This document discusses chronic pain in older adults. It notes that chronic pain is common in older populations, affecting 25-50% of community-dwelling elders and 45-50% of nursing home residents. The pathophysiology of chronic pain can involve nerve sensitization, nerve damage, and inflammatory mediators. Treatment of chronic pain in older adults requires special considerations due to age-related changes in pharmacokinetics and pharmacodynamics. Non-pharmacological therapies and non-opioid medications are preferred, with opioids used cautiously at lower doses. Proper evaluation, treatment planning, and monitoring are important for safe and effective management of chronic pain in older patients.

1. Ravi Lakkaraju, MD
Poway Spine and Pain
Poway, CA

2.  The International Association for the Study of
Pain (IASP) defines pain as “an unpleasant
sensory and emotional experience associated
with actual or potential tissue damage”
 Pain is the single most common reason for
patients to seek medical attention

8.  2000 – 13.1% of population over 65
 2030 – 20% of population over 65
 25-50% of community elders suffer chronic
pain of some kind
 45-50% of Nursing home residents suffer
chronic pain

9.  Chronic pain effects approx. 100 million
Americans
 Roughly cost $635 billions annually
 Incidence greater than Diabetes, heart disease
and cancer combined.

10.  - sensitization of nociceptors
 - Nerve damage
 - Release of sensitizing humoral mediators

24.  In some conditions, nociception due to tissue
damage may occur, but the patient may not
perceive, or feel it
 i.e., diabetic peripheral neuropathy
 Conversely, the patient may perceive severe
pain with no demonstrable evidence of tissue
damage
 i.e., trigeminal neuralgia

25.  Nociceptive – somatic (superficial, deep) and
Visceral.
 Neuropathic – painful mononeuropathies,
polyneuropathies, Deafferentation pain,
sympathetically maintained pain, central pain.
 Mixed

27.  Acute pain
 Chronic pain
 Cancer pain
 Chronic non-cancer pain (CNCP)
 CPS (chronic pain syndrome)

29. 4 Basic Steps:
 Transduction
 Transmission
 Modulation
 Perception

30.  The process by which afferent nerve endings
participate in translating noxious stimuli (e.g.,
a pinprick) into nociceptive impulses
 Noxious stimulation is first carried by the
faster A-delta fibers and then by the slower C
fibers
 Local injury can cause nociceptors to become
hypersensitive to noxious stimuli, thereby
creating a condition called sensitization

31. • The process by which impulses are
sent to the dorsal horn of the spinal
cord and the brain
• Noxious stimulation is first carried
by the faster A-delta fibers and then
by the slower C fibers

32. • The process of dampening or amplifying pain-
related neural signals
• A variety of modalities can modulate these
pathways”, including:
• Systemic or neuro-axial injection of opioids
• Electric stimulation, TENS, Acupuncture, Massage.
• TCA’S, AED’s
• Stress, Anxiety
• Depression

33.  Refers to the subjective experience of pain
 Results from the interaction of transduction,
transmission, modulation
 Dependent on the psychological aspects of the
individual

35.  Neuropathic pain is pain due to damaged or
dysfunctional nerves
 The pathophysiology of neuropathic pain can have
both peripheral and central mechanisms
 it is doubtful that a single mechanism can account
for all cases
 The end result is pain that is experienced without
evidence of noxious stimulus

36.  - Enhanced pain intensity
 - Enlargement of pain areas
 - Widespread hyperalgesia
 - Enhanced disability

38.  - sensitization of central neural structures
 - Dysfunction of endogenous pain modulation

39.  - Psychophysical Assessments
 - Objective Assessments
 - Measuring spread of pain and referred pain
areas
 - Measurement of endogenous modulation
 - Measurement of Temporal Summation

48.  Can be classified mostly into 3 broad groups:
- Curative/Disease modifying
- Rehabilitative
- Palliative

49.  Simplest and preferred when the identifiable
pathophysiological process is present and
becomes the target of treatment.
 Typically pain should resolve once the
underlying process resolves
 Examples – ORIF, Appendectomy, Angioplasty
for ischemia
 Difficult to treat ‘upstream’ pathophysiologic
process

50.  Appropriate when 2 conditions apply
 - the curative model is not appropriate
 - major goal of treatment is improving patient’s
ability to function
- Examples – multidisciplinary pain rehabilitation
(PT, OT, counselling, biofeedback, CAM,
vocational rehab, etc.,)

51.  Combination of Medication management to
control pain
 And/or
 Less demanding rehabilitative therapies

52.  Low levels of pain can cause high functional
impact, depression
 Although pain threshold increases with age,
tolerance for pain decreases.

55.  Multiple pain complaints, multiple medical
problems, poor communication/under-
reporting
 Cognitive decline, depression, anxiety,
insomnia, fatigue
 Poor nutrition, poor tolerance to tests and
procedures.

56.  Can be more reliable than just pain reporting,
especially in low cognitive patients.
 Facial expressions
 Verbalizations
 Body movements

57.  Changes in interpersonal interactions
 Changes in activity patterns or routine
 Mental status changes

58.  Decreased renal function (decrease in
glomeruli, decrease in renal excretion, low
GFR, higher serum drug levels)
 Decreased hepatic function (decreased
Cyt.P450 oxidation causing higher serum drug
levels
 Decreased serum protein, decreased functional
binding to proteins – Less unbound drug,
increased CNS effect.

59.  Two metabolites – M3G, M6G (6 is more active
and leads to sedation, as this is renally
excreted)
 Elimination by hepatic metabolism to
glucuronides
 T1/2 is 2-4 hrs. may be elevated in elderly up
to 15 hrs.

60.  Metabolized to normeperidine
 Not reversible by naloxone
 This leads to respiratory depression and
excitatory neurotoxicity, anti-cholinergic
effects, urinary retention
 Blocks reuptake of NE and HT, can cause fatal
reaction with concomitant SSRI (Fluoxetine)

61.  Decreased nerve conduction velocity (loss of
myelin on axons, decrease axonal synapses)
 Elderly adults rely on C-fiber input when
reporting pain ; whereas, younger patients use
C and A-delta.

62.  TENS, heat, acupuncture, relaxation
techniques.
 Exercise – targeted therapies with realistic
achievable goals, should be integrated into
daily routine and ADL’s, progress slowly as
function and strength improve.
 PT / OT , custom adaptive equipment as
needed to decrease pain and improve function.

63.  ASA
 Acetaminophen
 NSAIDS
 Tramadol
 Opioids
 Anti-Depressants
 Anti-Epileptics
 Local Anesthetics / Topicals

64.  NSAIDS – exercise caution due to renal, GI and
CV risks
 Anti-depressants and Anti-convulsants -
adjunctive role in chronic pain especially
neuropathic pain states. Dosing limited by side
effects
 Topical anesthetic / NSAID patches – limited
penetration into the tissues, effective only at
superficial targets

67.  Equalizing the ‘Pain Pendulum’
 ‘Balance’ pain relief with risks associated with
opioids.
 (Not too much…not too little…just enough !!)

68.  Always administer tools for risk assessment
(COMM, DIRE, ORT, SOAPP, SOAPP-R)
 Have a clear written agreements / documentation
/ ‘opioid contract’
 All opioid contracts should be simple and written
at ‘6th or 7th’ grade level or even lower !
 Written consent from patient that ‘contract’ was
read and clearly understood by the patient.

69.  Opioid contract/Agreement sets precedence to
‘Rules/responsibilities on patients and reviews
risks involved. Not a binding agreement but a
good practice for every provider.
 Templates of medication agreements can be downloaded from www.SanDiego-
SafePrescribing.org
 Create function based treatment plans with
goals, e.g, begin PT, document improvement in
ADL’s and daily routine. Review partner or
care-giver input apart from patients self report.
Review therapy notes.

70.  Must have a good collaboration between
patient and clinician
 Apart from pain scores, goals should be
realistic, meaningful and verifiable.
 Treatment plan should be periodically re-
assessed, modified based on goals and
functional outcomes
 Always have a ‘Exit strategy’ or plan
termination that is mutually agreed upon by
the patient.

71.  works on 3 receptors- mu, kappa, delta.
 Exerts 3 actions – 1.inhibits transmission of
nociceptive input from the periphery to the
spinal cord, 2.activation of descending
inhibitory pathways that modulate
transmission in the spinal cord (pain
“dampening”), 3. Alteration of limbic system
activity.
 Thus, opioids modify sensory and affective
aspects of pain.

72.  Start at lowest possible dose for opioid –naïve
patients – ‘start low go slow’
 Opioid tolerant patients – select dose and
medication on case by case basis. When
converting from other opioid start at 50%
equianalgesic dose and titrate per response.
 May use ER/LA therapy alone, SA only, or a
combination of ER/LA with a SA opioid.
 Recommend not to use more than one SA
concurrently.

73.  SA opioids typically have rapid onset (10-60 min)
and relatively short duration (2-4 hrs)
 ER/LA opioids have relatively slow onset
(between 30 to 90 min) and relatively long
duration of action (4 to 72 hrs)
 Combination with non-opioid adjunctives can be
beneficial and can have opioid sparing effects. But
monitor for non-opioid drug toxicity.
 No ‘ceiling’ effect for opioid analgesic dosing.
 Selecting ‘Abuse-Deterrent’ formulations may
minimize the opioid abuse.

74.  Phenanthrene (Morphine, codeine, Thebaine,
Papaveretum)
 Semi-synthetic (hydrocodone, hydromorphone,
oxycodone, oxymorphone)
 Synthetic (Fentanyl, Demerol, methadone)

75.  Buprenorphine
 Butorphanol
 Nalbuphine

76.  3 principal classes
 - Mu 1, 2, 3
 . 1-supraspinal analgesia
 . 2-respiratory depression, physical dependence
 -Kappa
 . Sedation, spinal analgesia
 Delta – Anti-depressant, dependence, Analgesia

77.  Morphine dose is used as a ‘standard’ for dose
comparison of other opioids. Morphine
equivalent daily dose (MEDD)
 Recommend not to exceed >100 mg/day
MEDD
 exercise caution with morphine and Demerol
use in renal insufficiency patients. Most other
opioids eliminated by hepatic metabolism.
 Codeine is a prodrug and not all patients
convert it to an active form.

79.  When treating chronic pain with opioids, also
be prepared to proactively treat side effects.
 Common side effects include respiratory
depression, sedation, mental clouding or
confusion, nausea, vomiting, constipation,
pruritus and urinary retention.
 Side effects tend to subside with time with the
“exception” of Constipation.

80.  Periodic urine drug screens (should be performed
for the duration of COT)
 244 un-intentional Rx drug related deaths in San Diego county in 2014, 5723 ER
discharges related to pain killers in 2013
 Utilizing ‘CURES’/PDMP system for monitoring
and surveillance (CONTROLLED SUBSTANCE UTILIZATION REVIEW AND
EVALUATION SYSTEM). Register by Jan 1st, 2016.
 Can complete registration online at https://pmp.doj.ca.gov/pmpreg
 Perform Pill counts at each visit, especially in high
risk patients.

81.  July 2012, FDA released ‘final’ guidelines to
REMS for ER/LA formulations.
 2014-2015 – Government move to initiate an
action plan to formulate ‘National Pain
Strategy’(NPS)

82.  Urine drug screens typically done every 1-3
months.
 More frequently done in high risk patients, e.g,
 Prior history of addiction, past abuse, aberrant behavior, occupations demanding
mental acuity, elderly, unstable or dysfunctional social environment, comorbid
psychiatric or medical conditions
 Sometimes daily or weekly monitoring may be necessary for patients at very high
risk of adverse outcomes.
 Urine specimens can be adulterated and should be aware.
 Oral swab tests more easy to administer and can be more valuable than urine drug
screens.

83. DRUG METABOLITES
 Morphine
 Codeine
 Hydrocodone
 oxycodone
 Morphine, hydromorphone,
codeine
 Codeine, morphine,
hydrocodone
 Hydrocodone,
hydromorphone, 6-
hydrocodol
 Oxycodone, oxymorphone
 hydrocodone

84.  Screen for hypogonadism in patients on COT,
especially with signs and symptoms of fatigue, mood changes, decreased libido,
loss of muscle mass and osteoporosis.
 Perform opioid rotation if lack of efficacy, side-
effects of one opioid class, altered pharmaco-
kinetics, changes in absorption.

85. CHRONIC PAIN PATIENT ADDICTED PATIENT
 Medication use is not out of control
 Medication use improves quality of life
 Wants to decrease medication if adverse effects
develop
 Is concerned about the physical problem being
treated with the drug
 Follows the practitioner-patient agreement for
use of the opioid.
 May have left over medication
 medication use is out of control
 Medication use impairs quality of life
 Medication use continues or increases despite
adverse effects
 Unaware of or in denial about any problems that
develop as a result of drug treatment
 Does not follow opioid agreement
 Does not have left over medication. Loses
prescriptions. Always has a story about why
more drug is needed.

86.  Tolerance – decreased efficacy over time
 Dependence – tolerance +withdrawal
symptoms
 Addiction – ‘neurobiological disease’. Strong
genetic influence. Preoccupied with continued
use despite harm
 Pseudoaddiction – happens when pain is
undertreated. “drug seeking” or “clock
watching”. Usually resolves with effective pain
management.

87. 0
1,000
2,000
3,000
4,000
5,000
6,000
7,000
8,000
Total Female Male
Source: National Center for Health Statistics, CDC Wonder

88. 0
2,000
4,000
6,000
8,000
10,000
12,000
14,000
16,000
18,000 Total Female Male
Source: National Center for Health Statistics, CDC Wonder

89. 0
5,000
10,000
15,000
20,000
25,000
Total Female Male
Source: National Center for Health Statistics, CDC Wonder

92.  Reasons to terminate may include (healing or recovery
from the treatment condition, intolerable side-effects, lack of response, discovery of
abuse or misuse or addiction)
 Typically 10% dose reduction per week. Slower
taper will minimize unpleasant withdrawal
symptoms.
 Clonidine can be used. 0.1 – 0.2mg PO every 6
hrs daily or patch at 0.1mg/24 hours.
 Drug rehab - Methadone

93.  Respiratory depression usually preceded by
warning signs and can be prevented with
careful monitoring
 Take home Naloxone Rx for patients with high
risk for overdose
 . In 2014 FDA approved hand held auto-
injector (Evzio) and can be used at home by
family members or caregivers.

94.  Mu-1 agonist and NMDA antagonist
 Analgesic duration of 4-6 hrs
 Elimination t1/2 15-60 hrs
 Can cause QT prolongation, Torsade de pointes

95.  Has been long used to treat addiction.
 Long plasma elimination half life, relatively
short analgesic half life makes it optimal for
maintenance.
 Has opioid and non-opioid receptor effects
causing varied effects – ‘Broad spectrum
opioid’
 Metabolized by liver enzymes that differ from
those associated with most other opioids,
leading to drug-drug interactions.

96.  Significant genetic variations in the liver
enzymes that metabolize methadone
 Metabolism effected by cigarette smoking and
alcohol consumption.
 Lowest possible dose titration should be
followed even for opioid tolerant patients.

99.  1 provider and 1 pharmacy for all controlled
substances
 Use CURES/PDMP
 Use medication agreements when prescribing
‘COT’
 Don’t mix opioids and CNS
depressants/sedatives. Monitor polypharmacy
 Implement multidisciplinary approach to treat
chronic pain.