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Pain Management for Amputees. Dr Craig Davenport Rehabilitation Registrar Liverpool Hospital 19 th August 2005. Pain in the Amputee. Pre-operative pain – ischaemic, infection, trauma Early Post-op pain – somatic vs neuropathic, stump vs phantom limb

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Pain management for amputees

Pain Management for Amputees

Dr Craig Davenport

Rehabilitation Registrar

Liverpool Hospital

19th August 2005


Pain in the amputee
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


Stump pain
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


Phantom pain vs sensation
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)


Phantom limb pain
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


Plp onset
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)


Plp natural history
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)


Plp natural history1
PLP Natural History

  • Stump pain intensity tends not to correlate with PLP intensity

  • 2/3 experience telescoping of phantom limb


Also in kids
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


Why does pain occur
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


Why does pain occur1
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


Why does pain occur2
Why does pain occur?

Non-neurological factors:

  • Skin blood flow

  • Stump temperature

  • Muscle tension

    Psychological factors:

  • Stressors/ depression/ anxiety

  • Not personality types


Treatment approach
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


Treatment approach1
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


Non medical treatments
Non-Medical Treatments

  • TENS

  • Vibration Therapy

  • Acupuncture

  • Hypnosis

  • Biofeedback

  • Electroconvulsive Therapy

  • Mirror Treatment

  • Cognitive Behavioural Therapy

  • Farabloc (Conine 1993)


Peripheral stimulation
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


Potential drug treatments
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


Pre emptive analgesia
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)


Amitriptyline endep
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)


Other tca s
Other TCA’s

  • Nortryptiline

  • Imipramine

  • Doxepin


Gabapentin neurontin
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


Other anticonvulsants
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


Others
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


Pain and prostheses
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


Neuromas
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


Nasty interventions
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


Prognosis
Prognosis

  • When PLP persists 6 months, prognosis for spontaneous improvement is poor

  • Probably <10% have persistent severe pain


References
References

  • Bone et al, Reg Anaesth & Pain Med, 2002;27(5):481-6

  • Boyle et al, Oncology, 1982;10:301-312

  • Conine et al, Can J Rehab, 1993;6:155-61

  • Finsen et al, J of Bone & Joint Surg Br,1988;70:109-12

  • 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;21:267-78

  • Katz et al, J of Pain & Symp Man, 1991; 6:73-83

  • Kingery, Pain, 1997;73(2):123-39

  • Levy et al, APMR, 2001; 82(Suppl 1):S25-30

  • Malis et al, Cochrane database of Systemmatic Reviews, 2003(2):CD002918

  • Nikolajsen et al, Pain, 1996;67:69-77

  • Nikolajsen et al, Lancet,1997;350:1353-7

  • Pinzur et al, J Bone % Joint Surg Am, 1996;79:1752-3

  • Robinson et al, APMR,2004;85:1-6

  • Sherman et al, Pain,1984;18:83-95

  • Sherman & Sherman, Am J of Phys Med, 1983;62:227-38

  • Weinstein, 8th World Congress on Pain, 1996 pg376