Commentary on: "Early microscopic evidence for endothelial damage in arterial microanastomoses" by Benazzo et al.

Excerpt

This contribution presents evidence about possible microanastomotic factors related to early endothelial damage in arterial microanastomoses. There are two interesting points which the authors clearly demonstrate in this experimental study: (a) the anastomotic site appeared completely sealed with the cut ends protruding into the vessel lumen, and (b) the extensive areas of lack of endothelium with fibrin deposition between surgical microclamps on the inner surface of the artery. I believe the authors are overly enthusiastic in relating these factors to the no-reflow phenomenon, which has a more complex, functional, and anatomical pathophysiology. Failure of tissue perfusion with the passage of time despite a satisfactory arterial input heralds the onset of the no-reflow phenomenon. May et al. [7] demonstrated a progressive obstruction to blood flow with increasing periods of ischemia. They felt that ischemia induced the no-reflow phenomenon which was caused by cellular swelling, leakage of intravascular fluid, and intravascular aggregation with sludging and thrombus formation. Stagnation of blood within the free tissue transfer may also play a role in the development of the no-reflow phenomenon, either by increasing the hyperpermeability of the microcirculation [8] or by increasing the rate of thrombosis [5]. One other factor that could well influence the perfusion of tissue is the recently observed embolic events that follow microvascular anastomoses [2]. This contribution reinforces the already 30- to 40-year-old idea of Jacobson and Suarez [6], Chase and Schwartz [3], Cobbett [4], and Acland [1] who state that the microvascular surgeon must use a very meticulous microvascular technique to achieve the highest success rate in anastomosing vessels of small diameters. …