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Edema Venouslimphatic: Clinical Implications

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Edema Venouslimphatic: Clinical Implications EDEMA VENOUSLIMPHATIC: CLINICAL IMPLICATIONS. Marcello Izzo Contract Professor School of Specialization in Vascular Surgery University of Ferrara (Italy) Luigi Napolitano Specialist in Physical Medicine and Rehabilitation Oedema Center [Via ro ma 25-27, Nola (NA)] and ( V. Coscia, A. La Gatta, F.,V. Gasbarro)* *Vasae-Tech Center, University of Ferrara Edema (from the greek ??d?µa , swelling) is an increase of interstitial fluid located in different tissues, increased fluid extracellular. The edema may affect a single area, such as a leg, or it can be more or less widespread, in this case, before the swelling is clinically evident, they must accumulate several liters of fluid; for this reason the weight gain usually precedes the other manifestations of edema. The hydrops or hydropsy, indicates when the material serous spreads in an uncontrolled way in a body cavity, usually peritoneal; if the swelling affects all districts body is known as anasarca. The formation of interstitial fluid is controlled by the Starling equation: Net Ultrafiltration (F) = K [(PI cap - PI int) - s (PO-PO cap int)] where K = coefficient of capillary filtration; PI cap / int = hydrostatic pressure interstitial and blood; s = coefficient of theoretical restriction to the passage of proteins through the endothelial pores; PO cap / int = oncotic pressure blood and interstitial. The effective ultrafiltration pressure that takes place through the wall of capillaries [capillary hydrostatic pressure (PI cap) - interstitial hydrostatic pressure (PI int)], produces a ultrafiltration in extravascular direction, with loss of water containing small molecules. Contrary, the effective resorption pressure [oncotic plasmatic pressure (PO cap) - oncotic interstitial pressure (PO int)] draws interstitial fluid into the blood circulation. The amount of water absorbed and ultrafiltered are not identical: the amount of ultrafiltered water exceeds about 10% compared to that absorbed. The gross ultrafiltration is the amount of water ultrafiltered while the net ultrafiltration is the difference between gross ultrafiltration and amount of liquid absorbed. This net ultrafiltration corresponds to physiological lymphatic load water. Ultimately you get a state of non-equilibrium, continuous movement of water from the plasmatic compartment to the interstitial. This slight excess( net filtration ) is balanced by the proportion of liquid that returns to the circulation through the lymphatic. Thus any increase of oncotic pressure external to blood vessels (inflammation), or any reduction of oncotic blood pressure (cirrhosis) creates edema (Table 1). Tabella 1 | Cases of edema PHYSIOLOGY POSSIBLE CAUSE EFFECTS ? ? Capillary permeability (c) Cellulitis, arthritis, cyclic ormonal Inflammatory edema, “ idiopathic edema edema ” ? ?Pressure (capillary) venous (Pc) Cardiac insufficiency, venous Cardiac edema , venous edema insufficiency, abstinence syndrome ? ?Pressure oncotic tissue (?t) Drainage lymphatic insufficiency Lymphedema ? Pressure oncotic capillary (?c) Hypoalbuminaemia, nephrotic Hypoprotein edema syndrome insufficienza epatica An increase of hydrostatic pressure inside the blood vessels (phlebostasis) or a reduction of interstitial hydrostatic pressure have the same effect. The edema from lymphatic cases (lymphoedema) is a edema hyperprotein, and depends on alteration of the lymphatic vessels. It is characterized by a reduced ability to transport, from a normal lymphatic load and an edema high protein. If the permeability of the capillary walls increases, more fluid will tend to escape from the capillary, as happens in case of inflammation. In the latter case we speak of inflammatory edema or exudate. The non- inflammatory edema, caused by alteration of hemodynamic forces as "transudate". The transudate has a lower specific gravity 1012, is low in protein and contains no cells of inflammation. Contrary, the exudate is characterized by its high specific weight of more than 1020, is rich in protein and inflammatory cells . The venous edema, which is characterized by an ability to transport normal, a normal lymphatic load and a low concentration of protein, is an example, frequently in clinical practice, of edema from increased venules hydrostatic pressure. In fact, physiologically the pressure arterioles-capillary is approximately 32-35mmHg, while in the venules is approximately 12-15mmHg with a gradient of about 25mmHg. When you determine a venous stasis in chronic venous insufficiency, the venules hydrostatic pressure reaches values of about 35-50mmHg with the initiation of interstitial edema that may later become clinically evident. Thus will determine the Microangiopathic from chronic venous stasis, that prelude to trophic sequelae such as Lipodermatosclerosis (LDS) and varicose ulcers. In some cases, the venous hypertension in the venules side can achieve 120-122mmHg configured the framework of the “ vein malignant hypertension "that quickly leads to trophic ulcerative disorders. When the lymphatic transport capacity (safety valve of Földi) exceeds that of drainage of the lymphatic system, you have a stagnant liquid in the interstice, or else edema. According to the classification of Crockett, which is based on the concentration of proteins distinguish two types of edema. Edema low protein in which the concentration in g% is below 1.0, and edema high protein content which is greater than 1 g%. In low-protein edemas the budget trading disorders in the Starling-Landis system characterized 4 types of interstitial edema: a) edema of nephrosis and hepatic insuffic iency where the colloid-osmotic pressure (Pp) is low, this type of protein concentration is between 0,1-0,3 gr%; b) edema of cardiac insuffic iency where there is an increase of hydrostatic pressure (Pi), with protein concentrations between 0.3-0.5 g%; c) edema of lymphatic obstruction and insufficiency where in addition to an increase in hydrostatic pressure (Pi), there is an increase in capillary permeability. In this case, the protein concentration is between 0.6 and 0.9 g%; d) edema in the course of burns, allergies, and in this case, the important factor is an increase in capillary permeability with a protein concentration between 1 and 2 g%; this edema is borderline with lymphatic edema. In high protein edemas have lymphatic edema that occurs when transport capacity is greatly reduced by a disease of the lymphatic vessels or from trauma. In these cases, the lymphatic activity is no longer sufficient to carry the lymphatic physiology load of water and protein. Distinguish three pathogenetic cases: a) the lymphatic vessels interruption, with a protein concentration between 1 and 4 g%, b) the edema from impaired lymphatic function, containing between 1 and 3.5 g%; c) edema from lymphatic valve too low with 2% -3.5 g of protein. The increase in oncotic interstitial pressure determine greater water retention and starting to fibrotic changes typical of elephantiasis . A further classification of edema was made considering three different pathogenetic mechanisms related to the lymphatic system: dynamic insufficiency, mechanical insufficiency and insufficiency of the function of safety valve (ability to react to an increase of lymphatic load through a compensatory increase in lymphatic flow) . Regarding the dynamic insufficiency it must be presumed that the efficiency of the lymphatic pump is not unlimited; which means that an increase of lymphatic physiology load of water and / or protein may be offset by increased lymphatic activity, only until when the functional reserve of the lymphatic system is exhausted, that is up to the limit of transport capacity. If the physiological loads exceed the possibilities of transport capacity of the lymphatic system, resulting dynamic insufficiency that gives rise to the formation of an edema. In this form of insufficiency, the lymphatic activity is the transport capacity and, therefore, is defined as high flow insufficiency. [Fig 1] From a clinical perspective, the consequence of that insufficiency is represented by the following methods: a) orthostatic edema of the early stage of chronic venous insufficiency [CVI] b) hype proteic edema (nephrotic syndrome, enteropathy) c) early stage of acute inflammation. [Fig. 1] Dynamic insufficiency of limphatic system: an overrun of CT by the CL, produce a dynamic insufficiency or high flow. When CL CT exceeds the CT forms the edema. CT = Transport capacity of limphatic system. CL CL = Lymphatic physiology load. FLt = Time of formation of lymphedema. FLt The mechanical insufficiency or low flow insufficiency conversely, occurs when the transport capacity is greatly reduced by a disease of the lymphatic vessels or from trauma. In these cases, the lymphatic activity is no longer sufficient to carry the lymphatic physiology load of water and protein. [Fig 2]. The mechanical insufficiency produces a protein stasis in the interstice; which leads to increased of oncotic pressure [PO int] of interstitial fluid that limits the effective resorption pressure [PO cap - PO int]. It is present in secondary lymphedema post-surgical or post-traumatic and in lymphatics obstructions such as filariasis. Initially, the microcirculatory system works regularly and there is an functional overload of the venules portion. Later we see the failure with an increase of interstitial oncotic pressure, responsible for the flogosis which, in turn, if not controlled, can cause fibrosis and tissue sclerosis. [Fig. 2] Mechanical insufficiency of limphatic system: when the
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