Complex Regional Pain Syndrome in a College Athlete

Complex Regional Pain Syndrome in a College Athlete ANDREA WEBER, MS, ATC • Albright College HERB AMATO, DA, ATC • James Madison University C hronic...
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Complex Regional Pain Syndrome in a College Athlete ANDREA WEBER, MS, ATC • Albright College HERB AMATO, DA, ATC • James Madison University

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hronic pain and hyperactive pain are conditions that are frustrating to both the patient and the clinician. These disorders can be characterized by enigmatic etiologies, and they generally do not respond to conventional treatKey Points ment. They can be successfully treated, Complex regional pain syndrome however, and early de(CRPS) should be considered when tection and diagnosis an athlete presents with pain out of are critical to recovery. proportion to the underlying trauma. Athletic trainers Early recognition is critical to and therapists are ofsuccessful treatment and should ten able to evaluate an involve multiple tools, the most injury as soon as it ocimportant of which is the clinical curs and to follow its evaluation. progression throughout all phases of rehaAs athletic trainers and therapists, bilitation. This daily we must recognize signs and interaction is critical in symptoms that are abnormal in successfully managing response to even the most benign pain syndromes. The injuries. athletic trainer or therapist might be Athletes with CRPS should be treated the first clinician to as individuals, and a treatment note that an athlete is paradigm should be designed to not responding “norprogress rehabilitation within the mally” to an injury or confines of their pain. a rehabilitative activKey Words: chronic pain, dispropority. Complex regional tionate pain, multifaceted evaluation pain syndromes can and treatment be triggered by a variety of musculoskeletal injuries that we manage on a daily basis. Therefore, knowledge of the signs and symptoms of pain syndromes plays a critical role in early diagnosis and treatment. This article provides

information on the etiology, signs and symptoms, and treatment options for individuals with complex regional pain syndromes. Reflex sympathetic dystrophy (RSD), or complex regional pain syndrome Type I (CRPS I), is a complex pain phenomenon that is estimated to affect 6–8 million Americans (RSDnet.org, 2001). This disorder affects more women than men and afflicts both young and old (RSDnet.org). Despite its widespread existence, a definitive etiology and pathophysiology remains elusive. This condition often goes undetected, and it can become a source of debilitative chronic pain. The first widely accepted account of RSD was reported in 1864. Mitchell, Morehouse, and Keen (as cited in Colton & Fallat, 1996) described a burning pain that was secondary to gunshot wounds suffered by Civil War soldiers. Since this first account, numerous authors have reported similar pain patterns, and a variety of different names have been applied to the disorder. Over the past 140 years, the term reflex sympathetic dystrophy has become synonymous with causalgia, Sudeck’s atrophy, shoulder-hand syndrome, sympathetic paralysis, and algodstrophy, despite the fact that these disorders can involve signs and symptoms that differ from RSD. In an attempt to clarify terminology, the International Association for the Study of Pain (IASP) Subcommittee on Taxonomy defined RSD and causalgia as two separate entities (Bruehl, Harden, & Galer, 1999). RSD is described as a disorder, or group of disorders, that can develop as a result of trauma and might involve a nerve injury. Individuals with © 2002 Human Kinetics • ATT 7(4), pp. 18-24

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RSD experience pain, sensory abnormalities, abnormal blood flow and sweating, and changes in tissue and motor systems (Bruehl et al.). Causalgia, which closely resembles RSD in its signs and symptoms, is differentiated by the presence of a clearly definable nerve injury (Bruehl et al.). The IASP has adopted a new classification system, which categorizes both RSD and causalgia as complex regional pain syndrome (CRPS). RSD is Type I and causalgia, Type II CRPS. This was done to distinguish the features, location, and nature of the pain syndromes without respect to etiology (Bruehl et al., 1999). CRPS I will be used to describe the pain phenomenon formerly known as RSD, and CRPS will be used to describe the two disorders collectively.

Signs and Symptoms CRPS I can be divided into three stages that correspond to specific signs and symptoms (RSDnet.org, 2001). Each stage can vary in length and the number of signs and symptoms presented. Typical symptoms that characterize CRPS I are presented in the sidebar. The pain that typically accompanies CRPS I is usually most severe at night, and it can be either deep and stabbing or superficial in nature (RSDnet.org, 2001). Knowledge of the signs and symptoms and their progression is critical for proper management of CRPS I. Patients who are diagnosed early respond best to treatment, and they have the lowest rate of recurrence (RSDnet.org). The longer the disorder goes

Typical Symptoms of Complex Regional Pain Syndrome Type I Pain out of proportion to the injury Increased blood flow to the area Decreased range of motion Pain that is hyperreactive to nonnoxious stimuli (allodynia) Edema Variations in skin temperature Hyperhydrosis

unrecognized, the greater the likelihood of permanent trophic change (RSDnet.org). As few as 20% of individuals with CRPS I are able to fully resume prior activities, and it spreads to another area of the body in as many as 80% of all reported cases (RSDnet.org).

Diagnostic Tests Diagnosing CRPS is a complex task that involves many different strategies. The most useful tool is the clinical evaluation. Although distinguishing CRPS I from the other complex regional pain syndromes by signs and symptoms can be difficult, it can help determine the most appropriate next step. Gibbons and Wilson (1992) developed a scheme to help diagnose CRPS, which is shown in Table 1.

Table 1. Gibbons and Wilson’s Scheme to Diagnose Complex Regional Pain Syndrome Type I (CRPS I) Point System

Signs and Symptoms

Point-Total Interpretation

1 point if symptom is present

Allodynia/Hyperpathia

5 or more: probable CRPS

0 points if symptom is not present

Burning pain

3–4.5: possible CRPS

1/2 point if symptom presentation is ambiguous

Edema

Less than 3: no CRPS

Hair color/growth changes Sweating changes Temperature changes Radiographic changes Quantitative measurement of vasomotor/sudomotor disorder Bone scan consistent with CRPS

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Studies have demonstrated that radiographs of CRPS I patients usually show demineralization that is patchy or sparse in nature (Sintzoff, Sintzoff, Stallenberg, & Matos, 1997). An important point to remember is that individuals with CRPS I do not always exhibit osteoporosis. In addition, those who do present with osteoporosis do not necessarily have CRPS I. There are several other medical conditions that exhibit bone demineralization, such as hyperparathyroidism, which should also be considered. Three-phase radionuclitide bone scans can be beneficial in diagnosing CRPS I. Holder, Cole, and Myerson (1992) used bone scans as a means of diagnosing CRPS I of the foot in patients with signs and symptoms similar to those described by Gibbons and Wilson (1992). These investigators found that delayed scan images illustrated a diffuse pattern of increased tracer uptake. Although bone scans can be beneficial in diagnosing CRPS I, they are not 100% accurate and should be used in conjunction with other diagnostic procedures. Sympathetic blocks are the most definitive and frequently used tool for both diagnosing and treating CRPS I (Ladd, DeHaven, Thanik, Patt, & Feuerstein, 1989; Lankford, 1990; Schwartzman, 1996). They are typically administered as epidural lumbar blocks for individuals with lower extremity injuries and as stellate ganglion blocks for upper extremity injuries (Ladd et al; Lankford; Schwartzman). Regardless of which type of block is used and whether it employs an anesthetic or pharmacological approach, a positive test for CRPS I is one that decreases pain and causes an increase in temperature in the affected area (Lankford). These results are usually temporary but indicate the existence of CRPS I.

the entire upper extremity with minimal joint motion. Such a program usually consists of “scrubbing” and “carrying” components. The scrubbing phase involves the use of a coarse wire brush that the patient moves in a front-to-back motion over a piece of wood (Figure 1). Carrying involves the use of a weighted handbag or briefcase that is to be carried as often as possible by the patient. A stress-loading program for the lower extremity involves a gradual increase in weight-bearing status or isometric strengthening. Many rehabilitation programs also involve the use of a desensitization program (Stanton-Hicks et al., 1998). During desensitization a nonpainful stimulus such as a cotton ball or soft cloth is gently rubbed over the painful area (Figure 2). This is done to return sensory information to its uninjured level. As the individual is able to tolerate this exercise its intensity can be progressed to incorporate more coarse substances. Increasing active range of motion of involved joints is critical for successful treatment of CRPS I (Rogers & Valley, 1994). Because stiffness and trophic changes are normal symptoms of this disorder, immobilization of the extremity is contraindicated in most cases. Range-of-motion activities should be

Treatment Management of CRPS I, like its diagnosis, incorporates many different methods. Conservative methods that might work in some early cases include appropriate rehabilitation techniques, pharmacological intervention, and large-diameter-nerve stimulation (TENS). Some researchers have found that a “stress loading” rehabilitation program is very successful for treating CRPS I of the upper extremity. A stress-loading program described by Carlson and Watson (1988) consists of active exercises that require stressful use of 20 ❚ JULY 2002

Figure 1

A stress-loading exercise for the upper extremity.

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not respond to other treatments (Bruehl et al.; Rogers & Valley). The most important factor in treating patients with CRPS I is developing an effective treatment plan that facilitates performance of active functional exercises. Although each of the treatment options discussed can be beneficial, most successful treatment programs employ a variety of treatment options that include rehabilitation.

Etiology/Pathophysiology

Figure 2 Sensory desensitization of injured area with a cotton ball.

gentle and stay within a pain-free range. Aggressive range of motion or passive motion might exacerbate the condition. Using a TENS unit might alleviate pain sufficiently to permit performance of range-of-motion activities. TENS might modulate pain by stimulating largediameter afferents (Prentice, 1998), but it is rarely effective as the sole treatment option for individuals with CRPS I (Stanton-Hicks et al., 1998), and there is considerable variation in success rates of treatment plans that incorporate its use. Although rehabilitation can be successful in treating some cases of CRPS I, others are more resistant and require further intervention. In these cases, a sympathetic block is usually added to the treatment program. Sympathetic blockade affects only the sympathetic innervation. Because the motor and sensory innervation to the affected area are not altered, the individual retains normal motor control and might be better able to tolerate rehabilitation exercises. In many cases, a series of sympathetic blocks will be needed, which can be administered through the insertion of in-dwelling catheters that supply a constant sympathetic blockade (Bruehl et al., 1999; Rogers & Valley, 1994). Dorsal-column stimulators and sympathectomies have achieved varying levels of success and are usually reserved for extreme cases that do ATHLETIC THERAPY TODAY

Despite a considerable body of experimental research pertaining to CRPS I, an exact causal mechanism has not yet been discovered. Some investigators believe that individuals might have a physiological or psychological predisposition for developing it (Lankford, 1990; Stanton-Hicks et al., 1998). Determining the cause of CRPS I is further complicated by the variety of conditions believed to trigger the disorder. Softtissue injury, malignancy, myocardial infarction, stroke, severe head injury, operative procedures, fractures, and dislocations have all been found to precipitate CRPS I (RSDnet.org, 2001). Lankford has suggested that an abnormal sympathetic reflex is a contributory factor in the development of RSD (Lankford, 1990). A normal sympathetic reflex is associated with routing of injury-related afferent activity to the lateral horn of the spinal cord. Efferent sympathetic impulses are generated, which cause the peripheral nerves of the injured extremity to produce vasoconstriction (Figure 3). After a few hours, vasodilation occurs, which facilitates the healing process. An abnormal reflex fails to produce vasodilation, resulting in tissue ischemia, pain, and spasm (Lankford). A subsequent increase in activity of sympathetic nerves perpetuates the pain and spasm, which is believed to create the cycle of pain that CRPS patients experience. RSD, or CRPS I, is a persistent pain phenomenon that has an enigmatic etiology and pathophysiology. Clinicians should be aware of the signs and symptoms that typically accompany it. Early recognition and initiation of appropriate treatment are critical to successfully managing this condition. CRPS should be considered as a possible explanation for pain that is disproportionate to the associated trauma. Accurate diagnosis of CRPS I requires a multifaceted approach JULY 2002 ❚ 21

Figure 3 The figure on the left illustrates a normal sympathetic reflex. The figure on the right depicts an abnormal reflex in which excessive efferent information is sent to the periphery.

that combines clinical evaluation, radiographs, bone scans, and sympathetic blocks. The treatment plan should combine rehabilitation exercises, TENS, pharmacological agents, and sympathetic blocks. The factors most critical for successful recovery are early diagnosis of the condition and implementation of a variety of treatments.

Additional Information About Complex Regional Pain Syndrome and Reflex Sympathetic Dystrophy Can Be Found on the Web www.rsds.org www.home.ptd.net/~paulbarb/rsdweb.htm www.rsdcrps.com/

Case Report An 18-year-old Caucasian female NCAA Division I field-hockey player presented to the athletic training room after the winter break complaining of pain in her left ankle and foot. The athlete stated that while running at home she “twisted” her left ankle on an uneven area of sidewalk. She reported that swelling and discoloration were immediate in her ankle, and a physician in a hospital emergency room saw her 2 days subsequent to the injury. Radiographs failed to reveal a fracture in the left lower leg or foot, and the athlete was diagnosed as having a lateral ankle sprain. She was given crutches, a hard walking shoe, and an over-the-counter anti-inflammatory medication. At the time of the evaluation, the physician stated that he could not rule out the presence of a fifth-metatarsal stress fracture. The athlete presented to the athletic training room 16 days after the initial injury reporting a significantly 22 ❚ JULY 2002

www.rsdrx.com/ www.rsdhope.org/ www.ninds.nih.gov/health_and_medical/disorders/ reflex_sympathetic_dystrophy.htm

increased pain level in her left foot and ankle. She was still wearing the hard walking shoe, and she was nonweight-bearing with crutches. The athlete had no prior history of injury to her left foot or ankle. Evaluation revealed extreme point tenderness over the entire length of the fifth metatarsal and over the lateral ankle ligaments. Minimal swelling was present over the lateral malleolus. Active range of motion was mildly limited in dorsiflexion and plantar flexion, and inversion and eversion were markedly limited and rated as 2/5. Neurological-exam results were within normal limits. Dorsal pedal and posterior tibial pulses were strong and comparable to those of the uninvolved extremity.

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Because of persisting symptoms, a second set of radiographs was ordered to rule out a fifth-metatarsal stress fracture. The team orthopedic physician evaluated the athlete and interpreted the second set of radiographs as negative for bony injury. The physician suggested that she discontinue the use of crutches and the walking shoe. She was also instructed to begin ankle rehabilitation with an ankle stabilizer for support. Initial treatment followed a normal ankle-rehabilitation protocol. The athlete was unable to perform the rehabilitation exercises, and she was unable to discontinue using crutches and the walking shoe. She also reported being unable to sleep at night because of discomfort and pain that she qualified as extremely sharp and rated 8/10. A few days later she began to experience extreme numbness and a tingling sensation over the lateral side of her left ankle and the third, fourth, and fifth toes. She also reported that ice application, cold weather, and cold whirlpool sessions increased her pain levels. Movements of the water from the whirlpool turbine caused an increased pressure and pain that was qualified as achy and sharp. In addition, her left foot became hyperhydrotic when compared with the right. The existence of CRPS was suspected. One month after the initial injury, the athlete’s condition continued to deteriorate, and her pain levels reached 9.9–10+/10. The lateral aspect of her foot began to change in temperature and varied from warm to hot when compared with the medial aspect of the same foot. The foot continued to be very sensitive to touch, and even light brushing produced extreme pain. There was no change in dorsal pedal or posterior tibial pulses, and use of a transcutaneous electrical nerve stimulator (TENS) unit was initiated in an attempt to relieve her pain levels. Because there was no improvement in her condition, a bone scan was ordered to rule out further pathology. The results of the three-phase bone scan revealed changes that the radiologist believed were indicative of an early-phase complex regional pain disorder. The athlete was referred to a pain clinic that prescribed a personal TENS unit for her to wear six times daily for 1 hr at a time. She was also advised to continue using crutches and the walking shoe and to gradually progress her weight bearing and range-of-motion activities. Sensory-desensitization training, which involves using a nonnoxious stimulus to painful areas ATHLETIC THERAPY TODAY

in an attempt to break the abnormal pain cycle, was initiated over painful areas of her left foot with a cotton ball. Over the next 2 weeks, the athlete reported that using the TENS unit increased her pain. Also, the desensitization training was extremely painful—almost excruciating. Edema began to recur in the left ankle, and skin pallor became apparent. After a lumbar sympathetic block was administered, the athlete experienced a decrease in pain, and an increase in temperature of the left foot was noted. Her pain level returned to a level of 9.5/10 within 7 hr after administration of the sympathetic block, however, and a diagnosis of CRPS Type I was made. Over the next 2 months the athlete received a series of eight lumbar sympathetic blocks. After each block was administered, she experienced a decrease in pain symptoms that would last for a period of days to weeks. With this decrease in pain, rehabilitation was progressed and the athlete was able to discontinue the use of crutches. After administration of the sympathetic blocks, cold weather was the only stimulus that would increase her pain level. At the end of this 2-month training program, the athlete was able to run in a front to back pattern with the use of an ankle stabilizer. She was referred to a physical therapy clinic to complete the strengthening and proprioceptive phases of her rehabilitation during the summer break. On returning to school, she was able to complete all functional testing and she returned to play in collegiate field hockey without a recurrence of symptoms.

Acknowledgment Special thanks to Michael Dowens for his assistance with the graphics for this article. ❚

References Bruehl, S., Harden, R.N., Galer, B.S., Saltz, S., Bertram, M., Backonja, M., Gayles, R., Rudin, N., Bhugra, M.K., & Stanton-Hicks, M. (1999). External validation of IASP diagnostic criteria for complex regional pain syndrome and proposed research diagnostic criteria. International Association for the Study of Pain. Pain, 81(1-2), 147-154. Carlson, L.K., & Watson, H.K. (1988). Treatment of reflex sympathetic dystrophy using the stress-loading program. Journal of Hand Therapy, 1, 149-154. Colton, A.M., & Fallat, J.M. (1996). Complex regional pain syndrome. Journal of Foot and Ankle Surgery, 35(4), 284-296. Gibbons, J.J., & Wilson, P.R. (1992). RSD score: Criteria for the diagnosis of reflex sympathetic dystrophy and causalgia. Clinical Journal of Pain, 8(3), 260-263.

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Holder, L.E., Cole, L.A., & Myerson, M.S. (1992). Reflex sympathetic dystrophy in the foot: Clinical and scintigraphic criteria. Radiology, 184, 531-535. Ladd, A.L., DeHaven, K.E., Thanik, J., Patt, R.B., & Feuerstein, M. (1989). Reflex sympathetic imbalance: Response to epidural blockade. American Journal of Sports Medicine, 17(5), 660-667. Lankford, L.L. Reflex sympathetic dystrophy. (1990). In J.M. Hunter, MacKin, E.J., & Callahan, A.D. (Eds.), Rehabilitation of the hand (pp. 763-786). Philadelphia: Mosby Yearbook. Prentice, W.E. (1998). Neurophysiologic explanations of pain control. In J.M. Smith, V. Maliner, & C. Wells (Eds.), Therapeutic modalities in sports medicine (4th ed., pp. 39-41). St. Louis: McGraw-Hill. Rogers, J.N., & Valley, M.A. (1994). Reflex sympathetic dystrophy. Pain Management, 11, 73-83. RSDnet.org. The Internet source for reflex sympathetic dystrophy. Retrieved October 22, 2001, from http://www.rsdnet.org/RSDStages.html Schwartzman, R.J. (1996). Reflex sympathetic dystrophy. In J.L. Loscalzo, M.A. Creager, & V.J. Dzou (Eds.), Vascular medicine (pp. 1209-1221). Boston: Little, Brown.

Sintzoff, S., Sintzoff, S., Stallenberg, B., & Matos, C. (1997). Imaging in reflex sympathetic dystrophy. Hand Clinics, 13(3), 431-432. Stanton-Hicks, M., Baron, R., Boas, R., Gordh, T., Harden, N., Hendler, N., Koltzenburg, M., Raj, P., & Wilder, R. (1998). Complex regional pain syndromes: Guidelines for therapy. Clinical Journal of Pain, 14, 155166.

Andrea Weber is employed by Reading-Berks Physical Therapy and serves as an assistant athletic trainer at Albright College. She completed her undergraduate athletic training education at The Pennsylvania State University and received a master’s degree in kinesiology from James Madison University. Herbert Amato is an associate professor of health sciences at James Madison University and curriculum director of an approved undergraduate athletic training program. He has held athletic training positions at both the high school and the college level and was on the medical staff of the 1988 Olympic Team.

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