Ali R. Rahimi,MD,FACP,AGSFProfessor of Medicine

Mercer University School of MedicineClinical Professor

University of Georgia School of Pharmacy

Pain Managementin the Geriatric Population

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

Back pain

Abdominal Pain

Head pain

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 sufferingFamilial 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 Advanced age: >85 years old2 Poor cognitive function3 Minority status

Bernabei (1998), N = 13,625 cancer patients

Obstacles of geriatric pain management:1. Accessibility to treatment2. $$$3. SEs4. Comorbidities

Ex- NSAID use in pt w/ HTN or heart disease Ex- Acetominophen use in Liver dz pt

5. Interactions with the current meds6. Pts with cognitive impairments7. The assumption that pain is normal party

of aging8. Practitioner’s bias (pain seeker..)9. fear of legal repercussions…

It’s a risk factor!

Decreased activity bc of

pain

Myofacial deconditioning

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:

Tissue damage• Palliates/potentiates:

Worse with stress, pressureResponds better to opioids, NSAIDs

• Quality:Sharp, dull, stabbing, pressure, ache,

throbbing• Radiation:

Occasionally radiates (less well-defined), but not along an obvious nerve distribution

Easier to treat than Neuropathic!!

Differentiating between somatic, visceral, and neuropathic pain is ESSENTIAL to proper tailoring of pain treatments

Specific Goals:1- determining the presence and cause

of pain2- identifying exacerbaing comorbidities3- reviewing beliefs, attitudes and

expectations regarding pain

Overall: to decrease pain and increase function and quality of life!

Common pain syndromes in elderly

MUSCULOSKELETAL CONDITIONSOADegenerative disk dzOsteoporosis & FxsGout

NEUROPATHIC CONDITIONS:Biabetic neuropathyPostherpatic neuralgiaTrigeminal neuralgiaCentral poststroke painRadicular pain secondary to degenerative disc dz

RHEUMATOLOGIC CONDITIONS:RAPolymyalgia rheumaticsFibromyalgia

Aging takes a toll…In the PNS:

Loss of myelinated and unmyelinated fibersAxonal atrophy commonNerve conduction and endoneural blood flow are

reduced w/ ageLess 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

Sleep and pain Multiple studies have demonstrated the

comorbidity of pain and sleeplessness Pain is among the best predictors of sleep

disturbances among older adultsThus, 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 lifeOVERALL 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:OpiodsAnti-inflammatory agents (asa, NSAIDS,

cyclooxygenase [COX-2] inhinitors, steroids)

AcetaminophenTramadolMyo relaxantsTricyclic antidepressantsSRIsAntielileptic drugs (AEDs)

Non-pharmocologic approaches:Behavioral therapySpiritual counselingPhysical therapyPsychotherapySplintingSurgical correctionCold packsMeditation

Support groupsRadiation therapyAcupunctureHypnosisCultural healing ritualsHeat packsPrayerCommunity resources

How to choose an analgesic?

Mild to Moderate pain:AcetominophenAspirinNSAIDS

Moderate to severe:Use in combo with opioids

Severe pain:Opioids

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)CYP450

Excrition: renal

Can cause: GI irritation and bleeding. Use w caution in ppl with hx of gastric or peptic ulcercs.

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 effectsNo effect on platelet aggregation

Metab by liver Excretion: urine (metabolites can accumulate w renal impairment)

Hepatotoxic

Can take 500-1000mg orally q 6hrOlder 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 Excretion: urine

Adverse effects:n/v, bleedingHepato and nephrotoxicity

1.5 times higher risk of GI bleeding (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:PotenciesTime to onsetDurationResponse among patients

Common uses:After surgeriesPainful 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 paindecreased reaction to painincreased pain tolerance

OpioidsCornerstone of the analgesic regimen for

mod-sev pain

• MC ones:• Morphine• Oxycodone• Hydromorphone• Transdermal fentanyl

3 Main Opioid receptors:

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 pharmacokineticsPharmacokinetic 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 depressionsedationN/VConstipationUrinary retentionItching

1. Respiratory depressionCaused by directly acting on respiratory centerNaloxone 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 vomitingMC 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

cordto 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 retentioncauses increased smooth muscle tone increases sphincter tone

5. ItchingMechanism 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: MorphineMorphine = standard of opioids

BUT if pt doesnt respond well, they may switch to an equianalgesic dosage of:HydroporphoneOxycodoneFentanylOxymorphone 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:

MorphineHydrocodoneCodeineDextropropoxyphene

Typically combined with acetaminophen or an NSAID

Acetaminophen con Codeine• Advantages:

Low regulatory controlInexpensiveWidely available

• Disadvantages:10% cannot convert codeine to morphineMany 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!! ..1. Meperidine2. Propoxyphene3. codeine

1.Meperidine (DEMEROL)Low potency relative to morphineA short duration of action – so have to dose

it more frequentlyAnd 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 pain1.Toxicities assoc with it’s primary metabolite:

norpropoxyphene can cause cardiotoxicity and pulmonary edema

2.Half life: 6-12 hour;Metabolite half life 30-36 hours Pts with Dec Renal function or pts getting repeat doses:

higher risk

3.Puts geriatric pts at higher risks of falls (d/t CNS effects) 1. [study found that propoxy users have twofold higher risk for hip frature compared with

nonusers of analgesics]

4.ALSO, it has no clinical advantage over nonopioid analgesics such as acetominaphen

PG 289

3. CodeineMust 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. No ceiling effect2. Dose to pain relief without side effects3. Give orally when possible4. Sub-cutaneous administration is basically

equivalent to intravenous (and preferable)5. Treat constipation prophylactically6. 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

Anticonvulsants for shooting pain

GabapentinPregabalin

Steroids to decrease compression

Nerve infiltration by tumor or spinal cord compresion:

CorticosteroidsDeamethasonePrednisone

*Usu used for pts near end ofLife 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 antagonistButorphanolNalbuphinePentazocine

Mu antagonistsNalmefeneNaloxoneNaltrexone

Mu partial agonist/kappa antagonistBuprenorphine

When to refer:Pain not respsoning to opoiods at typical

dosesNeuropathic pain not responding to first

line treatmentsComples methadone management issuesIntolerable side effects from oral opioidsSevere pain from bone metsFor 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 opioidsThe 1998 guidelines recommended earlier

use of narcotics than is typical for treatment of younger patients because of the significant toxicities assoc with NSAIDS.

Trigeminal neuralgiaCharacterized 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 neuralgiaFollows outbreak of Herpes zosterSensory findings:

Allodynia (wind against skin hurts, sheet on area hurts etc) hyperalgesia

Post stroke painAn 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 painBone 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 >50Presentation:

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 pain50 studies total

21 concluded an increase in pain threshold with advancing age

3 reporeted a decrease17 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.