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The Ins and Outs of Pain

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Geared towards advanced pain nurses for the hospital-based and evidence-based management of pain. Overview of physiology, pathophysiology, assessment and management.

Geared towards advanced pain nurses for the hospital-based and evidence-based management of pain. Overview of physiology, pathophysiology, assessment and management.

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  • Pain is a frequent problem whether associated with advanced illness or other acute or chronic conditions,Weiss SC, Emanuel LL, Fairclough DL, Emanuel EJ. Understanding the experience of pain in terminally ill patients. Lancet. 2001;357(9265):1311-1315. PMID: 11343734.50% of 988 terminally ill patients reported pain. Of those patients experiencing moderate or severe pain,29% wanted more therapy, 61% wanted therapy to remain the same, 9% wanted less therapy or to stop their pain treatment altogether. Of these, 34% feared addiction, 31% were adverse to physical side effects (eg constipation), 33% averse to mental side effects (eg confusion) and 30% averse to additional pills or injections. Although the majority of patients had cancer, there was no association between disease and level of pain. We will briefly review the basic concepts important to understanding the physiology of pain This starts to build the common language we need when assessing and managing painWho in this room has experienced pain? Would you be willing to share you experience?
  • This is how the International Association for the Study of Pain has defined pain… recognizes that it is not only a sensory but also emotional experience Pain is the physical symptom that patients and families fear most Which is why I think the next definition is very useful. . .
  • …pain exists where ever they say it does, whenever they say it doesThis definition has been proposed by Margo McCaffery, a nursing leader in pain assessment and managementThis is the definition we should use at the bedside– because we need only accept the report of the patient to begin to comfort themAs clinicians we know that the same set of circumstances can cause significant pain in one person but little to no pain in another This sometimes affects our assessment of the situation So the final piece to pull this together is Dame Cicely Saunders concept of Total Pain
  • Dr. Saunders gives us the concept of Total Pain- which is the summation of all these domains: Physical symptoms, Emotional & psychological problems, Spiritual or existential distress and Social concerns.This recognizes that we are more than a physical body, and that other factors influence the sensation of painThe basic concepts we will discuss today provides a pathophysiologic basis which supports this model
  • Descartes:  “I feel pain, therefore, I am”This diagram represents the early concept of pain transmission A single nerve carries the impulse from the point of injury to the brain
  • New receptors, pathways, and hypotheses are being investigated everyday     We will not go into this diagram in any depth, but you can see that multiple connections,  neurotransmitters and pathways are represented Pain is much more than the early philosophers thoughtIt is important for all clinicians caring for the patient to have a basic understanding of pain and be able to talk to each other using the correct clinical language Let’s begin by defining some terms…
  • Let’s start with defining a nociceptorA nociceptor is a nerve that has developed to carry the pain signalSo imagine that I am one giant nociceptor . . . What am I doing when there is not an incoming pain stimulus . . . (resting quietly, scanning the environment) What happens when the person I (the nerve cell) belong to touches a hot stove? (nerve is stimulated by heat- a thermal stimulus)Discussion….(feel pain, withdraw hand, put in cold water, etc)So you have just defined the process of nociception . . . (the pain nerve cell being “turned on” and communicating with the rest of the body “pain”)Formal definition- primary afferent neurons that exist throughout the body and have the intrinsic ability to respond selectively to specific noxious stimuli (Pasero, McCaffery, Pain Assessment and Pharmacologic Management. 2011; page 1)
  • Nociception is the neural processing of noxious stimuliActivation of receptors in peripheral pain pathwaysTransmission of information about noxious stimuli to the brainSo, ULTIMATE DEFINTION: PAIN is the perception of nociception which occurs in the brain and includes 4 basic steps
  • This reflects “normal” pain, a healthy nervous system doing what it is designed to doLet’s walk through each step, one at a time…
  • Now our signal is climbing from the skin to the spinal cord and on to the processing and perception centers in the brain.Transmission is the process by which impulses are sent to the dorsal horn of the spinal cord, and then along the sensory tracts to the brainThe primary afferent neurons are active senders and receivers of chemical and electrical signals Their axons terminate in the dorsal horn of the spinal cord where they have connections with many spinal neuronsIn turn, spinal neurons have inputs from many primary afferents
  • This is the point in the process when we consciously know that we are in painExplains our individual response to a painful stimuliWhy we may respond differently to the same, repeated painful experienceRequires activation of higher brain structures, thalamus, limbic systemIncludes processes that influence movement, emotions and drivers related to painWe’ve only told part of the story, though; on it’s journey, our signal has interacted with Other trafficStreet signalsSwitching stationsEtc.
  • As the pain is translated and travels to the brain, multiple factors interact with the signal.This is where the pathophysiology meshes with the model of Total Pain Inhibitory mechanismLocal and descending processes occur in multiple sites from the periphery to the cortex, most importantly in the spinal cordInvolves the release of numerous neurochemicals endogenous opioids, serotonin, NorepinephrineHappens primarily in the dorsal horn but also affected by messaging from ascending and descending pathwaysWhat modulates pain?Stress, increasing tissue damage, disease progression . . . Leading to increasing painOpioids, electrical stimulation, hypnotherapy, psychological/social/spiritual support …. leading to decreasing painPsychological variables are important in the modulation of pain,  often increasing or decreasing painful sensations
  • To review, these are the 4 steps we have just discussedWe will add to these steps the physiologic and temporal classifications of painNow let’s move outside the body of our patient and look at the way that we, as clinicians, think about pain.
  • We, as a group, like to put things in boxes – to classify them. [CLICK] Let’s begin by looking at the different physiologic types of painWhen we think about pain from a physiologic standpoint, we think about it being nociceptive, neuropathic or mixedNociceptive painfollows the 4 basic steps we have just learned aboutThis is a healthy, intact nervous system doing what it is designed to doWe continue to develop an understanding of this type of pain and how the body reacts to painful stimuliNeuropathic pain does not follow the steps we have just learned aboutReflects a damaged or traumatized nervous systemWe do not know as much about neuropathic pain as we know about nociceptive painWe have to understand whether our patients have either nociceptive or neuropathic pain, or a combination of the two…referred to as “mixed” pain
  • Normal tissue responses to painful stimuli Described as sharp, aching or throbbingFurther subdivided into somatic and visceral painSomatic pain, mediated by the somatic nervous system, subserves skin, bone, and muscle Pain localization is precise and is often described as sharp, aching, or throbbing For example, describe the pain you have when you cut your finger (sharp, well localized, pinpoint with one finger)Visceral pain, mediated by the autonomic nervous system, subserves internal structures such as the visceral cavity It is typically difficultto localize or describe, and sometimes characterized as crampyFor example, describe the pain you have with diarrhea (crampy, deep, use the entire hand to show where pain is, radiates to back)We use the patient’s words and their actions, along with the pathology of the disease to accurately assess the pain
  • Neuropathic pain has been defined as a primary lesion or dysfunction of the nervous system Damaged caused by ischemia, compression, infiltration, metabolic injury, or transection Patients tend to describe neuropathic pain with words like burning, tingling, numbness, shooting, stabbing, or electric-like feelings Dysfunction of the nervous system repetitive nociceptive stimuli can create a condition where spinal cord neurons have increased sensitivity “central facilitation” nerves are undamaged, an abnormal signaling system a given noxious stimulus receives a larger response than normal (hyperalgesia)non-noxious light touch can stimulate pain pathways (allodynia)The N-methyl-D-aspartate (NMDA) receptor is thought to be involved in setting up this abnormal pathway Preliminary evidence suggests that if the initial nociceptive pain impulses are controlled, these neurological changes can be prevented Although neuropathic pain may respond well to opioids, adjuvant analgesics (tricyclic antidepressants, anticonvulsants, antiarrhythmics, etc.) are often required in combination with opioids to achieve adequate relief
  • What we are most often facing in advanced illnesses. A combination of both nociceptive and neuropathic pain
  • Returning to the ways in which we think about pain, [CLICK] let’s now consider the time course of the sensationacute or chronic
  • Sudden or recent onsetIdentifiable cause: injury, disease, medically causedShort duration usually < 1month Sympathetic responseFight or flight responsescharacteristic behavior: rubbing, moaning, crying, etcMay resolve spontaneouslyUsually responsive to medication therapy
  • Persistent: usually > 3 to 6 months; does not resolve spontaneously May not be an obvious cause for the reported pain May be due to a chronic disease or conditionProlonged Impairment: both physical and psychologicalUsually no sympathetic responseMay not APPEAR to be in pain when looking at themmay exhibit insomnia, anorexia, irritability, depressionChronic pain is often more challenging to manage
  • 5 elements we want to focus on for a pain assessmentTo many (if not most!), this will feel simplistic. However…All clinicians assess, all clinicians reportAnd we have consistencyAllows for accurate and safe treatment plans to be developedLet’s walk through each of these steps together.
  • Ask the patient to identify where the pain is felt There may be more than one placeAsk if the pain starts in one place and moves (radiates) to another
  • Ask for words used to describe the painThese words, along with the pathophysiology of the disease help determine if the pain is nociceptive, neuropathic, or mixed
  • Ask how the pain changes over timeThis is important because it helps identify the need for immediate release medication, extended release medication, or a combination of the two Constant pain is experienced throughout the day.There may be some variation in intensity, but the patient is in pain the entire dayBreakthrough pain describes an increase over the level of constant pain It may be due to certain activities (walking, bathing) or occur without any warningIntermittent acute (or incidental) pain describes pain that comes and goes, and fluctuates between being pain free and in pain
  • We think about pain severity as the “5th Vital Sign” and encourage clinicians to ask about pain severity at least each time any vital sign is measuredQuantify pain intensity; ask the patient to rate the pain This card has 3 severity scales available for use Numerical scale with anchors of 0 and 10Word descriptor scaleFaces scaleAssist the patient to use the scale that makes the most sense to themIn all cases, these scales are used by the patient to self report Do not use the Faces scale to “match” to the patient’s facial expression and use as a severity scale
  • San Diego Hospice pocket card with the PAINAD toolEach of the 5 elements is scored between 0-2, and then the 5 elements are added together for a total scoreYou must score all five elements to obtain the total scoreSuggestions for when to use the tool when the patient is at rest or during a pleasurable activitywhen the patient appears distressed or involved in a potentially painful activity (bathing, dressing, wound care, etc)This tool can be taught to all members of the team, including the familyThis gives us a “shared” language to evaluate potentially painful episodesIndividuals that know the patient will be able to provide useful information about “normal” behaviorsKeep in mind that “normal” behaviors may be related to long standing unrelieved painWarden V, Hurley AC, Volicer L. Development and psychometric evaluation of the pain assessment in advanced dementia (PAINAD) scale. J Am Med Dir Assoc. 2003;4:9-15.
  • The patient's report, combined with medication administration records or pain diaries, provides guidance on the effectiveness of the current plan and how the pain is changing with disease progressionDon’t assume that the patient is taking the medication as prescribed, ask them for details about dosingAsk about any affects that they don’t like because this will impact on a willingness to continue with the current plan or willingness to change the plan
  • Focused ExamGuarding?Pain with motion?Masses?PsychologicalAnxiousWithdrawnDepressedTogether with a careful physical exam and select laboratory and imaging studies, in which the benefits of the study outweigh the burdens, it is usually possible to identify the relevant pathophysiology leading to a pain stateIn different settings, there may not be any laboratory or imaging studies available so all your information comes from the patient’s self report and your examination, coupled with a knowledge of disease progression Why is it important to standardize the assessment…?
  • …so that we all speak the same language when it comes to pain.All members of the team have a role to play in pain assessment and management ((We have highlighted three of the roles, and identified the skills unique to that roleYou can see that some skills are shared by all disciplines, assess, monitor and communicateSome skills are unique to each disciplineWe need to identify what skills are needed, and who are the best members of the team to use the skill and provide the careThis touches on the idea of Scope of Practice, recognizing that this may differ based on a setting or a country, availability of team members, etc))
  • Let’s begin our pain management portion with a pet peeve…Narcotic, in the press & in law enforcement may refer to use of opioids, cannabinoids, cocainr, meth, benzos and even steroids (all subject to abuse).Opioid, includes endogenous and exogenous substancesMorphine is both an opioid and an opiate but fentanyl is only an opioid
  • A 3-step model to guide analgesic choice depending on the severity of the patient’s painThis ladder can be used for nociceptive and neuropathic painDepending on the severity of the pain, start management at the corresponding stepFor mild pain (1–3/10 on a numerical analogue scale), start at step 1For moderate pain (4–6/10), start at step 2 For severe pain (7–10/10), start at step 3 It is not necessary to traverse each step sequentially; a patient with severe pain may need to have step 3 opioids right awayThe addition of adjuvant analgesics is often critical to achieving an excellent outcomeAs you move between steps and between medications, approaches have been developed to switch opioids while maintaining analgesiaAlthough not displayed on this ladder, nonpharmacologic approaches may significantly increase the relief achievedAsk the group which step contains the most dangerous medications[CLICK] Step 1ASAInhibits thromboxane-induced platelet aggregation, producing an irreversible effect on platelets and a reported increase in bleeding time for up to 7 days after the last doseHigh risk for GI toxicity AcetaminophenHepatic effectNSAIDSRenal effectPlatelet effectCardiovascular effectGI effect
  • First Order Kinetics are important for all members of the IDT to understandOpioids, codeine, hydrocodone, hydromorphone, morphine, oxycodone, etc., all follow first-order kinetics and pharmacologically behave very similarlyThis curve represents a single, oral dose As we look at the graph, we see that the plasma concentration changes over timeincreases to a point during the absorption phasedecreases during excretion phaseAt the bedside, we can relate this curve to the reported pain relief: pain decreases with taking a dose, plateaus and then increases back to baseline (without a repeated dose of analgesic)
  • The second important pharmacology principles is the maximum concentration or the CmaxThis represents the maximum concentration of the drug for the dose just given [CLICK]At the bedside, this is where we see the expected maximum pain relief from the dose just given The Cmax is the parameter that determines the breakthrough dosing interval
  • Opioids reach their peak plasma concentration (Cmax) approximately 60 to 90 minutes after oral (including enteral feeding tube) or rectal administration[CLICK]
  • The analgesia associated with each opioid has a half-life (t½) that depends on the rate of liver metabolism andits rate of renal clearanceMost of the opioids we use (codeine, hydrocodone, hydromorphone, morphine, oxycodone), and their metabolites have a half-life of approximately 3-4 hours when renal clearance is normal It is the half life that determines the routine dosing scheduleWe teach that the number you need to remember for opioid half life is 4 hoursAt the bedside, this would be the duration we would expect for pain relief from a single dose
  • Opioids are metabolized in the liver and 90-95% excreted by the kidney Their metabolic pathways do not become saturated Liver conjugates morphine to an active metabolite, morphine-6-glucoronide, and an inactive metabolite, morphine-3-glucuronide, must be cleared renally20There is evidence that other opioids such as codeine, hydrocodone, hydromorphone, and fentanyl also have active metabolites21 Only methadone is excreted unchanged When dehydration or acute or chronic renal failure impairs renal clearance, the dosing interval for morphine must be increased, or the dosage size decreased, to avoid excessive accumulation of active drug If urine output is minimal (oliguria) or none (anuria), stop routine dosing and administer morphine only ‘as needed’ This is particularly important when patients are dyingOpioid metabolism is not usually affected by extensive liver metastases If hepatic function becomes severely impaired by hepatitis or there is clinical liver failure, increase the dosing interval or decrease the dose
  • The half-life is the parameter that guides routine dosingFor opioids (except methadone), the half-life is 4 hours Let’s look at why this matters…
  • For the patient with CONSTANT pain, non-scheduled dosing leads to return of pain prior to effective concentration of next breakthrough doseRequires patient educationVery difficult to achieve in the hospital given the other time demands on the floor nursing staff!![CLICK] with routine dosing, you can see that the steady state (represented by the line at the peak of the curves) results in each scheduled dose becoming effective before the prior dose is removed from the body.Speaking of steady state…
  • This graph demonstrates the plasma concentration increasing with routine dosing based on the half-life [CLICK]100%, or maximum plasma concentration is reached after 5 doses, when consistently given based on half lifeWhen dosed repeatedly, the plasma concentrations approach a steady state after 4 to 5 half-lives. Thus, steady-state plasma concentrations are usually attained within a day4 hr half life x  4 doses  = 16 hr4 hr half life x  5 doses  = 20 hourGiven this, I would like you to think about starting morphine drips. Often times, we will increase drips, we will titrate them up, when people have symptoms out of control.Can anyone think of a problem with this, knowing what we now know??When will that drip reach steady state…reach its maximum effect?
  • We work towards the steady state of plasma concentration to provide pain relief[CLICK] We try to avoid too little medication (trough) that leads to increased pain, or too much medication (peak) that leads to unwanted side effects This curve represents optimal dosing with the trough and the peak both staying within the therapeutic rangeLow end of the therapeutic range would be the plasma concentration needed to control painHigh therapeutic range would be the plasma concentration where side effects start to occur
  • How much of each drug, in each form, equals another.I would like to briefly spend some time working with two of these conversions so that we can see areas of misconception and areas prone to mistake.For each of the conversions, I will ask you to tell the group your first response without doing the calculation, what would you expect to hear?
  • To adjuvant……
  • Sarah has tremendous disease burden and non-opioid-responsive painWhat might be going on??…total pain.
  • Given the limited effectiveness of current treatments, combining different drugs may result in improved results at lower doses and with fewer side effectsLocally acting analgesics are attractive because they may cause minimal systemic side effectsThe lidocaine patch 5% has been shown to relieve localized pain in postherpetic neuralgia with no increase in side effects (NNT = 4.4)Capsaicin, an ingredient of hot peppers, has shown mixed results in RCTs, and some patients with postherpetic neuralgia have reported pain exacerbation
  • Evidence for multimodal pharmacology primarily inDiabetic peripheral neuropathyPost-herpetic neuropathy
  • Limited evidence of role for opioids in neuropathy20-30% improvement in painInconsistent beneficial effect on mood, QOL and disability
  • Methadone is a synthetic opioid potentially useful for controlling neuropathic pain because of its NMDA-antagonist propertiesIts long half-life (24–36 hours) necessitates extremely careful dose titrationTwo small RCTs of methadone demonstrated benefit in managing neuropathic pain and open-label experience suggests promise in a wide variety of neuropathic pain conditions
  • Gabapentin, an calcium channel antagonist has repeatedly demonstrated analgesic efficacy and improvements in mood and sleep in several RCTs (NNT = 3.8)Gaba: PHN, DPN, neuropathic cancer painLyrica: PHN, DPN, fibromyalgiaSafetyNot hepatically metabolizedNo drug interactionsSide-effects usually tolerable
  • GabapentinEasier to titrateFaster onsetImproves sleep and anxietyIntestinal transport saturates at ~1200mg…so more than this dose requires increased dose frequencyPregabalina gabapentin analogue with a similar mechanism, higher calcium-channel affinity and better bioavailabilitysuperior to placebo in several RCTs in diabetic peripheral neuropathy and postherpetic neuralgia (NNT = 4.2)More expensive
  • A couple of substances which theoretically increase inhibitory transmission are used for treating neuropathic painnoradrenalin and serotonin reuptake inhibitors (amitriptyline)Norepi reuptake inhibitor (desipramine, nortriptyline)duloxetine (Goldstein et al. 2005) venlafaxine (Rowbotham et al.2004) opioid receptor agonistsagents with GABAergic properties like baclofen or valproateTricyclic antidepressants have repeatedly been shown to reduce neuropathic painAnalgesic actions may be attributable to noradrenaline and serotonin reuptake blockade (presumably enhancing descending inhibition), NMDA-receptor antagonism and sodium-channel blockadeThe NNT is about 3 both for balanced noradrenaline and serotonin reuptake inhibitors (e.g., amitriptyline) and predominantly noradrenaline reuptake inhibitors (e.g., nortriptyline)Selective serotonin reuptake inhibitors (NNT = 6.7) and mixed serotonin–noradrenaline reuptake inhibitors (venlafaxine and duloxetine, NNT = 4.1–5.5) do not appear to be as effective as tricyclic antidepressantsUnwanted effects:CNSAnticholinergicNauseaCVSexual
  • Based on methodologically flawed trials, carbamazepine and phenytoin have NNTs of 2.1–2.3 for diabetic peripheral neuropathyBoth have significant adverse effects, making them generally poor candidates for first-line therapyCarbamazepine, however, is still considered first-line therapy for trigeminalneuralgia, a unique neuropathic pain condition (NNT = 1.7) Oxcarbazepine, a newer anticonvulsant structurally related to carbamazepine, may also be useful; however, only one RCT (in diabetic peripheral neuropathy) has been publishedRCTs of other anticonvulsants, including valproate, lamotrigine and topiramate, have had equivocal results(lamotrigine, topiramate, oxcarbazepine, tiagabine, levetiracetam, zonisamide, carbamazepine, phenytoin, valproate)
  • DexamethasoneFluorinated, which keeps it from crossing blood-brain barrier as easilyHigher risk of myopathyPharmacokinetics supports once-daily dosing, though often dose much more frequentlyStart with a powerful dose and taper until loss of beneficial effectRisks: myopathy, delirium (unpredictable unless they have a history of steroid-induced delirium, then they have a slightly increased risk for having it again), Cushingoid changes
  • LidocaineSodium channel blockerChallenge in the hospital due to monitoring and need for timely lithium blood level 8-10 hours after startingGood RCTs for neuropathic painOral version: mexiletineMexiletine, an oral antiarrhythmic agent and sodium-channel blocker, was superior to placebo in only 2 of 7 RCTsKetamineUsed as pain adjuvant as well as rapid depression mgmt. with some effectParenteral dosing usually results in dream-like state, higher doses may have frank hallucinationsEvidence primarily in mucositisAlso good for painful dressing changes
  • To adjuvant……
  • The perception that the administration of opioid analgesics for pain management causes addiction is a prevalent myth that inhibits adequate pain controlAddiction is a complex phenomenon It may be difficult to distinguish between true addiction, pseudoaddiction caused by undertreatment of pain, behavioral/family/psychological dysfunction, and drug diversion with criminal intentConfusion about the differences between addiction, tolerance, and physical dependence is in part responsible
  • Pharmacologic tolerance is the reduced effectiveness of a given dose of medication over time Clinical importance is rareTolerance to unwanted effects is observed commonly and is favorableTolerance to analgesia is rarely significant clinically when opioids are used routinely Doses may remain stable for long periods if the pain stimulus remains unchangedWhen increasing doses are required, suspect worsening disease rather than pharmacologic tolerance
  • Physical dependence is the result of neurophysiologic changes that occur in the presence of exogenous opioids Similar outcomes occur in the presence of exogenous hormones and other medications (beta-blockers, alpha-2 agonists, etc) Take-awaysPhysical dependence is not the same as addictionPhysical dependence is not evidence of addiction Its presence does not mean that opioids cannot be discontinued Withholding opioids after physical dependence develops results in transient withdrawal symptoms Abrupt opioid withdrawal may result in an abstinence syndrome characterized by tachycardia, hypertension, diaphoresis, piloerection, nausea and vomiting, diarrhea, body aches, abdominal pain, psychosis, and/or hallucinationsIf the pain stimulus decreases or disappears, opioid doses usually can be reduced in decrements of 50% or more every 2 to 3 daysIf the dose is lowered too quickly and abstinence symptoms occur, a transient increase in the opioid dose, treatment with clonidine, or a small dose of a benzodiazepine (eg, lorazepam) may be necessary to settle distressing symptoms
  • Drug diversion is the transfer of a prescription drug from lawful to an unlawful channel of distribution or useRecord keeping involves the pharmacist, clinicians and familyThe patient and caregivers must accept responsibility for the safekeeping of the medications and agree to only use for the intended symptom managementFrom Medscape NeurologyPrescription Drug Abuse and Diversion: An Expert Interview With James A. Inciardi, PhD, Darlene Foschini-Field, PhD; James A. Inciardi, PhD
  • Addiction, as the term is now used, is a complex phenomenon To manage pain effectively, physicians will need to educate patients, families, and other professionals about the inappropriate fear of addictionOpioids by themselves do not cause psychological dependence Four characteristics of addictionPsychological dependenceCompulsive useLoss of control over drugsLoss of interest in pleasurable activities
  • Its hallmark is psychological dependence on drugs and a behavioral syndrome characterized by compulsive drug use and continued use, despite harmAddiction is a rare outcome of pain management when there is no history of substance abuse
  • Since patients with histories of substance abuse can also develop significant pain, they deserve compassionate treatment of their pain when it occursMost will need to adhere to strict dosing protocols, and contracting may become necessaryPhysicians who are unfamiliar with these situations may need the help of specialists in pain management and/or addiction medicine
  • Transcript

    • 1. THE INS AND OUTS OF PAIN Kyle P. Edmonds, MD Fellow, Scripps Health & The Institute for Palliative Medicine at San Diego Hospice Adapted from the Palliative Care International Curriculum Series Editor, Frank R. Ferris, MD
    • 2. OBJECTIVES • Review the definitions, pathophysiology & classifications of pain. • Perform a standardized assessment of pain and state why it is important for team communication. • State how Cmax and half-life relate to opioid dosing. • Describe the hallmark of addiction and the low likelihood of occurrence in pain management.
    • 3. PAIN International Association for the Study of Pain ( IASP ): “An unpleasant sensory and emotional experience associated with actual or potential tissue damage.”
    • 4. PAIN Margo McCaffery: “Pain is whatever the person says it is…”
    • 5. TOTAL PAIN CICELY SAUNDERS 1964 Physical Social Patient with Pain Existential Emotional
    • 6. MECHANISM OF PAIN- DESCARTES
    • 7. NOCICEPTOR • Nerve cell • Activation • Thermal • Chemical • Mechanical • Transmits signal
    • 8. NOCICEPTION • Activation of receptors • Transmitting • Processing • Leads to pain perception
    • 9. BASIC STEPS: PAIN PROCESSING • Transduction • Transmission • Perception • Modulation
    • 10. PAIN TRANSDUCTION Mechanical Thermal Chemical Aδ or C fibers Judith A. Paice, AAHPM, 2008
    • 11. TRANSMISSION • Stimulus to cord • Cord to brain stem • Brain stem to higher cortex
    • 12. TRANSMISSION Somatosensory Cortex Associative Cortex Thalamus Judith A. Paice, AAHPM, 2008
    • 13. PERCEPTION • Experience • Conscious • Multidimensional • Interaction of transmission/transduction
    • 14. MODULATION • Changing • Inhibiting • Spinal cord level
    • 15. PAIN PROCESSING • Transduction • Transmission • Modulation • Perception
    • 16. CLASSIFICATION OF PAIN • Physiologic • Nociceptive • Neuropathic • Mixed • Temporal • Acute • Chronic
    • 17. NOCICEPTIVE PAIN • Somatic • Visceral • “Sharp” “Aching” “Throbbing”
    • 18. NEUROPATHIC PAIN • Damaged or dysfunctional nerves • Central • Peripheral • “Burning” “Tingling” “Numbness” “Electric”
    • 19. MIXED PAIN • Experiencing • nociceptive and • neuropathic
    • 20. CLASSIFICATION OF PAIN • Physiologic • Nociceptive • Neuropathic • Mixed • Temporal • Acute • Chronic
    • 21. TEMPORAL CLASSIFICATION: ACUTE • Sudden or recent onset • Identifiable cause • Short duration • Sympathetic response
    • 22. TEMPORAL CLASSIFICATION: CHRONIC • Persistent • May have no obvious cause • Prolonged functional impairment • No sympathetic response
    • 23. INTERVAL SUMMARY Understanding the pathophysiology leads to improved assessment and targeted management that will improve outcomes
    • 24. PAIN ASSESSMENT 1. Location 2. Description (type) 3. Change over time 4. Severity (0 – 10) 5. Effect of treatments • Benefit (+) • Unwanted effects (-)
    • 25. 1. LOCATION • Where is it ? • Does it move ?
    • 26. 2. DESCRIPTION • What does the pain feel like ? • Does it ever feel burning or shooting ? • How does the pain impact your life ?
    • 27. 3. CHANGE OVER TIME • Constant • Breakthrough • Intermittent acute
    • 28. 4. PAIN SEVERITY = 5TH VITAL SIGN 29
    • 29. 5. EFFECT OF TREATMENTS • Therapies tried • What worked ? • What didn‟t work ? • Any affects you didn‟t like ?
    • 30. EXAMINATION • General exam • Changes in behavior • Focused exam • Psychological exam
    • 31. INTERDISCIPLINARY TEAM • Physician •Assess •Diagnose •Prescribe •Monitor •Communicate • Nurse •Assess •Deliver •Monitor •Teach •Communicate • Pharmacist •Assess •Provide •Monitor •Teach •Communicate
    • 32. INTERVAL SUMMARY Assessment of pain requires a thoughtful history and physical. Standardizing the process helps prevent miscommunication.
    • 33. PAIN MANAGEMENT: DEFINITIONS • Opioid: anything that binds the opioid receptor • Opiate: derived from the opium poppy (Papaver somniferum) • Narcotic: archaic term, associated with illicit use 35
    • 34. PAIN MANAGEMENT PRINCIPLES • Don‟t delay control • Unmanaged pain nervous system changes • Treat underlying cause
    • 35. WHO LADDER 3, Pain 7 – 10 Morphine 2, Pain 4 – 6 Hydromorphone Fentanyl Codeine Oxycodone Tramadol Methadone A / Codeine ASA Levorphanol A / Hydrocodone Paracetamol / Acetaminophen ± Adjuvants A / Oxycodone 1, Pain 1 – 3 NSAID’s ± Adjuvants A / Dihydrocodeine ± Adjuvants WHO. Geneva, 1996.
    • 36. First Order Kinetics Plasma Concentration When biological effect follows plasma concentration Absorption 0 Excretion Time
    • 37. Maximum Concentration ( Cmax ) 10 Plasma Concentration 20 = maximum concentration during the dosage interval Cmax 0 4 Time ( hours )
    • 38. Time to Maximum Concentration ( t Cmax ) 10 Plasma Concentration 20 = time it takes to get to maximum concentration Cmax 0 1 Morphine PO / PR Cmax = 1 hour 4 Time ( hours )
    • 39. IV Time to Maximum Concentration ( t Cmax ) Plasma Concentration SC / IM Cmax 0 PO / PR Half-life (t1/2) Time
    • 40. Half-Life ( t ½ ) 10 Plasma Concentration 20 = time it takes for the body to excrete half the dose Morphine all routes t ½ = 4 hours 0 4 Time ( hours )
    • 41. CLEARANCE CONCERNS MORPHINE Liver Analgesia •Morphine  M3G . . . +  M6G . . . +++ CNS +++ + Urine 90 – 95 % Collins SL, et al. J Pain Symptom Manage. 1998. Mercadante S, Arcuri E. J Pain. 2004.
    • 42. PRINCIPLE FOR CONTINUOUS PAIN For constant pain • To achieve steady-state, dose routinely every halflife ( t ½ )
    • 43. CONTINUOUS PAIN PRINCIPLE
    • 44. Dosing every half-life ( t ½ ) Plasma Concentration Oral morphine = 4 hours 100% 97% 93.75% 87.5% 75% 50% 0 4 8 12 16 20 24 Time ( hours )
    • 45. Steady state after 5 half-lives Plasma Concentration Morphine ≈ 20 hours Concentration where side-effects start to occur Peak Trough 0 Concentration needed to control pain Time
    • 46. PRINCIPLE FOR BREAKTHROUGH PAIN • Dose once every Time to Cmax • PO 1h • Dose =10% of total 24 hr routine dose
    • 47. Breakthrough Pain Plasma Concentration PO / PR ≈ 1 hr Cmax 0 Time
    • 48. OPIOID ADVERSE EFFECTS Common • Constipation Uncommon • Bad dreams / hallucinations • Dry mouth • Delirium • Nausea • Myoclonus / seizure • Sedation • Pruritis / urticarial • Sweats • Respiratory depression • Urinary retention
    • 49. EQUIANALGESIC DOSES Oral/Rectal Analgesic IV/SC/IM 150 Codeine -- 15 Hydrocodone -- 15 Morphine 5 10 Oxycodone -- 3 Hydromorphone 1 51
    • 50. MORPHINE PO  OXYCODONE PO Morphine 15 mg PO = Oxycodone 10 mg PO • Patient is on Morphine ER 90mg BID PO • Oral Morphine Equivalent? • (90 mg x 2 = )180mg • This equals how much Oxycodone? • ( 180 mg x 15 / 10 =) 120mg • How much Oxycodone ER? • 60mg PO BID
    • 51. MORPHINE PO  HYDROMORPHONE IV Morphine 15 mg PO = Morphine 5 mg IV = Hydromorphone 1 mg IV • Patient is on Morphine IR 20mg q2hrs PO PRN • Now can‟t take PO, how much HM? • ( 20mg / 3 then 6.67 mg / 5 =) 1.3mg IV
    • 52. MORPHINE PO  HYDROMORPHONE IV Morphine 15 mg PO = Morphine 5 mg IV = Hydromorphone 1 mg IV • Patient is on Morphine ER 90mg BID (OME 180mg) • How much IV Hydromorphone in a day? • ( 180mg / 3 then 60 mg / 5 =) 12mg IV / 24hrs
    • 53. MORPHINE PO  HYDROMORPHONE IV Morphine 15 mg PO = Morphine 5 mg IV = Hydromorphone 1 mg IV • Patient is getting 8mg IV Morphine hourly PRN without relief • What is this equal to in Hydromorphone IV? • ( 8 mg / 5 =) 1.6 mg
    • 54. INTERVAL SUMMARY Understanding the way these medications enter and leave the body can help you safely and effective treat pain. Always have someone independently check your work when changing medications.
    • 55. SARAH, 43 YO • Metastatic colorectal CA • Sacral plexus destruction • Multiple opioid trials • Pain 6 / 10 • Drowsiness • Confusion
    • 56. “TOTAL PAIN” Disease Mgmt EOL Worry Physical Pain Practical Spiritual Psych Social 58
    • 57. ADJUVANT THERAPIES • Pharmacological • Interventional Anesthesia • Non-pharmacological • Acupuncture • Biofeedback • TENS • Counseling • Integrative therapies
    • 58. ADJUVANT EVIDENCE • Therapies extrapolated from non-cancer pain • Few RCTs • Very few comparative trials
    • 59. GUIDING THERAPY • Diagnosis • Assessment • Efficacy • Safety / tolerability • Ease of use • Cost
    • 60. OPIOIDS • Nociceptive pain > neuropathic pain • First-line for mod to severe neuropathic pain • Titrate to effect or side-effect
    • 61. METHADONE • Long half-life • NOT first order kinetics • Experienced palliative care / pain experts • Coanalgesic: 2.5 – 5+ mg • Cost PO << parenteral
    • 62. GABAPENTINOIDS • Sodium channel antagonist • Positive RCT‟s • NNT less favorable than TCAs • First-line 2º safety
    • 63. GABAPENTINOIDS… • Trial gabapentin •Start 100-300 mg qhs •Daily, increase 100 mg q8h •Effective 900 - 1800 mg / 24 hr •Max 3600 - 5400 mg / 24 hr • If ineffective, pregabalin •Start 25-75 mg q12h •Increase 25 mg q12h •Effective 100-150 mg / 24 hr •Max 300 - 600 mg / 24 hr
    • 64. ANTIDEPRESSANTS • 3º amine TCAs (amitriptyline) • 2º amine TCAs (desipramine, nortriptyline) • Mixed SNRIs (duloxetine, venlafaxine) • SSRIs (citalopram, paroxetine)
    • 65. OTHER ANTICONVULSANTS •  excitation • Limited data, trial-anderror • Newer drugs have better safety profiles
    • 66. CORTICOSTEROIDS • Limited data, widely used in • Bone pain • Neuropathic pain • Lymphedema • Other conditions • Dexamethasone • Start high dose 8+ mg daily • Taper to lowest effective dose
    • 67. OTHER OPTIONS • Lidocaine (IV or SC) • Sodium channel blockade • Good evidence • Ketamine (PO, IV, SC) • NMDA blocker • Dose-limiting psychological effects
    • 68. SARAH, 43 YO, CA COLON • Touch • Simplify meds ( ! ) • Address total suffering • Feb 14…Pain 6 / 10
    • 69. INTERVAL SUMMARY Sometimes the best long-acting medicine for a patient may not be an opioid. Poor opiateresponsiveness is a sign that multimodal therapies may be necessary to achieve pain relief.
    • 70. CLARIFYING ADDICTION
    • 71. TOLERANCE • Reduced effectiveness over time • Not clinically significant with chronic dosing • Suspect disease progression
    • 72. PHYSICAL DEPENDENCE • Process of neuro-adaptation • Abrupt cessation withdrawal • Titrate down if stopping • Avoid antagonists
    • 73. DRUG DIVERSION • Regulation • Record keeping • Accountability
    • 74. PSEUDO-ADDICTION • Most common cause of apparent drug „ failure ‟ is under-dosing • Behavior LOOKS like drug seeking
    • 75. ADDICTION: CHARACTERISTICS • Psychological dependence • Compulsive use • Loss of control over drugs • Loss of interest in pleasurable activities
    • 76. ADDICTION: HALLMARK • Continued use of drugs in spite of harm • Rare outcome of pain management
    • 77. SUBSTANCE USERS • Can have pain too • Treat with compassion • Consultation with pain or addiction specialists
    • 78. INTERVAL SUMMARY True addiction is rare in the management of pain and pain can occur in those with a history of substance use.
    • 79. SUMMARY • Pain may be nociceptive, neuropathic or both and the history tells you which. • A standardized approach to the assessment of pain helps prevent miscommunication. • For constant pain, dose on the half-life (q4hrs). For breakthrough pain, dose on the Cmax (routedependent). • True addiction is uncommon in pain management. 81
    • 80. THE INS AND OUTS OF PAIN Kyle P. Edmonds, MD Faculty, UCSD Division of Palliative Medicine 928.853.1483 Kyle.p.edmonds@gmail.com Kylepedmonds.com

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