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Neuropathic Pain - A Palliative Care Approach

Neuropathic Pain - A Palliative Care Approach. Dr Reema Patel Staff Grade in Palliative Medicine. Content. Introduction Pathophysiology of neuropathic pain Mana gement of neuropathic pain The evidence What to do in Clinical practice. What is Palliative Care?.

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Neuropathic Pain - A Palliative Care Approach

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  1. Neuropathic Pain - A Palliative Care Approach Dr Reema Patel Staff Grade in Palliative Medicine

  2. Content • Introduction • Pathophysiology of neuropathic pain • Management of neuropathic pain • The evidence • What to do in Clinical practice

  3. What is Palliative Care? • The active, total care offered to a patient and their families, when it is recognised that their illness is no longer curable • It concentrates on the quality of life and alleviation of distressing symptoms within the framework of a coordinated service WHO Classification

  4. What is pain? • “An unpleasant sensory and emotional experience associated with actual or potential tissue damage” Merksey 1979 • It is a subjective feeling, rather than objective

  5. Why is neuropathic pain important? • Relatively common and can be difficult to treat • 34% of cancer patients referred to pain service (Grond 1999) • 30% of lung cancer patients (Potter 2004) • Up to 40% of all cancer-related pain may have a neuropathic mechanism involved (Caraceni 1999)

  6. Definitions • Neuropathic pain • Pain initiated or caused by a primary lesion/dysfunction in the nervous system • Neuralgia • Pain in the distribution of the nerves • Analgesia • Absence of pain in response to stimulation which would normally be painful • Allodynia • Pain due to a stimulus that does not normally provoke pain

  7. Hyperalgesia • Increased response to stimulus that is not normally painful • Noxious stimulus • One which is damaging to normal tissue • Nociceptors • Receptor preferentially sensitive to noxious stimulus (thermal, chemical or mechanical)

  8. What is normal - how is pain conveyed? • Nociceptors - connect to nerve fibres and carry sensation of pain to the dorsal horn in the spinal cord • These signals then cross the spinal cord and are transmitted to the brain in the spinothalamic tract

  9. Normal Pain Pathways

  10. Nerve fibres • A fibres - small diameter, myelinated • C fibres - small diameter, unmyelinated • A fibres - large diameter, myelinated (Fordham 1986)

  11. A fibres • Mainly found in or just under the skin • Activated by noxious stimuli • Intense heat, cold, mechanical and chemical • Fast or first pain

  12. C fibres • Usually in a single receptive area • Convey messages generated by damaged tissue • Slow or second pain

  13. A fibres • Responds to light touch or mechanical stimulation (mechanoreceptors) • Vibration, touch and pressure • Not normally unpleasant

  14. As a rule, C fibres are opioid sensitive and A fibres are not

  15. What happens in neuropathic pain? • The nerve fibres are damaged or dysfunctioning • This causes over activity of the nerve (even after noxious stimulation has gone)

  16. Pathophysiology • The nerve can generate impulses randomly and “fire-off’ • There is failure or reduction of the usual inhibitory mechanisms (disinhibition) • The brain and spinal cord may become unusually sensitive (central sensitisation) to the nerve impulses (NMDA involved in this)

  17. Causes of nerve damage • Peripheral • Central (Scadding 2003)

  18. Peripheral causes • Trauma - post thoracotomy • Diabetes • Nutritional - alcoholic • Drugs - Cisplatin, Isoniazid • Infective - Guillain Barre • Direct infiltration - Pancoast’s tumour

  19. Central causes • Spinal cord compression • Multiple Sclerosis • Intrinsic spinal cord tumours and syringomyelia • Spinal root - disc prolapse, trigeminal neuralgia

  20. How does it feel? • Can be difficult to describe • ‘Shooting,’ ‘burning,’ ‘toothache,’ electrical impulse’ • Often in one set place • Can follow the path of the affected nerve (common in root pain from spinal cord compression)

  21. How do we treat it? • Often with multiple treatment modalities • Multidisciplinary team approach is also valuable in complex pain

  22. Treatment modalities • Psychological • Spinal (epidural or intrathecal) • Surgery (decompression) • Block (nerve, plexus, root) • Pharmacological • TENS • Topical

  23. TENS • Transcutaneous Electrical Nerve Stimulation • Works in 2 ways • Electrical impulses stimulate A fibres (mechanical) • A fibre activity is greater than A and C fibre ‘pain’ activity, thereby closing the ‘pain gate’ • Stimulates the body to release its own natural pain killers (endorphin and enkephalin)

  24. Gate theory of pain (Melzack and Wall) • Stimulating large A fibres can inhibit pain response via interneuron.

  25. What drugs do the Palliative Care Physicians use? • Recent questionnaire to doctors on the Specialist Register for Palliative Care (2005) • ‘What are your choices for managing NP in palliative care?’ • Asked to give 1st, 2nd and 3rd line choices • To state maximum dose used

  26. Results • 82 questionnaires sent out • 68% reply rate

  27. Most popular drugs • Gabapentin • Amitriptyline • Ketamine • Methadone • Dexamethasone • Clonazepam (excluding opioids other than methadone)

  28. Summary of anti-neuropathic agents • Pharmacokinetics • Dosing • Evidence

  29. 1. Gabapentin • Calcium channel blocker • It is excreted unchanged by the kidneys and hence accumulates in renal failure • Doses • Rapid • 300mg OD day 1, BD day 2 and TDS day 3, adding 300mg a day as required to 600-1200mg TDS • Slow • 100mg TDS Day 1, 300mg TDS day 7, 600mg TDS day 14, 900mg TDS day 21

  30. Gabapentin • Cochrane review, Wiffen 2005 • 14 studies included (one study acute pain, one study cancer-related pain) • NNT = 4.3 • Evidence to show that gabapentin is effective

  31. Pregabalin • Related to gabapentin • Sabatowski 2004 - large study (192) in post herpetic neuralgia • Significant response Vs placebo at 2 dose levels: 150mg/d and 300mg/d

  32. 2. Amitriptyline • Tricyclic antidepressant • Blocks pre-synaptic reuptake of serotonin and noradrenaline • Dose • 10mg ON initially, increasing to 150mg ON over 7-8 weeks

  33. 2. Amitriptyline • 1996 systematic review McQuay et al • 17 RCTs • NNT for TCAs = 2.9 • SSRI are less effective that TCAs • Efficacy in burning Vs shooting pain not supported

  34. 3. Ketamine • Partial NMDA antagonist • Useful in neuropathic, inflammatory or ischaemic pain • Can also be useful in terminal uncontrolled pain

  35. Ketamine • Routes • PO • 10mg QDS and increase by 10mg increments OD to BD up to 50mg QDS • CSCI (continuous sub-cut infusion) - • 50-100mg/24 hours, increasing by 50-100mg every 72 hours up to 500mg/24hrs Always co-prescribe an antipsychotic, either haloperidol or midazolam due to the common S/E of dysphoria

  36. NMDA antagonists - Ketamine • Cochrane review, Bell 2003 • 2 RCTs of adults with cancer pain on opioids receiving ketamine • Mercadante 2000 - in cancer NP; 10 patients unrelieved by morphine, given IV ketamine with significant pain relief. 6 patients suffered central adverse effects

  37. 4. Methadone • Opioid that acts as a NMDA receptor antagonist + serotonin re-uptake inhibitor • Long and variable half life • Inactive metabolites therefore lower toxicity in renal failure • Faecally excreted • Can take up to 10 days to reach steady state

  38. When to use methadone • Pain partially responsive to morphine • Renal failure • Morphine tolerance Specialist prescribing + requires hospital admission

  39. Conversion of methadone • Stop all opioids • Loading dose: 5 to 10% of the 24hour PO morphine or equivalent, to a max of 30mg • Same dose as PRN but 3hourly • On day 6, add total dose of methadone in last 24hours and give 12hourly

  40. Conversion of methadone • Dose changes are at a percentage increment as for morphine every 4-6 days • Re-assess as accumulation can occur up to 10days after commencing/dose changing • CSCI - half the dose and dilute (very acidic) • Can exacerbate asthma and can cause a diuresis

  41. Methadone • Nicholson systematic review 2004 • Cancer pain (not NP specifically) • 8 studies • ‘Not possible to draw conclusions on relative merits of methadone compared to other opioids in the management of NP pain’

  42. 5. Dexamethasone • Steroid • Used as adjunct for acute NP • Anti-inflammatory • Dose - 6 to 12 mg daily

  43. 6. Clonazepam • Benzodiazepine • GABA potentiating actions in CNS, notably spinal cord, hippocampus, cerebellum and cerebrum • Reduces neuronal activity • Dose • 500mcg ON increasing to 4mg (half life 20-60hours)

  44. Conclusions drawn • Large number of different agents used • Lack of concurrence particularly after 1st/2nd line choices • Maximum doses of drugs were low (when compared to evidence) • Evidence based on non-cancer, peripheral NP pain models

  45. What about opioids? Multiple mechanisms of pain • Used in conjunction with classical NP drugs • Kalso 2004 systemic review (15 RCTs) • Mean decrease in pain intensity in most studies was at least 30% both for NP and musculoskeletal pain • Opioids included oxycodone, morphine, methadone and fentanyl Therefore always worth trying opioids

  46. In clinical practice • Are neuropathic mechanisms present? • Pain in area of altered sensation • Rapidly escalating doses of opioids with no significant improvement in pain • S-LANSS questionnaire

  47. Leeds Assessment of symptoms and signs - self report (S-LANSS) • Scored out of 24 • Scores of 12 or more are strongly suggestive of neuropathic pain • Questionnaire has been validated in The Journal of Pain (Bennett M et al (2001, 2005)

  48. What can you do? • Identify NP (hx/ S-LANSS) • Think about WHO pain ladder initially (esp. if multiple mechanisms of pain) Non opioid, weak opioid, strong opioid If non-opioid responsive, or clearly NP process: • If mild pain and no CI, AMITRIPTYLINE • If moderate to severe pain, GABAPENTIN • Consider DEXAMETHASONE at the same time • If pain continues refer for specialist input

  49. Any Questions?

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