Your search

Under the direction of the German Society of Phlebology (Deutsche Gesellschaft für Phlebologie) and in cooperation with other specialist associations, the S1 guideline on intermittent pneumatic compression (IPC) was adopted in January 2018. It replaces the previous guideline from March 2005. The aim of the guideline is to optimize the indication and therapeutic use of IPC in vascular diseases and edema. An extensive literature search of MEDLINE, existing guidelines, and work relevant to the topic was performed. In view of the often methodologically weak study quality with often small numbers of cases and heterogeneous treatment protocols, recommendations can often only be derived from the available data using good clinical practice/expert consensus. Intermittent pneumatic compression is used for thromboembolism prophylaxis, decongestive therapy for edema, and to positively influence arterial and venous circulation to improve clinical symptoms and accelerate ulcer healing in both the outpatient and inpatient care setting. The therapy regimens and devices used depend on the indication and target location. They can be used as outpatient and inpatient devices as well as at home for long-term indications. A target indication is thrombosis prophylaxis. IPC should be used in severe chronic venous insufficiency (stages C4b to C6), in extremity lymphedema as an add-on therapy and in peripheral arterial occlusive disease (PAOD) with stable intermittent claudication or critical ischemia. IPC can be used in post-traumatic edema, therapy-resistant venous edema, lipedema and hemiplegia with sensory deficits and edema. Absolute and relative contraindications to IPC must be taken into account and risks considered and avoided as far as possible. Adverse events are extremely rare if IPC is used correctly. If the indication and application are correct-also as an add-on therapy-it is a safe and effective treatment method, especially for the treatment of the described vascular diseases and edema as well as thrombosis prophylaxis.

Whereas the blood microvasculature constitutes a biological barrier to the action of blood-borne insulin on target tissues, the lymphatic microvasculature might act as a barrier to subcutaneously administrated insulin reaching the circulation. Here, we evaluate the interaction of insulin with primary microvascular endothelial cells of lymphatic [human dermal lymphatic endothelial cells (HDLEC)] and blood [human adipose microvascular endothelial cells (HAMEC)] origin, derived from human dermal and adipose tissues, respectively. HDLEC express higher levels of insulin receptor and signal in response to insulin as low as 2.5 nM, while HAMEC only activate signaling at 100 nM (a dose that blood vessels do not normally encounter). Low insulin acts specifically through the insulin receptor, while supraphysiological insulin acts through both the IR and insulin growth factor-1 receptor. At supraphysiological or injection site-compatible doses pertinent to lymphatic microvessels, insulin enters HAMEC and HDLEC via fluid-phase endocytosis. Conversely, at physiologically circulating doses (0.2 nM) pertinent to blood microvessels, insulin enters HAMEC through a receptor-mediated process requiring IR autophosphorylation but not downstream insulin signaling. At physiological doses, internalized insulin is barely degraded and is instead released intact to the extracellular medium. In conclusion, we document for the first time the mechanism of interaction of insulin with lymphatic endothelial cells, which may be relevant to insulin absorption during therapeutic injections. Furthermore, we describe distinct action and uptake routes for insulin at physiological and supraphysiological doses in blood microvascular endothelial cells, providing a potential explanation for previously conflicting studies on endothelial insulin uptake.

The present study aimed to assess LV rotational mechanics by three-dimensional speckle-tracking echocardiography (3DSTE) in lipedema (n=25), lymphedema (n=26) patient groups with age- and gender-matched healthy controls (n=54). 3 lipedema and 4 lymphedema patients were excluded due to insufficient image quality for 3DSTE analysis. LV apical rotation (9.61 ± 4.25 degree vs. 6.40 ± 2.63 degree, p <0.05) and LV twist (13.83 ± 4.89 degree vs. 10.04 ± 3.56 degree, p <0.05) are impaired in lipedema patients as compared to matched controls; similar alterations in lymphedema were not found. Moreover, in some lipedema and lymphedema patients severe LV rotational abnormalities could be detected. Our results suggest that lipedema-associated impaired LV apical rotation and twist assessed by 3DSTE could be a novel differential diagnostic point between lipedema and lymphedema.

Surgical Treatment for Lipedema Abstract. Lipedema is a progressive disease that occurs in adolescence and affects one in nine women. The signs are limited to the lower limbs. Early signs are nonspecific, which is why the diagnosis is often ignored. Later, pain and heaviness of lower limbs become predominant. Finally, at an advanced stage, tissue fibrosis is associated with significant edema. At this stage, patients become severely disabled and bedridden. At the early stage, the treatment is conservative. Liposuction is indicated at the onset of pain. Its effectiveness pain and long-term control has been demonstrated on. Finally, late stages require heavy and complex surgeries combining dermolipectomy and liposuction.

Pain is an important criterion for diagnosing lipedema. This pain, however, has not been properly investigated or characterized in the literature, and in most cases, authors have settled for putting forward hypotheses. Comparison of these hypotheses with actual findings, if even available, it becomes obvious that many of these hypotheses cannot be correct. Hardly any of the tangible results seem to provide a solid basis for explaining lipedema-related pain. When examining lipedema-related pain reported in the pain literature, it becomes increasingly evident that dynamic mechanical allodynia, with Aß-fibers and probably tactile C (CT)-fibers, is Involved. It Is in principle possible to stimulate CT-fibers by manual lymphatic drainage (MLD), and this may explain the method's analgesic effects. Conversely however, this pain-relieving effect via CT-fibers seems to exclude the Involvement of small fiber neuropathy (SFN), and thus any direct nerve damage as the cause of pain in lipedema.

The use of velcro compression wrapping devices in the management of lymphoedema and chronic oedema is not a new concept. Wraps have been available for many years and are being used widely in clinic and community settings where bandaging or traditional compression garments are not suitable. Furthermore, they are becoming more common when treating venous disease, patients with wounds and lipoedema. The aim of this article is to introduce the reader and clinician to the new Haddenham easywrap and to demonstrate why it is different to any other velcro wrapping device available. Case studies will be utilised from clinicians currently using easywrap in clinical practice, with both therapist and patient feedback given to demonstrate the efficacy of this new velcro compression wrapping device.

Lower extremity edema is extremely common among patients seen across multiple specialties. The differential diagnosis is broad and ranges from simple dependent edema to more complex conditions such as chronic venous disease and lymphedema. Several key features from the history and physical exam can assist with the diagnosis. Imaging is rarely necessary at the initial visit unless venous thromboembolism is suspected. Treatment is specific to the etiology of the edema, but compression stockings, elevation, exercise, and weight loss remain the cornerstone in most cases.

Lymphatic vessels are lined by lymphatic endothelial cells (LECs), and are critical for health. However, the role of metabolism in lymphatic development has not yet been elucidated. Here we report that in transgenic mouse models, LEC-specific loss of CPT1A, a rate-controlling enzyme in fatty acid β-oxidation, impairs lymphatic development. LECs use fatty acid β-oxidation to proliferate and for epigenetic regulation of lymphatic marker expression during LEC differentiation. Mechanistically, the transcription factor PROX1 upregulates CPT1A expression, which increases acetyl coenzyme A production dependent on fatty acid β-oxidation. Acetyl coenzyme A is used by the histone acetyltransferase p300 to acetylate histones at lymphangiogenic genes. PROX1-p300 interaction facilitates preferential histone acetylation at PROX1-target genes. Through this metabolism-dependent mechanism, PROX1 mediates epigenetic changes that promote lymphangiogenesis. Notably, blockade of CPT1 enzymes inhibits injury-induced lymphangiogenesis, and replenishing acetyl coenzyme A by supplementing acetate rescues this process in vivo.

Eat to starve lymphedema and lipedema by having foods that fight these conditions (and cancer) and avoiding foods that contribute to symptoms or related conditions. Learn how food choices affect both conditions and how better nutrition can improve symptoms (including pain) and delay changes associated with progression to more advanced stages. Intended for anyone with, or at risk for, lymphedema or lipedema, caregivers, lymphedema therapists, and other health care providers. Signs of lymphedema and lipedema (painful fat syndrome) include swelling (edema), abnormal fat accumulation, pain, skin changes, and infections (cellulitis, wounds or ulcers) in affected areas. Lymphedema and lipedema are progressive conditions that can be depressing, disfiguring, disabling, and (potentially) deadly, without treatment. This guide explains why nutrition is an essential part of treatment and self-care for these conditions, what to eat, and how to change your eating pattern. It also covers vitamins, minerals, and supplements that may be beneficial. You may be at risk for lymphedema if you have chronic venous insufficiency, other venous disorders, heart disease, obesity, a cancer diagnosis (especially breast cancer, reproductive system cancers, or melanoma), or a family history of lymphedema or swollen legs. Eating wisely and maintaining a healthy body weight can help reduce your risk of developing lymphedema symptoms

Lipedema an often overlooked but treatable disease Lipedema is a painful disease that affects some women between puberty and menopause through a subcutaneous fat accumulation especially in the lower extremities. Patients suffer from pain and pressure tenderness. The larger fat accumulation, especially on the inside of the thighs and knees, causes walking difficulties. This can successfully be treated by liposuction with good long-term results in terms of pain reduction and prevention of osteoarthritis development in the knee and ankle joints.

BACKGROUND: Long-term results following liposuction in patients with lipoedema are available only for an average period of 4 years. OBJECTIVE: To find out whether the improvement of complaints persists for a further 4 years. METHODS: In a single-centre study, 85 patients with lipoedema had already been examined after 4 years. A mail questionnaire - often in combination with clinical controls - was repeated after another 4 years (8 years after liposuction). RESULTS: Compared with the results after 4 years, the improvement in spontaneous pain, sensitivity to pressure, oedema, bruising and restriction of movement persisted. The same held true for patient self-assessment of cosmetic appearance, quality of life and overall impairment. Eight years after surgery, the reduction in the amount of conservative treatment (combined decongestive therapy, compression garments) was similar to that observed 4 years earlier. CONCLUSION: These results demonstrate for the first time the long-lasting positive effects of liposuction in patients with lipoedema.

Compression therapy is a key component in the effective management of people with lower limb problems associated with venous, lymphatic and fat disorders such as lipoedema. Individuals with lymphoedema, venous ulceration and lipoedema often require long-term compression therapy to prevent and manage problems such as chronic ulceration and skin changes, persistent swelling and shape distortion. Challenges remain in achieving acceptable, safe, effective and cost-efficient compression therapy choices. Adjustable compression wrap devices using hook and loop fasteners, commonly called VELCRO brand fasteners, present new opportunities for improving treatment outcomes, supporting patient independence and self-management in the use of compression therapy. This paper reports the findings of an evidence review of adjustable compression wrap devices in people with lymphoedema, chronic oedema, venous ulceration and lipoedema. DECLARATION OF INTEREST: The authors have no conflict of interest to declare.

While there is no proven cure for lipoedema, early detection is key as specialist treatments, complemented by self-management techniques, can improve symptoms and prevent progression. There is no universal approach as the correct treatment or treatments will depend on each patient's particular circumstances; however, when chosen early and appropriately, interventions can provide huge benefits. The most common treatments in the management of lipoedema include compression, manual lymphatic drainage (MLD), tumescent liposuction, intermittent pneumatic compression therapy (IPC), kinesio taping, deep oscillation therapy, and cognitive behavioural therapy (CBT).

Lipedema is a chronic disorder characterized by abnormal distribution of subcutaneous adipose tissue on the proximal extremities, pain and capillary fragility. Its etiology is unknown but in analogy to central obesity, chronic low-level inflammation in adipose tissue has been suggested. There seems to be an increased propagation of pre-adipocytes into mature adipocytes contributing to the massive enlargement of subcutaneous adipose tissue. We investigated whether tyrosine kinases might be involved. Proteins from adipose tissue harvested during microcannular tumescent liposuction in lipedema and in lipomas were subjected to 10% polyacrylamide-gel, transferred to a polyvinylidenfluorid membrane and immunoblotted with indicated P-Tyr-100 antibody followed by enhanced chemiluminescence reaction. A survey of all blots did not reveal tyrosine-phosphorylated proteins with a molecular weight >100 kD in lipedema tissue and controls. These investigations suggest absence of activated growth factor receptors. Some signals indicating unspecific tyrosine-phosphorylation of smaller proteins were detected in tissue of both lipedema patients and controls. The present data suggest that there is no enduring activation of tyrosine kinase pathways of adipogenesis in lipedema as in lipoma controls.