Injury, serum lipids, fat embolism, and clofibrate.

The mechanism of fat embolism following injury has excited much controversy since it was first described by Zenker in 1862. Two theories seek to explain it-the classical mechanical theory, which is supported by Sevitt (1962), and the metabolic theory, which is supported by Evarts (1965). The mechanical theory suggests that following trauma fat is liberated from the marrow cavity into the venous sinusoids, whence it passes in the form of globules into the systemic circulation. The metabolic theory suggests that tissue injury may initiate changes in the physio-chemical state of the blood, and that this alters the emulsion stability of the blood lipids. Together with the activation of a lipid-mobilizing hormone by trauma this results in the formation of fat globules. Fat embolism follows trauma (usually to bones). There is a lucid interval of variable duration and then signs of respiratory and systemic fat embolism develop, together with changes in the mental state and level of consciousness; a petechial rash also occurs on the head, neck, and thorax. In this study, firstly, an attempt was made to try to establish whether there was any change in the serum non-cholesterol lipids after trauma; secondly, the incidence of all degrees of the syndrome of fat embolism was investigated; and, thirdly, the effect of Atromid (clofibrate) on the serum lipids and the incidence of fat embolism was studied. Clofibrate was used because it has an effect on the lipids of the hyperlipaemic patient and has also been found to depress postprandial lipaemia. Material and Methods The patients were inmates of the orthopaedic unit at St. James's Hospital, Leeds, either as a result of injury serious enough to warrant admission or because they were undergoing orthopaedic surgery. They were divided into two groups (Table I). One group received standard therapy, and the other received clofibrate as well, as soon as they were able to take capsules. The dosage of clofibrate used was 750 mg. by mouth followed by 500 mg. six-hourly for two days, then 250 mg. six-hourly for three days, then 250 mg. twice daily for two days, and finally 250 mg. daily for two days. The dose was tailed off to prevent any rebound effects. Eight patients who had had operations on non-bony structures also received clofibrate. Laboratory Estimations Plasma total lipids were estimated by the rapid turbimetric method of Kunkel et al. (1948), giving normal ranges between 340 and 640 mg./l00 …