Key result
Deformable emboli during cardiac surgery disrupt the blood-brain barrier, driving neurologic dysfunction and brain swelling.
Why the study?
The mechanisms by which macro and microemboli cause neurologic dysfunction during cardiac surgery and their impact on the brain remain incompletely understood.
Emboli during cardiac surgery cause neurologic damage not just through occlusion, but via endothelial disruption and blood-brain barrier breakdown.
Emboli may injure endothelium beyond ischemia; hypothesis-generating for targeted neuroprotection strategies in cardiac surgery.
Macro and microemboli can both cause significant neurologic dysfunction. The traditional belief in cardiac surgery was that the damage perpetrated by an embolus was caused by the occlusion of an arterial branch, resulting in an ischemic event and subsequent infarction. However, ongoing research has demonstrated that the mere passage of a deformable embolus (air, lipid, or semi-solid clot) will disrupt the endothelium as it is extruded through the vessel. A cascade of events follows endothelial irritation. In the closed environment of the brain, a disruption of the blood-brain barrier has been demonstrated after the passage of lipid microemboli. A significant breakdown of the blood-brain barrier causes marked brain swelling, increased intracranial hypertension, and a possible increase in the size of the lesions associated with larger occlusive emboli. Gaseous microemboli are also a well-documented endothelial irritant and can cause significant brain dysfunction. It is important to avoid delivering emboli of any size or composition to the cerebral vasculature in order to reduce the impact of cardiac surgery on the brain.
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David A. Stump (2005) conducted a review in Neurologic dysfunction associated with cardiac surgery. Emboli (macro and microemboli) was evaluated. The passage of deformable emboli during cardiac surgery disrupts the endothelium and blood-brain barrier, leading to significant neurologic dysfunction and brain swelling.
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