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      Assessment of the Peripheral Microcirculation Using Computer-Assisted Venous Congestion Plethysmography in Post-Traumatic Complex Regional Pain Syndrome Type I

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          Abstract

          In complex regional pain syndrome type I (CRPS-I), edema of the affected limb is a common finding. Therefore, the changes in macro- and microcirculatory parameters were investigated to elucidate the underlying pathophysiology. Twenty-four patients with post-traumatic CRPS-I and 25 gender- and age-matched healthy subjects were examined by means of an advanced computer-assisted venous congestion strain-gauge plethysmograph. The recording of the volume response of the forearm to a stepwise inflation of an occlusion cuff placed at the upper arm enabled the calculation of the arterial blood flow into the arm (Q<sub>a</sub>), the vascular compliance (C), the peripheral venous pressure (P<sub>v</sub>), the isovolumetric venous pressure (P<sub>vi</sub>; = hydrostatic pressure needed to achieve net fluid filtration) and the capillary filtration capacity (CFC) – an index of microvascular permeability. The study revealed no difference in any of the parameters between the right and left hand of healthy subjects. In CRPS-I patients, however Q<sub>a</sub>, P<sub>v</sub>, P<sub>vi</sub> and CFC were significantly (p < 0.01/0.001) elevated in the affected arm (Q<sub>a</sub> 11.2 ± 7.0 ml min<sup>–1</sup> 100 ml<sup>–1</sup>, P<sub>v</sub> 20.2 ± 8.1 mm Hg, P<sub>vi</sub> 24.7 ± 4.2 mm Hg, CFC 0.0058 ± 0.0015 ml min<sup>–1</sup> 100 ml<sup>–1</sup> mm Hg<sup>–1</sup>) compared to the unaffected arm (Q<sub>a</sub> 4.2 ± 2.4 ml min<sup>–1</sup> 100 ml<sup>–1</sup>, P<sub>v</sub> 10.0 ± 5.1 mm Hg, P<sub>vi</sub> 13.2 ± 3.7 mm Hg, CFC 0.0038 ± 0.0005 ml min<sup>–1</sup> 100 ml<sup>–1</sup> mm Hg<sup>–1</sup>) and the values obtained in healthy controls (Q<sub>a</sub> 5.1 ± 1.3 ml min<sup>–1</sup> 100 ml<sup>–1</sup>, P<sub>v</sub> 10.4 ± 4.3 mm Hg, P<sub>vi</sub> 15.7 ± 3.3 mm Hg, CFC 0.0048 ± 0.0012 ml min<sup>–1</sup> 100 ml<sup>–1</sup> mm Hg<sup>–1</sup>). Whereas the values in the unaffected arm of CRPS-I patients revealed no difference in Q<sub>a</sub>, P<sub>v</sub> and P<sub>vi</sub> but a lower CFC (p < 0.01) compared to those from healthy controls. These results suggest profound changes in both macro- and microvascular perfusion in the affected arm of CRPS-I patients. The high CFC contributes to the edema formation, and combined with the elevated P<sub>vi</sub>, they are in agreement with the hypothesis of an inflammatory origin of CRPS.

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          Most cited references 3

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          Reflex sympathetic dystrophy of the hand: an excessive inflammatory response?

          In 23 patients with reflex sympathetic dystrophy (RSD) of the hand, scintigraphy with indium-111 labeled human non-specific polyclonal immunoglobulin G (In-111-IgG) was performed to investigate whether inflammatory characteristics are present in RSD. Both blood flow and accumulation over 48 h were assessed. Nineteen patients had increased flow to the affected hand, and 3 had decreased flow. One patient had bilateral RSD. Exercise provoked aggravation of complaints and signs in all patients. The affected/non-affected hand ratio (target-to-background, T/B) immediately before and after exercise did not change significantly. The T/B ratios 48 h after In-111-IgG injection were significantly higher in patients with RSD less than 5 months than in patients with RSD existing 5 months or longer. The T/B ratios 24 and 48 h after In-111-IgG injection were not correlated with the flow T/B ratios. In fact, 2 of the 3 patients with a decreased flow showed excess accumulation on the late images. Significantly more patients with early RSD, existing less than 5 months, had a positive In-111-IgG scintigraphy (14 of 17) than the patients with late RSD (1 of 6). Increased vascular permeability for macromolecules, an important characteristic of inflammation, appears to play a role in the development of RSD. This phenomenon is not flow-dependent.
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            Peripheral sympathetic function as a predictor of complex regional pain syndrome type I (CRPS I) in patients with radial fracture.

            Complex regional pain syndrome type I (CRPS I) is a frequent complication after injuries of the upper limbs. The pathophysiology of this disease remains unclear, although disturbances of the sympathetic nervous system have been detected in several clinical studies, and sympathetic blocks resolve the symptoms in many of the cases. To investigate the meaning of sympathetic dysfunction at the beginning of the disease, 27 patients with distal radial fracture were examined prospectively during the course of the disease with regard to their clinical symptoms and their peripheral sympathetic nervous function. Sympathetic nervous function was examined by testing the vasoconstrictor response to sympathetic stimuli--recorded with laser Doppler fluxmetry--of the fingertips of both hands. Four patients developed CRPS I during the 12-week observation time and two patients presented an incomplete clinical CRPS I picture ('borderline patients'). The complaints of all patients (normal fracture patients, CRPS I patients, borderline patients) were similar during the first week after trauma with focus on pain, motoric disturbances and autonomic symptoms. After 1 or 2 weeks, a larger clinical difference developed between normal fracture patients and CRPS I or 'borderline patients'. In CRPS I patients and 'borderline patients', the sympathetic vasoconstrictor response was diminished or absent from the first posttraumatic day throughout the observation time, whereas the normal fracture patients revealed slightly impaired sympathetic nervous function on the first posttraumatic day and normal results during the rest of the observation time. With regard to the unaffected contralateral hand, CRPS I patients also showed impaired sympathetic nervous function. The results of the present study suggest that the disturbances in the sympathetic nervous system in CRPS I patients are systemic and not limited to the affected limb. Their occurrence before the clinical breakout of the disease may serve as a marker that might be useful for early therapy and lead to further understanding of the pathophysiology of CRPS I.
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              Reflex sympathetic dystrophy: model of a severe regional inflammatory response syndrome.

               R Goris (1998)
              The systemic inflammatory response syndrome (SIRS) and acute reflex sympathetic dystrophy syndrome (RSD) share clinical signs of severe inflammation, a protracted course, and a similar problem of impaired oxygen utilization. The difference is that SIRS patients have these signs and symptoms systemically and are severely ill in the intensive care unit (ICU), whereas acute RSD patients are in good health and their problems are limited to one extremity. Both conditions seem to be the result of an exaggerated inflammatory response. As RSD patients have a healthy contralateral extremity, they may be their own control in various flux studies. It is hypothesized that this situation is exquisitely suitable for studying the pathophysiology of severe inflammatory responses in humans. Only a few patients are required to perform studies of, for example, oxygen metabolism and cytokine or oxygen radical production. Assessment methods may be utilized, such as nuclear magnetic resonance spectroscopy, which cannot easily be performed in ICU patients.
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                Author and article information

                Journal
                JVR
                J Vasc Res
                10.1159/issn.1018-1172
                Journal of Vascular Research
                S. Karger AG
                1018-1172
                1423-0135
                2001
                October 2001
                17 September 2001
                : 38
                : 5
                : 453-461
                Affiliations
                Departments of aSurgery, and bAnesthesiology, Ludwig Maximilians University of Munich, Germany
                Article
                51078 J Vasc Res 2001;38:453–461
                10.1159/000051078
                11561147
                © 2001 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 2, References: 46, Pages: 9
                Categories
                Research Paper

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