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by the American Institute of Ultrasound in Medicine J Ultrasound Med 22:395-402 • 0278-4297
Doppler Sonographic Assessment of Posttraumatic Reflex Sympathetic DystrophyDepartments of Radiology (G.P.), Physical Medicine and Rehabilitation (Y.P.), and Nuclear Medicine (A.S.), Trakya University School of Medicine, Edirne, Turkey. Address correspondence and reprint requests to Gökhan Pekindil, MD, Celal Bayar Universitesi, Tip Fakültesi Radyoloji Anabilim Dali, Manisa, Turkey.
Objective. To reveal the arterial Doppler sonographic findings in cases of posttraumatic reflex sympathetic dystrophy. Methods. Eleven patients had hand reflex sympathetic dystrophy, and 9 had foot reflex sympathetic dystrophy. The duration of symptoms ranged from 1 to 28 weeks, and the history of fracture ranged from 6 to 48 weeks. Bilateral brachial or popliteal arteries proximal to injuries were evaluated by Doppler sonography with a 7.5-MHz linear transducer. All patients also had triphasic bone scintigraphy and extremity thermography. Results. Two patients had monophasic waveforms and 4 had low-pulsatility triphasic waveforms on the affected limbs when compared with the asymptomatic limbs. All opposite asymptomatic limbs had normal triphasic waveforms in these 6 cases. Spectral analysis revealed a loss or decrease of a normal reversed flow component with a reduced pulsatility index on the affected limb. Fourteen other patients had symmetric triphasic waveforms. We observed that the patients who had stage 1 reflex sympathetic dystrophy and warm limbs with durations of symptoms of more than 2 weeks had positive Doppler sonographic findings, whereas all patients with stage 2 reflex sympathetic dystrophy and all with normal skin temperature, regardless of stage, had normal waveforms. Conclusions. Doppler sonography revealed loss of normal triphasic arterial waveforms in some of the cases of stage 1 disease, whereas many cases of stage 1 disease and all cases of stage 2 disease had normal findings. Therefore, we think that Doppler sonography cannot be used for the diagnosis of reflex sympathetic dystrophy but may help in assessing hemodynamic stages of the disease.
Key Words: Doppler sonography • reflex sympathetic dystrophy • vascular sonography Abbreviations: PI, pulsatility index • RI, resistive index • RSD, reflex sympathetic dystrophy • TPBS, triphasic bone scintigraphy
Reflex sympathetic dystrophy (RSD) is a complication occurring after even minor injury or surgery to a limb. Recently it was named "complex regional pain syndrome 1."1 It consists of a painful, tender extremity associated with hyperesthesia, soft tissue swelling, dystrophic changes of the skin, vasomotor instability, stiffness of joints, and patchy osteoporosis in the affected part.2 Reflex sympathetic dystrophy is classically subdivided into 3 phases: a warm acute phase (stage 1) lasting 2 to 3 months, a phase of vasomotor instability (stage 2) lasting several months, and a cold end phase (atrophic). Although its pathogenesis is not yet clearly understood, a sympathetic nervous cause and an exaggerated regional inflammatory response to an injury have been suggested.3,4 The diagnosis of RSD has primarily been made on the basis of clinical, radiographic, and scintigraphic evaluation, with the standard of reference being relief of symptoms after invasive testing by methods such as differential neural blockades. It has been reported that many vascular abnormalities, such as transient vascular hyperpermeability, capillary and venous dilatation, arteriolar media and intima thickening, vasospasm, or both, and changes in blood flow, may be encountered in cases of RSD.4–8 These signs and symptoms occur in the area distal to the primary injury; therefore, we hypothesized that Doppler sonographic evaluation of the arteries of the affected limb proximal to the injury may give information about the local hemodynamic and vascular changes in patients with RSD.7 Although 2 previous case reports have supported this hypothesis, to our knowledge, spectral analysis of Doppler sonographic findings of RSD has not been reported previously in a prospective study.4,9 The aim of this study was to reveal the Doppler sonographic findings in patients with RSD.
This prospective study included 20 consecutive cases of postfracture RSD of the hand (11 cases) and foot (9 cases). An experienced physical medicine and rehabilitation specialist had determined the diagnosis of RSD according to the criteria established by the International Association for the Study of Pain.1 There were 12 men and 8 women (mean age, 41.7 years; range, 19–68 years). The time from the onset of symptoms to imaging ranged from 1 to 28 weeks (mean, 6.7 weeks). The patients were examined 6 to 48 weeks (mean, 15.7 weeks) after the fractures occurred. Staging was performed on the basis of the patients’ histories and clinical and radiologic findings. Sixteen patients had stage 1 RSD, and 4 had stage 2 disease. The skin temperature of the affected extremity was evaluated with thermography and defined as warm or cold if there was a difference greater than 0.4°C when compared with the opposite unaffected side. Bilateral upper or lower extremity arteries were evaluated with color Doppler sonography (Au-4 Idea; Esaote SpA, Genoa, Italy). In cases of unilateral upper extremity RSD caused by fractures distal to the elbow (on the wrist or hand), the brachial artery was sampled bilaterally at a location 3 to 7 mm above the antecubital crease in the brachial fossa with the patients in the supine position. In cases of unilateral lower extremity RSD caused by fractures distal to the knee (on the ankle or foot), the popliteal artery was bilaterally sampled in the popliteal fossa behind the knee with the patients in the prone position. A 7.5-MHz linear transducer was used with a range gate (1–2 mm) smaller than the vessel lumen. A wall filter of 50 to 100 Hz was used. The Doppler angle was within the range of 30° to 60°. Color Doppler sonography was not necessary, but it decreased the examination time, which averaged approximately 5 to 10 minutes. Scans were performed after a 10-minute rest in a temperature-controlled room. None of the patients had apparent signs of peripheral vascular disease or diabetes. The pulsatility index (PI) was determined by the software of the sonography unit. The PI values and waveforms of the brachial or popliteal arteries of both the diseased and opposite unaffected limbs were analyzed. The resistive index (RI) was measured in patients who had monophasic waveforms on the affected limbs. Six patients who had initially positive Doppler findings were also reevaluated with Doppler sonography after their symptoms improved. The follow-up period ranged between 6 and 12 months. All patients had bilateral triphasic bone scintigraphy (TPBS) performed within the same week of Doppler sonographic examination. All scintigraphic studies were performed with a large field-of-view gamma camera (Diagnost Tomo; Philips Medical Systems, Eindhoven, the Netherlands) equipped with a low-energy, parallel-hole, high-resolution collimator and a 20% energy window centered at 140 keV. After the injection of 15 mCi of technetium Tc 99m methylene diphosphonate, images of the affected and contralateral extremities were obtained in rapid sequences at 3 seconds per frame for 2 min. Thereafter, blood pool scintigraphy was performed with 300 kilocounts. A delayed static image for 5 min or 300 kilocounts was obtained 4 h later. Asymmetry in each phase of TPBS was graded as mild, moderate, or intense.
Clinical characteristics of the patients and the results of the scintigraphic and Doppler sonographic studies are presented in Table 1  .
Arterial Doppler sonography showed monophasic waveforms in 2 cases and low-pulsatility triphasic waveforms in 4 cases on the diseased side, whereas all had normal triphasic waveforms on the contralateral asymptomatic extremities (Figs. 1 and 2). Spectral analysis of these waveforms revealed a loss or decrease of the normal reversed flow component and increased peak systolic and, especially, enddiastolic velocities with spectral broadening and thus reduced PI values (2.4–3.9) in all 6 cases. The PI values of the opposite limbs were between 3.7 and 4.9 (mean, 3.93; Table 2). These decreases in PI ranged from 15% to 35% (mean, 24%) when compared with the opposite unaffected limbs. The increases in peak systolic and end-diastolic velocities ranged between 5% and 79% (mean, 23.7%) and 60% and 300% (mean, 122.5%), respectively, when compared with the opposite unaffected limbs. The RI values of 2 cases with monophasic waveforms were 0.77 and 0.89 in the affected limbs. The other 14 patients had normal symmetric triphasic waveforms in both diseased and unaffected contralateral extremity arteries, and the PI values ranged between 3 and 5.
When Doppler sonographic findings were compared with clinical stages and skin temperatures, we observed that the patients with positive Doppler sonographic findings had stage 1 RSD and warm extremities with durations of symptoms of 3 or more weeks. However, 10 other patients with stage 1 RSD, 3 of whom (patients 7, 8, and 18) having warm extremities with durations of symptoms of less than 3 weeks, had normal triphasic waveforms. All patients with stage 2 RSD and all with normal skin temperature, regardless of stage, also had normal waveforms. There was a correlation between the positive Doppler sonographic findings and moderately or intensely increased uptake at all phases of bone scans in 5 of 6 patients. However, there was discordance between waveform and uptake pattern at scintigraphy in a patient who had stage 1 disease with a warm extremity and low-resistance flow on Doppler sonography (patient 2). In this case, the bone scan showed only mildly increased uptake in the third phase. Otherwise, in another patient who had moderately increased uptakes at all phases of TPBS and a warm extremity (patient 18), Doppler sonography showed normal triphasic waveforms in both extremities. However, the durations of symptoms were 2 and 3 weeks in these 2 cases. In 13 other patients who had normal symmetric triphasic waveforms, bone scans showed no asymmetry or only mildly increased uptake in all 3 phases. In the follow-up period, Doppler sonography showed normal symmetric triphasic waveforms in all 6 patients who initially had asymmetric waveforms.
The extremity arteries have a high-resistance vascular bed at rest and therefore show sharp triphasic waveforms with initial rapid antegrade flow in systole, followed by retrograde (reversed) flow in early diastole and return of antegrade flow in late diastole. Because patients with RSD may have healthy contralateral extremities, as in this study, they may be their own controls in various flux studies, although both extremities can be affected. It is well known that the changes in vascular resistance of the receiving bed based on the pulsatility of the vessel and peripheral resistance may be reflected by the changes in PI and RI, respectively. In this study, we found decreases in PI and transformation of normal triphasic waveforms to monophasic or low-pulsatility triphasic waveforms in the affected limbs of the patients with stage 1 RSD and warm limbs for more than 2 weeks. These findings indicate decreased vascular resistance and increased blood flow to the affected limb. Mailis et al9 reported an increase in diastolic limb flow assessed by Doppler sonography in 2 patients with foot RSD. Goris4 assessed venous oxygen saturation and femoral artery flow with Doppler sonography in 8 patients with acute RSD and found tissue hypoxia despite increased arterial flow but did not give any information about the Doppler spectral analysis of the waveform. Nazarian et al10 assessed patients with RSD by power Doppler sonography and showed increased flow in the affected lower limbs. Conversely, al-Nahhas et al11 performed technetium Tc 99m methylene diphosphonate– labeled bone scintigraphy and Doppler sonography in patients with limb pain due to various causes (strain injury, RSD, and nonspecific pain) and showed increased arm blood flow on scintigraphy and Doppler sonography in cases of repetitive strain injury. However, they suggested that Doppler sonography failed to differentiate between different causes of pain.11 Other studies using several different methods, such as oscillography, plethysmography, skin temperature measurements, skin laser Doppler flowmetry, technetium Tc 99m human serum albumin–labeled dynamic vascular scintigraphy, technetium Tc 99m sestamibi–labeled muscle perfusion scintigraphy, and TPBS, have also shown increased blood flow in affected limbs in many cases of RSD, although there have been many discordant results.5,12–22 In this study, we also found that many patients with stage 1 disease had normal Doppler sonographic findings when they had no skin temperature differences or had warm extremities with durations of symptoms of less than 3 weeks. Quite variable blood flow appearances such as reduced or normal symmetric blood flow in the angiographic and blood pool phases of TPBS have been reported.18–22 In a previous study, we also reported that many patients with stage 1 RSD may have increased or normal muscle perfusion as shown on technetium Tc 99m sestamibi–labeled scintigraphy.17 Doppler sonographic findings were within normal limits in all patients with stage 2 disease in this study. We also previously reported normal muscle perfusion as assessed by technetium Tc 99m sestamibi–labeled scintigraphy in patients with stage 2 RSD.17 Many TPBS studies have also reported normal or decreased blood flow in stage 2 RSD18–22; however, Blockx and Driessens5 reported that both blood flow and volume decreased in stage 2 disease using technetium Tc 99m human serum albumin–labeled dynamic vascular scintigraphy. Consequently, the results of many different studies in the literature have shown that variations in blood flow may be encountered in affected limbs of patients with RSD and may be related to the disease stage. It must be emphasized that these different studies all depict flow in different ways. Recently it has been suggested that RSD is caused by an injury to a specific nerve or the C and A delta fibers that innervate the involved tissue.23 It is thought that the abnormal autonomic nerve flow may produce vasodilatation or vasoconstriction periods, or both, in the affected limb.24 From all these observations, it is also clear that not a single mechanism but, rather, a complex series of mechanisms is responsible for the hemodynamic changes seen in RSD.5 Moreover, the absence of population stratification according to disease stage makes interpretation of these results difficult.25 Pollock et al6 suggested that the temporal pathologic changes in the autonomic and vasomotor control mechanism might be associated with RSD. This suggestion supports the unexplored hypothesis that the underlying pathologic processes in RSD are dynamic, and that the stage is related to variable structural alterations over time.6 Abnormal fluctuations in sympathetic vascular control mechanisms may occur in these cases, and these would explain the several patterns of vascular response observed in many studies and would resolve discrepancies between studies that reported varying hemodynamic changes in patients with RSD.6 Conversely, accurate hemodynamic staging may be important for the choice of the right vasoactive treatment, for example, calcitonin (vasoconstrictive) versus guanethidine (vasodilative), in RSD.5 Our results also show that Doppler sonography may be used to monitor the hemodynamic changes during the follow-up period, because positive Doppler sonographic findings disappeared in all 6 of our patients who were treated, and symptoms were resolved. Tu et al26 used Doppler sonography to assess the effect of surgical sympathectomy on arterial blood flow in 8 patients with RSD. They found low PI values and biphasic waveforms in patients with warm, dry limbs, whereas high PI values and triphasic waveforms were found in those with cold, clammy limbs, which indicated failed sympathectomy.26 Finally, our results show that hemodynamic changes of the affected limb can be reflected by Doppler sonography in the first warm stage of RSD, especially after 2 weeks. We suggest that Doppler sonography cannot be used for the diagnosis of RSD but may help in staging of cases; moreover, as a noninvasive, easily performed, reproducible method, it can be used to assess different hemodynamic patterns of RSD. Thus it may help in choosing and monitoring treatment. However, we also think that a single method such as Doppler sonography may not completely reveal all blood flow changes seen during several stages of RSD, so a combination of testing techniques that reflects all the rapid fluctuations of blood flow may be required.6
Received November 5, 2002, from the Departments of Radiology (G.P.), Physical Medicine and Rehabilitation (Y.P.), and Nuclear Medicine (A.S.), Trakya University School of Medicine, Edirne, Turkey. Revision requested December 16, 2002. Revised manuscript accepted for publication January 2, 2003.
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Abstract
Introduction
