complex regional pain syndrome, CRPS, Allodynia, causalgia

1. Chairperson : Prof & HOD, Dr. Kiran kalaiah
Moderator : Prof, Dr. Mahesh K U
Presenter : Dr. Yashavardhan.T.M
Seminar presentation on topic: CRPS
DEPARTMENT OF ORTHOPAEDICS

3. IASP NOMENCLATURE
CRPS I = Reflex Sympathetic Dystrophy
CRPS II = Causalgia
The only difference between the two is the
inciting event: minor trauma (I) versus major
peripheral nerve injury (II).
Synonym: Algodystrophy, Sudeck’s atrophy,
sympathetically maintained pain, shoulder/hand
syndrome, transient osteoporosis, and acute
atrophy of bone.

4. 1864 - COLONEL WEIR
MITCHELL, MD
“SEVERELY PAINFUL
DYSTROPHIC SYNDROME
FOLLOWING BALLISTIC
INJURIES” IN CIVIL WAR
SOLDIERS: CAUSALGIA

5. Early 20th century Peter
Sudeck Described features
of pain, swelling, atrophy
etc. following minor injury to
limbs – hence this
phenomenon came to be
called “Sudeck’s atrophy”
PAUL SUDECK

6. JOHN BONICA
Promoted the term RSD
Described 3 stages

7. RENE LERICHE
Sympathetic nervous
system dysfunction as a
cause of pain.
Therapeutic surgical
sympathectomy

8. EPIDEMIOLOGY
CRPS I: 21 per 100,000
CRPS II: 4 per 100,000
Female-to-Male ratio: 3:1
Any age, but middle age predominates
Median 42 years
Onset 9 – 85 years of age
CRPS occurs in about 1-2% of patients who have had
fractures and in approximately 2-5% of patients after
peripheral nerve injuries

9. Causes:
1. Injury to pns in colles fracture with tight
plaster causing ischemia to dorsal radial nerve
of wrist.
2. Ephaptic crosstalk: insulting myelin sheath
layer damaged by injury allowing electrical
signals to jump from one nerve fibres to an
adjacent one. This causes the light touch and
temperature sensory signals to get mixed up
with pain messages.
PATHOPHYSIOLOGY

10. 3. Dorsal horn reorganisation: after nerve injury the
central connections for each sensory modality( light
touch, pain, vibration, temperature) unplugs like
telephone exchange and reconnects to wrong socket.
Thus light touch and temperature modalities
becomes painful.
4. SNS changes: increase in number of noradrenergic
receptors on the surface of peripheral nerve distal to
site of nerve injury. Their by causing receptor
sensitivity in periphery and causing firing off more
rapidly.

11. CLINICAL PRESENTATION
Precipitating event:
CRPS I
Minor trauma, contusion, sprain or strain
Fracture (especially colles fracture)
Post surgical
Immobilization
Less frequently: CVA, spinal cord injury
CRPS II
Documented peripheral nerve injury and concordant focal
deficits (but the signs and symptoms of CRPS are not limited to
the same distribution as the affected nerve.)

12. STAGE 1
Begins within days or week of the precipitation injury
1. Cold hyperalgesia: cold hurts
2. Mechanical hyperalgesia: movements causes pain
3. Vasomotor changes: colour changes red r blue skin colour
4. Sudomotor changes: excessive sweating
5. Sclerotomally mediated pain: pain does not follow the
particular nerve root.
6. Thermographic changes: increase in the temperature.
7. Radiographic: normal
8. Bone scan: increase uptake.
CLINICAL FEATURES

13. CLINICAL PRESENTATION
PAIN, PAIN, PAIN
Spontaneous, constant, burning, aching, throbbing
Disproportionate to the injury and persists beyond
normal or expected recovery period
Asymmetrical and not in the distribution of a
peripheral nerve. Worst distally.
Severe mechanical and thermal allodynia,
hyperalgesia, and hyperpathia

14. STAGE 2 (DYSTROPHIC)
6 WEEKS--1 YEAR
1. Pain becomes more severe
2. SKIN: Cool, moist, tight/shiny, swelling,
coarse/sparse hair, brittle nails, discolored, edema
3. SYMPATHETIC:
• VASOMOTOR: Mottled/cyanotic
• SUDOMOTOR: Hyperhydrosis
4. MOTOR: Weakness, decreased ROM
5. BONE SCAN: No longer helpful.
6. Radiogram: spotty wasting of bone[osteoporosis]

15. Stage 2 (Dystrophic)

16. Stage 2 (Dystrophic)

17. CRPS STAGE 3 (ATROPHIC)
6 MONTHS--FOREVER?
1. Pain is somewhat decreased (but still debilitating) less at rest,
worse with passive motion
2. Changes are irreversible, poor outcomes, permanent
disability
3. SKIN: Atrophy, “waxy”, very thin, ulcerations, brittle
nails
4. SYMPATHETIC: VASOMOTOR: Cold, intermittently
cyanotic/mottled
5. MOTOR: Decreased ROM, weakness, muscle & tendon
atrophy, contractures, dystonia, tremor. Nonfunctional
limb. STIFFNESS.
6. X-RAYS: Diffuse patchy osteoporosis (Sudeck’s Atrophy)

18. 1. MINOR CAUSALGIA: following injury to purely sensory nerve
2. MINOR TRAUMATIC DYSTROPHY: due to minor crush
injuries, sprain and fractures rather than any specific nerve injury.
3. MAJOR TRAUMATIC DYSTROPHY: develops after major
crush injury Or colle’s fractures
4. MAJOR CAUSALGIA: MITCHALL Et.al pointed out major
mixed nerve injuries. Most commonly median nerve and
sciatic nerve accounts 60% of cases.
5. SHOULDER HAND SYNDROME: as described by steinbroker,
LANKFORD CLASSIFICATION OF
RSD

19. • It is characterised by pain stiffness in the entire upper
extremity as a result of proximal injury to neck, chest
or shoulder or to a viscera lesions such as cervical
disc, heart attack, gastric ulcers, stroke or pan cost
tumour.
• Stiffness and pain in shoulder usually occurs first
following pain swelling and stiffness of wrist, hand
and fingers.
• fusiform swelling of the fingers and over the dorsum
of hand and wrist is characteristic.
SHOULDER HAND SYNDROME.

20. 1. MUSCULE TESTING: strength and range of motion can demonstrate joint
stiffness, myofascial contractures, mechanical allodynia and muscule
weakness.
2. Radiological examination: plain x ray shows osteopenia in affected limb only
after 2-4 weeks after the onset of symptoms.
3. Bone scans: increased uptake on the affected side is indicative od CRPS
induced osteopenia
bone scan is performed after administration of 15-20 mciof Tc 99m
labelled diphosphonates or polyphosphonates
First phase= immediately obtained consists of angiographic images
Second phase= 1-5 min after injection reflects regional blood pool distribution
Third phase= 1.5 hrs to 4 hrs reflects trace uptake by the bone it is more reliable
phase for conforming the clinical diagnosis, severity forms 54% -100%
DIAGNOSIS

21. 4. Modified sympathetic blockade testing: normal saline
solution is injected in control group and novacaine
(5% procaine ) is used as a pharmacological neural
blocker.
• The solution is injected into stellate ganglion when
the arm is involved or lumbar paravertebral ganglion
blockade when lower limb is involved.
• Patient can me monitored for pain, limb
temperature, pin prick response, motor function and
blood pressure changes.
• Pain relived by saline inj considered as psychological
origin.

22. 5. THERMOGRAPHY:
• Provides indispensable diagnostic and therapeutic
information.
• Both superficial and deep temperature changes
influences Infrared Testing, Inc test.
• The skin is perfect radiator b/t deep and surface of
heat, this radiator is 98% emissive efficiency.
• ITI records pathological temperatures at least as
deep as 27mm in extremities and deeper in the
breast.
• The pt is cooled down in a 20-21’C steady room for
30 min of equilibrium without clothing.

23. • No prior smoking for 90 min. A standard
sensitivity of 24-34’C was done, Two identically
reproducible images recorded on laser disc are
required.
• It will give excellent diagnostic information in
neuropathic pain. Such as cannot be achieved
by EMG r NCV
• ITI identifies hyperthermic foci of permanent
sympathetic system damage sparing pt from
further damage by trauma of sympathetic nerve
blocks.

24. CRPS I DIAGNOSTIC CRITERIA - IASP
1. The presence of an initiating noxious event or a
cause of immobilization.
2. Continuing pain, allodynia or hyperalgesia with
which the pain is disproportionate to the inciting
event.
3. Evidence at some time of edema, changes in skin
blood flow or abnormal sudomotor activity in the
painful region.
4. The diagnosis is excluded by the existence of
conditions that would otherwise account for the
degree of pain and dysfunction.
note: Criteria 2,3 and 4 are necessary for a diagnosis of complex regional pain
syndrome.
International Association for the Study of Pain: Diagnostic Criteria for Complex Regional Pain

25. CRPS II (CAUSALGIA) - IASP
1. The presence of continuing pain, allodynia or
hyperalgesia after a nerve injury, not necessarily
limited to the distribution of the injured nerve.
2. Evidence at some time of edema, changes in
skin blood flow or abnormal sudomotor activity
in the region of the pain.
3. The diagnosis is excluded by the existence of
conditions that would otherwise account for the
degree of pain and dysfunction.
note: All three criteria must be satisfied.
International Association for the Study of Pain: Diagnostic Criteria for Complex
Regional Pain Syndrome with 1997 ICD Codes
Merskey H, Bodguk N, eds. Classification of chronic pain, descriptions of chronic pain syndromes and
definitions of pain terms. Id ed. Seattle: IASP Press, 1994:40-3.

26. DIFFERENTIALS
1. Arthritis: atypical, Rheumatoid syndrome & Gout
2. Peri-arthritis, septic arthritis
3. Inflammation and infections
4. Bursitis
5. Capsulitis, tenosynovitis
6. Post herpetic neuralgia
7. Herniated disk
8. Nerve entrapment neuropathies
9. PVD

27. TREATMENT GOALS
Relief of pain
Return of function
Prevent or slow progression
IMPROVED
OUTCOME=
EARLY
TREATMENT

28. 1. NSAIDS
2. Pregabalin and gabapentine for neuropathic pain
3. Amitriptline (10-15mg) with Pregabalin or
gabapentine can drastically reduces allodynia
4. Katamine 30-80mg per day orally.
5. Nifidipine CCBS reduces peripheral vasoconstriction.
PAIN CONTROL:

29. • Vitamin C is a well-documented anti-oxidant capable
of stabilising reactive oxygen species (ROS), which
cause damage to membrane lipids and to the
microcirculation.
• In patients with burn injuries, high-dose vitamin C
supplementation decreases vascular permeability,
thereby limiting protein losses. Vitamin C diminishes
lipid peroxidation, the process by which ROSs damage
the vascular endothelial cells
• The endothelial barrier is also impaired in CRPS-I.
Burn injuries and CRPS-I share similarities, as both
involve inflammation and micro-angiopathy.
VITAMIN C

30. PHYSICAL THERAPY
• In the acute stage PT is the most important factor
in reversing the syndrome.
• Later, it can improve pain & function and help
prevent progression and migration.
• Aggressive PT may only be possible with
treatment of pain: pain meds, sympathetic
and/or somatic blockade.

31. • Safe, pain less and it uses pressurized o2 administered inside a
specifically designed chamber to deliver this life giving
elements to o2 starved tissues
• At this pressure o2 which normally delivered to tissues via the
haemoglobin in RBCs and other body fluids.
• Typical treatment session is 45 min to 2 hrs.
HYPERBARIC O2

32. • Similar to diving disorders
• Pressure changes can cause a squeezed or
barotrauma in tissue surrounding trapped air
inside the lungs, behind ear drum, inside Para
nasal sinuses and underneath dental fillings
• Temporary blurring of vision due to swelling
of lens resolves after 2-4 weeks. Also due to
optic neuritis.
COMPLICATIONS RELATED TO
HBO

33. 1. Under anti cancer drugs- doxorubicin &
cisplatin.
2. Disulfirum.
3. URTI
4. High fever
5. Emphysema with co2 retention
CONTRAINDICATIONS OF HBO

34. STELLATE GANGLION BLOCK

35. • Drugs such as bepuvicane 0.25% or lidocane
1%
• Onset of HORNERS syndrome is good
prognostic block, indicates sympathetic system
problem.
• Increases the body temperature by 1.5’C

36. • This techinique involves, 3 needles placed 5 cm laterally to midline
opposite the transvers process of L1,L2 and L3 or L2,L3 and L4
• When the transverse process are encountered, the needle are redirected
above or below and inserted to depth of 3.5 cm to 4cm so their tips
encounter the sympathetic trunk, lying along the anterolateral border
lumber vertebrae.
• 10 ml 1 % lidocane is injected into each needle with few moments a
sympathetic effects is appeared with warmth and drying of foot and relief
of pain.
LUMBAR SYMPATHETIC BLOCK

37. • It as been applied for treatment of causalgia since 1916
1. Surgical sympathectomy: it consists of section of sympathetic chain distal
to T3 ganglion and division of rami between T2 and T3 ganglia and their
respective intercostal nerves relives pain in upper extremity.
excision of L2 and L3 sympathetic ganglion through a high transvers
abdomen incision relives pain in lower limb.
LUMBAR SYMPATHECTOMY.

38. 2. Chemical sympathectomy: Alcohol based also
called as lytic blocks.
3. Radio frequency sympathectomy: heat
generating radio frequency electrodes causes
boiling hot temperature at targeted area which
coagulates kills nerve fibers and nerve cell.
4. Virtual sympathectomy:

39. PSYCHOLOGY (PSYCHIATRY)
Earlier anxiety progresses to severe depression. (Pain,
loss of work and self worth, financial loss, family
breakdown, pain behavior, medication dependence
and abuse)
Medical treatment of depression
Counseling, set realistic goals and expectations,
behavioral & cognitive therapies, biofeedback,
hypnosis.

40. CONTINUOUS INFUSION
• Tunneled epidural catheter. Patients who have a
good but short duration response to sympathetic
block or for sympathetic independent pain.
• May be left in place for several weeks.
• Titrate local anesthetic to sympathetic or somatic block with
minimal motor block.
• Physical therapy every waking moment!

41. • Implantable drug pumps may also be used to deliver
pain medication directly to the cerebrospinal fluid which
allows powerful opioids to be used in a much smaller
dose than when taken orally.
DRUG PUMP

42. SPINAL CORD STIMULATION
• Permanently implanted for control of chronic
neuropathic pain
• Tunneled percutaneous leads for several weeks in the
acute stage for therapeutic reversal for the disease. More
and more frequently used.
• Neuro-stimulation (spinal cord stimulator) may also be
surgically implanted to reduce the pain by directly
stimulating the spinal cord.
• • These devices place electrodes either in the epidural
space or directly over nerves located outside the central
nervous system.

43. THE FUTURE
• Education for earlier detection and
aggressive treatment.
• Better understanding of the
pathophysiology for development of
specific, targeted therapies.