Exaggerated Pain after Injury in the Athlete

Case Report A 46-year-old woman presents with right knee pain. The onset of pain was 10 d ago after a 20-min run. She admits having mild discomfort during the run but denies any specific injury. Her pain started to intensify over the previous 2 to 3 d, and it became severe and awoke her from sleep the morning of presentation. She describes her knee as red, swollen, and stiff. She is not able to straighten her knee because of pain. She has no history of a knee injury. She is status post open reduction internal fixation right distal tibia fibula fracture 22 months ago with hardware removal 14 months ago. Examination reveals an athletic woman in moderate distress. Gait is antalgic and there is visible knee swelling with mottled erythema. She has decreased range of motion due to pain and palpable warmth and allodynia. She was not able to tolerate any further examination. X-ray of the right knee was obtained and demonstrated mild medial joint space narrowing with early osteophyte formation. Patient was suspected of having complex regional pain syndrome (CRPS), and lidocaine 2% topical gel was prescribed along with desensitization home physical therapy exercises. She returned to clinic 1 wk later with 90% pain improvement. Patient’s gait was normal and examination was positive for mild medial knee swelling and palpable tenderness. She had full range of motion, no effusion, and ligaments were intact. She continued lidocaine gel, home desensitization exercises, and gradually returned to running over the next 3 to 4 wk. She has not had any recurrence of symptoms in 8 months. Introduction CRPS was described first in 1864 and since has been known by many different entities including reflex sympathetic dystrophy, causalgia, and posttraumatic dystrophy (6). This condition has been reported by several specialties and subspecialties including anesthesiology, family medicine, neurology, orthopedics, pain medicine, pediatrics, physical medicine and rehabilitation, and sports medicine. In 1994, new diagnostic criteria were proposed and the name change to CRPS was established (11). These diagnostic criteria were found to be sensitive, but not specific, so the International Association for the Study of Pain (IASP) developed a consensus statement, the ‘Budapest criteria,’ which were published in 2007. The ‘Budapest criteria’ added subgroups of patient-reported symptoms and clinician observed signs in order to make the criteria more specific. In addition, separate research criteria were proposed to make CRPS inclusion criteria more stringent, minimizing false positives in research samples (3). Definition Clinical criteria according to the IASP, which are not evidence based, are characterized by regional pain (not in a specific dermatome) that is disproportionate to any inciting event. Four symptom and sign categories exist: sensory, vasomotor, sudomotor, and motor. The patient must report at least one symptom in three of four categories, and the clinician must observe one sign in two of four categories (Table). Minor or major injury requiring immobilization often precedes symptoms, although the syndrome can occur also without a precipitating event. Two types are recognized: CRPS I, without distinct nerve injury; CRPS II, with named peripheral nerve injury.Table: Complex regional pain syndrome clinical diagnostic criteria, “Budapest criteria” (3).Pathophysiology Three main pathophysiology theories have emerged: neurogenic inflammation, autonomic dysfunction, and neuroplastic changes within the central nervous system (5). Each theory is not exclusive of the other two, and CRPS may be a combination of the given theories with one theory being more prominent depending on the individual’s signs and symptoms. There is evidence for familial occurrence (5). An association between HLA II loci DR15 and DQ1 has been found speculating a possible genetic predisposition (14). Diagnosis Since there is no definitive pathophysiology, there is no gold standard for diagnosis. Diagnosis is clinical; however laboratory, autonomic testing, and radiographic studies may aid in diagnosis and exclude other diagnoses. Early in the clinical course, as the case report mentioned illustrates, no testing is necessary and the radiograph performed did not aid in clinical decision making or treatment. It is important to note that length of symptoms is not part of the diagnostic criteria. CRPS was suspected in the provided case report because her pain seemed out of proportion to her history; she had allodynia, mottled erythema, and remote surgical history in the same limb. Acute signs and symptoms may differ from protracted cases. Meta-analysis by Capello et al. (1) found that bone scintigraphy had greater sensitivity and higher negative predictive value in diagnosing CRPS I compared to plain radiographs and MRI. However bone scintigraphy’s sensitivity declines 6 months after the onset of symptoms (4). CT scan is not recommended. Clinically there seems to be a precursor to CRPS that appears acutely in some athletes after injury or immobilization with only one or two of the signs or symptoms and not meeting IASP diagnostic criteria. For example, affected athletes may present with more swelling, pain, and/or exaggerated sensory changes that approach allodynia compared to other athletes with similar injuries. It is as if the body is hinting at CRPS but not evolving into CRPS after early intervention is applied. The IASP has accounted for these cases by forming a third diagnostic subtype CRPS-NOS (not otherwise specified), for those with fewer symptom and sign criteria, but presentation is explained best by CRPS. Differential Diagnosis Differential diagnosis includes acute joint injury, infection, reactive arthritis, synovitis, peripheral neuropathy, deep vein thrombosis, and nerve impingement or injury. Differential for the 46-year-old woman with symptoms primarily affecting her medial knee in the provided case report includes seroma, osteoarthritis, and medial meniscus, plica, medial collateral ligament, and patella pathology. Other considerations include the following: infection of skin, muscle, or bone, including gonococcus and Lyme disease; reactive arthropathies such as gout, pseudogout, rheumatoid arthritis, and lupus; transient synovitis and JRA in younger populations; nerve root and distal nerve impingement including thoracic outlet syndrome in upper extremity cases. Treatment When diagnosed early, desensitization techniques, compression socks, early mobilization, and oral and topical analgesics can be helpful. Please refer to the Appendix for a patient handout that can be used for home desensitization exercises. Serial follow-up and frequent reassurance, initially weekly until symptoms stabilize, is important in the management of CRPS. Symptoms not responsive to these interventions may require the clinician not experienced in the management of CRPS to consult a quality pain clinic or other physicians more experienced with additional treatment regimens. Levels of supportive evidence are variable and limited regarding treatment regimens. A meta-analysis conducted in 2010 by Tran et al. (13) found that only oral and intravenous bisphosphonates, but not calcitonin, have been proven to decrease pain and swelling and increase range of motion in patients with CRPS. Many other pharmacologic treatments including nonsteroidal anti-inflammatory drugs, opioids, topical dimethyl sulfoxide, tricyclic antidepressants, anticonvulsants, and limited amount of glucocorticoids have been used and show conflicting results in randomized controlled trials (RCTs) (13). Anecdotally many of these medications are used, show little likelihood for harm, and are recommended among expert clinicians in CRPS. Treatments such as intravenous regional blockage, lumbar sympathetic blocks, spinal cord stimulation, and epidural and intrathecal injections also show conflicting results in RCTs, but because of their invasiveness, they should be offered only after careful counseling. Interestingly, the benefits of physical and occupational therapy in RCTs remain unclear with some studies showing no benefit over the control group (7,8). Despite the lack of considerable supporting evidence, physical therapy is a widely used modality. The initial goal of therapy is desensitization, followed by range of motion, progression to functional activities, and finally return to sport. Patient education regarding diagnosis, treatment, and prognosis is recommended. The patient’s psychological well-being, especially as it relates to other comorbidities and/or as the result of pain needs to be assessed. If symptoms become prolonged, referral to psychiatry, counseling, and support groups may be beneficial. Prognosis Observationally early diagnosis and multidisciplinary treatment correlate with better outcomes. However cases may resolve spontaneously, and it is difficult to predict which will resolve and which will progress. Of those that resolve, 10% to 30% recur, with younger adults and children having a higher rate of recurrence (15,17). Recurrence can occur in the same limb or a previously unaffected limb, and it can be triggered by a new physical or emotional injury, cold exposure, or it can recur spontaneously. Prevention Early mobilization after fracture or soft tissue injury may reduce the risk of developing CRPS. Suspect CRPS in any injury that worsens with immobilization. Vitamin C supplementation at the time of fracture diagnosis and continued for 50 d has been shown to decrease the incidence of CRPS compared to placebo in patients with distal radius fractures. A dose of 500 mg daily is recommended (16). Conclusions The sports medicine physician is likely to encounter CRPS. CRPS should be included in the differential of any regional pain that is disproportionate in time or degree to the usual course of a known injury, trauma, following immobilization, and/or without known inciting event. A combination of abnormal sensory, vasomotor, sudomotor, and/or motor symptoms and clinical findings may be present. Being astute to the athlete’s clinical history and signs will ensure a timely diagnosis. Early diagnosis and comprehensive management is recommended in order to minimize symptoms, time away from sport, and long-term morbidity. The author declares no conflicts of interest and does not have any financial disclosures.