Introduction. Despite adequate postoperative care with compression garments, free flaps often remain oedematous. The cause is probably multifactorial, including inflammatory processes, hyperaemia and lymphatic stasis. Although lymphatic connexions are absent immediately after every free flap transfer, posttransfer oedema is often minimal or even absent. This establishment suggests the existence of an additional lymphatic outflow. Two hypotheses have been suggested: lymphangiogenesis and the presence of intra-tissular lymphovenous anastomoses. Material & method. In order to examine this second hypothesis, the following study was performed in 16 patients who underwent latissimus dorsi muscular flap or radial forearm flap transfer. After flap harvesting and pedicle dissection, the draining vein was isolated and cannulated. A solution of nanocolloids, labelled with Tc, containing 250µCu/0.1cc was injected into the flap, in four different spots. Blood samples from the cannulated draining vein were collected 0, 10, 20 and 30 minutes after IM injection. Radiation activity was measured postoperatively in the four blood samples and 24 hours after transfer in the muscular tissue, the axillary nodes and in the liver. Preoperatively as well as 18 hours postoperatively, a urine sample was taken and also examined for radioactivity. Results. Basal activity, measured after 0 minutes, was constant and ranged between 20 and 108cpm (M:75). However, 10, 20 and 30 minutes after injection, the measured activity reached respectively 22506, 35984 and 48585 cpm. After 24 hours, no activity could be found in the regional lymph nodes. In the liver, a noticable radioactivity was present. Radioactivity in the urine samples reached (8023 cpm). Discussion. These results strongly suggest that intra-tissular lymphovenous anastomoses exist, because literature has already proven that in this clinical setting direct intravascular injection or transendothelial passage can be excluded. Although the lymphatic flow in a transferred flap is disturbed and a certain degree of oedema installs, these lymphovenous anastomoses explain why lymphatic stasis remains limited. Moreover, during the late postoperative period, lymphangiogenesis will install and further reduce the lymphatic origin of free flap oedema. These lymphovenous connections may also explain why systemic metastasis develop in different clinical oncological situations.