Abstract
The recent change of the name of an American specialty board from ‘phlebology’ to ‘venous and lymphatic medicine’ (i.e. American Board of Venous and Lymphatic Medicine) reflects a broad change in contemporary concept regarding the venous-lymphatic circulation. Vein and lymphatic systems are delicately connected via the capillary system at the tissue level in order to transport venous blood and lymph fluid out of tissue. But their ‘mutual interdependence’ in this function has been benignly neglected for decades. Both systems, however, are ‘mutually complimentary’ only when they are functioning normally; when one of the two systems loses its normal function (e.g. chronic venous hypertension and lymphedema), such mutual interdependence generates a new problem; additional burdening/loading of the other system. Venous and lymphatic systems are, therefore, one ‘inseparable’ system so that the insufficiency or overload, either transient or permanent, to one of the systems allows the other to play an auxiliary role of fluid return via functional anastomosis. To accommodate a new concept to combine the venous and lymphatic systems as one new vascular specialty, a group of experts has developed a Core Content for training in venous and lymphatic medicine, published in a previous issue of Phlebology. 1 In fact, a close interrelationship between lymphatic and venous systems starts during embryological development, and subsequently results in an intimate anatomic structure of veins and lymphatics that together creates a physiological drainage function despite having entirely different rheodynamic conditions with different characteristics. Such a unique interrelationship plays an important pathophysiological role in any kind of edema. These points have several practical consequences concerning both differential diagnosis and management, some of which will be discussed below. New insights from basic research demonstrate that physiologically the main process responsible for interstitial fluid drainage is lymphatic transport and not venous capillary reabsorption as previously taught. 2 This means that lymphatics will always play a major role in any kind of edema. ‘Chronic edema’ persisting for more than three months, a common clinical entity seen by practicing phlebologists, may be defined as lymphedema, regardless of its primary cause. Edema develops when the increased lymphatic transport to compensate for the overload fails to adequately cope with increased fluid filtration into the tissue. An increased fluid extravasation is caused by a decrease of the intravascular oncotic pressure, increased permeability of the capillary membrane and, most importantly for phlebologists, an increase of venous pressure. 3 Edema due to reduced plasma osmotic pressure (hypoalbuminemia) may develop from various systemic causes: malnutrition, intestinal disease (malabsorption or protein loss), hepatic failure and nephrotic syndrome. A breakdown in the endothelial barrier causing increased capillary permeability may be due to inflammation and trauma facilitating the passage of plasma proteins and water across the capillary wall. Some drugs, e.g. calcium-channel blocking agents may also increase edema formation due to different mechanisms of action that interfere with permeability.
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