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
Pain:
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
Urandictionary.com:
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.
PAIN IS MC REASON FOR INDIVIDUALS
TO SEEK MEDICAL CARE
Definitions:
• Addiction: Psychological dependence on a drug.
• Physical Dependence:
Development of physical
withdrawal reaction upon discontinuation or antagonism of a
drug
• 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?
1
2
3
Advanced age: >85 years old
Poor cognitive function
Minority status
Bernabei (1998), N = 13,625 cancer patients
Obstacles of geriatric pain
management:
Accessibility to treatment
2. $$$
3. SEs
4. Comorbidities
1.
5.
6.
7.
8.
9.
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
peripherally
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
genearlly.
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
Neuropathic!!
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
pain
Overall: to decrease pain and increase function and
quality of life!
Common pain syndromes in elderly
MUSCULOSKELETAL CONDITIONS
OA
Degenerative disk dz
Osteoporosis & Fxs
Gout
RHEUMATOLOGIC CONDITIONS:
RA
Polymyalgia rheumatics
Fibromyalgia
NEUROPATHIC CONDITIONS:
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
ages.
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
observation):
Clinical observation examples:
increased incidence of silent MI in elderly patients
atypical presntation of an inflamed appendix, (absence of RLQ
pain)
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
sleeplessness
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
HOW TO QUANTIFY THE PAIN?
Details!
•Onset
•Duration
•Freq
•Intensity
•Locaiton
•Contributing factors
Troubleshooting pain assessment:
Demented/Confused patient:
Have to look for:
Agitation, agressiveness, etc.
Pain control vs quality of life
OVERALL GOAL:
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)
Acetaminophen
Tramadol
Myo relaxants
Tricyclic antidepressants
SRIs
Antielileptic drugs (AEDs)
Non-pharmocologic approaches:
Behavioral therapy
Support groups
Spiritual counseling
Radiation therapy
Physical therapy
Acupuncture
Psychotherapy
Hypnosis
Splinting
Cultural healing rituals
Surgical correction
Heat packs
Cold packs
Prayer
Meditation
Community resources
How to choose an analgesic?
Severe pain:
Opioids
Moderate to severe:
Use in combo with opioids
Mild to Moderate pain:
Acetominophen
Aspirin
NSAIDS
Drug Classes
Salicylates:
Salicylates
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.
CYP450
Acetominophen
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
NSAIDS
Antipyretic, analgesic and anti-inflammatory
properties
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
effects.
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
NSAID:
18 available in the US
All NSAIDS have similar mechanism of action BUT differ in:
Potencies
Time to onset
Duration
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
COX 2 NSAIDS:
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.
BY INCREASING SYSTEMIC VASCULAR RESISTANCE
and REDUCING RENAL PERFUSION
OPIOID:
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
Opioids
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
effect.
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
upward!!
2. Nausea and vomiting
MC SE
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:
Hydroporphone
Oxycodone
Fentanyl
Oxymorphone
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,
Hydrocodone
• 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!! ..
Meperidine
2. Propoxyphene
3. codeine
1.
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
1.
can cause cardiotoxicity and pulmonary edema
Half life: 6-12 hour;Metabolite half life 30-36 hours
2.
Pts with Dec Renal function or pts getting repeat doses: higher risk
Puts geriatric pts at higher risks of falls (d/t CNS effects)
3.
1.
4.
[
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:
1.
2.
3.
4.
5.
6.
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
1.
Tricyclic for dysesthetic pain
2. Anticonvulsants for shooting pain
3.
Steroids to decrease peri-tumor edema
Tricyclic for dysesthetic pain
Dysesthesia is pain not experienced by a normal nervous
system.
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
Alfentanil
Codeine
Hydrocodone
Ydromorphone
Fentanyl
Levorphanol
Meperidine
Methadone
Morphine
Opium
Oxycodone
Oxymorphone
Remifentanil
Sufentanil
Tramadol
Kappa agonist/mu antagonist
Butorphanol
Nalbuphine
Pentazocine
Mu antagonists
Nalmefene
Naloxone
Naltrexone
Mu partial agonist/kappa
antagonist
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)
hyperalgesia
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
claudication
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
pain
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.