Reflex Sympathetic Dystrophy
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Reflex sympathetic dystrophy applies to a variety of seemingly unrelated disorders having similar clinical features and reflecting the same fundamental disturbed physiology. The term reflex sympathetic dystrophy describes a disorder that is a reflexive response to a trauma, manifesting in the sympathetic nervous system, resulting in a dystrophy that can affect many types of tissues. There are numerous causes of this disease including sprains, dislocations, fractures, contusions, crush injuries, tight casts and extremity surgery. The diagnosis of severe RSD is rarely difficult to make, but less obvious cases are frequently misdiagnosed and thus mismanaged or neglected.
Mechanism
A sympathetic response to pain is a normal reflex. Pain impulses, conducted by A-delta and C fibers, synapse in the spinal cord in the intermediolateral cell column, from which efferent sympathetic impulses travel back to the extremity. In the normal progression to healing, this reflex arc eventually stops. If this sympathetic reflex arc continues, the tissues are subjected to vaso-constriction and tissue ischemia, causing more pain and thus increasing the barrage of afferent pain impulses traveling to the spinal cord and reactivating the sympathetic reflex.
Clinical Presentation
Trauma secondary to accidental injury is probably the most common cause of RSD. The hallmark of RSD is the lack or correlation between the initial injury and the magnitude of the symptoms. A seemingly inconsequential injury can progress to a permanent disability. RSD is manifested initially by pain, hyperesthesia and vasomotor disturbances followed by weakness, muscle atrophy and trophic changes involving the skin, muscles, bones and joints. Pain is the most prominent and characteristic feature. It is frequently described as burning or aching. It may vary from mild to excruciating and may be accompanied by recurrent paroxysmal aggravations. Initially, it involves just the injured extremity, but with time may spread to other sites such as the contralateral extremity.
Hyperesthesia is usually present, and the patient characteristically protects the extremity from contact. Vasomotor disturbances manifest as vasoconstriction (coldness and cyanosis) or vasodilation (warmth and redness to the extremity). Eventually, trophic changes progress to thin glossy skin, muscle atrophy and osteoporosis. The pain and physical signs do not conform to known patterns of nerve distribution, and have a disturbing tendency to spread proximally. Once RSD has become established, the syndrome will continue even after the precipitating pathology has healed.
Treatment
Sympathetic blocks and physical therapy are the mainstays of current therapeutic management. Most patients respond in an impressive manner to sympathetic blockade, and permanent resolution is possible if therapy is started before irreversible changes have occurred. A series of sympathetic blocks should be performed and continued until minimal discomfort persists. For upper extremity RSD, the site of block is typically the stellate ganglion. For lower extremity RSD, the site is usually the lumbar sympathetic chain.
Pharmacologic treatment of RSD includes multiple classes of medications. Tricyclic anti-depressants provide analgesia and mood elevation. Narcotics are notoriously ineffective in RSD and must be monitored closely when used in a long-term problem such as RSD. Procardia has been shown effective in promoting peripheral blood flow and reducing pain symptoms. Clonidine, as an oral medication or trans-dermal patch, can provide valuable adjunctive support. Neurontin, an anti-convulsant, has recently been shown effective in some cases of sympathetically-mediated pain.
Summary
RSD is a complex, chronic pain management problem that is difficult to diagnose and challenging to treat. The key to correct management includes early diagnosis leading to aggressive treatment.
STAGES OF REFLEX SYMPATHETIC DYSTROPHY
Stage l (acute phase): Vasodilation, Hyperemia, Edema, Burning Pain. Occurs 1-4 weeks after injury.
Stage 2 (dystrophic phase): Vasoconstriction, Cyanosis, Reduced Range of Motion, Patchy Osteoporosis. Occurs at 2-3 months.
Stage 3 (atrophic phase): Atrophic skin changes, Joint Contractures, Systemic Problems, Emotional Involvement. Occurs 6 months to years after injury.
Clinical Conditions That Can be Treated with Lumbar Sympathetic Blocks:
* Reflex sympathetic dystrophy
* Post-traumatic pain syndrome
* Circulatory insufficiency
* Causalgia
* Phantom limb pain
* Herpes zoster
* Post-herpetic neuralgia
* Intractable urogenital pain
* Limb amputation pain
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