Compression treatment following polytrauma and in endocrinopathies

Management of polytrauma patients will aim as much as possible at salvation of limbs and limb function if possible. The same applies to surgical reconstruction, for example of deglovement injury. Limb saving flaps and grafts may lead to complex loco-regional situations, with non-homogenic hardness or elasticity, fragility of tissues and dysfunctional skin. Inevitable damage to nerves, blood vessels or lymphatics prolongs healing or results in stiff scarred parts while other sites may be swollen (Figure 1). Sometimes, flaps and grafts appear to be undermined due to difficulties concerning adherence to the underlying tissues. Scarring may further impair elasticity or skin and limb functions. Following closure or healing of skin defects, rehabilitation exercises must start without compromising the fragile skin and eventually orthoses/prostheses will have to be accommodated. Therefore, compression treatment is sometimes needed to reshape or to protect the limb. The mobility and the need for compression may not be equal in the different compartments of the limb to be treated, and often compression devices will have to be adapted towards a combination of different materials and techniques, in order to deliver appropriate local pressure values. If the shape of the post-traumatic limb is too difficult to accommodate with standard devices, a silicone orthosis might help to reshape the leg in order to permit bandaging or donning of a compression stocking (Figure 2). At the same time this orthosis will equalize consistency of tissues and protect utterly fragile parts. The endocrinopathies considered in relation to compression therapy are mainly diabetes, thyroid disorders, morbid obesity and the metabolic syndrome, as they induce skin changes prone to collect and retain edema fluid, as well as vascular changes leading to hypertension and endothelial dysfunction. In peripheral arterial insufficiency, such as in hypertension, diabetes, peripheral arterial occlusive disease, it is important to keep in mind the territories of the affected angiosomes in order to adapt pressures accordingly. Compression affects the venous, arterial, lymphatic and capillary circulation. Not only the mechanical effects but also metabolic and behavioral changes on the cellular level have been described for endothelial cells, circulating leukocytes, or fibroblasts on the level of the microcirculation, being it primarily in phlebological patients. It has been shown that in patients with mixed disease [ankle-brachial index (ABI) 0.5-0.8] compression enhances arterial circulation by removal of edema through reduction in capillary filtration, increasing lymphatic drainage, a shift of fluid to non-compressed areas, and a breakdown of fibrosclerotic tissue (due to inflammatory mechanisms in venous disease). Endothelial dysfunction is strongly associated with both type-1 and -2 diabetes mellitus. In diabetic patients, the attention is cautiously focused on the micro-and macroangiopathy and on a peripheral sensory neuropathy considering the failure of perception under inappropriately high-pressure values. Multiple abnormalities in the skin microcirculation of the foot have been described in diabetics with neuropathy, and controversial results depending on the methods used are sometimes difficult to interpret.1 Peripheral autonomic neuropathy impacts on the regulation of flow in the small vessels of the skin including the lymphatics. These subjects may present edema due to several organ complications like heart or kidney failure, swelling secondary to the medication to treat these, or caused by the diabetic tissue alterations of the skin. Advanced glycation endproducts (and lipoxigenation), celland matrix alterations as well as deposition of a.o. amyloid [and glycosaminoglycans (GAGs)] make the skin and collagenous tissues thickCorrespondence: Mieke Flour, Schoonzichtlaan 43, B-3020 Herent, Belgium. Tel. +32.478.566780. E-mail: mie.flour@skynet.be