Experimentally Induced Cerebral Fat Embolism with Linoleic Acid: MR Imaging and Pathologic Correlation.
10.3348/jkrs.2000.43.5.527
- Author:
Jong Bae KIM
1
;
Hak Jin KIM
;
Yong KIM
;
Suck Hong LEE
;
Byeong Rae PARK
Author Information
1. Department of Diagnostic Radiology, Pusan National University, Pusan, Korea.
- Publication Type:Original Article
- Keywords:
Embolism, fat;
Brain, edema;
Embolism, experimental studies Brain, MR
- MeSH:
Animals;
Carotid Artery, Internal;
Cats;
Diagnosis;
Edema;
Embolism, Fat*;
Endothelial Cells;
Extracellular Space;
Hemorrhage;
Linoleic Acid*;
Magnetic Resonance Imaging*;
Neurons;
Vacuoles
- From:Journal of the Korean Radiological Society
2000;43(5):527-532
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To investigate the correlation between the MRI findings of cerebral fat embolism induced by injecting linoleic acid into ten cats, and pathologic diagnosis. MATERIALS AND METHODS: Using a microcatheter, 30 microliter of linoleic acid was injected into the internal carotid artery of ten cats. MR T2-weighted (T2WI), diffusion-weighted (DWI), and Gd-enhanced T1-weighted images (Gd-enhanced T1WI) were obtained after 30 minutes and after 2 hours of embolization. We pathlogically examined endothelial cell damage, cellular change, perivascular abnormality and fat vacuoles, and then determined the correlation between MRI and the pathologic findings. RESULT: After 30 minutes of embolization, lesions of very high signal intensity were detected by T2WI in six cats, and of slightly high signal intensity in two; in the remaining two, signal intensity was normal. DWI showed lesions of very high intensity in nine animals and of slightly high intensity in one, while Gd-enhanced T1WI showed well-enhanced lesions in nine and a minimally enhanced lesion in one. After 2 hours of embolization, T2WI revealed lesions of very high signal intensity in nine cats, and of slightly high signal intensity in one, while DWI detected lesions of very high signal intensity in all cats. On Gd-enhanced T1WI, lesions in all cats were well enhanced. According to the findings of light microscopic examination, infarcted lesions mainly involved the gray matter, but also some white matter. In the lesions, neurophil matrix edema, neuronal degeneration, perivascular swelling, the widening of extracellular space, extravascular hemorrhage, and fat vacuoles were evident. CONCLUSION: During the initial two hours following injection, MR imaging of cerebral fat embolism induced by linoleic acid through the internal carotid artery in cats showed high signal intensity on T2WI and DWI, and clear enhancement on Gd-enhanced T1WI. In cases involving cellular edema, cerebrovascular injury and extracellular space widening, the pathologic evidence suggested the coexistence of cytotoxic and vasogenic edema.
