Mechanism of cerebral fat embolism in subarachnoid hemorrhage: An experimental study
Özet
Subarachnoid hemorrhage (SAH) may cause neurogenic pulmonary edema (NPE), and chylomicron metabolism may be destroyed in injured lungs. We aimed to investigate the effect of neurogenic pulmonary edema (NPE), if present, on the development of cerebral fat embolism. This study has been conducted on 20 rabbits. Experimental SAH has been applied to half of the animals by injecting homologous blood into the cisterna magna, and the remaining half was applied only isotonic saline solution in the same manner under general anesthesia. After 20 days, all animals were killed. Their lungs and brains were examined histopathologically. Six animals died of SAH between 16 and 20 days, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. Fat globules were abundantly found in cerebral arteries of six of all the non-surviving animals. But, minimal histopathological changes were found in the lungs and brains of the surviving animals. Cerebral fat embolism was detected in only one animal that was given isotonic solution. SAH may cause NPE and result in lung tissue destruction. Chylomicron metabolism may be disordered in the destructed lungs and leakage of chylomicrons into systemic circulation may be facilitated via destroyed lung barrier. These pathologic processes may lead to cerebral fat embolism.
