An integrated theory of the no-reflow phenomenon and the beneficial effect of vascular washout on no-reflow.

OBJECTIVES

No-reflow is failure of perfusion in free tissue transfer despite adequate arterial inflow. The objectives of this study were to construct a theory of interactive mechanisms of the no-reflow phenomenon and to determine whether preischemic vascular washout could increase flap ischemia tolerance.

STUDY DESIGN

The evidence for the role of various mechanisms in the development of no-reflow is reviewed, and an integrated network proposed. A rat-groin free flap model is used to test preischemic vascular washout with normal saline, heparinized normal saline, lactated Ringer's solution, Tis-U-Sol, and Viaspan.

METHODS

The mean ischemia tolerance of this flap without any therapeutic intervention was first determined, using 22 animals. An additional 50 animals were used to compare with the control group the ischemia tolerance of flaps washed out with the above fluids before their ischemic period.

RESULTS

The critical ischemia time 50 (time after which half of the flaps are expected to survive and half, die) of the untreated flap is 23.4 hours in this model (P<.05). Flaps washed out with normal saline or lactated Ringer's solution have significantly worse ischemia tolerance (P<.0001). Flaps washed out with Tis-U-Sol or Viaspan behave similarly to the control group (P>.57). Flaps receiving preischemic washout with heparinized normal saline (4,000 units/L) had a significantly better outcome than the control group (P<.027).

CONCLUSIONS

Preischemic washout with normal saline, lactated Ringer's solution, or heparinized Tis-U-Sol is detrimental for flap survival after ischemia, Tis-U-Sol- and Viaspan-treated flaps do have ischemia tolerance similar to the control group, and flaps washed out with heparinized normal saline have a survival advantage in this model.