A possible mechanism for development of Legg-Calvé-Perthes syndrome following transient synovitis is the production of an effusion which acts as a tamponade of the intracapsular, subsynovial vessels to the femoral capital epiphysis. An intraarticular pressure of 150-200 mm Hg continuing for 10 to 12 h has been required to produce epiphyseal ischemia and subsequent osteonecrosis in animals. This study, on the hip of the immature pig, showed that an induced talcum synovitis did not increase intraarticular pressure. Autologous plasma was infused into synovitis-affected and normal hips to raise intraarticular pressures to 50, 100, and 200 mm Hg, respectively, in three groups of pigs. Decay of these joint pressures to 35 mm Hg occurred within a maximum of 132 min. This period is much less than the ischemia time required to cause osteocyte death. Decay of intraarticular pressure resulted from capsular stretching and efflux of the infusate from the joint. The data from this experiment do not support the theory that tamponade of the femoral capital epiphysis is the cause of osteonecrosis in Legg-Calvé-Perthes syndrome.