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At present, there is no proven cure for lipoedema. Nevertheless, much can be done to help improve symptoms and prevent progression. Many of these improvements can be achieved by patients using self-management techniques. This article describes the range of self-management techniques that community nurses can discuss with patients, including healthy eating, low-impact exercise, compression garments, self-lymphatic drainage, and counselling.

Frequently misdiagnosed as obesity, lipoedema is chronic condition involving an abnormal build-up of fat cells in the legs, thighs and buttocks that cannot be shifted by exercise or dieting. Estimated to affect up to 11% of the female population, the condition is widely unknown by health professionals. This means women typically wait for many years before diagnosis. This allows the condition to progress unchecked, resulting in unnecessary deterioration and the development of associated comorbidities, as well as significant pain and mental anguish. A free, 30-minute Royal College of General Practitioners (RCGP) e-learning course created in partnership with Lipoedema UK aims to rectify this situation by educating nurses, GPs and other health professionals on how to diagnose and manage lipoedema in primary care. This article aims to describe the condition of lipoedema, how to recognise/diagnose it, current treatment options and the findings of a 240-patient survey carried out by Lipoedema UK in 2013 that included documenting the difficulties for patients in obtaining a diagnosis as well as the mental and physical effects of the condition.

Liposuction surgically removes subcutaneous abdominal tissue (SAT) and has almost no effect on visceral abdominal tissue (VAT) depot. However, some authors suggest that deep layers of SAT are functionally similar to VAT and the amount of deep subcutaneous abdominal adipose tissue is strongly related to insulin resistance in a manner nearly identical to that of visceral adiposity. Moreover, SAT determines leptin secretion which indirectly reflects the level of insulin sensitivity in the body. Thus, the immediate removal of SAT could potentially affect metabolic profile of a patient. The current data are conflicting and cannot bring a clear evidence suggesting that liposuction itself results in important metabolic outcomes and, on the other hand, cannot exclude such a possibility. This review summarizes the liposuction-induced metabolic changes with regard to release of major adipokines and insulin sensitivity.

Background: Lipedema is a poorly known disorder of painful subcutaneous adipose tissue (SAT) likely affecting millions of women worldwide. Stage 1 lipedema has smooth skin with increased underlying fat, Stage 2 has indentations and nodules, and Stage 3 has large extrusions of skin and SAT. Women with lipedema have more SAT below the waist. As this gynoid fat is known to be cardioprotective, we aimed to determine if health declined with increasing stage and extent of lipedema SAT. Methods and Findings: Chart review from June 2012 to February 2013 at a tertiary academic center. Fifty women and one man were included in consecutive order. Fat was assessed in 29 areas for lipomas, size of the depot, and presence of lipedema fat. Pain was assessed by a numerical pain scale. Average age of patients was 50 ± 13 y; average body mass index was 38 ± 12 kg/m2. Median age of development of lipedema was 20 y. Pain occurred daily in 89.7%. None of the patients with Stage 1 lipedema had diabetes, hypertension or dyslipidemia. The amount of lipedema fat differed significantly between Stages of lipedema (p=0.003), with Stage 3 having significantly more. There was no difference in fat depot size or number of lipomas amongst Stages. Only one of 51 patients had type 2 diabetes. There was an increase in shortness of breath, palpitations, urination, and numbness in Stage 3. Conclusions: Lipedema fat can develop in any SAT location and increases in association with increasing signs and symptoms of systemic illness.

In many respects, lipedema of the arms and legs is still an underresearched disease within the lymphatic spectrum. It is clear that clinical symptoms frequently include symmetrical fat distribution in the arms and legs and pathognomonic tenderness in female family members. However, 75 years after the first descriptions provided by Allen and Hines, we still lack pathological evidence that would provide more insight than that offered by the theses proposed by Marsch and Brauer. We also lack information about hormonal influence on hyperplastic fatty tissue and the causes of obviously increased lymph formation in the fatty tissue in patients with lipohyperplasia dolorosa. Much more is known about the effects of combined decongestive therapy, which has been used since the 1960s. Moreover, since 1997, surgery has been used to successfully treat this disease presentation. The success rate in long-term observation (15 years) is 97%.

In the differential diagnosis of lymphedema, lipedema is often mentioned; however, in lipedema, there is initially no primary lymphatic impairment due to dysfunction. In the later stages of lipedema, obesity is often involved and will influence the patient negatively. In daily practice, contrary to the treatment point of view, a therapeutic approach of manual lymph drainage and compression therapy is often used for both lipedema and lymphedema, although these are two distinguishable diagnoses. Therefore, differentiating these two conditions is crucial for an optimal, dedicated treatment program. Because there is no consensus on the criteria for the diagnosis lipedema, a new method should be used to categorize and stratify patients to offer a dedicated treatment program and psycho-social support. The WHO method of International Classification of functioning, disability and health (ICF) is designed for a new approach of chronic diseases and can be of help in patients with lipedema. Lipedema is a debilitating, incurable chronic pathological condition that is often misdiagnosed or unrecognized. The most common form of symmetrical fat distribution is obesity. However, many diseases and syndromes, such as Cushing’s disease21 and polycystic ovary syndrome22, can lead to unusual fat deposition patterns. Lipedema almost exclusively affects women and is characterized by a bilateral, progressive accumulation and misdistribution of subcutaneous fat, usually below the waist. Only two cases of lipedema in male patients have been reported. The onset of lipedema is often soon after puberty; however, lipedema can develop later in life, such as during pregnancy or menopause. During the course of lip edema, very often a obesity component will be present. As a clinical syndrome, lipedema was first described as the presence of excessive fat deposits on the buttocks, thighs and legs associated with mild edema. Once accumulated, the excessive fat deposits respond poorly to vigorous dietary measures. Dietary measures predominately reduce fat in the areas of the body without lipedema. This process leads to an asymmetrical distribution of body fat between the upper body and lower extremities, a disproportional fat distribution. Because of the diet-resistant nature of lipedema part, many patients are reluctant to pursue stringent dietary measures, as this emphasizes the disproportionate body fat. Approximately 50% of lipedema patients have an elevated body mass index (BMI), which complicates the differentiation between lipedema and obesity (from the Latin obesus, grown fat by eating). Nevertheless, very often volume reduction of a lipedema leg is achieved after a conservative treatment program and weight reduction. In addition, large accumulations of subcutaneous fat deposits can mechanically compress existing and previously functional lymphatic structures, leading to a mechanical insufficiency and secondary lymphedema over time. In practice, diagnosing lipedema is often complicated, but lipedema must be differentiated from lipohypertrophy, lymphedema and obesity to provide the patient with adequate treatment options. The exact etiology of lipedema is still unknown, although recent research has suggested the involvement of several genetic factors. Because lipedema is often not recognized or misdiagnosed, the scarcely available prevalence figures are likely a significant underestimation. All of the current treatment options are non-curative, complex and require a multidisciplinary approach. Surgical treatment of the affected limbs occurs when conservative treatment options are no longer effective and daily functioning becomes severely compromised.

Edema is an accumulation of fluid in the interstitial space that occurs as the capillary filtration exceeds the limits of lymphatic drainage, producing noticeable clinical signs and symptoms. The rapid development of generalized pitting edema associated with systemic disease requires timely diagnosis and management. The chronic accumulation of edema in one or both lower extremities often indicates venous insufficiency, especially in the presence of dependent edema and hemosiderin deposition. Skin care is crucial in preventing skin breakdown and venous ulcers. Eczematous (stasis) dermatitis can be managed with emollients and topical steroid creams. Patients who have had deep venous thrombosis should wear compression stockings to prevent postthrombotic syndrome. If clinical suspicion for deep venous thrombosis remains high after negative results are noted on duplex ultrasonography, further investigation may include magnetic resonance venography to rule out pelvic or thigh proximal venous thrombosis or compression. Obstructive sleep apnea may cause bilateral leg edema even in the absence of pulmonary hypertension. Brawny, nonpitting skin with edema characterizes lymphedema, which can present in one or both lower extremities. Possible secondary causes of lymphedema include tumor, trauma, previous pelvic surgery, inguinal lymphadenectomy, and previous radiation therapy. Use of pneumatic compression devices or compression stockings may be helpful in these cases. (Am Fam Physician. 2013;88(2):102-110. Copyright © 2013 American Academy of Family Physicians.)

Edema of the limbs is a common reason for medical consultation, for which the lymphoscintigraphy is considered to be a reliable method for its differential diagnosis. OBJECTIVE: To evaluate the usefulness of radionuclide studies in the differential diagnosis of edema, and the diagnostic yield of different scintigraphic patterns. MATERIAL AND METHODS: A total of 61 patients, mean age 43 years, referred to our Department in the last three years for suspected lymphoedema, were considered. One patient was discarded due to lack of diagnosis, 56 had lower limb edema and 4 upper limb edema. After intradermal injection of two doses of (99m)Tc-nanocolloid, scintigraphic scans were made at 30 and 120minutes. The final diagnosis was based on imaging tests, clinical course, and response to treatment. We calculated the parameters of the diagnostic yield of four different scintigraphic patterns (presence of dermal backflow, asymmetry-alteration in inguinal/axillary nodes, presence of collateral pathways, and visualization of intermediate lymph nodes), considering them individually and jointly. RESULTS: The best diagnostic yield was achieved by considering dermal backflow and asymmetry in inguinal/axillary nodes (accuracy 88.9%, specificity 96.4%, PPV 95.5%). Evaluation of intermediate lymph nodes and presence of collateral pathways contributed little to the diagnostic yield, showing poor sensitivity and high false positive rates. CONCLUSION: The lymphoscintigraphy had high diagnostic yield, allowing early treatment of lymphœdema. The dermal backflow and asymmetry in inguinal/axillary nodes had the greatest diagnostic accuracy. Evaluation of intermediate lymph nodes and visualization of collateral pathways contributed little to improving the diagnosis.

The pathophysiology of skin diseases associated with monoclonal gammopathies is generally unknown. Our aim was to investigate whether a monoclonal gammopathy could be a causal factor in progressive lymphedema. We describe a 75 year old patient with a rapidly progressive lipo-lymphedema and a monoclonal gammopathy of unknown significance (MGUS) suspected as a key etiological factor. Dermal fibroblasts were cultured from lesional lower leg skin and non-lesional abdominal skin and compared to healthy control fibroblasts. We found 10-fold elevated basic fibroblast growth factor 2 (FGF-2) in the patient's serum and significantly increased basal FGF-2 production of lesional and non-lesional fibroblasts compared to healthy controls. Upon restimulation with patient or healthy control serum, lesional fibroblasts showed significantly increased proliferation rates and FGF-2 production in vitro. Non-lesional abdominal fibroblasts showed an intermediate phenotype between lesional and control fibroblasts. Our findings provide the first evidence that lesional dermal fibroblasts from lipo-lymphedema with plasma cell infiltration show increased proliferation and FGF-2 production and that both local tissue factors and altered FGF-2 serum levels associated with monoclonal gammopathies might contribute to this phenotype. Thus we propose a possible pathophysiologic link between the gammopathy-associated factors and the generation of lymphedema with initial fibrogenesis aggravating pre-existing lipedema.

Chronic edema is a multifactorial condition affecting patients with various diseases. Although the pathophysiology of edema varies, compression therapy is a basic tenant of treatment, vital to reducing swelling. Clinical trials are disparate or lacking regarding specific protocols and application recommendations for compression materials and methodology to enable optimal efficacy. Compression therapy is a basic treatment modality for chronic leg edema; however, the evidence base for the optimal application, duration and intensity of compression therapy is lacking. The aim of this document was to present the proceedings of a day-long international expert consensus group meeting that examined the current state of the science for the use of compression therapy in chronic edema. An expert consensus group met in Brighton, UK, in March 2010 to examine the current state of the science for compression therapy in chronic edema of the lower extremities. Panel discussions and open space discussions examined the current literature, clinical practice patterns, common materials and emerging technologies for the management of chronic edema. This document outlines a proposed clinical research agenda focusing on compression therapy in chronic edema. Future trials comparing different compression devices, materials, pressures and parameters for application are needed to enhance the evidence base for optimal chronic oedema management. Important outcomes measures and methods of pressure and oedema quantification are outlined. Future trials are encouraged to optimize compression therapy in chronic edema of the lower extremities.

Lipedema is a disproportional obesity due to unknown pathomechanism. Its major hallmark is frequent hematoma formation related to increased capillary fragility and reduced venoarterial reflex. Beyond microangiopathy, both venous and lymphatic dysfunction have also been documented. However, arterial circulation in lipedema has not been examined, and therefore we explored aortic elastic properties by echocardiography. Fourteen women with and 14 without lipedema were included in the study. Each subject consented to blood pressure measurement, physical examination, and transthoracic echocardiography. Aortic stiffness index (beta), distensibility, and strain were evaluated from aortic diameter and blood pressure data. Mean systolic (30.0 +/- 3.2 vs. 25.5 +/- 3.6, P < 0.05) and diastolic (27.8 +/- 3.3 vs. 22.3 +/- 3.1) aortic diameters (in mm) and aortic stiffness index (9.05 +/- 7.45 vs. 3.76 +/- 1.22, P < 0.05) were significantly higher, while aortic strain (0.082 +/- 0.04 vs. 0.143 +/- 0.038, P < 0.05) and distensibility (2.24 +/- 1.07 vs. 4.38 +/- 1.61, P < 0.05) were significantly lower in lipedematous patients compared to controls. Thus, lipedema is characterized with increased aortic stiffness.