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Quest for Quality: Linking Practice to Perception
INTEGRIS Baptist Medical Center
Day One
Pain Assessment and Analgesic Use
Chris Pasero, MS, RN-BC, FAAN
Lecture Outline
I.
Pain Assessment Guides Treatment: Initial and Ongoing (Pasero, McCaffery 2011)
A.
Harmful effects of unrelieved pain (see table in handout)
B.
The subjectivity of pain
1.
Molding: Controlling our patients’ expression of pain
2.
All guidelines agree: Self report is gold standard
C.
Comprehensive pain assessment
1.
Location
2.
Quality indicators; descriptions
3.
Intensity: Use rating scales in patients who can use them
4.
Onset, duration, variations
5.
What relieves; what aggravates
6.
Effects of pain; goal achievement: Assess during rest and activity
D.
Pain intensity ratings
1.
Purpose: A communication tool. Here’s where you are and here’s where
we’re hoping to go. Is what we’re doing helping? Documentation of
ratings facilitates evaluation of trends and treatment effectiveness
2.
0-10 NRS (Numerical [Pain] Rating Scale)
3.
0-10 Wong-Baker FACES Pain Rating Scale (age 3+ to adult); preferred
by African American children (Luffy, Grove 2003) and (Canadian)
parents, nurses, and children but smiling “no pain” resulted in higher
ratings (Chambers et al 2005)
4.
0-10 Faces Pain Scale - Revised (FPS-R) (age 3+) (Spagrud et al 2003)
5.
Culturally diverse populations: Use translated scales (multiple translations
available in Pasero, McCaffery 2011) and unbiased translators
a)
FPS-R: Preferred by African Americans and Hispanics (Jowers
Ware et al 2006); preferred by Chinese adults (Li et al 2007)
E.
Challenges in pain assessment: “Nonverbal” patients: Those who cannot report
pain using customary self-report pain rating methods, e.g., infants, toddlers,
cognitively impaired, unconscious, ventilated, dying patients
1.
Use the Hierarchy of Pain Measures as a framework (www.aspmn.org;
Herr 2006b; Pasero, McCaffery 2005b, 2011; Pasero 2009)
a)
Self report: Single most reliable indicator of pain
b)
Presence of condition or procedure thought to be painful
c)
Pain behaviors (e.g., cry, grimace, moaning, restlessness)
(1)
Surrogate report of pain behaviors
1
d)
2.
3.
Physiological signs (e.g., elevated heart rate, blood pressure): least
sensitive indicators of pain, particularly chronic pain (Arbour,
Gelinas, 2010; Pasero, McCaffery 2011)
e)
Analgesic trial to determine presence of pain
Pediatric pain indicators, assessment tools
a)
Rely on behaviors and parent reports; can be difficult to distinguish
pain from fear; neonatal “face of pain”
b)
Examples of pediatric behavioral scales (there are many others)
(1)
FLACC (preverbal: 2 months to 7 years): Face, Legs,
Activity, Cry, Consolability (Merkel, Voepel-Lewis 1997)
(2)
NIPS (Neonatal Infant Pain Scale) (facial expression, cry,
breathing, arms, legs, state of arousal); CRIES (neonatal:
32 weeks to term): Cry, Requires oxygen, Increased vitals,
Expression, Sleeplessness (Krechel, 1995)
(3)
PIPP (Premature Infant Pain Profile): Age, behavior, heart
rate, oxygen saturation, brow bulge, eye squeeze,
nasolabial furrow (Stevens, 1996) or COMFORT Behavior
Scale (van Dijk, 2005)
Cognitively impaired (Buffum et al 2007; Herr 2004a,b, 2006a,b; Feldt
2000a,b; Fuchs-Lacelle, Hadjistavropoulos 2004)
a)
Try a self-report pain tool
b)
Principles: Insure eyeglasses and hearing aids function, repeat
questions, allow time for response, enlarge font; assess during rest
and activity
(1)
Self-report with FPS-R: Preferred by cognitively intact and
impaired African Americans, Hispanics, and patients with
moderate-to-severe dementia (Jowers Ware et al 2006)
(2)
Self-report with Iowa Pain Thermometer (AGS 2002):
Several choices of descriptors, vertical preferred
c)
Consider behaviors
(1)
PAINAD scale: Breathing, negative vocalization, facial
expression, body language, consolability (0-2 ea; 0 to 10)
(Warden et al 2003)
(2)
Behavioral checklists
a)
PACSLAC (Fuchs-Lacelle, Hadjistavropoulos
2004) 60 possible pain behavior indicators
(i)
Facial expressions: 13
(ii)
Activity/body movement: 20
(iii) Social/personality/mood: 12
(iv)
Physiological/eating/sleeping changes/vocal
behaviors: 15
b)
Checklist of Nonverbal Pain Indicators (CNPI)
(Feldt 2000a,b): Assess during rest and movement;
0-1 each
(i)
Facial grimace or wince
(ii)
Vocal complaints (verbal)
2
II.
(iii) Nonverbal complaints (sounds)
(iv)
Bracing or guarding affected area
(v)
Restlessness (constant or intermittent)
(vi)
Rubbing affected area
c)
Non-Communicating Children’s Pain Checklist
(NCCPC) (Breau et al 2002) 0-3 each
(i)
Vocal: Crying, whimpering, whining
(ii)
Social: Not cooperating or interacting
(iii) Facial: Furrowed brow, pout, quiver
(iv)
Activity: Not moving, agitated
(v)
Body and limbs: Floppy, rigid, guards
(vi)
Physiologic signs: Breath holding, pallor
4.
PACU, critical care, others (Pasero, 2009a; Pasero, McCaffery 2011)
a)
Use various approaches to obtain self-report
b)
Consider underlying pathology and potential for pain; Thunder
Project II data (Puntillo et al 2001); was pain present prior to
sedation, loss of consciousness, coma?
c)
Make assumptions when appropriate; proceed with treatment
d)
Critical-Care Pain Observation Tool (CPOT) (Gelinas et al 2006,
2007, 2010): 0-8 behavioral scale, 2 points each category:
(1)
Facial expression
(2)
Body movements
(3)
Muscle tension
(4)
Vent tolerance/verbalization
5.
Underlying principles (Pasero, 2009a; Pasero, McCaffery 2005, 2011)
a)
A behavioral score is not a pain intensity rating. If a patient cannot
report pain intensity, the exact intensity is unknown
b)
Do analgesic trial to confirm presence of pain or make assumptions
when appropriate and proceed with treatment
c)
Use the analgesic trial to build treatment plan: Begin with
recommended starting doses (e.g., 2.5 mg/hr morphine in adults);
increase based on response; maintain if no response
Principles of Pain Management (Pasero, McCaffery 2011)
A.
Evaluate pain mechanisms to determine treatment options
1.
Nociceptive pain (physiologic; somatic, visceral): On-going activation of
pain-sensitive afferent neural pathways; CNS intact
2.
Pathologic pain (neuropathic): Due to lesion of peripheral or central
nervous system with multiple mechanisms; "sharp,” “shooting,” “electric,”
“continuous, burning” descriptors (Dworkin et al 2010)
3.
Review of nociception: “Normal pain transmission” from periphery to
CNS via ascending tract; descending inhibitory tract (modulation of pain)
B.
Use a multimodal approach (Kehlet, Wilmore 2004; Pasero 2003, Pasero,
McCaffery 2011; Schumann et al 2003)
1.
Rationale for use:
a)
Appropriate combinations attack more than one mechanism
b)
Synergistic action → ↓ doses → ↓ adverse effects
3
III.
2.
Current approach: Opioid only: Adverse effects are dose related
3.
3-step acute pain model (Crews 2002)
4.
World Health Organization Ladder: Stepwise approach (Foley 2006)
C.
Consider the type and intensity of pain to determine the appropriate route
(Stevens, Ghazi 2000)
1.
Oral: Preferred for all pain, especially persistent (chronic) pain
2.
IV: Severe, escalating pain
3.
Intraspinal (epidural, intrathecal)
4.
Perineural (continuous peripheral nerve block)
5.
Transdermal: First-line for some long-term persistent pain
6.
Topical
7.
Oral transmucosal (sublingual & buccal)
8.
Intranasal
9.
Subcutaneous
10.
Rectal
11.
Practice alert: The IM bolus technique is painful, unreliable, dangerous,
and not recommended
D.
Consider the characteristics of the pain to determine the frequency of dosing
1.
Intermittent pain: Treat PRN and prior to painful activities
2.
Persistent pain: Treat with continuous infusion (CI, basal rate), aroundthe-clock (ATC) oral or IV dosing.
a)
After titration with short-acting opioid, long acting formulations =
↑ adherence with fewer doses → better control
3.
Breakthrough pain: Treat with individualized supplemental (breakthrough,
rescue) doses (McCaffery, Pasero 2003; Pasero, McCaffery 2011)
a)
Oral: Provide 10%-15% of daily dose in short-acting opioid
b)
Parenteral (25%-50% of hourly requirement):
(1)
Opioid tolerant: Provide majority of dose by CI
(2)
If CI is used in opioid naive, use lowest effective dose
(assess sedation q 1 hr and dc if ↑ sedation)
c)
Adjust BTD whenever maintenance dose is adjusted
E.
Discuss goals of pain treatment, i.e., optimal function and QOL
1.
Level of pain relief that allows accomplishment of functional/QOL goals
2.
Pain > 3 interferes with activity/mood; > 5 interferes with QOL
3.
Tailor the treatment plan:
a)
Acute, short-term pain: Discuss realistic recovery/rehab milestones
and patient’s ability to achieve them
b)
Chronic pain: How has pain changed the patient’s life? What could
you do before that pain keeps you from doing now?
c)
End of life: Is there anything you want to accomplish before death
that pain would keep you from doing?
F.
Adjust treatment plan based on response: Level of function/QOL, pain relief, and
adverse effects. Find the right balance (individualize) for the patient. Pain
treatment goal is always optimal function and QOL
Use of Analgesics: Practical Tips (Fine, Portenoy 2006; Pasero, McCaffery 2011)
A.
Nonopioid analgesics (Pasero, McCaffery 2011)
4
1.
2.
3.
Agents in the nonopioid analgesic group:
a)
Acetaminophen: Tolerated well by most; can be combined with
any other analgesic
b)
Nonselective NSAIDs, e.g., ibuprofen, diclofenac, naproxen,
ketorolac
c)
COX-2 selective NSAIDs, e.g., celecoxib (Celebrex)
d)
All have a maximum daily dose
(1)
Ortho McNeil (Tylenol): 3000 mg/day, Fall 2011
Mechanisms of action (Boone 2007; Simon 2007)
a)
Acetaminophen: Theories; primary mechanism likely in CNS
b)
NSAIDs
(1)
Cyclooxygenase (COX) (enzyme) breaks down arachidonic
acid into prostaglandins
(2)
NSAIDs block prostaglandins by inhibiting COX
(3)
There are two isoforms of COX
a)
COX-1: Prostaglandins always present
b)
COX-2: Prostaglandins induced by
injury/inflammation
(4)
COX-1 inhibition → GI toxicity, platelet dysfunction
(5)
COX-2 inhibition → analgesia, antiinflammation
(6)
Nonselective NSAIDs inhibit COX-1 and COX-2
(7)
COX-2 selective NSAIDs inhibit just COX-2
(8)
COX selectivity is variable among the NSAIDs
NSAIDs: Adverse effects
a)
CV effects (Boone 2007; Clark et al 2004; Scheiman 2006; Schug,
Manopas 2007; Simon 2007)
(1)
May alter hemostatic balance
(2)
Rofecoxib and valdecoxib withdrawn; celecoxib retained;
avoid post CABG (Boone 2007)
(3)
Warning for all NSAIDs: Avoid in high risk CV patients
b)
GI effects (Laine 2003; Simon 2007)
(1)
NSAIDs block protective GI prostaglandins
(2)
GI toxicity is most common adverse effect of nonselective
NSAIDs; less common with COX-2 selective NSAIDs
(3)
High risk: Older adults, critically ill, history of intolerance
a)
Opioids may be safer in older adults (AGS 2009)
(4)
Do not combine two NSAIDs (↑ GI toxicity risk)
(5)
Consider proton-pump inhibitor, e.g., esomeprazole
(Nexium), omeprazole (Prilosec), in high risk patients
(Cryer et al 2006; Pasero, McCaffery 2011)
(6)
Topical NSAIDs (Rainsford et al 2008)
a)
Systemic absorption = 5-10% that of oral NSAIDs
b)
1% diclofenac sodium gel (Voltaren Gel)
(i)
Osteoarthritis; QID; max dose/joint (8 grams
upper; 16 grams lower); up to 32 grams/day
c)
1.3% diclofenac epolamine (FLECTOR Patch)
5
4.
5.
6.
(i)
Acute pain; BID application to painful area
c)
Renal effects are similar among the NSAIDs (Boone 2007)
d)
Bone healing: NSAID use (Einhorn, 2003; Gajraj 2003)
(1)
Withdrawal of COX-2 inhibition (NSAIDs) restores normal
healing after 14-21 days
a)
NSAIDs are rarely required for more than 14 days
after fracture or ortho surgery
(2)
Short-term NSAID treatment cause no discernable effect on
bone healing
(3)
Avoid in comorbid conditions that affect healing: smokers,
glucocorticoid use, metabolic bone disease
Parenteral nonopioids
a)
IV acetaminophen (Ofirmev)
(1)
Approved for adults and children ≥ 2 years old:
a)
Fever reduction; mild to moderate pain; moderate to
severe pain with adjunctive opioid analgesics
(2)
Single or repeat dosing; 15-min infusion
a)
Adults/adolescents > 50 kg: 1000 mg every 6 h or
650 mg every 4 h to maximum of 4000 mg/day
b)
Adults/adolescents < 50 kg and children ≥ 2 to 10
years: 15 mg/kg every 6 h or 12.5 mg/kg every 4 hr
to maximum of 75 mg/kg/day (3750 mg/day)
b)
IV ketorolac (Toradol) (Cepeda et al 2005)
(1)
Short term pain management (5 days)
(2)
< 65 y/o: 30 mg q 6 h (120 mg/day max; ≤ 105 mg/day
recommended); > 65 y/o: 15 mg q 6 h (60 mg/day max)
(3)
60 mg maximum if > 1.2 mg/dl serum creatinine
(4)
Pediatric dosing: 0.5 mg/kg q 6 h
(5)
Correct hypovolemia before administration
(6)
No advantage to ½ IM dose, ½ IV dose; give all IV
(7)
IV bolus ATC (not PRN), inject over at least 15 seconds
c)
IV ibuprofen (Caldolor) (Singla et al, 2010)
(1)
Approved for fever and acute pain in adults
(2)
400-800 mg over 30 min every 6 hrs
(3)
May preferable to ketorolac
a)
Less COX-1 selectivity (inhibition) than ketorolac
Intranasal ketorolac (Sprix Nasal Spray) (Brown et al 2009)
a)
Acute pain x up to 5 days
b)
< 65 yr: One 15.7 mg spray in each nostril q 6-8 h; ≥ 65 yr or < 50
kg: One 15.7 mg spray in one nostril q 6-8 h; 8 sprays/bottle
c)
26-36% opioid dose-sparing effect
Major benefits of nonopioids (Pasero, McCaffery, 2011)
a)
Opioid + NSAID + acetaminophen → up to 50% less opioid
(Ashburn et al 2004; Buvanendran et al 2003; Chen et al 2004;
Issioui et al 2002; Kehlet, Wilmore 2004; Marret et al 2005; Schug
2006; Schug, Manopas 2007; White 2005)
6
b)
B.
C.
D.
E.
Minimal or no effect on bleeding time: Acetaminophen,
nabumetone, meloxicam, choline magnesium trisalicylate,
magnesium salicylate, salsalate, COX-2 selective NSAIDs
c)
Start preop in surgical patients (Ashraf et al 2004; Buvanendran et
al 2003; Issioui et al 2002; Recart et al 2002)
Anticonvulsants: Carbamazepine (Tegretol), clonazepam (Klonopin),
oxcarbazepine (Trileptil), gabapentin (Neurontin), tiagabin (Gabatril), topiramate
(Topamax), pregabalin (Lyrica) (Dworkin et al 2010; Pasero, McCaffery, 2011)
1.
Calcium, sodium channel blockers; first line for neuropathic pain
a)
Starting dose varies; all require individualized titration
b)
Gabapentin 300 to 3600 mg/day; pregabalin 50 to 600 mg/day
c)
Adverse effects: Sedation, dizziness, unsteadiness, nausea
(1)
Adverse effects usually lessen with time
(2)
Slow titration if excessive adverse effects
2.
Anticonvulsants for acute pain management (Buvanendran 2007, 2010;
Grover 2009; Hurley 2006; Mathiesen 2011; Tiippana 2007; Zhang 2011)
a)
Opioid, nonopioid dose-sparing effect
b)
Acute burn pain (Gray 2005)
c)
May prevent chronic pain (Buvanendran 2010; Durkin 2010)
d)
Add to multimodal plan for high risk patients
Antidepressants: Secondary-amine TCAs: Nortriptyline (Pamelor), desipramine
(Norpramin); SNRIs: duloxetine (Cymbalta), venlafaxine (Effexor) (Dworkin et
al 2010) (use amitriptyline [Elavil] only if secondary-amine TCA unavailable)
1.
Block the reuptake of norepinephrine (NE) and serotonin; first line for
neuropathic pain
2.
Tricyclic antidepressants (TCA) dose varies: 5-25 mg to 200 mg hs
3.
Duloxetine (serotonin norepinephrine reuptake inhibitor-SNRI): Fewer
adverse anticholinergic effects than TCAs; up to 120 mg QD
4.
Adverse effects: Sedation, dizziness (orthostatic hypotension), dry mouth
Lidocaine patch 5% (Lidoderm) (Argoff et al 2004; Devors, Galer 2000; Habib et
al 2009; Pasero 2003; Pasero, McCaffery 2011)
1.
Postherpetic neuralgia (PHN), neuropathies, low back and neck pain,
migraine, variety of other acute and chronic pain conditions
2.
Analgesic, not anesthetic; minimal systemic absorption and adverse
effects
3.
Pliable adhesive; cut and apply directly to intact painful site
4.
Research shows 4 patches worn continuously (change q 24 hrs) is safe
Dual mechanism analgesics (Pasero, McCaffery 2011): Built-in multimodality
1.
Tramadol (Ultram, Ultracet) (AGS 2009; APS 2008; Dworkin et al 2010;
Fishman et al 2007)
a)
Dual mechanism of action: 1) mu opioid receptor; 2)
norepinephrine (NE) and serotonin reuptake inhibition
b)
Acute pain; second line for neuropathic pain
c)
50 mg/tablet (Ultram); tramadol + acetaminophen (Ultracet)
d)
Extended-release formulation: 100, 200, 300 mg
7
e)
F.
Slow titration to comfort or maximum daily dose of 400 mg; 300
mg in those older than 60; lowers seizure threshold (AGS 2009;
APS 2008, 2005; Bodalia et al 2003)
f)
Do not combine with other drugs that increase serotonin levels:
Serotonin syndrome (shivering, nausea, fever, confusion, delirium)
2.
Tapentadol (Nucynta) (Daniels et al 2009; Hartrick et al 2009; Kleinert et
al 2008; Pasero 2011)
a)
Dual mechanism: 1) mu opioid receptor; 2) NE reuptake inhibition
b)
NE targets analgesia; serotonin targets depression
c)
Effective for acute pain, chronic pain, and neuropathic pain
d)
50, 75, and 100 mg tablets; dosing interval every 4-6 hrs
e)
Extended-release formulation in development
Opioid analgesics (Pasero, McCaffery 2011)
1.
Large group of analgesics
a)
Opioids bind to mu, delta, or kappa receptor sites and block release
of neurotransmitters in peripheral and central nervous systems
b)
First line for moderate-severe physiologic (nociceptive) pain
c)
No ceiling on mu opioid analgesia; all of the first-line opioids
produce similar pain relief at steady state
2.
First-line (mu agonist) opioids for moderate-to-severe pain
a)
Morphine: Slow acting, long duration; metabolites M-3-G and M6-G (potent and analgesic) can accumulate with long-term use
b)
Hydromorphone (Dilaudid): Intermediate action and duration;
metabolite HM-3-G can accumulate with long-term use
c)
Fentanyl: Fast acting, short duration (except transdermal – see later
discussion); may be best choice for any organ failure; no clinically
relevant metabolites
3.
Opioid selection
a)
Consider drug characteristics
b)
Fentanyl for rapidly escalating severe pain; hemodynamic
instability; end-organ failure
c)
If relatively stable pain on admission, use the drug that will be
used for ongoing pain management
d)
Consider multiple patient characteristics
4.
Old stand-bys are not appropriate first-line opioids (Fick et al 2003)
a)
Meperidine (Demerol) produces toxic (CNS) metabolite
normeperidine
b)
Propoxyphene (Darvon, Darvocet) CNS and cardiotoxic:
Withdrawn from market in 2010
c)
Agonist-antagonist opioids (Stadol, Nubain, Talwin, Buprenex):
Ceiling on dose: Increases do not increase relief
(1)
Antagonize at mu opioid receptors: Can precipitate
withdrawal in opioid tolerant taking mu agonist opioids
(2)
Talwin causes hallucinations, nightmares, anxiety
(3)
Buprenorphine requires 10 mg naloxone to reverse
8
a)
5.
6.
Transdermal buprenorphine: Chronic pain (Gordon
et al 2010)
Opioid equianalgesia (see chart below and Pasero, McCaffery 2011)
a)
Doses that are approximately equal in ability to relieve pain
b)
Equianalgesic charts are not exact; are just guidelines
c)
Helpful when switching from one opioid or route to another
d)
Do not use equianalgesic chart to switch to methadone (see below
and multiple formulas in Pasero, McCaffery 2011)
Equianalgesic Dose Chart
Mu opioid
IM, IV, SC
PO
Morphine
10 mg
30 mg
Hydrocodone
--30 mg
Hydromorphone
1.5 mg
7.5 mg
Meperidine
75 mg
300 mg (NR)
Oxycodone
--20 mg
Oxymorphone
--10 mg
Fentanyl
100 mcg (1 mcg/h transdermal fentanyl is approx
equal to 2 mg/24 hours of oral morphine)
Example: Switching from one oral opioid to another oral opioid
Morphine to oxycodone
a) Determine total daily opioid dose (maintenance + breakthrough)
• 90 mg + 30 mg = 120 mg oral morphine/day
b) Find current opioid equianalgesic dose
• 30 mg of oral morphine
c) Divide 24 hr dose by equianalgesic dose = equianalgesic units
• 120 mg ÷ 30 mg = 4 equianalgesic dose units
d) Find new opioid equianalgesic dose
• 20 mg of oral oxycodone
e) Multiply new opioid equianalgesic dose by the number of current
opioid equianalgesic dose units = 24-hr dose of new opioid
• 20 mg x 4 units = 80 mg oxycodone
f) Decrease 24-hr dose by 25%-50%
• 80 mg x 0.25 = 20 mg → 60 mg
• 80 mg x 0.50 = 40 mg → 40 mg
g) Divide 24-hr dose of new opioid by number of doses to be
taken per day (q 12 hr dosing = 2 doses/day)
• 60 mg ÷ 2 = 30 mg q 12 hrs
• 40 mg ÷ 2 = 20 mg q 12 hrs
h) Recalculate BTD (10-15% of daily opioid dose)
• 60 mg x 0.10 = 6 mg
• 60 mg x 0.15 = 9 mg
BTD: 5-10 mg oxycodone q 2 h PRN (available strengths)
Fear of causing addiction: Major barrier to pain management
a)
The term “narcotic” is inaccurate, has negative connotation. Use
“opioid” with colleagues; “pain medication” or “pain medicine”
when talking with patients and their families
9
b)
Definitions (AAPM, APS, ASAM 2001)
(1)
Addiction: A primary chronic neurobiologic disease
characterized by impaired control over drug use,
compulsive use, continued use despite harm, and craving
(AAPM, APS, ASAM 2001); pattern of compulsive drug
use characterized by use of the opioid for effects other than
pain relief (APS, 2008). Taking an opioid for pain relief is
not addiction, no matter how long or what dose is taken
(2)
Physical dependence: State of adaptation manifested by a
specific withdrawal syndrome that can be produced by
abrupt cessation, rapid dose reduction, decreasing blood
level of the drug, or administration of an antagonist
(AAPM, APS, ASAM 2001)
(3)
Tolerance: State of adaptation in which exposure to a drug
induces changes that result in a diminution of one or more
of the drug’s effects over time (AAPM, APS, ASAM 2001)
a)
Treat analgesic tolerance by increasing dose or
opioid rotation: Opioids have no dose ceiling
(4)
Incidence of addiction when opioids are taken for pain
relief is rare in those with no history of addiction (<1%)
(Adriaensen et al, 2003; APS, 2008; Fields 2007; Jackson
2009; Mathias 2000;Rowbotham et al, 2008; Todd 2007 for
ED)
(5)
Rate of addiction to illicit drugs, prescribed opioids, and
alcohol in individuals taking long-term opioids is similar to
the general population (6-10%) (Nicholson, Passik, 2007;
Savage 2002)
(6)
Long-term opioid therapy: 3-year registry study long-term
CR oxycodone (Portenoy et al 2007): Prolonged relief,
tolerable adverse effects, modest need for dose escalation;
no evidence of new addiction
(7)
Pseudoaddiction: Iatrogenic syndrome created by
undertreatment of pain and characterized by patient
behaviors such as anger and escalating demands for more
or different medications; often results in suspicion and
avoidance by staff; can be distinguished from true addiction
in that the behaviors resolve when pain is effectively
treated (Weissman, Haddox 1989)
(8)
Guidelines for care (Pasero, McCaffery 2011)
a)
Realistic goal achievement: Short time with patient
precludes the possibility of a cure for addiction but
respectful care, support during hospitalization, and
referral for long-term plan is possible; do not
withhold opioids during periop period (May et al
2001; McCarter 2006)
10
b)
7.
8.
9.
10.
Use multidisciplinary approach to care if available,
e.g., addiction medicine specialist, social services
c)
Evaluation of abuse risk: SOAPP (Butler et al
2004), Opioid Risk Tool (Webster, Webster 2005)
d)
Use Federation of State Medical Boards Model
Guidelines for Use of Controlled Substances for
Treatment of Pain (www.FSMB.org) and
AAPM/APS Consensus Statement: Use of Opioids
for Treatment of Chronic Pain (www.painmed.org/)
e)
4 A’s (Passik 2004): Amount of relief; Activities;
Adverse effects; Aberrant drug-taking behaviors
f)
ASPMN position paper (www.aspmn.org) addresses
3 levels of addictive disease (Nichols, 2003)
Oral opioids (Hanks et al 2006; Sinatra, 2009)
a)
Available first-line opioids: Morphine, oxycodone,
hydromorphone, oxymorphone
b)
Faster onset and peak, shorter duration than modified-release
(1)
Onset 30-60 min; peak effect 60-90 min; duration 3-4 hrs
c)
Modified-release opioids: Overview (Hanks et al 2006)
(1)
Various terms depend on formulation: “controlled-release”;
“extended-release”; “sustained-release”; “long-acting”
(2)
Slow, more uniform release of drug over extended period
Modified-release oral opioid formulations (Blumenthal et al 2007;
Cheville et al 2001; Gimbel, Ahdieh 2004; Hale et al 2005; Kampe et al
2004; McIlwain, Ahdieh 2005; Roth et al 2000; Portenoy et al 2007)
a)
Morphine: MSContin, Oramorph (q 12 h); Kadian and Avinza (q
24 h; OK to sprinkle and to give per G-tube)
b)
Oxycodone: OxyContin q 12 h
c)
Oxymorphone: Opana (short-acting and ER q 12 h)
d)
Hydromorphone: Exalgo q 24 h
e)
80-90% of patients will benefit from more frequent dosing than
manufacturer recommends (Gallagher et al, 2007)
Tamper-resistant oral opioids
a)
Morphine (Embeda): Embedded naltrexone
b)
Oxycodone (OxyContin, Remoxy; Oxecta [fast-acting]):
Reformulated: Hard to cut, break, chew, crush, or dissolve
Methadone (APS 2005; Davis, Walsh 2001; Lynch 2005; Mercurio,
McPherson 2007) (See Pasero, McCaffery 2011 for extensive content)
a)
Inexpensive, mu opioid with NMDA antagonist activity; second
(Dworkin et al 2010) to fourth line (Moulin et al, 2007) for
neuropathic pain; sublingual for breakthrough (Hagan 2010)
b)
Long, variable half-life (12 to 190 hrs); longer than analgesic
duration so can accumulate; prolonged QT interval, multiple
incompatibilities (drug interactions)
c)
Controversy over potency (perhaps 5 to 10 times more than
morphine) and duration of analgesia unclear (4 to 12 hrs)
11
d)
11.
12.
13.
14.
Significant incomplete cross tolerance and no consensus on
method to use when switching to methadone: Morphine to
methadone ratios of 4:1 – 12. The higher the current morphine
dose, the lower the starting methadone dose
e)
Calculate total 24 hr oral morphine dose. If less than 90 mg/day,
use 4:1; if 90-300 mg/day, use 8:1; if greater than 300 mg/day, use
12:1 (APS 2005) OR calculate oral morphine dose then reduce
equianalgesic oral methadone dose by 90% (Indelicato, Portenoy
2002) (see also Pasero, McCaffery 2011)
f)
Divide 24-hr dose by 3 for 8-hr dose interval (APS 2005)
g)
Titrate very slowly; monitor response daily and especially on days
2 to 5; ↓ dose or stop if sedated
Transdermal fentanyl (TDF, Duragesic patch) (Allan et al 2005; Berliner
et al 2007; Pasero, McCaffery, 2011)
a)
Indications: Persistent (chronic) pain; unable to take oral opioids;
nonadherent patients; recovering addictive disease; opioid tolerant
children ≥ 2 years old with cancer pain (Finkel et al 2005)
b)
Gradual increase in serum concentration; levels off 12- 24 hr
c)
Relatively constant concentration during 48 to 72 hr application
period: Many require 48 hr change
d)
Base initial dose on current daily opioid dose: 2 mg/24 hr oral
morphine = 1 mcg/hr TDF; Provide fast-acting opioid for BTDs
e)
Increase dose if needed after 3 days then q 6 days
f)
Bypasses GI tract; no first pass effect; less constipation
g)
Patient preference: Fewer adverse effects, less stigma
h)
Plasma concentration lower in cachectic patients; more research
needed on this (Heiskanen et al, 2009)
i)
Avoid heat directly on patch
Oral transmucosal fentanyl “rapid onset” for breakthrough pain in opioid
tolerant patients: Ideal for severe, sudden onset pain
a)
Actiq (oral transmucosal) (Payne et al 2001)
(1)
Self-administered “sugar matrix on a stick”
(2)
Onset = 5-15 min; duration = 2.5-5 hrs
b)
Fentora (buccal) (Webster 2006)
(1)
Onset, duration faster than OTFC; 65% bioavailable
c)
BioErodible MucoAdhesive patch (BEMA, Onsolis)
Intranasal fentanyl (Lazanda): Breakthrough pain in opioid tolerant
a)
5 minute peak; 60 minute duration
b)
Start: 100 mcg spray x 1 in 1 nostril; wait 30 min to evaluate effect
c)
May increase in step-wise manner next episode: 100 mcg spray x 2
(1/nostril) → 400 mcg x 1 in 1 nostril → 400 mcg x 2 (1/ nostril)
IV opioids (Pasero, McCaffery, 2011; Sinatra, 2009)
a)
Used for rapid analgesia; moderate-to-severe pain (most common
for postop); anytime oral route cannot be used
b)
Drug solubility determines characteristics:
Onset
Peak
Duration
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G.
H.
I.
Morphine (hydrophilic)
8 min
30 min
2-3 h
Dilaudid (intermediate)
6 min
20 min
2-3 h
Fentanyl (lipophilic)
3 min
15 min
1-2 h
c)
First dose: Adult starting doses (pediatrics by kg or percentages):
(1)
Morphine 2 – 3 mg; hydromorphone (Dilaudid) 0.2 – 0.4
mg; fentanyl 25 – 50 mcg
(2)
Repeat previously safe dose
(3)
Risk of respiratory depression increases with > 10 mg
morphine; > 1.5 mg of Dilaudid; or > 100 mcg fentanyl
d)
IV opioid titration (Aubrun et al 2003; Dahmani et al 2001):
(4)
Insure multimodal approach is initiated (add nonopioids)
(5)
Push slowly and allow enough time to see effects
(6)
Stop if excessive sedation (sleep)
e)
Goal: Find a balance between pain relief and side effects
(1)
Pain control on a continuum
(2)
Relationship between pain ratings and dose is not linear.
(3)
Never dose to a specific pain intensity.
(4)
Remove pain intensity number goals (e.g., 4) from PACU
discharge criteria.
(5)
Pain control is a shared responsibility.
(6)
Goal: Effective and safe analgesia
f)
Titration for acute exacerbation of cancer pain in opioid tolerant
(Davis 2004)
(1)
1 mg IV morphine (or equiv) per min for 10 min until pain
relief (to 10 mg); repeat in 5 min if no relief (to 30 mg)
(2)
Calculate CI and BTD based on dose during titration
15.
Patient-controlled analgesia (PCA)
a)
Patient selection criteria: Must understand relationships between
pain, pressing a button and pain relief
b)
Authorized agent analgesia: parent-, caregiver-, nurse-activated
dosing (www.aspmn.org(Pasero, McCaffery 2005a; 2011)
c)
Use basal rates with caution (Pasero, McCaffery 2004)
d)
Oral PCA “MOD”: PRN dosing (Rosati et al, 2007): Secured,
programmable device allows patient access to PRN analgesia via
RFID technology; Patient enters pain rating
Continuous peripheral nerve block (perineural local anesthetic infusion of
bupivacaine [Marcaine] or ropivacaine [Naropin]) (Pasero, McCaffery 2011)
1.
Catheter(s) inserted next to or into site of innervation, e.g., nerve plexus,
surgical wound, for continuous local anesthetic infusion with or without
PCA; provide PRN rescue opioid doses; used for all types of pain
2.
Systemic local anesthetic toxicity is rare. Early: Metallic taste, ear ringing,
perioral numbness; Late: Irritability, slurred speech, seizures, CV collapse
Intraspinal analgesia (see Pasero, McCaffery 2011 for extensive content)
Minimize adverse effects to maximize outcome (Pasero, McCaffery, 2009; 2011)
1.
Use a multimodal pain treatment approach → ↓ doses
2.
Consider multimodal adverse effect treatment (Gan et al 2003; 2007)
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3.
IV.
Decrease opioid dose to reduce/eliminate adverse effect; seek lowest
effective opioid dose (Pasero, McCaffery 2011; Roberts et al 2005)
4.
Prevention of opioid-induced sedation and respiratory depression (Pasero,
2009b; Pasero, McCaffery 2002; 2011)
(1) Respiratory depression is rare in opioid tolerant
(2) At-risk populations: Infants < 6 months old, opioid naïve elders,
patients receiving other sedating drugs or with coexisting conditions
(3) Preventable: Sedation precedes opioid-induced respiratory depression
a. Use multimodal approach
b. Monitor sedation with a sedation scale and respiratory status q
1 h x 12 h, q 2 h x 12 h, then q 4 h if stable (risk ↑ first 24 h)
c. Use basal rates cautiously; decrease dose if excessively sedated
d. Assess risk factors; capnography in high risk
(4) Pasero Opioid-induced Sedation Scale (POSS) (Copyright 1994);
Nisbet & Mooney-Cotter, 2009 for reliability/validity)
S = Sleep, easy to arouse (Check respiratory depth and regularity,
compare to baseline, and if satisfactory, no action is necessary)
1 = Awake and alert (No action necessary; may ↑ opioid dose)
2 = Occasionally drowsy, easy to arouse (No action necessary;
may ↑ opioid dose)
3 = Frequently drowsy, arousable, falls asleep mid-sentence (Add
nonopioid and ↓ opioid dose 25% to 50%; ↑ monitoring until
sedation level is less 3)
4 = Somnolent, minimal or no response (Stop opioid, stimulate,
consider naloxone; restart opioid at 50% of original dose when
sedation level is less than 3 and respiratory status is satisfactory)
(5) Narcan administration: DILUTE 0.4 mg in 10 mL saline and give
SLOW IV push, TITRATE TO EFFECT (APS 2008); pediatrics (< 40
kg): 0.1 mg in 10 mL saline, titrate to effect
Nondrug Interventions (McCaffery 2002; Bruckenthal, 2010)
A.
Physical modalities
1.
Cold, heat, massage, TENS; acupuncture
2.
Physical therapy, aqua (hydro) therapy, functional restoration
B.
Cognitive-behavioral approaches
1.
Simple: Relaxation breathing, music, provide info, focusing, prayer
2.
Complex: Imagery, meditation, hypnosis, humor, therapeutic touch,
biofeedback, virtual reality
C.
Use to supplement, not replace, pharmacological interventions (APS 2002; 2005;
McCaffery 2002)
14