Coronary fat embolism following subarachnoid hemorrhage: an experimental study.

Abstract

Subarachnoid hemorrhage (SAH) can lead to neurogenic pulmonary edema (NPE), and chylomicron metabolism may be altered unfavorably in acute lung injury. This study aimed to investigate the possible effect of NPE on the development of coronary fat embolism. This study was conducted on 27 rabbits, 5 of which were used as the control (n=5). Experimental SAH was induced in 15 of the animals by injecting homologous blood into the cisterna magna, and the remaining 7 animals were administered only isotonic saline solution (Sham, n=7) in the same manner under general anesthesia. After 21 days, all the animals were euthanized, and their hearts, lungs, and brains underwent histopathological examination. Six animals died of SAH during the experiment, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. The histopathologic findings revealed minimal changes in the lungs, heart, and brains of the surviving animals; however, an abundant amount of fat globules was found in the coronary arteries of the six nonsurviving animals. There was a meaningful difference between the number of occluded coronary arteries with fatty globules in the surviving and nonsurviving animals (P<.001). However, the difference between the survivors and the isotonic-saline-injected group was not meaningful (P>.05). Coronary fat embolism was an important mortality factor following SAH (P<.005). In SAH-induced NPE, the leakage of chylomicrons into the systemic circulation may lead to coronary fat embolism, which has not yet been reported in the literature.