Quantitative assessment of microhemodynamics in ischemic skin flap tissue by intravital microscopy.

Abstract

Skin flaps are susceptible to ischemia, which may result in tissue necrosis particularly in areas deprived of their original anatomic blood supply. The pathophysiology of skin flap failure has been debated for many years, but due to methodological insufficiencies, every proposed theory has remained hypothetical. The aim of this study was to gain more evidence for the mechanisms involved in flap ischemia by assessing quantitatively hemodynamic parameters such as diameter, flow velocity, and volume flow in the microcirculation of a flap. To this end the authors developed a new island flap on the back of Syrian golden hamsters that allowed intravital microscopic investigation. The flap included an extended portion, which was deprived of its original anatomic blood supply. One hour after flap dissection, blood flow was 42% to 66% lower in all microvessels in the extended area than in the anatomically perfused part of the flap (p<0.05). In the entire microvasculature, a significant gradual decline of blood flow was observed over time. Any blood flow reduction was caused to a major extent by diminished flow velocity. At all times, microvascular diameters were slightly larger in the extended portion of the flap than in the anatomically perfused portion of the flap. The authors conclude that their new model is a unique tool for investigating microhemodynamic mechanisms involved in flap ischemia. This study reveals hypoperfusion of extended flap tissue, which is attributed to diminished arterial perfusion pressure but not to vasoconstriction or arteriovenous shunting.