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Results for “Reflex Sympathetic Dystrophy”

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PubMed1993

Epidural clonidine treatment for refractory reflex sympathetic dystrophy.

BACKGROUND: Intraspinally administered alpha 2-adrenergic agonists may relieve pain in sympathetically maintained pain (SMP) syndromes, such as reflex sympathetically dystrophy (RSD), by spinal, peripheral, and central nervous system actions. This study examined analgesic efficacy and side effects of epidurally administered clonidine in patients with severe, refractory RSD. METHODS: Twenty-six patients with severe chronic pain consistent with RSD were studied in a randomized, blinded, placebo-controlled design. Cervical or lumbar epidural catheters were inserted for patients with upper or lower extremity RSD, respectively, and patients received, in random order on three consecutive days, epidural injection of clonidine, 300 or 700 micrograms, or placebo. Pain (by visual analog score (VAS) and McGill Pain Questionnaire), sedation, blood pressure, and heart rate were monitored at specified intervals for 6 h after injection. Patients who responded to clonidine, but not placebo, then entered a trial of open-label, continuous epidural infusion of clonidine (10-50 micrograms/h). RESULTS: Clonidine, but not placebo, caused pain relief, sedation, and decreased blood pressure and heart rate after bolus epidural injection. The smaller clonidine dose (300 micrograms), produced pain relief and decreases in blood pressure and heart rate similar to those of the 700 micrograms dose, but with less sedation. Epidural clonidine was infused for a mean of 43 days in 19 patients at a mean rate of 32 micrograms/h for sustained analgesia. CONCLUSIONS: Transdermal clonidine has been demonstrated to produce analgesia in the area surrounding its application site in patients with SMP. The current study indicates that extensive analgesia may be obtained by epidural administration. Sedation and hypotension may limit bolus epidural clonidine administration for RSD. The role for chronic epidural infusion of clonidine has not yet been established.

Adult↗
PubMed2007

Reflex sympathetic dystrophy: a retrospective epidemiological study of 168 patients.

This is a retrospective epidemiological study. The objective is to determine the epidemiological characteristics including the patient demographics, etiological factors, duration of symptoms, treatment modalities applied and clinical outcome of the treatment in reflex sympathetic dystrophy (RSD). Medical records of the 168 patients managed in two tertiary hospitals with the diagnosis of RSD that was made according to both IASP criteria and three-phase bone scan were reviewed. The upper limb was affected 1.5 times as commonly as the lower limb. Of the 168 cases, 10.7% were non-traumatic. In 89.3% of the patients, RSD developed after a traumatic inciting event with a predominance of fracture. In 75.6% of the patients, RSD developed due to job-related injuries. The percentage of successful clinical outcome was 72%. The percentage of the patients that did not respond to therapy was 28%. The management period is long and this causes higher therapeutic costs in addition to loss of productive effort. However, response to therapy is good. On the other hand, in approximately one third of the patients, RSD does not improve despite all therapeutic interventions. In addition to compensation costs, this potentially debilitating feature causes RSD to appear as a socioeconomic problem.

Adolescent↗
PubMed1993

[Good results of treatment of reflex sympathetic dystrophy with a 50% dimethylsulfoxide cream].

In this open prospective study dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, was tested in a 50% concentration in a fatty cream base (cremor vaselini cetomacrogolis FNA) in a total of 37 patients suffering from reflex sympathetic dystrophy. Patients were selected according to an RSD screening protocol. They also received physiotherapy. Eligible patients presented with acute signs of RSD and needed to have a sensation of heat in the extremity, as well as at least two of the following symptoms: (distal) pain, redness, swelling, loss of function, hyperhidrosis or increased hair growth and/or nail growth. Endpoints were the clinical improvement of the patient together with the patient's assessment of the pain according to a Visual Analog Scale (VAS: 0-10; 0 = no pain, 10 = unbearable pain). Successful treatment was accomplished when the VAS was halved and clinical signs had improved. The results showed a significant improvement in VAS score from 5.3 (SD 2.9) to 0.9 (SD 1.3; p < 0.01) in a mean treatment time of 3.4 months (SD 1.9). Systemic side effects consisted of a sulfurous smell of the exhaled breath of 12 patients. Concerning local side effects a mild dry, scaling effect on the skin was seen.

Acute Disease↗
PubMed2004

Chronic post-ischemia pain (CPIP): a novel animal model of complex regional pain syndrome-type I (CRPS-I; reflex sympathetic dystrophy) produced by prolonged hindpaw ischemia and reperfusion in the rat.

A neuropathic-like pain syndrome was produced in rats following prolonged hindpaw ischemia and reperfusion, creating an animal model of complex regional pain syndrome-Type I (CRPS-I; reflex sympathetic dystrophy) that we call chronic post-ischemia pain (CPIP). The method involves placing a tourniquet (a tight fitting O-ring) on one hindlimb of an anesthetized rat just proximal to the ankle joint for 3 h, and removing it to allow reperfusion prior to termination of the anesthesia. Rats exhibit hyperemia and edema/plasma extravasation of the ischemic hindpaw for a period of 2-4 h after reperfusion. Hyperalgesia to noxious mechanical stimulation (pin prick) and cold (acetone exposure), as well as mechanical allodynia to innocuous mechanical stimulation (von Frey hairs), are evident in the affected hindpaw as early as 8 h after reperfusion, and extend for at least 4 weeks in approximately 70% of the rats. The rats also exhibit spontaneous pain behaviors (hindpaw shaking, licking and favoring), and spread of hyperalgesia/allodynia to the uninjured contralateral hindpaw. Light-microscopic examination of the tibial nerve taken from the region just proximal to the tourniquet reveals no signs of nerve damage. Consistent with the hypothesis that the generation of free radicals may be partly responsible for CRPS-I and CPIP, two free radical scavengers, N-acetyl-L-cysteine (NAC) and 4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl (Tempol), were able to reduce signs of mechanical allodynia in this model.

Animals↗
PubMed1984

Reflex sympathetic dystrophy in quadriplegia: case report.

A patient with quadriplegia developed severe localized unilateral hand pain associated with clinical evidence of abnormal sympathetic hand activity. Diagnosis revealed reflex sympathetic dystrophy (RSD), which was resolved with conservative management. The association of RSD with spinal cord injury has been reported only rarely. Since few speculations about this condition have been made, we suggest that unexplained painful syndromes in the extremities of patients with spinal cord injury be carefully evaluated to rule out the possibility of RSD.

Adolescent↗
PubMed1995

[Regional transient osteoporosis and reflex sympathetic dystrophy. Are they different entities or clinical variants of the same disease?].

We report a 50 years old male that evolved with alternating episodes of osteoporosis with pain, edema and erythema of both feet. The patient presented clinical and radiological evidences of both transient regional osteoporosis and reflex sympathetic dystrophy. The clinical evolution was documented with magnetic resonance imaging. The hypothesis that both entities could be different expressions of same syndrome is discussed.

Diagnosis, Differential↗
PubMed1989

Ketanserin in reflex sympathetic dystrophy. A double-blind placebo controlled cross-over trial.

Ketanserin, a selective S2 serotonergic antagonist, was assessed against placebo in a double-blind cross-over study of 16 patients with chronic peripheral burning pain. Nine of these had signs of reflex sympathetic dystrophy (RSD). All patients underwent 4 intravenous regional treatments, 2 with ketanserin (10 mg for upper limb pain, 20 mg for lower limb pain) and 2 with placebo. In those patients with RSD ketanserin and not placebo provided significant (P less than 0.05) sustained pain relief as assessed by linear analogue scales. In patients who did not fulfil the criteria for RSD no significant relief was seen with placebo or ketanserin. Following tourniquet release, drowsiness, shakiness and faintness were reported at a higher (P less than 0.05) frequency after ketanserin than after placebo. All side effects were mild and transient, and no changes occurred in heart rate or blood pressure following ketanserin that were significantly different from those seen following placebo. A role for serotonin in the pathogenesis of RSD is proposed.

Adult↗
PubMed2000

Reflex sympathetic dystrophy in hypophosphataemic osteomalacia with femoral neck fracture: a case report.

We report a male patient who presented with suspicion of skeletal metastases based upon an abnormal 99-mTc bone scan, which showed increased uptake at both femoral heads, left femoral neck, and several ribs. The images also suggested reflex sympathetic dystrophy, subcapital fracture of the left femur, and rib fractures. A diagnosis of hypophosphataemic osteomalacia was finally made.

Adult↗
PubMed1990

[Relationship between three phase bone scintigram and prognosis after sympathetic blockade in reflex sympathetic dystrophy of the hand].

We attempted to correlate the changes in three phase bone scintigram (TPBS) with prognosis after sympathetic blockade in reflex sympathetic dystrophy (RSD) of the hand. Subjects were 12 patients of RSD in acute or dystrophic stage, who all had increased images on TPBS. Either intravenous regional sympathectomy with guanethidine or stellate ganglion block was performed repeatedly. We compared TPBS obtained just before and after this series of sympathetic blocks and evaluated the eventual recovery of function of the hand. In 8 patients, blood flow (phase 1) image of TPBS decreased after the blockade. Of these patients, those who showed almost normalized tracer activity not only on flow image but on blood pool (phase 2) and delayed (phase 3) image, returned to normal. But others with normalized blood flow and still increased activity in blood pool and delayed image, remained with mild contracture of the hand. These results suggest that normalization of blood pool and delayed image on TPBS is a predictor of subsequent recovery after sympathetic blockade in RSD.

Adult↗