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This review paper presents a summary of concepts, ideas, theories, symptoms, stages, diagnostic procedures, and treatment modalities of a syndrome causing significant disability in a large segment of the American population. Diagnosis and early treatment will prevent significant and devastating disability in those individuals afflicted with this syndrome.
A 65-year-old female suffered trauma to her left hand on which acrodermatitis continua (psoriasis of Hallopeau) developed. It is suggested that the persistent pain of this skin condition, its poor response to treatment and her allied mental state led to the development of a severe algodystrophy with marked underlying osteoporosis.
The management of CRPS can be approached using objective criteria in a logical and systematic fashion. Frustration during treatment is common because: (1) the pathophysiology of CRPS is incompletely understood, (2) there is significant variation in presentation due to disparate premorbid anatomy and physiology, and (3) the natural history may be affected by incomplete treatment. Therapeutic efforts that should be effective may fail, and a trial-and-error approach to treatment is often mandatory. Early recognition of CRPS and prompt intervention, however, provide the best opportunity for clinical improvement.
RSDS is a complicated condition that requires early diagnosis and treatment for a favorable prognosis. The nurse should be alert to clinical signs in a patient with a traumatized area and report them to the physician as soon as possible. Management of the pain and establishment of trust will help promote successful physical therapy for the patient. The nurse should coordinate and manage the total care of the patient so that emotional and physical care can be at an optimum level for the patient and the patient's family.
Four female patients with Sudeck's atrophy (SA) were evaluated at our department. Sera of all patients were investigated for antibodies against Borrelia burgdorferi. In all patients elevated IgG antibody titers and in one patient also elevated IgM titer were found. In one patient structures identical with B. burgdorferi could be detected on histological sections from the skin of the affected limb. Our data and those of other authors suggest that a spirochetal infection can be regarded as an important etiopathogenetic factor in the development of SA.
A crossover study was performed for patients with RSD to evaluate the therapeutic efficacy of the hydroxyl radical scavenger DMSO. All patients were given DMSO locally 5 times a day during one week, and a placebo during one week. Before and after each treatment, subjective evaluation was performed by both the patient and the examinor as to clinical activity of RSD, and measurement was performed of the range of motion (ROM) of all joints in the affected extremity. DMSO was the most effective treatment as to improvement of ROM (p = 0.035) and as to overall improvement (p = 0.001). The efficacy of the hydroxyl radical scavenger DMSO indicates that RSD primarily involves an inflammatory process rather than a sympathetic reflex. As during the last 20 years no single report was published studying RSD in terms of inflammation, it is suggested that such studies are urgently needed to elucidate the real nature of RSD.
PURPOSE: To construct a questionnaire to measure skills in which notably both hands are active, which is suitable for patients with a disease of one or both hands and to research its response stability and possible improvements. METHOD: Using the Dutch elaboration of the ICIDH and then experts in a Delphi round, the questionnaire was constructed. Thereafter, test-retest and inter-observer reliability was examined. Fifty-four patients with RSD in one upper extremity and a normal contralateral extremity participated in the study, the first twenty to evaluate the construction of the questionnaire and the others to test reliability. RESULTS: The constructed Radboud skills questionnaire was reliable in terms of response stability (median coefficients of variation 2.2% to 6.6%). Correlation's between categories of items were fair to good. CONCLUSIONS: A useful questionnaire was constructed to map alterations in the level of disability in patients with a disease of one hand or both hands.
In 1864, W. Mitchell and colleagues first described the clinical syndrome which came to be known as 'causalgia'. Since that time, the concept of sympathetically related pain has evolved. There is general agreement that profound emotional and behavioural changes can follow these types of pain. Opinions have varied widely on the issue of a psychological etiology. It has often been suggested that certain personality traits predispose one to develop sympathetically related pain syndromes. A review of the literature reveals no valid evidence to substantiate this claim.
RSD is a symptom complex, representing an exaggerated response to injury or tissue damage. The amplification of the normal responses probably occurs both in the periphery and in the central nervous system. Diagnostic criteria are still under discussion, and treatment modalities are still directed toward the symptoms because the pathophysiology is not known. The pain of the condition may be sympathetically maintained of sympathetically independent (or both), and sympathetic blockade is useful in the former category. Treatment modalities must be directed toward optimizing both comfort and function of the affected extremity. Such treatment programs might occur in a multidisciplinary setting.
In some patients, ongoing and evoked neurogenic pain is relieved by pharmacological or destructive block of the sympathetic innervation of the affected part. In others, sympatholysis is ineffective. The present report shows that these two groups of patients can be distinguished by a safe and simple diagnostic test. Individuals in whom the pain was transiently relieved by intravenous phentolamine (Regitine) were very likely to respond favourably to subsequent sympatholytic treatment with i.v. regional guanethidine. Individuals in whom the phentolamine test was negative did not enjoy pain relief from this type of sympatholysis.
In summary, RSD is pain of neuropathic origin. The diagnosis is often obscure and requires a complete history, physical, and psychological evaluations. The diagnosis depends on symptoms (burning pain, allodynia and hyperpathia); signs (edema, sudomotor changes, temperature changes); and objective measurements, such as skin temperature, QSART, radiographs, and triple-phase bone scans; as well as the clinical response to a sympathetic block. Management of RSD should be designed to promote restoration of function utilizing physical therapy made possible by sympathetic, central, or peripheral nerve blockade. Medications may include nonsteroidal anti-inflammatory drugs, tricyclic antidepressants, and vasoactive drugs. Psychologic support is an important part of the patient's rehabilitation. Dorsal column or peripheral nerve stimulators, sympathectomies, and narcotics should be considered only when other more conservative measures have failed.
The chronic pain syndrome encompassed by the term RSD is poorly understood. The confusion is caused in large part by frequent misdiagnosis and excessive use of sympatholytic procedures in inappropriate circumstances. Recently, pain specialists have redefined the specific criteria for regional pain syndromes having sympathetic maintaining factors, emphasizing application of placebo testing in diagnosis and attention to anatomic principles in pharmacologic and surgical treatment. The authors believe that three-phase bone scanning is a valuable adjunct to clinical judgment in making the proper diagnosis. Current thinking suggests that sympathetic maintained pain exists but that it may comprise only approximately 10% of regional pain cases. Once the appropriate diagnosis is made, classically described sympatholytic procedures are reasonably used. Alternative techniques, such as spinal cord stimulation, may have an important role in refractory cases of sympathetically maintained pain.
This study evaluates quantitative and qualitative patterns of bone scintigraphy and correlates them to laboratory findings and clinical signs to reveal possible inflammatory reactions in RSD. Activity ratios between the affected hand/foot and the contralateral side were calculated in 99mTc DPD-bone scintigraphy for five phases (arterial: 0-30 sec, early blood pool: 0.5-5 min. late blood pool: 5-15 min, 3 hrs early bone, 24 hrs late bone phase) and the presence of five scintigraphic signs in the bone phases was assessed. Activity ratios of all phases correlated with ESR those in the early and late bone phase correlated with alpha 2 globulin and beta globulin concentrations and those in the arterial, the early and late blood pool phase with the gamma globulin concentrations, respectively. Clinical features such as pain, swelling, physical force, temperature differences and the duration of symptoms did not correlate to the activity ratios. However, three signs in the bone phase were negatively correlated to albumin concentrations. Positive correlations were found for alpha 2, gamma globulin concentrations, ESR, neutrophil cell counts and individual uptake patterns. We conclude that the quantitative analysis of five phase bone scintigraphy in RSD reveals different aspects of tracer kinetics and provides different pathophysiological information. Lateralization of regional hyperemia, increased micro vascular permeability and bone metabolism in RSD parallels shifts in protein concentrations and blood cell counts that are suggestive of a subacute inflammatory process, even in patients with no overt signs of inflammation.
OBJECTIVE: To assess the sensitivity, specificity, and predictive value (PV) of stress infrared telethermography (IRT) in the complex regional pain syndrome, type I (CRPS-I). METHODS: One hundred eighty-five consecutive patients (47 men, 138 women) with 205 pairs of chronically painful limbs (upper, lower, or both) were examined by pain specialists in neurology, physiatry, and anesthesia, who then reached a consensus diagnosis. A clinical diagnosis of CRPS-I required at least two of the following observations: burning pain, vasomotor changes, diaphoresis, trophic changes, allodynia. Patients with only one criterion were classified as possible CRPS-I; those with none were judged not to have CRPS-I. Patients and 24 asymptomatic control subjects underwent stress IRT, which was considered positive for CRPS-I if it showed three of the following: quantitative thermal emission of > or = 1.00 degree C, abnormal distal thermal gradient patterns, presence of a "thermal marker," and abnormal response to functional cold water autonomic stress testing. RESULTS: By clinical criteria, CRPS-I was diagnosed in 73 pairs of limbs; not CRPS-I was diagnosed in 70; and 62 pairs had possible CRPS-I. Excluding possible CRPS-I cases, there were 5 false-negative stress IRTs (sensitivity 93%) and 7 false-positive results (specificity 89%). Based on estimated 50% prior probability for our population, the positive PV is 90% and the negative PV 94%. None of the control subjects exhibited thermographic evidence of CRPS-I. CONCLUSION: Stress IRT is a sensitive and specific indicator of CRPS-I.
CRPS-I consists of post-traumatic limb pain and autonomic abnormalities that continue despite apparent healing of inciting injuries. The cause of symptoms is unknown and objective findings are few, making diagnosis and treatment controversial, and research difficult. We tested the hypotheses that CRPS-I is caused by persistent minimal distal nerve injury (MDNI), specifically distal degeneration of small-diameter axons. These subserve pain and autonomic function. We studied 18 adults with IASP-defined CRPS-I affecting their arms or legs. We studied three sites on subjects' CRPS-affected and matching contralateral limb; the CRPS-affected site, and nearby unaffected ipsilateral and matching contralateral control sites. We performed quantitative mechanical and thermal sensory testing (QST) followed by quantitation of epidermal neurite densities within PGP9.5-immunolabeled skin biopsies. Seven adults with chronic leg pain, edema, disuse, and prior surgeries from trauma or osteoarthritis provided symptom-matched controls. CRPS-I subjects had representative histories and symptoms. Medical procedures were unexpectedly frequently associated with CRPS onset. QST revealed mechanical allodynia (P<0.03) and heat-pain hyperalgesia (P<0.04) at the CRPS-affected site. Axonal densities were highly correlated between subjects' ipsilateral and contralateral control sites (r=0.97), but were diminished at the CRPS-affected sites of 17/18 subjects, on average by 29% (P<0.001). Overall, control subjects had no painful-site neurite reductions (P=1.00), suggesting that pain, disuse, or prior surgeries alone do not explain CRPS-associated neurite losses. These results support the hypothesis that CRPS-I is specifically associated with post-traumatic focal MDNI affecting nociceptive small-fibers. This type of nerve injury will remain undetected in most clinical settings.
For the patient presenting with early symptoms (< 6 months) I usually start treatment with a dose pack of methylprednisolone, analgesics, and daily occupational/physical therapy for 2 weeks (Fig. 2). If they do not respond within the first week, I add stellate ganglion blocks and acupuncture to the treatment regimen. For patients presenting with established chronic pain, I immediately start them on a dose pack of methylprednisolone for 1 to 2 weeks, a nonsteroidal anti-inflammatory such as indomethacin, 50 mg 3 times a day for 10 days and then switch to 75 mg twice daily until there is a response. Amitriptyline is helpful for sleep and depression and also has a beneficial effect on blood flow. Calcium channel blockers (nifedipine) may help improve peripheral circulation by its effect on vascular smooth muscle. In this patient group, I almost always start stellate ganglion blocks on the first visit. I have the patient try at least 2 blocks before deciding whether or not blocks are helpful. Many patients will not respond to the first block, but will start to respond after the second block. If the blocks are helping, I recommend 3 blocks a week, every other day for 3 weeks. Patients get the most benefit from their blocks if they have occupational or physical therapy immediately following the block. Surgical sympathectomy may be helpful but only in patients who have responded to sympathetic blockade.
Early diagnosis of RSD is essential. A keen clinical awareness of this problem is required by all hand surgeons. RSD is a clinical diagnosis that may be supplemented by digital temperature, three-phase bone scan, and digital radiographs of the hand. A thorough examination is necessary to identify untreated or inadequately treated sources of RSD. Once diagnosed, prompt treatment of RSD is beneficial. Patients are referred to our anesthesia department for diagnostic and therapeutic stellate ganglion blocks. A trial of 2 to 3 blocks is attempted initially. After successful block is performed, as measured by a Horner's sign and extremity temperature, the patient is brought to the hand clinic where active range-of-motion exercises are started. A stress loading program is an important and essential part of our treatment protocol. Sympathetic blocks are performed on a biweekly basis until the pain is relieved. Consideration is given to long-acting stellate ganglion blocks with a continuous catheter infusion for patients who show a limited, but short-lived response to stellate ganglion blocks. For RSD that does not respond to the stellate ganglion block, we generally perform a bretylium intravenous regional block. Patients with RSD are referred to our hand psychologist for counseling, psychotherapy, relaxation therapy, and possibly biofeedback. We use a multitherapy approach with all available modalities to achieve the best success in breaking the cycle of pain and returning the patient to normal, productive function.
The striking similarity of certain pain symptoms and neurologic changes in RSD and the findings of severe thoracic outlet and inlet syndrome were the reason why clinical diagnostic studies of this dystrophy were also completed by radiologic examinations of the vessel system. Surprisingly, more or less striking and differently configurated stenoses in the area of the subclavian vein, with a resulting impairment of the venous run-off, were found. Those findings have been documented in 20 of 21 patients with RSD since 1984 by functional venography and, in the meantime, they were confirmed intraoperatively in nine resistant cases. The stenoses led to a lesion-caused disproportion between increased arterial inflow and decreased venous outflow, with venous stasis. Consequently, they acted as a primary cause of an edema of the hand, with corresponding regional results, mainly on the function of the sympathetic nervous system. That shows a primarily increased activity in RSD that under the influence of local factors results in a pathologic positive feedback mechanism, as already was known. The stenosis of the subclavian vein, in my opinion, is the long-searched for cause of the so-called "individual predisposition." The use of functional venogram in diagnosis is essential because it gives important hints at the diagnostic and prognostic outlook for a possible surgical treatment of resistant RSD. It is also very important in understanding the pathogenesis. To improve the venous flow and diminish or interrupt the sympathetic efferences, we performed transaxillary decompression of the neurovascular bundle with additional upper thoracic sympathectomy in resistant cases of RSD. Nine patients experienced immediate improvement of the pain syndrome and edema, as well as the entire postoperative course. After an average follow-up of 7.5 years, we found an excellent result in seven patients, a good result in one, and a fair result in one. Intraoperative findings and the arteriograms we performed on seven surgically treated patients indicate the primarily increased sympathetic activity in RSD is mainly caused by irritations and compressions of the lower plexus roots as well as the postganglionic fibers in the area of the subclavian artery, mainly by the inner rim of the first rib and fibromuscular structures. So the two main pathogenetic factors of RSD are known, and now can be localized and documented radiologically. It now should be possible to study the pathophysiology of RSD in an appropriate animal model.