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CHRONIC PAIN MANAGEMENT

CHRONIC PAIN MANAGEMENT

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CHRONIC PAIN MANAGEMENT

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  1. CHRONIC PAIN MANAGEMENT PRESENTED BY: Dr CHITTRA MODERATED BY: Dr GIAN CHAUHAN

  2. DEFINITION • IASP defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” • pain is always subjective and it is a sensation in part of the body, is unpleasant and also has an emotional component • If patients regard their experience as pain or if they report it in the same way as pain caused by tissue damage, it should be accepted as pain • ASA defines chronic pain as “pain of any etiology not directly related to neoplastic involvement, associated with chronic medical condition or extending in duration beyond the expected temporal boundary of tissue injury and normal healing, and adversely affecting the function or well-being of individual” • IASP defines it as “pain without apparent biological value that has persisted beyond the normal tissue healing time usually taken to be 3 months”

  3. PREVALENCE • 20% to 60% • higher prevalence in women and the elderly CLASSIFICATION Malignant nonmalignant inflammatory musculoskeletal neuropathic (arthritic) (low back pain) post herpetic phantom limb CRPS diabetic headaches visceral

  4. BIOPHYSICAL CONCEPT • Chronic pain patients have in common complex influences of biologic, cognitive , emotional , and environmental factors • patients have limited mobility, lack of motivation, depression, anger, anxiety, and fear of reinjury, these hamper return to normal work or recreational activities • may become preoccupied with pain and somatic processes, which disrupt sleep ,cause irritability and social withdrawal • The interplay between these biologic, psychological, and social factors results in persistence of pain and illness behavior • Management of pain addresses physical, psychological, and social skills and underscores patients' active responsibility to regain control over life by improving function and well-being

  5. PATHWAY OF CHRONIC PAIN

  6. CHRONICITY Repeated nociceptor stimulation sensitize both peripheral and central neurons (activity-dependent plasticity) progressive increase in output in response to persistent nociceptor excitation is known as“wind-up sustained by transcriptional changes in the expression of genes coding for various neuropeptides, transmitters, ion channels, receptors, and signaling molecules in both nociceptors and spinal neurons physical rearrangement of neuronal circuits by apoptosis, nerve growth, and sprouting occurs in the peripheral and central nervous systems

  7. PATIENT EVALUATIONHISTORY • Mode of onset • site • chronicity and duration • character and severity(visc pain- dull aching, neuralgic pain – stabbing, myofascial pain) • investigations, operations, drugs,treatments done • associated factors ( premonitory symptoms,pptfactors,environmental factors, family history,pat medical and surgicl history, psychiatry history, medications drugs ,alcohol abuse, kinesiophobia

  8. PHYSICAL EVALUATION GPE (Skin lesions, jt deformities etc) PAIN RELATED BEHAVIOUR (facial expression, emotional) SYSTEMIC EXAMINATION NEUROLOGICAL EXAMINATION cranial nerve fxn msc strength grading DTR Sensation musculoskeletal system

  9. CRANIAL NERVE EXAMINATION OLFACTORY: • Familiar odors, individual nares OPTIC: • Vision, fundus, fields of vision OCULOMOTOR,TROCHLEAR,ABDUCENS • ptosis, light response, nystagmus, fields of gaze, asymmetric extraocular movements TRIGEMINAL NERVE • jaw msc strength • superficial pain and touch senation in each branch

  10. The ophthalmic, maxillary, and mandibular nerves provide sensation to the eye and forehead, midface and upper jaw, and lower jaw, respectively

  11. FACIAL Corneal reflex, symmetry ACOUSTIC Sense of hearing, bone and air conduction GLOSSOPHARYNGEAL Gag reflex, ability to swallow VAGUS Palate and uvula inspection, nasal twang SPINAL ACCESSORY Trapezius and SCM strength HYPOGLOSSAL Tongue inspection and strength

  12. MOTOR SYSTEM

  13. DTR SCALE

  14. SENSORY SYSTEM Pain,touch,temperature vibration ,proprioception

  15. MUSCULOSKELETAL SYSTEM Inspection Palpation Movement Range of motion

  16. SPECIFIC TESTS SLRT Spinal flexibility Tinel’s test Phalen’s test Adson’s test

  17. PAIN MEASUREMENT AND ASSESSMENT CATEGORY SCALE RUPEE ANALOG SCALE NUMERICAL RATING SCALE VISUAL ANALOG SCALE DESCRIPTOR DIFFERENTIAL SCALE

  18. ASSESSING PAIN IN PRE-SCHOOLERS THE OUCHERS SCALE HAPPY-SAD FACE SCALES COLOR ANALOG SCALE POKER CHIP TOOL LADDER SCALE LINEAR ANALOGUE SCALE

  19. RADIOGRAPHY AND IMAGING OPERATING ROOM FLUOROSCOPY: Anterior elements Posterior elements Space components Procedures performed: Caudal epidural steroids/catheter placement Celiac plexus block Hypogastric plexus block Sympathetic plexus block Trigeminal ganglion block Stellate ganglion block Transforaminal steroid injection

  20. EPIDUROGRAPHY Opacification of epidural space with aqueous contrast medium SPINAL ENDOSCOPY Percutaneous minimally invasive endoscopic investigation of epidural space to enable color visualisation anatomical structures inside the spinal canal Direct drug application Direct lysis of scarring Placement of catheter and electrode system

  21. CT Trauma Abscess Neoplasm Metastasis LAP Superior bone detail MRI More contrast resolution Better soft tissue detail

  22. BONE SCAN Imaging of entire skeleton Early detection of abnormal areas Metastaic disease CRPS Joint diseases

  23. MULTIMODAL MODALITY • facilities to evaluate and treat biomedical, psychosocial, and occupational aspects • Pain physician, psychologist, physical therapist, and occupational therapist SINGLE MODALITY MANAGEMENT • used as part of multimodal management

  24. TREATMENT OPTIONS pharmacologic management ablative techniques acupuncture blocks (i.e., joint and nerve or nerve root) botulinum toxin injections electrical nerve stimulation epidural steroids with or without local anesthetics intrathecal drug therapies minimally invasive spinal procedures physical or restorative therapy psychologic treatment trigger point injections

  25. PHARMACOLOGIC MANAGEMENT NSAIDs opioid therapy Serotonergic drugs anticonvulsants anti-depressants benzodiazepines NMDA receptor antagonists skeletal muscle relaxants topical agents

  26. NSAIDS • NSAIDs inhibit COXs • COX-1 and COX-2, are constitutively expressed in peripheral tissues and in central nervous system • By blocking one or both enzymes prostaglandin formation diminishes • Less severe pain states ( early arthritis, headache,backache) are commonly treated with nonselective NSAIDs or antipyretic analgesics mostly used orally • ↓Sensitization of sensory neurons,↑ Inhibition of spinal neurons • COX-2 expression is constitutive in many tissues, gastrointestinal epithelium, vascular endothelium, spinal cord and inhibition of COX-2 may exacerbate inflammation, impair ulcer healing • Selective COX-2 inhibitors confer an increased risk for thrombosis, myocardial infarction, renal impairment, hypertension, stroke, and liver toxicity

  27. OPIOIDS ASA RECOMMENDS: • controlled or extended release opioid therapy provides effective pain relief for patients with low back pain or neuropathic pain for assessment periods ranging from 1 to 9 weeks, with nausea or vomiting and constipation as side effects • Tramadol provides effective pain relief for assessment periods ranging from 4 to 6 weeks • immediate release opioids, transdermalopioids, and sublingual opioids provide relief for back, neck, leg, and neuropathic pain for assessment periods ranging from 2 weeks to 3 months • Dizziness, somnolence, and pruritus are among reported side effects associated with opioid therapy

  28. All three receptors (µ, δ, κ) mediate analgesia, but with differing side effects • Tolerance and physical dependence may occur with prolonged administration of pure agonists, and abrupt discontinuation or administration of an antagonist can result in withdrawal syndrome • Proposed mechanisms involved in pharmacodynamic tolerance include opioid receptor–G protein uncoupling, decreased receptor internalization/recycling, and increased sensitivity of the NMDA receptor • Increased nociceptive stimulation by tumor growth, inflammation, or neuroma formation are possible reasons for increased dose requirements

  29. Opioids are effective in periphery ,at neuraxis and systemically • Systemically and spinally administered opioids can produce similar side effects, depending on the dosage and rostral/systemic redistribution • most effective drugs for severe acute and cancer-related chronic pain • prevalence of addiction is as high as 50% in patients treated with opioids for chronic nonmalignant pain • Thus, consistent with the multifactorial nature of chronic pain, it is highly questionable whether opioids alone can produce an analgesic response • Thus, the use of opioids as a sole treatment modality in chronic nonmalignant pain is not recommended

  30. SEROTONERGIC DRUGS • monoamine neurotransmitter found in sympathetic nervous system, gastrointestinal tract, and in platelets • Within the dorsal horn of the spinal cord, serotonergicneurons contribute to endogenous pain inhibition • 5-HT1B/1D agonists are effective against neurovascular headaches • Triptans inhibit neurogenic inflammation via 5-HT1D receptors on trigeminal afferents, with additional sites of action on thalamic neurons and in the periaqueductal gray matter • Activation of vascular 5-HT1B receptors constricts meningeal and coronary vessels • Triptans can be applied orally, subcutaneously, or transnasally and have been used for the treatment of migraine • All triptans narrow coronary arteries via 5-HT1B receptors by up to 20% at clinical doses and should not be administered to patients with risk factors or coronary, cerebrovascular, or peripheral vascular disease

  31. ANTIEPILEPTIC DRUGS • used for treatment of neuropathic pain resulting from lesions to peripheral or central nervous system • cause may beectopic activity in sensitized nociceptors from regenerating nerve sprouts, recruitment of previously “silent” nociceptors, or spontaneous neuronal activity • increased expression and trafficking of ion channels (e.g., Na+, Ca2+, TRP) and increased activity at glutamate receptor sites • stabilization of neuronal membrane by blockage of pathologically active voltage-sensitive Na+ channels (carbamazepine, phenytoin, lamotrigine, topiramate), blockage of voltage-dependent Ca2+ channels (gabapentin, pregabalin), inhibition of presynaptic release of excitatory neurotransmitters (gabapentin, lamotrigine), and enhancement of the activity of GABA receptors (topiramate) • Their most common adverse effects are impaired mental and motor function which limit their clinical use, particularly in elderly patients • Serious side effects have been reported, including hepatotoxicity, thrombocytopenia, and life-threatening dermatologic and hematologic reactions

  32. Carbamazapine: • first line treatment for trigeminal neuralgia • used in acute onset PDN, post herpetic,central pain, phantom limb, neural invasion by tumor,radiation fibrosis • monitor CBC, LFT, every 3 mnths • 100mg bd/day ↑by 100 mgbd-tds weekly to 600-800mg/day OXCARBAZEPINE: • 300mg hs weekly↑ 300mg/day max 1200mg/day

  33. GABAPENTIN • First choice for neuropathic pain in eldrly, PDN, post herpetic neuralgia and radiculopathy • 300mg hs-↑1st week to 300mg bd, ↑3rd week to 300mg tds-↑ max of 1200-1600mg/d • effect starts in 3 or 4 days and pain relief in 2 weeks • dizziness, seadtion, nausea, rashes PREGABALIN

  34. ASA recommends: • delta calcium-channel antagonists provide effective neuropathic pain relief for assessment periods ranging from 5 to 12 weeks • a meta-analysis found that sodium-channel antagonists provide effective pain relief for assessment periods ranging from 2 to 18 weeks

  35. ANTIDEPRESSANTS • used for treatment of neuropathic pain – post herpetic, PDN- tension headache migraine,atypical facial pain- 1st line of treatment • nonselective norepinephrine/5-HT reuptake inhibitors (amitriptyline, imipramine, clomipramine, venlafaxine), preferential norepinephrine reuptake inhibitors (desipramine, nortriptyline), and selective 5-HT reuptake inhibitors (citalopram, paroxetine, fluoxetine) • The reuptake blockade leads to stimulation of endogenous monoaminergic pain inhibition in the spinal cord and brain • In addition, tricyclic antidepressants have NMDA receptor antagonist, endogenous opioid–enhancing, Na+ channel–blocking, and K+ channel–opening effects that can suppress peripheral and central sensitization • require monitoring of plasma drug concentrations to achieve optimal effect and avoid toxicity, unless sufficient pain relief is obtained with low doses • Patients with ischemic heart disease may have an increased risk for sudden arrhythmia, and patients with recent myocardial infarction, arrhythmia, or cardiac decompensation should not take tricyclic antidepressants at all • Adverse events include sedation, nausea, dry mouth, constipation, dizziness, sleep disturbance, and blurred vision

  36. amitryptilline • 10mg/d hs-inc 25mg/d after 1 wk, 2-3 wks inc 50mg/d- max 75mg/day ASA recommends: • tricyclic antidepressants provide effective pain relief for variety of chronic pain etiologies for assessment periods ranging from 2 to 8 weeks, with dry mouth and somnolence or sedation as reported side effects • selective serotonin–norepinephrine reuptake inhibitors provide effective pain relief for variety of chronic pain etiologies for assessment periods ranging from 3 to 6 months

  37. NMDA RECEPTOR ANTAGONISTS NMDA receptors involved in central sensitisation and wind up long term potentiation of pain ASA RECOMMENDS: • dextromethorphan and memantine are equivocal regarding pain relief for patients with diabetic neuropathy, postherpetic neuralgia, or other neuropathic pain conditions (phantom limb pain, peripheral nerve injury, and CRPS) • provide pain relief for neuropathic pain for assessment periods ranging from 2 to 16 weeks

  38. TOPICAL AGENTS • many chronic pain syndromes depend to some degree on peripheral activation of primary afferent neurons • Localized administration can potentially optimize drug concentrations at site of pain generation while avoiding high plasma levels, systemic side effects, drug interactions, and need to titrate doses into therapeutic range • Topical NSAIDs are effective for a limited period (2 weeks) for chronic musculoskeletal pain • Local adverse effects included rash and pruritus • topical tricyclic antidepressant (doxepin) has shown efficacy in mixed group of patients with neuropathic pain and, as a mouthwash, in patients with chemotherapy-induced oral mucositis

  39. Topically applied capsaicin interacts with nociceptive neurons via the vanilloid receptor (TRPV1) • after repeated application depletion of substance P in sensory neurons, direct neurotoxic effect that results in degeneration of small-diameter sensory nerve fibers • supplement for treatment of neuropathic pain in a small number of patients unresponsive to or intolerant of other therapeutic approaches

  40. Topical formulations of local anesthetics block Na+ channels in primary afferent neurons,reduces impulse generation in both normal and damaged sensory neurons • Such neurons exhibit spontaneous and ectopic firing, which possibly contributes to certain conditions of chronic neuropathic pain • pain relief can be achieved with local anesthetic concentrations below those that totally block conduction of impulses • lidocaine patches and gels showed pain reduction in patients with postherpetic neuralgia and allodynia • patients with painful diabetic polyneuropathy, CRPS, postmastectomy syndrome, or post-thoracotomy syndrome can achieve relief of pain

  41. Topically applied or locally injected opioids produce analgesia by activating opioid receptors on primary afferent neurons • upregulationand accelerated centrifugal transport of opioid receptors in sensory neurons and facilitation of access of opioid agonists to their receptors by disruption of the perineural barrier • Intra-articular morphine produces analgesia in chronic rheumatoid and osteoarthritis

  42. OTHER ANALGESICS • Baclofen activates GABAB receptors presynaptically and postsynaptically, leads to decrease in excitatory and an increase in inhibitory neurotransmission • trigeminal neuralgia and central neuropathic pain • side effects are drowsiness, dizziness, and gastrointestinal distress • Botulinum toxin is assumed to inhibit release of acetylcholine at neuromuscular junction ,alleviate muscle spasticity • Side effects include pain and erythema at the injection site and unintended paralysis of adjacent muscles

  43. THANKS