1. Pain Management for Older Adults
Update July 2012
Miriam B. Rodin, MD, PhD
Division of Geriatrics and Gerontology
St Louis University Medical School
Weeks Conference 5/10/2019

2. No conflicts of interest to declare

3. OBJECTIVES
Describe the different kinds of pain: somatic, visceral, neuropathic
Distinguish acute, cancer and chronic non-cancer pain.
Understand the indications for opioid therapy
Describe at least 2 opiate tolerance syndromes.
Formulate an approach to chronic pain in older adults
Use a guide for titration of opiates.
If respiratory depression you should use NALAXONE.
Unless you have hx of addiction it is very less likely to develop addiction. You will have tolerance, not dependence.
Hydromorphone, recommended in kidney failure.

4. This is no different than in the general population using a Medicare database the point is that it is up..

5. WHO 3-step ladder So how should we treat pain in older adults?
The same way EXCEPT
The WHO 3-step ladder was conceived for the management of CANCER pain, not acute (i.e. surgical) pain OR chronic pain. Cancer pain or pain due to progressive cancer does not get better, it gets worse and requires continuous active assessment and management that employs all available techniques. Ultimately there is no absolute ceiling on use of opiates in cancer pain. However, just increasing the dose is going to fail. Most physicans have had no specific training in how to manage opiates.
Except for cancer pain and end-of-life there is NO role for LA opiates
Source: World Health Organization. Technical Report Series No. 804, Figure 2. Geneva: World Health Organization; Reprinted with permission.

6. Sympathetic Maintained
Types of Pain:
NOCICEPTIVE
NEUROPATHIC MIXED
Somatic
bones, joints
connective tissues
muscles
Deafferentation
(phantom limb)
Sympathetic Maintained
Peripheral
Visceral
Organs – heart, liver, pancreas, gut, etc.

7. Where does it hurt? “All over” while rubbing their belly

8. Visceral Pain Described as: deep, cramping, squeezing, pressure
Distribution: poorly localized
Referred: Heart attack to stomach or arm
Colicky: Bowel obstruction, gallstone
Diffuse: Peritonitis, liver metastasis
Caused by infiltration or distention of abd or thoracic viscera, or inflammation.
Mediated by the large slow C-fibers
Analgesics: anti-inflammatories including steroids; anticholinergics (antispasmodics) VAGOLYTICS
Watch out for orthostatic blood pressure.

9. Somatic pain Mediated by A-fibres: nociceptors in MSK tissue.
Descriptors: sharp, or deep, dull, gnawing
Distribution/Examples:
Well localized—patients can often point with one finger to the location of their pain
bone mets, sprained ankle, toothache
Analgesics: NSAIDS, acetaminophen, opioids
Post operative pain is MOSTLY MSK associated with the incision. Should be getting better within a few days. Hospital discharge < 10days of opiates.

10. Neuropathic pain Due to nerve injury/degeneration, central/peripheral
Described as: burning, shooting or electric
Distribution:
Dermatomal: constant burning, shooting, paroxysmal or lancinating e.g. post-herpetic neuralgia
Stocking-glove regional: burning, pricking, numb e.g. diabetic neuropathy of LEs,
Mononeuropathy or plexopathy: Nerve root compression due to pressure, infiltration: malignancy, fracture
Analgesics: 1st line membrane stabilizers e.g. TCAs or AEDs
Plexopathy (compression of nerve plexus due to malignancy, abscess or fracture)

11. Begin to develop tolerance to narcotics after about 6 weeks, Diagnostically continuous pain days.

12. How the pain gets to your brain
This is less than half the story. Peripheral pain receptors include A-delta pain receptors, very fast, you pull your hand away from the radiator before you feel the burn. A-beta receptors are light touch. A-fibres decuss to the homunculus, the detailed surface anatomical map in the parietal lobes of your brain.
Pressure and temperature receptors shown here are threshhold driven, it doesn’t hurt until the stimulus rises above a certain level. C-fibres are slow. They feed into a diffuse network of areas in the brain.
Remember that every area of your brain talks to every other area of the brain eventually so the parietal lobes talk to the amygdala, the frontal lobes, the hippocampus etc etc. then what?
How the pain gets to your brain

13. In other words it’s really complicated
Then what. Most of the neocortex is inhibitory, why, because you would go nuts from all the cross-talking going on up there. Pain afferent sends signal to the spinal cord. They can end in any of the 5 layers of the dorsal horns. There an intermediate neuron synapses with a spinal ascending neuron. That neuron rises to the brain stem, the medulla and synapses with a 3rd neuron that decusses, crosses over to the other side. In the thalamus it synapses with the 4th afferent neuron that goes up into the somatosensory cortex (parietal lobe). Think of the laser cables the phone company used before there was the cloud.
At each synapse, more than one neuron can get in. At each level of synapse a different set of excitatory and inhibitory neurotranmitters are used.
Then the processed signal is responded to by the neurons descending from the brain. Notice that acute sharp pain, the hot radiator, you react BEFORE your brain knows it: There are short circuits that go only as far as the medulla, or even only around the spinal cord, short interneurons. More complicated signals are processed and descending signals, mostly inhibitory, come back: The body will naturally dull the pain.
ENDOGENOUS ENDODORPHINS (Runners’ high)

14. So painkillers act at different places in ascending pain pathway BUT they can also act on the descending pathways.
Correction: Tylenol acts centrally in the brain mechanism unknown

15. Pain History and Physical
Pain Characteristics – onset, duration, location, quality, intensity, associated symptoms, exacerbating and relieving factors. What have you done for it?
Current medical condition, medications
Physical exam including orthostatic vitals, mood, mobility
Impact of pain on function – work, daily activities, personal relationships, sleep, appetite, emotional state
Patient (and family’s) expected goals/specific fears for treatment

16. Acute vs. Chronic Pain Acute pain Chronic Pain
Etiology is often evident
Accompanied by autonomic nervous system changes: elevated BP, HR, RR & O2 consumption, decreases GI motility, diaphoresis, myardiasis, m spasm
Patient shows sign of pain, like grimacing
Pain which persists beyond 1-3 months
Often fails to demonstrate autonomic symptoms
Pt may look more like they are depressed than in pain
Often associated with MDD
Pt often succumb to pain and may lose hope.
Acute injury begins to subside rapidly. A trip to the dentist, the pain rarely lasts more than 3 days. A hip replacement should be subsiding after a week. What about RECURRENT injuries eg occupational injuries like Carpal Tunnel? Recurrent localized inflammation?
Chronic pain is pain that persists longer than days by convention despite healing of the initial injury or apparent resolution of the problem eg gall bladder surgery.
Need to carefully examine the treatment history. Is it just “still there” and I canfeel it or has there been continuous and perhaps even escalating use of pain killers?

17. Principles of Chronic Pain Management
Multimodal Therapy
Establish Expections
Non-opiate analgesics
Mind-body work
Physical therapy
Supportive psychotherapy
Complementary therapy
Manipulation and massage
Desensitisation
Local injection
Opiates rotation rather than escalation
Identify most important aspect of discomfort
Agree on a metric
How good is better?
Establish a common language of descriptors
Establish expectations for follow up and communications

18. Page 2
                                                                                                                                                                                                                             
Left upper corner is a picture of one postulated mechanism for how continuous pain blockade with opiates induces the neural pathways to remodel both peripherally and centrally to restore pain sensation BECAUSE pain serves a useful purpose, it’s an attempt to heal. The result of neural remodeling and acquired tolerance of opiates uniquely, the syndrome of opiate-induced pain syndromes has been described. It is usually constant, since there is no stimulus, and poorly localized, since remodeling has bypassed the anatomical pathways and typically dull, burning or hard to describe.
It’s complicated. After 6 weeks, remember that the body will send afferents of it’s own to block pain. But the flip side is that the brain expects some pain. I don’t expect that you can read this. It is one model of how opiate tolerance develops, the “gate mechanism.” And the photo is from a mouse. If you continuously blockade an afferent synapse, that neuron or a neighboring neuron will put out little tendrils to re-establish the connection. But the essential connection between the initial site of injury and where the efferent signal goes is lost.
Opiate tolerance: after about 6 weeks
Pain becomes dull
Hard to localize
Takes larger and large doses to knock it down.

19. Damaged tissue can continue to hurt
Damaged tissue can continue to hurt. Recurrent injury can create a LEARNED pattern of pain. Hyperalgesia and allodynia are 2 well described chronic pain associated syndromes which if treated like acute pain and prolonged opiates lead to further complications that we are only now beginning to understand, that is, both the science of it and social impact.
If in the history there is an acute pain months to years ago “where it all started” AND there has been continuous treatment with narcotics LOOK for OPIATE INDUCED pain syndromes.
A continuous dose of 60 morphine mg equivalents beyond days or even longer is highly suspicious.

20. Opiates act on mu-receptors
Mu-receptors are located in the brain and in the ascending and descending tracts.
There are sub-types of mu-receptors that mediate opiate responses:
Euphoria
Analgesia
Sedation
Constipation (in the visceral innervation of the bowel)
Nausea
As tolerance develops the first “side effect” to fade is sedation then euphoria. Oxycodone 120mg/d? No I’m not sleepy. It still hurts, increase the dose.

21. And the delta and the kappa receptors which are more the domain of anaesthesioloigsts than internists.

22. Not all opiates are the same
If one “stops working” do not increase it, rotate it.
Methadone is messy but it has NMDA (glutamate is an excitatory NT) blockade activity
Use a validated conversion calculator and don’t trust yourself to remember where the decimal goes. (Fentanyl)
Google: narcotic converter
If a reasonable dose isn’t working DO NOT escalate, rotate.

23. SELECTION OF ASSESSMENT TOOLS BASED ON COGNITIVE ABILITY
PAIN SCALES
SELECTION OF ASSESSMENT TOOLS BASED ON COGNITIVE ABILITY
Cognitive ability
Recommended assessment tool
Adult patient with no cognitive impairment
Brief pain inventory and standard pain scales
Adult patients with cognitive impairment
Standard four-point verbal rating scale for pain
Adult patients who are unable to communicate
Observer rating using the four-point verbal rating scale for pain
Caraceri et al 2002

24. Use a standard scale to track the course of pain
Numeric and Verbal Analog Pain scale
Faces Pain Scale and Pain Thermometer
Pain Intensity Scales: they assess intensity not the impact of pain on the patient.
Source: Acute Pain Management Guideline Panel. Acute Pain Management in Adults: Operative Procedures. Quick Reference Guide for Clinicians. Rockville, MD: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research. February AHCPR Pub. No
In general, short simple verbal rating scales (e.g. no pain, slight pain, moderate, or severe pain) which focus on intensity are probably the easiest and most appropriate for use in those with acute pain. Studies have documented over a 70% completion rate. Numeric pain intensity scales as well as VAS have been found in the literature to be the more difficult scales to use in the elderly, regardless of cognitive status. Physiologic measures such as blood pressure and pulse are not reliable markers as they can vary depending on medications, comorbidities, or the normal aging process in general.
The point with the numeric 1-10 scales is the numbers mean different things to different people. Pick “what number is it today?” “Is that good enough?” How much is good enough?” Strive for good enough.

25. Pain Intensity Scales: they assess intensity not the impact of pain on the patient. That is why we should use the multidimensional scale to assess total pain.
“But I’m not sad, I just hurt.”

26. PATIENT WITH COGNITIVE IMPAIRMENT (or small children)
PAIN ASSESSMENT IN ADVANCED DEMENTIA (PAINAD) SCALE

27. Non Verbal Signs of Pain
Cornell Pain Inventory

28. The Chronic Pain Cycle
There is always a large overlay of emotional, psychiatric and social stuff in the cycle.

29. Remodeling of afferent
and inhibitory pathways

31. Approach to Chronic Pain in Older Adults
Pain history: Is it acute or chronic?
Standardized pain scale
Comprehensive medical hx & review ALL drugs
What else have you tried for relief?
Social impact of pain: isolation? IADL? Work?
Physical exam: Locate, elicit, soothe, performance
Diagnostic investigations if needed: There is usually quite a thick sheaf of previous labs and imaging.
Set a goal: What level of pain is acceptable to you if ZERO is not an option

32. Approach to Chronic Pain in ALL Adults
Nociceptive component: Tylenol 3-4 g/d scheduled
Neuropathic component: TCA or gabapentin or duloxetine (SNRI)
Revisit after 2-4 weeks. Relief?
NSAIDS, topical agents
Adjunctive therapies
Physical therapy, supervised exercise, yoga, t’ai ch’i
Massage, TENS, heat or cryo therapy, US
Relief?
Low potency opioids prn to scheduled
Supportive psychotherapy anxiety/depression
The biggest mistake I see in prescribing is orders

33. Mrs. S says her knee hurts: The first mistake in pain management:
Tylenol 500 mg 1-2 tabs po q 4-6hrs prn
Norco 5/325 mg po 1-2 tabs po q 4-6hrs prn
What’s wrong with this?
Everything.
What’s the diagnosis?
What if it’s septic what about fever?
What if it’s arthritis and inflamed?
What is prn and according to whom?
PRN means Probably Never
Tylenol toxicity.

34. The right answer to Mrs. S knee pain:
Examine. Xray if needed. It’s her OA.
Tylenol 650 mg tid while awake scheduled
Can increase to q 6hr scheduled if pain is waking her at night.
Topical mentholated cream, NSAID (if her insurance will pay for it), non-pharmacological interventions
If no contraindication, naprosyn 375 or 500mg bid x 7d
o/w oxycodone nmt 5mg po q 6 prn, revisit pill count in 7d.

35. Suspect Opiate Induced Hyperalgesia when:
Using high potency opioids > 6 months
Taking > equivalent of oxycodone 30 mg/d or MSIR 45 mg/d for > 3 months and asking for escalation
Multiple prescribers

36. Approach to Chronic Pain in Everybody Regardless of Age
When a durable response is achieved:
Negotiate gradual taper of opioids, “Save it for a rainy day.”
Continue adjunctive therapies and non-opiates.
If an adequate dose is not effective
Dose escalation is excessive or ineffective:
Suspect drug diversion
Suspect drug tolerance / dependence
Suspect opiate-induced pain syndromes
I received a nice consultation for pain management for an 83 y/o lady afflicted with fibromyalgia who was in somuch pain she could not carry on daily activities.
She was taking 90mg methadone daily
60mg of oxycodone daily
Some tylenol, some NSAIDs
Muscle relaxants, sleep aids (benzo and antihistaminic)
She said she wasn’t depressed.
Today she attends water aerobics several times a week, yoga, book club and takes 30mg oxycodone most days. I won’t argue with her about it.

37. Suspect drug diversion if
Utox is negative or
Elderly patient is always accompanied by a younger person who verbalizes the pain for them
Multiple prescribers

38. Adjuvant Medications: in order
Topicals
Tylenol
NSAIDS, Celecoxib, steroids
Anticonvulsants
Antidepressants
Anticholinergics
Anxiolytics
Muscle relaxants
Antihistamines

39. Summary Pain is a normal bodily function.
Chronic pain indicates that normal pain physiology has changed either by pathway remodeling or drug induced changes.
Chronic pain is defined by >3 months duration, no obvious localizable cause
Approach to chronic pain should be systematic and step-wise.
Approach to chronic pain should be multimodal and multidisciplinary.

40. Thanks!