Complex regional pain syndrome

Complex regional pain syndrome

1. Complex Regional Pain Syndrome
Ashraf Abdelaziz MD
Al-Azhar University

2. Case
•53 y male complains of severe wrist pain
–History of casting because distal radius fracture
–Burning pain for one year
–Numbness and tingling
–The pain increased by touching his skin
–His hand is ‘dark red’ and often swollen
–Weakness in the extremity.

3. Definition
International Association for Study of Pain defines CRPS as:
“continuous pain in a portion of an extremity after trauma,
which may include fracture but does not involve a major nerve,
associated with sympathetic hyperactivity.”

4. CRPS
•Complex: Varied and dynamic clinical
presentation
•Regional: Non-dermatomal distribution of
symptoms
•Pain: Out of proportion to the inciting events
•Syndrome: Constellation of symptoms and
signs

5. Historical Perspective
•During the AmericanCivil War (1864), Silas Mitchell observed a
chronic pain syndrome in soldiers who suffered traumatic injuries
•He described this syndrome using the term Causalgia.

6. •At the beginning of the 20th century, Paul Sudeckidentified the
localized bone atrophy by x-rays (sudeck’satrophy)
•Because the inflammatory irritation which involves nutritional
problems and in consequence resorption of bone

7. •In1917aFrenchsurgeonnamedRene
Lericheimplicatedthesympathetic
nervoussysteminCausalgia
•Hetreatedthesepatientswithsurgical
sympathectomy

8. •In the 1950’s, John Bonicaintroduced the phrase reflex
sympathetic dystrophy

9. •Many terms used to describe the condition:
»Sudeck’sdystrophy
»Post-traumatic dystrophy
»Acute atrophy of the bone
»Algodystrophy
»Algoneurodystrophy
»Chronic traumatic edema
»Postinfarctionalsclerodactyly
»Post-traumatic algodystrophy
»Post-traumatic osteoporosis
»Post-traumatic spreading neuralgia
»Post-traumatic sympathetic dystrophy
»Pseudodystrophy
»Reflex neurovascular dystrophy
»Shoulder hand syndrome
»Sympathalgia
»Traumatic angiospasm
»Traumatic vasospasm

10. Epidemiology
•Incidence: 5/100,000/year
•The mean age: 36 -46 years
•Women : 80%
•60% occurs in the upper extremities
•40% occurs in the lower extremities
•Incidence after fracture (16%–46%)
•Strain or sprain (10%–29%)
•Post surgery (3%–24%)
•Contusion or crush injury (8%–18%).

11. •There is nocorrelation between the severity of trauma and the degree
of CRPS symptoms.
•No psychological factor predisposing for CRPS has been
identified
•However 80% of CRPS patients had ‘stressful life events’ close to the
time of diagnosis.

12. •Two types of CRPSbased on the presence of a nerve injury
•CRPS type I: often involves only one limb with pain, minor
edema,after a period of immobilization.
•CRPS type II: presence of a known injury to a nerve.

13. Classification
Lankford and Evans Stages of CRPS
•Acute: 0-3 months, burning, swelling, warmth, hyperesthesia, cold
intolerance, joint stiffness
Normal x-rays, +ve three-phase bone scan
•Subacute (dystrophic): (3-12 months), worsening pain, cyanosis,
stiffness, skin atrophy
Subchondral osteopenia on x-ray
•Chronic(atrophic): > 12 months, Diminished pain, glossy skin, joint
contractures
Extreme osteopenia on x-ray

14. Clinical presentation
•Characteristic triad of symptoms comprising autonomic, sensory, and
motor disturbances

15. •Distal edema –80%
•Skin temperature changes –80%
•The affected hand is initially warm.
•Skin color changes
•Initially red, becomes pale in chronic cases
•Sweating
•Increased sweating more common
•Nail and hair changes
•Increased growth in early disease

17. •Spontaneous pain:
•Burning, aching, throbbing, shooting, or deep pressure pain
•Hyperalgesia
•Motor changes:
•Weakness, distal tremors, dystonia
•As a part of the clinical presentation or a result of disuse
painful limb

18. •Bony changes:
•Osteoporosis –periarticular distribution
•Joint stiffness

19. •Patients often have associated psychological disturbances
•These are generally consequences of the disorder

20. Pathophysiology
•Three main hypotheses
•Neurogenic inflammation
•Autonomic dysfunction
•Neuroplasticchanges within the CNS

21. Diagnosis
•Diagnostic criteria for CRPS:
•Presence of an initiating cause of immobilization
•Continuing pain, allodynia, with pain disproportionate to any
event
•Evidence of edema, changes in skin blood flow, or abnormal
sudomotoractivity in the wrist.

22. •A modified diagnostic criteria (2007) to increase specificity (‘Budapest
criteria’):
•Pain is disproportionate to any inciting event
•Must report at least threesymptoms of the fourfollowing
categories:
–Sensory: hyperalgesia, allodynia
–Vasomotor: temp. skin, color changes or asymmetry
–Sudomotor: edema, sweating changes or asymmetry
–Motor: decreased range of motion, weakness, tremor, dystonia,
trophic changes

23. At least one sign in twoor more of the following categories:
▪Sensory: hyperalgesia or allodynia
▪Vasomotor: temperature asymmetry, skin colourchanges
▪Sudomotor: oedema, sweating changes, or sweating
▪Motor: decreased range of motion, motor dysfunction, or trophic
changes.

24. Diagnostic tests
•Three-phase bone scintigraphy:
•Significant uptake in the metacarpal bones
•high sensitivity and specificity for CRPS
•The best timing in the subacute (up to 1 year) phase

25. •Plain radiographs and MRI have not been shown to be sensitive or
specific for CRPS

26. •Diagnostic tests
•Sympathetic ganglia block
•Regional intravenous block
•Phentolamineinfusion test (alpha-1 receptor antagonist)

27. Management of CRPS
•Therapy is directed at managing the signs and symptoms of the
disease
•A multiple approaches
•Drugs therapy
•Physical therapy
•And psychological therapy is most appropriate

28. •Drugs demonstrated to be effective for CRPS based on randomized
controlled trials:
–Steroids(oral): anti-inflammatory, neuronal membrane stabilizer
–Vitamin C (oral): antioxidant
–Alendronate(IV): osteoclast inhibitor
–Bretylium(IV): Autonomic ganglia blocker
–Ketansarin(IV): serotonin and alpha receptor antagonist
–Phentolamine(IV): alpha-1 receptor antagonist
–Lidocaine(IV): sodium channel blocker
–DMSO (topical): free radical scavenger
–Calcitonin(intranasal): osteoclast inhibitor
–Clonidine (epidural): alpha-2 receptor agonist
–Baclofen(intrathecal): GABA-B receptor agonist
Drugs therapy

29. Physical therapy
•Early physical therapy is essential to avoid atrophy and
contractures.
•Physical therapy to :
❖Reduce pain
❖Improve functionand coordination ability of the limb
•The patients should take an active role in their care

30. Psychological therapy
•Psychological dysfunction is a reflection of the
disease.
•Pain coping skills
•Relaxation training
•Cognitive behavioral therapy
•Mirror therapy
Mirror therapy

31. Invasive therapy
Sympathetic nerve blocks
•Diagnostic and therapeutic
•Helping patients to tolerate physical and occupational
therapy

32. Peripheral nerve stimulator
•Programmable stimulators placed on affected nerves
•Electrodes are placed along the course of peripheral
nerves to control pain..
•Types
–Transcutaneous electrical stimulation (TENS)
–Peripheral nerve stimulation
–Spinal cord stimulation

33. •Surgical/chemical sympathectomy
•Surgical sympathectomy appears significantly more effective
than chemical sympathectomy
–Excision
–Electrocautery

34. Surgical decompression
•Indications
–CRPS with known nerve involvement (e.g. carpal tunnel release if
median nerve involved)
–Treatment of associated nerve problems.

35. •Most studies indicate that patients with early diagnosis and treatment
(within 6 to 12 months) have an overall good outcome.
•Spontaneous resolution can occur if CRPS is diagnosed and managed
early

36. Summary
➢CRPS is a complicated chronic pain syndrome
➢Variable clinical presentation and complicated diagnostic
criteria.
➢Diagnosis is made on a clinical criteria
➢Treatment is best managed with a multiple approaches including
medications, interventional procedures, physical therapy and
psychological therapy

37. ارك

ش
Thank you