DRAINAGE DEFECT , VENOUS ECTASIA  AND TRANSPARIETAL PRESSURE
C.Franceschi
Institute of arteriovenous malformations and complex venous insufficiency. Hospital Saint Joseph. 7 Rue Pierre LAROUSSE 75014 Paris France 

Clinical symptoms of  venous insufficiency are due to a trans-parietal pressure ( TPP) excess . TPP depends in the difference between intra and extra venous pressure. TPP excess does not allow a correct drainage of the tissues, and expands the veins size.. The defect of drainage is responsible of oedema, and trophic damages ( hypodermitis, necrosis, ulcer). This effect is amplified by excessive capillary permeability. Dilatation of veins due to TPP excess is responsible of varicose veins. It is increased by parietal compliance excess.
TPP correction can be reached by extra venous pressure(EVP) enhancement and/or by intravenous pressure(IVP) reduction. What ever are the causes of TPP excess, some non invasive but quite efficient techniques can be easily performed , as banding ( EVP enhancement) and/or leg raising ( IVP reduction by hydrostatic pressure ( HP) lessening). However, banding and especially leg raising are not comfortable and cannot permit a normal and active life. So, the invasive reduction of IVP has to be done. The assessment of haemodynamic disorder by specific instrumental investigation is necessary to check  over the cause of IVP excess and perform , if possible, the appropriate therapy. It can be desobstruction and/or by-pas in case of obstruction, valve repair and/or closed shunt disconnection, blood column fractionating, If so, the symptoms have to reduce  and instrumental control has to assess normal haemodynamic data. On the contrary, the non respect of drainage as phlebectomy, stripping, sclerosis of draining veins leads to aggravate the status of the concerned tissues and develops recurrence of varicose by regional IVP excess due to increase of residual pressure in badly drained territories. That is the reason why therapy has to preserve the ways of drainage meanwhile correcting the initial cause of IVP excess.