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Reflex sympathetic dystrophy, or as it is now known, complex regional pain syndrome, Type 1, is an unusual complication of a variety of injuries whose development should be suspected in the presence of disproportionate pain coupled with autonomic disturbance. Early recognition and treatment with multimodality therapy offer a high probability of recovery.
Reflex sympathetic dystrophy (RSD) is currently defined as CRPS type I (complex regional pain syndrome). Due to the lack of comprehensive understanding of underlying pathophysiological mechanisms, a wide variety of therapeutic approaches are proposed, all of them being of unpredictable and variable efficacy. This is also due to the lack of controlled studies and randomized therapeutic trials. Most of the so-called "efficient" treatments are in fact based on anecdotal case reports and/or uncontrolled studies with small number of cases. Sympathetic blocks and active physiotherapy are, for many authors, the cornerstones of the efficient management. The role of prevention must be strongly emphasized, focusing, if RSD occurs following surgery, on the importance of pre- and postoperative efficient analgesia.
Reflex sympathetic dystrophy (RSD) progresses at a slow to moderate pace and was rarely diagnosed until the mid-1980s. Thermography, better documentation, and research of this disease has made diagnosis easier. Patients with RSD may be seen by the PACU nurse, who needs to be aware of the disease's progression and treatment to better guide the patient's plan of care.
Reflex sympathetic dystrophy (RSD) is a chronic pain syndrome with prominent cutaneous findings. Atrophy has been considered to be the most common manifestation of the disease. We catalogued the abnormal skin conditions in RSD by means of chart review. Vascular problems were most common, followed by inflammatory diseases, infections, and atrophic diseases. Atrophic disease accounts for a minority of the skin problems seen in RSD. Most cutaneous complaints were related to vascular disease, particularly edema.
Reflex sympathetic dystrophy syndrome is a peculiar rheumatological pathology whose diagnosis at times is evident, but other times it is complex. This difficulty compels us to have a good knowledge of the syndrome and to take it into account when faced with any rheumatological differential diagnostic. In this work we revise the major aspects of diagnostic.
Reflex sympathetic dystrophy (RSD) is a relatively common disabling disorder of unknown pathophysiology. From a cohort of 52 patients, carefully selected to fulfill the recently formulated diagnostic criteria for RSD, venous blood samples were taken for typing of class I and II major histocompatibility antigens. The frequency of HLA-DQ1 was found to be significantly increased compared with control frequencies. The association provides an indication for an organic basis of RSD.
Reflex sympathetic dystrophy presents with pain out of proportion to the cause, loss of function, and significant evidence of an autonomic disorder. These findings are often accompanied by psychological disturbances, which can dominate the condition. There are differences in the symptoms and signs during childhood. It is more frequent among girls than boys, and the legs are more often affected than the arms; and trophic changes may be absent. There may be no history of trauma, and the response to treatment is often satisfactory. There are a number of theories on etiology. A disorder of the sympathetic nervous system with increased activity has been suggested, but on the evidence available super-sensitivity to neurotransmitters is more likely. Also there may be a spinal, as well as a peripheral, component to the sensitivity. Other suggestions include the release of a pain substance, a disturbance of natural opioid metabolism, and an exaggerated inflammatory response. The diagnosis is mainly clinical, supported by X-ray examination, bone scans with Technetium 99m labelled diphosphonates, and a characteristic scintograph pattern. Laser Doppler flowmetry can also, be useful. The most effective preventative measure is control of pain and early mobilisation. Many treatments have been tried, but the response is variable. Drugs include analgesics, non-steroid anti-inflammatory drugs, anti-depressants, and steroids. Betablockers, with gradually increasing doses may help; as may vasodilators. Calcitonin, by intramuscular injection has been given a particularly favourable report. Physiotherapy is of prime importance. Some treatments are only likely to be considered in older children. Blocking of sympathetic pathways can be tried with paravertebral or epidural injections of local anesthetics. Regional intravenous injections of alpha adrenergic blocking agents distal to a tourniquet can relieve pain, but usually only transiently; and ketanserin may act favourably as a serotonin antagonist. Surgical sympathectomy can also be considered.
Reflex sympathetic dystrophy (RSD) usually follows traumatic injuries or neurologic disorders. The authors report a rare case of RSD that followed intraarterial administration of cocaine in a patient with a history of intravenous drug abuse. The cocaine was self-administered inadvertently into the femoral artery rather than the femoral vein. Despite the intense pain, swelling, and dermatologic changes that followed, the diagnosis of RSD was not considered until scintigraphic studies suggested it. A combination of normal radiographs, a normal leukocyte study, and an abnormal bone scan in the region of tenderness and swelling excluded other possibilities and suggested RSD. In our patient, RSD was likely caused by an ischemic autonomic injury from the vasoconstrictor action of cocaine. Clinical follow-up and relief using phentolamine, an alpha-adrenergic blocker and vasodilator, made the diagnosis of RSD most likely.
Reflex sympathetic dystrophy (RSD) may be a misdiagnosis or at least not descriptive enough in patients with atypical hand posture and atypical edema. Seven patients with the previous diagnosis of RSD were investigated further because of inconsistent clinical picture with the underlying pathology and bizarre course of the disease. Four patients had clenched fist and three had factitious edema. These seven patients underwent psychological examination, and MMPI was applied to all. In two of these no psychological disorder was obtained according to DSM-IV. One patient could not adapt to MMPI. In two anxiety disorders, in one depression, and in one patient conversion disorder was diagnosed. We suggest that these patients are not motivated enough to improve their conditions and expectations of such patients may show some differences depending on the environment.
Reflex sympathetic dystrophy (RSD), an unusual diagnosis in general paediatrics, is well recognised by paediatric rheumatologists. This study reports the presentation and the clinical course of 46 patients (35 female, age range 8-15.2) with RSD. The patients saw professionals from an average of 2.3 specialties (range 1-5). Twenty five (54%) had a history of trauma. Median time to diagnosis was 12 weeks (range 1-130). Many children had multiple investigations and treatments. Once diagnosis was made, treatment followed with physiotherapy and analgesics. Median time to recovery was seven weeks (range 1-140), with 27.5% relapsing. Nine children required assessment by the child and adolescent psychiatry team. This disease, though rare, has significant morbidity and it is therefore important to raise clinicians' awareness of RSD in childhood. Children with the condition may then be recognised and referred for appropriate management earlier, and spared unnecessary investigations and treatments which may exacerbate the condition.
Reflex sympathetic dystrophy (RSD) is a disorder that can potentially result in permanent impairment. Because there are no adequate comparative studies regarding the additional value of physical therapy (PT) or occupational therapy (OT) for reducing the severity of permanent impairment in RSD, we prospectively investigated their effectiveness. At two university hospitals, we randomly assigned 135 patients with RSD of one upper limb, existing for <1 yr, to PT, OT, or control therapy (CT). One year after inclusion, impairment percentages were calculated according to the general method of the American Medical Association's Guides to the Evaluation of Permanent Impairment. For statistical evaluation, the Wilcoxon's signed-rank test (two-sided; alpha = 0.05) was used. The mean whole body impairments were as follows: PT, 21.6% and 19.1%; OT, 22.8% and 22.1%; CT, 22.0% and 22.1% (intention-to-treat and per protocol analysis, respectively). There were no significant differences between the groups. We conclude that impairment percentages in RSD patients treated with PT or OT did not differ significantly from those treated with CT at 12 months after inclusion.
Reflex sympathetic dystrophy (RSD) is a clinical syndrome defined in the English literature by pain, dystrophic tissue changes and local disturbance of autonomic function in a limb or part of a limb. Algodystrophy is the common name used for the condition in the French literature, in which the concept also includes the "transient regional osteoporosis" and the "regional migratory osteolysis". We want to discuss three points: 1) Are the RSD, transient regional osteoporosis and migratory osteolysis different diseases or different manifestations of a single condition? We believe that an objective differentiation is not possible between them. Our report about 28 cases of polytopic RSD shows the frequent association in the same patient of these manifestations and we believe that this represents the broad spectrum of a single disease. 2) Is the accepted classic pathophysiologic mechanism of RSD accurate? The conception of a disturbance of autonomic function is not easily linked with its association with conditions such as diabetes, hyperthyroidism, hyperlipidaemia and others. Even more difficult to explain is the association with malignancy and osteomalacia. The deposit of immunoglobulins that we have demonstrated in two cases in the palmar fascia of RSD associated with malignancy suggests a possible immunological mechanism. 3) What are the limits of RSD? The association between RSD and aseptic necrosis of the hip has been reported. Are they two different conditions or is the aseptic necrosis only a more developed form of RSD? Finally, we report the first single case of Munchausen syndrome mimicking a RSD of the hand with the same clinical, radiological and scintigraphic appearance.
Reflex sympathetic dystrophy can be elicited by various factors (e. g. trauma, herpes zoster, myocardial infarction). Independent of kind and site of a lesion, symptoms occur most often in the whole distal part of the affected extremity. There in most cases, a triad of autonomic, motor and sensory disturbances can be found clinically. For early diagnosis--beside clinical investigation--a comparative measurement of skin temperatures on both sides of finger or toe tips, respectively, is recommended. Hereby the clinical finding of a warmer or colder extremity can be proved, which supplies evidence of a disturbed skin blood flow. In case, the above mentioned triad and a disturbance of skin circulation is found, diagnosis of sympathetic reflex dystrophy can be made with great certainty. With regard to the underlying pathophysiology, symptoms can be explained at this time satisfactory only by the assumption of a vicious circle. Starting from a painful event (e.g. trauma, mark in a plaster cast, nerve lesion or myocardial infarction) a functional disturbance of the sympathetic nervous system is initiated. This results in a disturbance of the circulation in all of the affected tissues (skin, muscle, bone and joint), which finally gives rise to an abnormal excitation of afferent receptors, particularly of nociceptors. This excitation maintains the disturbance of the sympathetic nervous system at central nervous level (vicious circle). The most relevant pathomechanism in this process seems to be the occurrence of an imbalance between the activity of sympathetic vasoconstrictor neurons supplying arteries and those, supplying veins. A sympatholytic therapy, if applied in time, is able to cut off the vicious circle, which may lead to a restitutio ad integrum. Further investigations will show to what extent psychological factors are involved in developing the central nervous disturbance of the sympathetic nervous system and may also show if in addition the motor system is affected.
Reflex sympathetic dystrophy syndrome is comprised of a variety of changes in vasomotor and trophic responsivity, as well as, stiffness, edema and severe pain. This study examined 20 patients with reflex sympathetic dystrophy syndrome who had failed to respond to a variety of techniques commonly used to treat this disorder. These patients had documented histories of reflex sympathetic dystrophy syndrome ranging from 18 to 60 months. All had been referred for psychological evaluation and provision of pain management. A combination of thermal biofeedback, relaxation training, and supportive psychotherapy were used to reduce subjective pain. The results indicate that patients were able to significantly increase their initial (p less than 0.0001) and postrelaxation (p less than 0.0001) hand temperatures, as well as to significantly reduce their subjective pain ratings (p less than 0.0001). This reduction in pain was maintained at 1-year telephone follow-up, with 14 of the 20 patients returning to work by that time. This intervention was effective as a pain reduction strategy for our patients with reflex sympathetic dystrophy syndrome who had failed to benefit from other treatments.
Reflex sympathetic dystrophy syndrome is a difficult condition to treat. Many modalities have been proposed, all of them being clinically effective but whose efficacy is often difficult to assess, and has not been properly compared. A regimen of physical therapy (pressure therapy, antalgic electrotherapy and exercise therapy) with or without calcitonin was investigated in 24 patients randomly assigned to 2 groups, one given physical therapy alone (Group I) and the other physical therapy plus salmon calcitonin 100 MRC units daily for 3 weeks (Group II). Efficacy assessment was based on clinical (pain, oedema and movement in the affected parts), biochemical (blood and urinary phosphorus and calcium levels, plasma 25-OH-D, plasma parathyroid hormone (PTH), creatinin, alkaline phosphatases and urinary hydroxyproline) and scintigraphic parameters, as well as on the patient's ability to resume working. There was significant improvement in pain in the Group II patients after one week of treatment. As a result the authors advocate the use of calcitonin in addition to physical therapy in reflex sympathetic dystrophy syndrome - and even of calcitonin alone where physical therapy is not possible.
OBJECTIVES: Reflex sympathetic dystrophy (RSD) is, from the onset, characterized by various neurological deficits such as an alteration of sensation and a decrease in muscle strength. We investigated if afferent A-beta fibre-mediated reflexes are changed in lower extremities affected by acute RSD. METHODS: The involvement of these fibres was determined by analyzing reflex responses from the tibialis anterior (TA) and biceps femoris (BF) muscles after electrical stimulation of the sural nerve. The reflexes were studied during walking on a treadmill to investigate whether the abnormalities in gait of the patients were related either to abnormal amplitudes or deficient phase-dependent modulation of reflexes. In 5 patients with acute RSD of the leg and 5 healthy volunteers these reflex responses were determined during the early and late swing phase of the step cycle. RESULTS: No significant difference was found between the RSD and the volunteers. During early swing the mean amplitude of the facilitatory P2 responses in BF and TA increased as a function of stimulus intensity (1.5, 2 and 2.5 times the perception threshold) in both groups. At end swing the same stimuli induced suppressive responses in TA. This phase-dependent reflex reversal from facilitation in early swing to suppression in late swing occurred equally in both groups. CONCLUSIONS: In the acute phase of RSD of the lower extremity there is no evidence for abnormal A-beta fibre-mediated reflexes or for defective regulation of such reflexes. This finding has implications for both the theory on RSD pathophysiology and RSD models, which are based on abnormal functioning of A-beta fibres.
Reflex sympathetic dystrophy syndrome is a troublesome, complex disorder that presents with chronic, unexplained aching or burning pain, the intensity of which is incommensurable with the original injury. Six diagnostic criteria have been described by Genant et al: pain and tenderness in the extremities; swelling of soft tissue; diminished motor function; trophic skin changes; vasomotor instability; and patchy osteoporosis. Currently, the most widely accepted etiology is an initial vasomotor reflex spasm occurring after an injury to the extremity, followed by a loss of vascular tone, persistent vasodilation, and rapid bone resorption.
Reflex sympathetic dystrophy syndrome is a devastating disease that is difficult to diagnose and treat. Presented here is a review of the literature explaining its clinical and radiographic findings, pathogenesis, diagnosis, and treatment modalities.