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Low Back Pain Sasikaan Nimmaanrat, MD, FRCAT, MMed (Pain Mgt)
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General Concepts of Pain & Chronic Pain
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Pain An unpleasant sensory & emotional experience associated with actual or potential tissue damage or described in terms of such damage
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Descartes (Cartesian)’s Model of Pain
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The Main Ascending & Descending Spinal Pain Pathways
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Chronic Pain and Consequences
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Biopsychosocial Model
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Low Back Pain
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Treatment In the absence of “red flags”, treatment should consist of appropriate medications for both – –Nociceptive pain – –Neuropathic pain
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Treatment Patient activity is often limited because of pain, so sufficient analgesia becomes extremely important to maintain appropriate activity.
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Treatment Chronic back pain management is based on 3 principles 1. 1. Management of nociception 2. 2. Psychological and behavioral therapy 3. 3. Rehabilitation
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Management of Nociception Sufficient analgesia using – –Medications – –Procedures – –Both
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Psychological and Behavioral Therapies Chronic pain with all of its losses is commonly associated with comorbid disorders – –Anxiety – –Depression – –Sleep disturbance
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Pharmacotherapy
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Mechanistic Approach to Pain Treatment Brain Central sensitization Peripheral sensitization PNS PGEr Na+ TTXr NK-1 VR-1 NGF Opioid NSAIDs COXIBs Opioids Capsaicin Clonidine Na+ TTXr,TTXs TCA CBZ OXC TPM LTG Mexiletine Lidocaine Ca++ : NMDA: PGE: TCAs SNRIs Opioids Tramadol Clonidine Baclofen Clonazepam NE / 5HT, GABA Opioid receptors Descending inhibition Spinal cord GBP/ Pregabalin Ketamine, TPM Dextromethorphan Methadone NSAIDs / COXIBs
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Pharmacological Intervention Non-opioids – –Paracetamol – –NSAIDs – –Selective COX-2 inhibitors Opioids – –Weak opioids – –Strong opioids Adjuvants –Antidepressants –Anticonvulsants
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Non-opioids
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Paracetamol (acetaminophen) Effective analgesic with antipyretic activity Does not inhibit COX in peripheral tissues -> lack of anti-inflammatory activity Require up to 4 gm/day for at least a week to affirm its effectiveness
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Paracetamol Generally well tolerated Most serious adverse effect of acute overdosage is a dose-dependent (150 mg/kg), potentially fetal, hepatic necrosis Insufficient glutathione (liver disease, alcohol consumption> 3 units/day, malnutrition etc.)
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NSAIDs / COXIBs
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Selective COX-2 Inhibitors (COXIBs) Short-term use – gastric ulcer rates similar to placebo Do not impair platelet function Contraindicated in pts with – –Ischaemic heart disease – –Cerebrovascular disease – –Peripheral arterial disease
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COXIBs Exercise caution in pts with risk factors for heart disease – –Hypertension – –Hyperlipidaemia – –DM – –Smoking
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COXIBs The CV risks may increase with dose & duration of exposure The shortest duration possible & the lowest effective daily dose should be used
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Topical Analgesics Lignocaine patch 5% & topical capsaicin – –FDA approval for postherpetic neuralgia (PHN) Lignocaine patch 5%: focal peripheral neuropathy Topical capsaicin: painful diabetic neuropathy (PDN)
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Opioids
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Opioids in the Management of Chronic Non-cancer Pain: An Update of American Society of the Interventional Pain Physicians (ASIPP) Guidelines Pain Physician 2008; 11: S5-S62.
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Indications & Medical Necessity Pain of moderate to severe degree Suspected organic problem Documentation of failure to respond to non-controlled substances, adjuvants, physical therapy & interventional techniques
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The 4 As Continued opioid prescription requires monitoring of “the 4As” – –Analgesic – –Activity – –Aberrant behavior – –Adverse effect
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Treatment Objectives Pain relief Improved physical function Improved psychosocial function
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Discontinuation of Opioids Evidence of diversion or illegal use warrants an immediate discontinuation of opioids Clonidine po or transdermal 0.1 mg can be offered to counteract the majority of withdrawal symptoms
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Classification of Opioids Weak opioids (mild - moderate pain) – –Codeine – –Tramadol Strong opioids (moderate - severe pain) – –Morphine – –Fentanyl
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Codeine Derivative of morphine Potency 1/10 of morphine (CYP2D6) 10-20% of population lack of CYP2D6 Dose limiting side effects – –Constipation – –Vomiting – –Sedation
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Tramadol Atypical centrally-acting analgesic – –μ agonist (tramadol & M1) – –Serotonin & noradrenaline reuptake inhibitor Potency 1/20 – 1/5 of morphine Effective treatment of NeP (NNT 3.5, 3.8) Adverse effect (AE) profiles different from other opioids – –Less respiratory depression – –Limited effects on GI motor function – –Most common AE: nausea & vomiting
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Morphine Full μ agonist Standard opioid which others are compared Relatively water soluble Metabolised by hepatic conjugation – –Morphine-3-glucuronide – –Morphine-6-glucuronide
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Morphine M3G – –Very low affinity for opioid receptors – –No analgesic activity – –May antagonise analgesic effects of morphine – –May responsible for neurotoxic symptoms (hyperalgesia, allodynia & myoclonus, sometimes asso. with high doses of morphine)
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Morphine M6G – –An agonist at μ receptors – –More potent than morphine & excreted via kidney – –Repeated use of morphine, M6G responsible for significant amount of analgesic activity Predictors of higher M3G & M6G concentrations – –Impaired renal function – –Oral route (1 st pass metabolism) – –Higher doses – – ↑ ed patient age
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Pethidine Potency 1/10 of morphine Multiple disadvantages Active metabolite – norpethidine Neuroexcitation – –Nervousness – –Tremors – –Twitches – –Multifocal myoclonus – –Seizures
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Pethidine Impaired renal function increases T 1/2 of norpethidine Not reversed by naloxone & may increase the problems related to norpethidine toxicity Should be discouraged in favour of other opioids
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Fentanyl μ agonist High lipid solubility Potency 100X of morphine Rapid onset, short duration of action Various routes of administration – –Oral transmucosal – –Parenteral (IV, IM, S/C) – –Epidural / intrathecal – –Transdermal (transdermal therapeutic system – TTS)
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Reservoir DesignD-TRANS ® Matrix Design Fentanyl TTS
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Fentanyl Lollipop
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Adjuvants
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Neuropathic pain Medical management Nerve blocks (LA, steroid) Surgery (decompression, neuroaugmentation) Membrane stabilizing agents enhancement DH inhibition OXC CBZ Phenytoin Valproate Lidocaine Mexiletine Corticosteroids Amitryptyline Desipramine Fluoxetine Imipramine Nortryptyline Paroxetine OXC, Clonazapam Gabapentin / Pregabalin Baclofen Antiepileptics Antiarrhythmics Antidepressants Antiepileptics GABA-B agonists
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Therapeutic Procedures
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Epidural steroid injection Caudal epidural injection Lumbar selective nerve root injection Sacral nerve root injection Lumbar facet joint injection Facet joint denervation Ablative procedures for discogenic pain Vertebroplasty Intraspinal neurolytic procedure Epiduroscopy Epidural decompressive neuroplasty Sacroiliac joint injection Spinal cord stimulation Neuroaxial infusion system Trigger point injection Psoas muscle injection Pyrifomis muscle injection
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Epidural Steroid Injection
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Key learning points – –Multiple structures account for low back pain – –Epidural depot steroids relieve radicular pain caused by nerve root pathology, but not “unspecific” low back pain – –Epidural steroid injections are generally safe in the hands of well-trained, experienced physicians, with experience in resuscitation routines
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Epidural Steroid Injection Complications – –Epidural infection – –Epidural hematoma – –Spinal cord injury – –Total spinal anesthesia – –Intravenous injection (local anesthetic toxicity)
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Epidural Steroid Injection Complications – –Persistent paresthesia & worsened of pain from needle trauma – –Inadvertent dural puncture (at least 1% in experienced hands) – –Corticosteroids on the meninges leading to arachnoiditis – –Adrenocortical suppression is certainly possible & is one of limiting factors for repeating this procedure
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Epidural Steroid Injection Evidence for efficacy – –Substantial evidence for at least short-term efficacy – –Pts with leg pain only have the best long-term outcomes – –Efficacy is also better in pts without previous surgery – –Pts with spinal stenosis usually have less favorable prognosis, unless there is acute increase in recent pain
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