Pain Management in the Geriatric Population

1. Pain Managementin 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

2. 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.

3. 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.

4. PAIN IS MC REASON FOR INDIVIDUALS TO SEEK MEDICAL CARE Abdominal Pain Back pain Head pain

5. 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

6. Pain can be assoc w/: • Psychologic and physical disability • a source of individual suffering • Familial distress

7. 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 old 2 Poor cognitive function 3 Minority status • Bernabei (1998), N = 13,625 cancer patients

8. Obstacles of geriatric pain management: • Accessibility to treatment • $$$ • SEs • 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…

9. It’s a risk factor! Myofacial deconditioning Decreased activity bc of pain Gait distrubances INJURIES from falls

10. 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.

11. 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

12. Nociceptive Pain: Easier to treat than Neuropathic!! • Origin: • 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

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

14. Specific Goals: • 1- determining the presence and cause of pain • 2- identifying exacerbaing comorbidities • 3- reviewing beliefs, attitudes and expectations regarding pain • Overall: to decrease pain and increase function and quality of life!

15. 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

16. 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!

17. 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 painthat (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.

18. 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.

19. 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

20. 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

21. HOW TO QUANTIFY THE PAIN?

22. Details! • Onset • Duration • Freq • Intensity • Locaiton • Contributing factors

23. Troubleshooting pain assessment: • Demented/Confused patient: • Have to look for: • Agitation, agressiveness, etc.

24. Pain control vs quality of life • OVERALL GOAL: • to abolish pain with minimal adverse effects. • Ex- Patient with COPD and pain: • Cant treat their pain too vigorously bc we will exacerbate the COPD symptoms

25. Treating the pain:

26. Pharmacologic approaches: • Opiods • Anti-inflammatory agents (asa, NSAIDS, cyclooxygenase [COX-2] inhinitors, steroids) • Acetaminophen • Tramadol • Myo relaxants • Tricyclic antidepressants • SRIs • Antielileptic drugs (AEDs)

27. Non-pharmocologic approaches: • Behavioral therapy • Spiritual counseling • Physical therapy • Psychotherapy • Splinting • Surgical correction • Cold packs • Meditation • Support groups • Radiation therapy • Acupuncture • Hypnosis • Cultural healing rituals • Heat packs • Prayer • Community resources

28. How to choose an analgesic? Severe pain: Opioids Moderate to severe: Use in combo with opioids Mild to Moderate pain:Acetominophen Aspirin NSAIDS

29. Drug Classes

30. Salicylates:

31. 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.

32. 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

33. 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, bleeding • Hepato and nephrotoxicity 1.5 times higher risk of GI bleeding (more so in the elderly) Concurrent use of PPI for prevention

34. 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

35. 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

36. 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

37. Opioids • Cornerstone of the analgesic regimen for mod-sev pain • MC ones: • Morphine • Oxycodone • Hydromorphone • Transdermal fentanyl

38. 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

39. 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.

40. 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.

41. Adverse effects: • Respiratory depression • sedation • N/V • Constipation • Urinary retention • Itching

42. 1. Respiratory depression • Caused by directly acting on respiratory center • Naloxoneis 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: • Impariedresp function • Sleep apnea • Or bronchial asthma Not common if begin with low dose and titrate upward!!

43. 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.

44. 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.

45. 4. Urinary retention • causes increased smooth muscle tone • increases sphincter tone

46. 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

47. 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)

49. Opioid Combos~ • Full opioid agonists: • Morphine • Hydrocodone • Codeine • Dextropropoxyphene Typically combined with acetaminophen or an NSAID

50. Acetaminophen con Codeine • Advantages: • Low regulatory control • Inexpensive • Widely available • Disadvantages: • 10% cannot convert codeine to morphine • Many drugs interfere with conversion