COMPLEX REGIONAL PAIN SYNDROME

 INTRODUCTION:

Complex regional pain syndrome (CRPS) first came into picture in 19th century and was then known as CAUSALGIA (Injuring the nerves). This consisted of vague symptoms with or without dermatomal distribution. Then it was called as Sudeck’s Atrophy or Shoulder Hand Syndrome. Later now it is known as Complex Regional Pain Syndrome.

The International Association for the Study of Pain has proposed dividing CRPS into two types :

TYPE I: REFLEX SYMPATHETIC DYSTROPHY (RSD)

• No specific nerve involvement.
• Pain state maintained by a sympathetic efferent activation by the circulating catecholamines or by a neuro-chemical activation. (Catecholamine: A protein synthesized by adrenal gland, it is associated with any kind of injury).
•  RSD develops after a noxious event which is associated with a spontaneous pain or allodynia or hyperalgesia. (allodynia: abnormal hypersensitivity) differential diagnosis can be Trigeminal Neuralgia.
• RSD is not specific to a particular distribution (pain is vague in nature).
• Associated odema is present.
• Abnormal skin blood flow because of vasomotor changes.
• There are abnormal pseudomotor activities like trophic changes in skin.

TYPE II: CAUSALGIA

• Specific nerve injury.
• Most common nerves to get involved are median and tibial nerves. e.g. Tarsal Tunnel Syndrome.
• Same symptoms like Carpal Tunnel Syndrome. Pain along the nerve’s distribution.
• Odema, abnormal blood flow and psedomotor changes are same as in Reflex Sympathetic Dystrophy.

PATHOPHYSIOLOGY of CRPS :

Inappropriate continuation of sympathetic activity leads to vasodialation which results in odema and because of this odema there is a capillary collapse. This will lead to ischemia which causes pain leading to an increases in sympathetic activity and the cycle continues.

This is called as a Positive Feedback Loop.

EPIDEMIOLOGY of CRPF :

Females are three times more vulnerable than males.

Causalgia in nerve injury or any other bone injury like Colle’s fracture happens because of  tight cast application. Now a days the incident is much less because of improvement in management of Colles’s fracture.

SIGNS & SYMPTOMS of CRPF :

PRIMARY SIGNS :

• Pain: Constant, aching and burning pain). There is strong correlation between psychologial status and pain.
• Odema: Which gradually spreads proximally. In earlier stages it is soft. Later stages it is hard or brawny.
• Stiffness: Increase with swelling. Early mobilization is always advised. If stiffness goes untreated it can lead to fibrous ankylosis.

SECONDARY SIGNS :

• Associated osteopenia.
• Vaso-motor changes which lead to loss of skin creases.
• Hyperhydrosis.
• Loss of skin hairs.
• Nail changes like brittleness.
• Elongated long finger hairs.
• Shiny skin.
• Discoloration of skin.
• Fibrosis of palmar fascia.

OTHER ASSOCIATED SIGNS :

• Tremors
• Disuse Atrpohy.
• Dystonia or RSD hand or Dystonic hand. (Dystonia: abnormal variation in tone at times it can be hypertonic flaccid).

DIAGNOSTIC CHARACTERISTICS OF RSD :

• Normally associated with a provocative injury.
• Hyperalgesia.
• Allodynia.
• Pain which is not associated with dermatomal distribution.
• Pseudomotor and vasomotor changes.
• Radiographs showing osteoporotic and osteopenic changes.

STAGES OF RSD :

STAGE I :

Traumatic stage initiated after an injury.

1. Duration is from 0-3 months post injury.
2. Signs: pain, hyperalgesia, allodynia. The affected part becomes pale and it is cold on palpation.
3. Sometimes there can be cyanosis.
4. Oedema is soft which can distribute proximally.
5. Periarticular swelling which can lead to a joint stiffness.
6. Trophic changes which like fast growing nails,long finger hairs.
7. Relative disuse of the part.
8. Patient keeps it in particular position just to avoid any painful stimulation.
9. Ragiographs implement osteopenic changes.

STAGE II :

Called as Dystrophic Phase.

1. Duration : 3-6 months.
2. Skin becomes warm.
3. Swelling (diffused) which leads to obliteration of the skin creases.
4. Skin becomes shiny.
5. Associated hyperhydrosis.
6. Fine tremors.
7. Nails become brittle
8. Cracked nails or grooved nails.
9. Radiographs show osteoporotic changes.

STAGE III :

1. Atrophic stage.
2. Lasts for 6-12 months.
3. Skin becomes pale, cold, dry but shiny.
4. Because of disuse there is decreased muscle mass.
5. Oedema becomes hard or brawny which leads to gross joint stiffness.
6. There can be ankylosis of the joints presence of fibrous joints.
7. Associated changes in dystonic parts (hands or feet).
8. Associated tremors.

TREATMENT :

Primary goals :

• Early mobilization.
• Active assisted range of motion exercises. (NEVER GIVE PASSIVE ROM EXERCISES IN EARLY STAGES)
• To reduce or relieve odema.
• To improve local circulation and mobilization of the adjacent joints.

STAGE I TREATMENT :

• No heat is given.
• Cryotherapy helps.
• Faradism under pressure to reduce odema with compression bandage and active assisted exercises.
• Load assisted exercises: lighter resistance elastic bands. For gripping : soft ball squeezing exercises.

STAGE II TREATMENT :

• Iontophoresis : for hyperhydrosis.
• Continue with cryotherapy.
• Mobilization of major joints to relieve stiffness.
• Whirlpool bath to reduce odema.
• Fine motor skill training.
• Steriognosis (identification of shapes) training.
• Start strengthening exercises.

STAGE III TREATMENT :

• Major aim in this stage is to improve range of motion. Over pressure should not be applied because of presence of fibrous joints, ankylosed joints can lead to breakage of bones and fractures.

THOSE ABOVE ARE COLLECTED FROM SOME BOOKS AND WEBSITES..

THANK YOU,

SRIKUMARAN PHYSIOTHERAPY CLINIC & FITNESS CENTER