Reflex Sympathetic Dystrophy

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Reflex Sympathetic Dystrophy (Complex Regional Pain Syndrome)

In 1598, Pare first recorded awareness of the condition. Then, later during the American Civil War, Reflex Sympathetic Dystrophy (RSD) was recognized and described. The hallmark of Complex Regional Pain Syndrome (CRPS) is severe, spontaneous pain associated with local features of autonomic dysfunction that occurs after trauma or operation to a limb. It is defined as a disordered response by an extremity to a noxious (hurtful) stimulus.

The exact cause is unknown.

The five major signs and symptoms are:

  • Pain out of proportion to the injury
  • Edema
  • Autonomic dysfunction
  • Movement disorder, and
  • Trophic changes

Causes of CRPS include accidental trauma. Injury may be the result of fractures, dislocations or sprains, amputations, crush injuries or even minor cuts of the toes or feet. Other etiologic (causative) factors include surgical procedures, diabetes mellitus, hemiparesis, venipuncture, and infections. It usually results from incomplete nerve trauma or soft tissue injury, and most commonly affects the hands and feet.

Genant proposed criteria for diagnosis of RSD which included pain and tenderness in the extremity, soft-tissue swelling, decreased motor function, trophic skin changes, vasomotor instability and patchy oteoporosis.

Histological findings on synovial biopsies characteristic for RSD that Kozin noted include proliferation and disarray of synovial lining cells, increased numbers of small blood vessels, mild perivascular inflammatory infiltrate and synovial edema.

Stages of RSD (CRPS)

  1. STAGE I occurs between 1-3 months. The foot displays soft, puffy edema, antalgic guarding of the part, pronounced pain, allodynia(hyperesthesia to light touch-pressure), hyperhidrosis(excessive perspiration); spotty osteoporosis on radiographic inspection; pain aggravated by movement and emotional stress.
  2. STAGE II occurs between 3-6 months. Edema is still present, range of motion decreases, dystonia (impairment of muscle tone), mottled or cyanotic coloration, and progressive spotty bone demineralization noted radiographically. Hair growth is decreased, nails are brittle, and there is muscle wasting causing limited joint mobility.
  3. STAGE III occurs between 6-9 months. There is a cool, dry foot with pallor;with the skin slightly taut, waxy and thin; stiffness and disability are pronounced, marked disuse atrophy of bone (Sudek's atrophy).

Techniques to confirm clinical diagnosis

Plethysmography(the determination of changes in volume by using an instrument for recording variations in volume of an organ, part, or limb) and venous blood gas measurement for determination of vasoconstriction.

Thermography or videothermogram to evaluate near-surface blood flow. A positive thermogram will show significant coolness in the affected extremity.

Xenon clearance or laser Doppler to measure peripheral blood flow.

Serologic tests, such as antinuclear antibody and rheumatoid factor (are usually negative).

Plain film radiographic examination reveals patchy osteoporosis, which may progress to a diffuse ground-glass appearance.

Three-phase Technetium bone scan, showing diffuse uptake in the blood flow, pool and delayed phase. In the delayed phase, periarticular uptake is noted in the affected part.

Other studies include electromyography(the recording and study of the electrical properties of skeletal muscle) and nerve conduction velocity studies, arteriography(radiography of an artery or arterial system after injection of a contrast medium into the blood stream), and erythrocyte sedimentation rate. The results of these studies are negative. Quantitative bone density testing is also used.

Pharmaceutical treatment for CRPS is Prednisone, Elavil, Procardia, NSAIDS(Non-Steroidal Anti-Inflammatory Drugs), Neurontin, Dilantin

PHYSICAL THERAPY treatment may be administered including, massage, ultrasound, ROM(range of motion) exercises, splint, hydrotherapy and contrast baths, transcutaneous electrical nerve stimulation (TENS), trigger point electrical stimulation, acupuncture.

Other forms of treatment include chemical sympathectomy, epidural block, lidocaine, morphine pump, and amputation

References

  • Banks, Alan S., et al McGlamry's Comprehensive Textbook of Foot and Ankle Surgery. Philadelphia:Lippincott Williams and Wilkins, 2001.
  • Kozin F. Reflex sympathetic dystrophy syndrome:a review. Clin Exp Rheumatol 1992;10:401-409.
  • Schwartzman RJ, McLellan TL. Reflex sympathetic dystrophy.Arch Neurol 1987;44:555-561.
  • Schwartzman RJ. Reflex sympathetic dystrophy. Curr Opin Neurol Neurosurg 1993;6:531-536.
  • Stanton-Hicks MD. Upper and lower extremity pain. In: Raj P, ed. Practical Management of pain. St. louis:Mosby-Year-Book, 1992:312-328.
  • Bej MD, Schwartzman RJ. Abnormalities of cutaneous blood flow regulation in patients with reflex sympathetic dystrophy as measured by laser Dopler fluxmetry. Arch Neurol 1991;48:912-915.
  • Amadio PC, Mackinnon SE, Merritt WH, et al. Reflex sympathetic dystrophy syndrome:consensus report on an ad hoc committee of the American Association for Hand Surgery on the definition of reflex sympathetic dystrophy syndrome. Plast Reconstr Surg 1991;87:371-375.
  • Schwartzman RJ. The diagnosis and staging of RSD: an overview of the problem. Reflex sympathetic dystrophy: current strategies in diagnosis and treatment. Paper presented at Jefferson Medical College, Philadelphia, April 10, 1992.