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Quieting Down Opioid Prescribing Quieting Down Opioid Prescribing

Quieting Down Opioid Prescribing - PowerPoint Presentation

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Quieting Down Opioid Prescribing - PPT Presentation

Maria Foy PharmD BCPS CPE Pharmacy Care CoordinatorPalliative Care Abington Hospital Jefferson Health Tanya J Uritsky PharmD BCPS CPE Clinical Pharmacy Specialist Pain Management and Palliative Care ID: 908530

opioid pain therapy dose pain opioid dose therapy taper 2015 effects treatment risk due patient daily clin chronic 30mg

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Slide1

Quieting Down Opioid Prescribing

Maria Foy, PharmD, BCPS, CPEPharmacy Care Coordinator/Palliative CareAbington Hospital Jefferson Health

Tanya J. Uritsky,

PharmD

,

BCPS, CPE

Clinical Pharmacy Specialist, Pain Management and Palliative Care

Hospital of the University of

Pennsylvania

Slide2

Disclosures

Tanya Uritsky has nothing to discloseMaria Foy is on the speaker’s bureau for Astra Zeneca

Slide3

Goals and Objectives

At the completion of this activity, the participant should be able to:Recommend

an opioid de-escalation protocol based on current opioid dosage and length of therapyProvide dosing for inpatient ketamine during the de-escalation processUtilize co-analgesics for the treatment of chronic pain

Slide4

Question

Symptoms of central sensitization may include (select all that apply):AllodyniaHyperalgesia

SwellingBradycardia

Slide5

Pain System Changes and Opioids

Tanya J. Uritsky, PharmD, BCPS, CPE

Slide6

The Pain Pathway

Bingham B, et al. , Nature Clinical Practice, 2009; 5(1):1-37. Accessed at: www.nature.com/clinicalpractice/rheum

Slide7

“Inflammatory Soup”

Lower threshold for activation

Increased rate of firingPlays a role in allodynia, hyperalgesia and in central sensitizationPeripheral Sensitization

Slide8

Central Sensitization

Amplification of neural signaling that elicits pain hypersensitivityAn uncoupling of the clear stimulus-response relationship that defines nociceptive pain

Manifests as:Hyperalgesia/secondary hyperalgesiaAllodyniaProlonged pain after transient stimulusCan persist long after healing of the injuryWoolf CJ. Pain, 2011;152(3 Suppl):S2-S15.

Slide9

Taking A Closer Look

Pain afferents - Glutamate, Substance P, Calcium

Central -NMDA activation, reduced endogenous opioid, reduced serotonin/5HT2A up-regulation, norepinephrine changes, dopamine changes Microglial Cells/Astrocytes -glutamate, cytokines, K/Ca channel dysregulationRaouf, et al. 2010

Slide10

Glial Cell Activation

Adapted from: https://

www.practicalpainmanagement.com/pain/other/glial-cell-activation-neuroinflammation-how-they-cause-centralized-pain, online May 2015; accessed September 21, 2017NeuroinflammationChronic FatigueDepressionCentralized PainInsomniaOverstimulation of sympathetic nervous systemIntellectual Decline

Pituitary Over-Stimulation

Activated Glial Cells

Slide11

Pain Memory

Adapted from: https://www.practicalpainmanagement.com/pain/other/glial-cell-activation-neuroinflammation-how-they-cause-centralized-pain, online May 2015; accessed September 21, 2017

Slide12

What You See

Major SymptomsConstant painInsomnia, depression, fatigueSecondary SymptomsAnxiety, anorexia, hopelessness, allodynia

BehaviorReclusiveness, immobilityBecoming house/bed boundSympathetic Nervous System ExcitationHypertension, tachycardia, hyperthermia, hyperhidrosis, mydriasis, etc.https://www.practicalpainmanagement.com/pain/other/glial-cell-activation-neuroinflammation-how-they-cause-centralized-pain, online May 2015; accessed September 21, 2017

Slide13

But Why?

Lowers pain threshold Stress

Poor sleepOperant learningIndividual beliefs and expectations Predictors of chronic painAnxiety disorderPhysical, psychological, emotional trauma or abuseDepression

Slide14

The Common Denominator

Central Sensitization

PTSDFibromyalgiaChronic Fatigue SyndromeMigrainesTension HeadacheFunctional GI disorders

Multiple Chemical Sensitivities

Restless Legs Syndrome

Myofascial Pain Syndromes

Temporomandibular Disorders

Interstitial Cystitis

Primary Dysmenorrhea

Slide15

Treatments of Central Sensitization

KetamineGabapentinPregabalinDuloxetine, milnacipran

, lamotrigineCox-2 inhibitorsCognitive Behavioral TherapyAerobic exercise/physical therapyChronic pain rehabilitationMassage therapyRelaxationAcupuncture

Slide16

Question

Common attributes of both central sensitization and addiction are:A. ConfusionB. Allodynia

C. HyperalgesiaD. Environmental Factors

Slide17

When should opioid

tapering be considered?Lack of functional improvementPain not effectively treated

Intolerable side effectsPatient preferenceUnacceptable risk Nonadherence with treatment planConcern for OUD or SUDAberrant behaviors Concomitant medicationsHigh-dose opioid therapyPsychologic comorbiditiesMayo Clin Proc. 2015;90(6):828-842; VA/DoD 2017

Risks

Benefits

Slide18

General Principles

Recommendations vary in guidelines and primary literatureLimited evidence exists comparing tapering strategiesMust be patient-centered – no single strategy will apply to all patients

Mayo Clin Proc. 2015;90(6):828-842; VA/DoD 2017

Slide19

Opioid De-escalation

Should only be attempted after a discussion with patient and shared decision-making regarding a treatment plan:

Consider non-opioid and non-pharmacologic therapeutic options for pain controlDiscuss options for treatment for concomitant substance use disorder, as necessaryRecommend options for mental and behavioral health treatment, as appropriate Mayo Clin Proc. 2015;90(6):828-842; VA/DoD 2017; Ment Health Clin. 2015;5(3):102-108; VA PBM Academic Detailing Service 2016

Slide20

Opioid De-escalation

Initial rate of reduction can be variable and is related to risk stratificationPatient risk (OUD, mental health conditions, other comorbidities, illicit behaviors)

Duration of opioid therapy Opioid formulationReduction of 5-20% every 4 weeks is commonOften first reduce the dose of the medication to the smallest commonly available unit dosage and then increase the amount of time between doses PRN use of short-acting therapy generally does not need to be tapered

Slide21

Factors Determining Taper Duration

Faster taper recommendedSlower taper required

Lower risk patientLonger opioid treatment durationLong-acting opioid therapyConsider 10-25% reduction every 4 weeksMayo Clin Proc. 2015;90(6):828-842; VA/DoD 2017; Ment Health Clin. 2015;5(3):102-108; VA PBM Academic Detailing Service 2016 Higher risk patientShorter opioid treatment durationShort-acting opioid therapyConsider > 25% initial dose reduction

Slide22

Taper Examples

Slowest taper

Slow taperFast TaperRapid TaperDurationYearsMonths to yearsWeeksDaysMethodReduce by 2-10% every 1-2 monthsReduce by 5-20% every 4 weeks

Reduce by 10-20% every week

Reduce by 20-50% of first dose if needed, then reduce by 10-20% daily

Adapted

from: VA PBM

Academic

Detailing

Service 2016

Slide23

Patient Case

RA is a 59 yo WM with a history of chronic lumbar pain from a MVA, for which he has been prescribed opioid therapy for the last nine years. Pain is thought to be primarily neuropathic in origin. Patient and provider are concerned about worsened pain and function, despite recent opioid

dose increases. Patient’s provider would like to taper RA’s opioid therapy in favor of alternatives for pain and requests your assistance.

Slide24

Patient Case

Active problemsChronic low back painDepressionHypertensionHyperlipidemia

Pertinent labs are WNLUDS, PDMP, refill history have been appropriateCurrent medications:Morphine SR 30mg TIDSertraline 50mg daily Lisinopril 10mg dailyAtorvastatin 40mg dailyAspirin 81mg daily

Slide25

Patient Case

How quickly should RA’s therapy be tapered?Rapidly over the next two weeks, due to his high riskQuickly over the next month, due to his concern for adverse effects

Slowly over the next several months, due to his duration of therapyVery slowly over the next year, due to his high opioid dose

Slide26

Patient Case

How quickly should RA’s therapy be tapered?Rapidly over the next two weeks, due to his high riskQuickly over the next month, due to his concern for adverse effects

Slowly over the next several months, due to his duration of therapyVery slowly over the next year, due to his high opioid dose

Slide27

Possible Taper Schedule

Current regimen: morphine SA 30mg TIDMonth 1: 30mg QAM, 15mg at noon, 30mg QPMMonth 2: 30mg QAM, 15mg at noon, 15mg QPMMonth 3: 15mg TIDMonth 4: 15mg Q12HMonth 5: 15mg once daily, then stop

Mayo Clin Proc. 2015;90(6):828-842; VA/DoD 2017; Ment Health Clin. 2015;5(3):102-108; VA PBM Academic Detailing Service 2016

Slide28

How might this tapering plan differ if a fast taper were required due to patient risk?

Slide29

What additional pharmacotherapy could you recommend for RA?

Slide30

Withdrawal Symptom Management

Withdrawal symptoms are not life-threatening, but may occur even with a gradual taperShort-term medications may be considered to limit withdrawal symptomsDo NOT use benzodiazepines or opioids to manage withdrawal symptoms

Slide31

Withdrawal Symptom Management

Symptom

Possible Treatment Aches, pains, myalgias NSAIDS, acetaminophenDiarrhealoperamideConstipationlaxative - reduce and stop with time

Nausea,

vomiting

Prochlorperazine

, haloperidol, ondansetron

Anxiety, irritability, lacrimation, cramps, rhinorrhea, diaphoresis, insomnia

Hydroxyzine, quetiapine

Insomnia

trazodone

Autonomic symptoms (hypertension, nausea, cramps, diaphoresis, tachycardia)

clonidine;

r

eassess in 3 to 7 days

- t

aper upon symptom resolution

Adapted

with

permission

from:

Ment

Health

Clin

. 2015;5(3):102-108.

Slide32

Co-analgesic Therapy

Maria Foy, PharmD, BCPS, CPE

Slide33

Patient-Centered Non-Opioid Therapies

Based on focused history, diagnoses, pain assessment, pain type Nociceptive (arthritis, joint/muscle pain)

 acetaminophen, NSAIDsNeuropathic (diabetic neuropathy, PHN)  anticonvulsants, antidepressantsPatient-specific risk for adverse eventsHistory of GI bleed, renal or hepatic dysfunction, age, uncontrolled hypertensionPatient-specific indications for dual benefit of a particular medicationInsomnia, obesity, depression, anxietyStart one new agent at a timeMay trial multiple agents in a therapeutic category

Slide34

Options for Alternative Therapy

N-methyl-D-aspartate (NMDA) antagonistsAcetaminophenNon-steroidal anti-inflammatory agents (NSAIDs)Tricyclic antidepressants (TCAs)Serotonin-norepinephrine reuptake inhibitors (SNRIs)

AnticonvulsantsTopicals

Slide35

NMDA Antagonists

Activation of N-methyl-D-aspartate (NMDA) receptors associated with hyperalgesia, neuropathic pain, and reduced functionality of opioid

receptorsAntagonists may play a role in improvement Limiting factors for useSide effects (CNS effects, cardiovascular, GI)Provider expertise and training Ketamine and methadone most commonly usedUS Pharm. 2011;36(5):HS4-HS8; Comprehensive Treatment of Chronic Pain by Medical, Interventional, and Integrative Approaches 2013

Slide36

Ketamine for Chronic Pain

FDA approved indicationsAnesthetic agent for diagnostic and surgical procedures not requiring muscle relaxation

Induction of anesthesiaA supplement to low potency anestheticsNitrous oxide Off Label UsesPrevention/reversal of central sensitizationTreatment of pain not responding to opioidsTreatment for neuropathic painTreatment for acute pain in opioid tolerant patients

Slide37

Ketamine Dosing

Indication

Initial DoseMax DoseRouteCommentsRefractory pain0.1 mg/kg/hr0.5 mg/kg/hrIV/SCContinuous infusionPost-op pain < 50 kg0.1-0.2 mg/kg/hr0.2 mg/kg/hrIV

Continuous infusion

Post-op

pain

> 50 kg

4 mg/

hr

10 mg/

hr

IV

Continuous infusion

Complex Regional Pain Syndrome

10 mg/

hr

30 mg/

hr

IV

Initial:

continuous infusion

Maintenance: intermittent infusions

Slide38

Ketamine Adverse Effects

Hypotension , hypertension, tachycardiaPsychomimetic effects (hallucinations, dreamlike state)Increased intracranial pressureExcessive sedationExcessive salivationNausea, vomiting

Tonic clonic movement, tremors, diploplia

Slide39

Ketamine Clinical Pearls

Ketamine produces opioid sparing effectsConsider decreasing opioid dosing by 25-50% at initiation of ketamine therapy, followed by 25% every 12-24 hours as toleratedSigns of withdrawal

indicate too rapid of a opioid dose reduction. Treat with a slower taper or bolus dose of ketamineCo-administration of a benzodiazepine or haloperidol is recommended to prevent or minimize psychomimetic effects Consider lorazepam 0.5-1 mg IV/po q6-8h Give dose prior to initiation of infusionIf significant adverse reactions occur, stop the infusion. Side effects should subside in 15-30 minutes

Slide40

Methadone

3 mechanisms of analgesia Mu receptor agonist, NMDA receptor antagonist, norepinephrine reuptake inhibitorVariable half life Average of 24 hours, range of 8-56 hoursMultiple cytochrome P450 drug-drug interactions

Can prolong the QTC intervalHigher dosingCongenital predisposition to pro-longed QTCDose increases should not occur before a minimum of 5-7 daysPain control at day 3 can identify risk of overdose at day 5

Slide41

Acetaminophen

Dose: 650-1000mg Q4-6 hoursRecommend scheduled use, not PRNLimit to 3-4g/day in healthy patients, 2g/day in hepatic impairmentBe aware of duplication of therapy

No antiplatelet effect (< 2g/day)

Slide42

Acetaminophen Toxicity

Acute hepatotoxicity Seen with ingestion of 7.5-15 gramsFatal at 20-25 g

Heavy alcohol consumption, fasting, or malnutrition may increase metabolism to toxic metaboliteChronic toxicity Ingestion of >4 g/day chronicallyArguments to lower maximum dose ongoingConsuming >2 alcoholic drinks/day with doses greater than 2 g/dayAlcoholic liver disease

Slide43

NSAIDs

Naproxen, ibuprofen, meloxicam, diclofenac, sulindac, etodolac, indomethacin Caution in renal disease, cardiovascular disease, heart failure, history of GI bleed

Consider celecoxib in patients with history of GI intolerance

Slide44

NSAID Adverse Effects

NSAID therapy adverse effects (AE) associated with various body systemsGastrointestinal, CardiovascularHepatic, Renal,Central Nervous, RespiratorySpecial considerations for children and pregnant or lactating women

Chronic therapy and higher doses associated with increased AE risk

Slide45

Tricyclic Antidepressants

Tertiary amines Amitriptyline, imipramine Slightly more efficacious for pain, but less well toleratedSecondary amines

Nortriptyline, desipramineMore well toleratedDose at bedtime, due to likelihood of sedation (antihistaminergic properties)Consider in:Younger patients for neuropathic painPatients with concomitant insomnia or depressionCaution in:Elderly because of anticholinergic effectsCardiovascular disease

Slide46

TCA Adverse Effects

SedationDry mouth,

Blurred visionConfusion, deliriumConstipationOrthostatic hypotensionWeight gainCardiovascular effectsConduction blocksTachycardiaVentricular arrhythmias

Slide47

Selective Norepinephrine Reuptake

InhibitorsDuloxetine, venlafaxine, desvenlafaxine, milnacipran

, levomilnacipranConsider for neuropathic pain in patients with concomitant depression/anxietyMay increase blood pressureNausea and vomiting common DuloxetineAlso indicated for musculoskeletal pain and fibromyalgiaAvoid in hepatic insufficiency, CrCl <30 mL/minVenlafaxine IR product dosed BID or TIDAdjust dose based on renal functionAbrupt withdrawal associated with serious abstinence syndrome

Slide48

Anticonvulsants

Gabapentin, pregabalin, topiramate, oxcarbazepine, carbamazepine, lamotrigine,

valproic acidGabapentin generally first line Renal dose adjustment requiredTitrate to a target dose of 1800 mg/day in divided dosesMax dose 3600 mg/dayPregabalin may be preferred over gabapentinImproved tolerability, faster onset, and ease of titrationRenal dose adjustment requiredMonitor for sedation, fluid retention

Slide49

Anticonvulsants

Monitor for cognitive effects, especially with topiramateConsider

topiramate Obese patients due to appetite suppressionConcomitant substance use disorders (smoking cessation, alcohol use disorder, others)MigrainesCaution with carbamazepine due to drug-drug interactions

Slide50

Topicals

Diclofenac gel or patch, menthol/methyl salicylate cream, trolamine salicylate cream, capsaicin cream or patch, lidocaine gel, cream, or patchGood options in patients at high risk for side effects from other agents

Diclofenac gel, capsaicin cream must be reapplied 3-4 times daily for optimal benefitDiclofenac gel ideal in patients who cannot take oral NSAIDs (minimal systemic absorption)Capsaicin cream onset of action: 2 – 4 weeksAvoid use with irritated or broken skin

Slide51

Back to RA

Active problemsChronic low back painDepressionHypertensionHyperlipidemia

Pertinent labs are WNLUDS, PDMP, refill history have been appropriateCurrent medications:Morphine SR 30mg TID  tapering plan in placeSertraline 50mg daily Lisinopril 10mg dailyAtorvastatin 40mg dailyAspirin 81mg daily

Slide52

What additional pharmacotherapy could you recommend for RA?

Stop sertraline, start duloxetine 30mg daily x 1 week, then increase to 60mg dailyConsider cross taper of morphine to methadone, following baseline EKGStart meloxicam 30mg daily with food

Both A and B

Slide53

What additional pharmacotherapy could you recommend for RA?

Stop sertraline, start duloxetine 30mg daily x 1 week, then increase to 60mg dailyConsider cross taper of morphine to methadone, following baseline EKGStart meloxicam 30mg daily with food

Both A and B

Slide54

Self Assessment

Which of the following should be considered when determining the speed of an opioid taper?Patient genderDuration of opioid treatment

Opioid dose

Slide55

Self Assessment

Which of the following should be considered when determining the speed of an opioid taper?Patient genderDuration of opioid treatment

Opioid dose

Slide56

Key Takeaways

Opioid tapers must be individualized for patient needsRecommend slower tapers for those with a longer duration of opioid therapy and with lower risk of useConsider rapid tapers for higher risk patientsOptimization of non-opioid therapy can assist in tapering efforts

Ketamine use is becoming more common for treatment of refractory pain and for opioid sparing effects

Slide57

References

Berna C, Kulich RJ, Rathmell JP. Tapering long-

term opioid therapy in chronic noncancer pain: evidence and recommendations for everyday practice. Mayo Clin Proc. 2015;90(6):828-842.Kral LA, Jackson K, Uritsky T. A practical guide to tapering opioids. Ment Health Clin. 2015;5(3):102-108.VA/DoD clinical practice guideline for management of opioid therapy for chronic pain. Washington, DC: Veterans Health Administration; 2017.Dowell D, Haegerich TM, Chou R. CDC Guideline for Prescribing Opioids for Chronic Pain United States, 2016. MMWR Recomm Rep 2016; 65(1);1–49.

VA PBM Academic Detailing Service. Pain management opioid taper decision tool

A VA clinician’s guide. Washington, DC; Veterans Health Administration; 2016.

Vorobeychik

Y, Willoughby CD, Mao J. NMDA Receptor Antagonists in the Treatment of Pain. In: Deer T. et al. (

eds

) Comprehensive Treatment of Chronic Pain by Medical, Interventional, and Integrative Approaches. New York, NY. Springer. 2013.

Jamero D, Borghol A, Vo N, Hawawini F. The emerging role of NMDA antagonists in pain management. US Pharm. 2011;36(5):HS4-HS8.