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When Pain Becomes a Disease Than a Symptom! Dr R Jayamaha MBBS(Col), MD(SL), FIPP(USA) Consultant Physician Special Interest in Interventional Pain Practice.

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Presentation on theme: "When Pain Becomes a Disease Than a Symptom! Dr R Jayamaha MBBS(Col), MD(SL), FIPP(USA) Consultant Physician Special Interest in Interventional Pain Practice."— Presentation transcript:

1 When Pain Becomes a Disease Than a Symptom! Dr R Jayamaha MBBS(Col), MD(SL), FIPP(USA) Consultant Physician Special Interest in Interventional Pain Practice Teaching Hospital, Kandy

2 History of Pain… Pain; Gods Punishment? In 1591 Eufan MacAyane of Edinburgh, a young mother, was dragged from her home and taken away. Her pleas for mercy were ignored, and she was thrown into a pit and buried alive.

3 So What Was Her Crime? She had just given birth to twin sons and during her difficult labor she had asked for pain relief. The church’s teachings of the day regarded the pain of childbirth as a punishment justly inflicted by God!

4 The concept that pain is a visitation from a just God dates at least from the earliest days of Christianity Genesis 3:16

5 It may be even older….. Among Egyptian papyri from as much as 4500 years ago there are clear descriptions of what would have been painful surgical procedures. Although certain herbs were available at that time, that could relieve pain, and were discussed in other papyri, the surgical descriptions themselves make no mention of them.

6 By A.D. 150 to A.D. 200 a few Greek and Roman surgeons were giving herbs that not only relieved pain but also put the patient to sleep, thereby approaching the capabilities of modern anesthetists. In fact Dioscorides, a Greek army surgeon who was first to use the term Anesthesia

7 But these isolated measures did not spread in Christian Europe In later centuries Muslim physicians did begin to use various herbs for the relief of pain, soaking a sponge in the appropriate herbs to be inhaled by the patient known as soporific sponges. They were introduced in Christian Europe by monks between the fourteenth and seventeenth centuries.

8 So…. What is Pain?

9 By Definition Pain is… “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage, or both.” International Association for the Study of Pain ( IASP:2001)

10 Pain is what the patient says it is! Never deny patients symptoms for “?FUNCTIONAL ILLNESS”

11 PAIN Biological Psychological Social

12 Classification Aetiological –Nociceptive pain Is pain from pain receptor stimulation. It may be somatic pain from activation of receptors in the musculoskeletal system or visceral pain which arises from receptors in the viscera. –Neuropathic pain Is due to changes in the peripheral or central nervous system. –Idiopathic pain? Is pain without a known cause, and is not a diagnosis of psychogenic pain. Chronological –Acute (<3months) A response to injury or illness Time limited Usually responsive to treatment Inadequate treatment delays recovery –Chronic (>3months) A state in which pain persists beyond the usual course of an acute disease or healing of an injury, or that may or may not be associated with an acute or chronic pathologic process that causes continuous or intermittent pain over months or years

13 Types of Pain Acute Pain /Physiological Pain Nociceptive Symptom of a disease Treatment of diseases cures pain & it is self-limiting. Simple relationship between pain and tissue damage Proportionate to the clinical finding Chronic Pain /Pathological Pain Mostly Neuropathic A disease itself (a disease of nervous system). Difficult to treat & sustaining. Dissociated relationship between pain and tissue damage Disproportionate to the clinical finding

14 PAIN: an Alarm? True for Acute Pain which is an ALARM. Chronic Pain is a false alarm; it is a disease.

15 Acute Pain (Nociceptive) Chronic Pain (Neuropathic) without ongoing tissue damage (Nociceptive) Pain Chronic Pain (Neuropathic) with ongoing tissue damage (Nociceptive) - Mixed

16 Why Bother So Much? In US………….  It is estimated that approximately 1/3 of the population suffers from chronic pain and up to 9% of adults suffer from moderate to severe non-cancer related chronic pain (American Pain Society [APS], 2002).  In addition, chronic pain is estimated to affect 15% to 20% of children (Goodman & McGrath, 1991).

17 Pain – 76.2 million people, National Centers for Health Statistics Diabetes – 20.8 million people (diagnosed and estimated undiagnosed), American Diabetes Association Coronary Heart Disease (including heart attack and chest pain) and Stroke – 18.7 million people, American Heart Association Cancer – 1.4 million people, American Cancer Society

18 Statistics on Duration Adults 20 years of age and over who reported having pain said that it lasted: –Less than one month – 32% –One to three months – 12% –Three months to one year – 14% –Longer than one year – 42% The suicide rate among pain patients is almost 20 times greater than all other patients because of inadequate relief.

19 Inadequate Pain Treatment Can Lead To… Lost productivity Excessive healthcare expenditures Needless suffering Domestic and occupational problems Increased thoughts and risk of suicideIncreased thoughts and risk of suicide (American Pain Society, 2001: National Conference of State Legislatures, 1999) The economic burden of chronic pain as high as $100 billion annually in US

20 How is pain processed? Pain results from a series of exchanges among three major components of your nervous system: –Nociceptors / Peripheral nerves (transduction/ transmission) –Spinal cord (+Modulation/neuroplasty) –Brain (Perception/reorganization)

21 Nociceptors Most concentrated in areas prone to injury Such as fingers and toes. When nociceptors detect a harmful stimulus They generate a pain message in the form of an electrical impulse along a peripheral nerve to your spinal cord and brain. They can be epicritic (A-δ/ Fast) or protopathic (C- Slow) pains.

22 Spinal cord Nerve fibers that transmit pain messages enter the spinal cord in an area called the dorsal horn. There, they release chemicals (neurotransmitters) that activate other nerve cells in the spinal cord, which process the information and then transmit it up to the brain.

23 Gate-Control Theory: Ronald Melzack (1960s) Described physiological mechanism by which psychological factors can affect the experience of pain. Neural gate can open and close thereby modulating pain. Gate is located in the spinal cord.

24 Gate-Control Theory Brain Spinal Cord Gating Mechanism Transmission Cells From pain fibers From other Peripheral fibers To brain Brain Spinal Cord Gating Mechanism Transmission Cells From pain fibers From other Peripheral fibers To brain Gate is openGate is closed

25 Three Factors Involved in Opening and Closing the Gate The amount of activity in the pain fibers. The amount of activity in other peripheral fibers Messages that descend from the brain.

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27 The Brain When messages travel up the spinal cord, it arrives at the thalamus –a sorting and switching station deep inside your brain. The thalamus forwards this message simultaneously to three specialized regions of the brain: –Somatosensory cortex - the physical sensation region –Limbic system - the emotional feeling region –Frontal cortex - the thinking region The brain then responds to pain by sending down messages which moderate the pain in the spinal cord.

28 What is Sensitization? Sensitization is a phenomenon of inappropriate or disproportionate response to normal stimulus Peripheral Sensitization Central Sensitization

29 Peripheral sensitization Sensitization of primary afferent terminals. Active nociceptors become sensitized and sleeping nociceptors awaken. Damaged axons sprout, forms collaterals. Ectopic discharges along nerve axon, terminals & at DRG. SNS fibers invade DRG- CRPS Phenotypic switch in expression of neuropeptides like Sub P, CGRP.

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31 Central Sensitization Central Re-organisation. Wind up (summation of signals) Up-regulation of NMDA receptor Ectopic activity Depression inhibitory synapses Activation of WDR cells.

32 Results of Sensitization 1.Increased intensity of pain. 2.Increased area of pain. 3.Increased duration of pain. 4.Allodynia 5.Decreased tolerability to pain. 6.Development of psychological problems (e.g.. depression due to decreased serotonin level). 7.Pain become non-responsive to conventional analgesics. PainSensitization Decreased tolerance

33 Symptoms of chronic pain Pain in the area of neuro-deficit. Allodynia, Hyperalgesia Character of pain: Burning, shooting, electric shock-like, stabbing pain. Associated symptoms: Numbness, tingling, pruritus, feeling of pin & needles. SMP: redness, edema, painful joint movements, decreased skin temperature, fall of hairs.

34 Consequences of Unrelieved Pain Cardiovascular Hypercoagulability Increased heart rate, blood pressure Increased cardiac workload Increased oxygen demand Increased risk of myocardial infarction

35 Consequences of Unrelieved Pain Respiratory Diminished respiratory function Decreased alveolar ventilation Pneumonia Atelectasis Pulmonary embolism Hypoxia Slowed wound healing

36 Consequences of Unrelieved Pain Gastrointestinal Delayed gastric emptying Decreased motility Illus Anorexia/weight loss

37 Consequences of Unrelieved Pain Musculoskeletal Muscle spasm Impaired muscle function Decreased mobility Decreased ability to ambulate Diminished short- and long-term recovery & rehab

38 Consequences of Unrelieved Pain Cognitive Mental status changes Confusion Sleep disturbance Depression Behavior disturbances Anxiety Anhedonia

39 Consequences of Unrelieved Pain Personal Inability to perform ADL’s/loss of independence Impaired relationships with family/friends Impaired intimacy/sexual activity Social Isolation Anger Loss of self-esteem

40 Pain Assessment Type of Pain & Aetiology Severity of Pain Disability (Physical/ Psychological) Treatment in Progress

41 Pain Assessment Pain Scales No one will treat hypertension without BP measurement BUT everyone tends to treat without measuring it…..

42 Treatment of ( Mainly Chronic) Pain: MUTIMODAL APPROACH

43 Treatment Strategies 1.Eliminate barriers to effective pain management 2.Clarifying controversial issues in pain management 3.Non-medicinal treatment methods 4.Appropriate medications for pain relief 5.Interventional pain management

44 1.Barriers to Effective Pain Management Care ProvidersCare Providers: Inadequate knowledge re: pain and its management, fear of side effects, fear of regulatory retributions PatientsPatients: Exaggerated fear of addiction, belief that pain is normal/inevitable part of aging Health Care SystemHealth Care System: dissuades opioid use, under- utilization of pain specialists due to insufficient knowledge of benefit

45 Treatment Strategies 1.Eliminate barriers to effective pain management 2.Clarifying controversial issues in pain management 3.Appropriate medications for pain relief 4.Non-medicinal treatment methods 5.Interventional pain management

46 2.Controversial Issues in Pain Management Addiction Primary, chronic, neurobiologic disease, characterized by a persistent pattern of dysfunctional opioid use with Preoccupation with obtaining opioids despite adequate analgesia Pseudo-addiction A set of behaviors a person exhibits to obtain adequate pain relief like becomes focused on obtaining meds, clock watching, may seem to be “drug seeking”, may resort to doctor shopping, deception, to obtain adequate relief. Behaviors resolve when pain treated effectively Dependence A state of adaptation manifested by a specific drug class withdrawal syndrome produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist. Tolerance A state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time. Tolerance may develop with opioid side effects (e.g. respiratory depression, drowsiness). Exceeding tolerance can be fatal.

47 “Controlled substances have legitimate clinical usefulness and the prescriber should not hesitate to consider prescribing them when they are indicated for the comfort and well being of the patient.” D.E.A. Physician’s Manual

48 Treatment Strategies 1.Eliminate barriers to effective pain management 2.Clarifying controversial issues in pain management 3.Appropriate Non-Medical & medications for pain relief 4.Interventional pain management

49 Acute Pain (Nociceptive) Chronic Pain (Neuropathic) without ongoing tissue damage (Nociceptive) Pain Chronic Pain (Neuropathic) with ongoing tissue damage (Nociceptive) - Mixed

50 Treatment of Acute Pain Source + Pain Control Non Pharmacological methods NSAIDs for a very short period Paracetamol in adequate doses Tramadol + Paracetamol in adequate doses Regional analgesia Treatment of Chronic Pain with Tissue Damage Source + Pain Control + Correcting neuropathy/ central sensitization Treatment of Chronic Pain Without Tissue Damage Correcting neuropathy/ central sensitization Treatment for peripheral sensitization Na-Channel blocker, Ca-Channel blocker Treatment for central sensitization NMDA antagonist, Ca-Channel blocker, Opioids, drugs inhibiting Sub P, drugs enhances inhibitory synapses. Restoration of descending inhibitory pathways Tramadol OR Tricyclics Aims of Medical Treatment

51 Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery? Surgical Destruction of Neuro-pathways Treatment of Pain Missing link Between Med & Sx Mx

52 Diet (e.g.. Migraine) Exercise Biofeedback/relaxation training Acupuncture Consistent sleep/wake cycles Non Pharmacological

53 Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery? Operation Treatment of Pain

54 NSAIDs are the most widely prescribed drugs for the treatment of acute and chronic pain, which account for about 6 to 7 billion dollars P.A in sales worldwide.

55 Appears to be more involved than previously thought peripheral action only. Multiple isoforms of cyclooxygenase

56 NSAIDs: Mechanism of Action Inhibits cyclooxygenase- prevents sensitization of peripheral Nociceptors by diminishing PG formation- most commonly stated. Cellular effects unrelated to PGs-inhibits release of inflammatory mediators from neutrophils & macrophages. Also produces analgesia through CNS mechanism- by reversing inhibition by PGs of opioid-mediated pain modulation

57 I- Aspirin- irreversible inhibition of both COX-1 & COX-2. II- Ibuprofen-reversible competitive inhibition of both isoforms. III-Flurbiprofen-slower time dependent inhibition of both isoforms. Also enhances NO production in gastric mucosa IV-Celecoxib- largely COX-2 selective COX selectivty- 4 classesCOX selectivty- 4 classes

58 Gastrointestinal effects. Cardiovascular effects. Renal toxicity Renal impairment in 18%, ARF in 6% using NSAIDs. Clinically significant in patients with Heart failure, Renal insufficiency & Liver disease Hepatic toxicity. Liver related side effects reported in 3% users. Sulinduc creates higher risk of hepatic damage, although mild& reversible. Diclofenac with fulminant hepatitis reported Allergy and hypersensitivity. Hematologic effects. Aspirin inhibits platelet activation irreversibly- takes 7-10 days to recover. Non-aspirin NSAIDs include reversible platelet inhibition – resolves when drug is eliminated Most NSAIDs potentiate anticoagulant activity of warfarin. CNS effects. Toxicity

59 Age > 50 yearsAge > 50 years Past history of peptic ulcerPast history of peptic ulcer Steroid useSteroid use Alcohol useAlcohol use Multiple NSAIDs useMultiple NSAIDs use First 3 months of useFirst 3 months of use NSAIDs- GI toxicity Risk The ARAMIS model for estimating risk of Gastric ulceration while taking nonselective NSAIDs. A score > 1.5 is considered high risk and a contraindication for the use of nonselective NSAIDs. The scale is for chronic use over a 12 month period. Step 1 Start at a score of 0 Step 2 Add 0.3 for every 5 y of patient’s age over 50 y Step 3 Add 1.2 if the pt is receiving a corticosteroid Step 4 Add 1.4 if the pt has reported a previous NSAID- related GI side-effects Step 5 Add 0.5 if the pt has sustained disability

60 Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery Operation Treatment of Pain

61 OPIOIDS CLASSIFICATION NATURAL Morphine. Codiene. Theibene. SEMISYNTHETIC Pethidine. Oxycodone. SYNTHETIC Fentanyl. PURE AGONIST Morphine. Fentanyl. PARTIAL AGONIST Buprenorphine. AGONIST- ANTAGONIST Nalbuphine. ANTAGONIST Naloxone Naltrexone. Mu Analgesia Respiratory depression. Nausea, Vomiting. Kappa Hallucination. Delta Spinal Analgesia. Endogenous Endorphines Enkephalines Dynorphines

62 Codeine About 1/10th the potency of morphine lower efficacy than morphine about 10% converted to morphine by CYP450 2D6 10% of patients do not possess this enzyme

63 Tramadol Opioid receptor agonist (mu and delta) NE and 5-HT reuptake blocker (antidepressant) α-2 adrenoceptor agonist These actions are synergistic for analgesia

64 Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery Operation Treatment of Pain

65 Anticonvulsants Traditionally used for neuropathic pain-carbamazepine and phenytoin. Newer agents- gabapentin, pregabalin, lamotrigine. Gabapentin and carbamazepine- are more evidence based. Pregabalin and lamotrigine- no systematic review or meta-analysis of trials available at present. Pregabalin – higher doses(300 to 600 mg/day) produces more consistent results than lower doses(75 to 150 mg/day). Complications: sedation-somnolence, fatigue, dry mouth etc. Antidepressants Also traditionally used for neuropathic pain. TCAs may be most effective classes of drugs. Amitriptyline – NNT=2, desipramine-NNT=2.1 Not effective in HIV-related neuropathies. Other Rx Lidocaine and mexiletine are equivalent to morphine, gabapentin, TCAs. Lidocaine IV up to 5mg/kg over 3 to 45 min. Mexiletine 100 to 200mg three times per day(upto 675mg TID reported). Lidocaine 5% transdermal also effective  2-adrenergic receptor agonist- clonidine NMDA receptor antagonist (Ketamine..) capsaicin

66 Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery Operation Treatment of Pain

67 End of Pharmacotherapy ??? *finally, there is some evidence for a variety of (new) drugs

68 Non- opioids Weak opioids +/- non- opioids Strong opioids Recovery Operation Treatment of Pain World of Misery Non-pharmacological methods

69 Treatment Strategies 1.Eliminate barriers to effective pain management 2.Clarifying controversial issues in pain management 3.Appropriate medications for pain relief 4.Non-medicinal treatment methods 5.Interventional pain management (IPM)

70 Non- opioids Weak opioids +/- non- opioids Strong opioids Recovery Operation Treatment of Pain Non-pharmacological methods

71 Interventional Pain Management are some minimally invasive procedures done under image guidance which gives permanent/long term pain relief by stopping nociceptive inputs or correcting neuropathy. It fills the gap between pharmacologic management of pain & more invasive operative procedure. (The missing link)

72 Interventional Pain Management John Bonica ‘The Godfather ‘of Interventionalism Norman Harden Center for Pain Studies Rehabilitation Institute, Chicago Northwestern University

73 The Evidence

74 few RCTs of Interventions in Pain…so far! Randomization Ethics Control ? Blinding Impossible ? Economic Referral Bias What outcome?

75 Flavors of interventions: Injections (squirt) – Local/Spinal/ ITDD Ablation (burn) – Cryo/RF Electro-stimulation (shock) – Peripheral / cord Stimulation Surgery (slash)

76 Pros & Cons Bridges the gapBridges the gap Targeted therapyTargeted therapy Invasive but Safe in Skilled handsInvasive but Safe in Skilled hands CostCost Patient/Procedure selectionPatient/Procedure selection

77 Scope for IPM….. Neuralgias e.g. Trigeminal Neuralgia, Post Herpetic neuralgia, Migrain/CH, IFP Chronic spinal Pain XDs e.g. Facet J. A, Discogenic Pain, FBSS Vertibroplasty Complex Regional Pain XD Cancer Pain

78 Most Important Consideration of IPM….. Correct Procedure on Correct patient.

79 Questionnaire…? wathupitiwala\Wathupitiwala.doc 1. Pleases select the type of your practice General Practitioner12% Specialist88% Other (please specify) 2. If you consider all pain syndromes… All can be treated successfully Many can be treated successfully56% Some can be treated successfully38% A few can be treated successfully6%

80 3. Why in your opinion some patients cannot be cured of pain? Wrong diagnosis34% Wrong / inadequate treatment (including not enough drug categories/ groups) 50% Late presentations 19% Pain has become a disease 37% There is a missing link between medical& surgical management of pain 35% Drug addicted patients 3% 4. Can you enumerate such difficult situations (mainly chronic pain condition) you came across and how did you manage get away with those (chronic) patients? a b c

81 5. If your patient has a chronic pain, If he/she is not a drug addict and if Psychiatric assessment is normal,…also if there is no medically or surgically correctable cause....what can you offer them? Ignore their complains and discharge from follow up9% Continue a cocktail of analgesics/adjuvant drugs27% Prescribe them anti-depressants anyway35% Continuously investigating them for a cause35% Other (please specify) 6. What are the various modalities of pain treatment available except treating underlying condition, specifically for chronic pain conditions? TENS (transcutaneous electrical nerve stimulation) therapy 56% Meditation65% Relaxation / Distraction techniques 65% Visual imagery, as simple as picturing a peaceful scene, for example 37% Biofeedback, which teaches control over muscle tension, temperature, heart rate and more 53% Heat, cold or irritant application 65% Manipulation and massage 60% Surgically destroying pain pathways60% Other (please specify) 22%

82 7. If your patient is not benefiting all these and not consenting or not a candidate for surgery…is there a possible escape route? Yes69% If "Yes" what would be that possible modality??? No31%

83 Thanks


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