The incidence and importance of fat embolism is being increasingly recognized since the introduction of better methods of diagnosis. That depot fat, particularly that in bone marrow, can enter the circulation after local trauma is beyond dispute. But fat embolism has been present at autopsy following a wide variety of conditions, including (1) metabolic disturbances (diabetes, cardiovascular-renal syndrome); (2) poisonings (phosphorus, alcohol, chloroform, carbon monoxide, potassium chloride); (3) toxemias from acute and chronic infections; (4) toxemias from tissue destruction (burns),3,4 and (5) from use of pump oxygenator in extracorporeal circulation.1 The mechanism by which fat embolism occurs is not always clear.
Lehman and Moore stated in 1927 that ether vapor in the blood stream produced fat embolism in the presence of post-absorptive lipemia. They believed that the ether in the circulating blood dissolved the circulating chylomicra, and the the ether vapor tension in the blood was lowered in
DAVIES JI, PELTIER LF. Deep Ether Anesthesia and Fat EmbolismResults of Experiments with Lipemic Dogs. Arch Surg. 1961;82(3):417-419. doi:10.1001/archsurg.1961.01300090087016