Pain Management in the Geriatric Population

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Transcript Pain Management in the Geriatric Population

Pain Management
in the Geriatric Population
Ali R. Rahimi,MD,FACP,AGSF
Professor of Medicine
Mercer University School of Medicine
Clinical Professor
University of Georgia School of Pharmacy
 Webster:
 a : usu. localized physical suffering associated with a bodily
disorder; also : a basic bodily sensation induced by a noxious
stimulus, received by naked nerve endings, characterized by
physical discomfort (as pricking, throbbing, or aching), and
typically leading to evasive action
 b : acute mental or emotional distress or suffering
 What happens when you reach into the blender to dislodge a
stuck icecube without unplugging it first.
Pain & elderly
 Pain is what many people say they fear most about dying.
 Pain is undertreated at the end of life
 Older patients are likely to have a increased pain threshold
but to be less toleant to severe pain.
• Addiction: Psychological dependence on a drug.
• Physical Dependence:
Development of physical
withdrawal reaction upon discontinuation or antagonism of a
• Tolerance: Need to increase amount of drug to obtain the
same effect
• Pseudoaddiction: Behavior suggestive of addiction
occurring as a result of undertreated pain
Pain can be assoc w/:
 Psychologic and physical disability
 a source of individual suffering
 Familial distress
Pain in nursing home patients
30% reported daily pain
26% of these patients received no analgesia
Only 26% of them received strong opioids
 What predicted inadequate pain management?
Advanced age: >85 years old
Poor cognitive function
Minority status
Bernabei (1998), N = 13,625 cancer patients
Obstacles of geriatric pain
Accessibility to treatment
2. $$$
3. SEs
4. Comorbidities
Ex- NSAID use in pt w/ HTN or heart disease
Ex- Acetominophen use in Liver dz pt
Interactions with the current meds
Pts with cognitive impairments
The assumption that pain is normal party of aging
Practitioner’s bias (pain seeker..)
fear of legal repercussions…
It’s a risk factor!
Myofacial deconditioning
Decreased activity
bc of pain
Gait distrubances
INJURIES from falls
Types of pain:
 Nociceptive pain-
Nerves responding appropriately
to a painful stimulus
 Neuropathic pain-
results from NS dysfunction,
and may originate centrally or
 Somatic pain-
originates in the skin, bones, myo, and
connective tissue, and usually is
located specifically.
 Visceral pain-
originated in internal body structures
and organs, and is located more
Neuropathic pain:
• Origin:
 Nerve damage
• Palliates/potentiates:
 Set off by unusual stimuli, light touch, wind on skin, shaving
(trigeminal neuralgia)
• Quality:
 Electric, burning, tingling, pins & needles, shooting (system
isn’t working right)
• Radiation:
 Nerve-related pattern
Nociceptive Pain:
• Origin:
Easier to treat than
 Tissue damage
• Palliates/potentiates:
 Worse with stress, pressure
 Responds better to opioids, NSAIDs
• Quality:
 Sharp, dull, stabbing, pressure, ache, throbbing
• Radiation:
 Occasionally radiates (less well-defined), but not along an
obvious nerve distribution
 Differentiating between somatic, visceral, and neuropathic pain is
ESSENTIAL to proper tailoring of pain treatments
Specific Goals:
 1-
 2 3-
determining the presence and cause of pain
identifying exacerbaing comorbidities
reviewing beliefs, attitudes and expectations regarding
 Overall: to decrease pain and increase function and
quality of life!
Common pain syndromes in elderly
Degenerative disk dz
Osteoporosis & Fxs
Polymyalgia rheumatics
Biabetic neuropathy
Postherpatic neuralgia
Trigeminal neuralgia
Central poststroke pain
Radicular pain secondary to degenerative disc dz
Aging takes a toll…
 In the PNS:
Loss of myelinated and unmyelinated fibers
Axonal atrophy common
Nerve conduction and endoneural blood flow are reduced w/ age
Less nerve regeneration observed
 progressive loss of serotonergic and noradrenergic neurons in the
superficial lamina of the spinal dorsal horn, and bc serotonin and
norepineph have important roles in the descending inhibitory
control pathways, such a loss may upset the natural endogenous
pain-suppressing mechanisms.
 Therefore, pain treatment of the elderly obviously
differs from that of young patients!
Models of the prevalence of pain
 1- Pain increases with age and then decreases at older ages (ie, 70 and
beond). They suppose that this pain typically has a mechanical etiologic
component and possibly is assoc with the occupational envioroment
 2- pain increases with age. This has a mechanical etilogic component but
also an assoc with increasing prevalence of degenerative dz, particulary at older
 3- age-independent pain that (obviously) lacks a mechanical etiologic
component. (ie- risk factors that are constant throughout the life course)
 4- A decrease in pain prevalence at older ages. It is not clear whether
the trajectory is caused by age-related changes in pain and pain perception, or
by changes in pain reportin.
Effect of age on human (via clinical
 Clinical observation examples:
 increased incidence of silent MI in elderly patients
 atypical presntation of an inflamed appendix, (absence of RLQ
 Study example: (pg 208)
 Yunis compared elderly and young patients with
fibromyalgia. They found that chronic head aches,
anxiety, tension, mental stress and poor sleep were all
less common in the elderly patients w this condition.
Lonliness and pain
 The comorbidity of pain and psychological distress is WELL
DOCUMENTED The feeling of lonliness is the single most important predictor
of psychologic state of distress in older persons.
 A study by Eisenberger supported the
hypothesis that Pain distress and social
distress share neurocognitive substrates
Study on page 193
Sleep and pain
 Multiple studies have demonstrated the comorbidity of pain and
 Pain is among the best predictors of sleep disturbances among
older adults
 Thus, it appears that improved pain leads to improved
sleep, and impoved sleep leads to
improved pain!
Study =pg 193
•Contributing factors
Troubleshooting pain assessment:
 Demented/Confused patient:
 Have to look for:
Agitation, agressiveness, etc.
Pain control vs quality of life
 to abolish pain with minimal adverse effects.
 Ex- Patient with COPD and pain:
o Cant treat their pain too vigorously bc we will exacerbate the
COPD symptoms
Treating the pain:
Pharmacologic approaches:
 Opiods
 Anti-inflammatory agents (asa, NSAIDS, cyclooxygenase
[COX-2] inhinitors, steroids)
Myo relaxants
Tricyclic antidepressants
Antielileptic drugs (AEDs)
Non-pharmocologic approaches:
Behavioral therapy
Support groups
Spiritual counseling
Radiation therapy
Physical therapy
Cultural healing rituals
Surgical correction
Heat packs
Cold packs
Community resources
How to choose an analgesic?
Severe pain:
Moderate to severe:
Use in combo with opioids
Mild to Moderate pain:
Drug Classes
 Analgesic, antipyretic, anti-inflammatory and anti-rheumatic activity.
 MOA:
 Inhibits prostaglandin synthesis producing analgesic.
antiplatelet effect by inhibiting the production of thromboxane
 Much higher levels needed for anti-inflammatory effect than for anti-platelet, anti-pyretic
and analgesic effects.
 Metab: Gut & plasma (ASA); liver (salicylate)
 Excrition: renal
 Can cause: GI irritation and bleeding.
 Use w caution in ppl with hx of gastric or peptic ulcercs.
 analgesic and antipyretic agent
 MOA:
 Inhibits central prostaglandin synthesis with minimal inhibition of peripheral
prostaglandin synthesis
 Antipyretic effect by direct action on the hypothalamic heat-regulating center
 Benefits:
 Absorbed rapidly
 No gastric mucosa effects
 No effect on platelet aggregation
 Metab by liver
 Excretion: urine (metabolites can accumulate w renal impairment)
 Hepatotoxic
Can take 500-1000mg orally q 6hr
Older pts and Pts with liver dz: do not exceed 2g/day
 Antipyretic, analgesic and anti-inflammatory
 MOA:
 Reduce central and peripheral prostaglandin synthesis but they do not
inhibit the effects of the prostaglandins already present, resulting
in analgesia, followed by relatively delayed anti-inflammatory
 Metab: liver
1.5 times higher risk of GI bleeding
 Excretion: urine
 Adverse effects:
 n/v, bleeding
 Hepato and nephrotoxicity
(more so in the elderly)
Concurrent use of PPI for prevention
18 available in the US
 All NSAIDS have similar mechanism of action BUT differ in:
Time to onset
Response among patients
 Common uses:
 After surgeries
 Painful chronic conditions (ex- OA)
 Benefit more notable when used in combo w an opiod.
 Opiod SEs like sedation, n/v decreased when used w NSAID
 Purpose in pharmacology unclear
 Only available: celecoxib
 Cox2 and NSAIDS are CI in pts with cardiac disease!
 estimated to be responsible for up to 20 percent of hospital admissions for congestive heart failure.
 a chemical that works by binding to opioid receptors, which
are found principally in CNS and the GI.
 Hence, the GI Ses
 Effects:
 decreased perception of pain
 decreased reaction to pain
 increased pain tolerance
 Cornerstone of the analgesic regimen for mod-sev pain
• MC ones:
• Morphine
• Oxycodone
• Hydromorphone
• Transdermal fentanyl
3 Main Opioid receptors:
 Mu, delta and kappa receptors.
 Mu agonists:
produce analgesia
affect numerous body systems
influence mood & reward behavior
 Delta agonists
produce analgesia
not a lot on market
 Kappa agonists
produce analgesia
may cause less resp depression and miosis
psych effects, can produce dysphoria
 Opioids LACK the adverse renal, and hematologic
effects of NSAIDs
 MU-receptor agonists are MC used
 although drugs may interact with more than one type of receptor.
 Ex- the mu receptor antagonist and kappa receptor agonist
drugs were deigned to cause less respiratory depression.
Opioids pharmacokinetics
 Pharmacokinetic properties of an opioid can dictate the
circumstance which they are appropriate in:
Ex- Lipid-soluble drug such as fentanyl, which diffuse rapidly acros the BBB, are preferable if
analgesia is required immediately before a short, painful procedure.
 Elimination half life very short:
 So, steady state reached in a day or less!
 Thus, you can adjust the dose daily knowing we are seeing it’s
Adverse effects:
 Respiratory depression
 sedation
 N/V
 Constipation
 Urinary retention
 Itching
1. Respiratory depression
 Caused by directly acting on respiratory center
 Naloxone is specifically used to counteract life-threatening
depression of the central nervous system and respiratory system
 Therapeutic doses of morphine can affect:
 Resp rate, minute volume tidal exchange
 Although, tolerance to this effect is usually achieved
with repeated doses of opioids.
Avoid/Monitor in pts with:
 Imparied resp function
 Sleep apnea
 Or bronchial asthma
Not common if
begin with low
dose and titrate
2. Nausea and vomiting
 Likely due to changing blood serum levels , not problem @
steady state
 The freq of nausea and vomiting is higher in ambulaory
patients (vestibular component?)
 Antiemetics (metoclopramide or droperidol) can be used
along with the opioid.
3. Constipation:
 Acts on receoptors of GI tract and spinal cord
 to produce decrease in peristalsis and intestinal secretions
 Tolerance to this effect is not common Result- prescribe prophylactic laxatives
 … use stood softener AND a stimulant laxative.
4. Urinary retention
 causes increased smooth muscle tone
 increases sphincter tone
5. Itching
 Mechanism not fully known~
 Hypot: related to the release of histamine from mast cells.
 If itching is with rash- consider allergy.
 Can use an antihistamine to treat this
Opioids: Morphine
 Morphine = standard of opioids
 BUT if pt doesnt respond well, they may switch to an
equianalgesic dosage of:
Or methadone
 If pt has diminished renal function, they may benefit from:
 Oxycodone or hydromorphone (bc these don’t have clinically
significant active metaolites)
Opioid Combos~
 Full opioid agonists:
 Morphine
 Hydrocodone
 Codeine
 Dextropropoxyphene
Typically combined with
acetaminophen or an NSAID
Acetaminophen con Codeine
• Advantages:
 Low regulatory control
 Inexpensive
 Widely available
• Disadvantages:
 10% cannot convert codeine to morphine
 Many drugs interfere with conversion
Acetaminophen with Oxycodone,
• Oxycodone combination contains 325 mg acetaminophen
• Hydrocodone combination contains 500 mg acetaminophen
• No clear advantage between the two
Three mu=receptor agonist to avoid
whenever possible!! ..
2. Propoxyphene
3. codeine
1.Meperidine (DEMEROL)
 Low potency relative to morphine
 A short duration of action – so have to dose it more frequently
 And a toxic metabolite (normeperidine)
 Ex- meperidine 75mg = 5-7.5 mg of morphine
 can cause irritability and seizures
2. Propoxyphene (DARVOCET)
 treat mild to mod pain
Toxicities assoc with it’s primary metabolite: norpropoxyphene
can cause cardiotoxicity and pulmonary edema
Half life: 6-12 hour;Metabolite half life 30-36 hours
Pts with Dec Renal function or pts getting repeat doses: higher risk
Puts geriatric pts at higher risks of falls (d/t CNS effects)
study found that propoxy users have twofold higher risk for hip frature compared with nonusers of analgesics
ALSO, it has no clinical advantage over nonopioid analgesics
such as acetominaphen
PG 289
3. Codeine
 Must be converted to morphine by means of the cytochrome
P-450 pathway to provide analgesia.
 Lots of Caucasians are poor metabolizers of this isoenzyme
-thus cant make the conversion!
 So, they do not get any of the codeine’s benefit but still suffer
the Side effects.
Principles of opioid use:
No ceiling effect
Dose to pain relief without side effects
Give orally when possible
Sub-cutaneous administration is basically equivalent to
intravenous (and preferable)
Treat constipation prophylactically
Full opioid agonists are best choice for severe pain..
Where to start?
Treating Chronic pain:
Basal pain medicine plus a different therapy for spikes:
 Predictable spikes - Short-acting agent prior to event
 Unpredictable spikes - Short-acting agent readily available (prn)
Treating Neuropathic Pain;
Opioids and NSAIDS less effective
Classes of Agents
Tricyclic for dysesthetic pain
2. Anticonvulsants for shooting pain
Steroids to decrease peri-tumor edema
Tricyclic for dysesthetic pain
 Dysesthesia is pain not experienced by a normal nervous
 Eg- neuropathic burning from chemotherapy
 Considered "Dante-esque" pain.
• Amitriptyline
• Nortriptyline
• Desipramine
Anticonvulsants for shooting pain
 Gabapentin
 Pregabalin
Steroids to decrease compression
 Nerve infiltration by tumor or spinal cord compresion:
 Corticosteroids
 Deamethasone
 Prednisone
*Usu used for pts near end of
Life bc of detrimental SE of
Long term steroid use.
Opioid analgesics available in US
Mu agonists
 Kappa agonist/mu antagonist
 Butorphanol
 Nalbuphine
 Pentazocine
 Mu antagonists
 Nalmefene
 Naloxone
 Naltrexone
 Mu partial agonist/kappa
 Buprenorphine
When to refer:
 Pain not respsoning to opoiods at typical doses
 Neuropathic pain not responding to first line treatments
 Comples methadone management issues
 Intolerable side effects from oral opioids
 Severe pain from bone mets
 For a surgical or anesthesia-based procedure, intrathecal
pump, nerve block, or rhizotomy
When to admit:
 For severe exacerbation of pain that is not responsive to
previous stable oral opioid around-the-clock plus
breakthrough doses.
 Pateints whose pain is so severe that they cannont be cased
for at home
 Uncontrollable side effects from opioids, including nausea,
vomiting, and altered mental status
Good to know..
 Older individuals tend to be more sensitive to
benzodiazepines and opiods.
 Pain from bone mets more susceptible to NSAID pain relief
than opioids
 The 1998 guidelines recommended earlier use of narcotics
than is typical for treatment of younger patients because of
the significant toxicities assoc with NSAIDS.
Trigeminal neuralgia
 Characterized by: severe, unilateral facial pain described as
lancinating electrics shock-like jolts in one or more
distributions of the trigeminal nerve.
 Maxillary and Mandibular divisions = MC
 Careful clinical evaluation and MRI is recommended
Postherpetic neuralgia
 Follows outbreak of Herpes zoster
 Sensory findings:
 Allodynia (wind against skin hurts, sheet on area hurts etc)
Post stroke pain
 An underrecognized consequence following storke
 May present as shoulder pain in the paretic limb or present as
central poststroke pain.
 Characterized as pain that is severe and persistnet w
accompanying sensory abmomalities
 Ex- the guy from Oceanside.
Metastatic bone pain
 Bone pain that is worse at night, when laying down or not
assoc with acute injury
 Pain that gradually but rapidly increase in intensity or with
weight-bearking or activity.
 Freq sites:
 Hips, vertebrae, femur, ribs, and skull
Temporal Arteritis:
 More than 95% of TA are ppl >50
 Presentation:
 New onset headache, malaise, scalp tenderness and jaw
 PE: indurated temporal arterly that is tender with a diminihed
or abent pulse
 Irreversible bliness is consequence of untreted.. So timely
assesment and tx is
Pain perception in rats:
 When nociception is tested in mice using an electrical
current, it seems that there are age related changes in
nociception .
 The graphic representaion of electical thresholds needed to
induce a vocal reponse was of a U-shap pattern. (high pain
tolerance in young and old- lower in the middle aged)
Effect of age on human experimental
 50 studies total
 21 concluded an increase in pain threshold with advancing age
 3 reporeted a decrease
 17 noted no change
 However,
 Temporal vs Spatial summation:
 It was fround that temopral summation to a heat pain stimulus, for
example, is more pronounced in the elderly as compared with
younger subjects. Whereas spatial summation is not significantly
influenced by age.