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Pain Management for Amputees Dr Craig Davenport Rehabilitation Registrar Liverpool Hospital 19 th August 2005.

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Presentation on theme: "Pain Management for Amputees Dr Craig Davenport Rehabilitation Registrar Liverpool Hospital 19 th August 2005."— Presentation transcript:

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2 Pain Management for Amputees Dr Craig Davenport Rehabilitation Registrar Liverpool Hospital 19 th August 2005

3 Pain in the Amputee Pre-operative pain – ischaemic, infection, trauma Early Post-op pain – somatic vs neuropathic, stump vs phantom limb Late post-op pain – stump vs phantom limb

4 Stump Pain Somatic stump pain usually resolves as the wound heals Can trigger Phantom pain Prolonged stump pain usually attributable to local pathology – delayed wound healing, infection, surgical complications, poor prosthetic fit, neuromas, adherent scars Late onset stump pain - neuromas, prosthetic fit, claudication, bony overgrowth, osteoarthritis, tumour recurrence

5 Phantom Pain vs Sensation Phantom limb Sensation – almost universal doesn ’ t correlate with pain reports Non-painful phantom sensations of 3 types: Kinetic senstations (movement) Kinesthetic (size,shape,position) Exteroceptive (touch, pressure, temperature, itch, vibration)

6 Phantom Limb Pain Phantom pains often described as crushing, toes twisting, hot iron, burning, tingling, cramping, shocking, shooting, “ pins & needles ” Tends to localise to more distal phantom structures (eg fingers and toes) prevalence in early stages 60-80% Independent of age in adults, gender, level or side of amputation

7 PLP Onset Mostly onset immediately after amputation, some at two weeks. Rarely months later 1/3 maximal immediately post-op and generally resolved by 100 days ½ slowly peaked then improved within 100 days ¼ slower rise toward maximal pain (Weinstein, 1996)

8 PLP Natural History Tends to diminish in severity and frequency over time, with resolution over several weeks to 2 years One study – 72% at 8 days, 65% at 6 months, 59% at 2 years (Jensen, 1985) Duration of episodes vary - continuous 12%, days 2%, hours 37%, seconds 38% (Sherman & Sherman,1983) 50% had decreasing PLP with time 50% no change or increase over time (Sherman et al, 1984)

9 PLP Natural History Stump pain intensity tends not to correlate with PLP intensity 2/3 experience telescoping of phantom limb

10 Also in Kids PLP also occurs in children, often under- recognised 70-75% at 7 years after amputation, but none severe (Boyle et al, 1982) Less in congenital limb deficiency

11 Why does pain occur? Peripheral neuropathic mechanisms: immediate nerve injury discharge local nociceptive substances deafferentation ectopic firing neuromas Ephatic transmission b/w sensory and sympathetic fibers

12 Why does pain occur? Spinal cord: Expansion of receptive fields Low-threshold inputs when high-threshold inputs lost Disinhibition Brain: Cortical engram generates pain in absence of stimuli Cortical reorganisation

13 Why does pain occur? Non-neurological factors: Skin blood flow Stump temperature Muscle tension Psychological factors: Stressors/ depression/ anxiety Not personality types

14 Treatment Approach Non-Medical and Medical/Surgical Prevent contractures Limit oedema Adequate Post-op Analgesia Desensitisation - massage/bandaging Get patient moving, distraction helps Early prosthetic training

15 Treatment Approach Somatic Pain – non-pharm, simple analgesics, NSAIDs, tramadol, opioids Neuropathic/Phantom Limb Pain – follow neuropathic pain principles – Non-pharm, TCA’s, anticonvulsants, local anaesthetics

16 Non-Medical Treatments TENS Vibration Therapy Acupuncture Hypnosis Biofeedback Electroconvulsive Therapy Mirror Treatment Cognitive Behavioural Therapy Farabloc (Conine 1993)

17 Peripheral Stimulation Controlled trial of TENS/sham/largactil showed benefit at 16 weeks; no difference beyond 12 months, improved stump healing (Finsen,1988) Auricular TENS – controlled trial showed beneficial (Katz, 1991) Vibration & Acupuncture only case reports

18 Potential Drug Treatments Epidural anaesthesia Amitriptyline (Tricyclic antidepressants) Anticonvulsants – carbamazepine, gabapentin Clonazepam Opioids/Tramadol Mexiletine/lignocaine Beta/alpha blockers - clonidine Intrathecal opioids/ lignocaine Capsaicin cream, NSAID cream IV Ketamine Sympathetic ganglion block

19 Pre-emptive Analgesia Pre-operative anaesthesia: Early trials looked promising but less robust Better designed trials did not show benefit in PLP (Nikolajsen 1997) Peri-op regional nerve blocks – decreased use of opioids in early post-op period (Pinzer, 1996)(Fisher, 1991)

20 Amitriptyline (Endep) Well documented for neuropathic pain (Kingery, 1997) Generally considered effective Dose 10mg up to 150mg (75mg in elderly) Recent RCT in PLP  no benefit (Robinson 2004)

21 Other TCA’s Nortryptiline Imipramine Doxepin

22 Gabapentin (Neurontin) Evidence in neuropathic pain RCT in PLP benefit at 6 weeks (Bone 2002) 100mg tds up to 1200mg tds Relatively well tolerated Main side effects are dizziness/somnolence/memory impairment Not subsidised by PBS for pain  $150/mth

23 Other Anticonvulsants Carbamazepine (Tegretol) – cheap; proven in neuropathic pain, nasty haematological S/E’s Lamotrigine (Lamictal)– emerging evidence for neuropathic pain Valproate (Epilim)– lacks evidence, not very effective

24 Others Capsaicin – no RCT for PLP; unpleasant IV calcitonin (post-op) – unknown mechanism; reduced early PLP, longer term effect lacks evidence (Jaeger, 1992) Mexiletine – open label study in PLP; risk of sudden death Beta-blockers – limited reports Benzodiazepines – clonazepam limited reports IV Ketamine – reduces ‘wind-up’ – short-term reduction in PLP (Nikolajsen 1996) Opioids – probably have a role Tramadol – alternative to opioids NSAIDs not effective

25 Pain and Prostheses Use of Prosthesis – may increase or decrease pain Poor prosthetic fit may irritate stump tissues or neuroma  revise socket Musculoskeletal pain due to altered biomechanics  PTK/thigh lacer Sensitive stump may require altered prosthetic prescription  Silicon liner, Thigh Lacer Stump bandaging/ hard casting may reduce pain

26 Neuromas localized pain, sharp/shooting/paraesthesia Reproduced by local palpation, relieved by LA injection Tinel ’ s sign Try socket relief and local steroid/LA injection Ablation – Phenol alcohol injection into neuroma Surgery – not much evidence, high recurrence rate

27 Nasty Interventions Stump surgery – for defined pathology  bury nerve terminal in bone, excise bony spurs DREZ lesioning Sympathectomy – conclusive evidence lacking (Mailis 2003) Spinal cord stimulation – works but expensive, infection risk Deep Brain or Motor Cortex Stimulation – works but effect decreases with time Cordotomy/thalamotomy

28 Prognosis When PLP persists 6 months, prognosis for spontaneous improvement is poor Probably <10% have persistent severe pain

29 References Bone et al, Reg Anaesth & Pain Med, 2002;27(5):481-6 Boyle et al, Oncology, 1982;10: Conine et al, Can J Rehab, 1993;6: Finsen et al, J of Bone & Joint Surg Br,1988;70: Fisher et al, Anaesth Analg, 1991;72:300-3 Halbert et al, Clin Journal of Pain, 2002; 18:84-92 Jaeger et al, Pain, 1992;48:21-7 Jensen et al, Pain, 1985;21: Katz et al, J of Pain & Symp Man, 1991; 6:73-83 Kingery, Pain, 1997;73(2): Levy et al, APMR, 2001; 82(Suppl 1):S25-30 Malis et al, Cochrane database of Systemmatic Reviews, 2003(2):CD Nikolajsen et al, Pain, 1996;67:69-77 Nikolajsen et al, Lancet,1997;350: Pinzur et al, J Bone % Joint Surg Am, 1996;79: Robinson et al, APMR,2004;85:1-6 Sherman et al, Pain,1984;18:83-95 Sherman & Sherman, Am J of Phys Med, 1983;62: Weinstein, 8 th World Congress on Pain, 1996 pg376


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