contemporary pain assessment and management in today’s adult and geriatric population christine...

Contemporary Pain Assessment and Management in Today’s Adult and Geriatric Population

Christine Coletta-Hansen ANP-BC, ACHPN

Palliative Care Nurse PractitionerGrand View Medical Center

Course Objectives At the end of this lecture participants

will be able to : Verbalize understanding of the holistic impact of chronic

pain in today’s adult and geriatric population (10 min.) Verbalize at least 3 reliable/valid pain assessment

tools/techniques that can be used in the adult or cognitively impaired populations (10 min)

Compare/contrast different opioid analgesics to assist in choosing appropriate pharmacotherapy depending on individual patient needs.(90 min)

Discuss co-analgesia options according to pain etiology.(30 min)

Create a plan to provide pain management to patients at risk for addiction.(40 min)

Facts and Figures about Pain in America An estimated 75-150 million

Americans suffer chronic long lasting pain

1 of 7 PCP office visits are due to pain

More than 50 million are partially or fully disabled from the pain

Pain affects up to 80% patients with Stage IV CHF

Pain Facts cont. National study of 2.2 million SNF

residents showed 41.2% complained of moderate to severe pain 60 & 180 days post initial assessment.(Jakobsson et al 2003)

70% of those approaching end-of-life admit to moderate to severe pain

94% of cancer patients report experiencing moderate to severe pain (EPIC 2007)

Definition of Pain McCafferty: clinical definition Scientific definition:

Changing view per Perry Fine, MD 2006

“A condition of malfunctioning of the PNS/CNS system as well as dysregulation of other systems (Immune/Neuroendocrine/Sleep/Mood)

Pain and the Patient

Chronic Pain Alters Brain Functional MRI performed in people

suffering chronic pain show a state of constant activity in areas that should be at rest.

Frontal cortex, associated with emotion, is constantly active causing problems with attention, sleep and causing depression

Growing Evidence Chronic pain is now believed to be

a systemic or multisystem impairment that arises from an initial trigger or injury to the nervous system that for reasons that are unclear does not recover

Peripheral and Central Pathways for Pain

Ascending Tracts Descending Tracts

Cortex

Midbrain

Medulla

Spinal Cord

Thalamus

Pons

Factors for Pain Assessment Assess pain for:

Intensity and location Descriptors, duration Alleviating and aggravating factors Accompanying symptoms Effect on quality of life (Goal

Attainment Scale; J. Farrar) Patient’s goal for pain control Previous effective (non)/pharmacologic tx

Ongoing Monitoring of Chronic Pain Patients (Passik & Weinreb, 2000)

“4 A’s” Analgesia ADL’s Adverse effects Aberrant drug taking behaviors PDAT (Passik et al 2004)

Multidimentional assessment of pain relief, side effects, physical and psychological function and aberrant drug related behaviors

Chronic Pain Principles Treat pain by least invasive route first

(IV still takes 10 hrs to reach steady state)

Give medication around the clock (use long acting formulations when possible)

Always have breakthrough medications available

Give medications by the “Ladder” Individualize the dose to meet patient

needs/goals Utilize multidisciplinary approach

Pain Types &Drug Classes Used to Treat Them Nociceptive (Bone, Muscle,

Visceral, etc.) (dull, achy, throbbing, nagging) Inferred tissue damage; localized;

afferent Neuropathic (CNS or PNS)

CRPS, phantom pain=CNS Neuropathies=PNS

Idiopathic Psychogenic (team approach

necessary)

Pain assessment tools

Pain Assessment Tools(Standardized throughout the institution)

MCGill Pain Inventory Wong-Baker Faces Scale VAS/Pain thermometer Pediatric/Adolescent Color Intensity Scales Verbal Descriptor Scale Goal Attainment Scale

Elderly Attitudes Toward Pain Treatment Don’t want to bother anyone Believe pain is a normal part of the

aging process Don’t want to be a “bad patient” Fear becoming overmedicated or

addicted Fear pain means illness is

worsening

Chronic Pain in the Elderly-Mixed/Unspecified Pain may have mixed or unknown causes

(also, multiple locations) Treatment is unpredictable and various

approaches may be needed Some pain syndromes may be psychologically

based and traditional analgesia may not be indicated

Polypharmacy and drug interaction risks pose increased challenges in the elderly.

Geriatric Pain Assessment Tools

Impaired Cognition/MMSE 12

Geriatric Pain Assessment Tools

Pain Assessment in the Nonverbal Patient (Herr et al, 2006)

Make all attempts for the patient’s self-report

Search for potential causes of pain (if needed, assume pain is present)

Observe patient behaviors New onset confusion or agitation

Surrogate reporting of pain behaviors/activity changes

Attempt an analgesic trial

Pain Assessment Tools for Nonverbal or Cognitively Impaired Adults

ADD: Assessment of Discomfort in Dementia Protocol

CNPI: Checklist of Nonverbal Pain Indicators

NOPPAIN: Nursing Assistant Administered Instrument to Assess Pain in Demented Individuals

PACSLAC: Pain Assessment Scale for Seniors with Severe Dementia

PAINAD: Pain Assessment in Advanced Dementia Scale

All are referenced in the bibliography

WHO Stepladder Step I (beware of combination

products)NSAIDS/Cox-2/APAP Step II Step III Opioids (“the good, the bad and the

ugly”): Merperidine (normerperidine/CNS toxicity); propoxyphene (norpropoxephene/CNS/Renal toxicity; 1 IN 20 DRUG

RELATED DEATHS ARE FROM THIS DRUG); equipotency of ASA (650 mg)/merperidine (oral); morphine (metabolites) & renal insuff.

Adjuvants

Nonopioid Analgesics Acetaminophen (paracetamol)

Minimal anti-inflammatory effects Fewer adverse effects than other nonopioid

analgesics Adverse effects

Renal toxicity Risk for hepatotoxicity at high doses

Increased risk with liver disease or chronic alcoholism

??? effect on platelet function New recommendations as low as 2600

mg/24h

Use of NSAIDS in the Elderly

Avoid using high dose, long term NSAIDS

GI complications up to 40%. Use PPI’s Dehydrated patients & renal failure Use NSAIDS PRN rather than around the

clock Topical NSAIDS give 70x more direct

joint delivery than oral route Dicolfenec gel/spray; Ketoprofen

2009 NSAID formulation IV ibuprofen(Caldalor) infused over 30

min. Comes in 400 mg/4ml or 800 mg in 8 ml. $13.00/dose

Only injectable drug for fever No 5 day limit like ketorolac Costs 9x more than ketorolac therefore

stay with it for short term use in patients at low risk for GI bleeding or renal dysfunction.

Consider IV ibuprofen if longer IV treatment is needed.

NSAID patch(s) diclofenac epolamine topical patch 1.3%

(Flector) 1 patch/2xday to INTACT skin No bathing/showering diclofenac (Voltaren) gel 1% measured 4

gm for LE and 2 gm for UE diclofenec spray has an even faster onset

of analgesia; (Pennsaid) 1.5% 40 gtts qid

Tramadol (non-schedule opioid) Blocks reuptake of seratonin and

norepinepherine. Mu-receptor agonist as well Tramadol (Ultram) 37.5 mg effective; ER (more

somulence nausea and dizziness) ER (100/200/300 mg available) 200-400 mg in 4 divided doses Caution with SSRI use*******

(seizures/seratonin syndrome) Side effects are dizziness, constipation,

drowsiness, tremor, HTN, seizures. High (up to 28%) discontinuation rate

Seratonin syndrome 50% is antidepressant related, especially when

combined with Tramadol or methadone. High seizure risk Can occur within minutes to hrs after starting ALTERED MENTATION, HYPERACTIVITY,

AKASTHESIA, MYOCLONIS, DIAPHORESIS, HYPERTHERMIA

Tramadol, SSRI, SSNRI,TCA’s, opiates, antihistamines, CNS stimulants, tryptans

Tapentatol (Nucynta) For ACUTE PAIN Schedule II; similar to tramadol (mu

agonist and affects NE as well. 50/75/100 mg; may take up to 600

mg/day Dose q 4-6h No renal or hepatic challenge 100 mg = Oxycodone IR 15 mg but is 2x

the cost

Equianalgesic Table

PO/PR (mg) Analgesic SC/IV/IM (mg)

30 Morphine 107.5 Hydromorphone 1.520 Oxycodone -20 Methadone 10

10 Oxymorphone 1 30 Hydrocodone -

Opioid allergies Most reactions are

“pseudoallergies”: histamine release/puritis, etc.

For a true opioid allergy use a drug from a different class. Patients allergic to codeine CAN usually take fentanyl, methadone but NOT morphine, hydrocodone or oxycodone.

Drug conversion Hints (McPherson 2010)

Oral/rectal same MSO4= 1:3 (IV to oral) Fentanyl: 50% of TDD oral morphine

(25 mcg fentanyl is 50 mg MSO4 TDD) Hydromorphone 5:1 or 3.7:1 (M:HM) Oxycodone 1.5:1(M:O) Tramadol 10:1 (T:M)

Chronic Pain and Opioids Opioids can relieve moderate to severe

pain For occasional chronic recurrent pain

not controlled by NSAIDS, use opioids PRN

Opioids: no ceiling or maximum dose For continuous pain—Sustained release Use breakthrough medications (1/3 –1/2

q. 12 h. dose) “Start low and go slow” Remember cross tolerance/opioid

rotation (20-25% of equianalgesic dose)

Pharmacogenomics of Opioids Genetic polymorphisms >1% of normal

population (1 out of 10 get poor response)

Sensitivity of mouse strains to morphine (ranges from 0-90% based on strain of mouse)

Codeine Poor metabolizers

2% Asians/African Americans 10% Caucasians 20% Middle Eastern

Chronic Pain and Opioids cont. 10 days or longer withdrawl

syndrome will occur therefore: Decrease dose by 50% and give q. 6

h. x 2 days then reduce by an additional 25% every 2 days.

Opioid Options (Amabile, 2006)

Morphine: IR/SR (MSContin, Avinza, Kadian/Embeda)

Oxycodone: IR/SR(OxyContin) Hydromorphone: IR only for now Oxymorphone (Opana) Methadone: (1/2 life of approx. 30 hrs) Fentanyl: high 1st pass effect and low oral

bioavailability. Highly lipophyllic.

Opioid Induced Hyperalgesia (Ballantine 2006)

NMDA receptor mechanisms are involved in the development of hyperalgesia/sensitization (as are opioid metabolites)

NMDA receptor is also involved with opioid tolerance (desensitization).

Dilemma: Increasing the dose of opioid can either improve or worsen pain

Weaning at times may actually improve analgesic effect.

Hyperalgesia: neuroplastic change in pain perception

Opioids: Compare/Contrast Morphine: “gold standard”. Avinza/Kadian/MS Contin/Embeda

(sequestered naltrexone core; REMS. $250.00 vs $90.00 for regular ER formulation)

Oral, rectal, parenteral Metabolite(morphine 3-glucuronide) can cause

seizures, myoclonis, puritis, dysphoria, headache, and hyperalgesia. Risk is increased if low GFR!!!

Avoid in renal failure Crosses Blood brain barrier in 96 min(fentanyl in 6

min)

Opioids: Compare and contrast cont.

Hydromorphone/Dilaudid: IR only Synthetic opioid Oral, rectal, parenteral, intranasal SR recalled by FDA in 2005 due to interactions with

ETOH leading to rapid drug release Metabolite hydromorphone-3-glucuronide causes

same side effects as MSO4 but hydromorphone is more potent therefore requiring less dosing with less adverse outcomes.

Cautious use in renal failure

Opioids: Compare/Contast cont..

Oxycodone: IR/SR Oxy Contin

Synthetic Not renally cleared therefore may be

advantageous in dialysis patients but use cautiously

Less nausea, vomiting Combunox (5 mg with 400 mg

Ibuprofen)

Oxycodone New black box warning for interactions with

CYP3A4 drugs (pathway for metabolizing oxycodone)

Increasing levels with inhibitors (macrolides, antifungals or protease inhibitors)

Decreasing levels with carbamazapine, phenytoin, rifampin (decreases level by 50%)

To avoid, prescribe morphine, codeine, hydromorphone or tapentadol (fentanyl, hydrocodone tramadol and propoxyphene are also 3A4 affected.

Opioids: Compare/Contrast cont….

Methadone (synthetic opioid) ½ life 20-36 hrs. NMDA antagonist and inhibits

serotonin and norepinephrine and therefore helpful in neuropathic pain syndromes

Cheap CLOSE MONITORING. QT prolongation

a risk as are mult. drug interactions (rare if <50 mg/day)

Methadone cont. 80 % oral bioavailability (bid or tid dosing basal with ½ dose q

3 hrs prn BTP); plasma levels do NOT correlate well with drug interactions

Lipophilic Excretion is mostly fecal therefore utilized with renal

failure patients Analgesic properties in 30 minutes; for approximately

4-8 hrs 50% of all deaths occur in the first 2-3 weeks of use (dosed

too quickly) Side effects: “spacy/fuzzy” feeling, drowsiness, constipation,

dry mouth, N/V, puritis, urinary retention: 98% reaches CNS Tablets (5/10 mg); Diskets (40 mg); Solution 5/10 mg

/5ml; powder for rectal compounding; topical gel 20 mg/ml—poor response) and IV

Drugs that may Increase Methadone Effects (www.zerodeaths.org) (www.torsades.org)

Ciprofloxacin Diazepam Diltiazem Actue ETOH Fluconazole Haloperidol Ketoconazole Macrolides SSRI’s Benzodiazepines Verapamil

Drugs that may decrease Methadone Effects (Leavitt 2005)

Barbituates Carbamazepine Cocaine Dexamethasone Chronic ETOH Heroin Phenytoin Rifampin Spironolactone Tobacco Lopinavir & Ritonavir

Methadone Dosing Opioid naiive patient

Start 5 mg po bid

Opioid tolerant patient Usually do not do equianalgesic conversions Start 5-10 mg po tid with breakthrough available Titrate q 3-7 days (after steady state is achieved

to avoid toxicity that can occur 20 hrs out) DO NOT COMBINE WITH BENZOS Caution in patients with sleep apnea, respiratory

infection

Morphine to Methadone conversion

MDD MSO4 <1 gm/day 10:1 MDD MSO4 1-2 gm/day 20:1 MDD MSO4 >2 gm/day 30-40:1

Don’t adjust in <5-7 days Stop methadone then 12 hrs later

switch

Methadone Good choice if:

MSO4 allergy Renal issues Neuropathic pain Adverse drug rxn Refractory pain Cost LA preferred

Methadone Bad choice if:

< 1 week to live Drug interactions Syncope Cognitive impairment Non-adherent

Opana oxymorphone HCl (Opana) Extended relief (5

mg/10mg/20mg/40mg) 12 hr dosing (long ½ life: 9-11 hrs) IR (5mg/10 mg) Only for non-opioid naïve patients who are

not allergic to codeine(metablolite of oxycodone)

Resp. depression is a risk in the debilitated elderly

2x oxycodone; 3x MSO4

Oxymorphone cont. Opana and Opana ER should be

taken 1 hr. prior to meals or 2 hrs after meals (otherwise dangerously increases blood levels) Titrate by 10 mg q 12 hrs q 3-7 days to

relief Structurally RT hydromorphone Numorphan. (Injectable oxymorphone:

10mg/ml)

Opioids: Compare/Contrast cont…

Fentanyl: IR/SR Lipophilic., parenteral, spinal, transdermal,

transmucosally, nebulized Transdermal may not be appropriate choice

if “unstable” pain, fever, diaphoresis, morbid obesity, cachexia, ascites due to altered absorption

“clean” drug; considered safer with dialysis NEWER RESEARCH WITH REGARD TO

CACHEXIA (Journal of Pain; Kalso, E. 2009)

TD Fentanyl titrations Increase TDF in 3 days then q 6 d

as needed Increase by 25-50 mcg/hr but do

not exceed 100% per dose increase

20% of the population will need patch change q 48 hrs

IV:TDF is 1:1 ratio conversion

Oral Fentanyl (Actiq)

Recommended consumption time of “lollipop” is 15 minutes (suck between cheek and lower gum)

Titrate as needed (Start with 200mcg units)

Redosing may occur 30 min. after start of last dose

Ordered for up to 4 units per day Used for breakthrough pain in patients

already tolerant of opioid administration

Fentanyl film (Onsolis)

Fentanyl film for BTP in opioid tolerant patients

Wet mouth; pink side up on finger, press and hold to cheek for 5 sec.

Dissolves in 15-30 min 200/400/600/800/1200 mcg 200 mcg to start (may repeat in 2 hrs;

MAX 4/day)

Rapid Acting Opioid fentanyl buccal tablet (Fentora) 100/200/400/600/800 mcg

For breakthrough pain in opioid tolerant patients (60 mg MSO4/day; 25 mcg fentanyl/hr; 30 mg oxycodone/day)

Starting dose 100 mcg/onset 15 min.

Redosing may occur in 30 minutes/duration 60 min.

Mean is 400 mcg/breakthrough episode

Buccal fentanyl cont. 200-400 mcg Actiq similar to 100mcg

Fentora Remove from blister and place entire

tablet above rear molar between upper cheek and gum and allow to dissolve.

DO NOT spit, suck, chew or swallow tablet After 30 minutes, may swallow remainder

with water

Rule of Thumb If >200 mg oral morphine per day

think: Time to add co-analgesics Opioid rotate ?opioid non-responsive pain Evaluate pain intensity rating: if

<5/10 increase does by 25-50% and if >6/10 increase by 50-100%

Opioid Side Effects Well known

Constipation, sedation, confusion, puritis (histamine release), nausea, respiratory depression, dysphoria

With chronic use (>1 week) most side effects subside with the exception of constipation.

Chronic opioid use: decrease in testosterone/bone loss

Treating Side Effects Prevent constipation with prophylactic bowel

regimen Encourage adequate fluid intake Treat mild sedation(psychostimulants), severe

nausea (neuroleptics, anticholinergics antihistamines, prokinetics, corticosteroids, benzodiazepines, 5-HT3 antagonists), puritis (avoid antihistamine; opioid rotate or/paroxetine/lorazepam), and myoclonis(clonazepam/anticonvulsants/baclofen)

Breakthrough Pain (BTP) (Passik, Moyer, 2006)

Defined as transient increase in intensity of moderate or severe pain occurring in the presence of well-established baseline pain

Typically rapid in onset (3 min.) and lasting short duration (30 min.). May be visceral, somatic, neuropathic

If due to movement/activity it is referred to as “incident” pain.

May be due to inadequate dosing, idiopathic, or “end of dose” pain.

Dose 10-20% of long acting dose q 4 hrs prn

Structured Opioid Therapy for Chronic Pain

1. Pt. reports pain2. Rehabilitative approach3. Medication management (goal

directed/carefully monitored)4. Titrate to effective dose then maintain5. Provide prescriptions on a monthly basis

assessing pain/effect on well-being6. ? Random drug screening7. Increase dose if unstable pain and monitor

for side effects8. If treatment fails wean or “opioid swap”.

Summary of Evidence Supporting Long-Term Opioid Use (Ballantyne, 2006)

Many authors report prolonged and satisfactory analgesia for up to 6 years using moderate doses of opioids (195 mg MSO4 or equivalent)

Some failed pt’s improve when taken off opioids

Question if tolerability can be overcome in every pt. with dose escalations

Addiction rates now reportedly range from 5-25%

Neuropathic Pain: Opioid Effectiveness ( Gimbel, Richards, Portenoy, 2003)

Many recent studies suggest that opioids provide superior analgesic efficacy when compared to placebo

With neuropathic pain syndromes, higher opioid doses may be needed.

Neuropathic Pain Central vs Peripheral Neuropathic Pain Scale/Pain Questionnaire Exam

Pinprick hyperalgesia (exaggerated pain following pinprick)

Straight leg raise (lumbar nerve root) Myofacial trigger points Tinnel’s sign

Adjuvant/ Co-Analgesics Defined as drugs with other

indications that may be analgesic in specific circumstances

Numerous drugs in diverse classes Sequential trials are often needed

Adjuvant Analgesics for Neuropathic Pain

Anticonvulsants Gabapentin commonly used

Favorable safety profile (rare drug interactions) and positive relief in PHN/diabetic neuropathy. Does not always work

Usual effective dose: 600–3600 mg/d and sometimes higher (mean >1800 mg/day); ? Effect >900 mg TDD

Analgesic effects established for phenytoin, carbamazepine, valproate, clonazepam, Trileptal (does not affect bone marrow) and lamotrigine (slow titration needed)

Pregabalin therapeutic usually >150 mg po bid

Pregabalin

Does not effect dopamine or seratonin or noradreniline

PNH and fibromyalgia indications

S/E: Edema and weight gain along with other anticholinergic s/e

Typical dose 300-600 mg/day (mean >1800 mg qd)

Start 50 mg po qd then bid then up to 100 mg tid

Adjuvant Analgesics for Neuropathic Pain

Local anesthetics(sodium channel blockade)

Oral therapy with mexiletine, tocainide, flecainide

IV/SQ lidocaine also useful (1 hr infusion; results can be fast; may get q 6 weeks)

Useful for any type of neuropathic pain

Multipurpose Adjuvant AnalgesicsAntidepressants (use also with

concominant depression; often better than anticonvulsant co-analgesics))

Enhance the descending pain inhibitory system Best evidence: 30 amine TCAs (eg, amitriptyline) Can

alter cardiac conduction. OBTAIN ECG due to alpha blockade.

20 amine TCAs (desipramine, nortriptyline) better tolerated and also analgesic

Some evidence for SSRI/SSNRIs/atypical antidepressants (eg, paroxetine, venlafaxine, maprotiline, bupropion, Cymbalta, others) and these are better tolerated yet

s/e: Cant see, spit, pee, s#%t; often dose related

duloxetine (Cymbalta)

SNRI DPN indicator 20/30/60 mg caps 60 mg qd-bid is typical dosing s/e: insomnia, somnolence, HA,

nausea, xerostomia, constipation, liver issues

Pharmacological Interventions Lidoderm Patches Emla; Emu cream Alpha blockers (clonidine) Ketamine gel Capsaicin tid or qid

Qutenza :New use of 30-90 min application for 1 treatment session with potential pain relief for up to 3 months

Qutenza (8% capsacin patch) For tx. neuropathic pain In office procedure Clean area and apply local

anesthetic. Apply patch for 60 min then remove (may burn) and apply cooling gel. Pain relief lasts 2-12 weeks

Proposed for foot neuropathy

Ketamine Anesthetic; NMDA receptor

antagonist Used as a local anesthetic for

neuropathic pain syndromes Doses: 20 mg/cc; 50 mg/cc; 100

mg/cc Used TID Apply directly to pain site

Ketamine IV Can be used for neuropathic pain

resistant to opioids as well as to attempt to reverse tolerance of opioids

Can cause hallucinations and dysphoria therefore most are placed on a benzodiazepine in conjunction.

Lidoderm/Lidocaine Patch 5% Used for treatment of peripheral

neuropathies Apply to skin at the site of treatment Up to (3) patches may be applied only

once for up to 12 hours within a 24 hour period

May be cut smaller prior to removal of the liner

There is enough drug in patch to last 24 -72h

Lidocaine IV For neuropathic pain resistant to opioids Can be 1x dosing and repeated q 6 weeks or

may be added to IV opiate infusions 125-200 mg Lidocaine over 30 minutes Lidocaine 75 mg/hr. cont. infusion Lidocaine 2mg/kg IV over 30 min Toxicity rare if <4-6 mcg/hr (dizzy, oral

numbness, myoclonis, seizures

MRI burn warning Recent studies suggest

transdermal patches (Flector/some Fentanyl/NTG and scopalamine) have been known to have metallic particles in their formulations and have been known to cause burns during MRI procedures.

Remove and replace after MRI

Adjuvant Analgesics for Neuropathic Pain

Miscellaneous drugs Calcitonin

RCTs in CRPS and phantom pain Bone pain Limited experience

Baclofen RCT in trigeminal neuralgia 30–200 mg/d or higher Taper before discontinuation FYI: TMJ relatively unresponsive to

opioids

Adjuvant Analgesics for Cancer Pain For bone pain

Bisphosphonates (eg, pamidronate, clodronate), calcitonin, radiopharmaceuticals (eg, Sr89, Sm153)

For bowel obstruction pain Anticholinergics, octreotide

Adjuvant Analgesics for Musculoskeletal Pain

“Muscle relaxants” Refers to numerous drugs, eg,

cyclobenzaprine, carisoprodol (new documentation of WD syndromes), orphenadrine, methocarbamol, chlorzoxazone, metaxalone

Centrally-acting analgesics Do not relax skeletal muscle

Antispasmodics Baclofen/Lioresal

5 mg/tid

Methocarbamal/ Robaxin 1.5 mg/qid

Orphenadrine/Norflex 100 mg/bid

Carisoprodol/Soma 350 mg/ tid and hs

Cyclobenzaprine/ Flexaril 10 mg/ tid

Diazepam/Valium2-5 mg/tid

Corticosteroids Useful for neuropathic pain. Immunosuppression and endocrine effects

limit long-term use Proximal muscle wasting occurs after 4-6 wks

of Tx.

Dexamethasone has least mineralcorticoid effect due to long duration of effect(60 hr ½ life)

Once/day dosing 8-20 mg At times high dose rapid taper is most

effective (up to 100 mg/day then titrate down to 2 mg/day)

cannabis (Sativex)

Oral spray Peak 30 min. s/e: dizziness,

dry mouth, nausea, fatigue

For neuropathic pain

Smoked MJ is actually better and may become a C2 drug soon in some states)

Chronic Pain-Nonpharmacologic Options Heat/Cold Massage Acupuncture TENS Exercise Relaxation Techniques/ CBT Touch therapies

Interventional Medicine

Transforaminal lumbar epidural steroid injections via fluroscopy

Epiduroscopy Intradiscal electrothermal therapy Kyphoplasty/Vertebroplasty Surgeries Radiofrequency neuroablation Intra-articular corticosteroids Intra-articular viscotherapy Intrathecal Infusions

Dealing With Addiction

Pain Related terms Cont. Addiction: overwhelming involvement with

obtaining and using a drug for its psychic effects, not for medical reasons. It is a CHRONIC disease

Physical Dependence: after repeated administration of a drug, withdrawal symptoms occur when it is not taken

Pseudoaddiction: Iatrogenic syndrome of behaviors developing in direct consequence of inadequate pain management.

UNIVERSAL PRECAUTIONS FOR ALL PATIENTS

Addiction Prevalence and REMS

Evolving The new worldwide trend is

nonmedical use of prescription drugs (NMUPD) and soon is projected to exceed illicit drug use.

Common: analgesics, stimulants, sedatives, tranquilizers

Predisposing factors Genetic factors account for 40-50% individual

risk Further influenced by environment

(availability, peer pressures, stressors, sociocultural and legal)

Prolonged use show long-lasting changes in the brains of those with SUD’s causing neurophysiologic reinforcement.

APS definition of Opioid Abuse A primary, chronic neurobiological

disease with genetic, psychosocial, and environmental factors characterized by: Impaired control over use Compulsive use Continued use despite harm Craving

Risk Stratification

Low Risk: No personal/family history of SUD and no comorbid psychiatric condition.

Moderate Risk: + past history of SUD, + family history of SUD and/or comorbid psychiatric condition

High Risk: Active addiction and/or major psychiatric disorder.

Teens/Young Adult

Teens and SUD In one recent survey more than 2.1

mill teens abused prescription drugs (VICODIN, OXYCODONE, sleeping pills, anti-anxiety, and stimulants.

50% of these teens admitted to abusing 2 or more of these drug classes along with alcohol and MJ at the same time

PARENT MEDICINE CABINETS!!!

Addiction stats 40-60 % of all patients hospitalized

due to a trauma are substance abusers

25% of all hospitalized patients are suspected substance abusers

Largest growing population is prescription abusers

Statistics An estimated 20% of patients

seen in primary care have SDA’s and yet one recent survey noted that substance abuse was only diagnosed in 9% of general medicine visits (Muher 2010)

Most popular illicit drugs were marijuana (3.9 mill), pain relievers (1.7 mill), and cocaine (1.6 mill)

Statistics cont. In 2007 approximately 22.3 million

adults were classified as having substance dependence or abuse disorders.

Of these adults, 15.5 mill abused alcohol alone and 3.2 million were abusing alcohol and other substances.

Addiction: Evolving View Research into genetics and

neurobiology. Relationships between exposure to

drug therapies and previously undetermined predispositions to addiction/chemical dependency (variability in opioid receptors and how flexible and changeable those receptors are over time)

New tools are being developed to aid in this risk assessment

Opioid Therapy and Chemical Dependency Risk of addiction: Evolving view

Acute Pain: Unlikely Cancer Pain: Very Unlikely Chronic non-cancer pain:

Surveys of patients without abuse or psychopathology show rare addiction

Surveys including patients with abuse history show mixed results

Differential Diagnoses Pseudoaddiction Self-medication for depression/anxiety Spiritual distress Boredom Loneliness Personality or Psychiatric disorder Criminal Intent Delirium

Risk Assessment Tools DAS-I DIRE SOAPP CAGE-AID (cut down; annoyed, guilty, eye-

opener); 2 or more affirmative is + predictor) These tools are believed to have an 83%

positive predictive value in the general population

Screening for Potential Risk: Tools (referenced in bibliography)

SOAPP: Screening and Opioid Assessment for Patients with Pain Tool (24 items)

ORT: Opioid Risk Tool (5 items)

SISAP: Screening Instrument for Substance Abuse Potential (5 items)

PMQ: Pain Medication Questionnaire (26 items)

NIDA Modified ASSIST Tool and Interventions Step 1: Ask Step 2: Advise Step 3: Assess Step 4: Assist Step 5: Arrange http://www.drugabuse.gov/

nidamed/screening/nmassist.pdf

Pain Management in Pt’s at Risk for Developing Addiction (Newman, 2004)

Research suggests at –risk patients do well with controlled programs and should not compromise pain management attempts

Patients have decreased pain threshold, hyperalgesia, and 72% lifetime comorbidity between substance abuse and psychiatric disorders.

How Do We Best Treat Pain? Acknowledge that treatment of pain is

necessary. Admit that withholding pain medication can be

quite harmful Begin to use chronic opioids in controlled

settings for appropriate patients Screen for addiction potential of all patients Keep in mind an interdisciplinary team

approach may be necessary

Conflict

Relapses Relapses are predicted by stressors

(such as poorly treated pain, as well as other emotional/physical stressors)

THE GOALS IS TO PREVENT RELAPSE

Monitoring Drug-Related Behaviors

Probably more predictive of addiction

Selling prescription drugs Forging prescriptions Stealing or “borrowing” drugs from another person Injecting oral formulation Obtaining prescription drugs from nonmedical source“Losing” prescriptions repeatedly

Probably less predictive of addiction

Aggressive complaining Drug hoarding when symptoms are milder Requesting specific drugs Acquiring drugs from other

medical sources Unsanctioned dose escalation once or twice

Monitoring Drug-Related Behaviors (cont.)

Probably more predictive of addiction

Concurrent abuse of related illicit drugs Multiple dose escalations despite warnings Repeated episodes of gross

impairment or dishevelment

Probably less predictive of addiction

Unapproved use of the drug to treat another symptom Reporting of psychic effects not intended by the clinician Occasional impairment

Chronic Opioid Therapy in Substance Abusers

Good outcome (N = 11)

Primarily alcohol

Good family support

Membership in AA or similar groups

Bad outcome (N = 9)

Polysubstance Poor family support No membership in support groups

Dunbar SA, Katz NP. J Pain Symptom Manage. 1996;11:163-171.

Treatment Approach Open posture Acceptance/tolerance Exaggerated drug use suggestions

to encourage pt’s to be more forthcoming

Current use/dosing for baseline meds.

Ethics of the Treatment Agreement Pain Management “contract” Provides structure, expectations of both

parties and consequences of aberrant drug behaviors. NOT PUNATIVE!

Treatment Agreement Plan to also:

Prevent SUD Identify factors suggestive of relapse Structure to provide opioids for

treatment of chronic pain while preventing the risk of relapse

Plan if relapse occurs and needs to be managed

Addictions Risk: Structured Approach to Treatment Select and monitor patients

carefully Use multidisciplinary approach Wean therapy when goals are not

reached through repeated, varied, thorough attempts S/S of withdrawal Methadone maintenance and

treatment of pain

Treatment 1. Frequent assessment for abuse during

routine visits 2. Monitoring for and treating s/e of SAD’s 3. Education regarding side effects and

treatment options 4. Coordination with specialty services 5. Use of community supports (AA/NA) 6. Prevention of exacerbations 7. Team approach to behavioral changes

Addiction Implications for Pain Therapies

Future research addresses hopeful outcomes that we will be better able to predict what patients will do better with which therapies to mitigate and manage addiction over the long term (Fione, 2006).

Set clear guidelines Maximize non-pharmacological therapies Urine tox. screens and treatment agreements

If need further testing Gas Chromatography/Mass spectrometry

Remember to order fentanyl/methadone/oxycodone/merperidine separately (not structurally like morphine)

Treatment of Opioid Addiction Methadone Maintenance program/MMT (MUST BE

SEPARATE from pain treatment in order to continue in structured addition therapy with supports)

Suboxone (Buprenorphine)/BMT Buprenorphine/naloxone 4:1 ratio sublingual Physicians must meet criteria to prescribe according

to the Drug Abuse Treatment Act of 2000 or take an 8 hr course to become certified to prescribe (limit of 30 patients)

Daily dosing of 0.6-1.2 mg/d (8 mg is equipotent to 30-60 mg oral methadone)

Ceiling dose is 12 mg (no effect above that dose) Vivitrol (IM monthly Naltrexone) Counseling, CBT, group therapy

Non-opioid treatment Vivitrol ( 380 mg q 4 wk IM alternating

buttocks each time) or ReVia (oral) are NALTREXONE

Blocks opioid receptors however cravings continue.

ReVia dosing is 12.5 mg day 1, 25 mg day 2, 50 mg day 3, 100 mg day 4

Clonidine (Catapres): decrease craving Dosing 0.1-0.3 mg po q 4 h then taper over next 10-

14 days

Opioid Addiction Treatment/OAT The use of opioid analgesia may cause

addiction relapse. Moreover the evidence suggested that UNRELIEVED PAIN can trigger relapse.

Remember OAT should not be used for analgesia

Aggressively treat pain with conventional opioids using SCHEDULED doses rather than prn dosing.

For those of BMT remember that there is increased competition for mu receptors

BMT and chronic pain treatment options 1. Continue BMT and titrate short acting

opioids to pain relief 2. Divide BMT dose to 6-8 hr intervals 3. DC BMT, implement opioid analgesia, and

restart BMT when opioid analgesia no longer needed.

4. In the hospitalized patient, DC BMT, institute MMT, add short acting opioids to treat pain and have naloxone at bedside. Convert back to BMT as approaching discharge

CMS codes for Abuse Screening and Treatment Refer to codes and CPT codes at http://sbirt.samhsa.gov/coding.htm

Conclusions