Optimizing Management of Lymphedema Editorial Summary Lymphedema is a major global condition defined as progressive swelling of the body part which is in part due to disruption of the lymphatic system. This article is going to discuss the pathophysiology of lymphoedema, the demographics of the condition and its management. There will be a deep overview of the importance of the endothelial or Calix layer as well as the importance of the starling model of capillary fluid change. A detailed look at the lymph circulation including the capillaries and lymphatic endothelial cells and its relevance to lymphedema. There will also be a focus on hyperglycaemia and diabetes in lymphoedema In this article. The role of albumin and glycocalyx as well as sodium are explored. The clinical characteristics and management will also be analysed.
Introduction
L
ymphedema affects 140-300million patients worldwide. It is defined as the progressive swelling of a body part, usually an extremity following developmental (primary lymphedema) or acquired (secondary lymphedema) disruption of the lymphatic system resulting in lymph accumulating in the interstitial space.1 This article discusses the pathophysiology of lymphedema, demographics of this condition and its management.
Endothelial Glycocalyx Layer In 1894, Starling proposed a model of capillary fluid exchange, based on hydrostatic and oncotic pressures in the blood capillaries and interstitium, with the capillary acting as a semiporous membrane, through which fluid moves freely in and out.2 In 1940, Danielli introduced the concept of a protein-based lining of vessels which played a vital role in fluid filtration, and in 1966, Luft visualised this layer using electron microscopy.2 The “endothelial glycocalyx layer” (EGL) was then recognised as controlling the movement of proteins and fluid across the blood capillary wall, through dynamic and complex processes.2
Dr M. Mark Melin M Health Fairview Wound Healing Institute, University of Minnesota Physicians Minneapolis MN, United States
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The endothelial glycocalyx is a complex carbohydrate-rich gel-like layer lining the luminal surface of blood vessels functioning as a barrier between the blood and vessel wall.3 The glycocalyx layer is composed of membrane-bound proteoglycans, secreted glycosaminoglycans (GAGs), sialic acidcontaining glycoproteins, and glycolipids
Wound Masterclass - Vol 1 - December 2022
associated with the endothelial surface.3 The main proteoglycans of the endothelial glycocalyx are membrane-spanning syndecans and glycosylphosphatidylinositol-linked glypicans which carry the two main GAGs, heparan sulphate and chondroitin sulfate.3 In 2010, it was demonstrated that there was no net resorption of fluid back to the venous side of the blood capillaries and there is only diminishing net filtration across the capillary bed.2 Capillaries and venules can only resorb fluid in extreme situations.2 An acute reduction of transendothelial pressure, for example caused by precapillary vasoconstriction, post-capillary vasodilation, haemorrhage or hypovolaemia will allow transient venous absorption preserve blood volume.2 This challenges the previously accepted view regarding Starling forces.2 Acting as a complex molecular sieve, the EGL precisely regulates fluid and protein movement through the capillary wall into the tissues and prevents movement of proteins and fluid back into the venous side of the capillaries, even when interstitial tissue hydrostatic pressure is increased, or capillary oncotic pressure is higher than the tissue oncotic pressure (Figure 1).2,4 All fluid and blood proteins moving into the interstitium each day must be removed via reabsorption through the lymphatic capillaries alone.2 Thus, all oedemas fall on a continuum of lymphedema, and can lead to chronic inflammation and tissue thickening caused by accumulation and degradation of proteins.2 Glycocalyx and endothelial cell damage occur in several clinical situations including ischemia– reperfusion injury, hypoxia/reoxygenation,
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