Pulmonary fat embolism was first recognized clinically in 1862(1) by German investigators. Since that time the problem has been studied and all features of the condition have been described (2–4). I t is the purpose of this report to present the pulmonary roentgen manifestations of traumatic fat embolism. Materials and Methods The material for this study was selected from 10 cases of clinical traumatic fat embolism admitted to the Massachusetts General Hospital during the past eight years (Table I). The chest radiographs were reviewed and 6 of satisfactory quality were found. In the remainder of the cases either no chest films were made or those which were obtained were unsatisfactory. To evaluate the frequency of occurrence of this condition, clinical records of all fracture cases admitted to the wards over a period of four and a half years were reviewed. A comparison of the radiographic patterns of embolic fat in lungs has been carried out both clinically and by experimental studies in rabbits. The Entity and the Pathophysiological Sequence (Fig. 1) Fat embolism follows the liberation of large quantities of fat droplets into the circulatory system after severe bone or soft-tissue trauma with or without fracture. This fat, which normally lies in the intra-cellular space, is liberated into the extracellular fluids, and, with the increased tissue pressure and disruption of small capillaries coincident to the trauma, is carried into the circulation. These free intravascular fat droplets are not of physiological chylomicron size (less than 1 micron) but are much larger (7 to 15 microns) (5). They are transported by the venous system to the right heart and the pulmonary capillary bed. Here the globules of fat can alter the viscosity of blood as well as occlude small vessels. They are further emulsified into smaller droplets which pass through the pulmonary circulation into the systemic circulation as small emboli to multiple organs. Other pathways such as the lymphatics exist, but are no doubt of lesser significance. An intracardiac shunt may enhance systemic embolization. Clinical Features Following injury, there is usually a lucid period of several hours to several days, after which the clinical syndrome evolves. Either pulmonary symptoms or centralnervous-system symptoms may dominate, or lung manifestations may appear first, followed by the neurological complex. The Pulmonary Manifestations: The clinical aspects are essentially those of pulmonary embolism and acute cor pulmonale. There is sudden onset of cough, dyspnea, and tachypnea, sometimes with air hunger and deep, gasping respiration. Cough, sputum, pleuritic chest pain, and rarely hemoptysis may be present. Other findings include diffuse râles and rhonchi, pleural friction rubs, and a sudden rise in temperature; the pulse may be weak, rapid, and irregular. These findings, particularly the rise in vital signs (Fig. 2), represent the well known clinical signs of pulmonary embolism.