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The spreading of focal brain edema induced by ultraviolet irradiation.

Focal brain edema limited to one cerebral hemisphere was produced by ultraviolet irradiation of the exposed cortex. Tissue water content was determined by the gravimetric method which allows microsampling. Therefore, the spread of edema around the small necrotic area could be mapped more precisely than by determination of dry weight which calls for larger samples. As early as 30 min following irradiation, hyperemia and swelling of the brain are observed under the operating microscope. This correlates with venous stasis, hyperemia, and broadened perivascular spaces around venules and large capillaries accompanied by a marked rise in the specific weight of the tissue. After 4 h an edema front can be observed spreading from the perinecrotic zone in which there is a marked rise in endothelial cell vesicular activity. Edema reaches maximum levels in the deep white matter at 48 h post irradiation with normalisation of the tissue water content after 96 h. The velocity at which the edema front spreads from the cortex to the periventricular area lies in the range of 0.25 mm/hr. Edema reabsorption coincides with signs of retrograde micropinocytosis in endothelial cells.

Animals↗

Sulfidopeptide-leukotriene peptidases in pulmonary edema fluid from patients with the adult respiratory distress syndrome.

The human pulmonary edema fluid concentrations of LTC4 and of LTD4 and LTE4, derived peptidolytically from LTC4, were assessed by radioimmunoassays of the mediators resolved by reverse-phase high-performance liquid chromatography. The mean pulmonary edema fluid concentration (+/- SD) of LTD4 of 19.2 +/- 25.6 nM for 12 patients with the adult respiratory distress syndrome and of LTE4 of 192 +/- 309 nM for 10 of the patients were significantly higher (P less than 0.005 and P less than 0.05) than those of 2.2 +/- 2.4 and 11.0 +/- 18.2 nM, respectively, for 10 patients with cardiogenic pulmonary edema, whereas the lower mean concentrations of LTC4 were not significantly different for the two groups. Pulmonary edema fluid from five patients with adult respiratory distress syndrome, one with cardiogenic pulmonary edema, and one with an indeterminate syndrome contained similar concentrations of peptidoleukotriene peptidases. The LTC4 and LTD4 peptidolytic activities in ARDS fluids were 81 and 142 kD, respectively, by gel filtration. The extents of peptidolysis of [3]LTC4 and [3]LTD4 by 100 microliter of pulmonary edema fluid attained respective mean maximum levels of 74.5 +/- 2.9% (N = 5) and 37.7 +/- 10.2% (N = 4) after 30 min at 37 degrees C and were inhibited by serine-borate and by cysteine, respectively. The predominance of LTD4 and LTE4 over LTC4 in states of altered pulmonary vascular pressure and permeability thus is attributable to two distinct peptidases.

Adolescent↗

Relationship of perfusion to edema in the 9L gliosarcoma.

The relationship between tumor perfusion and edema was analyzed, with edema characterized as tumor wet/dry weight ratio. Perfusion of subcutaneous 9L gliosarcoma was measured by injection of 133Xe in saline into the tumor core, followed by gamma camera imaging of 133Xe washout kinetics. A significant inverse correlation was found between edema and tumor perfusion (p < 0.0002), suggesting that edema can limit tumor perfusion, perhaps through a mechanism of increased interstitial fluid pressure. The perfusion rate of highly edematous tumors was reduced to less than 10% of the perfusion rate of less edematous tumors (p < 0.001). It was also found that tumor edema increased significantly with increasing tumor volume (p < 0.001), which could account for the finding that perfusion declined significantly with increasing tumor volume (p < 0.02). These findings are potentially important because it is possible to quantify tumor edema in vivo, with millimeter resolution, using 1H magnetic resonance imaging (MRI). Thus MRI may provide a non-invasive technique for characterizing tumor perfusion or tumor drug delivery.

Animals↗

[Unexplained edema in females--diuretic-induced or idiopathic?].

Both women with diuretic induced edema and with idiopathic edema present a typical history leading to the diagnosis in most cases. These women are almost exclusively in the reproductive age and they tend to have some other characteristics in common additionally. There is controversy whether idiopathic edema exists as a syndrome with multifactorial pathogenesis or if fluid retention in these women is due to diuretic abuse. In either case the use of diuretics is not indicated as they can increase and perpetuate the edema and moreover may bring about impairment of renal function. Abstinence of diuretic intake is the only way out of the vicious circle of fluid retention induced by intermittent diuretic intake resulting in intermittent edema and prostrained use of diuretics. Therapy of idiopathic edema is difficult; it includes physical therapy, psychotherapy and pharmacotherapy with aldosterone antagonists or ACE-inhibitors in some severe cases.

Diuretics↗

Nitric oxide modulates pancreatic edema formation in rat caerulein-induced pancreatitis.

This study was designed to investigate the role of nitric oxide (NO) in the formation of pancreatic edema in caerulein-induced pancreatitis in rats. Pancreatitis was produced by two intraperitoneal injections of caerulein, and plasma amylase concentration, pancreatic edema index (pancreatic wet weight/body weight), and Evans blue extravasation (as a measure of vascular permeability) were evaluated 5 h after the first injection. Four doses (1, 2.5, 5, and 10 mg/kg) of NG-nitro-L-arginine (L-NNA), an NO synthase inhibitor, were subcutaneously administered at -0.5, 0.5, 1.5, 2.5, and 3.5 h after the first injection of caerulein. L-NNA significantly lowered the edema index, the wet/dry weight ratio of the pancreas, and Evans blue extravasation in the rats with pancreatitis. The maximal effect was obtained by L-NNA at a dose of 2.5 mg/kg; this inhibited the increase in pancreatic edema formation from the control value by 60%-70%. Intraperitoneal injections (20 mg/kg, five times) of L-arginine, a substrate for NO production, partly reversed the L-NNA-induced inhibition of pancreatic edema formation, but D-arginine, an enantiomer of L-arginine, did not show any effect. Plasma amylase concentrations were not significantly affected by any dose of L-NNA, nor were they affected by L- or D-arginine. These findings strongly suggest that endogenous NO plays an important role in the formation of pancreatic edema in caerulein-induced pancreatitis in rats, probably by increasing vascular permeability and protein extravasation.

Acute Disease↗

Peripheral edema after esophagectomy.

Patients who have undergone major surgery such as esophagectomy may develop peripheral edema in the immediate postoperative period, the cause of which is not fully understood. The purpose of this study was therefore to determine the mechanism of this phenomenon. Finger edema was measured as a marker for peripheral edema before and after esophagectomy in eight patients. Plasma interleukin-6 (IL-6) was also measured by an enzyme-linked immunosorbent assay. Finger edema markedly increased in the immediate postoperative period and remained significantly elevated until after postoperative day (POD) 3 compared to the preoperative value (P < 0.05). Plasma IL-6 also markedly increased in the immediate postoperative period and remained significantly elevated on POD 2 compared to the preoperative value (P < 0.05). The degree of finger edema highly correlated with the level of plasma IL-6 (r = 0.71, P = 0.0001). These findings indicate that peripheral edema after esophagectomy might be caused by a proinflammatory cytokine response.

Body Weight↗

The cuff leak test to predict failure of tracheal extubation for laryngeal edema.

OBJECTIVE: Laryngeal edema secondary to endotracheal intubation may require early re-intubation. Prior to extubation the absence of leak around an endotracheal tube may predict laryngeal edema after extubation. We evaluated the usefulness of a quantitative assessment of such a leak to identify the patients who will require early re-intubation for laryngeal edema. METHODS: This prospective study included 76 patients with endotracheal intubation for more than 12 h. The leak, in percent, was defined as the difference between expired tidal volume measured just before extubation, in volume-controlled mode, with the cuff inflated and then deflated. The best cut-off value to predict the need for re-intubation for significant laryngeal edema was determined and the patients were divided into two groups, according to this cut-off value. RESULTS: Eight of the 76 patients (11%) needed re-intubation for laryngeal edema. Patients requiring re-intubation had a smaller leak than the other patients [9 (3-18) vs 35 (13-53)%, p<0.01]. The best cut-off value for gas leak was 15.5%. The high leak group included 51 patients, of whom only two patients (3%) required re-intubation. The low leak group included 25 patients, among whom six patients (24%) required re-intubation ( p<0.01). The sensitivity of this test was 75%, the specificity 72.1%, the positive predictive value 25%, the negative predictive value 96.1% and the percent of correct classification 72.4%. CONCLUSIONS: A gas leak around the endotracheal tube greater than 15.5% can be used as a screening test to limit the risk of re-intubation for laryngeal edema.

Aged↗

Assessing pulmonary permeability by transpulmonary thermodilution allows differentiation of hydrostatic pulmonary edema from ALI/ARDS.

OBJECTIVE: To test whether assessing pulmonary permeability by transpulmonary thermodilution enables to differentiate increased permeability pulmonary edema (ALI/ARDS) from hydrostatic pulmonary edema. DESIGN: Retrospective review of cases. SETTING: A 24-bed medical intensive care unit of a university hospital. PATIENTS: Forty-eight critically ill patients ventilated for acute respiratory failure with bilateral infiltrates on chest radiograph, a PaO(2)/FiO(2) ratio < 300 mmHg and extravascular lung water indexed for body weight >/= 12 ml/kg. INTERVENTION: We assessed pulmonary permeability by two indexes obtained from transpulmonary thermodilution: extravascular lung water/pulmonary blood volume (PVPI) and the ratio of extravascular lung water index over global end-diastolic volume index. The cause of pulmonary edema was determined a posteriori by three experts, taking into account medical history, clinical features, echocardiographic left ventricular function, chest radiography findings, B-type natriuretic peptide serum concentration and the time-course of these findings with therapy. Experts were blind for pulmonary permeability indexes and for global end-diastolic volume. MEASUREMENTS AND RESULTS: ALI/ARDS was diagnosed in 36 cases. The PVPI was 4.7+/-1.8 and 2.1+/-0.5 in patients with ALI/ARDS and hydrostatic pulmonary edema, respectively (p<0.05). The extravascular lung water index/global end-diastolic volume index ratio was 3.0 x 10(-2)+/-1.2 x 10(-2) and 1.4 x 10(-2)+/-0.4 x 10(-2) in patients with ALI/ARDS and with hydrostatic pulmonary edema, respectively (p<0.05). A PVPI >/= 3 and an extravascular lung water index/global end-diastolic index ratio >/= 1.8 x 10(-2) allowed the diagnosis of ALI/ARDS with a sensitivity of 85% and specificity of 100%. CONCLUSION: These results suggest that indexes of pulmonary permeability provided by transpulmonary thermodilution may be useful for determining the mechanism of pulmonary edema in the critically ill.

Capillary Permeability↗

A lung ultrasound sign allowing bedside distinction between pulmonary edema and COPD: the comet-tail artifact.

OBJECTIVE: Acute cardiogenic pulmonary edema and exacerbation of chronic obstructive pulmonary disease (COPD) can have a similar clinical presentation, and X-ray examination does not always solve the problem of differential diagnosis. The potential of lung ultrasound to distinguish these two disorders was assessed. DESIGN: Prospective clinical study. SETTING: The medical ICU of a university-affiliated teaching hospital. PATIENTS: We investigated 66 consecutive dyspneic patients: 40 with pulmonary edema and 26 with COPD. In addition, 80 patients without clinical and radiologic respiratory disorders were studied. MEASUREMENTS: The sign studied was the comet-tail artifact arising from the lung wall interface, multiple and bilaterally disseminated to the anterolateral chest wall. RESULTS: The feasibility was 100%. The length of the examination was always under 1 min. The described pattern was present in all 40 patients with pulmonary edema. It was absent in 24 of 26 cases of COPD as well as in 79 of 80 patients without respiratory disorders. The sign studied had a sensitivity of 100% and a specificity of 92% in the diagnosis of pulmonary edema when compared with COPD. CONCLUSIONS: With a described pattern present in 100% of the cases of pulmonary edema and absent in 92% of the cases of COPD and in 98.75% of the normal lungs, ultrasound detection of the comet-tail artifact arising from the lung-wall interface may help distinguish pulmonary edema from COPD.

Adolescent↗

Correlation between the degree of contrast enhancement and the volume of peritumoral edema in meningiomas and malignant gliomas.

Peritumoral edema and contrast enhancement of brain tumors are both thought to be due to breakdown of the blood-brain barrier (BBB); however, the exact mechanism by which these two phenomena occur and whether there is a quantitative or etiological relationship is not known. Our purpose was to determine whether the relationship between the breakdown of the BBB, defined radiologically as the degree of contrast enhancement, and the volume of surrounding edema is different for high-grade gliomas and meningiomas. We analyzed 13 meningiomas and 23 gliomas. A direct linear relationship between the degree of contrast enhancement (dC) and volume of peritumoral edema (V) with a high correlation coefficient (R = 0.66, P = 0.0006) was established for gliomas. A mathematical relationship between dC and V could not be established for meningioma. The findings for gliomas offer indirect radiological evidence that the defect in the BBB which causes edema is quantitatively and etiologically related to the defect in the BBB responsible for contrast enhancement. For meningiomas, the lack of a relationship between dC and V implies either that the mechanisms responsible for formation of edema and contrast enhancement are fundamentally different or that a physical barrier in certain meningiomas limits propagation of edema into the adjacent white matter.

Adolescent↗

Bone marrow edema syndrome of the foot: one year follow-up with MR imaging.

OBJECTIVE: To describe the MR findings of bone marrow edema syndrome (BMES) of the foot and its evolution at 1 year follow-up. DESIGN AND PATIENTS: Twenty-five of 32 patients with disabling foot and ankle pain unrelated to trauma diagnosed as BMES when MR imaging demonstrated a bone marrow edema pattern in one or more bones without any radiological or underlying clinical cause, were re-evaluated by MR imaging 1 year later. RESULTS: On the initial MR examinations an average of 4.7 individual bones were involved by bone marrow edema. Soft tissue edema was present in every patient and joint effusion in 10 patients. MR imaging at 1 year showed resolution of bone edema in 18 patients (72%), partial improvement in five (20%) and no improvement in two (8%). Six patients (24%) developed similar symptoms in the other foot during follow-up. Ten of 17 available plain radiographs showed some loss of radiodensity. Further bone marrow edema developed in bones of the same foot that were initially normal, or in uninvolved distant bone marrow areas in the same affected bone, in six of seven patients on follow-up MR imaging. CONCLUSIONS: The evolution of the MR findings of BMES of the foot is to complete resolution or partial improvement at 1 year in the majority of cases. Migration to the other foot occurs in up to a quarter of patients.

Bone Marrow Diseases↗

Shifting bone marrow edema of the knee.

OBJECTIVE: The purpose of our study is to describe shifting bone marrow edema in the knee as the MR imaging feature of intra-articular regional migratory osteoporosis of the knee. PATIENTS AND METHODS: Five men, aged 45-73 years, were referred by orthopedic surgeons for MR imaging evaluation of knee pain, which had been present for 2 weeks to 6 months. One patient had a prior history of blunt trauma. None had risk factors for osteonecrosis. Four patients had two MR examinations and the patient with prior blunt trauma had four. Plain radiographs were obtained in all patients. RESULTS: In all cases, a large area of marrow edema initially involved a femoral condyle, with migration of the bone marrow edema to the other femoral condyle, tibia, and/or patella occurring over a 2- to 4-month period. Adjacent soft tissue edema was present in all five patients, while none had a joint effusion. Radiographs of two patients showed generalized osteopenia. CONCLUSION: In the absence of acute trauma or clinical suspicion of infection, a large area of bone marrow edema without a zone of demarcation may represent intra-articular regional migratory osteoporosis. Demonstration of shifting bone marrow edema on follow-up examinations suggests this diagnosis.

Aged↗

[Incidence and extent of postoperative macular edema following vitreoretinal surgery with and without combined cataract operation].

PURPOSE: In the majority of patients with full-thickness macular hole, closure can be achieved with vitreoretinal surgery techniques. However, postoperative function is variable and the prognostic determinants for visual acuity are incompletely understood. We evaluated the incidence and extent of macular edema after macular foramen surgery with and without combined cataract-surgery. METHODS: Between October 1997 and March 2001 macular foramen surgery was performed in 125 eyes from 116 patients. Fluorescein angiograms with sufficient quality were obtained from 59 eyes using a confocal scanning laser ophthalmoscope (Heidelberg Retina Angiograph, HRA, Heidelberg Engineering, Heidelberg) and were evaluated by two independent observers. RESULTS: Angiographic macular edema was noted on average 4.2 months after the operation in 47 out of 59 (79.7%) eyes. The incidence of macular edema was 87% in eyes after a combined cataract operation compared to 66.7 % in eyes with no simultaneous operation ( p=0.735). Mean postoperative visual acuity was 0.4 (min 0.1-max 1.2) with no significant difference between eyes with (4.1 lines) and without macular edema (3.5 lines) with regard to visual improvement from baseline. CONCLUSIONS: The results indicate a high incidence of macular edema in eyes after macular hole surgery with subsequent anatomical success. Apparently, the presence of macular edema is not associated with short term visual impairment. Furthermore it seems that a combined cataract operation compared to a consecutive procedure is not associated with disadvantages regarding the functional outcome.

Aged↗

[Diagnosis and follow-up of non-diabetic macular edema with optical coherence tomography (OCT)].

INTRODUCTION: Objective and quantitative follow-up of macular edema with present clinical methods is limited. We studied to what extent optical coherence tomography (OCT) may be clinically useful in diagnosis and follow-up of non-diabetic macular edema. PATIENTS AND METHODS: We evaluated 106 eyes with non-diabetic macular edema retrospectively considering diagnosis, foveal retinal thickness in OCT, fluorescein angiographic findings and visual acuity. RESULTS: In 60 of 61 eyes (98%) the diagnosis of macular edema was confirmed by fluorescein angiography. There was only a minor correlation between visual acuity and foveal retinal thickness (r=0.32, p=0.001). Follow-up of 24 eyes showed a statistically significant decrease of foveal retinal thickness under therapy from 420+/-165 microm to 354+/-165 microm (p=0,035) as well as a small improvement in visual acuity from 0.30 to 0.38 (p=0.025). CONCLUSION: OCT can diagnose macular edema non-invasively and thus may replace fluorescein angiography as an invasive method. The reduction of macular edema in the course of therapeutic measures can be documented objectively with OCT.

Diabetic Retinopathy↗

Visual outcome of patients with macular edema after pars plana vitrectomy and indocyanine green-assisted peeling of the internal limiting membrane.

PURPOSE: To evaluate the efficacy of inner limiting membrane (ILM) peeling in persistent macular edema. METHODS: This retrospective review analyzed a series of 23 eyes from 23 patients with persistent macular edema treated by pars plana vitrectomy (PPV) with indocyanine green (ICG)-assisted peeling of the ILM. Thirteen female and 10 male patients with a mean age of 57.2+/-15.6 (24-77) years underwent operation between May 2000 and October 2001. The main diagnoses were uveitis (anterior, intermediate, posterior and panuveitis) ( n=9), central retinal vein occlusion (CRVO) (n=4), diabetic retinopathy (DR) ( n=5), vitreoretinal traction syndrome ( n=2), and Irvine-Gass syndrome ( n=3). Nine eyes had undergone phacoemulsification (PE) previously and two eyes had been subjected to combined PE and ILM peeling. The eyes were tamponaded with gas (3), silicone oil (5) or air (11). In four cases no endotamponade was used. Improvement in visual acuity of 2 lines or more was regarded as significant. RESULTS: Visual acuity improved after 3 months in 9 of the 23 patients. After 6 months and at the follow-up, a significant improvement was found in 6/21 and 7/21 patients. This improvement was predominantly seen in patients with uveitis (5/9), or diabetic maculopathy (3/5); One patient with Irvine-Gass syndrome showed a significant reduction, one with vitreoretinal traction an improvement in visual acuity. The group of patients with CRVO showed no significant change during the follow-up. The choice of endotamponade did not alter the visual acuity outcome. CONCLUSIONS: Different patient groups respond differently to ILM peeling. Although overall significant visual acuity improvement was observed in only one third of all cases 12 months after ILM peeling for persistent macular edema, patients with uveitis and nonproliferative diabetic maculopathy demonstrated a benefit. The lack of long-term improvement in the majority of cases is in accordance with the hypothesis that ILM peeling may reduce the intraretinal edema, but does not affect the underlying mechanism causing macular edema. So far, only diabetics have shown improvement (still unproven) from ILM peeling, and this study provides no justification for extending the treatment to macular edema of other causes. Large-scale investigations are needed to evaluate the efficacy in certain diagnosis groups.

Adult↗

Repeated topical application of growth hormone attenuates blood-spinal cord barrier permeability and edema formation following spinal cord injury: an experimental study in the rat using Evans blue, ([125])I-sodium and lanthanum tracers.

The neuroprotective efficacy of growth hormone on a focal spinal cord trauma induced alteration in the blood-spinal cord barrier (BSCB) and edema formation was examined in a rat model. Under Equithesin anaesthesia, one segment laminectomy was done over the T10-11 segments. Spinal cord injury was produced by making an incision into the right dorsal horn of the T10-11 segments (2 mm deep and 4 mm long). The animals were allowed to survive 5 h after injury. Highly purified rat growth hormone [rGH, 25 microl of a 1microg/ml solution) was applied over 10 sec topically on the exposed surface of the spinal cord 30 min before injury. The identical doses of the rGH were repeated 0 min, 30 min, 60 min, 120 min, 180 min and 240 min following injury. Saline (0.9% NaCl) treated traumatised rats at identical intervals served as controls. Traumatised rats treated with saline exhibited marked edema formation and extravasation of Evans blue and ([125])Iodine tracers in the spinal cord. At the ultrastructural level, perivascular edema and exudation of lanthanum across the endothelial cells was quite frequent in the spinal cord. Pretreatment with rGH significantly attenuated the edema formation and the extravasation of tracers in the spinal cord. In these rats, perivascular edema and infiltration of lanthanum across the endothelial cells was not much evident. These observations show that the rGH has the capacity to reduce the early manifestations of microvascular permeability disturbances and edema formation following trauma and further suggest a possible therapeutic potential of the hormone for the treatment of spinal cord injuries.

Animals↗

Role of norepinephrine and excitatory amino acids in edema of the spinal cord after experimental compression injury in rats.

The role of norepinephrine and excitatory amino acids in edema of the spinal cord after an acute experimental compression injury was studied in rats. Control rats received the compression injury only. Intraspinal norepinephrine was depleted in one rat group by injection of 6-hydroxydopamine (6-OHDA) into the subarachnoid space to selectively destroy catecholamine neurons and in a third group MK-801 was administered intravenously to block receptors for N-methyl-d-aspartate (NMDA), an excitatory amino acid. Recovery from motor paralysis and suppression of edema of the spinal cord were then compared in the three groups. Significant recovery from motor paralysis was found 12 h after injury in the 6-OHDA-treated rats, compared with the controls, and 24 h after injury in the MK-801-treated rats. Edema of the spinal cord was significantly suppressed for up to 24 h after injury in the 6-OHDA-treated rats. The MK-801-treated rats showed no significant suppression of the edema until 24 h after the spinal cord injury. It was concluded that norepinephrine is primarily involved in the formation of vasogenic edemas, which develop in the early stages after an injury, whereas excitatory amino acids affect the formation of cytotoxic edemas, which develop at a relatively later stage.

Analysis of Variance↗

Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome: ultrasonography as a diagnostic tool.

Remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome is characterized by symmetrical synovitis and swelling of both the upper and lower extremities. The anatomical determinant of RS3PE is predominantly extensor tenosynovitis as revealed by magnetic resonance imaging (MRI). Given the cost constraints, time, and expertise required in carrying out MRI and ease in diagnosing tenosynovitis by ultrasound, we utilized high-frequency ultrasonography (USG) for evidence of tenosynovitis of the distal tendons in patients with RS3PE. Diagnosis of tenosynovitis was made on the basis of anechoic or hypoechoic signals around the tendon sheaths in both transverse and longitudinal planes. Flexor and extensor tendons at the wrist and metacarpal heads and extensor digitorum longus (EDL) tendons at the ankle were evaluated with a 7.5-10-MHz linear probe. There were ten patients (seven males) with a mean age of 59.5 years (range: 52-78 years) and mean disease duration of 6.1 months (range: 1.5-12 months). Disease onset was acute in all of the cases. Pitting edema of the hands was present in all except two patients whereas four patients, in addition, had edema of the feet. Edema was symmetrical in seven patients. Inability to make a complete fist was noted in all. Tenosynovitis of extensor and flexor tendons at the wrist and the metacarpal heads was documented in all patients with edema of the hands. In seven cases extensor tendon tenosynovitis was more prominent compared to the flexor tendons. Tenosynovitis of EDL tendons was detected in six cases. Dramatic relief with low-dose prednisolone was noted in all patients within 6 weeks of therapy. At a mean follow-up of 10.1 months all patients had marked relief in edema of extremities and improvement in the grip strength. Our study confirms that tenosynovitis of both flexor and extensor tendons at the wrist and extensor tendons of the feet is the hallmark of RS3PE syndrome. USG is a reliable and cost-effective modality for evaluation of patients with suspected RS3PE.

Aged↗