Can read freely here https://sethiortho.blogspot.com/ Complex Regional pain syndrome Silas Mitchell Causalgia. Burning pain after a tramatic nerve injury combined with vaso motor, sudomotor and trophic changes , Paul Sudeck identified the localized bone atrophy by x-rays (sudeck’s atrophy) Because the inflammatory irritation which involves nutritional problems and in consequence resorption of bone In 1917 a French surgeon named Rene Leriche implicated the sympathetic nervous system in Causalgia He treated these patients with surgical sympathectomy In the 1950’s, John Bonica introduced the phrase reflex sympathetic dystrophy Complex: Varied and dynamic clinical presentation Regional: Non-dermatomal distribution of symptoms Pain: Out of proportion to the initiating events Syndrome: Collection of symptoms and signs CRPS – I Common presentation than CRPS -II Reflex sympathetic dystrophy CRPS – II Causalgia Develops after injury to a peripheral nerve or main branches Incidence - 2.5 - 5/100 000 Incidence after fracture (16 –46%) Strain or sprain (10 –29%) Post surgery (3 –24%) Contusion or crush injury (8 –18%) Upper limb : lower limb- 3: 2 Female : male ratio - 3: 2 Old > young (Common 50 – 60 yrs ) Multifactorial origin Definitive cause still remains unknown Three main hypotheses Autonomic dysfunction Neurogenic inflammation Neuroplastic changes within the CNS Increased Sympathetic activity Upregulation of adregenic receptors Adregenic receptor expression on nociceptive fibres In chronic stage of CRPS Acute tissue damage mediated classical inflammation Cytokines – IL-1,IL-6 and TNF Lowering pain threshold of nociceptive nerve endings Peripheral sensitization Neurogenic inflammatory response Neuropeptides and cytokines released by nociceptors Substance P, bradykinin and glutamate Lower the pain threshold/ vasodilation/oedema Peripheral sensitization Early onset of distal odema – 80% Changes / asymmetry skin colour - 40% Initially red, becomes pale in chronic cases Autonomic disturbances Sensory changes Motor disturbances Trophic changes Changes/ asymmetry skin temperature – 80% Affected limb initially warm later become cold Sudomotor changes Hypohidrosis – Early diminished sweating Hyperhydrosis - Increased sweating more common

1. Complex Regional
pain syndrome
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Sethinet presentations

2. Introduction - CRPS
• Mostly associated with minor trauma/ Immobilization
• Severity of the pain is high and continuous
• There is no correlation between the severity of trauma and the degree of CRPS
symptoms
• Debilitating type pain -
• Associated with sensory, vasomotor, sudomotor and trophic disturbance

3. Historical Perspective
• American Civil War (1864), Silas Mitchell observed a
chronic pain syndrome in soldiers who suffered traumatic
injuries.
• He described this syndrome using the term Causalgia.
• Burning pain after a tramatic nerve injury combined
with vaso motor, sudomotor and trophic changes

4. Historical Perspective
At the beginning of the 20th century, Paul Sudeck identified
the localized bone atrophy by x-rays (sudeck’s atrophy)
Because the inflammatory irritation which involves
nutritional problems and in consequence resorption of
bone
In 1917 a French surgeon named Rene Leriche implicated
the sympathetic nervous system in Causalgia
He treated these patients with surgical sympathectomy

5. Historical Perspective
• In the 1950’s, John Bonica introduced the phrase
reflex sympathetic dystrophy
• In 1994- IASP – Proposed the term CRPS

6. Complex Regional Pain Syndrome
• Complex: Varied and dynamic clinical presentation
• Regional: Non-dermatomal distribution of symptoms
• Pain: Out of proportion to the initiating events
• Syndrome: Collection of symptoms and signs

7. Types – based on presence of nerve injury
• CRPS – I
• Common presentation than CRPS -II
• Reflex sympathetic dystrophy
• CRPS – II
• Causalgia
• Develops after injury to a peripheral nerve or main branches

8. Epidemiology
• Incidence - 2.5 - 5/100 000
• Incidence after fracture (16 –46%)
• Strain or sprain (10 –29%)
• Post surgery (3 –24%)
• Contusion or crush injury (8 –18%)
• Upper limb : lower limb- 3: 2
• Female : male ratio - 3: 2
• Old > young (Common 50 – 60 yrs )

9. Pathology
• Multifactorial origin
• Definitive cause still remains unknown
• Three main hypotheses
• Autonomic dysfunction
• Neurogenic inflammation
• Neuroplastic changes within the CNS

10. Autonomic dysfunction
Increased Sympathetic activity
• Upregulation of adregenic receptors
• Adregenic receptor expression on nociceptive fibres
In chronic stage of CRPS
Vasoconstriction Hypoxemia Acidosis Free radicals
formation Oxidative stress

11. Inflammation
• Acute tissue damage mediated classical inflammation
• Cytokines – IL-1,IL-6 and TNF
• Lowering pain threshold of nociceptive nerve endings
• Peripheral sensitization
• Neurogenic inflammatory response
• Neuropeptides and cytokines released by nociceptors
• Substance P, bradykinin and glutamate
• Lower the pain threshold/ vasodilation/oedema
• Peripheral sensitization

12. Central sensitization
• Increase excitability of 2ry nociceptive neurons in the spinal cord
• Alternation in nocieceptive processing in the CNS
Hyperalgesia – Increased pain from noxious stimuli
Allodynia – Pain in response to non noxious stimuli

13. Clinical Presentation
1. Autonomic disturbances
2. Sensory changes
3. Motor disturbances
4. Trophic changes

14. Autonomic disturbance
• Early onset of distal odema – 80%
• Changes / asymmetry skin colour - 40%
Initially red, becomes pale in chronic cases
• Changes/ asymmetry skin temperature – 80%
Affected limb initially warm later become cold
• Sudomotor changes
• Hypohidrosis – Early diminished sweating
• Hyperhydrosis - Increased sweating more common

15. Sensory and motor
disturbance
Sensory
• Pain – deep ache/ burning pain
• Allodynia
• Hyperalgesia
• Hyperresthesia – increased sensation – cold/warm
Motor
• Weakness
• Tremor
• Dystonia

16. Other clinical features
• Trophic changes
• Nail growth
• Hair growth
• Hyperkeratosis
• Psychological changes
• Fear
• Anxiety
• Depression
• Bony changes:
• Osteoporosis
• Joint stiffness

17. Lankford and Evans Stages of CRPS
• Acute
• 0-3 months
• Burning type pain
• swelling
• Hyperesthesia
• Subacute / dysrophic
• 3-12 months
• Worsening of pain
• Stiffness
• X-ray –subchondral osteopenia

18. Lankford and
Evans Stages of
CRPS
• Chronic / atrophic
• > 12 months
• Skin and joint contracture
• Extreme osteopenia in X ray

19. Differencial diagnosis
• Deep vein thromposis
• Thrombophlebitis
• Cellulitis
• Lymphedema
• PVD
• Dupuytren`s contractures
• RA

20. Diagnosis
• No pathognomonic signs/symptoms
• No definitive diagnostic test
• Diagnosis based clinical evaluation
• Budapest criteria - IASP -2007
• Sensitivity – 85%
• Specificity – 69%

21. IASP Diagnostic criteria -2007 - Budapest criteria
• Continuous Pain is disproportionate to any inciting event
• Symptoms - Must report at least one symptoms in three of four following categories:
• Sensory: hyperalgesia, allodynia
• Vasomotor : temp /skin, color changes or asymmetry
• Sudomotor : edema, sweating changes or asymmetry
• Motor/ Trophic :
Motor - Decreased ROM, weakness, tremor, dystonia,
Trophic – Skin, hair, nails changes

22. IASP Diagnostic criteria - Budapest criteria
• Signs – must meet at least one sign in two or more of four categories
• Sensory: Evidence of hyperalgesia or allodynia
• Vasomotor : Asymmetry in skin temperature/ colour/
• Sudomotor : evidence of odema /sweating changes
• Motor / trophic–
Motor - Evidence of decrease ROM, Motor dysfunction
Trophic – skin changes , hair and nail growth

23. Management of CRPS
• Therapy is directed at managing the signs and symptoms of the disease
• A multi disciplinary approaches
• Early treatment is necessary to achieve complete recovery and prevent damage
• Management
1. Medical and non medical pain therapy
2. Physical therapy
3. Psychological therapy

24. Treatment goal
• Pain relief
• Functional recovery of the affected limb
• Psychological improvement

25. Pharmacotherapy
Anti inflammatory drugs – inhibit inflammation
• NSAIDS and steroids – Can use in early stage of the disease
• No effect on neuropathic pain
Opioids - inhibit pain pathway
• Tramadol and morphine
• Can use moderate to severe pain
• Efficacy in neuropathic pain

26. Pharmacotherapy
Antiepileptics – inhibit pain pathway and plasicity
• Gabapentin, Pregabalin
• No effect on CRPS type I
• Efficacy in neuropathic pain
• Can use chronic and acute condition
Free radicals scavenger – reduce pain and inflammation
• Vitamin C and N- acetyl cysteine
• Effective on acute phase
• Decrease the recurrence of symptoms
Antidepressants
• Amitriptyline imipramine venlafaxine
• effcacy in neuropathic pain

27. Pharmacotherapy
Bisphosphonates – Alandronate, pamidronate
• Reduce bone turnover
• Have anti nociceptive effect
• Effective in acute and subacute phase
NMDA agonist – change central sensitization
• Ketamine - chronic CRPS
• Dose and length is still unclear
Topical anesthetics
• Lidocaine cream
• Trans dermal absorption patches

28. Pharmacotherapy
Calcitonin – intranasal spray
• Regulate bone metabolism
• Analgesic effects
Vasodilators
• Alpha adregenic antagonist- Clonidine transdermal patch
• Calcium channel blockers – Nifidipine -control extreme vasoconstriction
Muscle relaxants
• Intrathecal/ oral baclofen - dystonia

29. Physical therapy
• Early rehabilitation – good functional restoration
• Not always possible – severe pain/ psychological disorder
• Advantages
• Prevent muscle atrophy
• Prevent contracture
• Control oedema
• Improve joint mobility
• Pain relief – desensitization of affected limb

30. Psychological therapy – IASP recommendations
<2months – does not need
> 2months with pain-
• Need psychological evaluation and Identify and treat the psychological disease
• identify the factors determine the disability of the patient
• Treatment options are
• Counseling
• Behavioral modification
• Relaxation therapy
• Self hypnosis

31. Interventional Techniques
Nerve stimulation – Nerve stimulator placed in the spinal cord, peripheral nerve
• More effective
• High complications
Sympathetic nerve block
• Indicated for patient with Refractory to drug treatment
• Improve short term pain relief and mobility
• Effectiveness is greater in Early stage
Surgical / chemical sympathectomy
• High risk of recurrence between 6 months to 2 yrs
Amputations – indications
• limb dysfunction , severe Pain
• Gangrene / infection / Ulcer
High chance of phantom limb pain and recurrence in residual limb

32. Emerging treatments
Hyperbaric oxygen therapy
• Anti noceciptive effect
• Reduce edema and increase ROM
• A RCT study – Done on 71 patients with CRPS, 97% rapid and marked
improvement in pain seen at the end of the first day

33. Emerging treatments….
Botulinum toxin
• Pain relief in neuropathic pain
• A Study 97% reported pain relief
• Can use to treat the fixed dystonia

34. Emerging treatments…..
Plasma exchange therapy
CRPS also have autoimmune etiology
A study –
• 91 % of pateints reported significant median pain reduction
• Weekly plasma exchange reduce pain in 45% of patient

35. Prognosis
Still difficult to predict …
Good outcome
• 1st yr – 74%
• 6th yr – 36%
Returns to work – vary
Recent study -
• Permanent inability to work – 31%
• Partially inability to work – 28%

36. Thank you