessment as well as pain intensity to base analgesic regimen adjustments
consideration of impact of new medical or surgical issue or non-opioid responsive pain if unexpected pain levels despite Rx
consider psych factors/past experiences contributing to pain experience; non-pharmacological interventions for them
all pts on opioids are @ risk of OIVI; monitor (minimum SS). mitigate & have strategies for managing OIVI where possible.
-Pharmacologic therapies:
multi-modal analgesics & Rx for their side-effects
titratable dose regiments
avoid long-acting opioid preparations unless a demonstrated need, close monitoring & a cessation plan in place
Analgesic stewardship programs
order sets are recommended (combine meds, monitoring & meds for adverse effects)
-deliver of safe & effective acute pain management:
hospitals to ensure necessary governance, HCW training, staffing & documentation for opioid & specialised analgesia delivery techniques
multi-D approach for pts w complex medical & psych co-morbidities
ANZCA-accredited hospitals must have an acute pain service with: qualified staff w expertise in acute pain Mx, close multi-D liaison, protocols for Rx & adverse reactions, regular R/V, after hours r/v service
QA: regular audits for effectiveness of Rx & adverse events (outcomes overseen by qualified specialist & hospital R/V committee w mechanism to deal w & prevent adverse event recurrence.
research, education ongoing
ANALGESIC STEWARDSHIP:
opioid stewardship= coordinated interventions designed to improve, monitor & evaluate use of opioids to support & protect human health
strives for a balance btwn analgesia sufficient to facilitate pt recovery & restoration of function & minimisation of analgesia-related harms to pts & others
relies on education but also system-focused strategies such as forcing functions, barriers & automation & also standardisation & protocols, warnings, reminders & checklists.
so it’s both individual practitioners & healthcare system as a whole.
considers before, during admission & at time of discharge.
Pre-op strategies:
pt assessment, education re: the surgical procedure & postop care incl pain expectations (helps reduce preop anxiety & postop pain along with emphasis re: pain relief assisting functional recovery & that it’ll be reduced but not likely to be eliminated), discussion of analgesia techniques/risks/side effects, expectation that if postop opioids it’s short-term w dose decrease as recover, identification of pts who may benefit from weaning of pre-op opioids, referral to chronic pain or addiction medicine. consider referral to psych (if anx/depression/catastrophic thinking/pre-existing chronic pain/preadmission opioids; these pts are @ risk high pain scores & opioid requirements, PPOU, opioid misuse, persistent postsurgical & post-trauma pain).
recognition of pts @ higher risk of poorer postop pain control:
younger female, smoking, preop anxiety & depression, pain catastrophising, preop pain & preop opioid use. pts w acute pain trajectories not decreasing over the first few postop days are predictive of chronic postsurg pain & persistent postdischarge opioid use
regular pain assessment is vital however chasing unidimensional pain scores w opioids & raising expectations in pts, carers & staff that arbitrarily define “acceptable” levels of pain or even elimination of pain can lead to prescription of excessive opioid & risk OIVI, persistent postdischarge opioid use & opioid misuse & diversion.
more important than unidimensional pain scores is assessment of how acute pain affects function. functional limitation due to pain means that re-evaluation of therapy is required.
to assist w achieving functional goals, time prn IR opioid so the near maximum effect of the dose occurs @ the time of the designated activity (“activity-based analgesia”).
also assess efficacy of analgesia.
unexpected pain despite appropriately-prescribed Rx or pain that suddenly increases suggests development of new med/surg issue, psychological issue or pain thats not opioid responsive, for which alternate analgesia should be considered.
pain scores shouldn’t be disregarded, but pain score trajectory assists w Ax of pt progress.
Most significant opioid adverse effects:
- OIVI: due to sedation, depression of central resp drive, UA obstruction. risks hypoxic brain damage & death. peak risk is within 24hrs of surgery, most events are preventable.
can usually avoid w careful titration of dose against effect, careful observation & monitoring.
SNORING should not be assumed to be normal sleeping; such pts should have their level of sedation assessed on a regular basis.
RR & SpO2 aren’t direct measures of adequacy of ventilation, there’s no good evidence or correlation w PaCO2 (a direct measure of OIVI)
-Pt-related risk factors (*assume all pts are @ risk!)
older age
female
sleep disordered breathing
obesity
renal impairment
pulm disease (esp COPD)
cardiac disease
DM
HTN
neurologic disease
2+ comorbidities, genetic variations in opioid metabolism
opioid-tolerant (likely due to differential tolerance to opioids)
-Modifiable risk factors:
co-administration of sedatives
multiple opioids (this DOESN’T include verified doses of opioids pts took for Mx of chronic pain)
continuous infusion of opioids
initiation of long-acting opioid preparations
multiple prescribers
inadequate nursing Ax or responses
reliance on a unidimensional pain scores alone to Ax adequacy of analgesia, “chasing” pain scores
using opioids for pain that’s not opioid-responsive
OIVI risk is less w tramadol, tapentadol & patches of buprenorphine
To manage OIVI risk:
-avoid modifiable risk factors
-appropriate monitoring & early escalation of care where OIVI noted
SEDATION SCORE is the most important assessment marker for detecting OIVI; should measure at time of admin & then at time of peak effect, eg. IR PO or subcut dose, re-Ax SS @ 1hr.
Sedation scores:
0= wide awake
1= easy to rouse
2= easy to rouse but unable to stay awake
3= difficult to rouse
2 indicates early OIVI so titrate opioids so that SS is always <2
2. persistent post-discharge opioid use
3. opioid misuse & diversion
“standard orders”
- Persistent postdischarge opioid use
may occur in up to 25% of pts
pt risk factors:
psychological comorb (anx, dep, catastrophic thinking, PTSD)
preop BZD or antidepresants
preop tobacco, ETOH & substance use
pre-existing chronic pain
preadmission opioid use
lower age
female
lower household income
*weaning opioid doses prior to surgery could be of benefit!
pts w minor surgery may be just as vulnerable to PPOU as major
modifiable risk factors:
long-term preadmission opioids
psych comorbidities
unrealistic expectations
chasing pain scores- unidimensional reliance
abnormal pain/opioid dose trajectories (not decreasing)
over-reliance on opioids
SR opioid preparations
large numbers of tablets on discharge
repeat opioid prescriptions
lack of deprescribing advice
mitigating harm:
-avoid modifiable risk factors
-pt & carer education
-GP communication
-referral to specialist services (eg. chronic pain, psych, addition medicine)
peripheral regional analgesia hasn’t been shown to reduce the incidence of PPOU
CONSIDER TRANSITIONAL PAIN SERVICE: monitor postdischarge opioid use assist weaning
- Opioid misuse & diversion
ensure prescription of discharge opioid is not in excess of the number used by the pt.
educate pt re: safe storage & where to securely dispose of excess medication.
risk of misuse & diversion is less w tramadol, tapentadol & bup (patches only)
can screen for risk opioid misuse: Revised Opioid Risk Tool: questions related to personal or FHx ETOH, illegal or prescription drugs, age, Dx eg. OCD, bipolar. Anx/depression scored separately. Score <=2 suggests low risk, >=3 suggests high risk future opioid misuse.
Many issues w ppl who are opioid-tolerant prior to admission:
-likely to report higher pain scores, have higher opioid requirements, greater risk OIVI & PPOU
-Incr OIH & physical dependence so incr pain sensitivity & risk of opioid withdrawal if opioid abruptly ceased or reduced in dose.
-LT opioid use also incr risk SSI, earlier revision rates for major joints, longer hospital stay, greater risk non-home D/C, higher readmission & healthcare costs.
-CAN REDUCE THESE RISKS EVEN TO LEVELS SIMILAR TO OPIOID-NAIVE PTS BY WEAN OR CEASE OPIOIDS IN THE MONTHS PRIOR TO ADMISSION
-Any weaning needs to be slow, achievable & pt cenred (rapid tapers risk mental health crises, illicit drug use & suicide.
-evidence shows that tapering of opioid doses in pts w chronic pain usually leads to reduction or no change in their pain, rather than worsening.
Opioid dosing:
age a better predictor of opioid requirements than weight (brain sensitivity to opioids increases)
initial dose based on age, adjust according to comorbidities (eg. renal impairment)
avoid long-acting opoids (incl patches & methadone) for acute pain unless demonstrated need, close monitoring avail & cessation plan. risks incl: incr risk OIVI & other opioid-related adverse effects, less effective pain relief incr risk PPOU.
impossible to predict dose appropriate, slow onset & offset makes rapid & safe titration impossible. it’s the same as “background infusion”, markedly incr risk OIVI.
if significant multi trauma or burns, long-acting opioid may temporarily be appropriate after careful Ax but communicate to rehab service/GP re: temporary basis. atypical better (lower risk OIVI & misuse/diversion cf conventional opioids).
pts on long-acting pre-op opioids: tolerant & physically dependent so after verifying drug & dose, continue.
opioid-fre analgesia/anaesthesia techniques as yet have limited good evidence- it does lead to reduced N&V but no evidence to show clinically sig benefits wrt pain relief & opioid use or discharge opioid prescribing/PPOU.
opioid-sparing:
paracetamol, NSAIDs (if haem instability risk, avoid NSAIDs if eGFR <80mL/min), gabapentinoids no longer recommended for routine use in acute pain (statistically but not clin sig reduction postop pain/opioid use, no reduction in CPSP, incr dizziness, visual disturbance & OIVI, risk abuse/misuse), ketamine reduces postop pain & opioids, small reductions in PONV, reduced CPSP after some OTs.
Mg++ small reduction postop opioids, low quality evidence.lignocaine limited benefit so far, dexmed may reduce PONV but risk brady/hypoT.
Use protocols/gjidelines & order sets
prep for discharge soon after admission- daily R/V of pain trajectory & function, consider eraly referral to addiction or pain specialist if 2+ psychoacive drugs in combo, if has sig psych illness, illicit drugs or evidence high-risk Bx.
opioid weaning should commence even before D/C.
base d/c opioid on number of tablets taken day before d/c & pt age (ie. if used no opioid the day before discharge, don’t given any for d/c). for chn, dispense the smallest possible volume. consider interval dispensing for @-risk pts.
discussion & written info for pt & carer, w info incl aim of pain relief is to restroe function; prn if needed prior to activity. do not nec need to take prns on the clock if functioning well.
opioid NOT to be used to aid sleep.
max 1 week w progressive decrease.
recognition of OIVI & need to avoid BZD gabapentinoids, ETOH, cannabis).
risk opioid misuse & addiction, opioids only to be taken by the person for whom they are prescribed, for the reason prescribed & in doses no higher than prescribed.
secure storage & excess meds disposed of safely (risk poisoning/diversion/misuse)
incr risk fatal crash: impair driving, cognitive reasoning similar to ETOH. worse psychomotor impairment in first few weeks following initiation of prescription opioid or if a chronic dose is increased. Should not drive while taking an opioid prescribed for ongoing management of acute pain after surgery or injury as is the case for other complex tasks or making key decisions.
d/c advice to see Dr if significant pain continues.
material in the pts language & appropriate reading level.
must communicate w pts GP or other treating Dr w clear plan for analgesia reduction after D/C (info mirroring the advice given to the pt).
expectations that:
opioids should be short-term only, daily dose trajectories should trend down
repeat prescriptions for opioid are major modifiable risk factor for PPOU & incr risk opioid misuse.
pts still taking opioid beyond usual healing time may benefit from specialist r/v; if developed CPSP non-opioid meds may be more appropriate
day stay analgesia for pts with OS or obese?
ideally should not include opioids
IT_PM 1.9
Outline the risks associated with and the monitoring requirements for patients receiving patient-controlled analgesia (PCA), opioid infusions or continuous regional analgesia for acute pain management
Operator-related:
programming errors (distractions, inexperienced staff)
wrong medication
wrong route
prescription errors eg. background rate too high
inappropriate monitoring (eg. lack of SS monitoring
Pt-related:
family or pt tempering
pt mistaking pca for nurse-call button
Equipment/practice environment
cracks in syringes/cartridge
“runaway” pumps/spontaneous triggering, frayed wire in demand apparatus–> triggering
uncontrolled siphoning of syringe contents
recommendations: antisiphon valves (& don’t position syringe above pt level & ensure no cracks in syringe & ensure engaged) & anti-reflux (one-way) valve if not on dedicated line
opioid used:
drug interactions or inappropriate cessation of drugs which should not continue w PCA
error reporting database systems, Q&S reporting, audit & education to ratify risk factors & limit risk future adverse events
pump programming eg. w preselected medication concentrations/dosages, “soft” & “hard” limit ranges
“smart pump” technology may reduce programming errors & improve pt safety
hospital-wide safety improvement program (equipment, guidelines, education, monitoring)
Conuous infusion constant blood levels after 4-5 half-lives, avoids issues w peaks & troughs of intermittent admin however varied pt response & variable intensity of acute pain may cause inadequate levels or delayed onset adverse effects
5-fold incr risk OIVI (need closer monitoring). adding continuous infusion incr OIVI, doesn’t improve pain relief or sleep or reduce number of PCA demands.
PCA labour intensive & issues w dexterity/cognition but more appropriate to intermittent nature of acute pain, lock-out for safety if used appropriately (pt only). IV PCA better analgesia than conventional parenteral opioid regimen. IV PCA higher opioid consumption, pruritis but not other opioid-related adverse effects or hospital LoS. Higher pt satisfaction w PCA
adding naloxone to PCA morphine doesn’t have analgesic benefit but may decr nausea & pruritis.
subcut PCA may be as effective as IV PCA. subcut time to reach max serum concentration (median) morphine 15min. variable rate absorption.
s/c oxycodone peak venous [] after 22mins.
Methadone:
Fully synthetic mu opioid agonist
Full agonist
High potency, high affinity
R enantiomer MOP & DOP agonist
NMDA antagonist: S enantiomer
Serotonin & NAdr reuptake inhibitor
Ketamine analgesic dose 0.1-0.3mg/kg/hr
Using IV methadone in OT:
T1/2 keo= 8 mins with methadone (similar to oxycodone), so clinical onset 6-10mins
Offset by redistribution bloodstream to fat/muscle, redistribution half life 6mins (so expect peak Resp depression to be within 30mins of IV)
IV; initially (about 30 mins) dist to fat & muscle. Phase 2 cleared by liver (takes more like 24hrs). Need drug to be in therapeutic analgesic range. Higher dose 0.2mg/kg (about 15mg 70kg pt) provides analgesia up to 24hrs, while lower dose (eg. 5mg) offset by redistribution & lower 2nd-phase plasma level, more like 3-4hrs analgesia.
Larger dose in OT may reduce opioid dose 24hrs.
Use for surgery expected to have high levels of pain. Opioid-sparing opioid.
Young robust 20mg
Middle-age 15mg
Fragile 10mg
Give up front, possibly trickle in small doses
PACU: 2.5mg 15-minutely prn IV or could just use oxycodone protocol
On ward, po IR opioids
Used in ORT.
Highly fat soluble.
Initial offset due to distribution to fat & muscle (rather than Cl, as per most opioids)
Takes about 1 week with repeated dosing to saturate fat & muscle w drug (then stops working due to Cl by liver)
Metabolised by liver to INACTIVE metabolites (by CYP3A4>1A2,2D6)
Kidneys minimally involved; useful in CKD
- Complex pharmacology; T1/2elim about 24hrs (vs 4-8hrs w others)
- Many interactions (liver enzymes), incl tramadol & SSRIs, eg. rifampicin
- QT prolongation
- Converting doses non-linear & one-way
60-100mg for withdrawal (suppress cravings, reduce mortality)
More like 20mg analgesia
Chronic methadone user peri-op:
-main issues:
-opioid tolerant & methadone tolerant
-fat & muscles saturated w methadone, any additional to bloodstream then cleared by liver
-multimodal: simple, regional, advanced (ketamine)
-dosing of IR difficult; risk under-doing it & having PACU pain crisis. Risk of using IV methadone= over-doing it & sleepy
-continue regular methadone, divide over BD dosing (prevent withdrawal, keep in therapeutic range for more of the day
-generally require slightly higher doses of their prn breakthrough analgesia (oxycodone)
-if NBM: PO-IV bioavailability approx 80% (40-100!), changes in liver enzymes w chronic methadone use. More of the methadone taken PO metabolised by liver before reaches bloodstream (lower BA with chronic use, 50%). If changing from PO to IV in chronic user then, give the dose BD & decr by 1/3. PCA for additional analgesic needs.
MONITOR FOR WITHDRAWAL (SCALE, STAFF EDUCATION): chills, fever, body aches, diarrhoea, tachycardia, tremore, yawning, rhinorrheoa/lacrimnation, piloerection, insomnia, muscle pain, nausea, agitation, mydriasis, sweating, depression/anxiety/restlessness.
-regional catheter if laparotomy, likely to HDU in the first 24-48hrs post-op.
Pregnancy: methadone Elim half-life much shorter (about 8hrs vs 24). Consequence= pregnant pt needs higher doses, or BD, esp towards end of pregnancy.
Methadone Cat C, caused or suspected of causing harm but not malformation, thought to be reversible.
