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KNOW YOUR PAIN 2015 CHRONIC PAINfinal2.pptx

The document discusses various aspects of pain management, particularly chronic pain and its classifications, emphasizing the complexities of diagnosis and treatment. It illustrates specific case studies demonstrating effective interventions like nerve blocks and pharmacotherapy for different types of pain, highlighting common misconceptions surrounding pain and its treatment. The document underscores the significance of comprehensive pain assessment and the psychosocial effects of living with chronic pain, advocating for a multi-faceted approach to effective management.

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KNOW PAIN PROGRAMME DR SANTOSH KUMAR SHARMA ASST PROF DEPT OF ANAESTHESIOLOGY, CCM & PAIN MEDICINE BRD MEDICAL COLLEGE GORAKHPUR
THE PROBLEM  75 yrs,female from maharajganj, rt sided trigeminal neuralgia for 5 yrs. Came to the OPD crying with sari’s pallu in her mouth. Had not eaten for 3 days. Pain relieved instantly by trigeminal block. She didn’t believe that her pain had gone. Came for follow up after 8 mts. (pic follows)  55 yrs, female from nepal, lt sided ca breast postoperative with ulcer on breast and motor weakness, lymphedema and severe burning pain of left upper limb for 1 yr. treated by stellate ganglion block 3 sittings. Had 40-50% pain relief. Lost to follow up after the earthquake in nepal (pic follows).  21 yrs,male from bansgaon, driver by occupation, with low back pain radiating to left leg upto the great toe for 2 months. SLR positive same side. Spectacular results with pharmacotherapy within a month time. No need for any intervention.
Pt with trigeminal neuralgia Pt with carcinoma breast
Pain is a more terrible lord of mankind than death itself.” Albert Schweitzer
Total care emotional spiritual physical social ‘‘Pain management continues to be the most difficult problem facing medicine today.’’ Jason R. Bauer and Charles E. Ray, Jr. WHY ………….?
MYTHS ABOUT PAIN  A symptom of a disease  It always comes with tissue damage  Always a friend, it warns us of our disease  It never kills  It is inevitable in many conditions and we need to accept it.  Extended rest and reduced activity is all that is needed to treat pain  Pain: "You should snap out of it. It's all in your head". If cause not identified, pain is functional and you need a psychiatric evaluation
MYTHS ABOUT PAIN SPECIALITY  Manage pain not the disease  Useful when no treatment is available  It has to be morphine or neurolysis  There has to be 100% pain relief (‘Techno-fix’)
DISCUSSION POINTS • What is pain? • Burden of chronic pain. • Newer concepts in pathophysiology of pain. • Diagnosis of chronic pain. • Newer concepts of analgesic therapy. • Newer drugs to manage pain. • Interventional Pain Management to diagnose & treat pain.
IASP Definition of Pain “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp- pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013.
PAIN ACUTE PAIN (NOCICEPTIVE) CHRONIC PAIN WITH TISSUE DAMAGE (NOCICEPTIVE + NEUROPATHIC) CHRONIC PAIN WITHOUT TISSUE DAMAGE (NEUROPATHIC)
CLASSIFICATION OF PAIN According to Pain duration  Acute pain: pain of less than 3 months duration  Chronic pain: pain lasting for more than 3 months, or persisting beyond the course of an acute disease, or after tissue healing is complete.  Acute-on-chronic pain: acute pain flare superimposed on underlying chronic pain
CLASSIFICATION OF PAIN According to pathology  Nociceptive: represents the normal response to noxious insult or injury of tissues such as skin, muscles, visceral organs, joints, tendons, or bones.  Somatic: musculoskeletal (joint pain, myofascial pain), cutaneous; often well localized  Visceral: hollow organs and smooth muscle; usually referred  Neuropathic: pain initiated or caused by a primary lesion or disease in the somatosensory nervous system.  Diabetic neuropathy  post herpetic neuralgia  spinal cord injury pain  phantom limb (post-amputation) pain  post-stroke central pain.
CLASSIFICATION OF PAIN According to pathology (contd)  Inflammatory: a result of activation and sensitization of the nociceptive pain pathway by a variety of mediators released at a site of tissue inflammation.  Appendicitis  Osteoarthritis  Rheumatoid arthritis  Central sensitization/dysfunctional pain: May be caused by persistent neuronal dysregulation or dysfunction  CRPS  Fibromyalgia
Inflammatory Pain Pain 2015: Towards a New Classification Nociceptive stimulus Physiological Pain Inflammatory lesion (OA, spondylitis, infection) Nerve lesion (diabetes, PHN, radiculopathy, trauma…) Neuropathic Pain Fibromyalgia IBS CRPS 1 Myofascial Pain Dysfunctional Pain
ACUTE Vs CHRONIC PAIN CHARACTERISTIC ACUTE PAIN CHRONIC PAIN Cause Generally known Often unknown Duration of pain Short, well-characterized Persists after healing, >3 months Treatment approach Resolution of underlying cause, usually self-limited Underlying cause and pain disorder; outcome is often pain control, not cure
Mixed Type Caused by a combination of both primary injury and secondary effects NOCICEPTIVE Vs NEUROPATHIC PAIN Nociceptive Pain Caused by activity in neural pathways in response to potentially tissue-damaging stimuli Neuropathic Pain Initiated or caused by primary lesion or dysfunction in the nervous system Postoperative pain Mechanical low back pain Sickle cell crisis Arthritis Postherpetic neuralgia Neuropathic low back pain CRPS* Sports/exercise injuries *Complex regional pain syndrome Central post- stroke pain Trigeminal neuralgia Distal polyneuropathy (eg, diabetic, HIV)
NOCICEPTIVE Vs NEUROPATHIC PAIN Serra J. In: Serra J (ed). Tratado del dolor neuropático. Panamericana; Madrid, Spain: 2006. Nociceptive Neuropathic Definition Pain caused by physiological activation of pain receptors Pain initiated or caused by a primary lesion or dysfunction in the peripheral or central nervous system Mechanism Natural physiological transduction Ectopic impulse generation, central sensitization, and others Localization Local + referred pain Confined to innervation territory of the lesioned nervous structure Quality of symptoms Ordinary painful sensation New strange sensations Treatment Good response (conventional analgesics) Poor response (conventional analgesics)
POSSIBLE DESCRIPTIONS OF NEUROPATHIC PAIN  Sensations  Numbness  Tingling  Burning  Paresthesia  Paroxysmal  Lancinating  Electric like  Raw skin  Shooting  Deep, dull ache  Signs/Symptoms  Allodynia: pain from a stimulus that does not normally evoke pain  Thermal  Mechanical  Hyperalgesia: exaggerated response to a normally painful stimulus
WHY SHOULD PAIN BE TREATED? CONSEQUENCES OF CHRONIC PAIN 1. Douglas C et al. J Neurosci Nurs 2008; 40(3):158-68; 2. Tang NKY et al. J Sleep Res 2007; 16(1):85-95; 3. Hawker GA et al. Osteoarth Cartil 2008; 16(4):415-22; 4. Munce SE et al. J Occup Environ Med 2007; 49(11):1206-1211; 5. Stewart WF et al. JAMA 2003; 290(18):2443-54; 6. Ritzwoller DP et al. BMC Musculoskelet Disord 2006; 7:72-81. Healthcare costs6 Presenteeism and absenteeism4,5 Disability4 Reduced social activities3 Disrupted daily routine3 Decreased quality of life3 Anxiety2 Depression2 Sleep disturbances2 Chronic pain1
DOMAINS OF CHRONIC PAIN Social Consequences  Marital/family relations  Intimacy/sexual activity  Social isolation Socioeconomic Consequences  Healthcare costs  Disability  Lost workdays Quality of Life  Physical functioning  Ability to perform activities of daily living  Work  Recreation Psychological Morbidity  Depression  Anxiety, anger  Sleep disturbances  Loss of self-esteem
WHY SHOULD PAIN BE TREATED? PAIN IS LINKED TO DEPRESSION Trivedi MH. Prim Care Companion J Clin Psychiatry 2004; 6(Suppl 1):12-6 Prevalence of pain in depressed patients is 15–100% Prevalence of major depressive disorder in patients with chronic pain is 15–50% • Depressive symptoms rather than major depressive disorder • Mostly musculoskeletal pain • Mostly in patients with multiple pain symptoms
CONSEQUENCES OF UNTREATED & UNDER TREATED ACUTE PAIN Extensive and Persistent cascade of neurochemical mediators triggered by tissue injury leads to a long-term, permanent, neurological change that can lead to SENSITIZATION ALLODYNIA HYPERALGESIA MAY evolve into chronic pain Person is less tolerant to pain, area & intensity of pain increases, character of pain changes, and psychological changes occur.
PHYSIOLOGY OF PAIN PERCEPTION  Transduction  Transmission  Modulation  Perception  Interpretation  Behavior Injury Descending Pathway Peripheral Nerve Dorsal Root Ganglion C-Fiber A-beta Fiber A-delta Fiber Ascending Pathways Dorsal Horn Brain Spinal Cord Adapted with permission from WebMD Scientific American® Medicine.
Central sensitization Peripheral sensitization CNS PNS CNS central nervous system “Healthy” nociceptors Normal transmission Central reorganization Abnormal nociceptors Physiologic state Nociceptive Pain Neuropathic Pain PNS peripheral nervous system Pathologic state Pappagallo M. 2001.
MECHANISMS OF PAIN: NEUROPLASTICITY HOW DOES A CHRONIC PAIN STATE DEVELOP?  Peripheral Sensitization - Injury causes release of “sensitizing soup” - Reduction in threshold and increase response of nocioceptors  Central Sensitization - Membrane excitability, synaptic recruitment and decreased inhibition - Uncoupling of pain from peripheral stimuli
SENSITIZATION IS A CONSTANT FEATURE OF CHRONIC PAIN PERIPHERAL SENSITIZATION  Up regulation of nociceptors  SNS connecting with somatic fibres (CROSS TALK)  Sprouting of damaged axons and ectopic discharge CENTRAL SENSITIZATION  Central reorganisation  Activation of the N- methyl-D-aspartate (NMDA) channel,  Increase in intracellular Ca2+,  Wind-up/wide dynamic range (WDR) neuron sensitization
INADEQUATE CHRONIC PAIN TREATMENT  Breivik et al., EJP 2006;10:287-333. Percentage of chronic pain suffers who reported that their pain is inadequately controlled in 16 countries
PREVALENCE OF CHRONIC PAIN Tsang A et al. J Pain 2006; 9(10):883-91.
PREVALENCE OF CHRONIC PAIN IN INDIA Dureja GP, Jain PN, Shetty N, Mandal SP, Prabhoo R, Joshi M, Goswami S, Natarajan KB, Iyer R, Tanna DD, Ghosh P, Saxena A, Kadhe G, Phansalkar AA. Prevalence of chronic pain, impact on daily life, and treatment practices in India. Pain Pract. 2014;14(2):E51-62.
5–20% OF THE GENERAL POPULATION MAY SUFFER FROM NEUROPATHIC PAIN Summary of Selected Prevalence Studies Adapted from: Bouhassira D et al. Pain 2008; 136(3):380-7; de Moraes Vieira EB et al. J Pain Symptom Manage 2012; 44(2):239-51; Elzahaf RA et al. Pain Pract 2013; 13(3):198-205; Johayon MM, Stingl C. Psychiatr Res 2012; 46(4):444-50; Torrance N et al. J Pain 2006;7(4):281-9; Toth C et al. Pain Med 2009; 10(5):918-29;
PAIN IS NOW THE 5TH VITAL SIGN (Adopted by the American Board for Hospital Accreditation) Lynch ME, et al. Pain Res Manage Vol 11 No 1 Spring 2006.
COMMON CAUSES OF CHRONIC PAIN 1. Chronic pain Neuropathic pain Cancer pain Headache Low back pain Musculoskeletal Pain Arthritis Pain RA, OA Psychogenic pain Metabolic Pain Osteomalacia Osteoporosis Gout
Common descriptors Shooting Electric shock-like Burning Tingling Numbness Post herpetic neuralgia Lumbar radicular pain Chronic post- surgical pain Post-stroke pain Diabetic peripheral neuropathy RECOGNIZING NEUROPATHIC PAIN
LOW BACK PAIN  FACET JOINT ARTHROPATHY (15- 45%)  INTERNAL DISC DISRUPTION (25 -40%)  SACRO ILIAC JOINT ARTHROPATHY (15 -30%)  DISC PROLAPSE/HERNIATED DISC/ SLIPPED DISC (2-5%)  CRPS/RSD (2 -8%)  OSTEOPOROTIC COMPRESSION FRACTURE (3-5%)  FIBROMYALGIA & MYOFASCIAL PAIN (2-5%)  SPINAL CANAL STENOSIS (2-3%)  SPONDYLOLYSTHESIS (2-3%)  TUMORS & INFECTION (<1%)  OTHERS (LIKE FBSS <1%)
POSTSURGICAL NEUROPATHIC PAIN  Post mastectomy syndrome- seen after breast surgeries from lumpectomy to radical dissection. Disruption of neural pathways (intercostobrachial nerve) is the cause  Post neck dissection- severe ipsilateral face and neck pain due to damage to cervical plexus  Post thoracotomy syndrome- pain along the intercostal nerves near the scars  Phantom pain
DIAGNOSIS AND MANAGEMENT OF CHRONIC PAIN
Basic Approach to Patient Management Comprehensive Pain Assessment National Pharmaceutical Council, Joint Commission on Accreditation of Healthcare Organizations. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, VA: 2001; Passik SD, Kirsh KL CNS Drug 2004; 18(1):13-25. Characterize pain location, distribution, duration, frequency, quality, precipitants Take detailed history (e.g., comorbidities, prior treatment) Conduct physical examination Clarify etiology, pathophysiology Complete risk assessment Assess effects of pain on patient’s function PAIN PHYSICIAN
THE 3L APPROACH TO DIAGNOSIS1 Patient verbal descriptors of pain, questions and answers Nervous system lesion or disease Sensory abnormalities in the painful area Listen1,2 Look1,4 Locate1,3 1. Freynhagen R, Bennett MI. BMJ 2009; 339:b3002; 2. Bennett MI et al. Pain 2007; 127(3):199-203; 3. Freynhagen R et al. Pain 2008; 135(1-2):65-74; 4. Freynhagen R et al. Curr Pain Headache Rep 2009; 13(3):185-90.
PAIN HISTORY  Taking History of a Pain patient “Healing begins with history”  Cornerstone of accurate Pain diagnosis is relevant medical history.  No expensive investigation can substitute the role of history.
PAIN HISTORY WORKSHEET  Location/distribution  Onset  Frequency/variation  Intensity  Type  Aggravating and relieving factors  Impairment and disability  Previous pain treatments  Other conditions/treatments  Response to treatment  Impact of pain on daily living, psychological status and quality of living
LOCATE THE PAIN *In cases of referred pain, the location of the pain and of the injury or nerve lesion/dysfunction may not be correlated Gilron I et al. CMAJ 2006; 175(3):265-75; Walk D et al. Clin J Pain 2009; 25(7):632-40. Body maps are useful for the precise location of pain symptoms and sensory signs.*
DETERMINE PAIN INTENSITY International Association for the Study of Pain. Faces Pain Scale – Revised. Available at: http://www.iasp pain.org/Content/NavigationMenu/GeneralResourceLinks/FacesPainScaleRevised/default.htm. Accessed: July 15, 2013; Iverson RE et al. Plast Reconstr Surg 2006; 118(4):1060-9. 0 0–10 Numeric Pain Intensity Scale No pain 1 2 3 4 5 6 7 8 9 10 Moderate pain Worst possible pain Simple Descriptive Pain Intensity Scale No pain Mild pain Moderate pain Severe pain Very severe pain Worst pain Faces Pain Scale – Revised
PHYSICAL EXAMINATION  Conduct comprehensive physical and neurological exams when evaluating and identifying patient’s subjective complaints of pain1  Should serve to verify preliminary impression from history and guide the selection of laboratory and imaging studies2  Identifying the pain generator (with supporting history) 1. American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiology 1997; 86(4):995- 1004; 2. Brunton S. J Fam Pract 2004; 53(10 suppl):S3-10.
PAIN DIAGNOSIS  Confirm or exclude underlying causes  There is no single diagnostic test for pain  Multiple tests may not be helpful  Plain X-rays with multiple views  MRI  CT  CT myelogram  Nerve conduction velocity  Electromyography  DIAGNOSTIC BLOCK American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiology 1997; 86(4):995-1004; Brunton S. J Fam Pract 2004; 53(10 Suppl):S3-10. CT = computed tomography; MRI = magnetic resonance imaging
IDENTIFY AND TREAT UNDERLYING CAUSE Forde G, Stanos S. J Fam Pract 2007; 56(8 Suppl Hot Topics):S21-30 Whenever possible, it is important to identify and treat the underlying cause of pain!
Evaluate for patients presenting with pain the presence of red flags! Initiate appropriate investigations/ management or refer to concerned specialist Littlejohn GO. J R Coll Physicians Edinb 2005; 35(4):340-4. BE ALERT FOR RED FLAGS
GOALS IN THE TREATMENT OF NEUROPATHIC PAIN 2o goals *Note: pain reduction of 30–50% can be expected with maximal doses in most patients Argoff CE et al. Mayo Clin Proc 2006; 81(Suppl 4):S12-25; Lindsay TJ et al. Am Fam Physician 2010; 82(2):151-8. 1o goal: >50% pain relief* … but be realistic! Sleep Mood Function Quality of life
MULTIMODAL PAIN MANAGEMENT
MULTIMODAL TREATMENT OF NEUROPATHIC PAIN Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006. Pharmacotherapy Stress management Occupational therapy Biofeedback Complementary therapies Physical therapy Education Lifestyle management Sleep hygiene
Non-opioids like Aspirin, Paracetamol Diclofenac Weak opioid +/- non- opioid +/- adjuvant Strong opioids like morphine pethidine fentanyl Inter- ventional Pain Manage- ment STEP-I STEP-II STEP-III STEP-IV WHO ANALGESIC LADDER
PAIN TREATMENT CONTINUUM Least invasive Most invasive Psychological/physical approaches Topical medications *Consider referral if previous treatments were unsuccessful. Systemic medications* INTERVENTIONAL TECHNIQUES* Continuum not related to efficacy
Diagnostic blocks Epidural steroids Radiofrequency technigues Neurostimulation techniques Neuroaxial medication Interventional Therapies ADJUVANT ANALGESICS + PATIENTS EDUCATION
PHARMACOTHERAPY IN PAIN MANAGEMENT
MECHANISM-BASED PHARMACOLOGICAL TREATMENT OF NEUROPATHIC PAIN Spinal cord Nociceptive afferent fiber SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant Adapted from: Attal N et al. Eur J Neurol 2010; 17(9):1113-e88; Beydoun A, Backonja MM. J Pain Symptom Manage 2003; 25(5 Suppl):S18-30; Jarvis MF, Boyce-Rustay JM. Curr Pharm Des 2009; 15(15):1711-6; Gilron I et al. CMAJ 2006; 175(3):265-75; Moisset X, Bouhassira D. NeuroImage 2007; 37(Suppl 1):S80-8; Morlion B. Curr Med Res Opin 2011; 27(1):11-33; Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7. Descending modulation Central sensitization Ectopic discharge Peripheral sensitization Brain Medications affecting descending modulation: • SNRIs • TCAs • Tramadol, opioids Medications affecting central sensitization: • α2δ ligands • TCAs • Tramadol, opioids Medications affecting peripheral sensitization: • Capsaicin • Local anesthetics • TCAs Nerve lesion/disease Nerve lesion/disease Central sensitization Nerve lesion/disease
ASSESSMENT OF PAIN PATHOPHYSIOLOGY CAN HELP GUIDE APPROPRIATE MEDICATION THERAPY Nociceptive pain Neuropathic and central sensitization/ dysfunctional pain Lack of response to non-opioid Tx α2δ ligands Antidepressants Opioids For management of moderate to severe pain in appropriate patients Most opioid treatment guidelines for chronic pain recommend use for patients after inadequate response to non-opioid therapy* Mild Moderate Severe *Selected on the basis of the pathophysiology of patient’s pain, provided there are no contraindications for its use Coxib = COX-2-specific inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug Chou R et al. J Pain 2009; 10(2):113-30; Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7. Acetaminophen nsNSAIDs
PHARMACOLOGICAL MANAGEMENT OF NEUROPATHIC PAIN Initiate treatment with one or more first-line treatments • α2δ ligands (gabapentin, pregabalin) • SNRIs (duloxetine, venlafaxine) *Use tertiary amine TCAs such as amitiptyline only if secondary amine TCAs are unavailable Note: there is insufficient support for the use of nsNSAIDs in neuropathic pain nsNSAID = non-specific non-steroidal anti-inflammatory drug; SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant Dworkin RH et al. Mayo Clin Proc 2010 ; 85(3 Suppl):S3-14; Freynhagen R, Bennett MI. BMJ 2009; 339:b3002. • TCAs* (nortriptyline, desipramine) • Topical lidocaine(for localized peripheral pain) • If there is partial pain relief, add another first-line medication • If there is no or inadequate pain relief, switch to another first-line medication If first-line medications alone and in combination fail, consider second-line medications (opioids, tramadol) or third-line medications (bupropion, citalopram, paroxetine, carbamazepine, lamotrigine, oxcarbazepine, topiramate, valproic acid, topical capsaicin, mexiletine) STEP 1 STEP 2 STEP 3
PRESCRIBING RECOMMENDATIONS FOR FIRST-LINE MEDICATIONS SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant Dworkin RH et al. Mayo Clin Proc 2010; 85(3 Suppl):S3-14. Medication Starting dose Titration Max. dosage Trial duration α2δ ligands Gabapentin 100–300 mg at bedtime or tid ↑ by 100–300 mg tid every 1–7 days 3600 mg/day 3–8 weeks + 2 weeks at max. dose Pregabalin 50 mg tid or 75 mg bid ↑ to 300 mg/day after 3–7 days, then by 150 mg/day every 3–7 days 600 mg/day 4 weeks SNRIs Duloxetine 30 mg qd ↑ to 60 mg qd after 1 week 60 mg bid 4 weeks Venlafaxine 37.5 mg qd ↑ by 75 mg each week 225 mg/day 4–6 weeks TCAs (desipramine, nortriptyline 25 mg at bedtime ↑ by 25 mg/day every 3–7 days 150 mg/day 6–8 weeks, with ≥2 weeks at max. tolerated dosage Topical lidocaine Max. 3 5% patches/day for 12 h max. None needed Max. 3 patches/day for 12–18 h max. 3 weeks
BUT… PATIENTS WITH CHRONIC PAIN OF JUST ONE TYPE OF PAIN PATHOPHYSIOLOGY MAY BE RARE Dowd GS et al. J Bone Joint Surg Br 2007; 89(3):285-90; Vellucci R. Clin Drug Investig 2012; 32(Suppl 1):3-10. • Therapies that will work better for a particular patient are likely to depend on the mechanisms contributing to the patient’s pain • Patients may have different pathophysiologic mechanisms contributing to their pain • e.g., complex regional pain syndrome has multiple potential mechanisms, including nerve injury and inflammation – “mixed pain state” • Patients with mixed pain may benefit from combination therapy
INTERVENTIONAL PAIN MANAGEMENT
Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery Operation TREATMENT OF PAIN
Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery Operation TREATMENT OF PAIN World of Misery
Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids +/- adjuvant Strong opioids Recovery Operation TREATMENT OF PAIN
Interventional Pain Management are some minimally invasive procedures 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. TREATMENT OF PAIN
INTERVENTIONAL TECHNIQUES IN THE MANAGEMENT OF CHRONIC PAIN MINIMALLY INVASIVE PROCEDURES  Injections of drugs to target areas  Ablation of targeted nerves (neurolytics, radio frequency)  Implantation of intrathecal infusion pumps  Implantation of spinal cord stimulators  Some surgical techniques (IDET, annuloplasty, nucleoplasty)
EVIDENCE BASED GUIDELINES FOR INTERVENTIONAL PAIN MEDICINE  EFNS guidelines on neurostimulation therapy for neuropathic pain. Cruccu et all. Eur J Neurology 2007;14:952-70.  Polyanalgesic consensus conference 2007: recommendations for the management of pain by intathecal (intraspinal) drug delivery: Report of an interdisciplinary expert panel. Deer et al. neuromodulation 2007;10:300-328  Evidence-based guidelines for interventional pain medicine according to clinical diagnoses. Van Kleef et al. Pain Practice 2009;9:247-51.  Evidence based medicine. Trigeminal neuralgia. Van Kleef et al. Pain Practice 2009;9:252-9.  Comprehensive evidence-based guidelines for interventional techniques in the management of chronic pain. Manchikanti et al. Pain Physician 2009;12: 699.
ADVANTAGES OF INTERVENTIONAL PAIN MANAGEMENT Reduction in pain Return to work Reduction in oral medication Improved quality of life
RADIOFREQUENCY TECHNIQUES The use of high frequency electric current to produce controlled thermocoagulation Sweet and Wepsic, 1974 (Gasserian ganglion) Shealy, 1975 (spinal pain) Sluijter and Mehta, 1981 (needles) Sluijter, 1998 (pulsed radiofrequency) RF
PAIN MANAGEMENT AS A MEDICAL SPECIALTY
WHAT IS GOING ON ?  Pain as a 34th speciality  Pain as a 5th vital sign  Incorporated in undergraduate studies  National/international policy on pain  Training programs  Evidence based guidelines of management
THESE PHYSICIANS OFTEN SPECIALIZE IN PAIN MANAGEMENT  Anesthesiologists  Neurosurgeons  Neurologists  Orthopedic surgeons  Physiatrists (PM&R)  Rheumatologists Other pain specialists  Acupuncturists, chiropractors, physical therapists, psychiatrists, psychologists, or professional counselors
MOTTO OF PAIN MANAGEMENT  Relief of pain shall be a basic human right  Treat pain from the diagnosis till end  Patient assessment: paramount  Mechanism based approach  Believe the patient  Encourage patient participation  Be consistent, not variable  Empower the pt. to choose the course of treatment  Deliver the intervention timely  Treat the pt. as a whole
SNAP SHOTS FROM PAIN OT
TRANSFORAMINAL NERVE ROOT BLOCK INDICATION: RADICULAR PAIN FROM NERVE ROOTS
INTERLAMINAR EPIDURAL STEROID INJECTIONS • Interlaminar Epidural
CAUDAL EPIDURAL INJECTION
SACROILIAC JOINT INJECTION FABER TEST
FACET JOINT BLOCK
DISC PROCEDURE
TRIGEMINAL GANGLION BLOCK
STELLATE GANGLION BLOCK
INDICATIONS  CRPS I AND II  NEUROPATHIC PAIN ,UPPER EXTREMITY  HEADACHE  VASCULAR INSUFFICIENCY
RADIOFREQUENCY LESIONING OF STELLATE GANGLION Neuropathic pain of the face, neck and arm
LUMBAR SYMPATHETIC BLOCK
INDICATIONS  CRPS I AND II  NEUROPATHIC PAIN ,LOWER EXTREMITY  VASCULAR INSUFFICIENCY
LUMBAR SYMPATHETIC BLOCK FOR PERIPHERAL VASCULAR DISEASE BEFORE AFTER
USG GUIDED STELLATE GANGLION BLOCK
COELIAC PLEXUS BLOCK
INDICATIONS  MALIGNANCY OF FOREGUT  CHRONIC PANCREATITIS
CT GUIDED COELIAC PLEXUS BLOCK Intra aortic approach
INDICATIONS  PELVIC MALIGNANCY  ENDOMETRIOSIS  PID
GANGLION IMPAR BLOCK
INDICATIONS  MALIGNANT PERIANAL PAIN  VISCERAL PAIN
USG GUIDED SUBACROMIAL BLOCK
GENICULAR NERVE RADIOFREQUENCY ABLATION
SPINAL CORD STIMULATOR IMPLANTATION
STEPS OF SCS IMPLANTATION
VERTEBROPLASTY FOR COMPRESSION #
INDICATIONS  METASTASES  OSTEOPOROSIS  OSTEOGENESIS IMPERFECTA  MULTIPLE MYELOMA
VERTEBROPLASTY L2
INTRATHECAL PUMPS
SUMMARY  Pain is an enormous global health problem affecting all populations & affects every aspect of a patient’s life  Comprehensive pain assessment is important & includes detailed history of pain, pain assessment tools and physical examination  Whenever possible, it is important to identify and treat the underlying cause of pain  Be alert for red flags and evaluate for patients presenting with pain the presence of red flags  Assessment of pain pathophysiology can help guide appropriate medication therapy  Drugs include acetaminophen, NSAIDS, Opioids, A2δ ligands e.g gabapentin, pregabalin and antidepressants- e.g. Amitryptiline
SUMMARY  Neuropathic pain is pain caused by a lesion or disease of the somatosensory system  Neuropathic pain can be distinguished from nociceptive pain through common verbal descriptors and simple bedside tests  Non-pharmacological therapies, including patient education, are important components of neuropathic pain management  interventional approach can be diagnostic/break pain cycles  Interventional Pain Management works in most situations where all other options has failed. Long term analgesia and cure is possible  Multimodal approach is necessary for chronic pain  Non-adherence to chronic pain medication is common  Simplifying regimens, imparting knowledge, modifying patient beliefs and human behaviour and providing communication and trust may help overcoming barriers to treatment
TAKE HOME MESSAGE MANY MECHANISMS SO MANY METHODS (MULTIMODAL APPROACH)
PAIN SOCIETIES:  AMERICAN ACADEMY OF PAIN MEDICINE  INTERNATIONAL ASSOCIATION FOR THE STUDY OF PAIN (IASP)  AMERICAN SOCIETY OF INTERVENTIONAL PAIN PHYSICIANS (ASIPP)  INDIAN SOCIETY OF THE STUDY OF PAIN (ISSP)  WORLD INSTITUTE OF PAIN (WIP) SCOTTIE DOG- THE PAIN MASCOT WIFE PAIN- NO TREATMENT
All the happiness that Mankind can gain lies not in pleasure but in relief from pain -John Hayden CURE SOMETIMES, RELIEVE OFTEN,COMFORT ALWAYS
KNOW YOUR PAIN 2015 CHRONIC PAINfinal2.pptx

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KNOW YOUR PAIN 2015 CHRONIC PAINfinal2.pptx

  • 1.
    KNOW PAIN PROGRAMME DRSANTOSH KUMAR SHARMA ASST PROF DEPT OF ANAESTHESIOLOGY, CCM & PAIN MEDICINE BRD MEDICAL COLLEGE GORAKHPUR
  • 2.
    THE PROBLEM  75yrs,female from maharajganj, rt sided trigeminal neuralgia for 5 yrs. Came to the OPD crying with sari’s pallu in her mouth. Had not eaten for 3 days. Pain relieved instantly by trigeminal block. She didn’t believe that her pain had gone. Came for follow up after 8 mts. (pic follows)  55 yrs, female from nepal, lt sided ca breast postoperative with ulcer on breast and motor weakness, lymphedema and severe burning pain of left upper limb for 1 yr. treated by stellate ganglion block 3 sittings. Had 40-50% pain relief. Lost to follow up after the earthquake in nepal (pic follows).  21 yrs,male from bansgaon, driver by occupation, with low back pain radiating to left leg upto the great toe for 2 months. SLR positive same side. Spectacular results with pharmacotherapy within a month time. No need for any intervention.
  • 3.
    Pt with trigeminalneuralgia Pt with carcinoma breast
  • 4.
    Pain is amore terrible lord of mankind than death itself.” Albert Schweitzer
  • 5.
    Total care emotional spiritual physical social ‘‘Pain managementcontinues to be the most difficult problem facing medicine today.’’ Jason R. Bauer and Charles E. Ray, Jr. WHY ………….?
  • 6.
    MYTHS ABOUT PAIN A symptom of a disease  It always comes with tissue damage  Always a friend, it warns us of our disease  It never kills  It is inevitable in many conditions and we need to accept it.  Extended rest and reduced activity is all that is needed to treat pain  Pain: "You should snap out of it. It's all in your head". If cause not identified, pain is functional and you need a psychiatric evaluation
  • 7.
    MYTHS ABOUT PAINSPECIALITY  Manage pain not the disease  Useful when no treatment is available  It has to be morphine or neurolysis  There has to be 100% pain relief (‘Techno-fix’)
  • 8.
    DISCUSSION POINTS • Whatis pain? • Burden of chronic pain. • Newer concepts in pathophysiology of pain. • Diagnosis of chronic pain. • Newer concepts of analgesic therapy. • Newer drugs to manage pain. • Interventional Pain Management to diagnose & treat pain.
  • 9.
    IASP Definition ofPain “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp- pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013.
  • 10.
    PAIN ACUTE PAIN (NOCICEPTIVE) CHRONIC PAINWITH TISSUE DAMAGE (NOCICEPTIVE + NEUROPATHIC) CHRONIC PAIN WITHOUT TISSUE DAMAGE (NEUROPATHIC)
  • 11.
    CLASSIFICATION OF PAIN Accordingto Pain duration  Acute pain: pain of less than 3 months duration  Chronic pain: pain lasting for more than 3 months, or persisting beyond the course of an acute disease, or after tissue healing is complete.  Acute-on-chronic pain: acute pain flare superimposed on underlying chronic pain
  • 12.
    CLASSIFICATION OF PAIN Accordingto pathology  Nociceptive: represents the normal response to noxious insult or injury of tissues such as skin, muscles, visceral organs, joints, tendons, or bones.  Somatic: musculoskeletal (joint pain, myofascial pain), cutaneous; often well localized  Visceral: hollow organs and smooth muscle; usually referred  Neuropathic: pain initiated or caused by a primary lesion or disease in the somatosensory nervous system.  Diabetic neuropathy  post herpetic neuralgia  spinal cord injury pain  phantom limb (post-amputation) pain  post-stroke central pain.
  • 13.
    CLASSIFICATION OF PAIN Accordingto pathology (contd)  Inflammatory: a result of activation and sensitization of the nociceptive pain pathway by a variety of mediators released at a site of tissue inflammation.  Appendicitis  Osteoarthritis  Rheumatoid arthritis  Central sensitization/dysfunctional pain: May be caused by persistent neuronal dysregulation or dysfunction  CRPS  Fibromyalgia
  • 14.
    Inflammatory Pain Pain 2015: Towardsa New Classification Nociceptive stimulus Physiological Pain Inflammatory lesion (OA, spondylitis, infection) Nerve lesion (diabetes, PHN, radiculopathy, trauma…) Neuropathic Pain Fibromyalgia IBS CRPS 1 Myofascial Pain Dysfunctional Pain
  • 15.
    ACUTE Vs CHRONICPAIN CHARACTERISTIC ACUTE PAIN CHRONIC PAIN Cause Generally known Often unknown Duration of pain Short, well-characterized Persists after healing, >3 months Treatment approach Resolution of underlying cause, usually self-limited Underlying cause and pain disorder; outcome is often pain control, not cure
  • 16.
    Mixed Type Caused bya combination of both primary injury and secondary effects NOCICEPTIVE Vs NEUROPATHIC PAIN Nociceptive Pain Caused by activity in neural pathways in response to potentially tissue-damaging stimuli Neuropathic Pain Initiated or caused by primary lesion or dysfunction in the nervous system Postoperative pain Mechanical low back pain Sickle cell crisis Arthritis Postherpetic neuralgia Neuropathic low back pain CRPS* Sports/exercise injuries *Complex regional pain syndrome Central post- stroke pain Trigeminal neuralgia Distal polyneuropathy (eg, diabetic, HIV)
  • 17.
    NOCICEPTIVE Vs NEUROPATHICPAIN Serra J. In: Serra J (ed). Tratado del dolor neuropático. Panamericana; Madrid, Spain: 2006. Nociceptive Neuropathic Definition Pain caused by physiological activation of pain receptors Pain initiated or caused by a primary lesion or dysfunction in the peripheral or central nervous system Mechanism Natural physiological transduction Ectopic impulse generation, central sensitization, and others Localization Local + referred pain Confined to innervation territory of the lesioned nervous structure Quality of symptoms Ordinary painful sensation New strange sensations Treatment Good response (conventional analgesics) Poor response (conventional analgesics)
  • 18.
    POSSIBLE DESCRIPTIONS OFNEUROPATHIC PAIN  Sensations  Numbness  Tingling  Burning  Paresthesia  Paroxysmal  Lancinating  Electric like  Raw skin  Shooting  Deep, dull ache  Signs/Symptoms  Allodynia: pain from a stimulus that does not normally evoke pain  Thermal  Mechanical  Hyperalgesia: exaggerated response to a normally painful stimulus
  • 19.
    WHY SHOULD PAINBE TREATED? CONSEQUENCES OF CHRONIC PAIN 1. Douglas C et al. J Neurosci Nurs 2008; 40(3):158-68; 2. Tang NKY et al. J Sleep Res 2007; 16(1):85-95; 3. Hawker GA et al. Osteoarth Cartil 2008; 16(4):415-22; 4. Munce SE et al. J Occup Environ Med 2007; 49(11):1206-1211; 5. Stewart WF et al. JAMA 2003; 290(18):2443-54; 6. Ritzwoller DP et al. BMC Musculoskelet Disord 2006; 7:72-81. Healthcare costs6 Presenteeism and absenteeism4,5 Disability4 Reduced social activities3 Disrupted daily routine3 Decreased quality of life3 Anxiety2 Depression2 Sleep disturbances2 Chronic pain1
  • 20.
    DOMAINS OF CHRONICPAIN Social Consequences  Marital/family relations  Intimacy/sexual activity  Social isolation Socioeconomic Consequences  Healthcare costs  Disability  Lost workdays Quality of Life  Physical functioning  Ability to perform activities of daily living  Work  Recreation Psychological Morbidity  Depression  Anxiety, anger  Sleep disturbances  Loss of self-esteem
  • 21.
    WHY SHOULD PAINBE TREATED? PAIN IS LINKED TO DEPRESSION Trivedi MH. Prim Care Companion J Clin Psychiatry 2004; 6(Suppl 1):12-6 Prevalence of pain in depressed patients is 15–100% Prevalence of major depressive disorder in patients with chronic pain is 15–50% • Depressive symptoms rather than major depressive disorder • Mostly musculoskeletal pain • Mostly in patients with multiple pain symptoms
  • 22.
    CONSEQUENCES OF UNTREATED& UNDER TREATED ACUTE PAIN Extensive and Persistent cascade of neurochemical mediators triggered by tissue injury leads to a long-term, permanent, neurological change that can lead to SENSITIZATION ALLODYNIA HYPERALGESIA MAY evolve into chronic pain Person is less tolerant to pain, area & intensity of pain increases, character of pain changes, and psychological changes occur.
  • 23.
    PHYSIOLOGY OF PAINPERCEPTION  Transduction  Transmission  Modulation  Perception  Interpretation  Behavior Injury Descending Pathway Peripheral Nerve Dorsal Root Ganglion C-Fiber A-beta Fiber A-delta Fiber Ascending Pathways Dorsal Horn Brain Spinal Cord Adapted with permission from WebMD Scientific American® Medicine.
  • 24.
  • 25.
    MECHANISMS OF PAIN:NEUROPLASTICITY HOW DOES A CHRONIC PAIN STATE DEVELOP?  Peripheral Sensitization - Injury causes release of “sensitizing soup” - Reduction in threshold and increase response of nocioceptors  Central Sensitization - Membrane excitability, synaptic recruitment and decreased inhibition - Uncoupling of pain from peripheral stimuli
  • 26.
    SENSITIZATION IS ACONSTANT FEATURE OF CHRONIC PAIN PERIPHERAL SENSITIZATION  Up regulation of nociceptors  SNS connecting with somatic fibres (CROSS TALK)  Sprouting of damaged axons and ectopic discharge CENTRAL SENSITIZATION  Central reorganisation  Activation of the N- methyl-D-aspartate (NMDA) channel,  Increase in intracellular Ca2+,  Wind-up/wide dynamic range (WDR) neuron sensitization
  • 28.
    INADEQUATE CHRONIC PAINTREATMENT  Breivik et al., EJP 2006;10:287-333. Percentage of chronic pain suffers who reported that their pain is inadequately controlled in 16 countries
  • 29.
    PREVALENCE OF CHRONICPAIN Tsang A et al. J Pain 2006; 9(10):883-91.
  • 30.
    PREVALENCE OF CHRONICPAIN IN INDIA Dureja GP, Jain PN, Shetty N, Mandal SP, Prabhoo R, Joshi M, Goswami S, Natarajan KB, Iyer R, Tanna DD, Ghosh P, Saxena A, Kadhe G, Phansalkar AA. Prevalence of chronic pain, impact on daily life, and treatment practices in India. Pain Pract. 2014;14(2):E51-62.
  • 31.
    5–20% OF THEGENERAL POPULATION MAY SUFFER FROM NEUROPATHIC PAIN Summary of Selected Prevalence Studies Adapted from: Bouhassira D et al. Pain 2008; 136(3):380-7; de Moraes Vieira EB et al. J Pain Symptom Manage 2012; 44(2):239-51; Elzahaf RA et al. Pain Pract 2013; 13(3):198-205; Johayon MM, Stingl C. Psychiatr Res 2012; 46(4):444-50; Torrance N et al. J Pain 2006;7(4):281-9; Toth C et al. Pain Med 2009; 10(5):918-29;
  • 32.
    PAIN IS NOWTHE 5TH VITAL SIGN (Adopted by the American Board for Hospital Accreditation) Lynch ME, et al. Pain Res Manage Vol 11 No 1 Spring 2006.
  • 33.
    COMMON CAUSES OFCHRONIC PAIN 1. Chronic pain Neuropathic pain Cancer pain Headache Low back pain Musculoskeletal Pain Arthritis Pain RA, OA Psychogenic pain Metabolic Pain Osteomalacia Osteoporosis Gout
  • 34.
    Common descriptors Shooting Electric shock-like Burning Tingling Numbness Postherpetic neuralgia Lumbar radicular pain Chronic post- surgical pain Post-stroke pain Diabetic peripheral neuropathy RECOGNIZING NEUROPATHIC PAIN
  • 35.
    LOW BACK PAIN FACET JOINT ARTHROPATHY (15- 45%)  INTERNAL DISC DISRUPTION (25 -40%)  SACRO ILIAC JOINT ARTHROPATHY (15 -30%)  DISC PROLAPSE/HERNIATED DISC/ SLIPPED DISC (2-5%)  CRPS/RSD (2 -8%)  OSTEOPOROTIC COMPRESSION FRACTURE (3-5%)  FIBROMYALGIA & MYOFASCIAL PAIN (2-5%)  SPINAL CANAL STENOSIS (2-3%)  SPONDYLOLYSTHESIS (2-3%)  TUMORS & INFECTION (<1%)  OTHERS (LIKE FBSS <1%)
  • 36.
    POSTSURGICAL NEUROPATHIC PAIN Post mastectomy syndrome- seen after breast surgeries from lumpectomy to radical dissection. Disruption of neural pathways (intercostobrachial nerve) is the cause  Post neck dissection- severe ipsilateral face and neck pain due to damage to cervical plexus  Post thoracotomy syndrome- pain along the intercostal nerves near the scars  Phantom pain
  • 37.
  • 38.
    Basic Approach toPatient Management Comprehensive Pain Assessment National Pharmaceutical Council, Joint Commission on Accreditation of Healthcare Organizations. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, VA: 2001; Passik SD, Kirsh KL CNS Drug 2004; 18(1):13-25. Characterize pain location, distribution, duration, frequency, quality, precipitants Take detailed history (e.g., comorbidities, prior treatment) Conduct physical examination Clarify etiology, pathophysiology Complete risk assessment Assess effects of pain on patient’s function PAIN PHYSICIAN
  • 39.
    THE 3L APPROACHTO DIAGNOSIS1 Patient verbal descriptors of pain, questions and answers Nervous system lesion or disease Sensory abnormalities in the painful area Listen1,2 Look1,4 Locate1,3 1. Freynhagen R, Bennett MI. BMJ 2009; 339:b3002; 2. Bennett MI et al. Pain 2007; 127(3):199-203; 3. Freynhagen R et al. Pain 2008; 135(1-2):65-74; 4. Freynhagen R et al. Curr Pain Headache Rep 2009; 13(3):185-90.
  • 40.
    PAIN HISTORY  TakingHistory of a Pain patient “Healing begins with history”  Cornerstone of accurate Pain diagnosis is relevant medical history.  No expensive investigation can substitute the role of history.
  • 41.
    PAIN HISTORY WORKSHEET Location/distribution  Onset  Frequency/variation  Intensity  Type  Aggravating and relieving factors  Impairment and disability  Previous pain treatments  Other conditions/treatments  Response to treatment  Impact of pain on daily living, psychological status and quality of living
  • 42.
    LOCATE THE PAIN *Incases of referred pain, the location of the pain and of the injury or nerve lesion/dysfunction may not be correlated Gilron I et al. CMAJ 2006; 175(3):265-75; Walk D et al. Clin J Pain 2009; 25(7):632-40. Body maps are useful for the precise location of pain symptoms and sensory signs.*
  • 43.
    DETERMINE PAIN INTENSITY InternationalAssociation for the Study of Pain. Faces Pain Scale – Revised. Available at: http://www.iasp pain.org/Content/NavigationMenu/GeneralResourceLinks/FacesPainScaleRevised/default.htm. Accessed: July 15, 2013; Iverson RE et al. Plast Reconstr Surg 2006; 118(4):1060-9. 0 0–10 Numeric Pain Intensity Scale No pain 1 2 3 4 5 6 7 8 9 10 Moderate pain Worst possible pain Simple Descriptive Pain Intensity Scale No pain Mild pain Moderate pain Severe pain Very severe pain Worst pain Faces Pain Scale – Revised
  • 44.
    PHYSICAL EXAMINATION  Conductcomprehensive physical and neurological exams when evaluating and identifying patient’s subjective complaints of pain1  Should serve to verify preliminary impression from history and guide the selection of laboratory and imaging studies2  Identifying the pain generator (with supporting history) 1. American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiology 1997; 86(4):995- 1004; 2. Brunton S. J Fam Pract 2004; 53(10 suppl):S3-10.
  • 45.
    PAIN DIAGNOSIS  Confirmor exclude underlying causes  There is no single diagnostic test for pain  Multiple tests may not be helpful  Plain X-rays with multiple views  MRI  CT  CT myelogram  Nerve conduction velocity  Electromyography  DIAGNOSTIC BLOCK American Society of Anesthesiologists Task Force on Pain Management, Chronic Pain Section. Anesthesiology 1997; 86(4):995-1004; Brunton S. J Fam Pract 2004; 53(10 Suppl):S3-10. CT = computed tomography; MRI = magnetic resonance imaging
  • 46.
    IDENTIFY AND TREATUNDERLYING CAUSE Forde G, Stanos S. J Fam Pract 2007; 56(8 Suppl Hot Topics):S21-30 Whenever possible, it is important to identify and treat the underlying cause of pain!
  • 47.
    Evaluate for patients presentingwith pain the presence of red flags! Initiate appropriate investigations/ management or refer to concerned specialist Littlejohn GO. J R Coll Physicians Edinb 2005; 35(4):340-4. BE ALERT FOR RED FLAGS
  • 48.
    GOALS IN THETREATMENT OF NEUROPATHIC PAIN 2o goals *Note: pain reduction of 30–50% can be expected with maximal doses in most patients Argoff CE et al. Mayo Clin Proc 2006; 81(Suppl 4):S12-25; Lindsay TJ et al. Am Fam Physician 2010; 82(2):151-8. 1o goal: >50% pain relief* … but be realistic! Sleep Mood Function Quality of life
  • 49.
  • 50.
    MULTIMODAL TREATMENT OFNEUROPATHIC PAIN Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006. Pharmacotherapy Stress management Occupational therapy Biofeedback Complementary therapies Physical therapy Education Lifestyle management Sleep hygiene
  • 51.
  • 52.
    PAIN TREATMENT CONTINUUM Least invasive Most invasive Psychological/physicalapproaches Topical medications *Consider referral if previous treatments were unsuccessful. Systemic medications* INTERVENTIONAL TECHNIQUES* Continuum not related to efficacy
  • 53.
    Diagnostic blocks Epidural steroids Radiofrequencytechnigues Neurostimulation techniques Neuroaxial medication Interventional Therapies ADJUVANT ANALGESICS + PATIENTS EDUCATION
  • 54.
  • 55.
    MECHANISM-BASED PHARMACOLOGICAL TREATMENT OFNEUROPATHIC PAIN Spinal cord Nociceptive afferent fiber SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant Adapted from: Attal N et al. Eur J Neurol 2010; 17(9):1113-e88; Beydoun A, Backonja MM. J Pain Symptom Manage 2003; 25(5 Suppl):S18-30; Jarvis MF, Boyce-Rustay JM. Curr Pharm Des 2009; 15(15):1711-6; Gilron I et al. CMAJ 2006; 175(3):265-75; Moisset X, Bouhassira D. NeuroImage 2007; 37(Suppl 1):S80-8; Morlion B. Curr Med Res Opin 2011; 27(1):11-33; Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7. Descending modulation Central sensitization Ectopic discharge Peripheral sensitization Brain Medications affecting descending modulation: • SNRIs • TCAs • Tramadol, opioids Medications affecting central sensitization: • α2δ ligands • TCAs • Tramadol, opioids Medications affecting peripheral sensitization: • Capsaicin • Local anesthetics • TCAs Nerve lesion/disease Nerve lesion/disease Central sensitization Nerve lesion/disease
  • 56.
    ASSESSMENT OF PAINPATHOPHYSIOLOGY CAN HELP GUIDE APPROPRIATE MEDICATION THERAPY Nociceptive pain Neuropathic and central sensitization/ dysfunctional pain Lack of response to non-opioid Tx α2δ ligands Antidepressants Opioids For management of moderate to severe pain in appropriate patients Most opioid treatment guidelines for chronic pain recommend use for patients after inadequate response to non-opioid therapy* Mild Moderate Severe *Selected on the basis of the pathophysiology of patient’s pain, provided there are no contraindications for its use Coxib = COX-2-specific inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug Chou R et al. J Pain 2009; 10(2):113-30; Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7. Acetaminophen nsNSAIDs
  • 57.
    PHARMACOLOGICAL MANAGEMENT OF NEUROPATHICPAIN Initiate treatment with one or more first-line treatments • α2δ ligands (gabapentin, pregabalin) • SNRIs (duloxetine, venlafaxine) *Use tertiary amine TCAs such as amitiptyline only if secondary amine TCAs are unavailable Note: there is insufficient support for the use of nsNSAIDs in neuropathic pain nsNSAID = non-specific non-steroidal anti-inflammatory drug; SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant Dworkin RH et al. Mayo Clin Proc 2010 ; 85(3 Suppl):S3-14; Freynhagen R, Bennett MI. BMJ 2009; 339:b3002. • TCAs* (nortriptyline, desipramine) • Topical lidocaine(for localized peripheral pain) • If there is partial pain relief, add another first-line medication • If there is no or inadequate pain relief, switch to another first-line medication If first-line medications alone and in combination fail, consider second-line medications (opioids, tramadol) or third-line medications (bupropion, citalopram, paroxetine, carbamazepine, lamotrigine, oxcarbazepine, topiramate, valproic acid, topical capsaicin, mexiletine) STEP 1 STEP 2 STEP 3
  • 58.
    PRESCRIBING RECOMMENDATIONS FOR FIRST-LINEMEDICATIONS SNRI = serotonin-norepinephrine reuptake inhibitor; TCA = tricyclic antidepressant Dworkin RH et al. Mayo Clin Proc 2010; 85(3 Suppl):S3-14. Medication Starting dose Titration Max. dosage Trial duration α2δ ligands Gabapentin 100–300 mg at bedtime or tid ↑ by 100–300 mg tid every 1–7 days 3600 mg/day 3–8 weeks + 2 weeks at max. dose Pregabalin 50 mg tid or 75 mg bid ↑ to 300 mg/day after 3–7 days, then by 150 mg/day every 3–7 days 600 mg/day 4 weeks SNRIs Duloxetine 30 mg qd ↑ to 60 mg qd after 1 week 60 mg bid 4 weeks Venlafaxine 37.5 mg qd ↑ by 75 mg each week 225 mg/day 4–6 weeks TCAs (desipramine, nortriptyline 25 mg at bedtime ↑ by 25 mg/day every 3–7 days 150 mg/day 6–8 weeks, with ≥2 weeks at max. tolerated dosage Topical lidocaine Max. 3 5% patches/day for 12 h max. None needed Max. 3 patches/day for 12–18 h max. 3 weeks
  • 59.
    BUT… PATIENTS WITHCHRONIC PAIN OF JUST ONE TYPE OF PAIN PATHOPHYSIOLOGY MAY BE RARE Dowd GS et al. J Bone Joint Surg Br 2007; 89(3):285-90; Vellucci R. Clin Drug Investig 2012; 32(Suppl 1):3-10. • Therapies that will work better for a particular patient are likely to depend on the mechanisms contributing to the patient’s pain • Patients may have different pathophysiologic mechanisms contributing to their pain • e.g., complex regional pain syndrome has multiple potential mechanisms, including nerve injury and inflammation – “mixed pain state” • Patients with mixed pain may benefit from combination therapy
  • 60.
  • 61.
    Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids+/- adjuvant Strong opioids Recovery Operation TREATMENT OF PAIN
  • 62.
    Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids+/- adjuvant Strong opioids Recovery Operation TREATMENT OF PAIN World of Misery
  • 63.
    Non-pharmacological methods Non- opioids Weak opioids +/- non- opioids+/- adjuvant Strong opioids Recovery Operation TREATMENT OF PAIN
  • 64.
    Interventional Pain Managementare some minimally invasive procedures 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. TREATMENT OF PAIN
  • 65.
    INTERVENTIONAL TECHNIQUES IN THEMANAGEMENT OF CHRONIC PAIN MINIMALLY INVASIVE PROCEDURES  Injections of drugs to target areas  Ablation of targeted nerves (neurolytics, radio frequency)  Implantation of intrathecal infusion pumps  Implantation of spinal cord stimulators  Some surgical techniques (IDET, annuloplasty, nucleoplasty)
  • 66.
    EVIDENCE BASED GUIDELINESFOR INTERVENTIONAL PAIN MEDICINE  EFNS guidelines on neurostimulation therapy for neuropathic pain. Cruccu et all. Eur J Neurology 2007;14:952-70.  Polyanalgesic consensus conference 2007: recommendations for the management of pain by intathecal (intraspinal) drug delivery: Report of an interdisciplinary expert panel. Deer et al. neuromodulation 2007;10:300-328  Evidence-based guidelines for interventional pain medicine according to clinical diagnoses. Van Kleef et al. Pain Practice 2009;9:247-51.  Evidence based medicine. Trigeminal neuralgia. Van Kleef et al. Pain Practice 2009;9:252-9.  Comprehensive evidence-based guidelines for interventional techniques in the management of chronic pain. Manchikanti et al. Pain Physician 2009;12: 699.
  • 67.
    ADVANTAGES OF INTERVENTIONAL PAINMANAGEMENT Reduction in pain Return to work Reduction in oral medication Improved quality of life
  • 68.
    RADIOFREQUENCY TECHNIQUES The useof high frequency electric current to produce controlled thermocoagulation Sweet and Wepsic, 1974 (Gasserian ganglion) Shealy, 1975 (spinal pain) Sluijter and Mehta, 1981 (needles) Sluijter, 1998 (pulsed radiofrequency) RF
  • 69.
  • 70.
    WHAT IS GOINGON ?  Pain as a 34th speciality  Pain as a 5th vital sign  Incorporated in undergraduate studies  National/international policy on pain  Training programs  Evidence based guidelines of management
  • 71.
    THESE PHYSICIANS OFTENSPECIALIZE IN PAIN MANAGEMENT  Anesthesiologists  Neurosurgeons  Neurologists  Orthopedic surgeons  Physiatrists (PM&R)  Rheumatologists Other pain specialists  Acupuncturists, chiropractors, physical therapists, psychiatrists, psychologists, or professional counselors
  • 72.
    MOTTO OF PAINMANAGEMENT  Relief of pain shall be a basic human right  Treat pain from the diagnosis till end  Patient assessment: paramount  Mechanism based approach  Believe the patient  Encourage patient participation  Be consistent, not variable  Empower the pt. to choose the course of treatment  Deliver the intervention timely  Treat the pt. as a whole
  • 73.
  • 75.
  • 76.
    INTERLAMINAR EPIDURAL STEROIDINJECTIONS • Interlaminar Epidural
  • 77.
  • 78.
  • 79.
  • 81.
  • 82.
  • 84.
  • 85.
    INDICATIONS  CRPS IAND II  NEUROPATHIC PAIN ,UPPER EXTREMITY  HEADACHE  VASCULAR INSUFFICIENCY
  • 86.
    RADIOFREQUENCY LESIONING OFSTELLATE GANGLION Neuropathic pain of the face, neck and arm
  • 87.
  • 88.
    INDICATIONS  CRPS IAND II  NEUROPATHIC PAIN ,LOWER EXTREMITY  VASCULAR INSUFFICIENCY
  • 89.
    LUMBAR SYMPATHETIC BLOCKFOR PERIPHERAL VASCULAR DISEASE BEFORE AFTER
  • 90.
    USG GUIDED STELLATEGANGLION BLOCK
  • 92.
  • 93.
    INDICATIONS  MALIGNANCY OFFOREGUT  CHRONIC PANCREATITIS
  • 94.
    CT GUIDED COELIAC PLEXUSBLOCK Intra aortic approach
  • 96.
  • 97.
  • 98.
    INDICATIONS  MALIGNANT PERIANALPAIN  VISCERAL PAIN
  • 99.
  • 100.
  • 102.
  • 103.
    STEPS OF SCSIMPLANTATION
  • 104.
  • 105.
    INDICATIONS  METASTASES  OSTEOPOROSIS OSTEOGENESIS IMPERFECTA  MULTIPLE MYELOMA
  • 106.
  • 107.
  • 108.
    SUMMARY  Pain isan enormous global health problem affecting all populations & affects every aspect of a patient’s life  Comprehensive pain assessment is important & includes detailed history of pain, pain assessment tools and physical examination  Whenever possible, it is important to identify and treat the underlying cause of pain  Be alert for red flags and evaluate for patients presenting with pain the presence of red flags  Assessment of pain pathophysiology can help guide appropriate medication therapy  Drugs include acetaminophen, NSAIDS, Opioids, A2δ ligands e.g gabapentin, pregabalin and antidepressants- e.g. Amitryptiline
  • 109.
    SUMMARY  Neuropathic painis pain caused by a lesion or disease of the somatosensory system  Neuropathic pain can be distinguished from nociceptive pain through common verbal descriptors and simple bedside tests  Non-pharmacological therapies, including patient education, are important components of neuropathic pain management  interventional approach can be diagnostic/break pain cycles  Interventional Pain Management works in most situations where all other options has failed. Long term analgesia and cure is possible  Multimodal approach is necessary for chronic pain  Non-adherence to chronic pain medication is common  Simplifying regimens, imparting knowledge, modifying patient beliefs and human behaviour and providing communication and trust may help overcoming barriers to treatment
  • 110.
    TAKE HOME MESSAGE MANYMECHANISMS SO MANY METHODS (MULTIMODAL APPROACH)
  • 111.
    PAIN SOCIETIES:  AMERICANACADEMY OF PAIN MEDICINE  INTERNATIONAL ASSOCIATION FOR THE STUDY OF PAIN (IASP)  AMERICAN SOCIETY OF INTERVENTIONAL PAIN PHYSICIANS (ASIPP)  INDIAN SOCIETY OF THE STUDY OF PAIN (ISSP)  WORLD INSTITUTE OF PAIN (WIP) SCOTTIE DOG- THE PAIN MASCOT WIFE PAIN- NO TREATMENT
  • 112.
    All the happinessthat Mankind can gain lies not in pleasure but in relief from pain -John Hayden CURE SOMETIMES, RELIEVE OFTEN,COMFORT ALWAYS