Many hypotheses have been proposed to explain the clinical features and laboratory findings during chronic venous insufficiency (CVI). Edema is known to occur primarily as a result of the increase in venous pressure, accompanied by increased capillary permeability (PerM) and decreased blood colloid osmotic pressure as contributing factors. Nevertheless, there are many clinical and experimental observations which are not consistent with this accepted suggestion. Therefore, the diagnosis of edema is formulated, when edema has already occurred, i.e. only when the collection of the fluid exceeds a certain threshold and becomes clinically or instrumentally evident. The aim of this review was to clarify the pathophysiology of venous edema studying two fundamental processes: filtration and absorption that oversee the balance of intra- and extracellular fluids. In particular, we have described the alterations between filtration and absorption. The mechanisms involved in the CVI are several, starting from the structural rearrangement of the vascular endothelium up to the changes in intra and extracellular fluid. Evaluating the previous studies, we hypothesize that the venous edema is produced by the hydrostatic pressure prevailing on blood oncotic pressure, while the "intermediary" system or transduction system must be able to transform the physical stimulus induced by hypertension in a biochemical message promoting the cellular responses. Moreover, the chronic increase in shear stress, characteristic in CVI, prevails on calcium dependent mechanism, resulting in either hypertension, a mechanical stress, abolishes the Ca++ linked mechanism inducing a stable disassembly of adherens junction, or in the long run, the same mechanisms are unable to preserve the barrier integrity with a profound alteration of the vessel wall PerM, accompanied by leakage of macromolecules and blood cells. In conclusion, it is possible to assume that the essential sign in the venous chronic insufficiencies is not the edema, and then an excess of filtration, but the vessel wall permeation is the key factor to clarify the pathophysiological cascade and the clinical signs.