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As the science of wound healing has evolved over the past two decades, so has awareness of the "hidden epidemic" of lymphedema. Substantial information has been accumulated regarding the pathophysiology and therapy of lymphedema. Until recently, the relationship between wound healing and the negative effects of associated peri-wound lymphedema has received little attention. Identifying wound-related lymph stasis and safe mobilization of the fluid are fundamentals that must be addressed for proper therapy. Experience gained from the successful treatment of primary and secondary lymphedema has proven very useful in the applications to wound-related lymphedema. The mobilization of lymph fluid from the peri-wound area with the use of reasoned compression is essential for proper therapy of the open wound, as are appropriate bandage selection and safeguards for bandage application.
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HYPOTHESIS: The causes and management of lower limb lymphedema in the Western population are different from those in the developing world. OBJECTIVE: To look at the differential diagnosis, methods of investigation, and available treatments for lower limb lymphedema in the West. DATA SOURCE: A PubMed search was conducted for the years 1980-2002 with the keyword "lymphedema." English language and human subject abstracts only were analyzed, and only those articles dealing with lower limb lymphedema were further reviewed. Other articles were extracted from cross-referencing. RESULTS: Four hundred twenty-five review articles pertaining to lymphedema were initially examined. This review summarizes the findings of relevant articles along with our own practice regarding the management of lymphedema. CONCLUSIONS: The common differential diagnosis in Western patients with lower limb swelling is secondary lymphedema, venous disease, lipedema, and adverse reaction to ipsilateral limb surgery. Lymphedema can be confirmed by a lymphoscintigram, computed tomography, magnetic resonance imaging, or ultrasound. The lymphatic anatomy is demonstrated with lymphoscintigraphy, which is particularly indicated if surgical intervention is being considered. The treatment of choice for lymphedema is multidisciplinary. In the first instance, combined physical therapy should be commenced (complete decongestive therapy), with surgery reserved for a small number of cases.
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Aim: In pathophysiology of lipoedema, almost exclusively seen in women, lymphatic insufficiency might play a significant role. However, little is known about the pathophysiology of these abnormal localized depositions of body fat. We studied the involvement of the lymphatic system in lipoedema of the type Allen-Hines as well as of Typus Rusticanus Moncorps. Patients, methods: The standard (epifascial pathway) and a modified method (subcutaneous pathway) of lymphoscintigraphy was carried out with 28 patients suffering from lipoedema. Uptake percentages normalized to the injected dose were used as functional quantitative parameters. Visual assessment of both studies were done and scored. Patients with oedema of the legs because of venous insufficiency (Widmer stage II) served as a control group. Results: All patients of the control group and all patients with lipoedema of Typus Rusticanus Moncorps showed a normal standard lymphoscintigraphic study by visual scoring as well as by quantitative outcome. Lymph transport from the subcutaneous fat tissue was significant higher (p <0.012) in the group of patients with lipoedema diagnosed as type Allen-Hines than in Typus Rusticanus Moncorps. Conclusion: Epifascial lymph drainage in patients with lipoedema is not significantly disturbed. However, subcutaneous lymphatic drainage significantly differed in patients with lipoedema of type Rusticanus Moncorps in comparison with type AllenHines hinting at a differing lymphatic pathophysiology.
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PURPOSE: To evaluate the accuracy of computed tomography (CT) scan imaging in distinguishing lymphedema from deep venous thrombosis (DVT) and lipodystrophy (lipedema) in patients with swollen legs. MATERIAL AND METHODS: CT scans of the lower limbs were performed in 55 patients with 76 swollen legs (44 lymphedemas, 12 DVT and 20 lipedemas). Thirty-four normal contralateral legs were also similarly evaluated. Primary lymphedema was verified by lymphography or lymphoscintigraphy, whereas secondary lymphedema was documented by a typical clinical history. DVT was established by ultrasound Doppler imaging. The diagnosis of lipedema was made with bilateral swollen legs where lymphoscintigraphy and Doppler examination were both unremarkable. Qualitative CT analysis was based on skin thickening, subcutaneous edema accumulation with a honeycombed pattern, and muscle compartment enlargement. RESULTS: Sensitivity and specificity of CT scan for the diagnosis of lymphedema was 93 and 100%, respectively; for lipedema it was 95 and 100%, respectively; andfor DVT it was 91 and 99%, respectively. Skin thickening was found in 42 lymphedemas (95%), in 9 DVT (75%), and in 2 lipedemas (16%). Subcutaneous edema accumulation was demonstrated in 42 legs (95%) with lymphedema and in 5 (42%) with DVT but in none with lipedema. A honeycombed pattern was present only in lymphedema (18 legs or 41%); muscle enlargement was present in all patients with DVT, in no patient with lipedema, and in 4 (9%) with lymphedema. CONCLUSION: Edema accumulation is readily demonstrated with plain CT scan and is not present in lipedema. Specific CT features of the subcutaneous fat and muscle compartments allow accurate differentiation between lymphedema and DVT.
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"Lipedema," a special form of obesity syndrome, represents swelling of the legs due to an increase of subcutaneous adipose tissue. In 12 patients with lipedema of the legs and in 12 healthy subjects (controls), fluorescence microlymphography was performed to visualize the lymphatic capillary network at the dorsum of the foot, at the medial ankle, and at the thigh. Microaneurysm of a lymphatic capillary was defined as a segment exceeding at least twice the minimal individual diameter of the lymphatic vessel. In patients with lipedema, the propagation of the fluorescent dye into the superficial lymphatic network of the skin was not different from the control group (p > 0.05). In all 8 patients with lipedema of the thigh, microaneurysms were found at this site (7.9 +/- 4.7 aneurysms per depicted network) and in 10 of the 11 patients with excessive fat involvement of the lower leg, multiple microlymphatic aneurysms were found at the ankle region. Two obese patients showed lymphatic microaneurysms in the unaffected thigh and in only 4 patients were microaneurysms found at the foot. None of the healthy controls exhibited microlymphatic aneurysms at the foot and ankle, but in one control subject a single microaneurysm was detected in the thigh. Multiple microlymphatic aneurysms of lymphatic capillaries are a consistent finding in the affected skin regions of patients with lipedema. Its significance remains to be elucidated although its occurrence appears to be unique to these patients.
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OBJECTIVES: The purpose of this study was to define the relationships between the short saphenous vein (SSV) and the fasciae of the leg, including the muscular fascia (MF) and the membranous layer (ML) of the subcutaneous tissue. METHODS: Fascial relationships of the SSV were evaluated by means of dissection in 30 cadaveric limbs and by means of duplex sonography in 270 healthy limbs from living subjects. RESULTS: All along the leg, the SSV courses in a flat compartment delimited by the MF and the ML. Neither results from dissection nor results from sonographic examination demonstrated piercing of the MF by the SSV. A hyperechoic lamina similar to a ligament connects the SSV to the fasciae by which it is encased. An SSV tributary and collateral vessels course out of this space and are devoid of any fascial wrapping. CONCLUSIONS: The SSV does not correspond to the classical description of a "superficial" vein. In fact, from the anatomical point of view, the SSV is an interfascial vein, because it is encased by two connective fasciae, just like the greater saphenous vein. Fascial relationships of the SSV suggest that muscular contraction potentially influences the caliber and hemodynamics of the SSV. In addition, the ML is arranged as a sort of mechanical shield that could counteract dilative pathologic conditions in varicose limbs.
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Venous oedema, which occurs almost exclusively in the legs, develops due to increased venous pressure following valvular insufficiency, and is marked by blue discolouration, varicosities and, in chronic forms, by brown discolouration of the skin resulting from the deposition of haemosiderin. It is possible to confirm the condition by phlebological instrumental diagnosis. Primary lymphoedema also almost always occurs in the legs. It is caused by underdevelopment of lymphatic vessels, but the skin colour remains normal. It is recognisable by Stemmer’s sign and characteristic thickening of the skin over the toes resulting from subcutaneous protein fibrosis. Lymphoscintigraphy may be required for diagnosis in rare cases. Venous oedema and lymphoedema are found in both sexes, uni- or bilaterally. If bilaterally then usually asymmetrical. In contrast, lipoedema occurs in women only, thickening is always symmetrical, and the skin has a normal colour as in lymphoedema. The predisposing condition for lipoedema is lipohypertrophy of the extremities, a congenital accumulation of adipose tissue in the extremities that results in a disproportionate physical form with a relatively slim trunk. In one third of cases lipoedema is also observed in the arms. In contrast to lymphoedema, the hands and feet characteristically remain free of thickening and oedema.
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Diagnosis and treatment of the <<Lipedema Syndrome>> are now as ever connected with problems for the general physcician, but also for the experts in lymphology. Numerous open questions regarding etiology, diagnosis, and course of the disease as new therapetic concepts have lead to the idea, to include that subject again as one of the main topics into the program of the annual meeting of the German Society of Lymphology
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The role of operative management of "symptomatic" varicose veins in patients with lower extremity lymphedema or lipedema is controversial. We reviewed the clinical outcome of 261 patients between 1989-1997 at the Földiclinic with lower extremity lymphedema (68 patients), lipo-lymphedema or lympho-lipedema (103 patients) or lipedema (90 patients) who had undergone operation for varicose veins. In each group, the results were dismal as leg swelling worsened or was unchanged in greater than 90% whereas symptoms such as heaviness, fatigue, cramps (termed varicogenic symptomatology) were improved in less than 10%. These findings support that operations for varicose veins in the legs of patients with lymphedema, lipedema, or combinations of these disorders should be undertaken only if there is an absolute indication present (ascending phlebitis and/or bleeding). Otherwise, complete decongestive physiotherapy is still the best treatment approach for these groups of patients.
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Lipedema never reveals clinical picture of extreme lymphedema-elephantiasis, and skin signs and complications have not been observed. Aim of this paper is to present a case of lipedema with the initial lymphedema in which, after one episode of lymphangiitis and cellulitis, came to the rapid development of lymphedema followed by chyloderma. During the local treatment of extreme chyloderma with excessive exudation, semiocclusive synthetic dressings have been used for moist wound healing. The treatment was completed after 20 weeks with total epithelizsation, without maceration and irritation, without additional spreading of the chyloderma field, without wound infections, with fast and full relief of the pain. Lipedem with extreme lymphedema can be followed by skin complications of lymphedema like chylodermia.
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