Acute cerebral changes in experimental canine fat embolism

Abstract

Adult dogs, given 1 ml per kilogram body weight of Wesson oil i.v., were killed by injection of Nembutal after intervals varying from 22 hours to 9 days. The neurological deficit consisted of varying degrees of paralysis and decerebrate rigidity. Sudan-stained fat emboli were scattered through the brain, accumulated within circumscribed areas and around foci of degeneration. Lesions of the brain varied considerably in size and degree of tissue destruction. The temporal sequence of changes conformed with conventional patterns, except for minute lesions with reactive changes peripherally. Siderosis occurred from the second day and was more striking in the cerebellum than the cerebrum. It was tentatively explained as an instability of serum iron concentration with diffusion of iron compounds through damaged vascular walls. Fibrin was demonstrated perivascularly near the embolized part of the vessels in 2-day-old lesions. The conversion of fibrinogen was considered to be due to diffusion of plasma products at the sites of severe vascular damage, and admixture of thromboplastin within degenerating astrocytes. The glomeruli were clogged by discrete threads of fibrin attached to fat emboli. After repeated injections of fat, the cerebrum and cerebellum were damaged by hemorrhagic infarctions, the mechanism of which was not determined. Otherwise all foci seemed to have developed around vessels with arrested emboli, but the factors involved in the arrest were not understood. Many dogs suffered from chronic meningoencephalitis, choroiditis, and marked hydrocephalus. These changes were old and unrelated to the fat emboli.