EWMA 2020, 18-20 Nov


The talks will focus on

Diabetic foot ulceration (DFU) is known as one of the most severe complications of diabetes. Revascularization plays a crucial role in achieving ulcer healing. Non-surgical, minimally invasive, revascularization options for DFU have expanded over the last decade and have become a prominent tool to prevent amputation.
What is the role of endovascular treatment of the DFU now a days. When should we consider this option, what are the opportunities? Should we look at the location of the ulcer? What is the evidence of the intervention on angiosome-base.  

Systemic hyperbaric oxygen therapy (HBOT) has been proposed as a medical treatment for diabetic foot ulcers. The value of HBOT in the treatment of diabetic ulcers is still under debate. Available evidence suggests that HBOT may improve the healing of diabetic ulcers, but it comes from small trials with heterogeneous populations and interventions. As example the HODFU study (2010) showed that adjunctive treatment with HBOT facilitates healing of chronic foot ulcers in selected patients with diabetes. The DAMOCLES trial is performed in the Netherlands and it is unique for addressing patients with ischemic diabetic foot ulcers who may also receive vascular reconstructions. What are the results? How should we use the outcomes? What should be/is the role of HBOT treating DFU?

A series of multiple mechanisms can contribute to lack of healing in persons with DFUs. The association of diabetes with impaired wound healing and other vascular complications is a serious public health issue. For example Matrix Metalloproteinases (MMPs) play an integral role in wound healing. Their main function is degradation, by removal of damaged extracellular matrix (ECM) during the inflammatory phase, breakdown of the capillary basement membrane for angiogenesis and cell migration during the proliferation phase, and contraction and remodeling of tissue in the remodeling phase. For effective healing to occur, all wounds require a certain amount of these enzymes, which on the contrary could be very damaging at high concentrations causing excessive degradation and impaired wound healing. The imbalance in MMPs may increase the chronicity of a wound, a familiar problem seen in diabetic patients. What should we know about the molecular changes leading to stagnation? What are the possible treatment options?