- Email: [email protected]
Re: Urological Symptomatology in Patients with Reflex Sympathetic Dystrophy
1782
LETTERS TO THE EDITOR
recovery. How did the authors decide that patients with percutaneow nephrostomy recovered completely? We invite their comments about Double-J stent insertion following suture absorption. We replaced a Double-J stent in all patients in the belief that recovery will improve and, if insertion was not possible, we repaired the injury surgically. Even if we only performed percutaneous nephrostomy in cases with ureteral ligation our recovery rate (66.6%)was less than that of the authors (80%). Respectfully, M. Kamuran Bircan, Kenan Korkmaz and Hayrettin $ahin Department of Urology Dicle University School of Medicine 21280-Diyarbakir Turkey 1. Bircan, M. K., Ozttirk, O., Korkmaz, K. and $ahin, H.: Iatrojenik Ureter Ligasyonunda Tedavi Secenekleri. Urol. Biilteni, 3: 163. 1992.
RE: UROLOGICAL SYMPTOMATOLOGY IN PATIENTS WITH REFLEX SYMPATHETIC DYSTROPHY
M . B. Chancellor, P. J. Shenot, D . A . Rivas, S . Mandel and R. J. Schwartzman J. Urol., 155: 634-637, 1996 To the Editor. The authors attempted to determine the impact of reflux sympathetic dystrophy on lower urinary tract function. Their urodynamic study of 20 consecutive patients with neurologically verified reflex sympathetic dystrophy suggests a profound effect of this condition on detrusor and sphincteric function. Although the analogy with autonomic neuropathy from diabetes mellitus is tempting, this study raises some important issues related to the definition of reflex sympathetic dystrophy, study methodology and implications for the practicing urologist. At most pain management centers reflex sympathetic dystrophy is viewed as a rare disease that is difficult to diagnose and even more difficult to treat. Bonica originated the 3-step classification of reflex sympathetic dystrophy discussed by the authors.’ However, a major difficulty in diagnosing reflex sympathetic dystrophy is that its definition is qualitative and rather nonspecific. The International Association for the Study of Pain defmes reflex sympathetic dystrophy as “Continuous pain in a portion of an extremity after trauma which may include fracture but does not involve a major nerve, associated with sympathetic hyperactivity. The painful trauma, usually mild, is not associated with significant nerve injury. The pain is described as burning, continuously exacerbated by movement, continuous motion or stress.”2Therefore, nearly all acute chronic pain conditions can be interpreted to qualify in some respect to fit with this definition. The hallmark in the diagnosis of reflex sympathetic dystrophy has been relief of pain after a selective regional sympathetic block. Determination of efficacy of a sympathetic nerve block, as well as initial diagnosis of reflex sympathetic dystrophy should include a quantitative assessment of regional blood flow (laser Doppler study) and temperature of the affected and painful regions before and aRer the block. In this study there is no quantitative verification of reflex sympathetic dystrophy in any patient. There was no verification that the pain syndromes were not due to other causes, including localized nerve injury (electromyography or nerve conduction testing) or systemic diseases associated with secondary neuropathy. No quantitative small fiber neuropathy testing was done (quantitative thermal testing) to evaluate A-delta or C fiber pathology. Therefore, before considering any urodynamic changes associated with reflex sympathetic dystrophy, it is important to be certain that one has ruled out other causes of chronic pain and has established the diagnosis of reflex sympathetic dystrophy. In fact, one wonders how many patients with reflex sympathetic dystrophy and no urological symptoms have been seen at their regional center for the treatment of this disease. Without knowing the denominator in that study, it is extremely difficult to judge the importance of this report. Also, it would have been interesting methodologically to incorporate either an agematched or pain-matched control group to appreciate the relevance of the urodynamic findings reported.3 In their table depicting patient demographics, one also wonders if some medications used to treat pain in these patients with reflex sympathetic dystrophy might have altered bladder function. In par-
ticular, most pain management protocols rely heavily on tricyclic antidepressants and opiates, drugs known to decrease detrusor contractility substantially. In the 13 patients with detrusor hyperreflexia or detrusor-sphincter dyssynergia, we are concerned to see a significant incidence of prior orthopedic or back operations. Although the authors were careful not to incorporate patients after recent back surgery, one wonders what impact these prior operations might have had on the urodynamic findings. Finally, the absence of significant pelvic or suprapubic pain is surprising and does not substantiate the contention that reflex sympathetic dystrophy might be a possible etiology for interstitial cystitis.‘ If reflex sympathetic dystrophy is, indeed, a chronic pain syndrome characterized by continuous burning pain exacerbated by movement, how can it diffuse systemically to affect the bladder selectively? Also, if it were a chronic pain syndrome, one wonders what would be the implication of that diagnosis in the absence of a recognized and effective treatment for reflex sympathetic dystroPhY.5 ReSpedfUllY, Philippe E. Zimmern and Darrell Tanelian Department of Surgery Division of Urology Southwestern Medical Center 5323 Harry Hines Boulevard Dallas, Texas 75235-9110 1. Bonica, J.: Causalgia and other reflex sympathetic dystro hies. In: The Management of Pain. Philadelphia: Lea and Fekger, 1990. 2. International Association for the Study of Pain: Classification of chronic pain: description of chronic ain syndromes and definitions of pain terms. Prepared by tge Subcommittee on Taxonomy. Pain, 3:51, 1986. 3. Turner, J. A., Deyo, R. A., Loeser, J. D., Von Korf€, M. and Fordyce, W. E.: The importance of placebo effects in pain treatment and research. J.A.M.A., 271: 1609, 1994. 4. Atkins, R. M., Tindale, W., Bickerstaff, D. and Kanis, J . A.: Quantitative bone scintigraphy in reflex sympathetic dystrophy. Brit. J. Rheumatol., 3 2 41, 1993. 5. Tanelian, D. L.: Reflex sympathetic dystrophy: a re-evaluation of the literature. Pain Forum, submitted or publication.
Reply by Authors. We appreciate the enthusiastic and detailed comments regarding our recent investigation. Reflex sympathetic dystrophy is truly an enigmatic disease that is difficult and controversial with respect to diagnosis and treatment. Despite a thorough investigation, a consensus regarding any aspect of reflex sympathetic dystrophy among neurologists and anesthesiologists interested in pain management has proved to be elusive. All of our patients with reflex sympathetic dystrophy were diagnosed and referred for urological evaluation by 1 of us (R. J. S.) who is an internationally recognized authority on the disease. At most pain management centers reflex sympathetic dystrophy is seen commonly and is not considered a rare condition. The recent consensus statement in regard to reflex sympathetic dystrophy uses a revised taxonomic system for the disease.’ The process is initiated by trauma to C fibers in the soft tissue, or damage to a peripheral nerve or plexus. The symptoms are sensory abnormalities, including spontaneous burning pain, hyperalgesia, allodynia or hyperpathia; vascular and sweating abnormalities, including edema and trophic change in skin, subcutaneous tissue, joints and bone, and motor abnormalities, including dystonia, weakness and tremor.2 All of our patients had these symptoms and were extensively evaluated to rule out other causes of the symptoms. Our patients underwent myelography, followed by computerized tomography, electromyography and bone densitometry or plain films. Reflex sympathetic dystrophy is frequently not sympathetically maintained in its later stages. It is then sympathetically independent pain. Some patients were in the late stages of the illness and, consequently, were sympathetically independent. Therefore our evaluation of reflex sympathetic dystrophy conformsto common standards and the critique about our evaluation methodology is unfounded. In fact, the evaluation techniques presented by Zimmern and Tanelian deviate from those of most authorities on reflex sympathetic dystrophy. Our study has been criticized because of its retrospective nature and we readily acknowledgethis shortcoming. However, the majority of initial reports of newly recognized diseases or new manifestations of a previously recognized illness have been retrospective. Without first describing a syndrome or a disease, it would be almost impos-
LETTERS TO THE EDITOR
recovery. How did the authors decide that patients with percutaneow nephrostomy recovered completely? We invite their comments about Double-J stent insertion following suture absorption. We replaced a Double-J stent in all patients in the belief that recovery will improve and, if insertion was not possible, we repaired the injury surgically. Even if we only performed percutaneous nephrostomy in cases with ureteral ligation our recovery rate (66.6%)was less than that of the authors (80%). Respectfully, M. Kamuran Bircan, Kenan Korkmaz and Hayrettin $ahin Department of Urology Dicle University School of Medicine 21280-Diyarbakir Turkey 1. Bircan, M. K., Ozttirk, O., Korkmaz, K. and $ahin, H.: Iatrojenik Ureter Ligasyonunda Tedavi Secenekleri. Urol. Biilteni, 3: 163. 1992.
RE: UROLOGICAL SYMPTOMATOLOGY IN PATIENTS WITH REFLEX SYMPATHETIC DYSTROPHY
M . B. Chancellor, P. J. Shenot, D . A . Rivas, S . Mandel and R. J. Schwartzman J. Urol., 155: 634-637, 1996 To the Editor. The authors attempted to determine the impact of reflux sympathetic dystrophy on lower urinary tract function. Their urodynamic study of 20 consecutive patients with neurologically verified reflex sympathetic dystrophy suggests a profound effect of this condition on detrusor and sphincteric function. Although the analogy with autonomic neuropathy from diabetes mellitus is tempting, this study raises some important issues related to the definition of reflex sympathetic dystrophy, study methodology and implications for the practicing urologist. At most pain management centers reflex sympathetic dystrophy is viewed as a rare disease that is difficult to diagnose and even more difficult to treat. Bonica originated the 3-step classification of reflex sympathetic dystrophy discussed by the authors.’ However, a major difficulty in diagnosing reflex sympathetic dystrophy is that its definition is qualitative and rather nonspecific. The International Association for the Study of Pain defmes reflex sympathetic dystrophy as “Continuous pain in a portion of an extremity after trauma which may include fracture but does not involve a major nerve, associated with sympathetic hyperactivity. The painful trauma, usually mild, is not associated with significant nerve injury. The pain is described as burning, continuously exacerbated by movement, continuous motion or stress.”2Therefore, nearly all acute chronic pain conditions can be interpreted to qualify in some respect to fit with this definition. The hallmark in the diagnosis of reflex sympathetic dystrophy has been relief of pain after a selective regional sympathetic block. Determination of efficacy of a sympathetic nerve block, as well as initial diagnosis of reflex sympathetic dystrophy should include a quantitative assessment of regional blood flow (laser Doppler study) and temperature of the affected and painful regions before and aRer the block. In this study there is no quantitative verification of reflex sympathetic dystrophy in any patient. There was no verification that the pain syndromes were not due to other causes, including localized nerve injury (electromyography or nerve conduction testing) or systemic diseases associated with secondary neuropathy. No quantitative small fiber neuropathy testing was done (quantitative thermal testing) to evaluate A-delta or C fiber pathology. Therefore, before considering any urodynamic changes associated with reflex sympathetic dystrophy, it is important to be certain that one has ruled out other causes of chronic pain and has established the diagnosis of reflex sympathetic dystrophy. In fact, one wonders how many patients with reflex sympathetic dystrophy and no urological symptoms have been seen at their regional center for the treatment of this disease. Without knowing the denominator in that study, it is extremely difficult to judge the importance of this report. Also, it would have been interesting methodologically to incorporate either an agematched or pain-matched control group to appreciate the relevance of the urodynamic findings reported.3 In their table depicting patient demographics, one also wonders if some medications used to treat pain in these patients with reflex sympathetic dystrophy might have altered bladder function. In par-
ticular, most pain management protocols rely heavily on tricyclic antidepressants and opiates, drugs known to decrease detrusor contractility substantially. In the 13 patients with detrusor hyperreflexia or detrusor-sphincter dyssynergia, we are concerned to see a significant incidence of prior orthopedic or back operations. Although the authors were careful not to incorporate patients after recent back surgery, one wonders what impact these prior operations might have had on the urodynamic findings. Finally, the absence of significant pelvic or suprapubic pain is surprising and does not substantiate the contention that reflex sympathetic dystrophy might be a possible etiology for interstitial cystitis.‘ If reflex sympathetic dystrophy is, indeed, a chronic pain syndrome characterized by continuous burning pain exacerbated by movement, how can it diffuse systemically to affect the bladder selectively? Also, if it were a chronic pain syndrome, one wonders what would be the implication of that diagnosis in the absence of a recognized and effective treatment for reflex sympathetic dystroPhY.5 ReSpedfUllY, Philippe E. Zimmern and Darrell Tanelian Department of Surgery Division of Urology Southwestern Medical Center 5323 Harry Hines Boulevard Dallas, Texas 75235-9110 1. Bonica, J.: Causalgia and other reflex sympathetic dystro hies. In: The Management of Pain. Philadelphia: Lea and Fekger, 1990. 2. International Association for the Study of Pain: Classification of chronic pain: description of chronic ain syndromes and definitions of pain terms. Prepared by tge Subcommittee on Taxonomy. Pain, 3:51, 1986. 3. Turner, J. A., Deyo, R. A., Loeser, J. D., Von Korf€, M. and Fordyce, W. E.: The importance of placebo effects in pain treatment and research. J.A.M.A., 271: 1609, 1994. 4. Atkins, R. M., Tindale, W., Bickerstaff, D. and Kanis, J . A.: Quantitative bone scintigraphy in reflex sympathetic dystrophy. Brit. J. Rheumatol., 3 2 41, 1993. 5. Tanelian, D. L.: Reflex sympathetic dystrophy: a re-evaluation of the literature. Pain Forum, submitted or publication.
Reply by Authors. We appreciate the enthusiastic and detailed comments regarding our recent investigation. Reflex sympathetic dystrophy is truly an enigmatic disease that is difficult and controversial with respect to diagnosis and treatment. Despite a thorough investigation, a consensus regarding any aspect of reflex sympathetic dystrophy among neurologists and anesthesiologists interested in pain management has proved to be elusive. All of our patients with reflex sympathetic dystrophy were diagnosed and referred for urological evaluation by 1 of us (R. J. S.) who is an internationally recognized authority on the disease. At most pain management centers reflex sympathetic dystrophy is seen commonly and is not considered a rare condition. The recent consensus statement in regard to reflex sympathetic dystrophy uses a revised taxonomic system for the disease.’ The process is initiated by trauma to C fibers in the soft tissue, or damage to a peripheral nerve or plexus. The symptoms are sensory abnormalities, including spontaneous burning pain, hyperalgesia, allodynia or hyperpathia; vascular and sweating abnormalities, including edema and trophic change in skin, subcutaneous tissue, joints and bone, and motor abnormalities, including dystonia, weakness and tremor.2 All of our patients had these symptoms and were extensively evaluated to rule out other causes of the symptoms. Our patients underwent myelography, followed by computerized tomography, electromyography and bone densitometry or plain films. Reflex sympathetic dystrophy is frequently not sympathetically maintained in its later stages. It is then sympathetically independent pain. Some patients were in the late stages of the illness and, consequently, were sympathetically independent. Therefore our evaluation of reflex sympathetic dystrophy conformsto common standards and the critique about our evaluation methodology is unfounded. In fact, the evaluation techniques presented by Zimmern and Tanelian deviate from those of most authorities on reflex sympathetic dystrophy. Our study has been criticized because of its retrospective nature and we readily acknowledgethis shortcoming. However, the majority of initial reports of newly recognized diseases or new manifestations of a previously recognized illness have been retrospective. Without first describing a syndrome or a disease, it would be almost impos-