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We report on three patients of 201 who, after bone marrow transplantation (BMT), developed reflex sympathetic dystrophy (RSD). The syndrome occurred on days +40, +43, and +147, respectively, without known causes of RSD. The ankles, the feet, and the knees were affected. Long-lasting immobilization, slow bone marrow recovery, and other BMT-related factors could have predisposed to RSD.
We retrospectively reviewed the cases of fourteen patients who had reflex sympathetic dystrophy of the knee. All fourteen were hospitalized, and epidural block anesthesia was instituted with an indwelling catheter for an average of four days, during which continuous passive motion, manipulation (as necessary), stimulation of muscles, and alternating hot and cold soaks were used. The average length of follow-up was thirty-two months. Eleven patients had complete resolution of the symptoms, two had sufficient intermittent aching with changes in the weather to need medication, and one had no relief. The diagnosis was confirmed if the symptoms were relieved by a lumbar sympathetic block. Pain that was out of proportion to the severity of the injury was the most consistent finding, being present in all fourteen patients. However, variation in clinical severity is characteristic of the syndrome. Eleven of the fourteen patients had had a previous patellar operation. After the onset of the symptoms, nine patients had two or more arthroscopic examinations, without notable findings. All fourteen patients had had extensive physical therapy and medical treatment before the epidural block was performed.
A case report is presented of a 15-year-old girl with reflex sympathetic dystrophy (RSD). She was referred to hospital because of left upper limb pain. Her left upper limb was cold, edematous and blue with a limited active range of movement. The serum concentration of noradrenaline was lower on the painful side than on the healthy side, and neurotropin, which has an antinociceptive effect to hyperalgesia, was clearly effective. Early diagnosis and management is essential in the treatment of RSD and administration of neurotropin is a useful and non-invasive treatment without severe adverse effects.
OBJECTIVES: To examine the validity of several thermogram-derived indices of autonomic functioning in the diagnosis of reflex sympathetic dystrophy (RSD). DESIGN: A series of chronic pain patients were classified diagnostically based on thermogram results using discriminant function analysis, and validity measures (e.g., sensitivity, specificity) were used to determine the accuracy of computerized thermographic pixel analysis in discriminating RSD from other pathology. SETTING: The study was conducted at the Rush Pain Center, a multidisciplinary outpatient pain clinic. PATIENTS: A series of 46 chronic pain patients referred for suspected sympathetically mediated pain. INTERVENTIONS: All patients underwent computerized thermographic examination under a baseline condition after acclimating to a climate-controlled room, immediately after a cold challenge was applied to the contralateral uninvolved extremity (4 degrees C for 90 s) and 20 min after the cold challenge. OUTCOME MEASURES: Temperature during the three experimental periods, degree of temperature asymmetry between affected and nonaffected limbs during the three periods, response to cold challenge, and recovery following cold challenge were measured. RESULTS: Temperature asymmetry accurately discriminated between RSD and non-RSD patients, with the most accurate asymmetry measures obtained at baseline. Responses to cold challenge and actual temperature values did not discriminate between RSD and non-RSD pain patients. CONCLUSIONS: Thermography can be a useful component of RSD diagnosis. In situations where sensitivity and specificity are equally important, an asymmetry cutoff of 0.6 degree C appears optimal. If specificity (i.e., accurately ruling out non-RSD cases) is more important, a cutoff of 0.8 degree C or 1.0 degree C may be considered as well.
BACKGROUND: Sympathetic dysfunction in reflex sympathetic dystrophy (RSD) has been purported to consist of an afferently-induced increase in efferent sympathetic nerve impulses (somato-sympathetic reflex) and/or denervation-induced supersensitivity to catecholamines. In addition, both the central and peripheral nervous systems have been claimed to be involved. It was the aim of this study to obtain more insights into these underlying mechanisms. METHODS: In the affected extremeties of 42 patients with RSD we investigated as indirect measures of sympathetic (dys)function: (1) skin blood flow and the vasoconstrictive response to dependency of skin microvessels by means of laser Doppler flowmetry (distal to the site of trauma), (2) relative distention of the brachial artery and changes in relative distention consequent to a cold pressor test by means of ultrasonic vessel wall tracking (proximal to the site of trauma), and (3) arterial blood pressures by means of the Finapres technique. Both provocation tests induce a sympathetically mediated response. Patients were divided into three categories according to their perception of skin temperature in their injured limb (stage I, stationary warmth sensation; stage II, intermittent warmth and cold sensation; or stage III, stationary cold sensation). RESULTS: Distal to the site of trauma, when compared with controls, skin blood flow was increased at stage I and decreased at stages II and III, whereas the vasoconstrictive response to dependency was impaired at all three stages. Proximally, when compared with controls, relative distention of the brachial artery and its response to the cold pressor test were decreased at all three stages. No differences were observed in pulse pressure between patient groups and controls. CONCLUSIONS: These results suggest that sympathetic dysfunction in extremities of patients with RSD distal to the site of trauma consists of hypersensitivity to catecholamines at stages II and III as a result of autonomic denervation at stage I, whereas proximal to the site of trauma sympathetic nerve impulses may be increased at all three stages.
A 56-year-old woman presented with changes characteristic of the reflex sympathetic dystrophy syndrome (RSDS) but also frank synovitis of the left wrist, an elevated ESR and early damage of the left carpus on radiographs, suggesting septic arthritis. A dynamic scan showed changes characteristic of RSDS. A sample of synovium and bone from the wrist showed non-specific inflammation with partial destruction of cartilage by synovial pannus and involvement of subchondral bone by the inflammatory process. The search for the cause of infection was unsuccessful. Patchy osteopaenia developed 3 months after onset. At the 12 month follow-up, the course of disease was compatible with RSDS and destruction of the carpus had not progressed. Attention is drawn to the difficulty in reaching a precise diagnosis in early stages and the need to exclude infection.
Atypical presentations are common when spondyloarthropathy develops in older patients. We report two cases initially mistaken for reflex sympathetic dystrophy syndrome (RSDS). Both the patients were men, aged 62 and 75 years, respectively, with marked painful edema of a foot. One patient reported a moderate-energy trauma as the triggering event. Severe diffuse demineralization was noted on radiographs and diffuse hyperactivity on bone scans starting at the early vascular phase. These findings suggestive of RSDS led to treatment with calcitonin, griseofulvin, and pamidronate, all of which were ineffective. Laboratory tests showed severe inflammation, promoting investigations for other conditions. Spondyloarthropathy was diagnosed based on oligoarthritis with sacroiliitis, presence of HLA B27, and a favorable response to non-steroidal antiinflammatory therapy. In older patients, edema of the foot with severe demineralization and the laboratory evidence of inflammation should suggest a spondyloarthropathy.
OBJECTIVES: To construct a set of instruments to measure the level of impairment in reflex sympathetic dystrophy (RSD), to convert the scores for each instrument into one score and to derive a compounded impairment level sumscore (ISS), and to evaluate reliability, validity, and responsiveness of the ISS. DATA SOURCES AND EXTRACTION: Literature search in Medline (1985 to 1995), non-Medline journals, and references from these reports for measurement parameters and suitable, reliable, responsive, and validated instruments. DATA SYNTHESIS: Four measurement parameters (pain, active range of motion, temperature, and volume) and five measurement instruments were chosen to construct the ISS. All outcomes were converted into one score, resulting in an addable score. RESULTS: Forty-five patients with RSD of one upper extremity were evaluated. As expected for this heterogeneous index, the internal consistency of the ISS was poor to moderate. The ISS seemed to have content and concurrent validity. The responsiveness of the ISS was adequate. CONCLUSIONS: A multicomponent test was constructed to map alterations in the level of impairment in RSD patients. Each of the parameter scores could be translated into a uniform score. Adding the scores yielded the ISS.
OBJECTIVE: To determine the cost effectiveness and cost utility of acetylcysteine versus dimethyl sulfoxide (DMSO) for patients with reflex sympathetic dystrophy (RSD), from a societal viewpoint. DESIGN: An economic evaluation was conducted alongside a double-dummy, double-blind, randomised, controlled trial. Patients were followed for 1 year. The primary outcome measure was the Impairment-level Sum Score (ISS). Utilities were determined by the EuroQOL instrument (EQ-5D). Both cost-effectiveness and cost-utility analyses were performed. Differences in mean direct, indirect and total costs were estimated. Corresponding 95% confidence intervals were calculated by bootstrapping techniques. RESULTS: Both groups (DMSO, n = 64; acetylcysteine, n = 67) showed relevant improvement; no differences in effects were found. Only the total direct costs were significantly lower in the DMSO group for the period of 0-52 weeks. The incremental cost-effectiveness ratios showed that, in general, DMSO generated fewer costs and more effects compared with acetylcysteine. Post-hoc subgroup analyses on cost effectiveness suggested that patients with warm RSD could be best treated with DMSO and patients with cold RSD with acetylcysteine. These results were based on small subsamples. CONCLUSION: In general, DMSO is the preferred treatment for patients with RSD.
OBJECTIVE: To determine the clinical usefulness of skin temperature patterns for tracking reflex sympathetic dystrophy (RSD) by assessing (a) long-term relationships between changes in pain due to RSD and patterns of near surface blood flow and (b) relationships between site of pain and site of greatest asymmetries in near surface blood flow patterns. DESIGN: Multiple videothermographic evaluations of near surface blood flow patterns were performed on subjects diagnosed as having RSD. At each session, subjects filled in an outline of the body to show the location, intensity, and description of their pain. The thermograms were evaluated independently by two raters for location and intensity of pain, as well as location and degree of temperature asymmetries. SETTING: Two Army Medical Centers. SUBJECTS: Thirteen male and 16 female subjects were subsequently diagnosed as having RSD. OUTCOME MEASURES: Ratings of pain and videothermograms of the lower limbs were used as outcome measures. RESULTS: All but one subject were usually cooler on the most painful side by at least 0.5 degrees C. The amount of relative coolness was not proportional to pain intensity. There were no consistent overlaps between exact location of pain and greatest thermal asymmetry. Seven subjects were thermally symmetrical on at least one recording. Six subjects were warmer on the affected side on at least one recording. One subject was always warmer on the affected side. CONCLUSIONS: Videothermography is not an appropriate tool to use alone for either single session diagnosis or multi-session tracking of RSD.
BACKGROUND AND PURPOSE: This study was designed to investigate the correlation between reflex sympathetic dystrophy syndrome (RSDS) in hemiplegic patients and spontaneous electromyographic (EMG) activity, as well as to determine the predictive value of spontaneous EMG activity in early diagnosis of RSDS. METHODS: An EMG and nerve conduction velocity study of the weak upper limb was conducted on 70 hemiplegic patients at 3 to 4 weeks after cerebrovascular disease (either cerebral hemorrhage or infarction). Clinical assessment for development of the RSDS was done during the following 6 months. The correlation of RSDS development with the presence of spontaneous EMG activity and certain clinical parameters (including sex, age, side affected, cause of stroke, sensory impairment, spasticity, and shoulder subluxation) was analyzed statistically. RESULTS: Of the 46 patients who exhibited spontaneous activity, 30 (65%) developed clinical RSDS in their hemiplegic upper extremity, whereas only 1 (4%) of the other 24 patients with no spontaneous EMG activity developed clinical RSDS within 6 months after the onset of hemiplegia (P < .001). The correlation of RSDS development with the presence of shoulder subluxation and sensory impairment in the hemiplegic side was statistically significant. Neither age, sex, severity of spasticity, nor etiology of stroke had a significant correlation with the development of clinical RSDS. CONCLUSIONS: There is significant correlation between the presence of spontaneous EMG activity and the development of clinical RSDS in the hemiplegic upper extremity after stroke. It is concluded that spontaneous EMG activity in the hemiplegic hands of stroke patients might be a good predictor of the future development of clinical RSDS.
After closed hand trauma, a 17-year-old boy had acute inflammatory changes that resembled bacterial whitlows of the third and fourth right fingers. Clearing of the inflammatory changes was followed by the development of cyanosis, hyperhidrosis, and roentgenographic evidence of patchy osteoporosis in the involved extremity. Findings of a biopsy specimen revealed that the inflammatory lesions in the proximal nail folds were caused by proliferation of capillary vessels embedded in edematous loose connective tissue. This is the first report of cutaneous histopathologic findings in the first stage of reflex sympathetic dystrophy, although similar features have been described in synovial and bone biopsy specimens of patients with reflex sympathetic dystrophy.
In a series of 662 primary total knee arthroplasties, reflex sympathetic dystrophy (RSD) was diagnosed in five patients (0.8%), four of whom demonstrated marked limitation of flexion requiring manipulation during the early postoperative period. Limitation of flexion, along with excessive pain and cutaneous hypersensitivity, should alert the surgeon to the possibility of RSD. Classic posttraumatic RSD findings of objective vasomotor changes and radiographic osteopenia may be difficult to interpret in patients after total knee arthroplasty. Sympathetic blockade is the key diagnostic and therapeutic measure in the management of RSD. RSD should be considered in a differential diagnosis of early poor results after total knee arthroplasty.
Review of current medical literature reveals little understanding of the physiology underlying the complex signs and symptoms that accompany reflex sympathetic dystrophy (RSD). The author surveyed the osteopathic medical literature and found a significant body of research documenting the physiology of somatic dysfunction. The manifestations of upper thoracic somatic dysfunction are strikingly similar to those of RSD and may offer insight into its heretofore unexplained physiology of this disorder.
Diabetes mellitus and peripheral neuropathies are considered to be unusual causes of the reflex sympathetic dystrophy syndrome. Their coexistence in a patient with this syndrome is rare and considered to be incidental. We report a case in which remission of the syndrome accompanied the resolution of the diabetic neuropathy. A possible pathophysiologic mechanism connecting these conditions is discussed.
Recovery of motor function in spinal cord injury usually does not occur beyond 2 yr from the date of injury and is rare beyond 8 yr. We present a case of a gentleman with a right C-5 motor, left T-5 motor, bilateral T-5 sensory tetraplegia, sustained after a fall in September 1985, who developed reflex sympathetic dystrophy of his right arm. This pain failed to resolve during the next 8 yr, despite conservative treatment consisting of range of motion, contrast baths, transcutaneous electrical nerve stimulation unit, and tricyclic antidepressants. Furthermore, his pain was refractory to dorsal rhizotomy in 1987. Subsequent follow-up visits documented ongoing pain and weakness of the right arm, with a stable injury pattern. Approximately 8 yr after initial injury, the patient underwent a series of eight stellate ganglion blocks, with the surprising result of improvement in Kendall graded motor function. This improvement was enough to represent a change in the motor level of spinal cord injury from C-6 to C-7, with a resultant increase in functional abilities. The improvement of motor function after stellate ganglion blocks for treatment of reflex sympathetic dystrophy is unprecedented and indicates that its aggressive treatment in patients with myelopathies may hasten motor recovery and, thus, functional gains. Physiologic explanations for this phenomenon include (1) resolution of pain inhibition, (2) improvement in disturbed microcirculation, and (3) resolution of sympathetic inhibition of mu-motor neurons via internuncial neurons.
Eighty-five patients with cerebral vascular accidents were assessed with three-phase bone scintigraphy of the hands and with whole-body delayed bone imaging. Nine patients (10%) had normal three-phase bone images. Fifty-five patients (65%) showed decreased blood flow and blood-pool images of the hands and wrists with normal delayed bone scintigrams, indicating the effect of paralysis or disuse. Twenty-one patients (25%) had diffuse increased uptake with periarticular accentuation, felt to be bone-scintigraphic evidence of reflex sympathetic dystrophy of the hands and wrists; in two patients this occurred before its clinical appearance. Thirteen of the 21 reflex sympathetic dystrophy syndromes (RDS)-involved limbs (62%) had increased blood flow, whereas 8 (38%) had decreased flow. Gross limb blood flow appears to be related to the degree of muscle activity, but flow may be altered by the presence of sympathetic changes. A possible dissociation between whole-limb flow and bone blood flow in paralyzed limbs involved with RDS is discussed. The elbow was involved in only one case, and a true "shoulder-hand" distribution was seen in only 11 of 21 cases (52%). Five patients (6%) had leg involvement on whole-body imaging. Traumatic synovitis of the wrist, and trauma to subluxed shoulders, could be recognized on the delayed study.
A patient suffering from acute smoke inhalation also had a long medical history that included reflex sympathetic dystrophy syndrome of the left foot and ankle. The entire foot and ankle were tender and cool to palpation; range of motion was severely reduced. She was referred for hyperbaric oxygen therapy, and 15 min into the the first treatment (46 min at 60 fsw) she reported a lessening of the pain in her foot; moreover, the foot was less cyanotic and warmer to the touch. Subsequent treatments continued to improve her conditions and for longer periods of time.