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SYMPATHIC REFLEX DISTROPHY


SYMPATHIC REFLEX DISTROPHY / CAUSALGIA
Classified within the Post Traumatic Pain Syndromes, belonging to one of Medicine’s less comprehended clinical areas.

Diagnosis failure of these entities difficults the diagnosis and choosing the adequate treatment.

Confusion is made due to the existence of more than 30 terms to designate little variation of these syndromes (SYMPATHETIC REFLEX DISTROPHY, POST TRAUMATIC PAIN SYNDROME, PAINFUL POST TRAUMATIC OSTEOPOROSIS, POST TRAUMATIC SYMPATHETIC DISTROPHY, TRAUMATIC NEURALGY, CAUSALGIA, SUDECK’S SYNDROME, HAND-SHOULDER SYNDROME, ETC.)

All these denominations have disproportional pain, sympathetic dysfunction, late functional recovery and trophic alteration in common.

From the practical point of view, the acceptance of the term SYMPATHETIC REFLEX DISTROPHY to designate all post traumatic painful syndromes had great importance from the didactic point of view.

According to PSIA (PAIN STUDY INTERNATIONAL ASSOCIATION) the classification of chronic pain, since 1994, was established in type I - RPCS - REGIONAL PAIN COMPLEX SYNDROME and in type II RPCS (CAUSALGIA).
 
SYMPATHIC REFLEX DISTROPHY / VOLUME INCREASE OF THE AFFECTED SIDE
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Click on pictures for an amplified view

Click on pictures for an amplified view

 
RPCS TYPE I
In SYMPATHETIC REFLEX DISTROPHY, light to moderate lesions of extremities, or lesions in areas far from the dystrophy zone precede the symptoms appearance, these lesions do not have metameric distribution. In the electrophysiological exams there is no damage of a specific nerve and the clinical picture characterizes by a range of disautonomic motor sensorial symptoms together with a inflammatory process. Usually, RPCS presents paradoxally more severe symptoms than the causing trauma intensity. Sympathetic Reflex Dystrophy can happen due to lesion of soft parts, articulation or bones located anywhere, including face and torso. Orthopedic lesion of extremities can be the most important causing effect. The precipitating lesion can be light or moderate, making more difficult its relation with the syndrome. There is not an average interval between the lesion and symptom’s beginning, this can vary from immediately after trauma to months after it, what sometimes makes the causing effect identification harder.
 
RPCS TYPE II – CAUSALGIA
The first causalgia reports were made by Mitchell during the American civil war. The clinical picture featured intense burning with cutaneous hypersensibility to fine touch and it could be caused by movements, noises or even shocks. Autonomic symptoms could exist too. Curiously, causalgia symptoms only appear after partial lesion of the affected nerves and it never appears in complete lesions. Causalgia’s and sympathetic reflex dystrophy’s clinical presentations are very similar and what distinguishes them is the existence of lesion associated to a specific nerve in causalgia.

The distinction of post traumatic neuropathies that present extremely painful condition must be done, but without causalgia and sympathetic reflex dystrophy intensity and without the so important disautonomic inflammatory component.
 
SIGNS AND SYMPTOMS OF RPCS TYPE I AND II
The classic lesion that leads to causalgia’s arise is the high speed projectile lesion which causes partial lesion.

Extremities tissue damage, with or without nervous lesion evidence, is sometimes followed by diffuse burning pain and hyperalgesy in disparity with the trauma, if this one happens. This pain can be relieved by blocking the affected extremity’s efferent sympathetic activity. Hyperalgesia and spontaneous pain can be related to temperature decrease, hyperhidrosis and trophic alteration (muscular atrophy, bone demineralization).

Disestesy and pain are not necessarily restricted to the affected nerve and they can be so intense that the patient can not bare any contact with clothes. Any kind of stimulus to the member produces terrible pain. The extremity is protected by leaving the member in a position that prevents venous congestion, usually leaving the superior member flexed and adducted next to the torso.

Vasomotor dysfunction can occur under the form of vasoconstriction or vasodilatation. Vasoconstriction is more common so the hand extremities or the foot’s sole becomes shining, edemaciated, humid, cyanotic and cold when touched.

Autonomic symptoms such as generalized distal edema, extremely temperature sensitive extremity and hyperhidrosis can exist in different degrees.

Trophic alterations, in different degrees, are present almost every time, and if not treated in time, become irreversible as member atrophy and bone demineralization, which is evidenced in X-ray. Other trophic alteration may be present such as nail and hair growth, palmar or plantar fibrosis, thin skin and hypercheratosis.

In most of times, SYMPATHETIC REFLEX DISTROPHY is preceded by some kind of event like minor trauma, fracture, partial nervous lesion or other (shoulder trauma, myocardium infarct or even contralateral vascular brain damage).

Differential diagnosis must be done with pos traumatic neuropathy, fasceitis, osteomyelitis, peripheral neuritis, radicular compression and arthritis.
 
SYMPATHETIC NERVOUS SYSTEM FUNCTION
Sympathetic nervous system blocking or lesion has been used for years on causalgia and sympathetic reflex dystrophy treatment. Due to this factor, several authors consider autonomic disturbs as fundamental elements on the syndrome’s characterization, suggesting inclusive, that the sympathetic blocking may be an essential element to conclude the diagnosis. Other authors think that the hyperactivity of the sympathetic nervous system is not related to pain genesis and the sympathetic function must be rediscussed, or even dismissed.

The diagnosis must be based on anamnesis, signs, symptoms and on the response to sympathetic ganglion blocking with use of guanetidine. Fentolamine would be useful in the sympathetic nervous system (DMS) sustained division and independent pain of the sympathetic nervous system. (DIS)
 
TREATMENT
The main aim is pain relief and normal function reestablishment, or reestablishing the maximum of the affected member’s reminiscent functional potential, cutting as quick as possible the pain-immobilization-edema-alteration neurovegetative–disuse-pain cycle.

In a general way, treatment consists in using analgesics, non hormonal anti inflammatories, tricyclic antidepressives and fenotiazine associated to physical medicine and rehabilitation for a no longer than a month term.

In case of treatment failure, SYMPATHECTOMY IS INDICATED. This procedure can be done through radiofrequency or videothoracoscopy.

In superior members case, THORACIC SYMPATHECTOMY THROUGH VIDEOTHORACOSCOPY. The surgical blocking of sympathetic impulses to the affected member(s) interrupts the arc reflex, responsible for the causalgia syndrome.

Premature SYMPATHECTOMY prevents irreversible trophyc lesions incidence and does not allow definitive pain patterns establishment, which can become refractory even to sympathectomy if the definitive treatment is retarded.
 
PROGNOSIS
THORACIC SYMPATHECTOMY THROUGH VIDEOTHORACOSCOPY offers excellent results in pain relief although somatic pain can resist. Some residual symptoms can persist, due to the original injury, in soft tissues, muscles, bones, nerves and articulations.

SYMPATHECTOMY does not put away the need of a careful diagnosis and other pain and disability causes treatment.
 
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