I was giving a lecture on the pathology of cerebrovascular disease today, and showed a picture from Robbins of a brain with a shower of fat emboli after fracture of long bones. A student asked what the mechanism would be, pointing out that it would be difficult for marrow fat to get from the venous system of the leg into the arterial circulation of the brain without going through the filter of the pulmonary capillary bed.
The etiology of fat emboli after trauma is not clear. According to an article by Butteriss et al. in the American Journal of Neuroradiology, microemboli may pass into the systemic circulation either via cardiac or intrapulmonary right-left shunts or directly through the pulmonary capillary bed. Apparently a study of orthopedic surgery in dogs has shown that fat globules of <5 µm can traverse the pulmonary micovasculature. One could imagine these globules coalescing in the brain and causing significant infarcts, I suppose.
Whatever the mechanism, I imagine air emboli introduced when inserting or pulling out a central line might form in a similar manner.
(Source: D.J.A. Butteriss et al., Reversible Cytotoxic Cerebral Edema in Cerebral Fat Embolism . American Journal of Neuroradiology 27:620-623, March 2006.)
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According to Greenfield, the traumatized adipose tissue enters the venous circulation, facilitated by an increased tissue pressure at the site of truama. The fat globules are usually trapped by the lung. However, if the number of fat globules is large enough, and the trapping capacity of the pulmonary capillaries is exceeded, the fat can enter the systemic circulation, including the cerebral arteries. Fat emboli can also bypass the lungs via a patent foramen ovale or pulmonary arteriovenous shunt.
I emailed Tom Smith, neuropathologist at the University of Massachusetts, regarding this issue. Here is his response:
"Brian --
This is a great question, especially since I just had an autopsy case of cerebral fat embolization ("brain purpura") a few weeks ago!
Interestingly, as I was checking through the literature, I was somewhat surprised to learn that the exact mechanism of cerebral fat embolization is still not completely resolved. There are two major theories: mechanical and biochemical. Considering the mechanical theory, there are two possible ways that fat emboli can reach the brain from the venous circulation -- 1) via pulmonary-precapillary shunts or directly across the pulmonary-capillary bed or 2) via paradoxical embolization through a patent foramen ovale. The former has been "traditionally" advocated as the primary mechanism, since fat emboli can be observed in pumonary vessels, but there are very well documented reports of cerebral fat emboli occuring via paradoxical embolization as well -- see this reference from NEJM (http://content.nejm.org/cgi/content/full/329/13/926). Here is the biochemical theory -- "hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons. Acute-phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce and create the physiologic reactions described above. The biochemical theory helps explain nontraumatic forms of fat embolism syndrome" (this is a direct quote from eMedicine - http://www.emedicine.com/med/topic652.htm). I can't comment further on the so-called biochemical mechanism, but to me, the mechanical theory seems more plausable in cases of long bone fracture. You can occasionally seen bone marrow emboli in pulmonary vessels after CPR -- not the same mechanism as systemic fat embolization, but at least proves that fat-containing materials can make their way to the lungs.
I hope this is somewhat helpful!
Have a nice weekend.
Tom
Dude,
You misspelled "skeletal".
Dude
Dude,
Thanks for the pick-up on the mispelling. The error was corrected.
Dude
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What Doppler pattern is more likely to be find in Fat Cerebral embolism (hiperemic?)
Thank you
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