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A case of reflex sympathetic dystrophy following routine venipuncture is presented. This syndrome is characterized by pain, stiffness, and dysfunction of an extremity in response to a minor injury, and may lead to loss of the involved limb. The syndrome is poorly understood and often misdiagnosed. Early recognition and intensive physical therapy are most important in treating this disorder.
Concepts related to the pathophysiology of reflex sympathetic dystrophy syndrome (RSDS) are changing. Although sympathetic influences are still viewed as the most likely mechanism underlying the development and/or perpetuation of RSDS, these influences are no longer ascribed to an increase in sympathetic tone. Rather, the most likely mechanism may be increased sensitivity to catecholamines due to sympathetic denervation with an increase in the number and/or sensitivity of peripheral axonal adrenoceptors. Several other pathophysiological mechanisms have been suggested, including neurogenic inflammation with the release of neuropeptides by primary nociceptive afferents and sympathetic efferents. These neuromediators, particularly substance P, calcitonin gene-related peptide, and neuropeptide Y (NPY), may play a pivotal role in the genesis of pain in RSDS. They induce an inflammatory response (cutaneous erythema and edema) and lower the pain threshold. Neurogenic inflammation at the site of the lesion with neuromediator accumulation or depletion probably contributes to the pathophysiology of RSDS. However, no single neuromediator has been proved responsible, and other hypotheses continue to arouse interest.
Reflex sympathetic dystrophy (RSD) is characterized mostly by: (burning) pain, restricted range of motion, oedema and autonomic disturbances. Amputations in case of RSD patients should only be performed in cases of a dysfunctional limb, life threatening conditions such as untreatable infections or in cases in unbearable pain. The authors describe a patient in whom amputation became inevitable because of threatening infections.
The unusual case of reflex sympathetic dystrophy syndrome caused by an acute attack of gout is reported. The syndrome, involving the left ankle and hindfoot, developed twelve days after a classical gouty attack involving the first metatarso-phalangeal joint of the same foot. Diagnosis was based on X-ray and scintigraphic and MRI changes A prompt clinical remission was achieved with a short course of i.v. clodronate.
A study was conducted of 198 clients with reflex sympathetic dystrophy syndrome (RSDS) to gather demographic and descriptive data related to the occurrence of skin lesions. Participants ranged in age from 18-78 years, were predominantly women and represented all three stages of RSDS. Findings indicated that clients with RSDS develop distinctive skin lesions in addition to the cutaneous changes described in the literature. Skin lesions occur in the first and second stages of the syndrome. Skin lesions reportedly worsened in 135 clients (68%) when their pain became more severe, and correspondingly, seemed to improve as the pain decreased.
Reflex sympathetic dystrophy (RSD) is a syndrome characterized by pain out of proportion to injury, vasomotor and trophic changes, stiffness, and decreased function. It is important to separate the active disease process of RSD from its resultant state of contracture and fibrosis. Our treatment program is based on active "stress loading," which consists of active traction and compression exercises that provide stressful stimuli to the extremity without joint motion. Fifty-two patients with RSD were treated during a 3-year period. Their results and long-term follow-up on 41 patients are presented. The "stress loading" program has been used consistently during the past 20 years. The advantages of the program are its effectiveness, simplicity, safety, and noninvasiveness.
Reflex sympathetic dystrophy syndrome (RSDS), which probably has a multifactorial etiology, may appear after kidney transplantation. Its clinical manifestations include severe periarticular pain with inflammatory signs, especially in knees and ankles, causing functional disability. Symptoms develop during the first 3 months after transplantation and usually disappear 3 to 6 months later without sequelae. In renal transplant recipients it has previously been related to immunosuppressive treatment with cyclosporine. Therefore we had suggested that introducing tacrolimus could be a therapeutic option. We now present four cases of RSDS in kidney transplant recipients treated with tacrolimus. All but one patient were receiving tacrolimus monotherapy, excluding other drugs that might have been involved to cause the syndrome. It is also interesting that one of our cases develop RSDS long after transplantation when immunosuppressive treatment was changed. Symptoms correlated with an increase in alkaline phosphatase and with bone scintigraphy findings. All patients recovered without sequels 3 to 6 months afterward. In conclusion, RSDS is a relevant osteoarticular complication in patients receiving either anticalcineurinic drug (CyA or tacrolimus), even under monotherapy or with a low steroid dose.
The three-phase technetium bone scan has been recommended for use in the diagnosis of the reflex sympathetic dystrophy syndrome with a sensitivity and specificity of greater than 90%. A retrospective chart review was conducted of 63 patients who had three-phase technetium bone scan as part of a work-up for unexplained upper extremity pain, to determine the predictive value of the three-phase technetium bone scan in reflex sympathetic dystrophy syndrome, and what factors might affect it. The prevalence of definite or probable reflex sympathetic dystrophy syndrome, as assessed by Kozin's criteria, was 26% in this sample. The 3-hour delayed image demonstrated a sensitivity = 50%; specificity = 92%; positive predictive value = 67%, and negative predictive value = 84%. This was not improved using the data from the blood flow or pool phase. The sensitivity of 50% is lower than previous reports. The predictive value of the three-phase technetium bone scan was affected by the duration of symptoms and the age of the patient. Duration of symptoms less than 6 months, or ages more than 50 years substantially increased the sensitivity and positive predictive value of the three-phase technetium bone scan.
This case documents a patient with lumbosacral radiculopathy, reflex sympathetic dystrophy, and tarsal tunnel syndrome affecting one extremity. After lumbar laminectomy for L5-S1 radiculopathy, the patient developed foot pain diagnosed as secondary to reflex sympathetic dystrophy. Because of increasing foot pain despite long-term conservative therapy, the patient underwent further evaluation, including electrodiagnostic studies leading to the diagnosis of a superimposed tarsal tunnel syndrome. Following surgical decompression, pain decreased. Because of the unusual presentation, diagnosis and treatment of the tarsal tunnel syndrome was significantly delayed. To help understand the coexistence of these conditions, interrelating pathophysiologic mechanisms have been postulated, including the possibility that a "double-crush" phenomenon may have contributed to the development of tarsal tunnel syndrome. Earlier diagnosis and definitive treatment of the foot pain may have been possible had these mechanisms been better understood.
This report presents a brief review and an illustrative case summary of post-traumatic reflex sympathetic dystrophy. The manuscript is concerned with reviewing updated methods of properly diagnosing and treating such a complex condition. The case presented involves a young, healthy male patient, who after undergoing foot surgery, developed signs and symptoms of post-traumatic reflex sympathetic dystrophy.
It is suspected that some faults in the course of the treatment of traumas such as: reduction of fractures without sufficient anaesthesia, repeated reductions, tightness of casts, immobilization of fingers, ignoring patients' complaints of the pain and swelling about or painful rehabilitation may have effect on the development of the post-traumatic reflex sympathetic dystrophy. These opinions have not been confirmed by clinical trials. The incidence of above mentioned factors was analysed retrospectively in 165 patients with post-traumatic reflex sympathetic dystrophy within upper extremity and in 86 patients following fracture of distal radius without features of the condition (control group). It was found that the patients with reflex sympathetic dystrophy significantly more frequently complained of pain and swelling in the course of the treatment of trauma in the cast and they were subjected more frequently to painful rehabilitation after removing the cast. These factors appeared to have an effect on developing the reflex sympathetic dystrophy (comparing with the control group). The role of remaining factors that are often considered as significant in the development of reflex sympathetic dystrophy--painful and repeated reductions of fractures as well as immobilization of fingers-was not confirmed.
The lower leg skeletal muscles of 11 patients affected by reflex sympathetic dystrophy were investigated at rest by 31P nuclear magnetic resonance spectroscopy at a fieldstrength of 1.5 T. The results were compared with similar investigations of unaffected lower leg muscles of patients and volunteers. A significant increase was observed for the average tissue pH of the muscles of affected legs as deduced from the chemical shift of the resonance for inorganic phosphate. The average inorganic phosphate/phosphocreatine ratio of these muscles was also increased. The impairment of high energy phosphate metabolism, as deduced from the NMR data, may be caused by cellular hypoxia or diminished oxygen utilization, which would agree with previous findings that oxygen extraction is reduced in extremities affected by reflex sympathetic dystrophy.
UNLABELLED: The aim of our study was to evaluate Iloprost, a prostacyclin analog, for treatment of reflex sympathetic dystrophy in children not responsive to conservative treatment. Seven female patients with a mean age of 9 years (range, 6-11 years) diagnosed with reflex sympathetic dystrophy Stage II were treated with infusions of Iloprost given on three consecutive days. Additionally, all patients had physiotherapy and were offered psychologic consultation. One day after the final infusion, all seven patients were free of pain and achieved full weightbearing. The side effects of Iloprost were headache in all patients and vomiting in two patients. Two patients experienced relapse--one patient at 3 months and the other patient 5 months after primary treatment--but both were free of pain by 5 days after a second series of infusions. During a mean followup of 30 months all patients remained asymptomatic. Our preliminary results suggest that temporary sympathicolysis with Iloprost, physiotherapy, and psychologic counseling is a safe and an effective treatment of reflex sympathetic dystrophy in children with a long history of symptoms or in those who do not respond to conservative treatment. LEVEL OF EVIDENCE: Therapeutic study, Level IV (case series--no, or historical control group). See the Instructions for Authors for a complete description of levels of evidence.
BACKGROUND: Recently, a previously unrecognized posttransplant syndrome known as reflex sympathetic dystrophy syndrome of the lower limbs has emerged in patients receiving cyclosporine as immunosuppression. We describe herein this complication observed in a patient treated with tacrolimus after kidney transplantation. METHODS: A 49-year-old man received a kidney transplant from a cadaver donor and was treated with tacrolimus. Three months later, the patient complained of severe pain in the lower limbs that affected both knees and ankles. Bone scintigraphy and magnetic resonance were consistent with reflex sympathetic dystrophy syndrome. RESULTS: Laboratory tests that included creatinine, glomerular filtration rate, calcium, phosphate, urate, alkaline phosphatase, and parathormone were normal or near normal. Tacrolimus levels were around 13 microg/ml. Clinical improvement appeared slowly and spontaneously during the following 3 months, without appreciable changes in the tacrolimus level. CONCLUSIONS: In kidney transplant patients, tacrolimus could be a risk factor for the development of a reflex sympathetic dystrophy syndrome.
It is important for vascular surgeons to be familiar with reflex sympathetic dystrophy because they may be called on to participate in the evaluation and treatment of patients with this syndrome. Over a 3 1/2-year period, 35 patients, initially evaluated by a team of pain experts, were referred for surgical sympathectomy for reflex sympathetic dystrophy. All patients had at least one positive diagnostic sympathetic block before they were considered for surgical sympathectomy. With use of this team approach and careful patient selection, excellent results were obtained in 74%, good results in 17%, and poor results in 9%. Three patients required a repeat cervical sympathectomy after initial surgery failed to relieve their symptoms. One patient required a contralateral lumbar sympathectomy after ipsilateral sympathectomy was unsuccessful. Better results were obtained in patients treated earlier in their course and with extended surgical sympathectomy. Patients not responding to initial sympathectomy should be evaluated for the presence of residual functional sympathetic tissue, and if this is identified, further sympathectomy by an alternate approach appears justified.
Pseudodystrophy is a condition that in the past was regarded incorrectly as a kind of reflex sympathetic dystrophy. The difference between both diseases can be ascertained easily by a bone scintigraphy. Other clinical features of pseudodystrophy are discussed. Infrequent presentations of reflex sympathetic dystrophy are described: radial, parcellar, and zonal cases; vertebral localization; and other misleading conditions.
PURPOSE: There is considerable evidence that NMDA receptor antagonists can abolish nociceptor hypersensitivity in animals. In the present case report, two patients with reflex sympathetic dystrophy were treated with ketamine, a NMDA antagonist, morphine and bupivacaine. CLINICAL FEATURES: Two patients were referred suffering from severe pain, allodynia, hyperaesthesia, swelling and disability over their right lower legs, diagnosed as reflex sympathetic dystrophy. They had received conventional treatments with non-steroid anti-inflammatory drugs (NSAIDs), steroids, anticonvulsant, antidepressant, epidural lidocaine sympathetectomy and rehabilitation which failed to provide satisfactory pain relief. We administered subanalgesic doses of ketamine (7.5 mg), morphine (0.75 mg) and 6 ml bupivacaine 0.1% via a lumbar epidural catheter three times per day. After several courses of treatment over three and six months, satisfactory pain relief was achieved in each patient. Both are now able to walk with slight weight bearing with the assistance of crutch. The treatment is continuing with further improvement of symptoms and signs. CONCLUSION: Epidural coadministration of low doses of morphine, ketamine and bupivacaine provided effective pain relief in two patients. This suggests synergy from this combination that provides an alternative treatment for reflex sympathetic dystrophy.
Over a 12-year period, seven adolescent patients with reflex sympathetic dystrophy were seen in the Mayo Clinic Foot Clinic. The details of these cases are presented, and the literature pertaining to reflex sympathetic dystrophy in children is reviewed.