Fat emboli and shock

Abstract

Among the many explanations as to the cause of the circulatory failure in clinical as well as experimental shock, the theory that it is caused by fat embolism has been recently suggested. At least two distinct views as to the manner in which fat emboli may produce the circulatory failure are held: According to Porter (1), as we understand his view, fat, injected intravenously or gaining access to the venous circulation after fractures or laceration of the subcutaneous tissues, passes through the pulmonary vessels but lodges in the peripheral systemic vessels and thereby produces circulatory failure by some mechanism as yet not clearly explained. According to Bissell (2) the circulatory failure of postoperative or traumatic shock is caused by the lodgement of fat emboli in the pulmonary vessels, making it synonymous with pulmonary embolism.

During the past ten weeks we have re-investigated the following questions: (1) Is the mechanism by which the circulation fails after intravenous injection of oil the same as that following operation? (2) Is circulatory failure following fat injection primarily due to emboli of the pulmonary or systemic vessels? (3) Do fatcy emboli of the systemic vessels produce circulatory failure similar to that following operation and trauma? To do this the mean pressure in the carotid artery, pulmonary artery and the effective pressures in the left and right auricles were studied in naturally breathing animals.

Experiments showed that when the circulation fails during shock produced by exposing the intestines, the pressures in the systemic and pulmonary arteries fall and a marked reduction of the actual, as well as the effective venous pressures in the right auricle takes place. These dynamic changes, which we regard as characteristic of shock, do not occur when oil as such or in emulsion is injected intravenously.