The next in my occasional “Best Post Of The Month” series is for February, 2008:
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.)
3 comments:
Could it be patent foramen ovale in these patients, which might be doing the shunting of emboli!
I'm sure that in some patients the emboli are accounted for by patent foramena ovale (PFO). But only a minority of patients have PFO. Plus, we're talking about fat emboli here, presumably bone marrow fat. These patients do no have bone marrow emboli, as one sees at autopsy status post CPR, when broken ribs embolize bone marrow to the pulmonary vasculature. So, PFO cannot account for pure fat emboli. It's really a mystery as to what's going in on here.
Ok, is that the REAL you in this picture?! Truth be told, like the other one better. Goes with the blog image vs the clean cut professor type. LOL
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