Reflex Sympathetic Dystrophy Surgery 

  • Author: Satishchandra Kale, MD, FRCS(UK), Dip Sports Medicine(UK), MS(Orthopaedics), DOrtho; Chief Editor: Mary Ann E Keenan, MD   more...
 
Updated: May 14, 2010
 

Background

Reflex sympathetic dystrophy (RSD) is a condition that is often described under various synonyms that point to its incompletely understood etiology. In 1864, Weir Mitchell coined the term causalgia to designate severe pain following nerve injury. In 1900, Sudeck described regional demineralization accompanying posttraumatic pain. In 1923, Leriche described vasomotor disequilibrium.[1] In 1947, Evans introduced the term reflex sympathetic dystrophy. In 1993, the International Association for the Study of Pain renamed algodystrophy complex regional pain syndrome (also known as chronic regional pain syndrome or CRPS).

Reflex sympathetic dystrophy, or RSD, is type 1 CRPS. RSD can be considered an excessive sympathetic reaction of joints and periarticular soft tissues to any insult, traumatic or unknown.[2] This is quite different from causalgia (type 2 CRPS), in which the etiology is a partial nerve injury. RSD is characterized by pain, regional edema, joint stiffness, muscular atrophy, vasomotor disturbances (including temperature changes), trophic skin changes, (see image below) and regional skeletal demineralization seen on radiographs. These changes are aggravated by activity and extend over a larger area than the primary injury or surgery, including the area distal to this focus.[3, 4, 5, 6]

Reflex sympathetic dystrophy following surgery forReflex sympathetic dystrophy following surgery for Dupuytren contracture.

Because pathognomonic criteria are lacking for RSD, a taxonomic system based on clear definitions and objective quantification is desirable. Therefore, the current terminology of CRPS is increasingly being used as an umbrella to replace the myriad empirical descriptions used previously. No apparent relationship exists between the degree of initial trauma and severity of RSD, but RSD generally is more frequent following minor trauma or operations.

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Pathophysiology

Reflex sympathetic dystrophy (RSD, algodystrophy, complex regional pain syndrome [CRPS]) usually follows minor trauma or surgery. It also has been associated with various clinical conditions (eg, diabetes, parkinsonism). RSD begins with spontaneous pain associated with vasomotor and sudomotor disturbances.

Bonica described the progress of severe cases in 3 stages.[7] The acute stage of RSD is marked by pain, swelling, and warmth. Neurologic changes, such as hyperesthesia (glove and stocking distribution), incoordination, tremor, muscle spasms, and paresis, may be seen. The second dystrophic stage is characterized by cold skin with trophic changes. The final atrophic stage is manifested by muscle wasting and joint contractures. Symptoms usually are disproportionate to the cause and reflect disturbance of autonomic, sensory, and motor function.

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Epidemiology

Frequency

United States

According to various researchers, incidence of reflex sympathetic dystrophy (RSD) may be 2-17% following minor trauma or surgery. If causalgia is included in the broad definition, incidence can be as high as 32-35%. In the past, many subtle forms of RSD were missed, but with increased awareness of the condition, actual incidence may be much higher than initially thought.

International

There are no regions or population groups that have a predilection for reflex sympathetic dystrophy.

Mortality/Morbidity

Mortality associated with reflex sympathetic dystrophy (RSD) is negligible, though morbidity is extremely high. Despite good results following intravenous sympathetic blockade and intensive mobilization techniques, weakness of the extremity resulting from RSD is seen in almost 50-65% of patients, even 18-24 months following initial diagnosis. Full range of movement accompanying the above aggressive therapies is seen in 60-74% of patients. Prolonged morbidity is observed in about 50% of patients with psychiatric diathesis, workers' compensation claims, and lawsuits.[8]

Race

No particular race has a predilection for reflex sympathetic dystrophy.

Sex

Reflex sympathetic dystrophy is more common in women than in men; the male-to-female ratio is approximately 3:7. The ratio of upper extremity to lower extremity involvement is approximately 2:1. Even in children, girls are affected more frequently than boys, but peculiarly, the lower extremity is involved more frequently than the upper extremity.[9]

Age

Most patients with reflex sympathetic dystrophy (RSD) are aged 30-55 years, and the mean age is 45 years. With increasing awareness, RSD is being diagnosed in children more often; however, no studies exist pointing to a particular age distribution.

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Contributor Information and Disclosures
Author

Satishchandra Kale, MD, FRCS(UK), Dip Sports Medicine(UK), MS(Orthopaedics), DOrtho  Consultant Trauma and Orthopedic Surgeon, East and North Hertfordshire NHS Trust, UK

Satishchandra Kale, MD, FRCS(UK), Dip Sports Medicine(UK), MS(Orthopaedics), DOrtho is a member of the following medical societies: British Orthopaedic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

James F Kellam, MD  Vice-Chair, Department of Orthopedic Surgery, Director of Orthopedic Trauma and Education, Carolinas Medical Center

James F Kellam, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, Orthopaedic Trauma Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Samuel Agnew, MD, FACS  Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma, University of Florida at Jacksonville; Consulting Surgeon, Department of Orthopedic Surgery, McLeod Regional Medical Center

Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic Association

Disclosure: Nothing to disclose.

Dinesh Patel, MD, FACS  Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital

Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Mary Ann E Keenan, MD  Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania

Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association

Disclosure: Nothing to disclose.

References
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  2. Naleschinski D, Baron R. Complex Regional Pain Syndrome Type I: Neuropathic or Not?. Curr Pain Headache Rep. May 12 2010;[Medline].

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  4. Mitchell SW, Morehouse GR, Keen WW. Gunshot Wounds and Other Injuries of Nerves. Philadelphia:. JB Lipincott;1864.

  5. Mitchell SW. Injuries of Nerves and their Consequences. Philadelphia:. JB Lippincott;1972.

  6. Clinical Orthopaedics. Reflex sympathetic dystrophy. In: Bailliere's Clinical Orthopaedics. Vol 1. WB Saunders Co;1996.

  7. Bonica JJ, ed. The Management of Pain. 2nd ed. Philadelphia:. Lea & Febiger;1990:220-243.

  8. Allen G, Galer BS, Schwartz L. Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Pain. Apr 1999;80(3):539-44. [Medline].

  9. Wilder RT, Berde CB, Wolohan M, et al. Reflex sympathetic dystrophy in children. Clinical characteristics and follow-up of seventy patients. J Bone Joint Surg Am. Jul 1992;74(6):910-9. [Medline].

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  11. Herlyn P, Müller-Hilke B, Wendt M, Hecker M, Mittlmeier T, Gradl G. Frequencies of polymorphisms in cytokines, neurotransmitters and adrenergic receptors in patients with complex regional pain syndrome type I after distal radial fracture. Clin J Pain. Mar-Apr 2010;26(3):175-81. [Medline].

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  13. Wesseldijk F, Fekkes D, Huygen FJ, Bogaerts-Taal E, Zijlstra FJ. Increased plasma serotonin in complex regional pain syndrome type 1. Anesth Analg. Jun 2008;106(6):1862-7. [Medline].

  14. Higashimoto T, Baldwin EE, Gold JI, Boles RG. Reflex sympathetic dystrophy: complex regional pain syndrome type I in children with mitochondrial disease and maternal inheritance. Arch Dis Child. May 2008;93(5):390-7. [Medline].

  15. Genant HK, Kozin F, Bekerman C, et al. The reflex sympathetic dystrophy syndrome. A comprehensive analysis using fine-detail radiography, photon absorptiometry, and bone and joint scintigraphy. Radiology. Oct 1975;117(1):21-32. [Medline].

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  17. van Laere M, Claessens M. The treatment of reflex sympathetic dystrophy syndrome: current concepts. Acta Orthop Belg. 1992;58 Suppl 1:259-61. [Medline].

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  19. Zollinger PE, Tuinebreijer WE, Breederveld RS, Kreis RW. Can vitamin C prevent complex regional pain syndrome in patients with wrist fractures? A randomized, controlled, multicenter dose-response study. J Bone Joint Surg Am. July 2007;89(7):1424-31. [Medline].

  20. Ek JW, van Gijn JC, Samwel H, van Egmond J, Klomp FP, van Dongen RT. Pain exposure physical therapy may be a safe and effective treatment for longstanding complex regional pain syndrome type 1: a case series. Clin Rehabil. Dec 2009;23(12):1059-66. [Medline].

  21. Inchiosa MA Jr, Kizelshteyn G. Treatment of complex regional pain syndrome type I with oral phenoxybenzamine: rationale and case reports. Pain Pract. Mar-Apr 2008;8(2):125-32. [Medline].

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Reflex sympathetic dystrophy following surgery for Dupuytren contracture.
Radiograph of affected extremity, depicting regional osteopenia contrasted with normal radiographic appearance of the opposite extremity.
 
 
 
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